Annoying creationists

[Shalamar]

Don’t you know what the name of this thread is Shalamar? Here is how the proof goes. There are only two possible ways we got here. We were either created or we came about by abiogenesis and evolution. Panspermia just puts the creation or abiogenesis to another location. If you can prove either of the two propositions to be impossible, the other proposition is true by process of elimination. Abiogenesis and the theory of evolution have been eliminated. Shalamar, you were created and you should seek to know your Creator.

No. Thats flatly wrong. IF you can manage to disprove abiogenesis (Which isn't even a theory), and Evolution, then... you have managed to disprove abiogenesis, and Evolution. Thats it. That is ONLY it.

There is no 'process of elimination'. You still need to PROVE that creationism is correct. Disproving 'a' does not mean that 'b' is automatically true.

It just seems that you are a standard Creationist. You can't find proof for your beliefs, so you knock down what you feel to be false. Since you believe creationism to be true, that is what you strive towards. You try to make what you can uncover to fit your belief.

You are no scientist, and you haven't disproven anything. You've made ASSUMPTIONS that others here have pointed out as being false.

Please, try again, and provide me with proof of creationism.

[joobz]

Don’t you know what the name of this thread is Shalamar? Here is how the proof goes. There are only two possible ways we got here. We were either created or we came about by abiogenesis and evolution. Panspermia just puts the creation or abiogenesis to another location. If you can prove either of the two propositions to be impossible, the other proposition is true by process of elimination. Abiogenesis and the theory of evolution have been eliminated. Shalamar, you were created and you should seek to know your Creator.

Is that the same creator that approves of your continual derision, insults, lies, and general abuse of logic?

[kleinman]

Don’t you know what the name of this thread is Shalamar? Here is how the proof goes. There are only two possible ways we got here. We were either created or we came about by abiogenesis and evolution. Panspermia just puts the creation or abiogenesis to another location. If you can prove either of the two propositions to be impossible, the other proposition is true by process of elimination. Abiogenesis and the theory of evolution have been eliminated. Shalamar, you were created and you should seek to know your Creator.No. Thats flatly wrong. IF you can manage to disprove abiogenesis (Which isn't even a theory), and Evolution, then... you have managed to disprove abiogenesis, and Evolution. Thats it. That is ONLY it.

There is no 'process of elimination'. You still need to PROVE that creationism is correct. Disproving 'a' does not mean that 'b' is automatically true.

It just seems that you are a standard Creationist. You can't find proof for your beliefs, so you knock down what you feel to be false. Since you believe creationism to be true, that is what you strive towards. You try to make what you can uncover to fit your belief.

You are no scientist, and you haven't disproven anything. You've made ASSUMPTIONS that others here have pointed out as being false.

Please, try again, and provide me with proof of creationism.
What assumptions have I made? I have posted the data from a peer reviewed and published model of random point mutations and natural selection which show that combination selection pressures profoundly slow the evolutionary process and I have posted hundreds of real repeatable and measurable examples of mutation and selection which show the same thing. Mutation and selection can not evolve hundreds of genes simultaneously, it is a mathematical impossibility. I have also cited a paper which show that even if somehow ribose could be produced nonenzymatically, this molecule has a very short half life and would not even stay around for a hundred years let alone the billions of years evolutionists allege that the primordial soup would have taken to generate a living thing. All I have done is posted data which show that abiogenesis and the theory of evolution is false.

All I have strived for on this thread is to show how mutation and selection works. Thanks to Dr Schneider’s and Paul’s computer simulation and the hard work of numerous scientists, this has been accomplished.

Shalamar, there is another thread recently started by Gregoire where he cites a paper which alleges the stepwise evolution of the bacterial flagella. I posed this question of Gregoire and now I ask you. How was the DNA replicase system evolved in a stepwise manner, in particular could you tell us what helicase and gyrase were doing before DNA could be replicated?

[Apathia]

The Primordial Corps of Engineers:
http://h1.ripway.com/Apathia/TimeB.JPG
These guys have the map!

[delphi_ote]

Delphi, the whole concept of common descent by mutation and selection is nonsense. There is no mechanism that can do what you evolutionists allege.[/FONT][/SIZE]
I'm not asking about the mechanism. I'm asking a very clear, very simple question. Do you believe that all of the life on Earth come from a common ancestor? Answer with a YES or a NO. It's not that hard.

[kjkent1]

What assumptions have I made? ... All I have done is posted data which show that abiogenesis and the theory of evolution is false.You have assumed, inter alia:

1. that natural environments are never subjected to a dominant selective pressure. This assumption is necessary for you to assert that combination selective pressures prevent evolution from occurring in nature.

2. that only random point mutations contribute to evolutionary change. This assumption is necessary for you to assert that insufficient generational time exists in which for organisms to take on substantial morphological change.

3. that the fossil record does not show evidence of past evolutionary change. This assumption is necessary for you to impute the fossil record to divine intervention.

4. that retroviral insertions found in identical loci in organisms with a proposed common ancestor are not the result of common ancestry. This assumption is also necessary for you to impute the action of divine intervention.

5. that randomness is an illusion. This assumption is necessary for you to maintain your position that selective pressures do not produce multiple evolutionary possibilities -- which is necessary, because if randomness exists, then the creator is not almighty.

6. that your god will save you. This assumption is necessary to salve over your personal fear of death.

7. that only you are intelligent. This assumption is necessary to maintain your ability to ignore any contrary evidence, no matter how persuasive.

You really are one of the most narcissistic personalities I've ever encountered. Why if it weren't for your professed subservience to Christ, I'd half expect you to be hanging from the cross yourself!

[Dr Adequate]

So, kleinman's still sitting on his backside sniping aimlessly at the same half-a-dozen people while millions suffer and die needlessly.

And he still hasn't explained why.

Why, kleinman?

I've been reading this good book, and I found a bit in it that applies to you.

For the kingdom of heaven is as a man travelling into a far country, who called his own servants, and delivered unto them his goods.

And unto one he gave five talents, to another two, and to another one; to every man according to his several ability; and straightway took his journey.

Then he that had received the five talents went and traded with the same, and made them other five talents.

And likewise he that had received two, he also gained other two.

But he that had received one went and digged in the earth, and hid his lord's money.

After a long time the lord of those servants cometh, and reckoneth with them.

And so he that had received five talents came and brought other five talents, saying, Lord, thou deliveredst unto me five talents: behold, I have gained beside them five talents more.

His lord said unto him, Well done, thou good and faithful servant: thou hast been faithful over a few things, I will make thee ruler over many things: enter thou into the joy of thy lord.

He also that had received two talents came and said, Lord, thou deliveredst unto me two talents: behold, I have gained two other talents beside them.

His lord said unto him, Well done, good and faithful servant; thou hast been faithful over a few things, I will make thee ruler over many things: enter thou into the joy of thy lord.

Then he which had received the one talent came and said, Lord, I knew thee that thou art an hard man, reaping where thou hast not sown, and gathering where thou hast not strawed:

And I was afraid, and went and hid thy talent in the earth: lo, there thou hast that is thine.

His lord answered and said unto him, Thou wicked and slothful servant, thou knewest that I reap where I sowed not, and gather where I have not strawed:

Thou oughtest therefore to have put my money to the exchangers, and then at my coming I should have received mine own with usury.

Take therefore the talent from him, and give it unto him which hath ten talents.

For unto every one that hath shall be given, and he shall have abundance: but from him that hath not shall be taken away even that which he hath.

And cast ye the unprofitable servant into outer darkness: there shall be weeping and gnashing of teeth.

---

The only way the parable doesn't fit is that if what you claim is true, you are in the position, not of a man given one talent to invest, but hundreds, thousands, millions ... untold riches beyond my wildest dreams.

And you digged in the earth, and hid your lord's money.

[Dr Adequate]

What assumptions have I made? I have posted the data from a peer reviewed and published model of random point mutations and natural selection which show that combination selection pressures profoundly slow the evolutionary process and I have posted hundreds of real repeatable and measurable examples of mutation and selection which show the same thing. That's not what they show, and we know it, remember?

Mutation and selection can not evolve hundreds of genes simultaneously, it is a mathematical impossibility. But for some reason you can't show us any mathematics to back up your statements about mathematics.

I have also cited a paper which show that even if somehow ribose could be produced nonenzymatically, this molecule has a very short half life and would not even stay around for a hundred years let alone the billions of years evolutionists allege that the primordial soup would have taken to generate a living thing. I must have missed this bit of rubbish. Golly, you did find something else to be wrong about.

All I have strived for on this thread is to show how mutation and selection works. Perhaps first you should have tried to find out how it does, in fact, work.

Thanks to Dr Schneider’s and Paul’s computer simulation and the hard work of numerous scientists, this has been accomplished. Yes indeed. They have shown that mutation and selection work ... exactly as evolutionists claim. This is why they're all evolutionists, I guess.

Shalamar, there is another thread recently started by Gregoire where he cites a paper which alleges the stepwise evolution of the bacterial flagella. I posed this question of Gregoire and now I ask you. How was the DNA replicase system evolved in a stepwise manner, in particular could you tell us what helicase and gyrase were doing before DNA could be replicated? Yes, that was pointless, wasn't it?

[Paul C. Anagnostopoulos]

There are only two possible ways we got here. We were either created or we came about by abiogenesis and evolution.
Or both. If I were you, I'd go with both.

~~ Paul

[rocketdodger]

Ok, you are still sorting.

And that’s ok as well, it may not be realistic, but you are still doing a sort.


So you admit that my algorithm is in fact a sorting algorithm. Then, because my algorithm shows that for some n != 0, the sorting rate is higher under n +1 sorting conditions that n sorting conditions, you admit that your claim is WRONG. That being the case, I will quote you:

Since the foundation mechanism can not accomplish what is required for the theory of evolution to be plausible, every interpretation that evolutionists make of the evidence is called into question.

Kleinman, since your foundation mechanism no longer supports your theory, every interpretation of yours is called into question. How do you respond to this?

[kjkent1]

Or both. If I were you, I'd go with both.

~~ PaulLOL! Yes, that's true. Either because the creator uses abiogenesis and evolution to achieve its ends, or because an all powerful creator could create two sets of truths and bring them into being simultaneously -- despite their seeming contradictions.

Two different existences with point to point correspondence with the natural universe. And, the inhabitants of that universe could choose which existence is true and thereby subject themselves to its restrictions.

But, why stop there? Why not allow for an infinity of possible realities, all existing simultaneously!

Sounds like string theory or the many worlds interpretation. The only trouble is that if I step out in front of a speeding train, I still get crushed like a bug in at least one of those universes.

Sigh...life is just not fair.

[kjkent1]

So you admit that my algorithm is in fact a sorting algorithm. Then, because my algorithm shows that for some n != 0, the sorting rate is higher under n +1 sorting conditions that n sorting conditions, you admit that your claim is WRONG. That being the case, I will quote you:



Kleinman, since your foundation mechanism no longer supports your theory, every interpretation of yours is called into question. How do you respond to this?He'll probably respond with "the peer reviewed evidence shows that multiple pressures confound evolutionary change."

That is, when the evidence supports his model, he accepts it. But, when it doesn't, such as in cases where multiple resistance paths appear from a single selective pressure, or when the evidence of retroviral insertion suggests common ancestry, etc. -- kleinman rejects it.

That's the great thing about internet forums. Everyone gets to win their argument, because there's no judge.

[kleinman]

Delphi, the whole concept of common descent by mutation and selection is nonsense. There is no mechanism that can do what you evolutionists allege.I'm not asking about the mechanism. I'm asking a very clear, very simple question. Do you believe that all of the life on Earth come from a common ancestor? Answer with a YES or a NO. It's not that hard.
Delphi, do you believe there is some other mechanism than mutation and selection which can give common descent? Answer with a YES or a NO. It's not that hard.
What assumptions have I made? ... All I have done is posted data which show that abiogenesis and the theory of evolution is false. You have assumed, inter alia:
Objection, your honor, the defense lawyer is trying to introduce facts not in evidence.
I've been reading this good book, and I found a bit in it that applies to you.
Are you going to add this good book to the Help create a JREF recommended science books list?
The only way the parable doesn't fit is that if what you claim is true, you are in the position, not of a man given one talent to invest, but hundreds, thousands, millions ... untold riches beyond my wildest dreams.

And you digged in the earth, and hid your lord's money.
The only way your interpretation of this parable fits is The James Randi Educational Forum is the ground, and then you will have to explain why you have posted more than 10,000 times on this forum. Adequate, your interpretation of the both the Bible and the mathematics of mutation and selection both need some work. I encourage you to continue studying both.
There are only two possible ways we got here. We were either created or we came about by abiogenesis and evolution.Or both. If I were you, I'd go with both.
Paul, I am going to agree with you. Microevolutionary processes do occur but the concept of common descent is utter nonsense. Mutation and selection simply can not do it.
Ok, you are still sorting.

And that’s ok as well, it may not be realistic, but you are still doing a sort.So you admit that my algorithm is in fact a sorting algorithm. Then, because my algorithm shows that for some n != 0, the sorting rate is higher under n +1 sorting conditions that n sorting conditions, you admit that your claim is WRONG. That being the case, I will quote you:
I haven’t studied your computer code but essentially from your description you are doing something similar to Dr Schneider’s algorithm.
Since the foundation mechanism can not accomplish what is required for the theory of evolution to be plausible, every interpretation that evolutionists make of the evidence is called into question.Kleinman, since your foundation mechanism no longer supports your theory, every interpretation of yours is called into question. How do you respond to this?
If you want to understand how a computer simulation works, you need to do a parametric study of the model. You have not done this yet. All you have claimed is that you found a set of input values which shows something that you claims contradicts the principles of sorting/optimization. When analyzing stochastic systems, you may get particular cases that do not seem to fit the pattern. For example with Dr Schneider’s model, you can get significant differences in the generations for convergence based on the random seed used to initiate the calculation. I questioned Dr Schneider about this and whether it called the validity of his model into question. Dr Schneider responded by doing a series where he systematically examined the effect of random seed on the generation for convergence and he showed that it give approximately a bell curve distribution. You need to do this kind of study with your model to show that n+1 selection pressures evolve more quickly than n selection pressures. I think you are going to find that when you do this kind of parametric study with you model that n+1 selection pressures do no evolve more rapidly than n selection pressures. This will become especially apparent when as you increase G in your model (unless you uncouple the genome length from your computation by ignoring mutations at all loci except those where you are applying your selection pressures).
Kleinman, since your foundation mechanism no longer supports your theory, every interpretation of yours is called into question. How do you respond to this?He'll probably respond with "the peer reviewed evidence shows that multiple pressures confound evolutionary change."
Kjkent1, you are neither very good at mind reading or at pattern recognition. You should know by now that I respond to claims by evolutionists with citations which show how mutation and selection actually works. It is only when they accuse me of not having any mathematics that I respond with "the peer reviewed evidence shows that multiple pressures confound evolutionary change." So here are a couple of more citations which show how evolution by mutation and selection actually works, and the way it actually works is combination selection pressures profoundly slow the evolutionary process.
http://www.jci.org/cgi/content/full/117/9/2562 (http://www.jci.org/cgi/content/full/117/9/2562)

Molecularly targeted kinase inhibitor cancer therapies are currently administered sequentially rather than simultaneously. We addressed the potential long-term impact of this strategy in patients with chronic myelogenous leukemia (CML), which is driven by the fusion oncogene BCR-ABL. Analysis of BCR-ABL genotypes in CML patients who relapsed after sequential treatment with the ABL inhibitors imatinib and dasatinib revealed evolving resistant BCR-ABL kinase domain mutations in all cases. Twelve patients relapsed with the pan-resistant T315I mutation, whereas 6 patients developed novel BCR-ABL mutations predicted to retain sensitivity to imatinib based on in vitro studies. Three of these patients were retreated with imatinib (or the chemically related compound nilotinib) and responded; however, selection for compound mutants (2 or 3 BCR-ABL mutations in the same molecule) can substantially limit the potential effectiveness of retreating patients with inhibitors that have previously failed. Furthermore, drug-resistant mutations, when compounded, can increase oncogenic potency relative to the component mutants in transformation assays. The Aurora kinase inhibitor VX-680, currently under clinical evaluation based on its activity against the T315I mutation, is also effective against the other commonly detected dasatinib-resistant mutation in our analysis, V299L. Our findings demonstrate the potential hazards of sequential kinase inhibitor therapy and suggest a role for a combination of ABL kinase inhibitors, perhaps including VX-680, to prevent the outgrowth of cells harboring drug-resistant BCR-ABL mutations.
and
Although first reported in CML, resistant kinase domain mutations are increasingly common in other cancers treated with kinase inhibitors, such as gastrointestinal stromal tumor (16) and lung cancer (17, 18). Treatment strategies for these diseases, as with CML, are currently following a model of sequential therapy using second-line kinase inhibitors, since acquired resistance is associated with new kinase domain mutations in more than half of such patients. Our results suggest that secondary kinase domain mutations (in 17 of 17 consecutive CML patients studied) may be even more common in relapse to second-line kinase inhibitor therapy, reinforcing the critical role these targeted kinases play in propagating the malignant clone even after multiple rounds of therapy.

Consistent with preclinical predictions, mutations that confer clinical resistance to inhibitors that bind to the active conformation of the target kinase (such as dasatinib) appear to be restricted to contact residues and therefore are less numerous than those conferring resistance to inhibitors that exclusively bind an inactive conformation (such as imatinib). The high frequency of the T315I mutation in our analysis could reflect the high degree of dasatinib resistance conferred by this allele or may simply reflect the presence of an already evolving, but not dominant, T315I clone in imatinib-resistant patients.

Of particular concern is the strong selective pressure for compound drug-resistant mutants in the context of sequential cancer therapy in a substantial proportion of patients. (These mutants could emerge by selection of preexisting clones or generation of new mutations.) Compound mutants not only diminish the chance of retaining sensitivity to a hypothetical "third-generation" inhibitor due to their potential complexity but also carry the risk of creating novel kinase alleles with enhanced oncogenic potency. Prevention of selection for such compound mutants will likely require up-front combination therapy utilizing compounds that can collectively suppress all single point mutations. To this end, we have provided evidence that VX-680, which is undergoing clinical evaluation and has shown early efficacy in T315I-associated cases (10), can inhibit the kinase activity of the most common dasatinib-resistant mutants. Future studies will need to address the tolerability of such combinations and whether the potential benefit of preventing resistance is outweighed by additional toxicities. In addition, our analysis was focused primarily on advanced-phase CML (since these patients were the first to relapse). Although compound mutations were identified at the time of dasatinib failure in both chronic phase patients studied in this analysis, longer follow-up on a larger number of patients is required to discern the impact of sequential ABL kinase inhibitor therapy in early-stage CML.

Mathematical modeling studies have estimated that the probability of a single drug-resistant mutation is 10^–6 to 10^–7 per cell division (19). Therefore, identification of CML subclones with 2–3 mutations in a single molecule presumably requires an extraordinary number of tumor doublings, as well as the possibility of additional mutations in DNA mismatch repair that might increase the diversity of mutations generated. In addition, the fitness advantage observed with the triple compound mutant studied here may further increase the probability of such gain-of-function alleles expanding within individual patients, even without the selective pressure of kinase inhibitor therapy.

Targeted therapy of human malignancies is still in its infancy. Optimal patient management in the future will likely require periodic genotyping to determine the likelihood of response to a particular kinase inhibitor. Given the critical reliance of several malignancies upon key tyrosine kinases, the full therapeutic potential of small molecule tyrosine kinase inhibitors will not be realized until strategies are developed that can effectively prevent selection for drug-resistant kinase domain point mutations. CML has served as a valuable treatment paradigm for a growing number of malignancies associated with activated tyrosine kinases. Frontline combinations of ABL inhibitors, if proven to be acceptably safe, could substantially improve both the depth and durability of clinical responses in BCR-ABL–associated leukemias, particularly in advanced phases of the disease, where relapse typically occurs rapidly, by their ability to effectively eliminate BCR-ABL kinase domain point mutation as a mechanism of disease resistance. It is likely that other cancers being treated with kinase inhibitor therapy will benefit from a similar treatment strategy.
I thought I’d throw this citation in for those of you who think that mutation and selection is not deterministic.
http://www.bentham.org/dnag/samples/dnag1-1/Carvajal-Rodr%EDguez.pdf (http://www.bentham.org/dnag/samples/dnag1-1/Carvajal-Rodr%EDguez.pdf)
After treatment failure it is necessary the use of new drug combinations capable to overcome the emerged resistance. In order to design these new drug combinations two main approaches are used. The first approach consists on a phenotypic test in which the replication ability of virus variants is studied in vitro, via cell culture assays, in the presence or absence of drug. This approach is expensive and time consuming. The second approach is the use of genotypic assays in which viral sequences coding for the targets of a given drug are analyzed in order to detect mutations with low susceptibility to drugs. Although, this approach is faster and cheaper, a clear interpretation of results is not always possible due to the existence of many different mutations and mutation patterns that confer resistance. For instance, both the interaction between mutations (epistasis) and cross-resistance make difficult the interpretation of genotypic tests. Thus, the elucidation of results requires knowledge of the mutations selected due tothe effect of different antiretroviral drugs and of the potential for cross-resistance to other drugs conferred by certain mutations. Resensitization, the occurrence of a new mutation which annihilates a previous resistance effect [9], further complicate the scenario. So, the correlation of specific genotypes with resistant phenotypes after genotypic assays needs new computational methods that allow effective therapy design against drug resistant HIV variants [9-11].
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1480462 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1480462)
In the case of two antibiotics with distinct mechanisms of action, theoretical and empirical research supports the merits of combination therapy to both prevent treatment failure in individuals and control antimicrobial resistance at the population level; in other words, the same policy may satisfy both objectives (6–8). In other cases, the two objectives may be in conflict. For a bacterial pathogen that is increasingly resistant to a widely prescribed agent, promoting the use of a novel drug with activity against the resistant strains leads to fewer treatment failures and delivers benefits to current patients (4, 9). On the other hand, switching to a new drug imposes a selective pressure in favor of strains that are resistant to even the new antibiotic (10–12). Thus, we may expect that such a switch achieves the first objective at the expense of the second. Specifically, when considering two antibiotics within the same therapeutic class, high-level resistance is often conferred through sequential accumulation of chromosomal mutations or acquisition of new genetic material (8). This stepwise mechanism makes combination therapy or cycling of two antibiotics of the same class impractical. For example, resistance to fluoroquinolones in Streptococcus pneumoniae is mediated by chromosomal changes on two genes: DNA gyrase (gyrA) and topoisomerase IV (parC) (13). The first generation of fluoroquinolones, such as ofloxacin and ciprofloxacin, preferentially targets one of the two loci. Since 1994, however, a number of newer “dual-activity” fluoroquinolones, including levofloxacin (the second generation) and gatifloxacin and moxifloxacin (the third generation) (14), that demonstrate more comparable activity against both genes, have been developed. Because at least two mutations are usually required in order to confer a biologically significant resistance to these newer agents, the likelihood for a resistant strain to emerge during treatment of a fully susceptible infection is much lower (15–17). On the other hand, a strain already resistant to an “old” fluoroquinolone is only one mutation away from becoming resistant to the newer drugs, making selection of a fully resistant mutant more likely from such “precursor” strains.
Once again, the “theoretical and empirical research” supports that combination selection pressures profoundly slow the evolution of resistance. That’s how mutation and selection actually works. There are no selection pressures that evolve 10, 100 or the thousands of genes necessary to transform reptiles into birds.

[Shalamar]

Reptiles did not 'transform' into birds.

You really don't understand evolution, do you? That, or you are so forced into what you feel is right, you ignore anything else.

[Belz...]

This debate ended long ago once it was clear that combination selection pressures profoundly slow the evolutionary process.

Sorry, Alan. You don't get to decide what the evidence means and then ignore everything that other people are telling about said evidence while adding new evidence to it.

So you'll excuse me if I won't simply take your word over other people's.

This is clear both mathematically and empirically.

What's clear, mathematically, is that ev is incomplete, that under certain conditions it doesn't do what you claim it always does, and that similar programs disagree with you.

What's clear, empirically, is that your examples don't prove what you think they prove, that they are limited to a very narrow sample of possible examples and that those cited by other posters disagree with you.

I just keep posting real examples of combination selection pressures profoundly slowing evolution like a meteor shower falling on the heads of you evolutionists.

Good, that overwhelming selection pressure should mean that, by now, you'd only be left with evolutionists that agree with you. Of course, that hasn't happened, which is to show how weak the pressure is.

[rocketdodger]

If you want to understand how a computer simulation works, you need to do a parametric study of the model. You have not done this yet. All you have claimed is that you found a set of input values which shows something that you claims contradicts the principles of sorting/optimization.

No Kleinman, I already did a parametric study of my program, which you would know if you read my earlier posts in full. Regardless of genome size, pressure intensity, or any of the other variables, there is always a value of n != 0 such that average rate of fixation is higher under n + 1 pressures than n pressures.


When analyzing stochastic systems, you may get particular cases that do not seem to fit the pattern. For example with Dr Schneider’s model, you can get significant differences in the generations for convergence based on the random seed used to initiate the calculation.

Which is why I allow the user to specify the number of runs they want to make, where the random number generator is re-seeded between runs. The final result represents the average of these runs.


You need to do this kind of study with your model to show that n+1 selection pressures evolve more quickly than n selection pressures. I think you are going to find that when you do this kind of parametric study with you model that n+1 selection pressures do no evolve more rapidly than n selection pressures.

All of this is already accounted for, Kleinman.


This will become especially apparent when as you increase G in your model (unless you uncouple the genome length from your computation by ignoring mutations at all loci except those where you are applying your selection pressures)

I DO ignore mutations at non-targeted loci. Do you know why?

Because by definition a mutation at a loci not targeted by any selective pressures has no effect on the fitness of the individual.

If you are saying that every functional loci in a genome should have a stabilizing selective pressure applied to it, then I would agree. This directly contradicts your assertion that such a thing as single selective pressures exist at all, though, so why would you say such a thing? If my program was to be an accurate model of real mutation and selection, I would include this feature -- but since it is not intended to be, and including the feature would slow down the computation by orders of magnitude, I didn't include it.

It doesn't even matter, because regardless, my algorithm remains a sorting algorithm. Face it, Kleinman, you are just wrong. I have done the math. You have done no math. My math shows you to be wrong. Since you have no math to refute my math, I win.

[Belz...]

Delphi, the whole concept of common descent by mutation and selection is nonsense. There is no mechanism that can do what you evolutionists allege

That was not the question. Removing mutation and selection from the equation, do you agree that all life shares a common ancestor ?

If not, please explain the new species...

Shalamar, you were created and you should seek to know your Creator.

If only to smack him upside the head for doing such a mediocre job.

[Belz...]

Kleinman, would you mind explaining how HIV manages to evolve very quickly, again ? Do you contend that it's only under a very few selection pressures ?

[Belz...]

I thought I’d throw this citation in for those of you who think that mutation and selection is not deterministic.

Maybe you should've read past what you put in red:

Although, this approach is faster and cheaper, a clear interpretation of results is not always possible due to the existence of many different mutations and mutation patterns that confer resistance.

So, which is it ?

[kleinman]

Reptiles did not 'transform' into birds.

You really don't understand evolution, do you? That, or you are so forced into what you feel is right, you ignore anything else.
You are correct Shalamar, reptiles do not ‘transform’ into birds. Reptiles remain reptiles and birds remain birds. Now if I get the evolutionist (and SciFi channel) mythology correct, dinosaurs evolved into birds.

Oh, I don’t ignore anything else, I’m just focusing on the fundamental principle which you evolutionists propose is the foundation for the theory of evolution which is mutation and selection. When you examine the mathematical and empirical evidence of how mutation and selection actually works, you find that combination selection pressures profoundly slow the evolutionary process. Anytime you want to describe the selection pressure that would transform dinosaurs into birds, feel free to chime in. Oh, wait a minute, Kotatsu already answered that one. A dinosaur got chased into a tree and it was beneficial for the dinosaur to grow feathers and wings. Hey Kotatsu, was that a female or male dinosaur which got chased into the tree? Now Shalamar, kjkent1 has proven beyond a reasonable doubt that there is more than a single evolutionary pathway. So why don’t you give us another pathway for dinosaurs to transform into birds?

In the meantime, I’ll keep trying to explain to you evolutionists how mutation and selection actually works, that this system is nothing more than a sorting/optimization problem where multiple simultaneous optimizations conditions profoundly slow the sorting process. I don’t want to waste my talents, do I Adequate? Hey Adequate, you find any real examples of n+1 selection pressures evolving faster than n selection pressures yet? Here’s another real example which shows just the opposite.
http://jvi.asm.org/cgi/reprint/75/19/9502.pdf (http://jvi.asm.org/cgi/reprint/75/19/9502.pdf)
Highly active antiretroviral therapy (HAART) with reverse transcriptase inhibitors in combination with protease inhibitors has proven to suppress human immunodeficiency virus type 1 (HIV-1) replication to undetectable levels in patients (11, 12, 17). HIV-1 variants frequently evolve that escape HAART by developing resistance to the inhibitors used (4, 15, 19, 28, 40, 42). Of patients first treated with a single drug regimen and then going onto HAART, as many as 40% have a viral rebound within the first 3 years, and this number is likely to be higher outside of controlled studies (20, 35). Moreover, transmission of drug-resistant HIV has been observed and is likely to increase with more patients on combination therapy (25, 38).
Thus, there is a need to fully understand the sequence of molecular changes to HIV concomitant with development of resistance to protease inhibitors. In turn, this knowledge should facilitate the development of new inhibitors with activities against drug-resistant isolates.
So Adequate, what do you think monotherapy has done for the treatment of HIV? You evolutionists are so good at explaining how mutation and selection works. Explain that to the people with HIV who got monotherapy before they got combination therapy; that is if they are still alive.

[delphi_ote]

Delphi, do you believe there is some other mechanism than mutation and selection which can give common descent? Answer with a YES or a NO.
This question doesn't make sense! Mutation and selection did not cause common descent. Reproduction "caused" common descent. Mutation and selection caused the diversity of life. If you're asking if I believe there's another mechanism which could have produced that diversity, I would say no. It's possible, but I think it's very unlikely we will find a mechanism besides natural selection acting on mutations.

But you still have not answered my direct question. I'm not letting you off the hook. Let's try this again:
Do you believe that all of the life on Earth come from a common ancestor? In other words, is all life on earth part of one big family tree? Answer with a YES or a NO. No chickening out this time.

[Dr Adequate]

The only way your interpretation of this parable fits is The James Randi Educational Forum is the ground ... Yes, of course. Duh. The forums correspond, in the parable, to the earth in which you are burying your lord's money.

That's so clear and obvious, I'm astonished that you understood it.

Now, will you answer the question? Why are you hiding this life-saving discovery?

... and then you will have to explain why you have posted more than 10,000 times on this forum. Because in none of my posts do I claim to have made a discovery that will help millions of suffering and dying people, and so I feel no need to seek a wider audience for my views.

But you do make such a claim. So why should your supposedly awesome discovery be buried alongside my limericks, pictures of kittens, and jokes about spoonbenders and TV psychics?

[Dr Adequate]

So Adequate, what do you think monotherapy has done for the treatment of HIV? You evolutionists are so good at explaining how mutation and selection works. Explain that to the people with HIV who got monotherapy before they got combination therapy; that is if they are still alive. Since you ask, I think that combination therapy is better than monotherapy for HIV, just like every other evolutionist does, as you know perfectly well.

We even patiently explained to you why it's better, remember? About, I don't know, a hundred pages back?

Now, how about you answer my question?

[Kotatsu]

Delphi, do you believe there is some other mechanism than mutation and selection which can give common descent? Answer with a YES or a NO. It's not that hard.

Yes. Polyploidization can give common descent. If we find an animal or a plant which has a certain number of chromosomes, and another which have a number of chromosomes equal to a multiple of that first set, this would imply common descent of these two animals or plants even if there have been no other changes of the genome.

In the creature I did my master thesis on, Lumbriculus variegatus (1), we find diploid, triploid, tetraploid, and all the way up to 11-ploid individuals (2) which are --- as far as anyone has been able to tell --- morphologically identical (3). Certainly, these often do show some slight variation in the exact sequences (in nuclear regions, these differences are on the scale of one in 10.000 between individuals from Sweden and the US, presumably isolated for millions of years). However, as often as not, we find no differences in either the nuclear or the mitochondrial DNA. The only difference between them is the ploidy number.

There exists at least one mechanism by which 34 chromosomes (the diploid number of Lumbriculus variegatus can change into, say, 68, namely autopolyploidisation. If an lineage goes through autopolyploidisation, the descendants will be polyploid but otherwise genetically identical to their diploid ancestors. As these animals almost invariably are asexual (at least in Europe), relatives of these polyploid animals will often have the same genetic sequence, but differ in the number of chromosomes. Usually, no recombination occurs, as the asexual populations reproduce primarily through architomy; that is, the division of the body into two parts with subsequent regeneration of a head on the old tail and a tail on the old head (5).

Thus, without any mutation and selection, we can show that two Lumbriculus have a common descent simply by the fact that their genomes are identical, but their ploidy levels are not.

Now what?

---
(1) Also known as the Californian Black Worm, for some reason.
(2) After this ploidy level, the individual chromosomes are too small to count accurately, according to Christensen (1980), but there is no known mechanism, as far as I am aware, to stop polyploidisation from occurring past the point where it can be detected by the human eye. I can say with some confidence that there likely are Lumbriculus out there with higher ploidy levels.
(3) This is not entirely true, of course. They display an enormous variation in the number and position of the genital elements (4) and in their pigmentation. This has not yet been shown to have any correlation with ploidy level, however. Christensen (1980), however, stated that increased ploidy level seemed to decrease the efficiency of spermatogenesis, so there may be some ploidy-related effects in play.
(4) It should perhaps be explained that in the current taxonomy of Clitellata, families are roughly based on the number and position of the genital elements in almost all cases. If the genitals start in, say, segment 11, the worm can immediately be at least preliminarily assigned to a family. The variation in the Lumbriculus complex, however, is greater than the variation between families of other Clitellates, making them notoriously hard to assign to family level, had they not had a distinct pigmentation in the anterior end, and some other key characters. Recent progress by my old supervisor's group has shown, however, that these arrangements of families, though most often verified by genetic data, are not as reliable as hitherto thought. Some aberrant families have recently been shown to be parts of larger families, despite odd genitals.
(5) These also undergo morphallaxis, the process by which individual segments change morphologically, physiologically, and chemically to fit their new relative position in the new worm. Further, there are some queer limitations of how much will regenerate and so on, but I guess that by now, I have lost everyone's interest, so I will not go deeper into that unless asked to.

[joobz]

When you examine the mathematical and empirical evidence of how mutation and selection actually works, you find that combination selection pressures profoundly slow the evolutionary process.
Ok. Let's pretend you are correct.
Common descent isn't real.
Evolution doesn't happen.
Species remain what they are and do not change.
Just of out curiousity...

How do you explain the fossil record?
The evidence of species appearing and disspearing throughout history?
Similarities in gemones?
Chromosomal fusion of chimp genome?
emergence of multi-drug resistant bacteria?
Existence of viral dna in human genome and similarities with other species?
Existence of multiploidy and apparehent common descent?
The unusually high existence of sickle cell in african populations?
The existence of iRNA?
The fact that nothing has proven to be irreducibly complex in biology?
Why do the same proteins have multiple functions in different cells (e.g., PLA2/Prdx6)
nylon eating bacteria?
seperate species producing viable offspring?
symbiotic relationships in biology?
Why do mitochondria have thier own DNA?
Why do creatures reproduce sexually?
Why do some creatures reproduce by budding?
Why do cells, which divide, exchange DNA?
Why do cells exchange organelles?

[Kotatsu]

Anytime you want to describe the selection pressure that would transform dinosaurs into birds, feel free to chime in. Oh, wait a minute, Kotatsu already answered that one. A dinosaur got chased into a tree and it was beneficial for the dinosaur to grow feathers and wings. Hey Kotatsu, was that a female or male dinosaur which got chased into the tree?

Neither. That happened when God was still creating all animals individually, making the necessary mutations by hand.

Is it due to ill will that you display this lack of understanding of simple concepts, or are you like this in real life as well?

Let me explain one more time, while trying to find out exactly what part of the scenario it is you cannot understand:
Over a prolonged period of time a group of small dinosaurs gradually became arboreal.

Do you agree with this?

These arboreal dinosaurs were faced with a dilemma their terrestrial relatives did not have. Their environment contained huge holes; the trees were not a continuous mass as the ground was.

Do you agree with this?

Therefore, to get from one tree to another --- to escape from predators, to get more food, or just to move around --- they basically had two choices. They could either go down from the tree they were in, walk over to the next one, and climb that one. Or they could jump from one tree to another without touching the ground in between.

Do you agree with this?

Conceivably, some choose the former; these are not interesting for us, as they did not provide the ancestors of modern birds. Those who chose the latter, however, are what interests us. They found that when jumping from one tree to another, some always misjudged the distance, was caught by the wind, or something, and fell to the ground. Often, these animals did not survive because of the fall.

Do you agree with this?

The individuals who didn't fall to their death survived. This is a very simple concept, but essential. Some of these surviving individuals reproduced after having moved from one tree to another.

Do you agree with this?

Conceivably, there was a reason why some individuals managed to jump from one tree to another while others fell to their deaths. This reason may have been partly or totally based on the differences in the genome of the individuals.

Do you agree with this?

Over time, a larger percentage of those individuals or lineages which were better at judging the distance, keeping in the air, or possessed other necessary characters for moving about between trees survived to reproduce, whereas those lineages whose judgement or skills were not as good survived to a lesser extent.

Do you agree with this?

The genomes of these lineages, whether they survived or not, changed over time due to mutations.

Do you agree with this?

Some of these mutations provided a change in a character which made it easier to get from one tree to another without falling to your death. For instance, as MrScott showed, a single point mutation in modern hens make their feet grow feathers. While we cannot know the corresponding sequences of these arboreal dinosaurs, we can at least draw the conclusion that changes of this magnitude need to be based on extensive genetic change.

Here, I suspect you will disagree, if you haven't already.

The lineages in which these fortuitous mutations occurred --- and please notice that this is not limited to random point mutations --- were incrementally better equipped to move about in the trees. Thus, over time, they grew more plentiful than those lineages without the fortuitous mutations.

Agree?

As several factors weigh in on the success of moving from one tree to another, mutations which made this process simpler are conceivably numerous. In some lineages, one fortuitous mutation occurred, in others other fortuitous mutations occurred.

Agree?

These lineages could often interbreed, thus "collecting" or exchanging fortuitous mutations by sexual selection (all birds are sexual, and I assume here that dinosaurs were, too). Sometimes, this meant that one or more fortuitous mutation in one lineage was replaced by non-fortuitous ones in the progeny. In other cases, non-fortuitous mutations were replaced with fortuitous ones.

Agree?

The progeny of these latter cases were better equipped for moving about between trees than those of the former cases. This interbreeding continues over and over again, with approximately the same distribution of results.

Agree?

Now for the punch line: In the present case, one or several of these fortuitous mutations caused the "carrying area" of the scales to increase. Again, this is not necessarily a great change, as we have seen. These lineages became the precursor to birds, because these enlarged scales were precursors of feathers. Once this process had started, it was just a matter of what I believe you have referred to as "microevolution": just as different dogs have changed quite rapidly, changes in length and shape of these scales were just minor adjustments, because a character to improve upon had already developed: the scales.

As I have mentioned repeatedly before, this was not necessarily the best way to achieve greater survival to reproduction among arboreal animals, nor is it the only one in evidence today. Several other mechanisms have evolved, and some of them have even evolved on other dinosaurs (see Microraptor and its four wings, for example). However, that was the way it happened, and these changed scales have since been improved upon until they are well nigh unrecognisable as scales, and the birds well nigh unrecognisable as dinosaurs. But only "well nigh", because upon closer study --- and I am a birdwatcher with a great interest in dinosaurs, so I have taken time to study this closer --- the similarities are enormous. The gait, the stances, the general morphology --- in several different ways it is easy to come to the conclusion that dinosaurs are the ancestors of birds. And like a cherry on top, we also have an extensive fossil record describing exactly this change.

[Belz...]

Delphi, do you believe there is some other mechanism than mutation and selection which can give common descent? Answer with a YES or a NO. It's not that hard.


http://forums.randi.org/imagehosting/608045fd3950b30f8.gif (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=4645)

[Mr. Scott]

Now that we know how mutation and selection actually works, that is combination selection pressures profoundly slow the evolutionary process (and this has been shown numerous times both mathematically and empirically). And mutation and selection is the foundation mechanism for the theory of evolution. Since the foundation mechanism can not accomplish what is required for the theory of evolution to be plausible, every interpretation that evolutionists make of the evidence is called into question.

So, before you found out how mutation and selection work via Paul's model and combination thereapy, there was no reason for you to call into question evolutionists' interpretation of the evidence? Is that what you are saying?

[delphi_ote]

Yes. Polyploidization can give common descent.
Ah, so you took his question to mean "Is there another mechanism we can use to infer common descent?" I'm not sure if that's what he meant or not (figuring out his word salad is almost impossible sometimes,) but you gave a very interesting response.

We found a genome wide duplication event in the poplar genome project (http://www.sciencemag.org/cgi/content/abstract/313/5793/1596), which was probably caused by a paleopolyploid event sometime over the course of its divergence from its common ancestor with A. thaliana. Apparently these events happen very often in plants (http://upload.wikimedia.org/wikipedia/en/3/35/PaleopolyploidyTree.jpg). There has been some speculation that they are a major cause of speciation in plants.

[Dr Adequate]

The fact that nothing has proven to be irreducibly complex in biology? I disagree. Although most creationist example of irreducible complexity have been shot down, I would nominate the bones of the inner ear of mammals. Of course, we know how they evolved.

See here. (http://skepticwiki.org/index.php/Irreducible_complexity#Example:_The_Mammalian_Ear)

The example of obligate symbiosis is also given.

[kjkent1]

Objection, your honor, the defense lawyer is trying to introduce facts not in evidence.Overruled! I find Dr. Kleinman in contempt for wasting the the court's time by endlessly compounding his testimony. The witness is hereby disqualified as an expert on the subjects of evolutionary biology, genetics, mathematics, and HIV therapy.
I will only permit Dr. Kleinman to testify as an expert on the subject of being an annoying creationist.

On that subject, the witness is clearly without peer.

[Paul C. Anagnostopoulos]

So, before you found out how mutation and selection work via Paul's model and combination thereapy, there was no reason for you to call into question evolutionists' interpretation of the evidence? Is that what you are saying?
Crapmuffins! I knew it was my fault.

~~ Paul

[joobz]

I disagree. Although most creationist example of irreducible complexity have been shot down, I would nominate the bones of the inner ear of mammals. Of course, we know how they evolved.

See here. (http://skepticwiki.org/index.php/Irreducible_complexity#Example:_The_Mammalian_Ear)

The example of obligate symbiosis is also given.
good point. I was mentally stuck at the protein level. I guess if you are willing to ignore evolution, you will also consider organelles as irreducibly complex.

[kleinman]

Shalamar, you were created and you should seek to know your Creator.If only to smack him upside the head for doing such a mediocre job.
Why would you think that Shalamar is mediocre?
Kleinman, would you mind explaining how HIV manages to evolve very quickly, again ? Do you contend that it's only under a very few selection pressures ?
You should know the answer to that one Belz, the fewer the selection conditions, the faster it evolves.
I thought I’d throw this citation in for those of you who think that mutation and selection is not deterministic.Maybe you should've read past what you put in red:
Although, this approach is faster and cheaper, a clear interpretation of results is not always possible due to the existence of many different mutations and mutation patterns that confer resistance.So, which is it ?
Belz, how many variants are there, 10?, 100?, 1000?, millions? Consider that for hemoglobin, there are only a few hundred variants of this gene that still give viability. In time, most or all variants of viable resistant HIV genes will be identified.
Delphi, do you believe there is some other mechanism than mutation and selection which can give common descent? Answer with a YES or a NO.This question doesn't make sense! Mutation and selection did not cause common descent. Reproduction "caused" common descent. Mutation and selection caused the diversity of life. If you're asking if I believe there's another mechanism which could have produced that diversity, I would say no. It's possible, but I think it's very unlikely we will find a mechanism besides natural selection acting on mutations.
What sense are you making? All you need is reproduction for reptiles to evolve into birds? You have recombination and natural selection which can and does give great diversity. When I use the terminology “common descent”, I am talking about the notion of some life form that spontaneously arose in the primordial soup which through a sequence of mutation and selection evolves into the complex life forms we see today. That is an irrational and illogical notion.
But you still have not answered my direct question. I'm not letting you off the hook. Let's try this again:
Do you believe that all of the life on Earth come from a common ancestor? In other words, is all life on earth part of one big family tree? Answer with a YES or a NO. No chickening out this time.
I’m not afraid of answering the question. I’m actually a little surprised you don’t already know the answer. Why after 163 pages of discussion on this topic you would think my answer would be anything but no is quite mysterious. Why would you think I might say yes? Perhaps you think because humans and chimpanzees have the same insulin might make evolutionists think we arose from a common ancestor but then you have to show why humans and chimpanzees have different preproinsulin.
The only way your interpretation of this parable fits is The James Randi Educational Forum is the ground ... Yes, of course. Duh. The forums correspond, in the parable, to the earth in which you are burying your lord's money.

That's so clear and obvious, I'm astonished that you understood it.

Now, will you answer the question? Why are you hiding this life-saving discovery?
You are easily astonished but why would you think so little of the James Randi Educational Forum?
... and then you will have to explain why you have posted more than 10,000 times on this forum.Because in none of my posts do I claim to have made a discovery that will help millions of suffering and dying people, and so I feel no need to seek a wider audience for my views.
I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works. I’m not the only one who understands this. What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures. You have no empirical evidence of this yet you continue to believe it. I’ll continue working on you for now.
So Adequate, what do you think monotherapy has done for the treatment of HIV? You evolutionists are so good at explaining how mutation and selection works. Explain that to the people with HIV who got monotherapy before they got combination therapy; that is if they are still alive.Since you ask, I think that combination therapy is better than monotherapy for HIV, just like every other evolutionist does, as you know perfectly well.

We even patiently explained to you why it's better, remember? About, I don't know, a hundred pages back?

Now, how about you answer my question?
I posted a citation from a 50 year old Nobel laureate speech that said the same thing. Why haven’t you evolutionists explained this before? The theory of evolution by mutation and selection is your theory, why haven’t you done a better job explaining how mutation and selection actually works. Oh, that’s right; you say that n+1 selection pressures evolve more rapidly than n selection pressures. Adequate, you couldn’t be more wrong about how mutation and selection works. But I do like using an evolutionist dominated web site to do this.
When you examine the mathematical and empirical evidence of how mutation and selection actually works, you find that combination selection pressures profoundly slow the evolutionary process.Ok. Let's pretend you are correct.
Common descent isn't real.
Evolution doesn't happen.
Species remain what they are and do not change.
Just of out curiousity...
Joobz, you just love to speculate and extrapolate from your speculations. Take your list and account for the 150,000,000 base differences between humans and chimpanzees in 500,000 generations and don’t forget to tell us what the selection pressures and target genes for these selection pressures are.
Is it due to ill will that you display this lack of understanding of simple concepts, or are you like this in real life as well?
Kotatsu, once you understand that mutation and selection is simply a sorting/optimization problem, you will understand why this process can not transform large numbers of genes simultaneously. I harbor no ill will toward you or anyone else. I just think your ideas are illogical and irrational. They don’t make mathematical or empirical sense.
Now that we know how mutation and selection actually works, that is combination selection pressures profoundly slow the evolutionary process (and this has been shown numerous times both mathematically and empirically). And mutation and selection is the foundation mechanism for the theory of evolution. Since the foundation mechanism can not accomplish what is required for the theory of evolution to be plausible, every interpretation that evolutionists make of the evidence is called into question.So, before you found out how mutation and selection work via Paul's model and combination thereapy, there was no reason for you to call into question evolutionists' interpretation of the evidence? Is that what you are saying?
Before I looked at Dr Schneider’s and Paul’s model, I didn’t understand how mutation and selection worked. What their model showed was it took huge numbers of generation to evolve the binding sites on all but the tiniest genomes. I systematically studied each variable in the model in order to try to find out why this was happening. It was the multiple selection conditions that were doing this. That’s what prompted me do to a literature search to find out if there was empirical evidence of this. I have always been skeptical of the interpretation of the evidence presented by evolutionists but this is the first time I have done my own analysis of the evidence and it shows that evolutionists have the concept of mutation and selection backwards.
So, before you found out how mutation and selection work via Paul's model and combination thereapy, there was no reason for you to call into question evolutionists' interpretation of the evidence? Is that what you are saying?Crapmuffins! I knew it was my fault.
Paul, getting the credit and getting the blame is the same thing, it’s just how you interpret the evidence.
The fact that nothing has proven to be irreducibly complex in biology?I disagree. Although most creationist example of irreducible complexity have been shot down, I would nominate the bones of the inner ear of mammals. Of course, we know how they evolved.
So I guess you two are ready to explain to us what the components of the DNA replicase system were doing before DNA could be replicated. Tell us what the function of helicase and gyrase were. That should be a good story. Joobz, you can tell us this after you show us how ribose can be generated nonenzymatically.
Objection, your honor, the defense lawyer is trying to introduce facts not in evidence.Overruled! I find Dr. Kleinman in contempt for wastiong the the court's time by constantly compounding his testimony. The witness is hereby disqualified as an expert on the subjects of evolutionary biology, genetics, mathematics, and HIV therapy.
I will only permit Dr. Kleinman to testify as an expert on the subject of being an annoying creationist.

On that subject, the witness is clearly without peer.
I’ve appealed to a higher court and your decision has been overruled. So be prepared to be compounded.
http://www.natap.org/2005/HBV/092005_02.htm (http://www.natap.org/2005/HBV/092005_02.htm)
Background/Aims: Mathematical analysis of viral kinetics during lamivudine-adefovir combination therapy has not yet been performed in patients with lamivudine-resistant hepatitis B.

Conclusions: Although a recent study did not show any differences in the reduction of HBV DNA comparing monotherapy with adefovir dipivoxil to adefovir-lamivudine combination therapy in patients with lamivudine-resistant chronic hepatitis B, mathematical analysis of early viral kinetics suggests an additional effect of lamivudine on the infected cell loss during adefovir-lamivudine combination therapy.
And
In conclusion, I think that the differences between the population kinetics observed by Mihm and Tsiang probably reflect simple differences between quite small cohorts at baseline, and do not necessarily imply a beneficial effect of LAM on second phase kinetics during ADV treatment of YMDD infection. In this case, the raw data are more informative than the population delta. Nevertheless, other published and presented data (and the paradigm of HIV treatment) make me favour the maintenance of LAM after commencement of ADV for treatment of YMDD. For treatment-naive patients, the combination probably retards the emergence of YMDD species and may delay or prevent the emergence of ADV-resistant virus. Perhaps, trials in progress will show that combination treatment for HBV is superior to monotherapy, and will confirm that the treatment paradigm for HIV patients is relevant to the treatment of our patients with chronic hepatitis B infection.
http://jac.oxfordjournals.org/cgi/content/full/57/2/221 (http://jac.oxfordjournals.org/cgi/content/full/57/2/221)
A combination therapy may prove to be more effective than monotherapy in suppressing viral replication and may decrease or delay the incidence of drug resistance.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15067628&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15067628&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus)
BACKGROUND & AIMS: Lamivudine suppresses hepatitis B replication, but drug-resistant mutants emerge with long-term therapy. In vitro data suggest that lamivudine and famciclovir might synergistically inhibit hepadnaviral replication. We reviewed our experience with lamivudine and famciclovir in 24 patients with chronic hepatitis B infection. METHODS: Patients with chronic hepatitis B infection and detectable HBV DNA received lamivudine and famciclovir combination therapy. The primary end point was HBV DNA suppression at week 48. Follow-up was reviewed for those who remained on combination therapy beyond the first 48 weeks. RESULTS: Thirteen treatment-naïve HBeAg-positive subjects received 48 weeks of therapy; all had undetectable HBV DNA levels (less than 2.5 pg/mL) at week 48. Three patients underwent HBeAg seroconversion at week 48 and discontinued therapy. Ten patients remained on combination therapy; 3 developed YMDD (tyrosine-methionine-aspartate-aspartate) mutations at year 2, although HBV DNA levels remained below 2.5 pg/mL at a mean of 39 months. A second heterogeneous group of 5 subjects including interferon therapy failures and those with HBeAg-negative infection also received 48 weeks of combination therapy, with 1 subject developing redetection of HBV DNA by week 48. YMDD mutations were noted in the other 4 subjects at year 2, although just 1 subject had HBV DNA greater than 2.5 pg/mL at 39 months of therapy. CONCLUSIONS: In this small pilot study, 48 weeks of therapy with lamivudine and famciclovir was effective in suppressing HBV replication. A randomized controlled trial is required to define the role of combination therapy with lamivudine and famciclovir in delaying the clinical emergence of resistant strains.
Compounded you evolutionists again.

[joobz]

Joobz, you just love to speculate and extrapolate from your speculations. Take your list and account for the 150,000,000 base differences between humans and chimpanzees in 500,000 generations and don’t forget to tell us what the selection pressures and target genes for these selection pressures are.

So I guess you two are ready to explain to us what the components of the DNA replicase system were doing before DNA could be replicated. Tell us what the function of helicase and gyrase were. That should be a good story. Joobz, you can tell us this after you show us how ribose can be generated nonenzymatically.

So you can't answer any of my questions?

ETA: pretending your numbers are correct:
~4% difference between genomes over 500,000 generations (since the split is what I assume you are refering to) results in a 0.000008% change per generation. Considering that human genome variablity is somewhere arround 0.08% between individuals, this mutation rate relates to 1/10,000th of the variation between humans. These numbers are far from impossible.

[rocketdodger]

Does anyone else notice how Kleinman has been conveniently ignoring my last post?

[joobz]

Does anyone else notice how Kleinman has been conveniently ignoring my last post?
Even when kleinman responds, he ignores what is said.

[kjkent1]

I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works. I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works.All of which is entirely defeated by fact that ev and all of your citations show faster evolutionary change under the influence of a dominant pressure.

It's so obvious that this is what happens in natural environments that it should come as no surprise that all of your cited experiments show rapid change under that circumstance.

Even in a controlled environment, it is impossible to absolutely eliminate all but one selective pressure. The proof of this is that mutation itself occurs. The target organisms are under continuous attack from universal background radiation which contributes to mutational change. This itself is a selective pressure as well as the engine of genetic change.

The important criteria is not the number of pressures applied, but their relative intensity. Suppose that the most successful triple therapy test were run with two of the three therapies in homeopathic dosages. Do you seriously believe that the result would be the same as occurs with relatively similar dosages?

Both ev and reality are consistent -- evolution happens under a dominant selective pressure -- a circumstance which is relatively routine in nature.

It's a wonderful day that the annoying creationist bites the dust.

[kjkent1]

Does anyone else notice how Kleinman has been conveniently ignoring my last post?Religious fanatics are adept in their singular ability to slough off dissent. Almost as good as life insurance salespersons!

The preacher who is exposed as a charlatan will immediately admit his sins and then propose: "From whom you would rather learn to walk the road to salvation -- the saint or the sinner? Who would be the more likely person to show you the way?" Blah, blah, blah, blah!

[Shalamar]

If life, and as a result, humans, were 'created' and thus 'intelligently designed', then why did the designer do such a TERRIBLE job at it?

We are FAR too complex of beings, too many things go run, strange duplication of non essential parts, no backups for essential organs, and weird, strange crossing of plumping, where the same tubes deal with waste, and reproduction.

It seems Klienman thinks that evolution happens just like pokemon. Bang. One moment one species, another moment, a different one.

Too bad all the evidence points against creationism, and intelligent design.

[Kotatsu]

Ah, so you took his question to mean "Is there another mechanism we can use to infer common descent?" I'm not sure if that's what he meant or not (figuring out his word salad is almost impossible sometimes,) but you gave a very interesting response.

We found a genome wide duplication event in the poplar genome project (http://www.sciencemag.org/cgi/content/abstract/313/5793/1596), which was probably caused by a paleopolyploid event sometime over the course of its divergence from its common ancestor with A. thaliana. Apparently these events happen very often in plants (http://upload.wikimedia.org/wikipedia/en/3/35/PaleopolyploidyTree.jpg). There has been some speculation that they are a major cause of speciation in plants.

Well, as Kleinman apparently lack the mental skills to understand anything of what I said in my last two posts (as evidenced by his almost complete lack of response to them), I may as well ignore him, and continue talking to you.

I took his question to mean both any process which would give common descent and any process from which we may infer common descent, as the latter, it seems to me, is a subset of the former. Of course, just sexual reproduction, regardless of if mutations happen or not, will "give" common descent of the progeny of any given stage. Even asexual reproduction will do so, provided each individual gives rise to more than one progeny. That's how I see it, at least. In a sense, at least, common descent does not require evolution. Me and my sister would be of common descent even if our respective genomes were 100% identical, so his question is what we could expect of a man who has no idea what he is talking about.

However, if he means some mechanism or process or evidence we can use in present day organisms to infer common descent of at least some organisms (1), and we cannot use (random point) mutation and selection, then polyploidisation immediately springs to mind. Of course polyploidisation is often coupled to mutation and selection (2) (and to a change to an asexual lifestyle, at least in animals), but even without it, common descent could still be inferred.

I think it is telling that Kleinman choose not to comment on that post at all. My guess is that, again, he has no idea what is being talked about in his presence, and thus he runs below deck and closes the hatches behind him.

As for the last part of your post, I have seen that as well --- 80% of all flowers have polyploid forms or some such number (I think this number was from Otto and Whitton, 2000). The numbers in animals are less, which I have seen explained as a result of animals being less inclined to self-fertilize, but this is doubtlessly only part of the explanation. However, Okano (I think) found evidence that polyploidisation had occurred at least twice basally in the vertebrate phylum, but I don't know the details of it. I've also come to understand that it's more common in colder climates (Little et al., 1997 springs to mind, and also some papers the now infamous Paul Hebert were involved in, but I can't remember who were the first authors of those papers).

In all, I find polyploidisation extremely interesting, and sort of miss working with it. Do you work with it at present?

---
(1) Interesting side question: if we could show beyond any doubt that a certain group of organisms had evolved in a way that even someone as dense as Kleinman would accept it, would that be perceived as a localized evolution event or evidence that all organisms have evolved?
(2) Again, Song et al., 1999 is an excellent example of this. However, it is a study of allopolyploidisation, not autopolyploidisation.

[Kotatsu]

Kotatsu, once you understand that mutation and selection is simply a sorting/optimization problem, you will understand why this process can not transform large numbers of genes simultaneously. I harbor no ill will toward you or anyone else. I just think your ideas are illogical and irrational. They don’t make mathematical or empirical sense.

Do you have any useful response to my two longer posts? I mean the one about polyploidisation giving rise to common descent in a way we can actually measure and infer more easily than (random point) mutation and selection, and the elaboration of the dinosaur-to-bird evolutionary scenario I provided you with? If at any point in either of those two posts I am unclear or too technical --- I understand, for instance, if the polyploidisation post may be too convoluted for someone who has never specifically studied the area --- I would be happy to provide more details and explain it in simpler terms. Just say the word. Also: if you have problem accessing the papers I cite, I would be glad to send them to you. I wouldn't want to just copy and paste, sinc ethat could lead to allegations of cherry picking; far better for you to read the papers in full and get the whole picture.

[delphi_ote]

Well, as Kleinman apparently lack the mental skills to understand anything of what I said in my last two posts (as evidenced by his almost complete lack of response to them), I may as well ignore him, and continue talking to you.
Well, if he won't provide interesting answers or thoughts, maybe we can!
Of course, just sexual reproduction, regardless of if mutations happen or not, will "give" common descent of the progeny of any given stage. Even asexual reproduction will do so, provided each individual gives rise to more than one progeny. That's how I see it, at least. In a sense, at least, common descent does not require evolution. Me and my sister would be of common descent even if our respective genomes were 100% identical, so his question is what we could expect of a man who has no idea what he is talking about.
This was how I originally interpreted his question. You could imagine a universe where organisms were all related to each other, but didn't evolve. Instead of mutation and natural selection, you could have God the post-hoc Kludge Designer come in and incrementally "fix" his creation once in a while.
However, if he means some mechanism or process or evidence we can use in present day organisms to infer common descent of at least some organisms (1), and we cannot use (random point) mutation and selection, then polyploidisation immediately springs to mind. Of course polyploidisation is often coupled to mutation and selection (2) (and to a change to an asexual lifestyle, at least in animals), but even without it, common descent could still be inferred.
We could also use simple gene homology for this. It might not be a perfect model if we go at it blind to mutation mechanisms, but string similarity would certainly allow us to infer a tree of relationships among species.
I think it is telling that Kleinman choose not to comment on that post at all. My guess is that, again, he has no idea what is being talked about in his presence, and thus he runs below deck and closes the hatches behind him.
What about his inability to answer a direct question with a YES or a NO?
As for the last part of your post, I have seen that as well --- 80% of all flowers have polyploid forms or some such number (I think this number was from Otto and Whitton, 2000). The numbers in animals are less, which I have seen explained as a result of animals being less inclined to self-fertilize, but this is doubtlessly only part of the explanation. However, Okano (I think) found evidence that polyploidisation had occurred at least twice basally in the vertebrate phylum, but I don't know the details of it. I've also come to understand that it's more common in colder climates (Little et al., 1997 springs to mind, and also some papers the now infamous Paul Hebert were involved in, but I can't remember who were the first authors of those papers).
The image that I linked in my previous post includes more than one event in vertebrates! That's definitely something I'll have to read up on over Thanksgiving break!
In all, I find polyploidisation extremely interesting, and sort of miss working with it. Do you work with it at present?
No. I'm working on gene regulation in insects these days. Gene regulation is amazing, but I do miss investigating larger structural and comparative evolutionary questions about genomes. It was great to have such a deep sense of vast amounts of time in my every day work.

Fortunately, I think things will get interesting really fast with this insect stuff. We have a lot of fully sequenced genomes to work with these days, and the model organisms for development (fruit fly) and social behavior (honey bee) are closely related to all them.

[delphi_ote]

Perhaps you think because humans and chimpanzees have the same insulin might make evolutionists think we arose from a common ancestor but then you have to show why humans and chimpanzees have different preproinsulin.
I don't know anything about this protein. I went to NCBI. I got the sequence for human preproinsulin. I blasted (searched) it against the NR database (all the non redundant DNA we know of in the whole world.) Here are the first three hits:
ref|NP_000198.1| proinsulin precursor [Homo sapiens] >sp|P013... 214 2e-54
gb|AAP36446.1| Homo sapiens insulin [synthetic construct] >gb... 213 2e-54
ref|NP_001008996.1| proinsulin precursor [Pan troglodytes] >s... 212 5e-54

Pan troglodytes is chimp, in case you didn't know.

Here is the human amino acid sequence aligned against the chimp's:
Query 1 MALWMRLLPLLALLALWGPDPAAAFVNQHLCGSHLVEALYLVCGERGFFY TPKTRREAED 60
MALWMRLLPLL LLALWGPDPA+AFVNQHLCGSHLVEALYLVCGERGFFYTPKTRREAED
Sbjct 1 MALWMRLLPLLVLLALWGPDPASAFVNQHLCGSHLVEALYLVCGERGFFY TPKTRREAED 60

Query 61 LQVGQVELGGGPGAGSLQPLALEGSLQKRGIVEQCCTSICSLYQLENYCN 110
LQVGQVELGGGPGAGSLQPLALEGSLQKRGIVEQCCTSICSLYQLENYCN
Sbjct 61 LQVGQVELGGGPGAGSLQPLALEGSLQKRGIVEQCCTSICSLYQLENYCN 110

CURSES!!! OUR THEORY IS RUINED! HOW DID NATURE EVER CREATE SUCH DIVERSITY?!?!?!?!?!

ETA For those who are curious, here is the result of the chimp preproinsulin searched against the NR database:
ref|NP_001008996.1| proinsulin precursor [Pan troglodytes] >s... 215 7e-55
ref|NP_000198.1| proinsulin precursor [Homo sapiens] >sp|P013... 212 5e-54
gb|AAP36446.1| Homo sapiens insulin [synthetic construct] >gb... 212 6e-54

[Dr Adequate]

I haven’t made any discovery. Thank you. At last you admit the truth.

All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works. You know, we have read your posts, so we know that that isn't true.

For example, you've also misreported the facts, misinterpreted the facts, lied, talked gibberish, made silly mistakes in basic mathematics, and raved about cheese.

I’m not the only one who understands this. If you claim that there is one other person in the world who has fallen for your silly gibberish, perhaps you could name him.

What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures. What a silly lie. I claim no such thing.

Since you ask, I think that combination therapy is better than monotherapy for HIV, just like every other evolutionist does, as you know perfectly well. I posted a citation from a 50 year old Nobel laureate speech that said the same thing. Actually, if you ever take the trouble to read the speech you're lying about, you'll find that he said no such thing, principally because HIV was then unknown.

We even patiently explained to you why it's better, remember? About, I don't know, a hundred pages back? Why haven’t you evolutionists explained this before? We did. About, I don't know, a hundred pages back?

Oh, that’s right; you say that n+1 selection pressures evolve more rapidly than n selection pressures. Reciting the same silly lie twice in the same post won't make it any truer, it just makes you slightly more boring.

[Dr Adequate]

Before I looked at Dr Schneider’s and Paul’s model, I didn’t understand how mutation and selection worked...I haven’t made any discovery.

[Kotatsu]

This was how I originally interpreted his question. You could imagine a universe where organisms were all related to each other, but didn't evolve. Instead of mutation and natural selection, you could have God the post-hoc Kludge Designer come in and incrementally "fix" his creation once in a while.

Or not even that if we imagine that the environment the creatures live in is completely homogeneous all the time, and there are endless resources. Of course, that kind of universe is even more unlikely, but it could perhaps exist in theory.

We could also use simple gene homology for this. It might not be a perfect model if we go at it blind to mutation mechanisms, but string similarity would certainly allow us to infer a tree of relationships among species.

I haven't read much about this, but you mean the sequence in which the genes on a particular chromosome, say, occurs, no? That's basically just the same as the sequence similarities, but at a higher level --- at least theoretically. As such, it's subject to the same lame objections as Kleinman has towards nucleotide sequence similarities, i.e. that we have no mechanism to get from one state to another (which of course is not true in the real world, but seems to be true in whatever bizarre world Kleinman inhabits).

Thus, while I understand that it's a good example, I think that for the purpose of arguing with Kleinman, polyploidisation is actually a better one, as it is instantaneous, we have known mechanisms from it, it is not dependant on mutations and selection, or sexual selection, and so on. But I do see your point. To a person educated in these matters, your example is as good as mine.

What about his inability to answer a direct question with a YES or a NO?

Well, since he doesn't understand the subject you are asking about, he doesn't know what is the correct answer and what is the incorrect one, and thus he cannot chose the latter just to be contrary. He cannot answer it, because he might by mistake chose the option which is actually correct, and then we'll go on and on about that forever.

The image that I linked in my previous post includes more than one event in vertebrates! That's definitely something I'll have to read up on over Thanksgiving break!

I think the ones Okano (if that's his name, I can't remember really) were postulating were the one just "after" the [i]Amphioxus[/quote] and the one just "after" the lamprey. I seem to recall that his polyploidisation events were basal to all of Vertebrata, but I can't remember where I read about it.

Regardless of that, I have always believed that polyploidisation seems to be one of those things that are underrated unduly, just like sympatric speciation. It's stuff that I feel are probably much more common than most people think, but which are not as common in vertebrates as in invertebrates, and thus it is generally disregarded.

I have no hard data to back this up with, though, just a feeling. However, your tree seems to give some vague support to the feeling, as does several papers I have read over the last few years.

No. I'm working on gene regulation in insects these days. Gene regulation is amazing, but I do miss investigating larger structural and comparative evolutionary questions about genomes. It was great to have such a deep sense of vast amounts of time in my every day work.

Fortunately, I think things will get interesting really fast with this insect stuff. We have a lot of fully sequenced genomes to work with these days, and the model organisms for development (fruit fly) and social behavior (honey bee) are closely related to all them.

I have just recently started my PhD and work with co-evolution of shore birds and their lice, which I think will be extremely interesting. Nothing really revolutionary, I expect, as I approach the matter from a systematic and alpha-taxonomical point of view. However, I already have some great ideas to test, and I am becoming more and more satisfied with having been given this opportunity every day.

I think co-evolution is another thing Kleinman will have a hard time explaining satisfactorily (1). Why would the phylogenetic trees of parasites and those of their hosts ever be similar if the two groups had not evolved in parallel? The theory of evolution explains this elegantly, of course, but if you reject this theory, how do you explain it? My guess is that it will be called yet another example of wishful thinking or so, just like phylogenetic trees in general.

Isn't whole-genome sequencing immensely expensive?

---
(1) Meaning something he will dismiss with a platitude, an insult, or a simply misunderstanding of the concept.

[Kotatsu]

I don't know anything about this protein. I went to NCBI. I got the sequence for human preproinsulin. I blasted (searched) it against the NR database (all the non redundant DNA we know of in the whole world.) Here are the first three hits:
ref|NP_000198.1| proinsulin precursor [Homo sapiens] >sp|P013... 214 2e-54
gb|AAP36446.1| Homo sapiens insulin [synthetic construct] >gb... 213 2e-54
ref|NP_001008996.1| proinsulin precursor [Pan troglodytes] >s... 212 5e-54

Pan troglodytes is chimp, in case you didn't know.

What are the percentage matches? I never learn to find my way around GenBank, as I use it so rarely (there are extremely few sequences there for the Clitellates I work with, and I haven't started looking for lice sequnces yet).

Also, as I have reread the abstract you linked to, could you explain tandem gene duplication for me? I'm not familiar with that term.

EDIT:
Hooray! 300 posts, of which I estimate at least 200 have been in this thread!

[Belz...]

Yes. Polyploidization can give common descent.

But isn't that still mutation ?

[Dr Adequate]

But isn't that still mutation ? I'd have said so.

[Belz...]

Why would you think that Shalamar is mediocre?

Which such a bad grasp of grammar, Klein, it's no wonder you think evolution is mathematically impossible by reading examples that contradict this.

You should know the answer to that one Belz, the fewer the selection conditions, the faster it evolves.

Yeah, but that doesn't answer my question. Do you contend that HIV is naturally under only a very few pressures ?

Belz, how many variants are there, 10?, 100?, 1000?, millions? Consider that for hemoglobin, there are only a few hundred variants of this gene that still give viability. In time, most or all variants of viable resistant HIV genes will be identified.

Answer the question, Klein: is it deterministic or not ?

[Kotatsu]

But isn't that still mutation ?

Hmmm. When Kleinman says "mutation", I always think of that as short-hand for "random point mutation" as the dropping of these words are the only thing that differs between his ramblings today and those of a year ago. Maybe he doesn't mean that, though, and I have misinterpreted him. It's similar to how "slow and eventually stop" has gradually changed to "confound" over a similar amount of time.

And yes, they would count as mutations, or not as mutations, depending on what you really call a mutation. I believe it could be argued that mutations actually change something in the genome, which polyploidisation events, strictly speaking, don't. It would depend on context, I believe.

EDIT:
I would call the mutations if asked, but I could also see the need for a subgrouping of mutations that actually by definition alter the exact sequences (random point mutations, gene duplications and so on) and those that don't necessarily do that (polyploidisation, and possibly other processes)

[sol invictus]

What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures.
What a silly lie. I claim no such thing.


What was claimed is that n+1 selection pressures evolve more rapidly per pressure than do n. So if t(n+1) is the time it takes 90% of the population to evolve in response to n+1 pressures, then t(n+1)/(n+1) < t(n)/n.

I demonstrated that this is the case using kleinman's own model (which he proposed and incorrectly analyzed a few pages back), as did rocketdodger with a somewhat more realistic model.

[Dr Adequate]

Take your list and account for the 150,000,000 base differences between humans and chimpanzees in 500,000 generations. We did.

If the problems with your memory persist, consult a doctor.

A competent doctor.

[delphi_ote]

Or not even that if we imagine that the environment the creatures live in is completely homogeneous all the time, and there are endless resources. Of course, that kind of universe is even more unlikely, but it could perhaps exist in theory.
Imagining unreal universes is fun... but mostly useless.
Thus, while I understand that it's a good example, I think that for the purpose of arguing with Kleinman, polyploidisation is actually a better one, as it is instantaneous, we have known mechanisms from it, it is not dependant on mutations and selection, or sexual selection, and so on. But I do see your point. To a person educated in these matters, your example is as good as mine.
I totally agree with you. I was just pointing out that there are more "large" features on the genome that point to common heredity.
He cannot answer it, because he might by mistake chose the option which is actually correct, and then we'll go on and on about that forever.
I'm so glad we're not going on forever and ever now. :D
I think the ones Okano (if that's his name, I can't remember really) were postulating were the one just "after" the [i]Amphioxus and the one just "after" the lamprey. I seem to recall that his polyploidisation events were basal to all of Vertebrata, but I can't remember where I read about it.
If you find out, send me the link!
Regardless of that, I have always believed that polyploidisation seems to be one of those things that are underrated unduly, just like sympatric speciation. It's stuff that I feel are probably much more common than most people think, but which are not as common in vertebrates as in invertebrates, and thus it is generally disregarded.
I think most people's common understanding of evolution is biased toward "human-like" evolution. One example of this that pops to mind of is genetic algorithms. "Crossover" or "mating" was included from the very beginning of the field, but most of evolution's heavy lifting, so to speak, was conducted without any kind of "mating."
I have just recently started my PhD and work with co-evolution of shore birds and their lice, which I think will be extremely interesting. Nothing really revolutionary, I expect, as I approach the matter from a systematic and alpha-taxonomical point of view. However, I already have some great ideas to test, and I am becoming more and more satisfied with having been given this opportunity every day.
Very interesting! What is your field of study? I'm in bioinformatics, so all the research I've done has been from the computational side of things.
My guess is that it will be called yet another example of wishful thinking or so, just like phylogenetic trees in general.
That's the problem. This denialist mentality takes every piece of evidence and tries to pedantically attack every detail of it. They never take a step back and look at the big picture. They never think, "Wow, all this evidence from all these different fields is consistent."
Isn't whole-genome sequencing immensely expensive?
Yes, but it's getting cheaper by the minute! There was a time when I could list all of the genome sequencing projects going on off the top of my head. Now, there are too many to keep track of. Very exciting times!

[delphi_ote]

What are the percentage matches? I never learn to find my way around GenBank, as I use it so rarely (there are extremely few sequences there for the Clitellates I work with, and I haven't started looking for lice sequnces yet).
If you get to a point where you need help using or understanding any of the bioinformatics applications or databases, I'd be glad to assist!
Also, as I have reread the abstract you linked to, could you explain tandem gene duplication for me? I'm not familiar with that term.
As I understand it, it's exactly what it sounds like. Large stretches DNA get copied in 5' -> 3', 5'->3' order. Some of those regions contain genes. When this kind of mutation happens, the organism ends up with two tandem copies of that gene.

[Dr Adequate]

What was claimed is that n+1 selection pressures evolve more rapidly per pressure than do n. So if t(n+1) is the time it takes 90% of the population to evolve in response to n+1 pressures, then t(n+1)/(n+1) < t(n)/n. The word "rapidly" is rather ambiguous, since it can refer either to rate or to duration, and you must know by now that if kleinman can misunderstand something, he will.

In my own model, I continued the simulation to fixation of all alleles. Hence, my own statement of my result was that if the selection pressures are simultaneous, then the rate of evolution (fixations/generation) increases with the number of selection pressures.

Mind you, kleinman managed to misunderstand that too, as you can see by his absurd lies about what I "claim".

[Dr Adequate]

That's the problem. This denialist mentality takes every piece of evidence and tries to pedantically attack every detail of it. Pedantry implies a certain degree of precision. What denialists do is seize on each point separately and use their powers of incomprehension to rephrase it as a vague gray flabby mush of nonsense. Then they whine about how the mess they've made is nonsense.

[Kotatsu]

I totally agree with you. I was just pointing out that there are more "large" features on the genome that point to common heredity.

Indeed. The very existence of discrete chromosomes and not just some sort of gene soup, and the usage of the same bases everywhere and the fact that while the same code is not used to decipher these bases into amino acids in all groups of organisms, the different codes --- as far as I am aware --- are at least consistent within groups and a billion other things could also be used for this purpose.

f you find out, send me the link!

I am not sure if this is the article I was thinking of (as I haven't looked in this folder of articles for a year or so), but the guy's name was Ohno, not Okano (1), and he published a book called "Evolution of Gene Duplication" with which you may be familiar; I have never even seen the book. However, the only article I could find in my Endnote register was Furlong & Holland, 2004. Biological Journal of the Linnean Society 82, 425-430. Mind you, I haven't looked at more than the headline of the article yet, so it could be an entirely different article I was thinking about. I have a few folders filled with the little buggers...

I think most people's common understanding of evolution is biased toward "human-like" evolution. One example of this that pops to mind of is genetic algorithms. "Crossover" or "mating" was included from the very beginning of the field, but most of evolution's heavy lifting, so to speak, was conducted without any kind of "mating."

This miscomprehension is not limited to evolution. I think anyone who's ever worked with invertebrates (apart perhaps from insects and invertebrates we eat, such as clams) will sooner or later find that no one can really understand why they do it, unless they are scientists themselves. It's the "stuffed animal syndrome" --- people care about cute animals which can be made into stuffed toys. If they can't, or the animal is in any way ugly, bothersome, slimy or very small, there seems to be no understanding of why anyone would ever want to do any research on them...

And I made the "mistake" of moving from slimy worms to lice, and no one understand why.

Very interesting! What is your field of study? I'm in bioinformatics, so all the research I've done has been from the computational side of things.

My work is two-fold. First of all an alpha-taxonomic inventory of the feather lice parasitizing birds of Sweden and the other Nordic countries. This is done for the Swedish Taxonomy Initiative, which aims to catalogue all multicellular organisms here. Second, I will do phylogenetic work on some genera of lice infesting shore birds, primarily the subfamily Calidrinae (Charadriiformes: Scolopacidae). In both of these projects, there'll be some description of new species (I've already found 12 presumably undescribed ones!) and some morphological work. In the latter, I will also erect phylogenies over the relevant bird species, something which has not been done before, and then compare the trees (if I can ever get the bloody programs to work). I will work primarily with PAUP* and MrBayes, but also with some strange programs I've never used before, like TreeMap, TreeFit and Parafit, but I haven't got these to work yet.

I collect all my material myself, and am in the process of applying for money to go to Japan next autumn and collect from Siberian shorebirds. As a spin-off project, I'll also collect from species and genera of birds which occur both in Sweden and in Japan (such as Anas, Emberiza, Corvus, Parus and so on) to see if the lice fauna is homogenous on the same species of birds across Eurasia. Further on, I hope I'll be able to collect in Canada and Australia as well, and maybe Israel. It's hard work, but VERY fun. There are some pictures of the practical part of my work in the Forum picture thread (just click on my profile, I don't have that many posts), if you're interested.

That's the problem. This denialist mentality takes every piece of evidence and tries to pedantically attack every detail of it. They never take a step back and look at the big picture. They never think, "Wow, all this evidence from all these different fields is consistent."

It could be worse, though. I was in a debate on the forum of a Swedish TV channel once, arguing against a bunch of creationists. One kept explaining different stuff in nature --- "Spiders use five different kinds of nets for different purposes!" --- and claiming that evolution had no explanation for that ---- I find it quite obvious that spiders would not wrap their eggs in the same sort of net that they use to wrap their prey... --- while another kept repeating that he was "just a simple carpenter and couldn't understand all those difficult words, but he had a gut feeling I might be correct in the details but not in the big picture". In the end, I had to resort to invectives and eventually got myself banned, I believe.

Yes, but it's getting cheaper by the minute! There was a time when I could list all of the genome sequencing projects going on. Now, there are too many to keep track of. Very exciting times!

It would be very interesting to try that some day, if and when I could get the funding. With Clitellates, we usually use six genes --- COI, ITS1+5.8S.ITS2, 18S, 28S, 16S, and 12S --- and with lice five --- EF1a, COI, 16S, 18S, and 12S. To me, it's always seemed so uneconomical, as we get good results from just this data. However, whole genome sequencing would perhaps give much better data.

---
(1) The Okano I was thinking about worked with cement glands in barnacles, by the way.

[rocketdodger]

The word "rapidly" is rather ambiguous, since it can refer either to rate or to duration, and you must know by now that if kleinman can misunderstand something, he will.

In my own model, I continued the simulation to fixation of all alleles. Hence, my own statement of my result was that if the selection pressures are simultaneous, then the rate of evolution (fixations/generation) increases with the number of selection pressures.

Mind you, kleinman managed to misunderstand that too, as you can see by his absurd lies about what I "claim".

Exactly. This is why I have been careful to always say "rate" as well, just like Adequate.

It is a testimony to the stupidity of Alan Kleinman that he can take my statement "for some n != 0, the average rate of fixation under n + 1 pressures is higher than the average rate of fixation under n pressures" and twist it into "n + 1 pressures evolve faster than n pressures." How the f--- does a pressure even "evolve" anyway?

[Belz...]

This miscomprehension is not limited to evolution. I think anyone who's ever worked with invertebrates (apart perhaps from insects and invertebrates we eat, such as clams) will sooner or later find that no one can really understand why they do it, unless they are scientists themselves. It's the "stuffed animal syndrome" --- people care about cute animals which can be made into stuffed toys. If they can't, or the animal is in any way ugly, bothersome, slimy or very small, there seems to be no understanding of why anyone would ever want to do any research on them...

They don't ? I've always found ugly things fascinating !!!

And... shrimps are cute!

[sol invictus]

In my own model, I continued the simulation to fixation of all alleles. Hence, my own statement of my result was that if the selection pressures are simultaneous, then the rate of evolution (fixations/generation) increases with the number of selection pressures.


I didn't realize you had also done a simulation (I haven't read the entire thread)... in any case, thanks for the comment - your terminology is more precise and less susceptible to distortion than mine.


It is a testimony to the stupidity of Alan Kleinman that he can take my statement "for some n != 0, the average rate of fixation under n + 1 pressures is higher than the average rate of fixation under n pressures" and twist it into "n + 1 pressures evolve faster than n pressures."

Right - so we're all in agreement. I wonder whether I can reproduce your results in my simplistic model.

Question to both of you: does your rate scale as log(n)/n for large n?

[kleinman]

Joobz, you just love to speculate and extrapolate from your speculations. Take your list and account for the 150,000,000 base differences between humans and chimpanzees in 500,000 generations and don’t forget to tell us what the selection pressures and target genes for these selection pressures are.

So I guess you two are ready to explain to us what the components of the DNA replicase system were doing before DNA could be replicated. Tell us what the function of helicase and gyrase were. That should be a good story. Joobz, you can tell us this after you show us how ribose can be generated nonenzymatically.So you can't answer any of my questions?

ETA: pretending your numbers are correct:
~4% difference between genomes over 500,000 generations (since the split is what I assume you are refering to) results in a 0.000008% change per generation. Considering that human genome variablity is somewhere arround 0.08% between individuals, this mutation rate relates to 1/10,000th of the variation between humans. These numbers are far from impossible.
Have you asked any questions? All you have done is post a list of speculations.

So let’s consider your computations and assumptions you have made.
Horribly wrong assumptions in the joobz calculation:
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
10.) And the really, really horrible assumption is that n+1 selection pressures evolve faster than n selection pressures.

Hey joobz, when are you going to take up that $10,000 wager that you can’t prove your claim that my PhD thesis has mathematical or empirical irregularities. Let’s see you put your money where your big mouth is.
Does anyone else notice how Kleinman has been conveniently ignoring my last post?
I’m not ignoring your posts, we are just waiting for you to post your parametric studies of you model which show that n+1 selection pressures evolve more rapidly than n selection pressures. You could also post a real example of your model as well, that would be interesting. Wait a minute you did post the results from your parametric study, here it is:
I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.
I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works. I haven’t made any discovery. All I am doing is reporting the mathematical and empirical facts of how mutation and selection actually works.All of which is entirely defeated by fact that ev and all of your citations show faster evolutionary change under the influence of a dominant pressure.
That’s the point member of the bar. A single dominant selection pressure is the only case where you get rapid evolutionary change. Additional selection pressures whether weak or strong slow the sorting/optimization process.
Both ev and reality are consistent -- evolution happens under a dominant selective pressure -- a circumstance which is relatively routine in nature.
So defender of the mathematically illogical and irrational view of mutation and selection, it should be easy for you to tell us what that selection pressure is that transforms reptiles into birds.
If life, and as a result, humans, were 'created' and thus 'intelligently designed', then why did the designer do such a TERRIBLE job at it?
If life, and as a result, humans, were ‘mutated and selected’ and thus ‘evolved’, then why did evolution do such a TERRIBLE job at it?

Hey Shalamar, when was the last time an evolutionist opened a hospital? When you do, I have a suggestion for the name, “The Natural Selection Hospital of the Most Fit”.
Kotatsu, once you understand that mutation and selection is simply a sorting/optimization problem, you will understand why this process can not transform large numbers of genes simultaneously. I harbor no ill will toward you or anyone else. I just think your ideas are illogical and irrational. They don’t make mathematical or empirical sense.Do you have any useful response to my two longer posts? I mean the one about polyploidisation giving rise to common descent in a way we can actually measure and infer more easily than (random point) mutation and selection, and the elaboration of the dinosaur-to-bird evolutionary scenario I provided you with? If at any point in either of those two posts I am unclear or too technical --- I understand, for instance, if the polyploidisation post may be too convoluted for someone who has never specifically studied the area --- I would be happy to provide more details and explain it in simpler terms. Just say the word. Also: if you have problem accessing the papers I cite, I would be glad to send them to you. I wouldn't want to just copy and paste, sinc ethat could lead to allegations of cherry picking; far better for you to read the papers in full and get the whole picture.
Kotatsu, why don’t you tell us how polyploid genes are transformed into new genes? Once you figure out it requires mutation and selection then you can study how mutation and selection actually works.
Perhaps you think because humans and chimpanzees have the same insulin might make evolutionists think we arose from a common ancestor but then you have to show why humans and chimpanzees have different preproinsulin.I don't know anything about this protein. I went to NCBI. I got the sequence for human preproinsulin. I blasted (searched) it against the NR database (all the non redundant DNA we know of in the whole world.) Here are the first three hits:
Delphi, I already did the search and the results are already posted on this thread. So, there is diversity between human and chimpanzee preproinsulin but no diversity in the insulin of humans and chimps. Since you claim that humans and chimps came from a common ancestor, do care to show us how this happened?
I haven’t made any discovery.Thank you. At last you admit the truth.
But unlike you, I don’t perpetuate a myth that has led to the premature deaths of millions of HIV sufferers and others suffering from diseases that are subject to the principles of mutation and selection. Adequate, you have abandoned your profession as a mathematician and embraced an illogical and irrational belief system.
What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures.What a silly lie. I claim no such thing.
Sure you have Adequate, don’t you remember what you said about your silly graph? Here, let me remind you.
All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then I asked you for a real example of your model and you said this:
So far as I know, no-one has done the experiment.
Adequate, read on and I’ll post more citations which show the exact opposite of what you claim. Reality shows that combination selection pressures profoundly slow the evolutionary process. Adequate, how did you manage to get the mathematics of mutation and selection so wrong?

Here are some more examples of how mutation and selection actually works, and it works like Dr Schneider’s ev program works. Combination selection pressures profoundly slow the evolutionary, sort/optimization process.
http://www.blackwell-synergy.com/doi/full/10.1111/j.1469-0691.2006.01492.x (http://www.blackwell-synergy.com/doi/full/10.1111/j.1469-0691.2006.01492.x)
Although mutational resistance can be selected in vitro, it may not represent the most prevalent resistance mechanism in clinical isolates of a particular species. For example, chloramphenicol-resistant mutants of Staph. aureus have 23S rDNA mutations and may be cross-resistant to linezolid [44], but most clinically significant chloramphenicol resistance in this species is mediated by acetyltransferase enzymes [45]. However, in certain species, mutation is the main, or sole, cause of clinical resistance problems. One of the best examples is Mycobacterium tuberculosis. Resistance to all therapeutic agents in this species is mediated by mutations: i.e., rifampicin resistance in rpoB; isoniazid resistance in katC, inhA, oxyR, ahpC and furA; streptomycin resistance in rrs and rpsL; pyrazinamide resistance in pncA; ethambutol resistance in embB; and fluroquinolone resistance in gyrA and gyrB[46]. The treatment of tuberculosis requires combination therapy to tackle a difficult pathogen that causes prolonged disease [46,47]; monotherapy is not an option because of the very real risk of resistance emerging. Combination therapy decreases, but does not eliminate, this risk, which is influenced by the frequencies of mutation to resistance for each individual agent, and by the number of bacteria at a focus of infection [46].

Multidrug therapy is also recommended for Helicobacter pylori infections, typically comprising triple combination regimens, including two of clarithromycin, metronidazole, amoxycillin or tetracycline, plus a proton pump inhibitor [48]. Chromosomal mutations are responsible for resistance of H. pylori to clarithromycin (in 23S rRNA) [49–52], amoxycillin (changes in penicillin-binding protein 1) [53], metronidazole (in rdxA and other genes) [48], tetracycline (in 16S rRNA and other undefined genes) [54,55] and, in vitro, streptomycin (in rpsL) [56].
http://www.journals.uchicago.edu/CID/journal/issues/v41nS4/36160/36160.html (http://www.journals.uchicago.edu/CID/journal/issues/v41nS4/36160/36160.html)
Widespread drug resistance in parasites aggravates the burden of malaria. The extent of the problem is due mainly to the limited armamentarium of drugs used thus far to treat malaria and to policies and practices constrained by limited resources. All drugs in use are affected except, thus far, artemisinin derivatives. The scale and impact of resistance has been underestimated, leading to the continued use of failing drugs, which contributes to the rise in resistance and increased morbidity and mortality due to malaria. Pharmacological, epidemiological, and operational aspects factor the development and spread of resistance. Although the problem is complex, much can be done to reverse the course of events: adopt adequate tests to assess resistance, encourage and sustain development of new drugs, protect drugs against resistance through use of combinations, expand access to prompt and effective treatment, and promote evidence-based policies and sensible practices. The current situation favors the development of sensible strategies to restrain resistance.
and
De novo selection of resistant mutants. Resistance occurs as a result of spontaneously occurring mutations or gene amplification. Drug-resistant mutants are selected in the presence of levels of drug that are inadequate to suppress their growth. Considering the size of the malaria genome (3 × 10^7 bp), the number of parasites in 1 infected individual (10^8-10^12), and the mutation rate caused by replication errors by eukaryotic DNA polymerases (1 in 10^12), parasites with randomly mutated genomes are likely to occur in any infection. However, resistance is considerably rarer in vivo, being influenced by drug type, the underlying resistance mechanism, and the patient's state of acquired immunity. In some cases, there are mutations in the gene encoding the drug target. Single or multiple mutations of the same gene may accumulate, conferring increasing degrees of resistance. The DHFR of biguanide antifolates and the cytochrome b of atovaquone are particularly prone to resistance (per-parasite resistance mutation frequencies are 1 in 10^11 and 1 in 10^12, respectively). In other cases, resistance requires multigenic, independent mutations to be expressed. Typically, this applies to chloroquine (per-parasite resistance mutation frequency is 1 in 10^-19). These features explain why chloroquine was effective for several decades before it was rendered ineffective, whereas antifolates, even in combinations targeting 2 different enzymes (DHFR and DHPS), have a very short useful therapeutic life span.

Critical to what happens next is the number of parasites exposed to the drug and its pharmacokinetic and pharmacodynamic characteristics. Most vulnerable to resistance are those drugs with a slow onset of action (i.e., low killing rates or parasite reduction ratios) and slow elimination profiles (long half-lives), with a long "selective window" (corresponding roughly to the period during which levels are ~20%-80% of the drug's maximum inhibitory concentration) [26]. The antifolate combination pyrimethamine-sulfadoxine, with its long half-life and a resistance that develops through single-point mutations, is particularly prone to resistance
and
Preserving the life spans of both current and future antimalarial drugs is essential. Clearly, a move away from sequential monotherapy is now warranted and supported by evidence and is endorsed by the WHO [56]. The principle of combining drugs with different modes of action is common practice in other areas of infectious diseases, such as tuberculosis and HIV/AIDS, but is very recent in malaria.
and
ACTs are a way to enhance treatment efficacy, prevent or retard the development of drug resistance, and preserve valuable antimalarial drugs. The scientific rationale for using ACTs is sound for several reasons [57, 58]. In general, combining different drugs with independent modes of action will increase the chances of killing parasites and greatly decrease the probability that an infected patient will develop resistance to both drugs. In particular, artemisinins cause a rapid and substantial reduction in the parasite biomass, irrespective of the parasites' resistance to other antimalarials. The remaining parasites are then killed off by high concentrations of the companion drug.
This last citation for this post is for those of you who claim that I only consider point mutations.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1075723 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1075723)
Resistance to antiretroviral drugs is generally conferred by specific amino acid substitutions, rather than insertions or deletions, in reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1). The exception to these findings is the amino acid insertions found in the β3-β4 loop of the RT enzyme in response to treatment with nucleoside reverse transcriptase inhibitors. This insert consists most commonly of two amino acids, but we describe in detail the evolution of a variant with an 8-amino-acid (aa) insert in a patient treated with zidovudine (ZDV) and 2′-3′-dideoxycytidine (ddC). The 24-nucleotide insert is a partial duplication of local sequences but also contains a sequence segment of unknown origin. Extensive sequence analysis of longitudinal patient samples indicated that the HIV-1 population prior to the start of therapy contained not the wild-type amino acid 215T in RT but a mixture with 215D and 215C. Treatment with ZDV and subsequent ZDV-ddC combination therapy resulted in the evolution of an HIV-1 variant with a typical ZDV resistance genotype (41L, 44D, 67N, 69D, 210W, 215Y), which was slowly replaced by the insert-containing variant (41L, 44D, insert at position 69, 70R, 210W, 215Y). The latter variant demonstrated increased resistance to a wide range of drugs, indicating that the 8-aa insert augments nucleoside analogue resistance. The gain in drug resistance of the insert variant came at the expense of a reduction in replication capacity when assayed in the absence of drugs. We compared these data with the resistance and replication properties of 133 insert-containing sequences of different individuals present in the ViroLogic database and found that the size and actual sequence of the insert at position 69 influence the level of resistance to nucleoside analogues.
How can that be, combination therapy still works with HIV yet this virus does mutations other than point mutations?

Well, someday you evolutionists will learn how mutation and selection actually works. You could start with a study of Dr Schneider’s ev computer simulation of the process, then these hundreds of citations I have and will continue to post more will make sense to you. Then you will understand that Adequate’s claim that n+1 selection pressures evolve more rapidly than n selection pressures is nothing more than irrational and illogical thinking that if perpetuated will cause the unnecessary premature death of millions of people suffering from diseases subject to the principles of mutation and selection.

[sol invictus]

Sure you have Adequate, don’t you remember what you said about your silly graph?

Kleinman, surely you know the meaning of the word "rate"?

No one has said that the time required for n+1 mutations is less than the time for n. What has been said is that the RATE at which those mutations occur increases with n. As I have shown, and you agreed, that is true even in the simple model that you yourself proposed.

I'm sure you're capable of understanding that simple distinction.

[delphi_ote]

Delphi, I already did the search and the results are already posted on this thread. So, there is diversity between human and chimpanzee preproinsulin but no diversity in the insulin of humans and chimps.
By "diversity" you mean a few amino acid substitutions?! You realize the number of DNA mutations that requires is on the order of 10s, right? Is this really your argument? You don't understand how mutation could change a handful of amino acids over the course of millions of years?

This is officially the dumbest thing you've said in this entire thread.

[kleinman]

Sure you have Adequate, don’t you remember what you said about your silly graph?Kleinman, surely you know the meaning of the word "rate"?

No one has said that the time required for n+1 mutations is less than the time for n. What has been said is that the RATE at which those mutations occur increases with n. As I have shown, and you agreed, that is true even in the simple model that you yourself proposed.

I'm sure you're capable of understanding that simple distinction.
If you are talking about Dr Schneider’s peer reviewed and published model of random point mutations and natural selection, what it shows is that the ability of a system to sort and optimize is strongly dependent on the number of optimization conditions. The greater the number of optimization conditions, the more difficult for the sorting of mutations for each of the optimization conditions.

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs.

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then I asked you for a real example of your model and you said this:
So far as I know, no-one has done the experiment.
And rocketdodger said this:
The model is just a quick and dirty simulation of mutation and selection. It shows that additional selective pressures do not hinder the sorting mechanism like you claim it does. In particular, adding more and more pressures can easily bring the time to fixation per pressure down to within 200% of the time to fixation for a singly applied pressure. I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.
We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene.

[kjkent1]

That’s the point member of the bar. A single dominant selection pressure is the only case where you get rapid evolutionary change. Additional selection pressures whether weak or strong slow the sorting/optimization process.Yes, that "is" the point. Ev shows different convergence times when altering its mistake weights. Convergence appears to be normally distributed with the mean average at the point where all three selection pressures are equal. This is a clear indication that even the three selection pressures found in ev have different intensities.

You claim that convergence is much more rapid with only one pressure active. Assuming that pressure disabled is the negative extreme, and single pressure enabled is the positive extreme, then it is reasonable to assume that as relative intensity increases, generation time to convergence approaches the mean average.

So, it's not sufficient to simply state that multiple pressures confound evolutionary progress. The relative intensity of those pressures must be considered.

Also, ev's selective mechanism treats the weights as linear. That is, an n+1 mistake weight is 1 unit more selective than an n mistake weight. But, is this how real life selective pressures function? It could be that certain selective pressures are exponentially more powerful than others. I doubt that there's any research in this area, which means no way to know.

But, clearly, intensity is a very important factor, and you are discounting that factor to zero, by claiming that multiple selective pressures confound evolution. The fossil record shows otherwise.

So defender of the mathematically illogical and irrational view of mutation and selection, it should be easy for you to tell us what that selection pressure is that transforms reptiles into birds.
Behold, oh, obsessive-compulsive overconfident insulter of others who have reasonable counterarguments, The geologic record shows what selective pressures were at work throughout history. It is those pressures in concert with unpredictable mutation events which caused the transformation from one species to another.

And, the proof of this is the fossil record, which shows that such transformations took place during the same time that the geologic record shows the selective pressures which were at work.

Had there been a massive global flood only 6,000 years ago, we would see an entirely different geological record, and almost certainly an entirely different fossil record, too.

We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene. LOL! A day without kleinman's narcissism is like a day without sadness. Regardless, we have posted many citation which have disposed of your arguments. You just don't like them. And, as you view yourself as the sole arbiter of what is and is not true, you continue to misrepresent the facts -- said facts which may easily be witnessed by anyone with the energy to review this thread.

[rocketdodger]

Kleinman, you pathetic fool. You resort to quoting obsolete statements in order to disguise your stupidity?

Yes, I forgot the settings I used in a run -- so f---ing what? In a post since then, which I know you have read since you responded to it you idiot, I gave you the exact settings I used to get a set of results that prove you wrong.

Then, you claim my results must not be typical of even my own simulation, because they show you are wrong. In post #6516 I explicitly address all of the issues you brought up. Instead of responding to that, and admitting that you really are wrong, you blow a smokescreen by quoting statements made by Adequate and me that are no longer relevant.

The issue, Kleinman, is not that we have shown evolution speeds up under more selective pressures. We can't claim that, because nobody has actually tried to enumerate the selective pressures acting on populations. Duh. The issue is that both Dr. Adequate and I have shown you sorting algorithms, modeled on the general mechanism of mutation and selection, that are not always confounded by additional sorting conditions. It is this simple -- you have claimed time and time again that ALL sorting algorithms are confounded by additional sorting conditions. We have shown this to be untrue.

Both Adequate and I have studied our algorithms. Our results are not anomalies. We have shown you that all of the issues you claim could "affect" the results are in fact non-issues because we either already account for them or they would in fact not affect the results.

That is actually more than we need to do, because you have no proof at all of your own claim. All you have are studies featuring only a few pressures, and a program that features at most three pressures. You claim to have done parametric studies. How can you do a parametric study on the effects of adding selective pressures when the very program you are touting caps the number at 3? My parametric study of my program shows that for a genome of any appreciable size the threshold number of pressures where additional pressures start increasing the average fixation rate is well over 10. Do you have any data that can refute this? No, you don't. So until you can actually show me and everyone here why my algorithm is not a sorting algorithm, your theory is baseless.

Of course you will respond with some rubbish that has nothing to do with this, in order to dodge the issue once again. Don't you see how pathetic your debate tactics are? Given that you think you are actually right, it makes you look like an a--. Have we dodged ANY of the issues you bring up? NO. Have we ever mangled your words into something you don't actually mean? NO. If you are right about evolution, then why are you the one using the unfair debate tactics? One would think it would be the other way around.

[kleinman]

That’s the point member of the bar. A single dominant selection pressure is the only case where you get rapid evolutionary change. Additional selection pressures whether weak or strong slow the sorting/optimization process.Yes, that "is" the point. Ev shows different convergence times when altering its mistake weights. Convergence appears to be normally distributed with the mean average at the point where all three selection pressures are equal. This is a clear indication that even the three selection pressures found in ev have different intensities.

You claim that convergence is much more rapid with only one pressure active. Assuming that pressure disabled is the negative extreme, and single pressure enabled is the positive extreme, then it is reasonable to assume that as relative intensity increases, generation time to convergence approaches the mean average.
If you doubt my claim, set any two of the three weights for the selection pressures to zero and verify that the number of generations for convergence is far smaller than when trying to converge all three conditions simultaneously. This is true beyond a shadow of a doubt.
So, it's not sufficient to simply state that multiple pressures confound evolutionary progress. The relative intensity of those pressures must be considered.

Also, ev's selective mechanism treats the weights as linear. That is, an n+1 mistake weight is 1 unit more selective than an n mistake weight. But, is this how real life selective pressures function? It could be that certain selective pressures are exponentially more powerful than others. I doubt that there's any research in this area, which means no way to know.

But, clearly, intensity is a very important factor, and you are discounting that factor to zero, by claiming that multiple selective pressures confound evolution. The fossil record shows otherwise.
Kjkent1, it is that simple to say that multiple selection pressures confound the evolutionary process. This is how sorting/optimization problems work. Now your claim that the weight factor has a linear behavior is completely wrong. The weight factor has a highly nonlinear affect on the generations for convergence. That is why there is a huge difference between the generations for convergence when you set two of the three selection conditions to zero. If the weight factors were linear, setting two of the three conditions to zero should give a generations of convergence of 1/3 that of converging all three conditions simultaneously, instead, it take many orders of magnitude few generations to converge any one selection condition than all three selection conditions. That also happens to be what the hundreds of real examples of mutation and selection shows.

Now I can understand your desire to change the topic to evolutionist Rorschach tests but since we are talking about the mathematics of mutation and selection and the empirical evidence which shows that the evolutionist interpretation of this evidence is mathematically and empirically impossible.
So defender of the mathematically illogical and irrational view of mutation and selection, it should be easy for you to tell us what that selection pressure is that transforms reptiles into birds.Behold, oh, obsessive-compulsive overconfident insulter of others who have reasonable counterarguments, The geologic record shows what selective pressures were at work throughout history. It is those pressures in concert with unpredictable mutation events which caused the transformation from one species to another.

And, the proof of this is the fossil record, which shows that such transformations took place during the same time that the geologic record shows the selective pressures which were at work.

Had there been a massive global flood only 6,000 years ago, we would see an entirely different geological record, and almost certainly an entirely different fossil record, too.
Kjkent1, it’s all about what you obsess on. You are obsessing on a mathematically and empirically impossible idea. I’m not surprised that you would want to talk about a flood since the theory of evolution is sinking like the Titanic after hitting an iceberg. Only in this case it is a mathematical and empirical iceberg. Perhaps you would like to set up an orchestra on the deck of the theory of evolution so you could listen to some classical music as the theory sinks to the depths.
We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene. LOL! A day without kleinman's narcissism is like a day without sadness. Regardless, we have posted many citation which have disposed of your arguments. You just don't like them. And, as you view yourself as the sole arbiter of what is and is not true, you continue to misrepresent the facts -- said facts which may easily be witnessed by anyone with the energy to review this thread.
You find it narcissistic when I post real repeatable and measurable examples of mutation and selection? You evolutionists must hate yourselves. That explains why there are so many of you evolutionists. Misery loves company.

[kjkent1]

Kjkent1, it is that simple to say that multiple selection pressures confound the evolutionary process. This is how sorting/optimization problems work. Now your claim that the weight factor has a linear behavior is completely wrong. The weight factor has a highly nonlinear affect on the generations for convergence. That is why there is a huge difference between the generations for convergence when you set two of the three selection conditions to zero. If the weight factors were linear, setting two of the three conditions to zero should give a generations of convergence of 1/3 that of converging all three conditions simultaneously, instead, it take many orders of magnitude few generations to converge any one selection condition than all three selection conditions. That also happens to be what the hundreds of real examples of mutation and selection shows.Oh, my bovine excretionary friend, you are so mercifully free of the ravages of intelligence.

If you set all three selective weights to 1, the convergence will be identical to setting all three weights to 100, or to any other number. It's only when you set the weights to different numbers that you observe different generational times to convergence. This demonstrates both that the RELATIVE weight is significant, and that the various possible convergence outcomes are normally distributed centering around the mean of all three weights set to the same number.

It should be obvious that in the real world, various selective pressures will exhibit all sorts of different outcomes based on their relative weight. A meteor strike that upsets the global environment and radically changes the air temperature is much stronger than, shall we say, a one year drought that reduces water flow in a river by a few cubic meters per hour.

As for your reflections re narcissism, you really need to spend a little more time praying on the subject. The fact that you don't see just how arrogant you are, clearly must affect your ability to render care to your patients. Everyone makes mistakes, Alan -- even you. And, at the moment, you are making a big one by proclaiming that selective intensity is meaningless to the biological evolutionary process.

[Dr Adequate]

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs. I have not, of course, said that, which is why you cannot quote me saying that.

Adequate said this:
Yes, I said that. Because it's true.

That's why I said it, and why you can actually quote me saying it, and why you can't produce any counterexample.

And then I asked you for a real example of your model and you said this: Yes, I said that. Because it's true.

That's why I said it, and why you can actually quote me saying it, and why you can't produce any counterexample

We all wait for you evolutionists to post a single real example of your irrational and illogical thinking. But, alas for you, there are no examples of our "irrational and illogical thinking".

On the other hand, I continue to post citation after citation which shows that evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure targeting a single gene. We all know that this isn't true, remember?

[joobz]

Have you asked any questions? All you have done is post a list of speculations.Ah, can't find any problems with it can you? How sad for you.



So let’s consider your computations and assumptions you have made.
Horribly wrong assumptions in the joobz calculation:
this should be fun, considering I made none of these assumptions. Here we go:
1.) Mutation rate remains constant
No it doesn't you are correct. I was simply showing that the mutation rate must be equal to or faster than 0.0000085% base/generation change cummulatively. This allows for variation imposed emergence as well. Not very hard to acheive and mutation rate doesn't need to be constant.
2.) Mutation rate is known
I don't know it. I simply gave a change that would be needed. Is an average 0.0000085% base change/generation too fast?
3.) Number of selection pressures for all species for all time in all areas is known
It isn't known. You are correct. Is an average 0.0000085% base change/generation too fast?
4.) Number of selection pressures is constant
it isn't constant. you are correct. I'm glad we agree. Again, Is an average 0.0000085% base change/generation too fast?
5.) Selection pressure magnitude is constant and equal for all pressures
Again, you are correct. it isn't constant. you are correct. I'm glad we agree. Is an average 0.0000085% base change/generation too fast?
6.) Point mutations are the only mutation/adaptation mechanism
You are so right. variation mutations can occur in different individuals and recombine together. This means that the average 0.0000085% base change/generation isn't only in one individual and that varation in population can speed this along. WOW, I'm glad I didn't assume this was the only important method of adaption. That would be stupid. Who would make such a dumb conclusion?
7.) defining selection pressure is unimportant
I do assume this, you are correct. I'm only looking the seperation between human and chimp, and not considering relative selection pressures. I can assume based upon living habits that the protohuman protochimp populations filled different evolutionary nitches. So what bases were being fixed are different. Interestingly, the growth of variations can occur in both the chimp and human populations independantly. This allows for even more rapid seperation between species.
8.) slow equals stop
No obviously, I would never make this dumb statement. After allit 0.0000085% base change/generation is rather slow. But it most certainly isn't a stop.

9.) Mutation is non-random
Nope, I'm counting on it being rather random.

10.) And the really, really horrible assumption is that n+1 selection pressures evolve faster than n selection pressures.
Interestingly, my argument has nothing at all to do with this. Again, Is an average 0.0000085% base change/generation too fast?

Hey joobz, when are you going to take up that $10,000 wager that you can’t prove your claim that my PhD thesis has mathematical or empirical irregularities. Let’s see you put your money where your big mouth is.Why would I care about what is obviously unimportant and had little to no impact in the scientific community?

[Dr Adequate]

Kleinman, surely you know the meaning of the word "rate"?

No one has said that the time required for n+1 mutations is less than the time for n. What has been said is that the RATE at which those mutations occur increases with n. As I have shown, and you agreed, that is true even in the simple model that you yourself proposed.

I'm sure you're capable of understanding that simple distinction. What in the world makes you sure of that?

He seems to have a real mental block when it comes to math, even the grade-school stuff.

[Dr Adequate]

I didn't realize you had also done a simulation (I haven't read the entire thread) ... Yes, it appears that three of us have independently simulated mutation and selection and got the same results.

Results here. (http://forums.randi.org/showthread.php?p=3097224)

The function is here (http://forums.randi.org/showthread.php?p=2805700&highlight=begin#post2805700); call it from some sort of output routine with pop set as a constant.

... in any case, thanks for the comment - your terminology is more precise and less susceptible to distortion than mine. Which still doesn't make it kleinman-proof, as you can see --- the man is capable of misunderstanding anything, no matter how precisely stated.

Question to both of you: does your rate scale as log(n)/n for large n? I didn't think to look. It might be worth checking --- that looks like the sort of thing one might demonstrate directly from probability theory, without this fussing about with simulations.

[kleinman]

Kjkent1, it is that simple to say that multiple selection pressures confound the evolutionary process. This is how sorting/optimization problems work. Now your claim that the weight factor has a linear behavior is completely wrong. The weight factor has a highly nonlinear affect on the generations for convergence. That is why there is a huge difference between the generations for convergence when you set two of the three selection conditions to zero. If the weight factors were linear, setting two of the three conditions to zero should give a generations of convergence of 1/3 that of converging all three conditions simultaneously, instead, it take many orders of magnitude few generations to converge any one selection condition than all three selection conditions. That also happens to be what the hundreds of real examples of mutation and selection shows.If you set all three selective weights to 1, the convergence will be identical to setting all three weights to 100, or to any other number. It's only when you set the weights to different numbers that you observe different generational times to convergence. This demonstrates both that the RELATIVE weight is significant, and that the various possible convergence outcomes are normally distributed centering around the mean of all three weights set to the same number.
So is this how you draw the conclusion that ev treats the selection weights as linear? The convergence of ev is not linear with the weight factors, in fact the behavior is highly non-linear. Setting two of the three weight factors to zero demonstrates this fact. Nothing affects the generations for convergence in ev more than the number of selection conditions. Even when ev fails to evolve all three selection conditions simultaneously, single selection conditions still evolve to convergence with the selection condition.
It should be obvious that in the real world, various selective pressures will exhibit all sorts of different outcomes based on their relative weight. A meteor strike that upsets the global environment and radically changes the air temperature is much stronger than, shall we say, a one year drought that reduces water flow in a river by a few cubic meters per hour.
The principle that you are having difficulty understanding is if you take a given set of selection conditions then add an additional selection condition, it slows evolution of all the selection conditions. This is what ev is showing and this is what the citations I have posted is showing. This is how sorting/optimization problems work. There is nothing linear about the behavior of these problems. They are highly sensitive to the number of selection (optimization) conditions. Even only three selection conditions slow the evolutionary process profoundly as shown in ev and in the real examples of mutation and selection as well.
As for your reflections re narcissism, you really need to spend a little more time praying on the subject. The fact that you don't see just how arrogant you are, clearly must affect your ability to render care to your patients. Everyone makes mistakes, Alan -- even you. And, at the moment, you are making a big one by proclaiming that selective intensity is meaningless to the biological evolutionary process.
Only an evolutionist would think it is arrogant to show how mutation and selection works in reality. 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?
I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs.I have not, of course, said that, which is why you cannot quote me saying that.
No problem Adequate, here’s your post again and let’s here you contradict yourself again.
All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then Adequate goes on to say this:
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And
So far as I know, no-one has done the experiment.
and
and too bad you don’t have any empirical examples of your silly graph ...As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve more rapidly than n selection pressures or joobz’s speculation of abiogenesis by “cooperative” chemistry.
http://forums.randi.org/images/smilies/doglaugh.gif

[Dr Adequate]

What you do claim Adequate is that n+1 selection pressures evolve more rapidly than n selection pressures.
What a silly lie. I claim no such thing.
Sure you have Adequate What a silly lie. I have claimed no such thing.

[Dr Adequate]

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve more rapidly than n selection pressures ... What a silly lie. I claim no such thing.

[rocketdodger]

Yet more posts from Kleinman that contain no logical arguments whatsoever. And he still hasn't responded to the fact that the foundation of his theory has been demonstrated to be untrue (using independently created models, I would add).

Kleinman, how many posts will you make before you actually address the issue of your claim about sorting/optimization algorithms being proven false? Can you show anyone here why the algorithms Adequate and I use are not sorting algorithms?

[Belz...]

I see the laughing dog's been brought back into play.

We must be on to something.

[Belz...]

Yet more posts from Kleinman that contain no logical arguments whatsoever. And he still hasn't responded to the fact that the foundation of his theory has been demonstrated to be untrue (using independently created models, I would add).

Kleinman, how many posts will you make before you actually address the issue of your claim about sorting/optimization algorithms being proven false? Can you show anyone here why the algorithms Adequate and I use are not sorting algorithms?

Kleinman has a way of wording his theory, though, that seems well-learned to those who don't know better. That's why I was a little unsure at the beginning of this thread, because I couldn't spot anything wrong with his argument.

But once you learn more about the subject, Kleinman's flaws (or lies) become readily transparent.

[Dr Adequate]

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs. I have not, of course, said that, which is why you cannot quote me saying that. No problem Adequate ... Well, there is in fact a kind of teensy-tiny problem, which is that you have not, in fact quoted me "alleging" that "the greater the number of optimization conditions, the faster the sort occurs."

In fact, you have just quoted me as saying that:

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious. You even highlighted it in red, so that no-one could possibly miss out on the difference between what I actually claim, and what you claim I claim.

[Dr Adequate]

Let's help kleinman out by putting it in one post.

He can even link to it, if he ever learns to use the forum controls.

(1) With simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

(2) More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

[kleinman]

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve more rapidly than n selection pressures ...What a silly lie. I claim no such thing.
Not only did you say this, you admitted contradicted yourself when you then said that your silly graph shows that more optimization takes more time. Then when asked to present a real example of this, you finally admitted that you had no real examples of you irrational and illogical conclusion. Let’s remind the readers of what you said:
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then Adequate goes on to say this:
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And
So far as I know, no-one has done the experiment.
and
and too bad you don’t have any empirical examples of your silly graph ...[quote="Adequate"]As I have explained to you, I produced the model because I've not heard of this precise experiment being done.


If physicians and scientists listen to your irrational and illogical thinking, it would lead to increases in premature death of people suffering from diseases subject to the mutation and selection phenomenon. Fortunately they don’t as this following citation reveals.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1636340 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1636340)
[quote="Human cancers express a mutator phenotype"]The presence of large numbers of random mutations within tumors could limit the efficacy of targeted therapies. By the time a tumor is clinically detected it contains ≈10^9 cancer cells. The average frequency of random mutations in tumor samples we analyzed was 2.2 × 10^−6 per base pair. Thus, each cell would contain more than a thousand random mutations, and the entire tumor could harbor as many as 10^12 different single-nucleotide substitutions. Many of these mutations would alter the properties of the encoded proteins, including mutations that confer resistance to radio-, chemo-, and/or immunotherapy (36). Thus, increased genetic variability in newly diagnosed cancers could encompass a reservoir of mutations available for immediate clonal expansion upon initiation of treatment with any given agent, leading to rapid emergence of resistance. This concept provides a molecular basis for the observed clinical efficacy of combination therapy, because any single cell would be unlikely to contain mutations that confer resistance to agents with different mechanisms of cytotoxicity. It can be hypothesized that tumors with fewer random mutations should be treated more conservatively, whereas tumors with a higher frequency of random mutations should be treated more aggressively and with combination therapies. Thus, mutation frequency could provide a new index for stratification of tumors. One possibility is that mutation frequency will exhibit an overall positive association with tumor stage and grade, but that there will be significant variability within defined stages and grades. This variability, which may contribute to differences in within-group outcome, could help to guide therapy for individual patients.
Adequate, you don’t have a clue how mutation and selection actually works. Your posts reveal this. What is your PhD in, perpleximatics?

Now you evolutionist have a good weekend, my hope for you is that you not be subjected to n+1 selection pressures. I’ll be back next week to present more citations which show that combination selection pressures profoundly slow the evolutionary process.

[Dr Adequate]

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve ... Just for yucks and giggles, let's see if we can locate the only person on the entire Internet who has ever, ever, ever said that "selection pressures evolve".

By googling on the phrase "selection pressures evolve" (http://www.google.com/search?q=%22selection+pressures+evolve%22&hl=en&rls=com.microsoft:en-gb:IE-SearchBox&rlz=1I7SUNA&filter=0).

Oh look, it appears to be a chap who calls himself "kleinman". He seems to use the phrase quite a lot.

This guy "kleinman" seems to have a really radical take on biology. Specifically, he keeps getting it wrong at a very basic level.

[Dr Adequate]

Not only did you say this, you admitted contradicted yourself ... What a silly lie. I admitted no such thing, which is why you cannot quote any such admission.

[Dr Adequate]

If physicians and scientists listen to your irrational and illogical thinking, it would lead to increases in premature death of people suffering from diseases subject to the mutation and selection phenomenon. Fortunately they don’t as this following citation reveals. What a silly lie. We all know that combination therapy is effective and have explained to you why this is so.

[Dr Adequate]

Let’s remind the readers of what you said:

And then Adequate goes on to say this: Of course. I said both of those things because they are true.

All the cartoon laughing dogs in the world won't make them contradict one another.

Perhaps, given your math block, you should spend some time figuring out why not.

Adequate, you don’t have a clue how mutation and selection actually works. What a silly lie.

[Myriad]

I didn't think to look. It might be worth checking --- that looks like the sort of thing one might demonstrate directly from probability theory, without this fussing about with simulations.


I believe so. To be more specific, the total expected generations for n fixations should increase as the nth harmonic number (sum of the partial harmonic series 1 + 1/2 + 1/3 + ... + 1/n), which is approximated at large n by ln(n), though it doesn't actually converge on it (it converges on ln(n) plus the Euler-Mascheroni constant). So, the expected rate would be close to ln(n)/n.

This is assuming (I believe correctly, for your models) that as soon as any specific point mutation favored by a selection pressure occurs for the first time, it gets fixed in the population with a high degree of certainty. This would be the case provided that the chances of a favorable mutation being nullified by a simultaneous unfavorable one, and the chance of two simultaneous unfixed favorable mutations competing in the population, are negligible. (Which is the case if the mutation rate and/or the ratio of pressures to total genome length is sufficiently low.)

The rationale is that we're looking for the expected number of trials to get all of a specific set of n distinct "hits" in a random number generator that selects one of a superset of m possibilties. The expected time for the first hit is clearly m/n, after which the expected time for the second hit (with n-1 possible hit targets remaining) is m/(n-1), and so on until the nth hit which takes an expected m/1 = m trials. So the total expected time for n hits is m * (1/n + 1/(n-1) + ... + 1/2 + 1), which is m times the nth harmonic number.

Respectfully,
Myriad

ETA: It occurs to me that the conclusion remains the same even if the fixation probability is not close to one, as long as it's constant.

[Dr Adequate]

This is why I normally only post on this thread at weekends. The more often I explain precisely and carefully what I mean, the more opportunities kleinman has to tell mentally degenerate lies about what I mean. There's no helping him.

[Dr Adequate]

This is assuming (I believe correctly, for your models) that as soon as any specific point mutation favored by a selection pressure occurs for the first time, it gets fixed in the population with a high degree of certainty. No, not really. It's a population model, it incorporates genetic drift.

I think you'll find that this doesn't make much difference to the maths, though. There is still a probability that any given mutation will go on to fixation.

[sol invictus]

Not only did you say this, you admitted contradicted yourself when you then said that your silly graph shows that more optimization takes more time. Then when asked to present a real example of this, you finally admitted that you had no real examples of you irrational and illogical conclusion. Let’s remind the readers of what you said:

Kleinman, one word:

RATE

RATE is not the same as TIME.

Mutation rate is the number of mutations divided by time. TIME AND RATE ARE NOT THE SAME THING.

Are you capable of understanding that?

Stop making yourself look like an utter fool.

[Dr Adequate]

I believe so. To be more specific, the total expected generations for n fixations should increase as the nth harmonic number (sum of the partial harmonic series 1 + 1/2 + 1/3 + ... + 1/n), which is approximated at large n by ln(n), though it doesn't actually converge on it (it converges on ln(n) plus the Euler-Mascheroni constant). So, the expected rate would be close to ln(n)/n.

The rationale is that we're looking for the expected number of trials to get all of a specific set of n distinct "hits" in a random number generator that selects one of a superset of m possibilties. The expected time for the first hit is clearly m/n, after which the expected time for the second hit (with n-1 possible hit targets remaining) is m/(n-1), and so on until the nth hit which takes an expected m/1 = m trials. So the total expected time for n hits is m * (1/n + 1/(n-1) + ... + 1/2 + 1), which is m times the nth harmonic number.

Respectfully,
Myriad Ah, yes. Thanks.

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?

[sol invictus]

I believe so. To be more specific, the total expected generations for n fixations should increase as the nth harmonic number (sum of the partial harmonic series 1 + 1/2 + 1/3 + ... + 1/n), which is approximated at large n by ln(n), though it doesn't actually converge on it (it converges on ln(n) plus the Euler-Mascheroni constant). So, the expected rate would be close to ln(n)/n.

This is assuming (I believe correctly, for your models) that as soon as any specific point mutation favored by a selection pressure occurs for the first time, it gets fixed in the population with a high degree of certainty. This would be the case provided that the chances of a favorable mutation being nullified by a simultaneous unfavorable one, and the chance of two simultaneous unfixed favorable mutations competing in the population, are negligible. (Which is the case if the mutation rate and/or the ratio of pressures to total genome length is sufficiently low.)

<snip for brevity>

ETA: It occurs to me that the conclusion remains the same even if the fixation probability is not close to one, as long as it's constant.

Right - what you describe was exactly my model. If you ask what is the number of generations you have to wait so that every individual in a fraction f of the population has undergone n mutations, each mutation with probability (per generation) p, the answer is

t = log(n)/p - log(-log(f)) + order (1/n), valid for n>>1, p<<1.

So the RATE goes as p n/log(n), and increases with n.

[Dr Adequate]

Kleinman, one word:

RATE

RATE is not the same as TIME.

Mutation rate is the number of mutations divided by time. TIME AND RATE ARE NOT THE SAME THING.

Are you capable of understanding that? Is he capable of understanding grade school mathematics?

Does he understand the difference between generations and fixations per generation?

Apparently not.

As I said, I usually only post here at weekends. You may slowly be realising why.

Stop making yourself look like an utter fool. I believe that this point has also been explained to him.

This, too, went over his head.

If you haven't read this paper (http://gagne.homedns.org/~tgagne/contrib/unskilled.html), you may find that it gives you some sort of insight into what it's like to be kleinman.

[Dr Adequate]

I think I'll try the highlighting thing too. It can't do any harm.

Hello, kleinman.

Are you listening carefully?

(1) With simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

(2) More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

---

I bet he still doesn't understand.

[cyborg]

I bet he still doesn't understand.

Understanding is dangerous: he'd have to give up his Lord.

[Dr Adequate]

Understanding is dangerous: he'd have to give up his Lord. C'mon, we have plenty of Christians on the forum and they're not like this. He could understand grade-school math without abandoning his religion, lots of people do.

But in order to realise that there is something he needs to understand he'd have to give up something much more precious to him than his so-called religion --- his self-esteem.

Kleinman has shown no sign that he's ever had a glimpse of religious feeling. What kleinman apparently worships and exalts above all is the perfection and omniscience and glory of kleinman.

And now we want to explain to him the basic mathematics that he should have learned in grade school? Watch the cognitive dissonance set in.

[cyborg]

He could understand grade-school math without abandoning his religion, lots of people do.

No, he couldn't.

And now we want to explain to him the basic mathematics that he should have learned in grade school? Watch the cognitive dissonance set in.

Stop being nasty Dr A! Kleinman admitted he made a mistake when he said probabilities could be more than one.

(It is unfortunate for kleinman that it's a mistake any fourteen year old paying the minimal amount of attention to the very basics of probability would never make).

[rocketdodger]

If you haven't read this paper (http://gagne.homedns.org/~tgagne/contrib/unskilled.html), you may find that it gives you some sort of insight into what it's like to be kleinman.

Much obliged for that link Adequate -- very enlightening.

The interesting thing about those results is that they almost seem to suggest a correlation between modesty and competence. If so ... well we all know what a veritable fountain of modesty Kleinman is...

[Kotatsu]

Kotatsu, why don’t you tell us how polyploid genes are transformed into new genes? Once you figure out it requires mutation and selection then you can study how mutation and selection actually works.

Nothing in polyploidisation implies that the genes in the diploid genome needs to evolve into new genes. Polyploidisation occurs without random point mutations, and results in double copies of the same chromosomes within the same nucleus. What happens after that is entirely irrelevant to the question of whether or not polyploidisation implies common descent or not (Note: it does).

Of course, after a polyploidisation event, evolution continues pretty much as before, with random point mutations and whatnot (supposing, of course, that the polyploid individual survives to reproduce). One of the copies is then also freer to evolve away from the pre-polyploidisation sequence as the resulting amino acid sequence will still be produced by the other copy.

Kleinman, I have studied polyploidisation for quite some time. I know much, much more about how it works and what it implies than you do. Being a smug parrot does not lead anywhere, so try to read what I write and understand it.

And your slowness "argument" --- or rather assertion --- is invalidated by the paper by Song et al. which I have referred to numerous times. The speed of evolution within five generations in that experiment was much higher than you seem to be able to imagine, and quiet sufficient for driving the evolution of any given character.

[Belz...]

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.

[kjkent1]

Only an evolutionist would think it is arrogant to show how mutation and selection works in reality.Only a creationist would be arrogant enough to believe that he is the only person alive who knows how mutation and selection actually works.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?Logic, and that's all I need!

Your comments above suggest that if we conduct an experiment with one very strong therapeutic drug, and an infinity of other drugs administered in homeopathic quantities, that the evolutionary result will be "profoundly slow," to use your expression. But if we conduct the same experiment with one very strong drug and no other drugs, then the evolutionary result will be accelerated to the maximum possible.

Or to put it in mathematical terms: what is the intensity multiplier value that must accompany each selective pressure, that you contend is "the dominant parameter in the mathematics of mutation and selection?"

The above is what everyone here is concluding from your posts, so if the above is not representative of your position, now is your opportunity to explain exactly how selective a pressure must be, relative to any other selective pressure found in the same environment, before that pressure contributes to the "confounding" of the evolutionary process.

[Belz...]

If you haven't read this paper (http://gagne.homedns.org/~tgagne/contrib/unskilled.html), 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.

[Hellbound]

That's a very interesting link that concludes pretty much what I've said for some time: ignorance breeds confidence.

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 :)

[joobz]

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 :)
No, I'm confident that we know all there is to know about it.....oh crud.:p

[Myriad]

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?


Yes and no.

Normally I'm very good at explaining all kinds of things to all kinds of people. This is partly due, I think, to my association with developmentally disabled people, some of whom I've known since my own early childhood -- that is, for more than 40 years. This calls for an unusual combination of patience and creativity. If I've explained something 100 different ways, and they still don't get it, I'll try my damndest to come up with way 101. Given creativity without patience, one would likely give up too soon. Given patience without creativity, one can only repeat the same explanations that didn't work before.

I have managed (mostly in the original EvolutionIsDead thread) to explain a few things to Alan, including a little bit about what probabilities are (and hence, why they cannot exceed 1). My track record is better than most on that score.

The problem is, my explanations, however creative and patient, can do no good if Alan does not pay attention to them. Getting a point across to someone with, for instance, Down's Syndrome, one might encounter stubbornness, hostility, confusion, and prejudice comparable to or far in excess of Alan's. But in the end the Down's Syndrome guys want to get it right. They want to understand. If you have to explain something 47 times, they'll pay attention to the 47th explanation.

Once Alan showed that he was willing to respond to me without actually paying attention to what I wrote, I stopped addressing him. How can one engage in written discourse with someone who does not read? All the patience and creativity in the world won't help. Trying to offer a better explanation is as useful as pushing harder on a rope.

Absent the delusional pipe-dream of educating him, he ceases altogether to be annoying.

Respectfully,
Myriad

[cyborg]

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.

[drzeus99]

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.


Actually, most (if not all) creationists will NEVER learn that they are wrong. This is because they aren't open to logic, or more importantly, CHANGE. They are SO set in their ways and beliefs that NO amount of proof, evidence, logic, or reasoning will EVER change their set ways. IOW, it's almost always completely useless to even make the attempt.


Cheers,
DrZ

[Mr. Scott]

A question for Paul:

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.

S

[Paul C. Anagnostopoulos]

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.
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.

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.

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.

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.

Finally, we have had an ongoing backstory discussion about Rcapacity.

~~ Paul

[Dr Adequate]

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. 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.

It's lucky for him that he didn't start doing this when he was at school, or he'd still be resitting the seventh grade.

[UnrepentantSinner]

Oh the stupid... it hertz me braying.

http://www.christcenteredforums.com/forum/showthread.php/whats-wrong-evolution-3344/index.html

[rocketdodger]

Oh the stupid... it hertz me braying.

http://www.christcenteredforums.com/forum/showthread.php/whats-wrong-evolution-3344/index.html

It just makes me sad sometimes, to see people like this, who otherwise appear to be good, intelligent, and rational, throw it all away when it comes to the topic of religion.

It kind of makes you realize just how much this really is a sickness of the mind that needs to be healed worldwide.

[kleinman]

Are you listening carefully?

(1) With simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

(2) More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
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.

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?
Only an evolutionist would think it is arrogant to show how mutation and selection works in reality.Only a creationist would be arrogant enough to believe that he is the only person alive who knows how mutation and selection actually works.
Oh, I’m not the only one, check out the citations below.
A question for Paul:

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.
Yes Paul, explain to all the newcomers how I am misusing the ev mutation and selection sorting algorithm and that what ev really shows is how a human genome can evolve in a billion years based on the rate of information gain on a 256 base genome.
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.
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.
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.
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.
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.
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.
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.
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?
Finally, we have had an ongoing backstory discussion about Rcapacity.
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.

So how does mutation and selection actually work? Here are some more citations which show how.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10671334&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10671334&dopt=AbstractPlus)
Patients 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://jvi.asm.org/cgi/content/abstract/71/2/1089 (http://jvi.asm.org/cgi/content/abstract/71/2/1089)
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://www.pnas.org/cgi/content/abstract/93/4/1648 (http://www.pnas.org/cgi/content/abstract/93/4/1648)
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.
http://aac.asm.org/cgi/content/full/44/3/794?ck=nck (http://aac.asm.org/cgi/content/full/44/3/794?ck=nck)
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.
And
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. 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.

[rocketdodger]

While you wait for a real example of n+1 pressures evolving faster than n pressures (which we have shown you time and time again, by the way, you genius) we will be waiting for you to show us a real example of whatever it is you claim generated life as we know it.

Do you have a more probable explanation than evolution, Kleinman? We would all love to hear it. You see, the funny thing is, no matter how improbable you think you show the theory of evolution to be, it will still be more probable than whatever nonsense you claim should replace it.

[rocketdodger]

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.

No, no, and no. We have shown you over and over, in formal proofs and arguments, why you are wrong here. You have failed to counter even a single argument of ours.

1) We have shown you multiple sorting algorithms that are not always confounded by additional sorting conditions. You have failed to find any evidence that these are not sorting algorithms and show that your argument to the contrary is correct.

2) We have shown you multiple examples, in the real world, of n+1 selective pressures leading to faster evolution than n selective pressures. We have also shown you that every single citation you have given is from a study predicated on this fact. You have failed to provide any argument to the contrary.

3) We have shown you why the conclusions you reached using the ev program are utter nonsense. The programmer himself showed you. As before, you have failed to provide any argument to the contrary.

Your incompetence in mathematics and logic, as well as your complete inability to follow the arguments presented by others, has resulted in the mishmash of nonsensical posts that you contend are proof of your claims. Nobody else thinks so, Kleinman. In fact, your performance in this debate is so pathetic that the majority of us question whether you really are who and what you say you are.

[joobz]

I see kleinman is again attacking the stawman. I see you haven't justified your horribly wrong assumptions. Isn't it funny how you are unable to wish reality away?

[kjkent1]

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.You're welcome, however you continue to misunderstand the effect of setting a mistake count to zero.

When a mistake count is disabled, the ev organisms do not evolve to the "perfect creature" contemplated by the software, even though the software reports a "perfect creature." This is because when all three mistake counts are non-zero, "perfect" means a creature absent any missing or spurious bindings -- whereas when either missing or spurious bindings are set to zero, the "perfect creature," contains these errors, because they are not selected against.

If you want to conduct a realistic experiment, then set one or more of the mistake counts to zero, disable the "Stop on perfect creature" setting, and enable the "Stop on Rseq >= Rfreq." You will find that the creatures never converge, i.e., they do not evolve towards anything resembling a real-world genome.

Whereas, if you set the mistake counts to non-zero values -- no matter how disparate, then the creature will eventually converge to Rseq >= Rfreq.

The whole point of ev is to show information gain from a random start as measured by the Rseq ~ Rfreq relationship. Any setting which causes ev to terminate prior to that relationship being reached, is defective, because the final organism has no relationship to the real-world genomes that it supposed to be modeling.

Having said all of the above, I believe that you have demonstrated that "random point" mutation and selection cannot reasonably account for the entire history of evolutionary change. However, as you refuse to acknowledge that anything other than random point mutation exists in the real world, you are intentionally excluding the very evidence which would show you how mutation and selection accomplishes speciation in the generational time available.

Your citations to research shows that heavy selective pressure from multiple sources slows evolutionary change. But, none of those experiments attempt to demonstrate that natural environments do not routinely appear with only one dominant selective pressure. To the contrary, all of the organisms that the research tests exist precisely because those organisms change rapidly in response to a dominant selective pressure -- and the research demonstrates this rapid change by subjecting test organisms to a single dominant pressure, before subjecting the organisms to multiple pressures.

Kleinman, you have not disproved evolution -- you've proved it.

[Dr Adequate]

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. And then you wonder why people think that you're insane.

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? 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.

The same obscure Internet message board on which you've spent an entire year and (at a conservative estimate) half-a-million words explaining your ideas to a dozen people, all of whom keep laughing their heads off at your pathetic antics.

I should still be fascinated to know your reasons for doing this, but you're too ashamed to tell me, aren't you?

[Dr Adequate]

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. We know that you're talking bollocks, and if you could ever get your head round grade-school-level math, so would you.

But I don't think that you ever will.

[Dr Adequate]

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. Here's some serious, honest advice. No joke.

Take the passage that I've just quoted and show it to a doctor. Tell him that over the last year you've felt compelled to write half-a-million words of this stuff.

Ask him for help.

What's going on in your head is not right. I don't feel good myself, because it's wrong to laugh at the mentally disturbed, which is what I've been doing for the past year while participating on this thread.

There is something very wrong with you. You need help. I don't think that I can go on taunting you any longer. If I advise you that, in all seriousness, you are mentally ill, I don't mean it as a jibe or an ad hominem attack.

You are mentally ill. You need help.

Of course, your opinion will be that I'm wrong. If so, you have nothing to lose by showing this to a doctor. If I am right, as I am, you have the most precious thing in the world to gain.

You never came close to your ambition of being "annoying". But you have become an object of terrible, desperate pity.

I don't know if I can try to help you any more. Please try to help yourself.

[kleinman]

While you wait for a real example of n+1 pressures evolving faster than n pressures (which we have shown you time and time again, by the way, you genius) we will be waiting for you to show us a real example of whatever it is you claim generated life as we know it.
Only in your dreams have you shown n+1 selection pressure evolving more rapidly than n selection pressures, rocketwhomissesthetarget.
Do you have a more probable explanation than evolution, Kleinman? We would all love to hear it. You see, the funny thing is, no matter how improbable you think you show the theory of evolution to be, it will still be more probable than whatever nonsense you claim should replace it.
The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.
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.No, no, and no. We have shown you over and over, in formal proofs and arguments, why you are wrong here. You have failed to counter even a single argument of ours.
You have made one argument that n+1 selection pressures evolve more quickly than n selection pressures. This has been shown to be mathematically and empirically wrong. It is nonsense to think that a sorting problem speeds up by adding more sorting conditions.
I see kleinman is again attacking the stawman. I see you haven't justified your horribly wrong assumptions. Isn't it funny how you are unable to wish reality away?
It is true that the theory of evolution by mutation and selection is made of straw, that is why is blown away by the mathematical and empirical evidence.
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.You're welcome, however you continue to misunderstand the effect of setting a mistake count to zero.

When a mistake count is disabled, the ev organisms do not evolve to the "perfect creature" contemplated by the software, even though the software reports a "perfect creature." This is because when all three mistake counts are non-zero, "perfect" means a creature absent any missing or spurious bindings -- whereas when either missing or spurious bindings are set to zero, the "perfect creature," contains these errors, because they are not selected against.
Kjkent1, Paul and Dr Schneider’s confusing terminology of calling a zero mistake condition for a given set of selection conditions a “perfect creature” has also confused you. Ev is simply a sorting algorithm. It is designed with three sorting conditions. It is these three combined sorting conditions that slow down the convergence of ev. Setting two of the three sorting conditions to zero demonstrates this fact nicely.
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.And then you wonder why people think that you're insane.
You are the mathematician who believes in a mathematically impossible belief system. Why would someone spend years studying mathematical logic then abandon it for the irrational and illogical? You are spending too much time in your space zeppelin.
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?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.

The obscure Internet message board on which you've spent an entire year and (at a conservative estimate) half-a-million words explaining your ideas to two dozen people.
See, you can figure out something. I like posting here because I enjoy talking with such an interesting conversationalist as you. You are irrational and illogical but interesting none the less. So what’s our standing? Are we still 1464th most popular forum on the internet? Perhaps we can exceed the “Big Foot” thread on this forum. I’m sure you will help to reach that goal.

[Belz...]

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.

Translation: "Uh oh. I don't understand the difference, so I better come up with some clever insult, STAT."

[rocketdodger]

Only in your dreams have you shown n+1 selection pressure evolving more rapidly than n selection pressures, rocketwhomissesthetarget.

--bacteria in human body --> population under n selective pressures --> no evolution of penicillin resistance.
--bacteria in the same body after penicillin is taken --> population under n+1 selective pressures --> rapid evolution of penicllin resistance.

Remember, Kleinman? Apparently you have forgotten all of the convoluted twisting you performed to try to get out of the corner this example puts you in.

The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.

You haven't been able to back up your own arguments, which merely suggest evolution is improbable, never mind show evolution to be outright impossible. You clearly know nothing about probability theory.

But just to humor you, lets suppose you are right and that evolution is mathematically impossible. That means that either a) creationism is true or b) the molecules of our solar system just spontaneously assembled into the world as we know it.

We can calculate the probability of b). It is very low but still nonzero. Can you calculate the probability of a)? Let me know when you are finished.

You have made one argument that n+1 selection pressures evolve more quickly than n selection pressures.

We have made many such arguments, and none of them have been refuted in any way by you except by redefining selection pressure to be "relatively strong directional selection pressure that is one of the variables in a study I have cited."

This has been shown to be mathematically and empirically wrong.

By whom? Certainly not by you. Simply whining "no, thats not true" doesn't constitute a refutation, Kleinman.


It is nonsense to think that a sorting problem speeds up by adding more sorting conditions.

Really? Then surely you should be able to show Dr. Adequate and I why both of our algorithms are not sorting algorithms. Have you done this yet? No. Will you ever? I doubt it.

[Belz...]

You are the mathematician who believes in a mathematically impossible belief system. Why would someone spend years studying mathematical logic then abandon it for the irrational and illogical? You are spending too much time in your space zeppelin.

Klein, I think something broke in your mind around post 6614. I'm with Adequate. Get help.

[joobz]

It is true that the theory of evolution by mutation and selection is made of straw, that is why is blown away by the mathematical and empirical evidence.

So no justification for your assumptions then? I know why you haven't presented any, it's becuase you have no justification. They are horribly horribly wrong. You know enough to know that. This is the reason why you evade my question.

It is for that reason why I do not agree with Dr. Adequate. I don't think you are mentally deranged. I simply think you enjoy the attention.

[kleinman]

Only in your dreams have you shown n+1 selection pressure evolving more rapidly than n selection pressures, rocketwhomissesthetarget.--bacteria in human body --> population under n selective pressures --> no evolution of penicillin resistance.
--bacteria in the same body after penicillin is taken --> population under n+1 selective pressures --> rapid evolution of penicllin resistance.

Remember, Kleinman? Apparently you have forgotten all of the convoluted twisting you performed to try to get out of the corner this example puts you in.
This is where you have gotten it confused rocketwhomisses the target. The correct mathematics for this example is:
--bacteria in human body --> population under n selective pressures --> no evolution of penicillin resistance.
--bacteria in the same body after penicillin is taken --> population under n+1 selective pressures --> rapid evolution of penicllin resistance
-bacteria in vitro after penicillin is taken --> population under n+1-m selective pressures --> more rapid evolution of penicllin resistance than with n+1 selection pressures. Rocketwhomisses the target, you need to learn how to keep track of the number of selection pressures. This example show that when evolving a single strong selection pressure on the background of weak selection pressures, it only slows the evolution of that single strong selection pressure. Remove some of the weak selection pressures and that single strong selection pressure will evolve more quickly. Add a second strong selection pressure and you profoundly slow the evolution of both strong selection pressures.
The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.You haven't been able to back up your own arguments, which merely suggest evolution is improbable, never mind show evolution to be outright impossible. You clearly know nothing about probability theory.

But just to humor you, lets suppose you are right and that evolution is mathematically impossible. That means that either a) creationism is true or b) the molecules of our solar system just spontaneously assembled into the world as we know it.

We can calculate the probability of b). It is very low but still nonzero. Can you calculate the probability of a)? Let me know when you are finished.
Let’s see, I’ve used a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples of mutation and selection, all which show that combination selection pressures profoundly slow the evolutionary process. Rocketdodger, give us an estimate of the number of atoms in the earth. Then compute the probability that you can pick randomly one particular atom. The probably that the theory of evolution is true is hundreds of orders of magnitude less than that.

Rocketdodger, you always humor me. You whine quite a bit but I overlook this. I’ve already proved your theory is mathematically impossible, it’s your turn to prove my theory impossible.
You have made one argument that n+1 selection pressures evolve more quickly than n selection pressures.We have made many such arguments, and none of them have been refuted in any way by you except by redefining selection pressure to be "relatively strong directional selection pressure that is one of the variables in a study I have cited."
You can make up a story that you have written a model which shows that you sort mutations to n+1 selection conditions more rapidly than to n selection conditions but “I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was” doesn’t cut it.
This has been shown to be mathematically and empirically wrong. By whom? Certainly not by you. Simply whining "no, thats not true" doesn't constitute a refutation, Kleinman.
Sure it does when you back it up with the data from a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples of mutation and selection which shows the same thing. Now if you could post a real example where n+1 selection pressures sort mutations faster than n selection pressures then you would have a real counter argument, but of course, you don’t have any real examples of this.
It is nonsense to think that a sorting problem speeds up by adding more sorting conditions.Really? Then surely you should be able to show Dr. Adequate and I why both of our algorithms are not sorting algorithms. Have you done this yet? No. Will you ever? I doubt it.
Adequate has posted a silly graph and the only parametric study you have presented is this one:
I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.
You are the mathematician who believes in a mathematically impossible belief system. Why would someone spend years studying mathematical logic then abandon it for the irrational and illogical? You are spending too much time in your space zeppelin.Klein, I think something broke in your mind around post 6614. I'm with Adequate. Get help.
I think you have confused me with joobz. Joobz is the one who can’t brain. And I get lots of help from you evolutionists. Dr Schneider and Paul helped with their model of random point mutation and natural selection and then there is Delphi’s reference to Wikipedia fitness landscape and then there was kjkent1 pointing out the weights feature in ev and then there are the hundreds of real examples of mutation and selection I have been posting. It wouldn’t surprise me that many of the authors would call themselves evolutionists. Of course once they realize what combination selection pressures do to the mutation and selection process they would understand that common descent is a mathematical impossibility. I appreciate all the help you evolutionists give in this discussion. All I have to do is point out the mathematical and empirical facts of life of how mutation and selection actually works from the mathematical and empirical data you evolutionists so kindly produce.
It is for that reason why I do not agree with Dr. Adequate. I don't think you are mentally deranged. I simply think you enjoy the attention.
So what if I enjoy the attention. What does that make you since you have posted three times as many as I have? You evolutionists have failed at accurately describing how mutation and selection works. Dr Schneider’s model shows how mutation and selection works and so do the hundreds of citations which I have posted. That is why I am getting attention. You crybabies whine and complain about it but the mathematical and empirical evidence is there which show that combination selection pressures profoundly slow the evolutionary process. You can’t evolve the thousands of genes simultaneously necessary to transform reptiles into birds. You don’t have the selection pressures and you can’t transform all these genes simultaneously if you did. Common descent is a myth.

[Shalamar]

Please provide proof of Creationism.

[joobz]

So what if I enjoy the attention. Nothing. I didn't say there was anything wrong with being an attention seeker.

What does that make you since you have posted three times as many as I have?
My interests in this forum extend beyond you.

You evolutionists have failed at accurately describing how mutation and selection works. Dr Schneider’s model shows how mutation and selection works and so do the hundreds of citations which I have posted. That is why I am getting attention. You crybabies whine and complain about it but the mathematical and empirical evidence is there which show that combination selection pressures profoundly slow the evolutionary process. You can’t evolve the thousands of genes simultaneously necessary to transform reptiles into birds. You don’t have the selection pressures and you can’t transform all these genes simultaneously if you did. Common descent is a myth.
That's a lot of words used to evade my question. It would have been much simpler to say, "I have no justification for my assumptions."

[sol invictus]

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.

You really don't get it, do you?

Kleinman, will you actually put your money where your mouth is, or are you as much of a whining chicken**** as you sound? I'd like to make a bet with you, for real money. I'm tired of this BS nonsense you keep spouting.

Here are the rules: we have ten standard six-sided dice. On the first trial we roll all ten dice (that counts as one roll). Any die that comes up a 6 is removed and set aside and not rolled again, and then we roll the remaining dice (that counts as another roll). Again, any dice that read 6 are set aside with the others, and repeat until all the dice have come up 6 and been set aside. We keep track of how many rolls we had to make before all 10 dice read six. Let's call that number N10.

Now we do the same thing with 20 dice. Again, we keep track of how many rolls it takes before all 20 read 6 and have been set aside. Let's call that N20.

Now, I claim that the rate at which 6's come up will be faster for the case with 20 dice than for the case with 10. Specifically, I claim that 20/N20>10/N10. You have stated repeatedly that this is false. Therefore I propose we make this a bet.

You name the amount of money, up to $10,000 (if you want to bet more, I'm sure others will happily join). You and I perform this experiment, in the presence of observers. To avoid problems with statistical fluctuations one way or the other we can perform the experiment as many times as you like, and make the bet contingent on the average rates. Or we can do it only once - I'll take that risk. Or we can increase the number of dice, and compare the 100/N100 to 10/N10.

Do you accept?

PUT UP OR SHUT UP, KLEINMAN.

[kleinman]

What does that make you since you have posted three times as many as I have?My interests in this forum extend beyond you.
Just because you have an interest in mutation and selection doesn’t mean you have any understanding of the process. You have admitted that.
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.
I wonder how much you really understand about biomaterials when you post this kind of speculation.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
And then I wonder how much understanding of PDEs you have when you state that you can find irregularities in my PhD thesis yet won’t take me up on the $10,000 wager that you can’t find any mathematical or empirical irregularities. Let’s see where your interests take you.
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.You really don't get it, do you?
Sure I do, you evolutionists have no idea how mutation and selection actually works. This is why you can’t find a single citation which show that n+1 selection pressures evolve more quickly than n selection pressures. Now I see you want to do a little wagering.
Here are the rules: we have ten standard six-sided dice. On the first trial we roll all ten dice (that counts as one roll). Any die that comes up a 6 is removed and set aside and not rolled again, and then we roll the remaining dice (that counts as another roll). Again, any dice that read 6 are set aside with the others, and repeat until all the dice have come up 6 and been set aside. We keep track of how many rolls we had to make before all 10 dice read six. Let's call that number N10.
Don’t be silly sol. If you want to make a wager, let’s see you prove the theory of evolution is mathematically possible using probability theory. Lot’s of people have tried it. Let’s see if you can do it. Now that we know how mutation and selection actually works, probability theory alone is useless. Why don’t you tell us what the selection pressure was that evolved the first gene de novo? Or tell us what the selection pressure would be that would evolve any gene de novo. Tell us what the probability is for a 500 base gene to form by random additions of bases? There is where the wager is sol.

[joobz]

Just because you have an interest in mutation and selection doesn’t mean you have any understanding of the process. You have admitted that.

I wonder how much you really understand about biomaterials when you post this kind of speculation.
trying to change the subject again? Remember the question is can you justify ANY of your assumptions that make your theory plausible. I state again, the reason you avoid this is becuase you know better and that you understand what I ask kills your entire argument.


And then I wonder how much understanding of PDEs you have when you state that you can find irregularities in my PhD thesis yet won’t take me up on the $10,000 wager that you can’t find any mathematical or empirical irregularities. Let’s see where your interests take you.
Why do you make me repeat the embarrassing facts of your PhD? You had only two publications. Each with a different advisor and both were barely cited. This is the irregularity to which I spoke of. Everyone knows this is what I was refering to. Everyone here is capable of reading and understanding this point.

[rocketdodger]

This is where you have gotten it confused rocketwhomisses the target. The correct mathematics for this example is:
--bacteria in human body --> population under n selective pressures --> no evolution of penicillin resistance.
--bacteria in the same body after penicillin is taken --> population under n+1 selective pressures --> rapid evolution of penicllin resistance
-bacteria in vitro after penicillin is taken --> population under n+1-m selective pressures --> more rapid evolution of penicllin resistance than with n+1 selection pressures.



So adding selection pressures can both increase the rate of evolution or decrease the rate of evolution, depending on what those pressures are and how strong their relative magnitude is. Congratulations on disproving your own theory, you genius, and finally realizing what we have been trying to tell you.


Let’s see, I’ve used a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples of mutation and selection, all which show that combination selection pressures profoundly slow the evolutionary process.

I am no longer going to argue with you about your interpretation of these studies because you are incapable of discussing them intelligently. I am only going to argue with you about simple mathematics that can be demonstrated beyond a doubt. To that end, I am still waiting for you to show me why the algorithm I use in my simulation is not a sorting algorithm.

Rocketdodger, give us an estimate of the number of atoms in the earth. Then compute the probability that you can pick randomly one particular atom. The probably that the theory of evolution is true is hundreds of orders of magnitude less than that.

Fine. Lets say, to make sure we err conservatively, that this probability is 1.0 x 10^-999999999. Now tell me what the probability of creationism being true is.

Rocketdodger, you always humor me. You whine quite a bit but I overlook this. I’ve already proved your theory is mathematically impossible, it’s your turn to prove my theory impossible.

When did you prove my theory impossible? Did you refute any of my code, or even the general algorithm I used? The only thing you have said regarding my simulation, in fact, is that you agree it uses a true sorting algorithm. So if anything you proved your own theory wrong, you genius.

You can make up a story that you have written a model which shows that you sort mutations to n+1 selection conditions more rapidly than to n selection conditions but “I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was” doesn’t cut it.

You sad, pathetic, little liar. You know full well I have provided much more information than that -- look at post #6401.

But of course you know that, and you also know that my algorithm (and Dr. Adequates) shows your claim about sorting algorithms to be simply wrong. So instead of trying to find errors in our methods, which you know is futile, you try to smokescreen everyone away from the issue at hand. If this is an incorrect assessment of your tactics, prove me wrong. Show me why my algorithm is wrong and your claim is correct..

Sure it does when you back it up with the data from a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples of mutation and selection which shows the same thing. Now if you could post a real example where n+1 selection pressures sort mutations faster than n selection pressures then you would have a real counter argument, but of course, you don’t have any real examples of this.

Except for all of the studies you cite, which are predicated on the fact that organisms develop rapid resistance to human methods of eradicating them once those methods are introduced.


Adequate has posted a silly graph and the only parametric study you have presented is this one:

Who do you think you are foolling, you pathetic liar? I addressed this claim of yours regarding my parametric studies in post #6516 and post #6568. Don't you realize that lying about a person's prior posts doesn't work when the posts are in full view for everyone to see?

[kjkent1]

Kjkent1, Paul and Dr Schneider’s confusing terminology of calling a zero mistake condition for a given set of selection conditions a “perfect creature” has also confused you. Ev is simply a sorting algorithm. It is designed with three sorting conditions. It is these three combined sorting conditions that slow down the convergence of ev. Setting two of the three sorting conditions to zero demonstrates this fact nicely.Sure it's a sorting algorithm. But, when there is a condition set to zero, it sorts incorrectly.

It would be no different than if you had a program that sorted a random deck of cards back to its original order, and one of the sorting options was to disable the ability to distinguish suits. The program would still sort, but the suits would be incorrectly sorted, except by random accident.

You have it wrong, and you have had it wrong for 100s of pages in this thread. Being unwilling to admit error and learn from it is a huge defect for a scientist. But, you're wrong anyway, and everyone can see that you're not wearing any clothes.

[rocketdodger]

I wonder how much you really understand about biomaterials when you post this kind of speculation

Obviously more than you, Kleinman. It is not just speculation, it is fact. If your credentials weren't false, you would have taken organic chemistry in college, and would know this.

In chemistry, any reaction that can happen does happen, and the results are governed by the rules of chemical equilibrium and reaction kinetics. Don't you remember all of this Kleinman? Don't you remember how thermodynamically unfavorable reactions can be driven by applying Le Chatelier's principle and removing the products (such as through PRECIPITATION like joobz mentioned)? Don't you remember how chemical synthesis usually involves many such sub-reactions before the final product is reached?


Of course you don't remember, because you are a fraud and never learned it to begin with.

[sol invictus]

This is why you can’t find a single citation which show that n+1 selection pressures evolve more quickly than n selection pressures.

Then let's bet on it.

Put your money where your mouth is or shut it and stop lying, Kleinman. Or are you a hypocrite?

[Mr. Scott]

Before I looked at Dr Schneider’s and Paul’s model, I didn’t understand how mutation and selection worked.

(snip)

I have always been skeptical of the interpretation of the evidence presented by evolutionists but this is the first time I have done my own analysis of the evidence and it shows that evolutionists have the concept of mutation and selection backwards.

Precisely why were you skeptical of the interpretation of the evidence presented by evolutionarians before you looked at Dr. Schneider's and Paul's model?

[kleinman]

And then I wonder how much understanding of PDEs you have when you state that you can find irregularities in my PhD thesis yet won’t take me up on the $10,000 wager that you can’t find any mathematical or empirical irregularities. Let’s see where your interests take you.Why do you make me repeat the embarrassing facts of your PhD? You had only two publications. Each with a different advisor and both were barely cited. This is the irregularity to which I spoke of. Everyone knows this is what I was refering to. Everyone here is capable of reading and understanding this point.
You are as poor at doing your literature searches as you are in the mathematics of mutation and selection. You don’t know who my thesis advisor was and who wasn’t. You are simply a big mouth coward; everyone here is capable of reading and understanding this point.
This is where you have gotten it confused rocketwhomisses the target. The correct mathematics for this example is:
--bacteria in human body --> population under n selective pressures --> no evolution of penicillin resistance.
--bacteria in the same body after penicillin is taken --> population under n+1 selective pressures --> rapid evolution of penicllin resistance
-bacteria in vitro after penicillin is taken --> population under n+1-m selective pressures --> more rapid evolution of penicllin resistance than with n+1 selection pressures.So adding selection pressures can both increase the rate of evolution or decrease the rate of evolution, depending on what those pressures are and how strong their relative magnitude is. Congratulations on disproving your own theory, you genius, and finally realizing what we have been trying to tell you.
Wrong rocketdodger, adding selection pressures slows down the mutation and selection process, removing selection pressures speed up the mutation and selection process. Each additional selection pressure you add on to a population increases the difficulty of the population to sort beneficial and detrimental mutations. Sorting beneficial and detrimental mutations on a population with n weak selection pressures and a single strong selection pressure give a slower evolutionary process than the same population if subjected to n-m weak selection pressures and the same single strong selection pressure. The weak selection pressures serves to slow the evolution of the strong selection pressure.
Let’s see, I’ve used a peer reviewed and published model of random point mutations and natural selection and hundreds of real examples of mutation and selection, all which show that combination selection pressures profoundly slow the evolutionary process.I am no longer going to argue with you about your interpretation of these studies because you are incapable of discussing them intelligently. I am only going to argue with you about simple mathematics that can be demonstrated beyond a doubt. To that end, I am still waiting for you to show me why the algorithm I use in my simulation is not a sorting algorithm.
How could you argue about the results from ev. You don’t understand the model and you’ve never run a case. With respects to your model, you have yet to post a systematic study of your model. There is nothing to argue about your model.
Rocketdodger, give us an estimate of the number of atoms in the earth. Then compute the probability that you can pick randomly one particular atom. The probably that the theory of evolution is true is hundreds of orders of magnitude less than that.Fine. Lets say, to make sure we err conservatively, that this probability is 1.0 x 10^-999999999. Now tell me what the probability of creationism being true is.
Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is:
1 – (1.0 x 10^-999999999) ≈ 1
Rocketdodger, you always humor me. You whine quite a bit but I overlook this. I’ve already proved your theory is mathematically impossible, it’s your turn to prove my theory impossible.When did you prove my theory impossible? Did you refute any of my code, or even the general algorithm I used? The only thing you have said regarding my simulation, in fact, is that you agree it uses a true sorting algorithm. So if anything you proved your own theory wrong, you genius.
I proved your theory wrong when I showed you how mutation and selection actually works, both mathematically with Dr Schneider’s ev computer simulation of random point mutations and natural selection and empirically with the hundred of real examples of mutation and selection which I have cited. I then used your own estimate of the probability that the theory of evolution is true to show you that the probability that we were created is ≈ 1. How many different ways do I have to show you that we were created? You just won’t accept the mathematical and empirical facts. That’s why you can’t find a single real example of n+1 selection pressures evolving more rapidly than n selection pressures. It just doesn’t happen.

[joobz]

You are as poor at doing your literature searches as you are in the mathematics of mutation and selection. You don’t know who my thesis advisor was and who wasn’t. You are simply a big mouth coward; everyone here is capable of reading and understanding this point.
You have 2 publications listed on web of science, which typically ignores conference proceedings/abstracts. Why do you get so angry with me, when it was you who raised this issue in the first place. If you are embarrassed by your track record, why do you mention it?

You would save yourself much frustration and humiliation if you simply stuck to the topic at hand. I've asked 3 times now, what are your justifications for your model assumption?

You have never answered this question. Indeed, you failed to answer any question that clearly demonstrates your poorly conceived theory for what it is.

[Paul C. Anagnostopoulos]

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.
It's not simply "longer genomes," now is it? We can run one experiment with a longish genome that converges (Rcapacity >= Rfrequency), and another with the same length genome that does not (Rcapacity < Rfrequency). Therefore, obviously, there is another factor at work.

~~ Paul

[kleinman]

You are as poor at doing your literature searches as you are in the mathematics of mutation and selection. You don’t know who my thesis advisor was and who wasn’t. You are simply a big mouth coward; everyone here is capable of reading and understanding this point.You have 2 publications listed on web of science, which typically ignores conference proceedings/abstracts. Why do you get so angry with me, when it was you who raised this issue in the first place. If you are embarrassed by your track record, why do you mention it?

You would save yourself much frustration and humiliation if you simply stuck to the topic at hand. I've asked 3 times now, what are your justifications for your model assumption?

You have never answered this question. Indeed, you failed to answer any question that clearly demonstrates your poorly conceived theory for what it is.
You are the one who brought up my PhD thesis and you claimed you could find irregularities in it. So find the irregularities. Why do you continue to attribute Dr Schneider’s computer model to me? Can’t you even get that fact straight?
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.It's not simply "longer genomes," now is it? We can run one experiment with a longish genome that converges, and another with the same length genome that does not. Therefore, obviously, there is another factor at work.
That isn’t a profoundly longish genome is it? Paul, there is a way to determine what this factor is. You have to map out the fitness landscape. You do this by computing the mistakes in 4^G combinations of genomes. I’ll let you do the arithmetic on that one. What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

[joobz]

You are the one who brought up my PhD thesis and you claimed you could find irregularities in it. So find the irregularities. Why do you continue to attribute Dr Schneider’s computer model to me? Can’t you even get that fact straight?
So again, you wish to make yourself look foolish by repeating the same missinterpretation of my statements? Such actions only help to confirm Dr. Adequate's assessment of your mental health. Is that your goal?

Why do you try so hard to avoid answering my question? What are your justifications for your model? I've given you a list of nine assumptions that are required to make your analysis valid. Any one of them would being wrong would destroy your theory. Is this your way of finally admitting you've been wrong this whole time?

[rocketdodger]

Wrong rocketdodger, adding selection pressures slows down the mutation and selection process, removing selection pressures speed up the mutation and selection process.

Oh, so removing the penicillin selective pressure will speed up the evolution of penicillin resistance? Now I understand. So according to your theory, as long as we keep removing pressures, evolution will get faster and faster, until we get to zero pressures, at which point species must just pop into existence.


How could you argue about the results from ev. You don’t understand the model and you’ve never run a case.

I understand the model, and I ran the cases you told me to, which led to results different than yours, go figure.

With respects to your model, you have yet to post a systematic study of your model. There is nothing to argue about your model.

And you have yet to post a systematic study of ev. Who the hell cares? I told you already that every conceivable set of parameters you can give my simulation leads to the same conclusion -- for some n != 0, the rate of fixation under n+1 pressures is greater than the rate of fixation under n pressures. If you want the actual numbers from actual runs, fine. I will run the simulation a few times tonight on a wide variety of possible inputs and give you the results.

Will it matter? No, because you are full of sh--. Regardless of what I show you, you will cry about some other nonexistent problem and whine about how it must be throwing off my results. All of this, of course, without giving us a single mathematical explanation for why the results should be off, except the generic Kleinman cop-out that we all know so well -- "the mathematical and empirical evidence shows otherwise." Suuuuure.

Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is
1 – (1.0 x 10^-999999999) ≈ 1


Hahahahah. Nice creationist math there, genius. Try treating the two as independent events and see where that gets you. You do know about independent events in probability theory, right, grad-student?


You just won’t accept the mathematical and empirical facts.
I will accept any mathematical facts that you can show, Kleinman, using a mathematical proof, to actually be a mathematical fact. It is clear that you are a fraud and never wrote a thesis, because if you had, you would understand the concept of proof and how to construct a coherent argument.

I will also accept any empirical facts that you can show to actually be facts. That is why we have consistently asked you to prove to us why your theory is correct. Curiously, your only method of "proof" has been to regurgitate an assertion that your theory is correct.

That’s why you can’t find a single real example of n+1 selection pressures evolving more rapidly than n selection pressures. It just doesn’t happen.

Except in every single study you have cited, of course.

[rocketdodger]

What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

Do you even know what a fitness landscape looks like, Kleinman? Here is a hint for you -- regardless of the number of selective pressures, the landscape is always a convex shape. There is no such thing as local optima that the population can "get stuck on" or whatever nonsense it is that you assert.

If you think otherwise, please tell us all, what combination of mutations represent a local optima?

[kleinman]

Wrong rocketdodger, adding selection pressures slows down the mutation and selection process, removing selection pressures speed up the mutation and selection process.Oh, so removing the penicillin selective pressure will speed up the evolution of penicillin resistance? Now I understand. So according to your theory, as long as we keep removing pressures, evolution will get faster and faster, until we get to zero pressures, at which point species must just pop into existence.
No rocketdodger, you are attributing a property to mutation and selection that has no mathematical or empirical basis. Adding penicillin does not speed up the evolution of weak selection pressures. The evolution of resistance on the background of weak selection pressures slows the evolution of penicillin resistance. That is why you answered correctly when I asked you under what circumstances does penicillin resistance evolve more quickly, in vivo when there is an immune response against the bacteria or in vitro when there is no immune response. That’s the point rocketdodger; things don’t just pop into existence. There is a cause and effect relationship.
How could you argue about the results from ev. You don’t understand the model and you’ve never run a case.I understand the model, and I ran the cases you told me to, which led to results different than yours, go figure.
You are not doing something correctly with the model. A given set of input parameters always give identical output from the model. Those input parameters include the seed value for the random number generator.
With respects to your model, you have yet to post a systematic study of your model. There is nothing to argue about your model.And you have yet to post a systematic study of ev. Who the hell cares? I told you already that every conceivable set of parameters you can give my simulation leads to the same conclusion -- for some n != 0, the rate of fixation under n+1 pressures is greater than the rate of fixation under n pressures. If you want the actual numbers from actual runs, fine. I will run the simulation a few times tonight on a wide variety of possible inputs and give you the results.
Rocketdodger, that data from ev is on this thread. All you have posted is this:
I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.
This is your idea of a parametric study. This is the kind of sloppy analysis you evolutionists like to call science. Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.
What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.Do you even know what a fitness landscape looks like, Kleinman? Here is a hint for you -- regardless of the number of selective pressures, the landscape is always a convex shape. There is no such thing as local optima that the population can "get stuck on" or whatever nonsense it is that you assert.
Like I said, Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

[Paul C. Anagnostopoulos]

That isn’t a profoundly longish genome is it?
I'm not sure why it matters. Do you want to amend your statement to "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 really extra long genomes of extra big size."?

Paul, there is a way to determine what this factor is. You have to map out the fitness landscape. You do this by computing the mistakes in 4^G combinations of genomes. I’ll let you do the arithmetic on that one. What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.
I agree completely, Alan. It's a complicated landscape. What do you suppose creates those hills and valleys? You appear to think it's magic.

~~ Paul

[Paul C. Anagnostopoulos]

Adding penicillin does not speed up the evolution of weak selection pressures.
Please stop saying this. Selection pressures do not evolve. Please say what you actually mean, so at least we have a chance.

~~ Paul

[rocketdodger]

No rocketdodger, you are attributing a property to mutation and selection that has no mathematical or empirical basis. Adding penicillin does not speed up the evolution of weak selection pressures. The evolution of resistance on the background of weak selection pressures slows the evolution of penicillin resistance.

Will introducing penicillin to a population speed up the evolution of penicillin resistance, Kleinman? YES or NO?


This is your idea of a parametric study. This is the kind of sloppy analysis you evolutionists like to call science. Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

Can you show anyone here why the algorithms used by Dr. Adequate and myself are not sorting algorithms? YES or NO?

Like I said, Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

Can you show anyone here what distribution of mutations in a population might correspond to a local optima in the fitness landscape for that population? YES or NO? To make it simple for you Kleinman, lets suppose only two selective pressures of equal magnitude (A and B) are affecting the population.

[Paul C. Anagnostopoulos]

I ran two experiments with the standard model but a genome size of 4096:

weight width 7, site width 8 (Rcapacity >> Rfrequency): 124,827 generation to perfect creature

weight width 6, site width 7 (Rcapacity > Rfrequency): 131,375 generation to perfect creaure

weight width 5, site width 6 (Rcapacity > Rfrequency): 163,722 generations to perfect creature

weight width 4, site width 5 (Rcapacity > Rfrequency): 198,279 generations to perfect creature

weight width 3, site width 4 (Rcapacity = Rfrequency): still 16 mistakes after 1,000,000 generations

weight width 2, site width 3 (Rcapacity < Rfrequency): still 16 mistakes after 1,000,000 generations


~~ Paul

[UnrepentantSinner]

Klein, I think something broke in your mind around post 6614. I'm with Adequate. Get help.

I think you're being overly magnaimous since his is clearly a pre-existing condition. I can't even read Kleinmann's posts, but then again, I could never wade through the Unibomber's manifesto either. Dr. A's diagnosis is spot on.

[Mr. Scott]

Before I looked at Dr Schneider’s and Paul’s model, I didn’t understand how mutation and selection

worked.

(snip)

I have always been skeptical of the interpretation of the evidence presented by evolutionists but this is the first time I

have done my own analysis of the evidence and it shows that evolutionists have the concept of mutation and selection

backwards.

Precisely why were you skeptical of the interpretation of the evidence presented by evolutionarians before you looked at Dr. Schneider's and Paul's model?

[Kotatsu]

Common descent is a myth.

While what you say is usually nonsense, I am still waiting for you to comment on the discussion Delphi_ote and I had of random point mutation independent ways which implies common descent, such as gene order and polyploidisation events. Also, I have been waiting for some time to get an explanation for what exactly it is we see when we construct a phylogenetic tree based on gene data. Does the exact method we use to construct the phylogenies make any difference?

[Kotatsu]

Wow, one of you must have really pushed one of his buttons. He doesn't seem at all as comparatively cheery as he used to, and he doesn't even seem to put as much effort into his insults and lies. Or is it just the combined weight of the responses that's wearing him down?

That'd make sense, really. The more pressure he's under, the slower he thinks.

[Belz...]

Just because you have an interest in mutation and selection doesn’t mean you have any understanding of the process. You have admitted that.

Gosh, if you wanted to prove that you forgot what the context of Joobz' post was, you succeeded quite eloquently.

[Belz...]

Now that we know how mutation and selection actually works, probability theory alone is useless.

Fascinating. And how did you come to the conclusion that it was impossible ? Theory.

Why don’t you tell us what the selection pressure was that evolved the first gene de novo?

You understand nothing of evolution if you think that makes any sense at all.

Tell us what the probability is for a 500 base gene to form by random additions of bases?

Random ? Who said anything about random ?

You may have forgotten the "selection" part. You know, the part that ISN'T part of the definition of "beggaminases" that you so conveniently forgot ?

[Belz...]

Sure I do, you evolutionists have no idea how mutation and selection actually works. This is why you can’t find a single citation which show that n+1 selection pressures evolve more quickly than n selection pressures.

Of course we can. In fact, you keep finding those examples for us.

[Belz...]

Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is
1 – (1.0 x 10^-999999999) ≈ 1

False dichotomy.

[Belz...]

Wow, one of you must have really pushed one of his buttons. He doesn't seem at all as comparatively cheery as he used to, and he doesn't even seem to put as much effort into his insults and lies. Or is it just the combined weight of the responses that's wearing him down?

Check post 6614. Something definitely happened, there.

[kjkent1]

The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.Heck, that's easy, and I'm not even a mathematician:

Let math = The scientific study of the measurement, relationships, and properties of quantities and sets, using numbers and symbols.

Let God = an entity which cannot be measured scientifically.

Therefore, if the creator is God, and God is unmeasurable, then the creator is mathematically impossible.

OK, kleinman, it's your turn -- let's see your math for impossible evolution.

[kleinman]

What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.Do you even know what a fitness landscape looks like, Kleinman? Here is a hint for you -- regardless of the number of selective pressures, the landscape is always a convex shape. There is no such thing as local optima that the population can "get stuck on" or whatever nonsense it is that you assert.
Rocketdodger, you haven’t paid much attention to the citations posted so I’ll repeat one that show some graphics of a very simple fitness landscape for two selection conditions. I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes.
That isn’t a profoundly longish genome is it?I'm not sure why it matters. Do you want to amend your statement to "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 really extra long genomes of extra big size."?
Paul, I’m just pulling your leg for using the term “longish”. No, I am not going to amend the above statement. Are you claiming that ev does not converge to a local optimum, even when Rfrequency exceeds your Rcapacity value?
Paul, there is a way to determine what this factor is. You have to map out the fitness landscape. You do this by computing the mistakes in 4^G combinations of genomes. I’ll let you do the arithmetic on that one. What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.I agree completely, Alan. It's a complicated landscape. What do you suppose creates those hills and valleys? You appear to think it's magic.
Of course I don’t think it is magic. Ev’s complicated fitness landscape is caused by the same thing that causes complicated fitness landscapes in real cases of mutation and selection. There are more potential detrimental mutations at more loci than beneficial mutations at their relatively small number of loci, especially when you have combined selection pressures. You evolutionists like to ignore the detrimental affect of mutations but it is these detrimental mutations which confound the mutation and selection process.
Adding penicillin does not speed up the evolution of weak selection pressures.Please stop saying this. Selection pressures do not evolve. Please say what you actually mean, so at least we have a chance.
Each selection pressure imposes its own sorting condition on the mutation and selection process. Imposing a strong selection pressure on a population does not speed up the sorting process for the weak selection pressures. What the weak selection pressures give is a noisy background that slows the sorting process for the strong selection pressure. Certainly selection pressures do not evolve; they cause a population to evolve by sorting beneficial and detrimental mutations. I’ll try to better with my phraseology. If you are looking for a chance that mutation and selection can give common descent, you don’t have a chance. We now know how the mutation and selection sorting/optimization process works. This sorting/optimization process can barely sort beneficial and detrimental mutations for two targeted genes let alone the thousands of genes which would need to be transformed to evolve reptiles into birds.
I ran two experiments with the standard model but a genome size of 4096:

weight width 7, site width 8 (Rcapacity >> Rfrequency): 124,827 generation to perfect creature

weight width 6, site width 7 (Rcapacity > Rfrequency): 131,375 generation to perfect creaure

weight width 5, site width 6 (Rcapacity > Rfrequency): 163,722 generations to perfect creature

weight width 4, site width 5 (Rcapacity > Rfrequency): 198,279 generations to perfect creature

weight width 3, site width 4 (Rcapacity = Rfrequency): still 16 mistakes after 1,000,000 generations

weight width 2, site width 3 (Rcapacity < Rfrequency): still 16 mistakes after 1,000,000 generations
Your last two cases converge to a local optimum with 16 mistakes rather than a zero mistake local optimum. In order for the population to evolve to a perfect creature in these cases, the population must traverse a reduced fitness trough but the selection conditions prevent this. Take a look at the figures of fitness landscapes I reposted above. That should help you understand why ev behaves as it does. I think you look at this problem in the wrong way. Ev is really showing how few cases will actually converge to a perfect creature, most cases will not.
No rocketdodger, you are attributing a property to mutation and selection that has no mathematical or empirical basis. Adding penicillin does not speed up the evolution of weak selection pressures. The evolution of resistance on the background of weak selection pressures slows the evolution of penicillin resistance.Will introducing penicillin to a population speed up the evolution of penicillin resistance, Kleinman? YES or NO?
You don’t get a yes or no answer to this question. Sometimes you can introduce penicillin to a population and it wipes out the population. Sometimes you can introduce penicillin to a population for which it exerts no selection pressure and therefore does nothing to the population. If you want the fastest evolution of resistance to penicillin for population which is subject to the toxic effects of this drug, you subject the population to a sub-lethal concentration of penicillin while minimizing all other selection pressures and slowly increase the concentration of penicillin. That’s how mutation and selection actually works.
This is your idea of a parametric study. This is the kind of sloppy analysis you evolutionists like to call science. Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.Can you show anyone here why the algorithms used by Dr. Adequate and myself are not sorting algorithms? YES or NO?
It’s up to you two to show that your algorithms actually represent mutation and selection. You definitely haven’t shown that n+1 selection pressures evolve more rapidly than n selection pressures when you say this:
I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.
Like I said, Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.Can you show anyone here what distribution of mutations in a population might correspond to a local optima in the fitness landscape for that population? YES or NO? To make it simple for you Kleinman, lets suppose only two selective pressures of equal magnitude (A and B) are affecting the population.
This one you get a yes answer. See the citation and figures at the beginning of the post. I don’t think you appreciate how complex a real fitness landscape can be but there is an example of a simple fitness landscape for two selection pressures of equal magnitude for a computer simulation.
Precisely why were you skeptical of the interpretation of the evidence presented by evolutionarians before you looked at Dr. Schneider's and Paul's model?
My first real skepticism of abiogenesis and the theory of evolution occurred when I took courses in organic chemistry. In the laboratory we were required to synthesize a variety of more complex molecules from simpler molecules. In order to get a side group to bond to a particular site often required activating catalysts and shielding groups to prevent reactions at other sites. Often times the reactions would have to take place in strongly acidic then strongly basic solutions and visa versa. The idea that the complex organic molecules that form life can occur in some fanciful primordial soup is as joobz puts it, speculation.
Common descent is a myth.While what you say is usually nonsense, I am still waiting for you to comment on the discussion Delphi_ote and I had of random point mutation independent ways which implies common descent, such as gene order and polyploidisation events. Also, I have been waiting for some time to get an explanation for what exactly it is we see when we construct a phylogenetic tree based on gene data. Does the exact method we use to construct the phylogenies make any difference?
Oh, I thought I addressed this, several times, but I’ll address it again for you. So you have polyploidy, how do you transform those duplicated genes to a new form? Why Kotatsu, it requires mutation and selection and as we have seen over and over, transforming more than a single gene at a time profoundly slows the evolutionary process.

You can construct phylogenic trees based on similarities of genes. All that it shows is that living things can have some similarity in chemical structure. In order to use these phylogenic trees as evidence of common descent, you need to show how mutation and selection can accomplish the transformation from one form to another. The mathematical and empirical evidence of mutation and selection shows that it can not make the transformations.
Wow, one of you must have really pushed one of his buttons. He doesn't seem at all as comparatively cheery as he used to, and he doesn't even seem to put as much effort into his insults and lies. Or is it just the combined weight of the responses that's wearing him down?

That'd make sense, really. The more pressure he's under, the slower he thinks.
The only button you have pushed is the laughter button. Are you talking about the combined weight of the citations which show that n+1 selection pressures evolve more rapidly than n selection pressures? I don’t know how I can bear all zero of your citations.
Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is
1 – (1.0 x 10^-999999999) ≈ 1False dichotomy.
Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created. Since you evolutionists have shown that the sum of all probabilities is 1, it is a simple mathematical fact that probability that we were created based on rocketwhomissesthetarget’s own number is ≈ 1. Now you could change this if you can come up with an alternative explanation of how we got here. Wait a minute, you have, we have beggaminased.
The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.Heck, that's easy, and I'm not even a mathematician:

Let math = The scientific study of the measurement, relationships, and properties of quantities and sets, using numbers and symbols.

Let God = an entity which cannot be measured scientifically.

Therefore, if the creator is God, and God is unmeasurable, then the creator is mathematically impossible.

OK, kleinman, it's your turn -- let's see your math for impossible evolution.
Kjkent1, you are not able to measure God but you can measure the creation.

Now, it is not my math which shows the theory of evolution to be mathematically impossible, it is Dr Schneider’s mathematical model of mutation and selection which show how mutation and selection works. What Dr Schneider’s model shows is that combination selection pressures profoundly slow the mutation and selection process and that what real examples of mutation and selection shows. Here are a couple more real examples of mutation and selection which show that combination selection pressures profoundly slow the sorting of beneficial and detrimental mutations.
http://aac.asm.org/cgi/reprint/48/11/4226.pdf (http://aac.asm.org/cgi/reprint/48/11/4226.pdf)
Whether or not resistant mutants will be present before the start of antibiotic treatment of an initially susceptible population of bacteria depends on the size of the infecting population, the rate of mutation to resistance, and the amount of time that the population has been maintained. In the present investigation, we argue that for the treatment of chronic infections caused by hypermutable Pseudomonas aeruginosa of the sort frequently found in cystic fibrosis patients, mutants resistant to all single antipseudomonal drugs will almost invariably be present in a high proportion at the onset of treatment, and consequently, these strains should be considered resistant to all agents when they are used as monotherapy. Using a construct of P. aeruginosa strain PAO1 with a mutS deletion (strain PAO▲mutS), we show that when in vitro populations of less than 5 x 10^4 seemingly susceptible hypermutable bacteria are confronted with any of 11 antipseudomonal agents, mutants for which the MICs and the minimum bactericidal concentrations are in the range of clinical resistance will almost invariably ascend to dominance within 24 to 36 h. This does not occur for PAO1 without the mutS deletion. The results of our detailed analysis of this evolution of acquired resistance to two of these antibiotics, imipenem and ciprofloxacin, indicate that although the rates of mutation to resistance in PAO▲mutS are on the order of 1 x 10^6 per generation, resistant mutants are very likely to either be present in cultures of between 2 x 10^4 and 4 x 10^4 bacteria or arise after the bacterial populations are confronted with antibiotics. We also demonstrate with in vitro experiments that the problem of acquired resistance to treatment with single antibiotics can be thwarted by combination therapy with pairs of antibiotics of different classes with synergistic activities. We discuss the clinical implications of our analysis of these observations.
This following citation is for rocketwhomissesthetarget who thinks that weak selection pressures do not slow the evolutionary process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90521 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90521)
Understanding the mechanisms of the emergence of drug resistance and the factors that affect it will aid in the design of improved preventive strategies. This will occur by several means. Experimental data will help refine the mathematical models of the emergence of resistance and also provide a basis for predicting the probability of the development of resistance to new agents (10). Furthermore, the results of the drug combination experiments suggest that susceptibility results may not be a good indicator of the utility of antimicrobials for prevention of the emergence of resistance to other agents. Thus, drugs that are not considered highly active may still have a role in reducing or preventing resistance. The screening of antibiotics for the ability to reduce the level of resistance has been proposed by others (4, 10), and the results presented here lend support to that approach. However, the problem may be how to assess the emergence of resistance in a straightforward, reproducible, and clinically relevant manner (10).
Drugs which have weak selective affect still slow the evolution of resistance to strong selection pressures. That’s how the mutation and selection sorting/optimization process works mathematically and that’s how the process works empirically.

[sol invictus]

Creationism was proven impossible long ago.


Is God willing to prevent evil, but not able? Then he is impotent.

Is he able, but not willing? Then he is malevolent.

Is he both able and willing? Then whence is evil?

Is he neither able nor willing? Then why call him God?

[sol invictus]

It’s up to you two to show that your algorithms actually represent mutation and selection. You definitely haven’t shown that n+1 selection pressures evolve more rapidly than n selection pressures when you say this:

I offered you a bet on this using your own algorithm, the one you claimed demonstrated this "fact", and you won't take it. You won't take it because you are lying, you know you are lying, and you know you will lose.

Why do you keep lying?

[rocketdodger]

Rocketdodger, you haven’t paid much attention to the citations posted so I’ll repeat one that show some graphics of a very simple fitness landscape for two selection conditions. I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)

You stupid fool. That paper discusses the effects of applying a series of goals, one after the other, to the model population. The fitness landscapes they produce, which show local maxima, are simply the result of superimposing the landscapes of each individual goal.

If you consider all the goals at once, the landscape generated is simply a huge bulge -- one convex shape, with only a global maxima.

If you disagree, then give us all an answer to my question -- given two goals A and B, each of equal weight, what distribution would constitute a local maxima? Or in words you can understand, what location on the fitness landscape?

The top image shows the trajectory ...
...snip...
This is the same reason ev becomes very slow converging for longer genomes.

This paragraph of rubbish has nothing at all to do with the actual study you cited you fool.

[kleinman]

Creationism was proven impossible long ago.Is God willing to prevent evil, but not able? Then he is impotent.

Is he able, but not willing? Then he is malevolent.

Is he both able and willing? Then whence is evil?

Is he neither able nor willing? Then why call him God?
Both you and Epicurus fail to understand that God does not allow evil to go un-judged. God has His own perfect timing for judging and punishing evil. If God judged evil at the moment that it occurs, no one would survive, but with God there is forgiveness that He is to be feared. That is not my idea; it is what the Bible says. God judges with a perfect balance of justice and mercy on His perfect time scale. Too bad you have no understanding of the rate at which God does things but read the prophecy of Habakkuk in the Bible if you want to learn about this. Habakkuk asked the same questions that Epicurus asked, the difference is Habakkuk got the answer.
Rocketdodger, you haven’t paid much attention to the citations posted so I’ll repeat one that show some graphics of a very simple fitness landscape for two selection conditions. I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.You stupid fool. That paper discusses the effects of applying a series of goals, one after the other, to the model population. The fitness landscapes they produce, which show local maxima, are simply the result of superimposing the landscapes of each individual goal.

If you consider all the goals at once, the landscape generated is simply a huge bulge -- one convex shape, with only a global maxima.

If you disagree, then give us all an answer to my question -- given two goals A and B, each of equal weight, what distribution would constitute a local maxima? Or in words you can understand, what location on the fitness landscape?
Rocketwhomissesthetarget almost gets it right; these authors are accelerating the evolutionary process by applying the selection pressures sequentially. However, if you look at the fourth image down, the ‘Virtual’ varying landscape, you will see what the two superimposed fitness landscape with the two goals looks like. So go home and cry in your primordial soup. Then tomorrow morning go see your optometrist because you need new glasses.
The top image shows the trajectory ...
...snip...
This is the same reason ev becomes very slow converging for longer genomes.This paragraph of rubbish has nothing at all to do with the actual study you cited you fool.
How would you know? You don’t know anything about ev, you have admitted it already.
I am eager to participate in this discussion but I don't know the mathematical details of the topic, only general ideas. Paul, is there a good introductory source (assuming I am fluent in mathematics) where I can learn what this equation you guys are talking about represents? All this Rseq~ and Rfreq~ stuff is lost on me.
And now you are proving you are not fluent in mathematics. Where did you graduate from Rocketwhomissesthetarget, Mathishard University?

[joobz]

You stupid fool. That paper discusses the effects of applying a series of goals, one after the other, to the model population. The fitness landscapes they produce, which show local maxima, are simply the result of superimposing the landscapes of each individual goal.

If you consider all the goals at once, the landscape generated is simply a huge bulge -- one convex shape, with only a global maxima.

If you disagree, then give us all an answer to my question -- given two goals A and B, each of equal weight, what distribution would constitute a local maxima? Or in words you can understand, what location on the fitness landscape?
The funny part is that kleinman's stupid lie:

I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.
Was actually a confusion of references. I referenced both the paper he missquotes simultaneously along with the paper, "Evolution in the hypervariable environment of Madagascar" in PNAS (see link).

http://www.pnas.org/cgi/content/abstract/104/34/13723

I used those to papers to demonstrate that his assumption that
slection pressures are constant and known is completely and totally false. Since we know that weather can induce hypervariable environments and that these variable environments can accelerate evolutionary adaptation, his whole point is foolishly wrong.

He knows this. He knows better, but he'd rather believe and lie than know reality.

[Paul C. Anagnostopoulos]

Your last two cases converge to a local optimum with 16 mistakes rather than a zero mistake local optimum. In order for the population to evolve to a perfect creature in these cases, the population must traverse a reduced fitness trough but the selection conditions prevent this.
And that gobbledegook is called the Rcapacity problem.

~~ Paul

[rocketdodger]

Rocketwhomissesthetarget almost gets it right; these authors are accelerating the evolutionary process by applying the selection pressures sequentially. However, if you look at the fourth image down, the ‘Virtual’ varying landscape, you will see what the two superimposed fitness landscape with the two goals looks like.

They explicitly say, in great detail, how they temporally vary the goals back and forth in this experiment. This is not the fitness landscape produced when the model population is going for both goals at once -- they did not include that scenario in the experiment. Haven't you read the paper, Kleinman? Or did you just cite the first thing google found for you...

And if it was, it would be direct proof that your theory is wrong, because switching between the first and second goal allows the population to pull itself out of any local maxima they are in.

With regards to my earlier statement that local maxima do not exist in such graphs, I misspoke -- I was thinking of pressures as targeting single bases, rather than entire loci. In the latter case, there would be many possible combinations of mutations that would satisfy a given pressure, which would indeed lead to local optima. Unfortunately for you, Kleinman, local optima are completely irrelevant to evolutionary rate.

How would you know? You don’t know anything about ev, you have admitted it already.

Yes, I asked Paul for a reference on his program, I read it, and now I know what I wanted to know about it -- in particular, that you don't know wtf you are talking about. Congratulations on showing everyone the obvious, Kleinman.


And now you are proving you are not fluent in mathematics. Where did you graduate from Rocketwhomissesthetarget, Mathishard University?

I graduated from the University of Arizona. Where did you graduate from, Kleinman?

[rocketdodger]

You don’t get a yes or no answer to this question. Sometimes you can introduce penicillin to a population and it wipes out the population.
Sometimes you can introduce penicillin to a population for which it exerts no selection pressure and therefore does nothing to the population.
If you want the fastest evolution of resistance to penicillin for population which is subject to the toxic effects of this drug, you subject the population to a sub-lethal concentration of penicillin while minimizing all other selection pressures and slowly increase the concentration of penicillin. That’s how mutation and selection actually works.

Ok, lets rephrase: Will introducing a sub-lethal penicllin pressure increase the rate of evolution of penicillin resistance in a population? YES or NO?


It’s up to you two to show that your algorithms actually represent mutation and selection.

We never claimed they did. We only said they were modeled on mutation and selection. Our claim, which still stands, is that they are sorting algorithms. So far you have completely failed to show otherwise, which is pretty pathetic, considering my algorithm only has 4 steps.

You definitely haven’t shown that n+1 selection pressures evolve more rapidly than n selection pressures when you say this:

We only showed that in our simulations such a thing happens. We have no intent of proving it in reality, because we don't need to. You claimed all sorting algorithms are confounded by additional sorting conditions. We showed otherwise. Mutation and selection, in reality, is irrelevant to this claim of yours as well as our disproof of it.

And for the record, you are a lying, misinforming, manipulative troll. I posted an exact set of parameters for my simulation and I addressed your concerns regarding parametric studies of it, random number seed problems, etc, multiple times. Despite this, you keep repeating the initial statement of mine regarding having forgotten the parameters I used late one night to just make sure my program ran. Doing so illustrates nothing more than what a douchebag you are.

This one you get a yes answer. See the citation and figures at the beginning of the post. I don’t think you appreciate how complex a real fitness landscape can be but there is an example of a simple fitness landscape for two selection pressures of equal magnitude for a computer simulation.

Except, this is not an example of a fitness landscape generated by two simultaneous pressures. Regardless, I was incorrect about the lack of local maxima in such graphs.

All of this has nothing to do with the rate of fixation under multiple pressures.

Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created. Since you evolutionists have shown that the sum of all probabilities is 1, it is a simple mathematical fact that probability that we were created based on rocketwhomissesthetarget’s own number is ≈ 1.

Relying on false dichotomy only illustrates how pathetically desperate you are Kleinman. Treat the two as independent events. We are still waiting for a number you feel is an accurate probability of creationism being true.

[kjkent1]

Both you and Epicurus fail to understand that God does not allow evil to go un-judged. God has His own perfect timing for judging and punishing evil. If God judged evil at the moment that it occurs, no one would survive, but with God there is forgiveness that He is to be feared. That is not my idea; it is what the Bible says. God judges with a perfect balance of justice and mercy on His perfect time scale. Too bad you have no understanding of the rate at which God does things but read the prophecy of Habakkuk in the Bible if you want to learn about this. Habakkuk asked the same questions that Epicurus asked, the difference is Habakkuk got the answer.Tell that to every woman who's ever gone through labor.

God is a misogynist (Genesis 3:14-16), and a slaver (Exodus 21). You worship a monster. All history and his own writing demonstrates His incomparable evil.

[Kotatsu]

Oh, I thought I addressed this, several times, but I’ll address it again for you. So you have polyploidy, how do you transform those duplicated genes to a new form? Why Kotatsu, it requires mutation and selection and as we have seen over and over, transforming more than a single gene at a time profoundly slows the evolutionary process.

Cute. However, your stock answer doesn't in any way address what I am talking about, as the process I mention is independent of random point mutations and other kinds of mutations that alter the exact sequence. I am talking about the very process of polyploidisation, not what happens afterwards.

"I" transform the diploid genome into a polyploid one simply by doubling the copies of all involved chromosomes by one of several known mechanisms. When this occurs in only one of several individuals --- as is often the case --- we see diploid and polyploid individuals who have the exact same gene order and nucleotide sequences. No other mutations need to be involved. This is still evidence of common descent of these organisms.

I remind you also of the paper by Song et al. in which allopolyploids evolved "extensive genomic differences" which were expressed in at least five ecological or morphological traits. This occurred within five generations after the polyploidisation event. Apparently, these things can happen more rapidly than you can imagine.

And please don't take me on the "name the selection pressures and targeted genes" merry-go-round again --- at least not until you have read that article and understood it.

You can construct phylogenic trees based on similarities of genes. All that it shows is that living things can have some similarity in chemical structure. In order to use these phylogenic trees as evidence of common descent, you need to show how mutation and selection can accomplish the transformation from one form to another. The mathematical and empirical evidence of mutation and selection shows that it can not make the transformations.

The mathematical and empirical evidence shows that "we" can make those "transformations". I take it you have never seen an alignment of genes, have you?

Showing how this could work is rather easy. Take COI, for example, which I have worked with previously. When examining almost any given alignment of COI, you will notice a pattern. The differences between taxa almost invariably occur in every third position. A small amount occur in the positions before those, and almost none are in the positions after the first ones. This shows us that there is a higher tolerance for variation in every third position. Not surprisingly, when we translate these sequences into amino acids, the variable positions are third positions, the less variable positions are second positions, and the least variable positions are first positions. This makes sense, because variation in third positions is least likely to change the resulting amino acid, whereas variations in second and first positions are progressively more likely to change amino acid.

Thus, if we study this gene in organisms of a given genus, we will see slight differences between them. These differences are mainly in third positions, and can be adequately explained by random point mutations. These mutations may occur at any point in the gene, of course, but as first and second positions are more likely to change the amino acid, and thus the chemical and sterical properties of the protein, they are usually selected against.

This gives us a framework for phylogenetic research. Add sufficient taxa to your matrix, and compare the differences between the sequences. Many of the third positions will differ between closely related species. Most of them differ between more distantly related organisms, and with sufficient time of separation, second positions also show differences, and even first positions. When the taxa are too distantly related, of course, there is saturation, and COI cannot be used (but there are other regions used for those levels). However, the point is that these differences, which occur precisely by random point mutation and subsequent selection, form nested hierarchies. These are usually bifurcations, as is predicted from the more common ways of speciation.

These is no point along this road in which you are correct.

The only button you have pushed is the laughter button. Are you talking about the combined weight of the citations which show that n+1 selection pressures evolve more rapidly than n selection pressures? I don’t know how I can bear all zero of your citations.

I have posted five or six examples of how you are wrong in this regard. You have dismissed them without reading them, because you cannot understand what they are about. This is not my problem, obviously, but it is wrong to say that I have presented zero citations.

Also, the pressure I was referring to was that I believe there are more people arguing against you (or at least trying to, but your childish copy-paste-dismiss routine makes that kind of hard) than there used to be. We are your selection pressures, and in this limited context, you are correct. The evolution of your arguments has slowed and will presumably stop once we are enough people.

[Belz...]

Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created.

Yeah, that's what I said. False dichotomy.

[Belz...]

Both you and Epicurus fail to understand that God does not allow evil to go un-judged.

Funny, because lots of evil goes un-judged.

God has His own perfect timing for judging and punishing evil.

Which is retarded, because he knows in advance that evil will occur, yet he chooses to let it happen to people who don't deserve it.

Why is God evil ?

If God judged evil at the moment that it occurs, no one would survive

Why ? Is every evil punishable by death ?

Why is God evil ?

but with God there is forgiveness that He is to be feared.

Well, he blew that one, didn't he ?

Too bad you have no understanding of the rate at which God does things

Well that rate must be pretty slow, considering the number of selection pressures he's probably under, right ?

[Mr. Scott]

My first real skepticism of abiogenesis and the theory of evolution occurred when I took courses in organic chemistry. In the laboratory we were required to synthesize a variety of more complex molecules from simpler molecules. In order to get a side group to bond to a particular site often required activating catalysts and shielding groups to prevent reactions at other sites. Often times the reactions would have to take place in strongly acidic then strongly basic solutions and visa versa. The idea that the complex organic molecules that form life can occur in some fanciful primordial soup is as joobz puts it, speculation.[/SIZE][/FONT]

Were you fine with evolution before these experiments?

How old were you when this occurred?

Were you the only one in the class who first experienced "real skepticism" during that exercise?

Aren't you again confusing abiogenesis with evolution? This discussion is about evolution after abiogenesis occurred. Many Christians and world class scientists are fine with the idea that God took care of abiogenesis and sat back while it evolved into us. Nothing I know of in the genetic or geologic evidence contradicts this possibility.

What problem do you have with the theory that God started abiogenesis and let evolution run its course on its own?

[sol invictus]

Well that rate must be pretty slow, considering the number of selection pressures he's probably under, right ?

:)

[sol invictus]

That is not my idea; it is what the Bible says.

As little credibility as you have, kleinman, it's greater than that of some loser who wandered out into the desert 2,500 years ago and ate a bad cactus.

Read this. Who knows, you might learn something.

http://books.google.com/books?id=lu6ywyJr0CMC&dq=the+bible+unearthed&pg=PP1&ots=lPG0Nvh45B&sig=QX8sgw3N0KkGo9j6WxKzJlBfJVE&prev=http://www.google.com/search%3Fq%3Dthe%2Bbible%2Bunearthed%26ie%3Dutf-8%26oe%3Dutf-8%26aq%3Dt%26rls%3Dorg.mozilla:en-US:official%26client%3Dfirefox-a&sa=X&oi=print&ct=title&cad=one-book-with-thumbnail

Anyway, given that you have blind faith in religion, why do you need to lie about mathematics? Maybe your faith isn't so strong after all?

[rocketdodger]

I improved my program and now it generates results on par with what Dr. Adequate got.
Source code can be found here: www.jedi-arts.com/code/jev.cpp.
Executable (this was compiled on Vista so it might only work on 64 bit machines): www.jedi-arts.com/code/jev.exe.
Example input file (this must be placed in the same directory as the .exe): www.jedi-arts.com/code/data.txt.

Improvements --

*The ability to specify stabilizing pressures was added, so now Kleinman can't whine about us not accounting for detrimental mutations at non-targeted locations. In addition there is a "directionalWeight" parameter that allows you to jack up the relative intensity of directional pressures over the stabilizing pressures.

*The output, which was previously the average fixation rate as determined after all pressures had been fixed, is now simply the sum of all fixation activity in a given number of generations. "Fixation activity" is calculated as the inverse of the number of generations between a targeted mutation's first appearance and fixation. So for example if a targeted mutation first appears in generation 15, and gets fixed in generation 37, the fixation activity for the pressure is 1/(37 - 15). This is the most accurate measure of "rate of evolution" that I can think of.

*Because of the above change, each rep of a simulation always stops after a given number of generations, resulting in much faster simulation run times.

A selection of run results can be found at www.jedi-arts.com/code/sims.txt.

The results are clear. Regardless of the conditions, adding selective pressures can increase the amount of overall fixation in a given number of generations.

Intuitively, the additional fixation activity due to more pressures outweighs any slowdown in fixation time for each pressure. The larger the span of generations that you measure over (I used 10k generations for all of the above samples), the more profound this effect becomes.

[kleinman]

Your last two cases converge to a local optimum with 16 mistakes rather than a zero mistake local optimum. In order for the population to evolve to a perfect creature in these cases, the population must traverse a reduced fitness trough but the selection conditions prevent this.And that gobbledegook is called the Rcapacity problem.
No Paul, that’s what is called a simulation of reality. Here is a real example of this:
“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”
Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111
Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable.
You have to have a trajectory on the fitness landscape which allows the population to get to that local optimum. It is your Rcapacity concept which is nonsense.
Rocketwhomissesthetarget almost gets it right; these authors are accelerating the evolutionary process by applying the selection pressures sequentially. However, if you look at the fourth image down, the ‘Virtual’ varying landscape, you will see what the two superimposed fitness landscape with the two goals looks like.They explicitly say, in great detail, how they temporally vary the goals back and forth in this experiment. This is not the fitness landscape produced when the model population is going for both goals at once -- they did not include that scenario in the experiment. Haven't you read the paper, Kleinman? Or did you just cite the first thing google found for you...
Didn’t you know, joobz cited this article however he didn’t read it, he thought varying environments had to do with the weather. So let’s see what these authors have to say:
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
Simulations of biological evolution, in which computers are used to evolve systems toward a goal, often require many generations to achieve even simple goals. It is therefore of interest to look for generic ways, compatible with natural conditions, in which evolution in simulations can be speeded. Here, we study the impact of temporally varying goals on the speed of evolution, defined as the number of generations needed for an initially random population to achieve a given goal. Using computer simulations, we find that evolution toward goals that change over time can, in certain cases, dramatically speed up evolution compared with evolution toward a fixed goal. The highest speedup is found under modularly varying goals, in which goals change over time such that each new goal shares some of the subproblems with the previous goal. The speedup increases with the complexity of the goal: the harder the problem, the larger the speedup. Modularly varying goals seem to push populations away from local fitness maxima, and guide them toward evolvable and modular solutions. This study suggests that varying environments might significantly contribute to the speed of natural evolution. In addition, it suggests a way to accelerate optimization algorithms and improve evolutionary approaches in engineering.
And that’s what I have been saying for months now, single selection pressures evolve quickly. Single selection pressures toward a single goal applied sequentially is the only way you can achieve accelerated evolution. As soon as you combine selection pressures, the trajectory is confounded and the entire sorting/optimization process is profoundly slowed.
Oh, I thought I addressed this, several times, but I’ll address it again for you. So you have polyploidy, how do you transform those duplicated genes to a new form? Why Kotatsu, it requires mutation and selection and as we have seen over and over, transforming more than a single gene at a time profoundly slows the evolutionary process.Cute. However, your stock answer doesn't in any way address what I am talking about, as the process I mention is independent of random point mutations and other kinds of mutations that alter the exact sequence. I am talking about the very process of polyploidisation, not what happens afterwards.
Why don’t you mention that the majority of the examples of aneuploidy are harmful.
"I" transform the diploid genome into a polyploid one simply by doubling the copies of all involved chromosomes by one of several known mechanisms. When this occurs in only one of several individuals --- as is often the case --- we see diploid and polyploid individuals who have the exact same gene order and nucleotide sequences. No other mutations need to be involved. This is still evidence of common descent of these organisms.
Wheat evolving by polyploidisation into wheat is an example of “common descent”? So are you now going to make the leap and tell us that reptiles evolved into birds by polyploidisation? You evolutionists do love you speculations and extrapolations.
You can construct phylogenic trees based on similarities of genes. All that it shows is that living things can have some similarity in chemical structure. In order to use these phylogenic trees as evidence of common descent, you need to show how mutation and selection can accomplish the transformation from one form to another. The mathematical and empirical evidence of mutation and selection shows that it can not make the transformations.The mathematical and empirical evidence shows that "we" can make those "transformations". I take it you have never seen an alignment of genes, have you?
If you have the mathematical and empirical evidence, why are you always trying to inoculate yourself from having to specify the selection pressures and target genes to these pressures? I continue to post measurable and repeatable examples of mutation and selection which show combination selection pressures profoundly slow the evolutionary process while you continue to fail to post examples of mutation and selection which show otherwise and the examples you do post don’t define the selection pressures or the target genes for these selection pressures.
The only button you have pushed is the laughter button. Are you talking about the combined weight of the citations which show that n+1 selection pressures evolve more rapidly than n selection pressures? I don’t know how I can bear all zero of your citations.I have posted five or six examples of how you are wrong in this regard. You have dismissed them without reading them, because you cannot understand what they are about. This is not my problem, obviously, but it is wrong to say that I have presented zero citations.
None of your citations define the selection pressures and the target genes for these selection pressures. You post citations are not repeatable or measurable. The hundreds of citations I have and will continue to post more of all show how mutation and selection actually works. And the way this sorting/optimization problem works is that combined selection pressures have a profound slowing on the sorting of beneficial and detrimental mutations. The mutation and selection process can only sort mutations for a single selection condition targeting a single gene with any rapidity. As soon as two or more genes are targeted, the process is profoundly slowed. That’s how mutation and selection works mathematically and that’s how mutation and selection works empirically.
Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created.Yeah, that's what I said. False dichotomy.
We are all waiting for you to tell us any other possible way that we got here. Maybe you can make it a false trichotomy?
Both you and Epicurus fail to understand that God does not allow evil to go un-judged.Funny, because lots of evil goes un-judged.
How do you know? Do you think the fiend god gets away with evil?
My first real skepticism of abiogenesis and the theory of evolution occurred when I took courses in organic chemistry. In the laboratory we were required to synthesize a variety of more complex molecules from simpler molecules. In order to get a side group to bond to a particular site often required activating catalysts and shielding groups to prevent reactions at other sites. Often times the reactions would have to take place in strongly acidic then strongly basic solutions and visa versa. The idea that the complex organic molecules that form life can occur in some fanciful primordial soup is as joobz puts it, speculation.Were you fine with evolution before these experiments?
I never really gave much thought to the topic but now that I work in a profession which must deal with mutation and selection, I’ve decided to study the process in more detail. In addition, many evolutionists use the theory to argue there is no God. It is clear now that the theory of evolution by mutation and selection is mathematically and empirically impossible. The mutation and selection sorting/optimization process simply does not work the way evolutionists allege.
I improved my program and now it generates results on par with what Dr. Adequate got.
Then you get what Adequate got for all his real examples he posted of his model.
http://forums.randi.org/images/smilies/doglaugh.gif
And here is for all the data you have posted which shows that n+1 selection pressures evolve more quickly than n selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11448283&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11448283&dopt=AbstractPlus)
CONTEXT: The continued release of human immunodeficiency virus type 1 (HIV-1) into plasma at very low levels during highly active antiretroviral therapy (HAART) can be detected using specialized techniques, but the nature and significance of this low-level viremia, especially as related to acquisition of drug resistance mutations, are unclear. OBJECTIVE: To determine genetic resistance profiles of low-level plasma HIV-1 in patients with prolonged viral suppression (<50 copies/mL of plasma HIV-1 RNA) while receiving HAART. DESIGN AND SETTING: Cross-sectional study conducted at a US academic hospital from November 1999 to February 2001 using a novel method for amplification of low levels of viral genomes in plasma. PATIENTS: Eighteen HIV-1-infected patients (7 children and 11 adults), enrolled in a longitudinal study of HIV-1 reservoirs, who had suppression of viral replication while receiving protease inhibitor-containing combination therapy. Two patients (1 adult and 1 child) with less optimal suppression of viral replication were included to assess virus predominating when plasma HIV-1 RNA levels are low but detectable (<1000 copies/mL). Follow-up analyses were conducted in 3 patients. MAIN OUTCOME MEASURE: Detection of drug resistance mutations in clones amplified from low-level plasma virus. RESULTS: Viral sequences were amplified from 8 of the 18 patients with simultaneous plasma HIV-1 measurements of less than 50 copies/mL and from 2 patients with 231 and 50 copies/mL. Clones from 3 treatment-naive patients with less than 50 copies/mL of plasma HIV-1 RNA showed continued release, for as long as 42 months, of wild-type drug-sensitive virus. The 7 patients with prior nonsuppressive therapy, with viral loads below 50 copies/mL and during "blips" to 231 and 64 copies/mL, had only resistance mutations consistent with pre-HAART therapy (although reverse transcriptase inhibitor mutations may have continued to occur). New HAART-related mutations were seen in a control patient with prior viral load levels of about 400 to 1000 copies/mL. For phylogenetic analysis, sequences were available for both resting CD4(+) T cells and plasma HIV for 7 of 10 patients and showed patient-specific clustering of sequences and a close relationship between virus in the plasma and the latent reservoir. CONCLUSIONS: Based on the samples that could be amplified, low-level viremia in children and adults receiving HAART with prolonged suppression of viremia to less than 50 copies/mL of HIV-1 RNA may result primarily from archival, pre-HAART virus, reflecting earlier treatment conditions, and does not appear to require development of new, HAART-selected mutations reflecting partial resistance to therapy. Low-level viremia below 50 copies/mL may represent less of a concern regarding impending drug failure of current HAART regimens. However, the archival drug-resistant virus may be relevant regarding future treatment strategies.

“Antibiotic interactions that select against resistance”
Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgs
Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens. On a broader scale, such combinations are also important in understanding microbial ecology and evolution. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.
So here is an example where combination selection pressures not only slow the evolutionary process, it reverses the evolutionary process.

[Belz...]

We are all waiting for you to tell us any other possible way that we got here. Maybe you can make it a false trichotomy?


Just because you can't think of a third way doesn't mean there isn't one.

But that's besides the point, as anyone who's ever studied logic knows. You can't prove a theory by disproving another one.

Funny, because lots of evil goes un-judged.

How do you know?

Because to claim otherwise would be an argument from ignorance.

Do you think the fiend god gets away with evil?

He doesn't, because he doesn't exist.

[rocketdodger]

So you are only putting up single sentence dodges now. Getting tired of writing bullsh--, Kleinman? Just in case anyone might forget, I will recap the issues you keep dodging.

You claim sorting algorithms are always slowed by additional sorting conditions. Dr. Adequate and I have written independent programs which use sorting algorithms yet are not slowed by additional sorting conditions. You demand real world examples -- our programs are real world examples you fool. This issue is completely unrelated to evolution. It is about your claims regarding sorting algorithms.

You claim the probabililty of creation is greater than the probability of evolution. You have failed to come up with any sort of independent value for the probability of creation. Because you can't come up with a value, you rely on a false dichotomy. We are still waiting for you to show us how to generate a value independent of evolution.

You claim that the studies you cite show multiple selective pressures to slow evolution profoundly. They do no such thing. What they show is that lethal pressures, when combined, prevent populations from evolving resistance -- by killing them. If a population dies, obviously there will be no more evolution. The few studies you do cite that do not use lethal pressures fail to measure anything that could be construed as a "rate" of evolution.

You claim that the ev program can be used to generate data regarding the effects of the number of selective pressures on a population. The ev program only features 3 pressures, and they target the same loci. Only a fool would consider this a large enough input domain for generalizations about selective pressures in general. Furthermore, the model used in the ev program was never intended to show anything about selective pressures. Paul, the programmer who wrote the java version, has told you this. Yet, in your foolish vanity you presume to think you know, better than he does, what is in the source code.

[rocketdodger]

And that’s what I have been saying for months now, single selection pressures evolve quickly. Single selection pressures toward a single goal applied sequentially is the only way you can achieve accelerated evolution. As soon as you combine selection pressures, the trajectory is confounded and the entire sorting/optimization process is profoundly slowed.

My god, you are so dense. Did you not read the paper? They sped up evolution, compared to a single pressure, by temporally alternating the application of two pressures. If you think this finding helps your case, you are truly insane.

So here is an example where combination selection pressures not only slow the evolutionary process, it reverses the evolutionary process.

Evolution can't be reversed, you fool, any more than you can walk a negative distance. In that study they simply inverted the direction of a selective pressure. You seriously need to 1) read and 2) think before you cite.

[rocketdodger]

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11448283&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11448283&dopt=AbstractPlus)

What is this supposed to show? Once again, I must ask, did you even read the paper Kleinman?

Please tell me how this citation has any bearing on any arguments made in this thread.

[kleinman]

We are all waiting for you to tell us any other possible way that we got here. Maybe you can make it a false trichotomy?Just because you can't think of a third way doesn't mean there isn't one.

But that's besides the point, as anyone who's ever studied logic knows. You can't prove a theory by disproving another one.
Sure you can prove something by disproving something else, it called the process of elimination and the theory of evolution has been eliminated. So now we got here either by creation or something you can’t think of.
Funny, because lots of evil goes un-judged.How do you know?Because to claim otherwise would be an argument from ignorance.
Tell us of what evil that hasn’t gone un-judged?
Do you think the fiend god gets away with evil?He doesn't, because he doesn't exist.
How do you know he doesn’t exist?
You claim sorting algorithms are always slowed by additional sorting conditions. Dr. Adequate and I have written independent programs which use sorting algorithms yet are not slowed by additional sorting conditions. You demand real world examples -- our programs are real world examples you fool. This issue is completely unrelated to evolution. It is about your claims regarding sorting algorithms.
Adequate has posted a silly graph and you have posted the following:
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
Neither of you have done a systematic presentation of your models or given a real example of your models. On the other hand, I have posted hundreds of cases from ev including those which show that single selection conditions in the model evolve many orders of magnitude faster than all three selection conditions simultaneously. If you are having trouble running ev, either Paul or I can help you with this. In addition I have posted and will continue to post real examples which demonstrate what Dr Schneider’s peer reviewed and published model shows, which are combination selection pressures profoundly slow the evolutionary sorting/optimization process.
You claim the probabililty of creation is greater than the probability of evolution. You have failed to come up with any sort of independent value for probability of creation. Because you can't come up with a value, you rely on a false dichotomy. We are still waiting for you to show us how to generate a value independent of evolution.
Sure I have, you gave the probability of the theory of evolution to be true at 1.0 x 10^-999999999, the only other possibility is that we were created. So unless you want to claim that the probability that we are here is less than 1, then the probability that we were created is 1 – (1.0 x 10^-999999999) ≈ 1. Do you want to propose another way we came to be?
You claim that the studies you cite show multiple selective pressures to slow evolution profoundly. They do no such thing. What they show is that lethal pressures, when combined, prevent populations from evolving resistance -- by killing them. If a population dies, obviously there will be no more evolution. The few studies you do cite that do not use lethal pressures fail to measure anything that could be construed as a "rate" of evolution.
You still don’t understand that none of the drug therapies used to treat HIV kills the virus. They only inhibit the virus’s ability to reproduce. Either way, selection pressures can kill the members of the population or reduce the ability of members of the population to reproduce, the end result is the reduction in fitness of the population. Combination selection pressures reduce the fitness of a population to reproduce.
You claim that the ev program can be used to generate data regarding the effects of the number of selective pressures on a population. The ev program only features 3 pressures, and they target the same loci. Only a fool would consider this a large enough input domain for generalizations about selective pressures in general. Furthermore, the model used in the ev program was never intended to show anything about selective pressures. Paul, the programmer who wrote the java version, has told you this. Yet, in your foolish vanity you presume to think you know, better than he does, what is in the source code.
I though you said you understood how ev works. Every locus in the genome is subject to the selection pressures in ev when all three selection pressures are imposed. Only when you set selection pressures in the model to zero are only certain loci targeted. Apparently in your studies of ev you failed to read Dr Schneider’s publication on his model. He published the following statement concerning his model:
The weight matrix gene for an organism is translated and then every position of that organism's genome is evaluated by the matrix.
So you got this wrong about the ev model and Dr Schneider said the following for how he intended to have ev used.
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 added the highlighting for you rocketwhomissesthetarget. There are many interesting things you can learn about the mathematics of mutation and selection if you understand how ev works. So far, you have not demonstrated any of this understanding.
So here is an example where combination selection pressures not only slow the evolutionary process, it reverses the evolutionary process.Evolution can't be reversed, you fool, any more than you can walk a negative distance. In that study they simply inverted the direction of a selective pressure. You seriously need to 1) read and 2) think before you cite.
“Antibiotic interactions that select against resistance”
Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgs
Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens. On a broader scale, such combinations are also important in understanding microbial ecology and evolution. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.
Since simply color highlighting is not enough for rocketwhomissesthetarget, what do you think these authors mean byinversion of selection?

[rocketdodger]

Adequate has posted a silly graph and you have posted the following:

No. Both of us provided you with source code and a number of example outputs. I even compiled a .exe for you to run on your own.


Neither of you have done a systematic presentation of your models or given a real example of your models.

No. Both of us have described the workings of our model in great detail, in addition to providing the source code for you to examine. In addition, both of us have given you a real example of our models -- the programs we wrote according to them.

You just don't get it, do you? Forget about evolution, mutation and selection, beggaminuses, whatever. Concentrate on sorting algorithms. You claim sorting algorithms are always slowed by additional sorting conditions. Both algorithms we have shown you are sorting algorithms, and neither are slowed by additional sorting conditions. How can you explain this?


On the other hand, I have posted hundreds of cases from ev including those which show that single selection conditions in the model evolve many orders of magnitude faster than all three selection conditions simultaneously.

No. Nobody, not a single person in the history of this thread other than yourself, thinks these ev run cases show this. The extent of your argument here, Kleinman, is "I set two of the three doohickies that say 'pressure' to zero, and the thingy finishes sooner." Can you explain to all of us why setting the weight distribution to 10-1-1 instead of 10-0-0 completely refutes your claim?


Sure I have, you gave the probability of the theory of evolution to be true at 1.0 x 10^-999999999, the only other possibility is that we were created. So unless you want to claim that the probability that we are here is less than 1, then the probability that we were created is 1 – (1.0 x 10^-999999999) ≈ 1. Do you want to propose another way we came to be?

I see. You have used a probability independent of creationism to find the probability of creationism. The limits of your genius know no bounds, Kleinman.


You still don’t understand that none of the drug therapies used to treat HIV kills the virus. They only inhibit the virus’s ability to reproduce.

Which is why I said:
lethal pressures, when combined, prevent populations from evolving resistance -- by killing them.

Tell me, Kleinman, if a population stops reproducing, how can it evolve?


Either way, selection pressures can kill the members of the population or reduce the ability of members of the population to reproduce, the end result is the reduction in fitness of the population. Combination selection pressures reduce the fitness of a population to reproduce.

Yes, and when that fitness is reduced to stagnation, as in every study you are relying on, evolution will obviously proceed very slow. Kleinman, can you cite even a single real world study that doesn't involve pressures designed to destroy a population?


I though you said you understood how ev works. Every locus in the genome is subject to the selection pressures in ev when all three selection pressures are imposed. Only when you set selection pressures in the model to zero are only certain loci targeted. Apparently in your studies of ev you failed to read Dr Schneider’s publication on his model. He published the following statement concerning his model:

I said:
The ev program only features 3 pressures, and they target the same loci.

If all the pressures target all the loci, then they are... targeting the same loci. ??


So you got this wrong about the ev model and Dr Schneider said the following for how he intended to have ev used.

Do you see an "s" after "pressure" in that statement you quoted, you fool? To look at the effect of pressureS you need pressureS.


Since simply color highlighting is not enough for rocketwhomissesthetarget, what do you think these authors mean byinversion of selection?

I am just guessing, but I bet the same thing I meant when I saidIn that study they simply inverted the direction of a selective pressure..

Can you understand English? They took an environment selecting for individuals with resistance to a drug, introduced some more drugs, and the result was an environment selecting for the opposite -- individuals without the resistance.

[sol invictus]

]“Antibiotic interactions that select against resistance”[/SIZE][/FONT]
Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgs


Did you actually read that paper? It's pretty interesting, but it has no bearing on what you're trying to argue.

They started with two populations of e. coli - one resistant to doxycycline and one not. It was known that doxycycline suppresses the effects of Cipro, a more powerful antibiotic, when both are administered simultaneously to a wild (non-resistant) strain of e. coli. What they found here is that this effect - of doxycycline suppressing the effects of Cipro - didn't work for the resistant strain, meaning that the resistant strain was in sum more strongly affected by the combination than the non-resistant strain was. That's interesting because it may offer a way to fight resistant strains, which are a growing problem due to rapid evolution of bacterial strains.

Interesting result, but unfortunately for your argument it's got nothing to do with the rate of evolution of anything.

[joobz]

wow, a lot of words. A lot of obvious lies and a complete avoidance of justifing his theory assumptions.

[kleinman]

Adequate has posted a silly graph and you have posted the following:No. Both of us provided you with source code and a number of example outputs. I even compiled a .exe for you to run on your own.
So run your .exe, generate the data and prove to us that your model shows that n+1 selection pressures evolve more rapidly than n selection pressures. The following does not qualify as a number of example outputs:
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
I’ve already done a parametric study of a peer reviewed and published model of random point mutations and natural selection. You need to do the parametric study for your own model.
Neither of you have done a systematic presentation of your models or given a real example of your models.No. Both of us have described the workings of our model in great detail, in addition to providing the source code for you to examine. In addition, both of us have given you a real example of our models -- the programs we wrote according to them.

You just don't get it, do you? Forget about evolution, mutation and selection, beggaminuses, whatever. Concentrate on sorting algorithms. You claim sorting algorithms are always slowed by additional sorting conditions. Both algorithms we have shown you are sorting algorithms, and neither are slowed by additional sorting conditions. How can you explain this?
I don’t need to explain anything about your computer code. You need to do the parametric study and prove what you are saying. It’s not my job to find your coding and modeling errors. If you have developed a computer algorithm which accelerates sorting with additional sorting conditions, here’s your chance to win the Nobel Prize. You can then apply your logic to server software so that it runs faster the more users accessing the server.
On the other hand, I have posted hundreds of cases from ev including those which show that single selection conditions in the model evolve many orders of magnitude faster than all three selection conditions simultaneously.No. Nobody, not a single person in the history of this thread other than yourself, thinks these ev run cases show this. The extent of your argument here, Kleinman, is "I set two of the three doohickies that say 'pressure' to zero, and the thingy finishes sooner." Can you explain to all of us why setting the weight distribution to 10-1-1 instead of 10-0-0 completely refutes your claim?
I can’t help if you are so steeped in evolutionist dogma that you can’t recognize what the ev model shows.

Oh really, setting the weight factors to 10-1-1 instead of 10-0-0 completely refutes my claim? Why don’t you tell us what the other parameters you used when running these cases? Then we can compare the generations for convergence and see whether it refutes my claim, or did you:
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
The difference between what you have done and what I have done is that I have posted the data and parameters use to obtain the data. I have a large spreadsheet with all the data and parameters used to obtain the data from ev. We are not playing poker where you can bluff to win this debate, you have to produce the data and show how you obtained it. I have done this with ev and what this data shows is that the number of selection pressures profoundly slow the evolutionary process. Real measurable examples of mutation and selection show the same thing.
Sure I have, you gave the probability of the theory of evolution to be true at 1.0 x 10^-999999999, the only other possibility is that we were created. So unless you want to claim that the probability that we are here is less than 1, then the probability that we were created is 1 – (1.0 x 10^-999999999) ≈ 1. Do you want to propose another way we came to be?I see. You have used a probability independent of creationism to find the probability of creationism. The limits of your genius know no bounds, Kleinman.
There are only two possible ways that we could come to be. Either abiogenesis and evolution accomplished this or we were created. Too bad it can’t be decided with a coin flip, at least you would have a 50-50 chance to win this debate.
You still don’t understand that none of the drug therapies used to treat HIV kills the virus. They only inhibit the virus’s ability to reproduce.Which is why I said:lethal pressures, when combined, prevent populations from evolving resistance -- by killing them.Tell me, Kleinman, if a population stops reproducing, how can it evolve?
If the population has multiple simultaneous selection pressures, it doesn’t. You would have some understanding of this point if you studied how ev works. Ev does not cause extinction; the model lets half the population with the fewest mistakes to always reproduce. Still, the model comes to a virtual evolutionary standstill for all but the tiniest genomes when all three selection conditions are applied simultaneously. The model can not eliminate mistakes for all three selection conditions.
Either way, selection pressures can kill the members of the population or reduce the ability of members of the population to reproduce, the end result is the reduction in fitness of the population. Combination selection pressures reduce the fitness of a population to reproduce.Yes, and when that fitness is reduced to stagnation, as in every study you are relying on, evolution will obviously proceed very slow. Kleinman, can you cite even a single real world study that doesn't involve pressures designed to destroy a population?
The reason why evolution is reduced to stagnation in all the citations I have posted is because of combination selection pressures. It is a mathematical and empirical fact of life that the mutation and selection sorting/optimization process is reduced to stagnation by multiple simultaneous sorting conditions. Rocketdodger, selection pressures by definition reduce the fitness of a population to reproduce. Selection pressures are trying to destroy a population. There are no selection pressures that do not impair a populations’ ability to reproduce. If you think there are selection pressures which do not reduce the fitness of a population, tell us what they are.
Antibiotic interactions that select against resistance”
Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgs Did you actually read that paper? It's pretty interesting, but it has no bearing on what you're trying to argue.

They started with two populations of e. coli - one resistant to doxycycline and one not. It was known that doxycycline suppresses the effects of Cipro, a more powerful antibiotic, when both are administered simultaneously to a wild (non-resistant) strain of e. coli. What they found here is that this effect - of doxycycline suppressing the effects of Cipro - didn't work for the resistant strain, meaning that the resistant strain was in sum more strongly affected by the combination than the non-resistant strain was. That's interesting because it may offer a way to fight resistant strains, which are a growing problem due to rapid evolution of bacterial strains.

Interesting result, but unfortunately for your argument it's got nothing to do with the rate of evolution of anything.
Sol, I don’t have the body of the article available at this time but I do have an interview of the author which explains what they did:
http://pubs.acs.org/cen/news/85/i15/8515notw7.html (http://pubs.acs.org/cen/news/85/i15/8515notw7.html)
Using the right combination of antibiotics could curtail the development of drug-resistant bacteria, a new study shows.

Systems biology assistant professor Roy Kishony and grad students Remy Chait and Allison Craney at Harvard Medical School demonstrate that certain combinations of doxycycline and ciprofloxacin favor the growth of doxycycline-sensitive bacteria over doxycycline-resistant ones (Nature 2007, 446, 668). The combination is "suppressive," meaning that its bacteria-killing effect is weaker than that of the individual drugs.

The researchers tested the combinations against Escherichia coli strains that differ only in the presence or absence of a tetracycline efflux pump, which provides a common mechanism of resistance to tetracycline, doxycycline, and related antibiotics. In assays that measured selection for the gene responsible for this resistance, they found strong selection for doxycycline-resistant strains when they treated bacteria with doxycycline alone or in combination with erythromycin, which has a synergistic effect with doxycycline.

In contrast, the doxycycline-ciprofloxacin combination selects against the doxycycline-resistant bacteria at some concentrations. The resulting persistence of doxycycline-sensitive strains is counterintuitive. "The selection against resistance stems from the interaction between the antibiotics and is therefore largely independent of the underlying mechanistic way by which the bacteria become resistant," Chait says.

The observed effects work against only doxycycline-resistant bacteria. The authors suggest that such a strategy will work best with combinations of drugs where each one suppresses the other.

The clinical relevance of the findings is still uncertain. The current work involves antibiotic doses below therapeutic levels. "The suppressive condition that allowed for the observation of the effect is never used clinically," says Shahriar Mobashery, an antibiotic expert at the University of Notre Dame. Nevertheless, the study is "interesting conceptually," he says, and the phenomena "deserve further study and explanation."

Kishony's group plans to study higher drug concentrations that fully inhibit both the sensitive and resistant bacteria. "We hope that these findings may suggest avenues of research into new treatment strategies employing antimicrobial combinations with improved selection against resistance," Chait says.
Sol, this article demonstrates exactly that combination selection pressures profoundly slow the evolution of resistance.

[kjkent1]

The difference between what you have done and what I have done is that I have posted the data and parameters use to obtain the data. I have a large spreadsheet with all the data and parameters used to obtain the data from ev. We are not playing poker where you can bluff to win this debate, you have to produce the data and show how you obtained it. I have done this with ev and what this data shows is that the number of selection pressures profoundly slow the evolutionary process. Real measurable examples of mutation and selection show the same thing.
All default settings except:
4096 bases
24 Mutations per genome
Pause ONLY on Rseq >= Rfreq
Result: Convergence in 13,094 generations.
----
Same experiment except
Set spurious bindings inside binding site region to 0
Set spurious bindings outside binding site region to 0
Result: No convergence after 35,000 generations. None, zippo, nada!

The "perfect" creature is not perfect unless it is free of both missing and spurious bindings. Setting a mistake count to zero prevents the program from clearing that mistake from the genome.

Any experiment conducted with a mistake count set at zero will never evolve a "perfect creature." If you turn on "stop on perfect creature," the creature that is evolved is not perfect, BECAUSE it still contains errors!!! What ev reports is an error, because you have introduced a bug into the program.

The same result will be obtained no matter what settings you select, because any setting with a zero mistake count is an ERROR!

If you can't see this, then you're mentally ill, Alan. Everyone here understands this concept but you. Do you have a learning disability or what?

[rocketdodger]

So run your .exe, generate the data and prove to us that your model shows that n+1 selection pressures evolve more rapidly than n selection pressures. The following does not qualify as a number of example outputs:

You silly lying fool, how many times are you going to repeat that statement instead of addressing the issue? Here is a list of posts where I explicitly either give you example runs or speak in detail about the workings of my program: #6401, #6516, #6568, and most importantly #6676. Since you have replied to each of those posts, I know you saw them. Thus your insistance that I haven not provided more information than the statement I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was :( is nothing more than rhetoric trash that is obvious to everyone.

My program does not show that in reality n+1 selection pressures evolve more rapidly than n selection pressures. I have never claimed such a thing. I claimed that in the context of the model I used n+1 selective pressures lead to a higher average amount of fixation.

How can you be so dense that you miss this point that has been made by both Adequate and myself time after time after time? What our programs show is that adding sorting conditions does not slow down all sorting algorithms. We have both provided you with multiple sets of results. Take a look at www.jedi-arts.com/code/sims.txt for five sets of mine. When will you address this issue? Will you hide like a coward forever?

I’ve already done a parametric study of a peer reviewed and published model of random point mutations and natural selection.

Who cares? You can't use ev to research the effects of multiple selective pressures like you claim. Paul, the programmer of the simulation, has explained why in clear and easy to understand language. At best you can only look at 3 pressures at once, and they are not even independent pressures.

You need to do the parametric study for your own model.

I did. The results are at www.jedi-arts.com/code/sims.txt. There are five examples, which is all my program requires to illustrate what it was intended to illustrate. All I need is a single example anyway, but as it turns out, every run I make leads to the same conclusion.

The math is so simple even a drop-out like yourself should be able to handle it, Kleinman. When you only have one pressure, once its targets are fixed, nothing more can be done. If you add more, the amount they slow each other down is offset by the fact that you can work on fixing them all at once.

But you know all this already, and you know that your claim is wrong, so instead of addressing the issue here you will just dodge it.

You can then apply your logic to server software so that it runs faster the more users accessing the server.

THERE IS SUCH SOFTWARE YOU STUPID FOOL -- ITS CALLED DISTRIBUTED COMPUTING.

I can’t help if you are so steeped in evolutionist dogma that you can’t recognize what the ev model shows.

We know you can't. Someone that knew what they were talking about, on the other hand, would be able to help others see their point by explaining themselves.

Oh really, setting the weight factors to 10-1-1 instead of 10-0-0 completely refutes my claim? Why don’t you tell us what the other parameters you used when running these cases?

Using the default settings, it takes less than 20 generations to reach a perfect creature with 10-0-0. Using 10-1-1, it takes 316 generations. Ok. If your theory is true, then going to 10-10-10 will result in an "orders of magnitude" slowdown compared to 10-1-1. Except... with 10-10-10 it took 662 generations. That is merely double the time to convergence -- not quite "orders of magnitude" you genius.

And what is more... with 10-10-10 there is effectively three pressures where at 10-1-1 there was still effectively one -- a 300% increase. Yet it only took twice as long to converge, a 200% increase. So if we increased the number of pressures by 300% and convergence only took 200% longer... THE RATE OF CONVERGENCE INCREASED.

We are not playing poker where you can bluff to win this debate, you have to produce the data and show how you obtained it.

Both Adequate and I have done so, in multiple posts. Your lies don't fool anyone.

I have done this with ev and what this data shows is that the number of selection pressures profoundly slow the evolutionary process. Real measurable examples of mutation and selection show the same thing.

Really? Then how do you account for the ev results I just showed you? Wait, let me guess.. something about the population size not being high enough, or the number of binding sites not being high enough.. whine whine. Here is a question -- do you have any data on 10-1-1 and 10-10-10 available? Surely you must have done runs using those two weight distributions...

[sol invictus]

Sol, this article demonstrates exactly that combination selection pressures profoundly slow the evolution of resistance.

What are you talking about? It has nothing to do with evolution. All they found is that for some reason (which they don't understand) some bacteria are susceptible to that combination of antibiotics, and some aren't. Presumably there's some biochemical explanation.

So?

Are you capable of reading and understanding English?

[rocketdodger]

If the population has multiple simultaneous selection pressures, it doesn’t.

Oh, so a stagnant population that is not reproducing will still evolve, as long as there isn't multiple selective pressures acting on it? Since evolution depends on reproduction, I think you will have a hard time selling this claim to even fellow creationists...

You would have some understanding of this point if you studied how ev works.

But I do, and I did. And as we have all proved to you numerous times, ev does not show what you claim it does. Other than that, all you have are your cited studies, which all cause a population to either stagnate or die off immediately. The question still stands, Kleinman: Can you show us data from a study that did not use pressures designed to destroy a population?

The reason why evolution is reduced to stagnation in all the citations I have posted is because of combination selection pressures.

The reason evolution stops in the studies you cite is because the population stops reproducing or dies you fool. Mutation and selection doesn't happen when a population is not reproducing or dead.

It is a mathematical and empirical fact of life that the mutation and selection sorting/optimization process is reduced to stagnation by multiple simultaneous sorting conditions.

You keep saying this, but you have produced zero actual evidence. Fail. Try again.

Rocketdodger, selection pressures by definition reduce the fitness of a population to reproduce. Selection pressures are trying to destroy a population. There are no selection pressures that do not impair a populations’ ability to reproduce. If you think there are selection pressures which do not reduce the fitness of a population, tell us what they are.

You are clearly a fool who knows nothing about the mechanisms of evolution. Selective pressures by definition change the RELATIVE reproductive fitness of individuals in a population.

Some reduce the ability of a population as a whole to reproduce -- in particular, all of the pressures used in the studies you cite.

Others, rather than killing or impeding the reproduction of individuals, simply confer advantages or disadvantages to those individuals that exhibit their targets. For instance, suppose there is a population of bacteria living in a relatively weak food solution. Now add another type of food that they are only one point mutation away from being able to metabolize. Very quickly the population would evolve to be able to metabolize it. Are you suggesting that the addition of this new food pressure will reduce the population's reproductive fitness?

[tsig]

Sure you can prove something by disproving something else, it called the process of elimination and the theory of evolution has been eliminated. So now we got here either by creation or something you can’t think of.

Tell us of what evil that hasn’t gone un-judged?

How do you know he doesn’t exist?

Adequate has posted a silly graph and you have posted the following:

Neither of you have done a systematic presentation of your models or given a real example of your models. On the other hand, I have posted hundreds of cases from ev including those which show that single selection conditions in the model evolve many orders of magnitude faster than all three selection conditions simultaneously. If you are having trouble running ev, either Paul or I can help you with this. In addition I have posted and will continue to post real examples which demonstrate what Dr Schneider’s peer reviewed and published model shows, which are combination selection pressures profoundly slow the evolutionary sorting/optimization process.

Sure I have, you gave the probability of the theory of evolution to be true at 1.0 x 10^-999999999, the only other possibility is that we were created. So unless you want to claim that the probability that we are here is less than 1, then the probability that we were created is 1 – (1.0 x 10^-999999999) ≈ 1. Do you want to propose another way we came to be?

You still don’t understand that none of the drug therapies used to treat HIV kills the virus. They only inhibit the virus’s ability to reproduce. Either way, selection pressures can kill the members of the population or reduce the ability of members of the population to reproduce, the end result is the reduction in fitness of the population. Combination selection pressures reduce the fitness of a population to reproduce.

I though you said you understood how ev works. Every locus in the genome is subject to the selection pressures in ev when all three selection pressures are imposed. Only when you set selection pressures in the model to zero are only certain loci targeted. Apparently in your studies of ev you failed to read Dr Schneider’s publication on his model. He published the following statement concerning his model:

So you got this wrong about the ev model and Dr Schneider said the following for how he intended to have ev used.

I added the highlighting for you rocketwhomissesthetarget. There are many interesting things you can learn about the mathematics of mutation and selection if you understand how ev works. So far, you have not demonstrated any of this understanding.

“Antibiotic interactions that select against resistance”
Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgs

Since simply color highlighting is not enough for rocketwhomissesthetarget, what do you think these authors mean byinversion of selection?

Kman I don't know how you got here but I had a mother and father.

[tsig]

So run your .exe, generate the data and prove to us that your model shows that n+1 selection pressures evolve more rapidly than n selection pressures. The following does not qualify as a number of example outputs:

I’ve already done a parametric study of a peer reviewed and published model of random point mutations and natural selection. You need to do the parametric study for your own model.

I don’t need to explain anything about your computer code. You need to do the parametric study and prove what you are saying. It’s not my job to find your coding and modeling errors. If you have developed a computer algorithm which accelerates sorting with additional sorting conditions, here’s your chance to win the Nobel Prize. You can then apply your logic to server software so that it runs faster the more users accessing the server.

I can’t help if you are so steeped in evolutionist dogma that you can’t recognize what the ev model shows.

Oh really, setting the weight factors to 10-1-1 instead of 10-0-0 completely refutes my claim? Why don’t you tell us what the other parameters you used when running these cases? Then we can compare the generations for convergence and see whether it refutes my claim, or did you:

The difference between what you have done and what I have done is that I have posted the data and parameters use to obtain the data. I have a large spreadsheet with all the data and parameters used to obtain the data from ev. We are not playing poker where you can bluff to win this debate, you have to produce the data and show how you obtained it. I have done this with ev and what this data shows is that the number of selection pressures profoundly slow the evolutionary process. Real measurable examples of mutation and selection show the same thing.

There are only two possible ways that we could come to be. Either abiogenesis and evolution accomplished this or we were created. Too bad it can’t be decided with a coin flip, at least you would have a 50-50 chance to win this debate.

If the population has multiple simultaneous selection pressures, it doesn’t. You would have some understanding of this point if you studied how ev works. Ev does not cause extinction; the model lets half the population with the fewest mistakes to always reproduce. Still, the model comes to a virtual evolutionary standstill for all but the tiniest genomes when all three selection conditions are applied simultaneously. The model can not eliminate mistakes for all three selection conditions.

The reason why evolution is reduced to stagnation in all the citations I have posted is because of combination selection pressures. It is a mathematical and empirical fact of life that the mutation and selection sorting/optimization process is reduced to stagnation by multiple simultaneous sorting conditions. Rocketdodger, selection pressures by definition reduce the fitness of a population to reproduce. Selection pressures are trying to destroy a population. There are no selection pressures that do not impair a populations’ ability to reproduce. If you think there are selection pressures which do not reduce the fitness of a population, tell us what they are.

Sol, I don’t have the body of the article available at this time but I do have an interview of the author which explains what they did:
http://pubs.acs.org/cen/news/85/i15/8515notw7.html (http://pubs.acs.org/cen/news/85/i15/8515notw7.html)

Sol, this article demonstrates exactly that combination selection pressures profoundly slow the evolution of resistance.

Could you define "profoundly slow " ? Is it different than really slow or very slow or maybe
just stop?

Viva La Resistance!

[Kotatsu]

Why don’t you mention that the majority of the examples of aneuploidy are harmful.

Because it isn't true. If it were true, there would be virtually no polyploidisation events known. In the real world, however, as much as 80% of all flowering plants are believed to have both diploid and various polyploid populations. In animals, this number is less (this has been suggested to be because there is less selfing in animals, but I don't know if this is sufficient explanation), but nonetheless it occurs. Again, in Lumbriculus variegatus most populations I have looked at seem to be of various non-diploid ploidy levels.

But perhaps we misunderstand each other. Aneuploidy is not the same as polyploidy. I am talking about those cases where all the chromosomes are doubled, either by allopolyploidisation or by autopolyploidisation.

Wheat evolving by polyploidisation into wheat is an example of “common descent”?

Yes. What else would it be? An example of that some god creates every seed individually?

So are you now going to make the leap and tell us that reptiles evolved into birds by polyploidisation? You evolutionists do love you speculations and extrapolations.

If I had wanted to make that leap, I would have said so. I am merely pointing out that the concept of common descent does not rest exclusively on random point mutation and selection, but that, as always, other mechanisms can provide the same patterns as well.

And it certainly does not rely on your very flawed understanding of these mechanisms.

If you have the mathematical and empirical evidence, why are you always trying to inoculate yourself from having to specify the selection pressures and target genes to these pressures? I continue to post measurable and repeatable examples of mutation and selection which show combination selection pressures profoundly slow the evolutionary process while you continue to fail to post examples of mutation and selection which show otherwise and the examples you do post don’t define the selection pressures or the target genes for these selection pressures.

They do. The relevant selection pressure for the evolution of the advanced structures in some moth ears, for example, is predation by two different kinds of bats. The relevant selection pressure for the evolution of limpet shell structure is predation by different kinds of predators in different areas. The evolution in those phytophagous beetles are subject to hosts of selection pressures, including a range of new predators, the plants' own defense mechanisms, and other factors.

This data is not necessarily repeatable (even should such studies be ethically permissible), as I have explained to you before, because these pressures target the entire genome, and different structures could evolve to counter the same pressure at different times, just as for the various methods of how larger vertebrates move from tree to tree.

[Belz...]

Sure you can prove something by disproving something else

No, you can't. As usual you demonstrate your utter ignorance of how things work.

it called the process of elimination

That only works when you know exactly how many options you have.

and the theory of evolution has been eliminated.

It has ? Well, that's odd, because we've got a poster on this thread who's been claiming the same thing, and so far he hasn't been able to push his theory past rhetoric.

Oh, wait. That's you!

So now we got here either by creation or something you can’t think of.

Nice try, moonbat. It's YOUR onus to prove creation. I don't have to lift a finger.

Tell us of what evil that hasn’t gone un-judged?

Hasn't gone un-judged ? That's YOUR argument. Why would I want to prove YOUR point ?

How do you know he doesn’t exist?

It's my tentative conclusion until someone shows otherwise.

Or would you have me believe in Zeus, too ?

[Belz...]

Really? Then how do you account for the ev results I just showed you? Wait, let me guess.. something about the population size not being high enough, or the number of binding sites not being high enough.. whine whine. Here is a question -- do you have any data on 10-1-1 and 10-10-10 available? Surely you must have done runs using those two weight distributions...

Kleinman likes ev only when it suits him. Otherwise it's incomplete or "contrived".

[Belz...]

In animals, this number is less (this has been suggested to be because there is less selfing in animals, but I don't know if this is sufficient explanation), but nonetheless it occurs.

Selfing ?

[Belz...]

You evolutionists do love you speculations and extrapolations.

I don't suppose you'll speculate when I ask you how the universe was created ? How the soul operates ? What it does ? Why God made everything so that it looks like evolution works ?

[Kotatsu]

Selfing ?

Self-pollination.

[Paul C. Anagnostopoulos]

I swear I'm going to release a new version of Evj that does not use the term perfect creature. And I'm going to do it soon.

~~ Paul

[Belz...]

Self-pollination.

That's what I thought. Thanks.

[kleinman]

The difference between what you have done and what I have done is that I have posted the data and parameters use to obtain the data. I have a large spreadsheet with all the data and parameters used to obtain the data from ev. We are not playing poker where you can bluff to win this debate, you have to produce the data and show how you obtained it. I have done this with ev and what this data shows is that the number of selection pressures profoundly slow the evolutionary process. Real measurable examples of mutation and selection show the same thing.All default settings except:
4096 bases
24 Mutations per genome
Pause ONLY on Rseq >= Rfreq
Result: Convergence in 13,094 generations.
----
Same experiment except
Set spurious bindings inside binding site region to 0
Set spurious bindings outside binding site region to 0
Result: No convergence after 35,000 generations. None, zippo, nada!
So kjkent1, what is the lesson you want to teach from this single case? What is the selection pressure for Rseq >= Rfreq? Didn’t you know there is no selection pressure for Rseq >=Rfreq? Did the mistakes for this case go to zero? How about for the other experiment, did the mistakes go to zero? Perhaps you should continue your search for an example from ev where from the random initialization of the program you find a case where Rseq>=Rfreq, then you could claim it takes zero generations for convergence.
The "perfect" creature is not perfect unless it is free of both missing and spurious bindings. Setting a mistake count to zero prevents the program from clearing that mistake from the genome.

Any experiment conducted with a mistake count set at zero will never evolve a "perfect creature." If you turn on "stop on perfect creature," the creature that is evolved is not perfect, BECAUSE it still contains errors!!! What ev reports is an error, because you have introduced a bug into the program.
After all this time, you still don’t understand the mutation and selection sorting process. You can still obtain a perfect creature without selection, the probability is miniscule but it is probable. You can also obtain a creature with Rseq >= Rfreq without selection but the probability is also miniscule. The point that you refuse to understand is that these sorting/optimization problems become profoundly slow as the sorting requirements become more complex. Simple sorting conditions that require only a small number of mutations at the appropriate loci are the easiest to satisfy; complex sorting conditions which require many mutations at numerous different positions on the genome are much, much more difficult to satisfy. That is the lesson which ev teaches and that is the lesson which real examples of mutation and selection teaches. Transforming a reptile into a bird is a far more complex sorting/optimization problem than ev’s simple example. Besides the fact that there are no selection conditions that would do this, even if you could imagine the selection conditions, this sorting/optimization problem would take vastly more generations than ev’s simple sorting/optimization problem. Combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
If you can't see this, then you're mentally ill, Alan. Everyone here understands this concept but you. Do you have a learning disability or what?
Whatever learning disability I may have, it doesn’t compare with your disability in mathematics.
Sol, this article demonstrates exactly that combination selection pressures profoundly slow the evolution of resistance.What are you talking about? It has nothing to do with evolution. All they found is that for some reason (which they don't understand) some bacteria are susceptible to that combination of antibiotics, and some aren't. Presumably there's some biochemical explanation.
Certainly it has everything to do with evolution. These problems are all about a population finding a trajectory to a local optimum on a fitness landscape. When you have combination selection pressures, it interferes with the population finding a trajectory to a local optimum. That is what the mathematics shows and that is what the empirical evidence shows. That’s how the mutation and selection sorting/optimization problem works.
Could you define "profoundly slow " ? Is it different than really slow or very slow or maybe just stop?
Sure I’ll define “profoundly slow” for you; it’s too slow for the theory of evolution to be mathematically possible. Now if you read the thread, you will get some mathematical examples of this definition.
Why don’t you mention that the majority of the examples of aneuploidy are harmful.Because it isn't true. If it were true, there would be virtually no polyploidisation events known. In the real world, however, as much as 80% of all flowering plants are believed to have both diploid and various polyploid populations. In animals, this number is less (this has been suggested to be because there is less selfing in animals, but I don't know if this is sufficient explanation), but nonetheless it occurs. Again, in Lumbriculus variegatus most populations I have looked at seem to be of various non-diploid ploidy levels.
That explains the “Invasion of the Body Snatchers”, now do you want to explain how polyploidisation speeds up the evolutionary process, especially since in animals it is extremely harmful.
Sure you can prove something by disproving something elseNo, you can't. As usual you demonstrate your utter ignorance of how things work.
Sure I know how mutation and selection works. I have the mathematical and empirical evidence which shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
it called the process of eliminationThat only works when you know exactly how many options you have.
So let’s see, we have abiogenesis and evolution as one option, creation as a second option and the option you can’t think of. That should cover all the possible options.
and the theory of evolution has been eliminated.It has ? Well, that's odd, because we've got a poster on this thread who's been claiming the same thing, and so far he hasn't been able to push his theory past rhetoric.

Oh, wait. That's you!
All that mathematical and empirical evidence which shows how mutation and selection actually works, it’s so annoying to you evolutionists.
So now we got here either by creation or something you can’t think of.Nice try, moonbat. It's YOUR onus to prove creation. I don't have to lift a finger.
Moonbat? I don’t have to lift a finger either to prove creation; right now my job is to continue to post the evidence that the theory of evolution by mutation and selection is mathematically impossible. And you know what Belz, it’s really easy to find the evidence. Isn’t that annoying?
You evolutionists do love you speculations and extrapolations.I don't suppose you'll speculate when I ask you how the universe was created ? How the soul operates ? What it does ? Why God made everything so that it looks like evolution works ?
The difference here is that evolutionists like to call their speculations and extrapolations “science”. The problem for you evolutionists is that when mathematics and accurate measurement of how the mutation and selection sorting/optimization process works, it makes your speculations and extrapolations mathematically impossible.
I swear I'm going to release a new version of Evj that does not use the term perfect creature. And I'm going to do it soon.
That’s a good idea Paul, it is confusing terminology but it’s not going to change the mathematical fact of life that combination selection pressures profoundly slow the evolutionary process. Your Rcapacity label is not very informative either. Why don’t you call it the Robfuscation value, or perhaps the Rincomprehensible value.

In order to make the mutation and selection sorting/optimization process more comprehensible, here are so more examples of how it works.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11981365&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11981365&dopt=AbstractPlus)
CONTEXT: The Women and Infants Transmission Study is a prospective natural history study that has been enrolling HIV-1-infected pregnant women and their infants since 1989. OBJECTIVE: To evaluate the impact of different antiretroviral regimens on perinatal HIV-1 transmission at the population level. DESIGN: Prospective cohort study. Plasma HIV-1 RNA levels were serially measured in 1542 HIV-1-infected women with singleton live births between January 1990 and June 2000. MAIN OUTCOME MEASURE: HIV-1 status of the infant. RESULTS: HIV-1 transmission was 20.0% (95% confidence interval [CI], 16.1%-23.9%) for 396 women who not receiving prenatal antiretroviral therapy; 10.4% (95% CI, 8.2%-12.6%) for 710 receiving zidovudine monotherapy; 3.8% (95% CI, 1.1%-6.5%) for 186 receiving dual antiretroviral therapy with no or one highly active drug (Multi-ART); and 1.2% (95% CI, 0-2.5%) for 250 receiving highly active antiretroviral therapy (HAART). Transmission also varied by maternal delivery HIV RNA level: 1.0% for <400; 5.3% for 400 to 3499; 9.3% for 3500 to 9999; 14.7% for 10,000 to 29,999; and 23.4% for >30,000 copies/mL (p =.0001 for trend). The odds of transmission increased 2.4-fold (95% CI, 1.7-3.5) for every log10 increase in delivery viral load. In multivariate analyses adjusting for maternal viral load, duration of therapy, and other factors, the odds ratio for transmission for women receiving Multi-ART and HAART compared with those receiving ZDV monotherapy was 0.30 (95% CI, 0.09-1.02) and 0.27 (95% CI, 0.08-0.94), respectively. CONCLUSION: Levels of HIV-1 RNA at delivery and prenatal antiretroviral therapy were independently associated with transmission. The protective effect of therapy increased with the complexity and duration of the regimen. HAART was associated with the lowest rates of transmission.

Patrick E Duffy, Carol Hopkins Sibley. The Lancet. London: Dec 3-Dec 9, 2005. Vol. 366, Iss. 9501; pg. 1908
Jambou and colleagues' paper is a wake-up call; resistance to artemisinins may indeed be selected by uncontrolled use of artemisinins as monotherapy or in conjunction with ineffective partner drugs. We ignore this warning at the risk of a rapid demise of ACTs that are currently just being tested and deployed.

http://www3.interscience.wiley.com/cgi-bin/abstract/112773693/ABSTRACT?CRETRY=1&SRETRY=0 (http://www3.interscience.wiley.com/cgi-bin/abstract/112773693/ABSTRACT?CRETRY=1&SRETRY=0)
Multi-drug resistant hepatitis B virus (HBV) has been reported in hepatitis B patients who received sequential antiviral therapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine and adefovir have marked reduction in sensitivity to combination of lamivudine and adefovir, whereas constructs with mutations resistant to either drug remain sensitive to the other drug. We conducted this study to determine whether mutations conferring resistance to multiple antiviral agents co-locate on the same HBV genome in vivo and to describe the evolution of these mutations. Sera from six patients who had been found to have multi-drug resistant HBV mutations to lamivudine + adefovir, lamivudine + hepatitis B immunoglobulin (HBIG), or lamivudine + entecavir on direct sequencing were cloned after nested polymerase chain reaction (PCR). Analysis of 215 clones from 11 samples with multi-drug resistant mutations on direct sequencing showed that 183 (85%) clones had mutations to both therapies on the same genome; 31 clones had lamivudine-resistant mutants only. Clonal analysis of serial samples from three patients showed progressive evolution from all clones with lamivudine-resistant HBV mutations only to mixtures of clones that have multi-drug resistant mutations and clones that have lamivudine-resistant HBV mutations only, and ultimately all clones having multi-drug resistant HBV mutations. In conclusion, mutations conferring resistance to multiple antiviral agents co-locate on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing multi-drug resistant HBV. De novo combination therapy may prevent the emergence of multi-drug resistant mutants. (HEPATOLOGY 2006;44:703-712.)
Now I hope that all of you can remember something to be thankful for today. You all have a happy thanksgiving carving up a turkey and I’ll be back next week to continue carving up the theory of evolution turkey.

[Kotatsu]

That explains the “Invasion of the Body Snatchers”, now do you want to explain how polyploidisation speeds up the evolutionary process, especially since in animals it is extremely harmful.

What? It is not extremely harmful in animals, as evidenced by the fact that as many as 20% of all annelids have at least one polyploid form, and many have several. You simply ahve no idea about anything, do you?

[joobz]

I swear I'm going to release a new version of Evj that does not use the term perfect creature. And I'm going to do it soon.

~~ Paul
While you are at it, can you include a list of model assumptions made in evj and explain that ANY extrapolation that is made that exceeds the bounds of the assumptions is inherently wrong?

[Belz...]

Sure you can prove something by disproving something else

No, you can't. As usual you demonstrate your utter ignorance of how things work.

Sure I know how mutation and selection works.

Er... we were talking about the scientific method. Are you paying attention ?

I'm more and more of the opinion that you are either mentally ill, somehow, or a chatbot who just picks random words in my sentences and tries to answer as best you can. Nobody could be that thick.

it called the process of elimination

That only works when you know exactly how many options you have.

So let’s see, we have abiogenesis and evolution as one option, creation as a second option and the option you can’t think of. That should cover all the possible options.[/QUOTE]

Kleinman, if you had ever gone to school, which you haven't because you're either in an institute or a computer program, you'd know that that's completely irrelevant. The probaiblity of one isn't dependent upon the probability of the other.

All that mathematical and empirical evidence which shows how mutation and selection actually works, it’s so annoying to you evolutionists.

What mathematical evidence ? I've never seen a single equation from you.

What empirical evidence ? All the ones you've mentioned disprove your theory.

Of course, if you weren't a chatbot, you'd have a memory of these things.

I don’t have to lift a finger either to prove creation; right now my job is to continue to post the evidence that the theory of evolution by mutation and selection is mathematically impossible.

Then don't try to ascribe a probability to something you're not trying to prove, especially when you're not programmed to apply logic.

And you know what Belz, it’s really easy to find the evidence. Isn’t that annoying?

No, just sad that you think this is so. How much RAM are you using ?

The difference here is that evolutionists like to call their speculations and extrapolations “science”.

We call those "hypotheses".

The problem for you evolutionists is that when mathematics and accurate measurement of how the mutation and selection sorting/optimization process works, it makes your speculations and extrapolations mathematically impossible.

Even when such sorting/optimisation processes are shown to you to work differently ?

[kjkent1]

So kjkent1, what is the lesson you want to teach from this single case? What is the selection pressure for Rseq >= Rfreq? Didn’t you know there is no selection pressure for Rseq >=Rfreq? Did the mistakes for this case go to zero? How about for the other experiment, did the mistakes go to zero? Perhaps you should continue your search for an example from ev where from the random initialization of the program you find a case where Rseq>=Rfreq, then you could claim it takes zero generations for convergence.Alan, I don't no what's wrong with you, but you should consider getting professional help. If not psychological counseling, then at least take a computer programming class.

The reason why the mistakes quickly go to zero when you set the mistake count to zero is because ev NO LONGER COUNTS THOSE MISTAKES!

I hope that was simple enough for you. Your hypothesis, at least as far as ev is concerned, is based on your misunderstanding of how the software is constructed. Setting a mistake count to zero, means that ev won't recognize the existence of the mistake that would have otherwise been counted, and thus ev will report no mistakes, even though the mistakes are still there.

The genome that is created by ev when a mistake count is zeroed is a genome that does not represent a "perfect creature," i.e., one absent any mistakes.

The only accurate measurement of perfection in ev, once a mistake count is zeroed is the convergence from Rseq -> Rfreq. And since that convergence never occurs unless all three mistak counts are non-zero, your concluding that a creature is quickly created perfect is simply absurd.

Have someone teach you computer programming, because if you actually stepped through the program code, you would understand that you are making a spectacular mistake!

Happy Thanksgiving.

[rocketdodger]

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11981365&dopt=AbstractPlus

This abstract says nothing about evolution you fool. FAIL

[QUOTE]Patrick E Duffy, Carol Hopkins Sibley. The Lancet. London: Dec 3-Dec 9, 2005. Vol. 366, Iss. 9501; pg. 1908

From http://www.thebody.com/content/art13284.html:
Arteminisin is one of the most potent and fast acting malaria treatments available, killing up to 99.99 percent of parasites.

Gee, I wonder why combination therapy using Arteminisin and other such antimalarial drugs slows evolution... maybe because they destroy the population? FAIL

http://www3.interscience.wiley.com/cgi-bin/abstract/112773693/ABSTRACT?CRETRY=1&SRETRY=0

http://en.wikipedia.org/wiki/Lamivudine

http://en.wikipedia.org/wiki/Adefovir

http://en.wikipedia.org/wiki/Entecavir

All three drugs are viral inhibitors. And we know what immunoglobulins do.

Gee, I wonder why combination therapy using these treatments slows evolution.. maybe because they completely inhibit the population? FAIL

[Belz...]

Dodger, maybe you'd benefit from some time off this thread.

Maybe we all would.

[Dr Adequate]

Whatever learning disability I may have, it doesn’t compare with your disability in mathematics. But kleinman, do you not realise that the mental handicap that makes you unable to do mathematics also makes you incompetent to judge the mathematical abilities of others?

No, you don't, do you?

No-one can help you until you acknowledge that you have a problem. Admitting that you "may" have a learning difficulty is, I guess, a tentative first step towards accepting reality, but you've got a long way to go.

We're all here for you, though in my case only at weekends. If there's any really basic, easy, simple, straightforward mathematical principle you want explaining for the hundred-and-first time, don't hesitate to ask. Only this time, do try to listen to the answer.

[rocketdodger]

Dodger, maybe you'd benefit from some time off this thread.

Maybe we all would.

No doubt.

[Paul C. Anagnostopoulos]

Ah, you wimps. I've been here for 6,709 posts.

~~ Paul

[Belz...]

You're not impressing anyone, Paul. I've been here for 6710 !

[Dr Adequate]

I thought of another hypothesis to explain kleinman ... do you suppose that a right-sided stroke could have this effect?

[Belz...]

People with right-side strokes can learn to overcome this disability, so no.

[Dr Adequate]

People with right-side strokes can learn to overcome this disability ... (a) Not all of them; (b) only if they try.

[Belz...]

The point is, they CAN. ;)

[sol invictus]

Certainly it has everything to do with evolution. These problems are all about a population finding a trajectory to a local optimum on a fitness landscape. When you have combination selection pressures, it interferes with the population finding a trajectory to a local optimum. That is what the mathematics shows and that is what the empirical evidence shows. That’s how the mutation and selection sorting/optimization problem works.

It has as much to do with evolution as it does with petri dishes: without either, the experiment would have been impossible. But the result is simply that bacteria which are more resistant (than standard strains) to one antibiotic are less resistant to it combined with another.

So? What does that have to do with the rate of evolution under multiple pressures?

I think you are very, very confused.

[kleinman]

I hope you all had a wonderful thanksgiving. It seems though that you evolutionist still haven’t figured out how mutation and selection actually works so let’s have some leftover theory of evolution turkey. We are serving up the heart of the theory, mutation and selection. For those of you who still haven’t figured out how mutation and selection works, it is a sorting/optimization problem which is extremely sensitive to the number of selection conditions. A single selection condition which targets a single gene is the easiest case for a population to evolve resistance to that selection conditions. Each additional selection condition applied simultaneously makes it much more difficult for the population to evolve to these combined selection conditions. This is what Dr Schneider’s peer reviewed and published model or random point mutation and natural selection shows and this is what hundreds of real empirical examples of mutation and selection shows. Now let’s see how you evolutionists counter these mathematical and empirical facts of mutation and selection.
That explains the “Invasion of the Body Snatchers”, now do you want to explain how polyploidisation speeds up the evolutionary process, especially since in animals it is extremely harmful.What? It is not extremely harmful in animals, as evidenced by the fact that as many as 20% of all annelids have at least one polyploid form, and many have several. You simply ahve no idea about anything, do you?
Well now Kotatsu, not only have you explained “Invasion of the Body Snatchers”, you have now explained why annelids are more evolutionarily advanced than humans.
I swear I'm going to release a new version of Evj that does not use the term perfect creature. And I'm going to do it soon.While you are at it, can you include a list of model assumptions made in evj and explain that ANY extrapolation that is made that exceeds the bounds of the assumptions is inherently wrong?
Finally joobz acknowledges whose simulation of mutation and selection is showing that combination selection pressures profoundly slow the evolutionary process. It goes to show you even an alchemical engineer can learn something if you work with him long enough.

Paul, let’s see Dr Schneider and you list the assumptions that would eliminate the mathematical fact of life that the more complex the selection conditions the slower the process goes and at the same time Dr Schneider can take the rate of information gain on a 256 base genome and extrapolate that to a 3 gigabase genome.

Paul, the problem for you is not the term “perfect creature”. We can get past that confusing use of terminology. The problem for you evolutionists is how the mutation and selection sorting/optimization process works both mathematically and empirically. There is no way that you can extrapolate this process to explain how common descent could be achieved.
Er... we were talking about the scientific method. Are you paying attention ?

I'm more and more of the opinion that you are either mentally ill, somehow, or a chatbot who just picks random words in my sentences and tries to answer as best you can. Nobody could be that thick.
Belz, is that all you can do, to resort to name calling? If you can’t give an alternative to abiogenesis and evolution or creation as the way we came to be, admit it. In the mean time, I’ll continue to demonstrate with real examples of mutation and selection how this process works when there are combined selection pressures. Dr Schneider’s peer reviewed and published model of random point mutations and natural selection already demonstrates how the process works mathematically. That is how the scientific method works.
So kjkent1, what is the lesson you want to teach from this single case? What is the selection pressure for Rseq >= Rfreq? Didn’t you know there is no selection pressure for Rseq >=Rfreq? Did the mistakes for this case go to zero? How about for the other experiment, did the mistakes go to zero? Perhaps you should continue your search for an example from ev where from the random initialization of the program you find a case where Rseq>=Rfreq, then you could claim it takes zero generations for convergence.Alan, I don't no what's wrong with you, but you should consider getting professional help. If not psychological counseling, then at least take a computer programming class.

The reason why the mistakes quickly go to zero when you set the mistake count to zero is because ev NO LONGER COUNTS THOSE MISTAKES!
Kjkent1, when you reduce down the number of selection conditions and the number of generations required for convergence for a 16k genome with all three selection conditions goes from over 5,000,000 generations to at most a couple hundred generations for any of the single selection condition cases demonstrates that you need to learn how to count, let alone take a computer programming class.
From http://www.thebody.com/content/art13284.html: (http://www.thebody.com/content/art13284.html:)
Arteminisin is one of the most potent and fast acting malaria treatments available, killing up to 99.99 percent of parasites.Gee, I wonder why combination therapy using Arteminisin and other such antimalarial drugs slows evolution... maybe because they destroy the population? FAIL
Rocketdodger, you missed this quote from the same citation:
Jambou and colleagues' paper is a wake-up call; resistance to artemisinins may indeed be selected by uncontrolled use of artemisinins as monotherapy or in conjunction with ineffective partner drugs. We ignore this warning at the risk of a rapid demise of ACTs that are currently just being tested and deployed.
What you don’t understand Rocketdodger is that the remaining 0.01 percent of the population that isn’t killed can much more easily evolve resistance to a single selection pressure than it can against combination pressures. Dr Schneider’s computer simulation shows that even a population of 64 can easily evolve resistance to a single selection pressure in a small number of generations. This is how the mathematics of mutation and selection works. You don’t need huge populations to evolve against single selection pressures. It is when you combine selection pressures that you profoundly impair a populations’ ability to evolve against both conditions simultaneously.
Whatever learning disability I may have, it doesn’t compare with your disability in mathematics.But kleinman, do you not realise that the mental handicap that makes you unable to do mathematics also makes you incompetent to judge the mathematical abilities of others?
Adequate, I don’t have to judge your mathematical abilities on the topic of mutation and selection, you rightly judged yourself to be incompetent on the topic. Here is what you said about yourself:
And I, sir, am a mathematician, and I may be the greatest expert in the UK on certain aspects of non-associative algebras, and on absolutely nothing else ... oh, certain aspects of neoclassical economics ... uses of geometry in design ... OK, there are lots of things I'm an expert on ... none of which are relevant to our great struggle between truth and bullcrap.
So, now that we know that you have abandoned mathematical logic and reason for your mathematically irrational and illogical theory of evolution belief system, what do you have to say?
We're all here for you, though in my case only at weekends. If there's any really basic, easy, simple, straightforward mathematical principle you want explaining for the hundred-and-first time, don't hesitate to ask. Only this time, do try to listen to the answer.
So what is your advice on the theory of evolution by mutation and selection? You give us a silly graph.
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then Adequate goes on to say this:
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And
So far as I know, no-one has done the experiment.
and
and too bad you don’t have any empirical examples of your silly graph ...As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
So Adequate, you give us a silly illogical and irrational graph without a real example of what you are trying to demonstrate, you have lost contact with reality when you embraced the mathematically impossible theory of evolution.
Dodger, maybe you'd benefit from some time off this thread.

Maybe we all would.No doubt.
The problem for you evolutionists is not this thread; your problem is that you have lost contact with the mathematical and empirical truth of how the mutation and selection sorting/optimization process actually works.
Ah, you wimps. I've been here for 6,709 posts.
Perhaps you have a wider binding site width and they have a smaller Rcapacity value than you. Now don’t be so hard on your fellow evolutionists. If I recall you took a break or two to watch the sun over the primordial soup.
Certainly it has everything to do with evolution. These problems are all about a population finding a trajectory to a local optimum on a fitness landscape. When you have combination selection pressures, it interferes with the population finding a trajectory to a local optimum. That is what the mathematics shows and that is what the empirical evidence shows. That’s how the mutation and selection sorting/optimization problem works.It has as much to do with evolution as it does with petri dishes: without either, the experiment would have been impossible. But the result is simply that bacteria which are more resistant (than standard strains) to one antibiotic are less resistant to it combined with another.

So? What does that have to do with the rate of evolution under multiple pressures?

I think you are very, very confused.
It has everything to do with evolution under multiple pressures. Certainly, some combinations of drugs will interfere with the action of each other. Drugs that act during the reproduction phase such as the beta-lactams will not be as effective when used with drugs that interfere with protein synthesis thus making it less likely that the population would be reproducing. In these cases you are not using the drugs in combination. One drug is affecting a particular part of the population life cycle and the other drug is affecting a different phase of the life cycle. In addition, the combinations used in these studies were below therapeutic levels.
http://pubs.acs.org/cen/news/85/i15/8515notw7.html (http://pubs.acs.org/cen/news/85/i15/8515notw7.html)
Using the right combination of antibiotics could curtail the development of drug-resistant bacteria, a new study shows.

Systems biology assistant professor Roy Kishony and grad students Remy Chait and Allison Craney at Harvard Medical School demonstrate that certain combinations of doxycycline and ciprofloxacin favor the growth of doxycycline-sensitive bacteria over doxycycline-resistant ones (Nature 2007, 446, 668). The combination is "suppressive," meaning that its bacteria-killing effect is weaker than that of the individual drugs.

The researchers tested the combinations against Escherichia coli strains that differ only in the presence or absence of a tetracycline efflux pump, which provides a common mechanism of resistance to tetracycline, doxycycline, and related antibiotics. In assays that measured selection for the gene responsible for this resistance, they found strong selection for doxycycline-resistant strains when they treated bacteria with doxycycline alone or in combination with erythromycin, which has a synergistic effect with doxycycline.

In contrast, the doxycycline-ciprofloxacin combination selects against the doxycycline-resistant bacteria at some concentrations. The resulting persistence of doxycycline-sensitive strains is counterintuitive. "The selection against resistance stems from the interaction between the antibiotics and is therefore largely independent of the underlying mechanistic way by which the bacteria become resistant," Chait says.

The observed effects work against only doxycycline-resistant bacteria. The authors suggest that such a strategy will work best with combinations of drugs where each one suppresses the other.

The clinical relevance of the findings is still uncertain. The current work involves antibiotic doses below therapeutic levels. "The suppressive condition that allowed for the observation of the effect is never used clinically," says Shahriar Mobashery, an antibiotic expert at the University of Notre Dame. Nevertheless, the study is "interesting conceptually," he says, and the phenomena "deserve further study and explanation."

Kishony's group plans to study higher drug concentrations that fully inhibit both the sensitive and resistant bacteria. "We hope that these findings may suggest avenues of research into new treatment strategies employing antimicrobial combinations with improved selection against resistance," Chait says.
Ultimately, these authors recognize that combination therapies interfere with the evolution of resistance. Here are a couple of more examples which demonstrate how the mutation and selection sorting/optimization problem actually works, that is that combination selection pressures profoundly slow the populations’ ability to evolve against these selection pressures simultaneously.

A Fungal Achilles' Heel
Joseph Heitman. Science. Washington: Sep 30, 2005. Vol. 309, Iss. 5744; pg. 2175, 2 pgs Evolution of drug resistance in pathogenic fungi. Antimicrobial azole drugs (fluconazole) inhibit the activity of lanosterol 14-α-demethylase (Erg11) and block the production the membrane sterol ergosterol, inhibiting growth. Hsp90 and calcineurin are required for fungal cells to tolerate fluconazole, or to acquire and maintain drug resistance. Exposure to an Hsp90 inhibitor (geldanamycin) or calcineurin inhibitors (cyclosporin A or FK506) can enhance the effect of fluconazole, preclude or delay the onset of drug resistance, and reverse drug resistance.

Remarkably, Hsp90's function in drug resistance is exerted through calcineurin, a serine-threonine-specific protein phosphatase that is controlled by calcium and calmodulin, a calcium-binding protein. Calcineurin is the target of cyclosporin A and FK506, immunosuppressive drugs that revolutionized organ transplant therapy by inhibiting T cell activation (3). Calcineurin is essential for virulence of several pathogenic fungi including C. albicans and Cryptococcus neoformans (4-8) and also enables fungal cells to tolerate drugs that block ergosterol biosynthesis, even clinically derived resistant isolates (8, 9). Cowen and Lindquist marshalled genetic and epistasis evidence to implicate calcineurin as a relevant target for Hsp90 action in promoting drug resistance. This model is supported by prior biochemical and drug combination studies that revealed a direct physical and mechanistic relationship between Hsp90 and calcineurin in mediating drug tolerance (10, 11).

These discoveries have the potential to dramatically advance antimicrobial therapy. Azoles are fungistatic and not fungicidal, and therefore they inhibit the growth of fungal cells but do not kill them. Yet concomitant inhibition of either Hsp90 or calcineurin renders fluconazole and other drugs that target ergosterol biosynthesis fully lethal to fungal microbes (see the figure). This raises the prospect of developing potent drug combinations that enhance the intrinsic activity of drugs that target ergosterol biosynthesis while obviating (or at least reducing) the development of drug resistance. Small-molecule inhibitors and high-resolution x-ray crystal structures are known for both calcineurin and Hsp90 (12, 13). Cyclosporin A and FK506 have been in clinical use for one to two decades, whereas the Hsp90 inhibitor geldanamycin is in clinical trials as a novel chemotherapy agent. Geldanamycin appears to be well tolerated in humans, which bodes well for additional clinical indications as a potential antimicrobial agent (14). A variety of active geldanamycin analogs have been synthesized, broadening the potential to identify molecules with improved antimicrobial spectra, reduced side effects, or oral bioavailability. Given a recent report that geldanamycin combined with cyclosporin A exerts a synergistic toxic activity against P. falciparum (11), this potential therapeutic regime might be applicable to fungi and parasites.

The phenothiazinium chromophore and the evolution of antimalarial drugs
Mark Wainwright, Leonard Amaral. Tropical Medicine and International Health. Oxford: Jun 2005. Vol. 10, Iss. 6; pg. 501
Abstract (Summary)
The phenothiazinium salt methylene blue [3,7-bis(dimethylamino)phenothiazinium chloride] is the oldest known synthetic antimalarial drug, its clinical efficacy having been reported in 1891. The role of methylene blue in the evolution of the modern antimalarial armoury is often unappreciated, yet it can be linked directly to standard drugs such as chloroquine and its congeners. Also, in the face of increasing plasmodial resistance to modern antimalarials, phenothiazinium derivatives have again featured as lead compounds in drug research. The precise mode of action of methylene blue and its commercial analogues against Plasmodium spp. remains a cause for conjecture, having been variously described as nucleic acid intercalation, food vacuole basification, parasite redox cycle interference and haem polymerization inhibition. That the activity of the series may be due to more than one route - i.e. a multifactorial activity - underlines the utility of these compounds in antimalarial research either as single drugs or as adjuvants (partners in a drug combination), particularly in the face of resistant parasitic strains.[PUBLICATION ABSTRACT]
That’s how the mutation and selection sorting/optimization problem works, single selection conditions targeting single genes are the easiest conditions for a population to evolve against, as soon as you use combination pressures which target more than a single gene, the process is profoundly slowed. That’s how mutation and selection sorting/optimization work mathematically and that’s how mutation and selection sorting/optimization work empirically.

[Belz...]

Belz, is that all you can do, to resort to name calling?

Er... what name calling ?

If you can’t give an alternative to abiogenesis and evolution or creation as the way we came to be, admit it.

I can't think of an alternative.

That doesn't help you, though. And the fact that you don't understand why speaks volumes.

In the mean time, I’ll continue to demonstrate with real examples of mutation and selection how this process works when there are combined selection pressures.

Except that every example you've provided assumes evolution happens...

Dr Schneider’s peer reviewed and published model of random point mutations and natural selection already demonstrates how the process works mathematically. That is how the scientific method works.

How abouy Adequate's and Dodger's respective models ?

[joobz]

Finally joobz acknowledges whose simulation of mutation and selection is showing that combination selection pressures profoundly slow the evolutionary process. It goes to show you even an alchemical engineer can learn something if you work with him long enough.
Every model has assumptions. Paul's conclusions have remained within the bounds of the model's limitations. Perhaps you'd like to offer justifications for the ones you've made?


Don't worry, I really don't expect an answer from you. You've proven that you are incapable of presenting anything of substance.

[delphi_ote]

By "diversity" you mean a few amino acid substitutions?! You realize the number of DNA mutations that requires is on the order of 10s, right? Is this really your argument? You don't understand how mutation could change a handful of amino acids over the course of millions of years?

This is officially the dumbest thing you've said in this entire thread.
Hmm... it's been a week and no response? How sad!

[rocketdodger]

What you don’t understand Rocketdodger is that the remaining 0.01 percent of the population that isn’t killed can much more easily evolve resistance to a single selection pressure than it can against combination pressures.

What you don't understand, Kleinman, is that you are an idiot. The reason the population can evolve resistance easier is because if you add another such pressure, 99.99% more of the population gets killed off. That leaves 0.000001%.

Dr Schneider’s computer simulation shows that even a population of 64 can easily evolve resistance to a single selection pressure in a small number of generations. This is how the mathematics of mutation and selection works. You don’t need huge populations to evolve against single selection pressures. It is when you combine selection pressures that you profoundly impair a populations’ ability to evolve against both conditions simultaneously.

Dr. Schneider's simulation shows no such thing and you know it. Do the pressures in ev kill off the population? NO THEY DO NOT. Even if you were to set the mutation rate to zero in ev, the population's size would not change -- it never changes, you fool.

[kleinman]

Belz, is that all you can do, to resort to name calling?Er... what name calling ?
I'm more and more of the opinion that you are either mentally ill, somehow, or a chatbot who just picks random words in my sentences and tries to answer as best you can.
Belz, just because you are ignorant of the mathematics of mutation and selection, calling me either mentally ill or a chatbot is not going to increase your understanding of the topic. I’ll continue to give you empirical examples which demonstrate how the mutation and selection sorting/optimization process actually works
If you can’t give an alternative to abiogenesis and evolution or creation as the way we came to be, admit it.I can't think of an alternative.
That’s a start.
That doesn't help you, though. And the fact that you don't understand why speaks volumes.
Sure I understand Belz, no matter what mathematical or empirical evidence is presented to you about how mutation and selection actually works; you are going to deny the truth. You are not a scientist; you are an evolutionist religious zealot.
In the mean time, I’ll continue to demonstrate with real examples of mutation and selection how this process works when there are combined selection pressures.Except that every example you've provided assumes evolution happens...
Of course evolution by mutation and selection occurs. I have never said otherwise. What I have said is that the way the mutation and selection sorting/optimization process actually works, the theory of evolution and common descent are mathematically impossible. You don’t have the selection pressures and even if you did, you can’t transform the huge number of genes necessary to change a reptile population into a bird population. Belz, as much as you are committed to the theory of evolution and common descent, the mathematical and scientific evidence shows that it can’t happen.
Dr Schneider’s peer reviewed and published model of random point mutations and natural selection already demonstrates how the process works mathematically. That is how the scientific method works.How abouy Adequate's and Dodger's respective models ?
It is not my job to debug and correct programming errors that every evolutionist zealot comes up with. If they think they can prove that n+1 selection pressures evolve more quickly than n selection pressures, produce the data. Let them produce the parametric study of their models like I have done for Dr Schneider’s ev model and then they can try to find real examples of their models.

I took the time to study Dr Schneider’s model because it had been heavily scrutinized by many mathematicians and scientists. I saw Dr Schneider’s model as a plausible simulation of the mathematics of mutation and used the techniques I learned as an engineer to study the model. What these studies revealed is that the number of selection conditions dominates the mathematical behavior of these sorting/optimization problems. I then used my training as a physician and researcher to look for real examples of this mathematical finding and Belz, it was very easy to find huge numbers of real examples of mutation and selection that show the same behavior as Dr Schneider’s mathematical model.

Now if rocketdodger and Adequate want to argue that n+1 selection pressures evolve more quickly than n selection pressures, they need to produce the studies that show this. A single silly graph or a claim that he can show that n+1 selection pressures evolve more quickly than n selection pressures but he forgot what the parameters are does not cut it. In addition, neither promoter of the mathematically impossible has produced a single real example of their irrational and illogical proposal.
Finally joobz acknowledges whose simulation of mutation and selection is showing that combination selection pressures profoundly slow the evolutionary process. It goes to show you even an alchemical engineer can learn something if you work with him long enough.Every model has assumptions. Paul's conclusions have remained within the bounds of the model's limitations. Perhaps you'd like to offer justifications for the ones you've made?
This is why you are such a phony joobz. I have shown that Dr Schneider’s model takes huge numbers of generations to evolve all three selection conditions simultaneously and trivially small number of generations to evolve any one of the selection conditions alone and then post hundreds of real examples which demonstrate the same thing. When Dr Schneider makes a claim based on the rate of information gain for a 256 base genome and then proposes a human genome can evolve in a billion years based on this irrational extrapolation, you don’t make a peep. You are fatally biased in your speculations.
Don't worry, I really don't expect an answer from you. You've proven that you are incapable of presenting anything of substance.
Joobz, if you are so secure in your speculations, why don’t you take me up on that $10,000 wager that you could find irregularities in my PhD thesis. What I showed in my thesis was how to solve a PDE with an unknown spatially dependent physical property. Let’s see if you can even figure out what I did, let alone find an irregularity in my mathematics.
By "diversity" you mean a few amino acid substitutions?! You realize the number of DNA mutations that requires is on the order of 10s, right? Is this really your argument? You don't understand how mutation could change a handful of amino acids over the course of millions of years?

This is officially the dumbest thing you've said in this entire thread.Hmm... it's been a week and no response? How sad!
Delphi, the supplier of the Wikipedia reference to fitness landscape appears to have been going for the sterno again.
What you don’t understand Rocketdodger is that the remaining 0.01 percent of the population that isn’t killed can much more easily evolve resistance to a single selection pressure than it can against combination pressures.What you don't understand, Kleinman, is that you are an idiot. The reason the population can evolve resistance easier is because if you add another such pressure, 99.99% more of the population gets killed off. That leaves 0.000001%.
Rocketwhomissesthetarget, what you still don’t understand is that is what selection pressures do, they impair a populations’ fitness to reproduce. That’s how they work mathematically and that is how they work empirically. Even if only 0.000001% is remains of a population of 10^10 – 10^12 still leaves more than enough population to evolve to a single selection pressure. It is the second selection pressure which profoundly slows the ability of the population to evolve to both selection pressures simultaneously.
Dr Schneider’s computer simulation shows that even a population of 64 can easily evolve resistance to a single selection pressure in a small number of generations. This is how the mathematics of mutation and selection works. You don’t need huge populations to evolve against single selection pressures. It is when you combine selection pressures that you profoundly impair a populations’ ability to evolve against both conditions simultaneously.Dr. Schneider's simulation shows no such thing and you know it. Do the pressures in ev kill off the population? NO THEY DO NOT. Even if you were to set the mutation rate to zero in ev, the population's size would not change -- it never changes, you fool.
Rocketwhomissesthetarget, you are really slow to understand this mathematical and empirical problem. I have already posted the data which shows Dr Schneider’s model easily evolves a single selection condition even when it won’t evolve all three selection conditions simultaneously and the single selection pressures evolve in a trivially small number of generations. We can set up a remedial course for you so that you can learn how ev works.

Hey, rocketwhomissesthetarget, are you going to prove to us that n+1 selection pressures evolve more rapidly than n selection pressures? Let’s see you prove the irrational and illogical to be true.

[rocketdodger]

It is not my job to debug and correct programming errors that every evolutionist zealot comes up with.

It is if you disagree with or dispute our results.

If they think they can prove that n+1 selection pressures evolve more quickly than n selection pressures, produce the data.

We did. See www.jedi-arts.com/code/jev.cpp for my code and www.jedi-arts.com/code/sims.txt for five representative runs.

Let them produce the parametric study of their models like I have done for Dr Schneider’s ev model and then they can try to find real examples of their models.

We did, and we did. The real examples are the programs themselves. Can you show anyone why the algorithms used by Dr. Adequate and I are not sorting algorithms?

I saw Dr Schneider’s model as a plausible simulation of the mathematics of mutation and used the techniques I learned as an engineer to study the model. What these studies revealed is that the number of selection conditions dominates the mathematical behavior of these sorting/optimization problems.

You came to such a conclusion using a model that doesn't support more than 3 selection pressures, none of which are capable of targeting independent loci like real pressures? Tell us, Kleinman, what happens when you introduce a 4th pressure into an ev run? Also tell us what happens when you set one of the pressures in ev to target only a single loci.

I then used my training as a physician and researcher to look for real examples of this mathematical finding and Belz, it was very easy to find huge numbers of real examples of mutation and selection that show the same behavior as Dr Schneider’s mathematical model.

Can you cite a study which actually measures the percent fixation in a population after the introduction of multiple selective pressures?

In addition, neither promoter of the mathematically impossible has produced a single real example of their irrational and illogical proposal.

Can you show anyone why the algorithms used by Dr. Adequate and I are not sorting algorithms?

Rocketwhomissesthetarget, what you still don’t understand is that is what selection pressures do, they impair a populations’ fitness to reproduce. That’s how they work mathematically and that is how they work empirically. Even if only 0.000001% is remains of a population of 10^10 – 10^12 still leaves more than enough population to evolve to a single selection pressure. It is the second selection pressure which profoundly slows the ability of the population to evolve to both selection pressures simultaneously.

Prove it. Can you cite a study which actually measures the percent fixation in a population after the introduction of multiple selective pressures?

Rocketwhomissesthetarget, you are really slow to understand this mathematical and empirical problem. I have already posted the data which shows Dr Schneider’s model easily evolves a single selection condition even when it won’t evolve all three selection conditions simultaneously and the single selection pressures evolve in a trivially small number of generations. We can set up a remedial course for you so that you can learn how ev works.

Can you explain to everyone why setting the weights to 10-1-1 instead of 10-0-0 completely refutes your claim?

Hey, rocketwhomissesthetarget, are you going to prove to us that n+1 selection pressures evolve more rapidly than n selection pressures? Let’s see you prove the irrational and illogical to be true.

Can you show anyone why the algorithms used by Dr. Adequate and I are not sorting algorithms?

[kjkent1]

Kjkent1, when you reduce down the number of selection conditions and the number of generations required for convergence for a 16k genome with all three selection conditions goes from over 5,000,000 generations to at most a couple hundred generations for any of the single selection condition cases demonstrates that you need to learn how to count, let alone take a computer programming class.I can count just fine, Alan. Your contention is that ev demonstrates a sorting problem that shows that adding selective pressures, irrespective of their intensity, slows evolutionary change.

The fact is, that when you program ev with non-zero mistake weights, the intensity of the mistake has an effect on the generational time to convergence. However, ev doesn't have much of a differential, because the mistake count variable accepts numbers between only 1 - 100. The question is: what happens to convergence time as the differential in intensity increases?

Your cited publications provide the answer: an overwhelming selective pressure renders all other pressures meaningless for evolutionary purposes. Were this not true, then no resistance would develop among organisms subjected to single therapies -- either in vitro or in vivo.

Given the above facts, the only reasonable conclusion is that selective pressure intensity is the dominant selective property, and that it provides a natural mutational pathway which permits evolution to occur in the available time required.

All of your evidence points to this conclusion. Thanks for proving up evolution as mathematically possible!

[joobz]

This is why you are such a phony joobz.
I have shown that Dr Schneider’s model takes huge numbers of generations to evolve all three selection conditions simultaneously and trivially small number of generations to evolve any one of the selection conditions alone and then post hundreds of real examples which demonstrate the same thing. this is your problem. You have never done the latter. I've given you several references that explain clearly that variable environmental conditions (aka, changing selection pressures) greatly increases the rate of population adaptation. This is completely against your argument and what you show with ev. Ev assumes a constant steady pressure. This is merely one assumption built into ev. Since we know reality isn't this, and evidence supports the fact that changing conditions can result in a more rapid adaptation, You are simply wrong.

There isn't anything "phony" about it. Merely, the fact that you have overextended your argument to absurdity.

When Dr Schneider makes a claim based on the rate of information gain for a 256 base genome and then proposes a human genome can evolve in a billion years based on this irrational extrapolation, you don’t make a peep. You are fatally biased in your speculations. I didn't? I thought that it was a stretch to claim that. Oh well.

Joobz, if you are so secure in your speculations, why don’t you take me up on that $10,000 wager that you could find irregularities in my PhD thesis. What I showed in my thesis was how to solve a PDE with an unknown spatially dependent physical property. Let’s see if you can even figure out what I did, let alone find an irregularity in my mathematics.
Is your justification of your model assumptions? Maybe this is why you failed to write any substantial papers from your thesis. You lack the ability to address reviewer comments.

[delphi_ote]

Delphi, the supplier of the Wikipedia reference to fitness landscape appears to have been going for the sterno again.
You've been reduced to your broken record "insults" again. Let me run this through my translation software...
Yes, you completely demolished my argument about divergence between proteins. The divergence is extremely minor when you consider sequence similarity and millions of years of evolutionary divergence. Point mutations alone could certainly account for that. I regret ever bringing it up, so I'm going to act like a 12 year old to try and distract from the painful humiliation you've inflicted upon me.

[sol invictus]

Now if rocketdodger and Adequate want to argue that n+1 selection pressures evolve more quickly than n selection pressures, they need to produce the studies that show this. A single silly graph or a claim that he can show that n+1 selection pressures evolve more quickly than n selection pressures but he forgot what the parameters are does not cut it. In addition, neither promoter of the mathematically impossible has produced a single real example of their irrational and illogical proposal.

Both of them have done so, as have I - using the mathematical model that YOU YOURSELF proposed. It was trivial to do so, and the reason for it is obvious to anyone that understands probability even a little bit.

Now, are you going to put your money where your mouth is, kleinman? Will you bet on this?

As for that paper you cited, you are apparently unable to understand what they wrote, and I see no point in repeating myself yet again.

[kleinman]

It is not my job to debug and correct programming errors that every evolutionist zealot comes up with.It is if you disagree with or dispute our results.
You haven’t presented any results other than this:
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
That’s the parametric study you presented. It is this kind of slop that evolutionists like to call science.
I saw Dr Schneider’s model as a plausible simulation of the mathematics of mutation and used the techniques I learned as an engineer to study the model. What these studies revealed is that the number of selection conditions dominates the mathematical behavior of these sorting/optimization problems.You came to such a conclusion using a model that doesn't support more than 3 selection pressures, none of which are capable of targeting independent loci like real pressures? Tell us, Kleinman, what happens when you introduce a 4th pressure into an ev run? Also tell us what happens when you set one of the pressures in ev to target only a single loci.
Ev is public domain and Dr Schneider has posted the code online. Take his code, add a fourth selection condition and show us all that the Dr Schneider’s model converges more rapidly. Then you would be showing that adding a fourth drug to the treatment of HIV would speed up the evolution of the virus. So why don’t you do that rocketwhomissesthetarget?
I then used my training as a physician and researcher to look for real examples of this mathematical finding and Belz, it was very easy to find huge numbers of real examples of mutation and selection that show the same behavior as Dr Schneider’s mathematical model.Can you cite a study which actually measures the percent fixation in a population after the introduction of multiple selective pressures?
You don’t even know what the definition of fixation is.
Rocketwhomissesthetarget, what you still don’t understand is that is what selection pressures do, they impair a populations’ fitness to reproduce. That’s how they work mathematically and that is how they work empirically. Even if only 0.000001% is remains of a population of 10^10 – 10^12 still leaves more than enough population to evolve to a single selection pressure. It is the second selection pressure which profoundly slows the ability of the population to evolve to both selection pressures simultaneously.Prove it. Can you cite a study which actually measures the percent fixation in a population after the introduction of multiple selective pressures?
Do you want the mathematical example from ev or one of the hundreds of empirical examples which I have presented? Why don’t you tell us what the definition is for “fixation”.
Rocketwhomissesthetarget, you are really slow to understand this mathematical and empirical problem. I have already posted the data which shows Dr Schneider’s model easily evolves a single selection condition even when it won’t evolve all three selection conditions simultaneously and the single selection pressures evolve in a trivially small number of generations. We can set up a remedial course for you so that you can learn how ev works.Can you explain to everyone why setting the weights to 10-1-1 instead of 10-0-0 completely refutes your claim?
Why don’t you post the data? Or do you want me to post the data since you forgot what the parameters were?
Kjkent1, when you reduce down the number of selection conditions and the number of generations required for convergence for a 16k genome with all three selection conditions goes from over 5,000,000 generations to at most a couple hundred generations for any of the single selection condition cases demonstrates that you need to learn how to count, let alone take a computer programming class.I can count just fine, Alan. Your contention is that ev demonstrates a sorting problem that shows that adding selective pressures, irrespective of their intensity, slows evolutionary change.
If you could count, you would realize that evolving all three selection conditions simultaneously in more than 5,000,000 generations is a much, much larger number of generations than the less than 500 generations needed to evolve the three selection conditions individually.

That’s right kjkent1, adding selection conditions slow the sorting of beneficial and detrimental mutations. Of course, if you search really, really hard, you may be able to find a case in ev where Rseq>=Rfreq in 0 generations. The random initialization may give you one of these. Then you could use this case to construct a basis for the theory of evolution.
Your cited publications provide the answer: an overwhelming selective pressure renders all other pressures meaningless for evolutionary purposes. Were this not true, then no resistance would develop among organisms subjected to single therapies -- either in vitro or in vivo.
Really? I think if you read these citations carefully you will find that evolving resistance occurs more quickly in the controlled in vitro environment. Eliminating weak selection pressures from a population helps the population evolve to strong selection pressures.
When Dr Schneider makes a claim based on the rate of information gain for a 256 base genome and then proposes a human genome can evolve in a billion years based on this irrational extrapolation, you don’t make a peep. You are fatally biased in your speculations.I didn't? I thought that it was a stretch to claim that. Oh well.
Joobz finally makes a peep. I told Dr Schneider that once evolutionist discovered what his modeled showed, they would discredit it. Joobz, you are just a few years slow at it. Of course, what can you expect from someone who makes such weird speculations about abiogenesis?
Joobz, if you are so secure in your speculations, why don’t you take me up on that $10,000 wager that you could find irregularities in my PhD thesis. What I showed in my thesis was how to solve a PDE with an unknown spatially dependent physical property. Let’s see if you can even figure out what I did, let alone find an irregularity in my mathematics.Is your justification of your model assumptions? Maybe this is why you failed to write any substantial papers from your thesis. You lack the ability to address reviewer comments.
No joobz, my PhD thesis is just too difficult for alchemical engineers to understand.
You've been reduced to your broken record "insults" again. Let me run this through my translation software... Yes, you completely demolished my argument about divergence between proteins. The divergence is extremely minor when you consider sequence similarity and millions of years of evolutionary divergence. Point mutations alone could certainly account for that. I regret ever bringing it up, so I'm going to act like a 12 year old to try and distract from the painful humiliation you've inflicted upon me.
Don’t get angry with me just because you chose a field based on a mathematically and empirically impossible concept, if you weren’t drinking so much sterno than perhaps you could have made a more reasonable choice of careers. Your typical evolutionist response that millions of years make evolution true shows that you still don’t understand how mutation and selection actually works despite you gave us the Wikipedia citation for the fitness landscape. Delphi, sober up before your head blows up again.

[sol invictus]

You haven’t presented any results other than this:I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was



Just FYI - by repeatedly posting this and ignoring the fact that he shortly afterwards provided the parameters, you're simply proving to everyone reading the thread that you're a troll.

It weakens your credibility, or would if you had any left.

Now put up or shut up, little troll.

[kleinman]

Now if rocketdodger and Adequate want to argue that n+1 selection pressures evolve more quickly than n selection pressures, they need to produce the studies that show this. A single silly graph or a claim that he can show that n+1 selection pressures evolve more quickly than n selection pressures but he forgot what the parameters are does not cut it. In addition, neither promoter of the mathematically impossible has produced a single real example of their irrational and illogical proposal.Both of them have done so, as have I - using the mathematical model that YOU YOURSELF proposed. It was trivial to do so, and the reason for it is obvious to anyone that understands probability even a little bit.

Now, are you going to put your money where your mouth is, kleinman? Will you bet on this?

As for that paper you cited, you are apparently unable to understand what they wrote, and I see no point in repeating myself yet again.
Sure sol, here is the wager. Take ev with a genome length of 20,000 bases and if you show that it will converge to zero mistakes faster with all three of its selection conditions than it can for any of the three selection conditions alone then I’ll pay you $10,000. If you can't do this, you pay me $10,000. Put you money where your mouth is.

[joobz]

Joobz finally makes a peep. I told Dr Schneider that once evolutionist discovered what his modeled showed, they would discredit it. Joobz, you are just a few years slow at it. Of course, what can you expect from someone who makes such weird speculations about abiogenesis?It is my understanding that Dr. Schneider even admitted the overextention of his arguments. This isn't a big deal, because he allows for that and admits it.

however, I noticed, you ignored my destruction of your constant pressure assumption. Too bad reality doesn't ignore it. Sorry Kleinman, either you justify your arguments, or you are talking nonsense.

No joobz, my PhD thesis is just too difficult for alchemical engineers to understand.there there, kleinman. Still no justifications? Your arguments are fanciful and dumb. Why would you try to justify them?

[delphi_ote]

Don’t get angry with me just because you chose a field based on a mathematically and empirically impossible concept, if you weren’t drinking so much sterno than perhaps you could have made a more reasonable choice of careers. Your typical evolutionist response that millions of years make evolution true shows that you still don’t understand how mutation and selection actually works despite you gave us the Wikipedia citation for the fitness landscape. Delphi, sober up before your head blows up again.
Translating...
Let me start by projecting my own anger and frustration that my sterno world view doesn't correspond in any way with reality. I am too much of a sterno coward to admit that my sterno argument about proteins was blown out of the water by a simple search engine. A few point mutations could clearly sterno account for the divergence I said was impossible, so I need to dance away from that argument as quickly as possible. Maybe if I talk about all of these sterno other things, people will think I know what I'm talking about and sterno forget that delphi exposed my ignorance.
Sorry. My translation software seems to have trouble with the word sterno.

[kleinman]

Joobz finally makes a peep. I told Dr Schneider that once evolutionist discovered what his modeled showed, they would discredit it. Joobz, you are just a few years slow at it. Of course, what can you expect from someone who makes such weird speculations about abiogenesis?It is my understanding that Dr. Schneider even admitted the overextention of his arguments. This isn't a big deal, because he allows for that and admits it.
If you use a mutation rate of 1 mutation per million bases rather than Dr Schneider’s value of 1 mutation per 256 bases, Dr Schneider’s estimate for the evolution of a human genome goes from a billion years to 4 trillion years. If you used a genome length of any know free living organism, his estimate is worse than irrational.

Now the conclusion that I draw from his model is based on the affect of the combination selection pressures verses single selection pressures on the rate of convergence of Dr Schneider’s model. This conclusion leads to hundreds of real examples of mutation and selection which show the exact same behavior. You evolutionists have not been able to post a real example of mutation and selection which shows otherwise.
however, I noticed, you ignored my destruction of your constant pressure assumption. Too bad reality doesn't ignore it. Sorry Kleinman, either you justify your arguments, or you are talking nonsense.
If you think your speculations are true, post a real example where combination selection pressures evolve more rapidly than single selection conditions. Or are you still lost in your Madagascar rainforest?
No joobz, my PhD thesis is just too difficult for alchemical engineers to understand.there there, kleinman. Still no justifications? Your arguments are fanciful and dumb. Why would you try to justify them?
No joobz, this is dumb:
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

How could anyone with a knowledge of chemistry make such irrational speculations is something to marvel at. You can’t even tell us how ribose could form nonenzymatically.
Don’t get angry with me just because you chose a field based on a mathematically and empirically impossible concept, if you weren’t drinking so much sterno than perhaps you could have made a more reasonable choice of careers. Your typical evolutionist response that millions of years make evolution true shows that you still don’t understand how mutation and selection actually works despite you gave us the Wikipedia citation for the fitness landscape. Delphi, sober up before your head blows up again.Translating...Let me start by projecting my own anger and frustration that my sterno world view doesn't correspond in any way with reality. I am too much of a sterno coward to admit that my sterno argument about proteins was blown out of the water by a simple search engine. A few point mutations could clearly sterno account for the divergence I said was impossible, so I need to dance away from that argument as quickly as possible. Maybe if I talk about all of these sterno other things, people will think I know what I'm talking about and sterno forget that delphi exposed my ignorance.Sorry. My translation software seems to have trouble with the word sterno.
Sterno is not the only word your translation software is having trouble with. Your translation software seems to have been written by the same programmers who think n+1 selection pressures evolve more quickly than n selection pressures. Delphi, there is a 12 step program which can help you with your drinking problem.

[rocketdodger]

You haven’t presented any results other than this:I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was :(

Pathetic Liar.

Ev is public domain and Dr Schneider has posted the code online. Take his code, add a fourth selection condition and show us all that the Dr Schneider’s model converges more rapidly.?

I never claimed it converges more rapidly. That is why you cannot quote me as saying so you liar.

Then you would be showing that adding a fourth drug to the treatment of HIV would speed up the evolution of the virus. So why don’t you do that rocketwhomissesthetarget?

Except for the fact that the pressures in ev target the entire genome, the fact that the population size in ev remains constant, and the fact that fixation rate has little to do with convergence time, yes, it would be showing the same thing. You are a genius.

You don’t even know what the definition of fixation is.

http://en.wikipedia.org/wiki/Fixation_%28population_genetics%29

Do you want the mathematical example from ev or one of the hundreds of empirical examples which I have presented? Why don’t you tell us what the definition is for “fixation”.

I want an empirical example, since you are incapable of representing the results of ev correctly. So how about it, Kleinman? Can you cite a study which actually measures the percent fixation in a population after the introduction of multiple selective pressures?

Why don’t you post the data? Or do you want me to post the data since you forgot what the parameters were?

I already did, in a post you ignored:

Using the default settings, it takes less than 20 generations to reach a perfect creature with 10-0-0. Using 10-1-1, it takes 316 generations. Ok. If your theory is true, then going to 10-10-10 will result in an "orders of magnitude" slowdown compared to 10-1-1. Except... with 10-10-10 it took 662 generations. That is merely double the time to convergence -- not quite "orders of magnitude" you genius.

And what is more... with 10-10-10 there is effectively three pressures where at 10-1-1 there was still effectively one -- a 300% increase. Yet it only took twice as long to converge, a 200% increase. So if we increased the number of pressures by 300% and convergence only took 200% longer... THE RATE OF CONVERGENCE INCREASED.

[sol invictus]

Sure sol, here is the wager. Take ev with a genome length of 20,000 bases and if you show that it will converge to zero mistakes faster with all three of its selection conditions than it can for any of the three selection conditions alone then I’ll pay you $10,000. If you can't do this, you pay me $10,000. Put you money where your mouth is.

I won't take that bet, because - as everyone here agrees - it isn't true. Three conditions will take longer to converge than one.

The issue is whether they take three times longer or not, as you claimed.

RATE, kleinman - RATE.

Are you capable of understanding that elementary concept?

Now put up or shut up: will you bet that N+1 selection pressures fix at a slower RATE than N?

If not, then you have finally admitted that you've been wrong all along. I'm waiting for your answer.

[joobz]

If you use a mutation rate of 1 mutation per million bases rather than Dr Schneider’s value of 1 mutation per 256 bases, Dr Schneider’s estimate for the evolution of a human genome goes from a billion years to 4 trillion years. If you used a genome length of any know free living organism, his estimate is worse than irrational.

Now the conclusion that I draw from his model is based on the affect of the combination selection pressures verses single selection pressures on the rate of convergence of Dr Schneider’s model. This conclusion leads to hundreds of real examples of mutation and selection which show the exact same behavior. You evolutionists have not been able to post a real example of mutation and selection which shows otherwise.i'm sorry, but every post you have made to actual data has supported the evolutionary hypothesis. Nothing that you presented demostrate that
1.) # selection pressures remain constant and known
2.) slow = stop
3.) mutation rate remains constant
4.) only point mutation matters
5.) Selection pressure magnitude remains constant and known.
You have continually failed to answer my question.

What you say is just stupid. You haven't made an intelligent argument. You've only said stupid things. When we ask you to justify the stupid things you say, you reply with insults and stupidty.
such as:

If you think your speculations are true, post a real example where combination selection pressures evolve more rapidly than single selection conditions. Or are you still lost in your Madagascar rainforest?

No joobz, this is dumb:
[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

How could anyone with a knowledge of chemistry make such irrational speculations is something to marvel at. You can’t even tell us how ribose could form nonenzymatically.
All of those things you just said are stupid.
Why do you say stupid things?
Is Dr. Adequate correct in his description of your mental state?

[kleinman]

If you use a mutation rate of 1 mutation per million bases rather than Dr Schneider’s value of 1 mutation per 256 bases, Dr Schneider’s estimate for the evolution of a human genome goes from a billion years to 4 trillion years. If you used a genome length of any know free living organism, his estimate is worse than irrational.

Now the conclusion that I draw from his model is based on the affect of the combination selection pressures verses single selection pressures on the rate of convergence of Dr Schneider’s model. This conclusion leads to hundreds of real examples of mutation and selection which show the exact same behavior. You evolutionists have not been able to post a real example of mutation and selection which shows otherwise.i'm sorry, but every post you have made to actual data has supported the evolutionary hypothesis. Nothing that you presented demostrate that
1.) # selection pressures remain constant and known
2.) slow = stop
3.) mutation rate remains constant
4.) only point mutation matters
5.) Selection pressure magnitude remains constant and known.
You have continually failed to answer my question.
I understand that evolution is not your field because you have admitted this.
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.
So I’ll explain this so that even a novice like you can understand this.
All the real examples of mutation and selection cited had known number of selection pressures and all show that combination selection pressures. Many of these authors of these citations claim that the evolution of resistance can be stopped by combination therapy. You yourself posted a citation which shows that HIV does recombination and I have posted citations which show that HIV also does insertions and deletions. These examples show that point mutations alone are not required for combination selection pressures to profoundly slow the evolution of resistance. Other mechanisms of mutation do not change the fact that combination selection pressures profoundly slow the evolutionary process. Joobz, if there was any truth in your speculations, you would be able to post real examples of your speculations but you can’t. This is why you raise ridiculous speculations that the Madagascar rain forest and plate tectonics accelerates the evolutionary process. That is as weird as your speculations about cooperative chemistry. So here is another citation which shows that combination selection pressures profoundly slow the evolutionary process.
http://www.pnas.org/cgi/reprint/0600636103v1.pdf (http://www.pnas.org/cgi/reprint/0600636103v1.pdf)
In the case of two antibiotics with distinct mechanisms of action, theoretical and empirical research supports the merits of combination therapy to both prevent treatment failure in individuals and control antimicrobial resistance at the population level; in other words, the same policy may satisfy both objectives (6–8). In other cases, the two objectives may be in conflict. For a bacterial pathogen that is increasingly resistant to a widely prescribed agent, promoting
the use of a novel drug with activity against the resistant strains leads to fewer treatment failures and delivers benefits to current patients (4, 9). On the other hand, switching to a new drug imposes a selective pressure in favor of strains that are resistant to even the new antibiotic (10–12). Thus, we may expect that such a switch achieves the first objective at the expense of the second. Specifically, when considering two antibiotics within the same therapeutic class, high-level resistance is often conferred through sequential accumulation of chromosomal mutations or acquisition of new genetic material (8). This stepwise mechanism makes combination therapy or cycling of two antibiotics of the same class impractical. For example, resistance to fluoroquinolones in Streptococcus pneumoniae is mediated by chromosomal changes on two genes: DNA gyrase (gyrA) and topoisomerase IV (parC) (13). The first generation of fluoroquinolones, such as ofloxacin and ciprofloxacin, preferentially targets one of the two loci. Since 1994, however, a number of newer ‘‘dual-activity’’ fluoroquinolones, including levofloxacin (the second generation) and gatifloxacin and moxifloxacin (the third generation) (14), that demonstrate more comparable activity against both genes, have been developed. Because at least two mutations are usually required in order to confer a biologically significant resistance to these newer agents, the likelihood for a resistant strain to emerge during treatment of a fully susceptible infection is much lower (15–17). On the other hand, a strain already resistant to an ‘‘old’’ fluoroquinolone is only one mutation away from becoming resistant to the newer drugs, making selection of a fully resistant mutant more likely from such ‘‘precursor’’ strains.

In the presence of such a stepwise mechanism, does treatment success for today’s patients still inevitably lead to faster selection of resistance? It may do so, as argued above; however, a contrasting argument runs as follows: Because strains resistant to the older fluoroquinolones are the genetic precursors to higher-level resistance, early upgrade to the new agents could ‘‘block’’ the pathway toward selecting for highly resistant strains (18). Early use of the newer drugs also presents immediate benefits to patients. Therefore, an immediate switch to the more active drugs could achieve both better outcomes today and slower evolution of resistance tomorrow.
Hundreds of examples which show that combination selection pressures profoundly slow the evolutionary process. Where are all your citations joobz which show otherwise? Zero citations for your irrational and illogical theory verses a peer reviewed and published mathematical model which shows that combination selection pressures profoundly slow the evolutionary process and hundreds of real examples which show the same thing. Joobz, your speculations don’t constitute a mathematical or measurable repeatable scientific argument but that is understandable because you are a biased novice to the field of evolution. That’s a truthful admission on your part.

[joobz]

I understand that evolution is not your field because you have admitted this.

So I’ll explain this so that even a novice like you can understand this.
All the real examples of mutation and selection cited had known number of selection pressures and all show that combination selection pressures. Many of these authors of these citations claim that the evolution of resistance can be stopped by combination therapy. You yourself posted a citation which shows that HIV does recombination and I have posted citations which show that HIV also does insertions and deletions. These examples show that point mutations alone are not required for combination selection pressures to profoundly slow the evolution of resistance. Other mechanisms of mutation do not change the fact that combination selection pressures profoundly slow the evolutionary process. Joobz, if there was any truth in your speculations, you would be able to post real examples of your speculations but you can’t. This is why you raise ridiculous speculations that the Madagascar rain forest and plate tectonics accelerates the evolutionary process. That is as weird as your speculations about cooperative chemistry. So here is another citation which shows that combination selection pressures profoundly slow the evolutionary process.
http://www.pnas.org/cgi/reprint/0600636103v1.pdf (http://www.pnas.org/cgi/reprint/0600636103v1.pdf)

Hundreds of examples which show that combination selection pressures profoundly slow the evolutionary process. Where are all your citations joobz which show otherwise? Zero citations for your irrational and illogical theory verses a peer reviewed and published mathematical model which shows that combination selection pressures profoundly slow the evolutionary process and hundreds of real examples which show the same thing. Joobz, your speculations don’t constitute a mathematical or measurable repeatable scientific argument but that is understandable because you are a biased novice to the field of evolution. That’s a truthful admission on your part.
There you go again, saying stupid things. I don't want to think you are stupid, but you are really leaving me little choice.

How about you justify your assumptions now? This question will not go away. Neither will the other questions you have evaded by other posters here.

[kleinman]

Sure sol, here is the wager. Take ev with a genome length of 20,000 bases and if you show that it will converge to zero mistakes faster with all three of its selection conditions than it can for any of the three selection conditions alone then I’ll pay you $10,000. If you can't do this, you pay me $10,000. Put you money where your mouth is.I won't take that bet, because - as everyone here agrees - it isn't true. Three conditions will take longer to converge than one.

The issue is whether they take three times longer or not, as you claimed.
Ok, we have a bet, if ev takes more than three times longer to evolve all three selection conditions simultaneously for a G=20,000 bases than it takes to evolve each of the three selection conditions individually than you owe me $10,000. If ev evolves the three selection conditions singly in more than three times the sum of the number of generations for each of the selection conditions than it take for all three selection conditions simultaneously, than I owe you $10,000.

[sol invictus]

Ok, we have a bet, if ev takes more than three times longer to evolve all three selection conditions simultaneously for a G=20,000 bases than it takes to evolve each of the three selection conditions individually than you owe me $10,000. If ev evolves the three selection conditions singly in more than three times the sum of the number of generations for each of the selection conditions than it take for all three selection conditions simultaneously, than I owe you $10,000.

OK, now we're talking. That's the relevant question - whether the time to fix N conditions increases faster or slower than N. More simply, whether the RATE increases or decreases with N.

Why do you want to use 3 pressures, and not, say, 100? In my analysis the difference is much larger for larger numbers of pressures. Rocketdodger, if I recall correctly, also found that the rate only starts to increase at relatively large numbers of pressures.

Of course real evolution proceeded under a huge number of pressures, so I assume you won't object to increasing the number?

And why do you want to use ev, and not the model you proposed? I'm not necessarily opposed to using it, but I'd like to hear your reasons.

[delphi_ote]

Sterno is not the only word your translation software is having trouble with. Your translation software seems to have been written by the same programmers who think n+1 selection pressures evolve more quickly than n selection pressures. Delphi, there is a 12 step program which can help you with your drinking problem.
Sorry. Your distractions aren't working. Those two genes are clearly related by sequence. Plug your ears and spout all the nonsense you like. It's patently obvious you're ducking away from reality here.

[rocketdodger]

OK, now we're talking. That's the relevant question - whether the time to fix N conditions increases faster or slower than N. More simply, whether the RATE increases or decreases with N.

You are biting off more than you can chew, sol! I would not make the claim that the rate increases faster than N in general.

My claim, which my program backs up, is that for a given