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]

Annoying Creationists

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:

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.

~~ Paul

LOL! 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]

Annoying Creationists

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

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

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

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]

Annoying Creationists

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

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.