Annoying creationists

[Mr. Scott]

A single selection condition can be sorted for very rapidly by Dr Schneider’s sorting algorithm while all three selection conditions can only be sorted for rapidly only on extremely tiny unrealistic length genomes. This mathematical behavior that Dr Schneider’s mathematical model demonstrates is reflected in reality as demonstrated by more of these real examples of the mutation and selection sorting/optimization process.

Dr. Kleinman, I’m glad you brought this up because I am prepared to drive a silver spike through the heart of that argument.

Your error has to do with your equation of model execution time with the virtual time that it is modeling.

Nature does not execute a sort algorithm. The time it takes to sort a population in a computer in no way models the time needed to sort a population in nature. Organisms in a natural colony sort themselves instantaneously, whereas a computer model, by the nature of the usual computer program implementation, must execute an algorithm sequentially, and necessarily needs more CPU time as the number of items or selection conditions increases.

A computer program has to execute one instruction at a time, with a single CPU sequentially going through a sort algorithm step by step, item by item, and condition by condition. In nature, though, each organism has, in a sense, it’s own CPU, so a sort happens with massive parallelism. A colony of a trillion microbes has, in effect, a trillion processors running a trillion sorts all at the same time, and the number of conditions (selection pressures) would have no effect on the real time sort speed.

I’ll give you an example of how this works. Suppose a photographer needs one hundred students to line up for a photograph sorted by height. If the photographer were to make each comparison himself and order each swap himself and wait for each swap to occur before making the next comparison, it would take a very long time indeed for the hundred students to be sorted. Alternatively, the photographer could give the students the following instruction: “everyone please position yourself so that you have a taller person to your right and a shorter person to your left” and the students would sort themselves very, very quickly.

The first example is how Ev sorts -- laboriously, one comparison and swap at a time. The second example is how nature sorts -- every organism sorts itself, by reproducing or not reproducing according to how competition plays out, and the count of sort conditions would have no affect on the speed of that sort -- some die, some don't. No sort time is required.

In summary, though a condition (selection pressure) count may have a detrimental effect on computation time of a model like Ev, the time it takes for organisms to be selected or not because of multiple selection conditions in nature would not be similarly affected.

Now, Dr. Kleinman, if you were a real scientist and my argument were shown to be true, then you would thank me for advancing your knowledge in computer science and evolution. If you show me I’m wrong, I will thank you.

I await your refutation.

 

[kleinman]

Annoying Creationists

Once again, we have an evolutionist who thinks there is something unique about the mutation and selection sorting/optimization process. Somehow, evolutionists think that the sorting occurring with biological systems behaves differently from other sorting problems (or for that matter iteration problems or optimization problems) found in non-biological systems. All these mathematical problems are markedly slowed for more complex sorting conditions (or for iteration or optimization conditions). The computer model execution time and virtual time are directly correlated with real time. This is how Dr Schneider responded to this argument on his ev blog site, http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html

13) Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":

So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!

and

Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world.

1. The simulation was of phenomena in the "real" world.

2. Dr. Jones is invited yet again to do an experiment.

Dr Schneider is correct here. His sorting algorithm is exactly analogous to what happens in nature. Just because Dr Schneider’s algorithm can do generation cycles is some cases millions of times faster in the computer than could be done in real life, his model still properly models the mutation and selection sorting/optimization process.

Now the notion that there are trillions of sorting processes going on simultaneously is simply a fantasy that evolutionists try to use to justify their theory. Unfortunately for you evolutionists, there is no mathematical or empirical basis for this claim. In fact these types of claims obfuscate how the mutation and selection sorting/optimization process actually works as demonstrated by Dr Schneider’s mathematical computer simulation and the hundreds of real examples of mutation and selection which substantiates Dr Schneider’s simulation. Here are more examples which substantiate the result that Dr Schneider’s model demonstrates, which is that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://pathmicro.med.sc.edu/lecture/hiv14a.htm

These drugs are non-competitive reverse transcriptase inhibitors, that is they bind elsewhere than the active site of the enzyme.

Because of the problems with AZT and the other nucleoside analogs in the treatment of HIV, interest grew in another approach to inhibiting the same enzyme, reverse transcriptase. Alternative drugs might be useful in combination therapy since there is a limit to the number of mutations that reverse transcriptase can bear without losing function. Clearly, mutations resistant to a non-nucleoside non-competitive inhibitor of reverse transcriptase would be at a different site in the enzyme from the mutation that makes the enzyme resistant to a competitive nucleoside analog.

http://www.absw.org.uk/Briefings/insecticide_resistance.htm

Using high doses of insecticide should maximise kill of heterozygotes and this strategy was popular among theorists in the 1970s. But to be really effective, the dose was too high to be acceptable on either environmental or cost grounds. Another drawback was that uniform coverage of the crop was not assured. The high dose strategy could be revived though with transgenic plants if it is possible to maintain a high level of expression of the toxin gene. The other strategy is pyramiding which involves creating trangenic plants with genes for two different toxins. Insects resistant to one will be killed by the other, and vice versa. This provides a double hit strategy for seeing off heterozygotes and discouraging the spread of resistance genes. It also parallels the successful use of combination drug therapy in leprosy, TB and HIV/AIDS.

http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resistance&hl=en&ct=clnk&cd=297&gl=us

With its high mutation rate, small genome, and large population size, HIV is highly likely to generate resistance mutations (as we’ve seen with AZT)

What was needed was a way to increase the number of mutations that must arise in a virion’s genome to render it resistant to the drug

The key breakthrough was to use combination therapy, cocktails of multiple drugs acting together which are not only very effective, but which delay evolution of resistance

http://www.ann-clinmicrob.com/content/5/1/25

in this study the checkerboard analysis showed that amikacin in combination with cephalothin or dicloxacillin was synergistic against most of the resistant strains of S. aureus and coagulase-negative Staphylococcus. Vancomycin in combination with a beta-lactam (cephalothin or imipenem) showed additivity. An indifferent effect predominated for the combination vancomycin plus amikacin. Even though a synergistic effect is expected when using a beta-lactam plus amikacin combination, it is possible that the effect cannot be clinically achievable. Careful selection of antimicrobial combinations and initial MICs are mandatory for future evaluations.

Now if you evolutionists think there are trillions of sorting process going on simultaneously, present the mathematical and empirical basis for such a claim. Otherwise, all you do with such irrational and illogical claims is to contribute to the premature death of millions of people with diseases subject to mutation and selection. That includes stepfathers who die from cancer.

 

[kjkent1]

kleinman, scientific discovery marches on, despite your protestations to the contrary. You may want to check this link: http://www.livescience.com/health/080124-dna-telepathy.html. It discusses a weird, but empirically verifiable property of DNA, which may help explain how evolutionary processes get past your claims of statistical impossibility.

What is clear from the cited article is that we still don't know exactly how evolution works. We do, however, observe that it does work. As always, you are free to attribute the unexplained to God, while the scientist will attribute the unexplained to a lack of verifiable evidence.

In the end, it's still primarily a philosophy argument "in the gaps."

 

[kleinman]

Annoying Creationists

Now that’s a good one, DNA demonstrates telepathy. I guess you evolutionists forgot that there are electromagnetic fields around molecules. You evolutionists go further and further into the paranormal and have no idea about the basic science and mathematics of the mutation and selection sorting/optimization process. You go even further by indoctrinating naïve school children with this type of nonsense so they have no idea or foundation how to deal with diseases subject to the mutation and selection process. This is how evolutionist nonsense contributes to the premature death of millions of people suffering from disease subject to the mutation and selection sorting/optimization process. The theory of evolution is not only nonsense; it has and will continue to hurt millions of people.

 

[Belz...]

DNA demonstrates telepathy.

Yeah, like God.

 

[kleinman]

Annoying Creationists

You evolutionists can’t even explain how the mutation and selection sorting/optimization process works. What makes you think that you know how God works?

Here are more citations which show how the mutation and selection sorting/optimization work empirically. And it works the same as Dr Schneider’s ev model, which is that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://www.bmj.com/cgi/content/full/325/7374/1221?etoc

Artemisin combinations may delay and possibly reverse the development of drug resistance through a variety of mechanisms.

http://journal.paho.org/?a_ID=335

Suboptimal treatment regimens, such as monotherapy or dual therapy, treatment with poor-quality antiretroviral drugs, suboptimal dosing, and poor absorption, may increase the rate at which viral resistance evolves among treated individuals

http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html

The genetic instability of tumor cells renders them the ability to rapidly become resistant to many chemotherapies. As a result, there is great interest in selecting combination chemotherapeutic regimens that will overcome resistance and exert synergistic therapeutic activity.

Now since you evolutionists have no idea how the mutation and selection sorting/optimization process works, why don’t you speculate on how God works. Perhaps you can figure it out from your fossil Rorschach tests?

 

[rocketdodger]

Dr. Kleinman, I’m glad you brought this up because I am prepared to drive a silver spike through the heart of that argument.

Your error has to do with your equation of model execution time with the virtual time that it is modeling.

Nature does not execute a sort algorithm. The time it takes to sort a population in a computer in no way models the time needed to sort a population in nature. Organisms in a natural colony sort themselves instantaneously, whereas a computer model, by the nature of the usual computer program implementation, must execute an algorithm sequentially, and necessarily needs more CPU time as the number of items or selection conditions increases.

A computer program has to execute one instruction at a time, with a single CPU sequentially going through a sort algorithm step by step, item by item, and condition by condition. In nature, though, each organism has, in a sense, it’s own CPU, so a sort happens with massive parallelism. A colony of a trillion microbes has, in effect, a trillion processors running a trillion sorts all at the same time, and the number of conditions (selection pressures) would have no effect on the real time sort speed.

I’ll give you an example of how this works. Suppose a photographer needs one hundred students to line up for a photograph sorted by height. If the photographer were to make each comparison himself and order each swap himself and wait for each swap to occur before making the next comparison, it would take a very long time indeed for the hundred students to be sorted. Alternatively, the photographer could give the students the following instruction: “everyone please position yourself so that you have a taller person to your right and a shorter person to your left” and the students would sort themselves very, very quickly.

The first example is how Ev sorts -- laboriously, one comparison and swap at a time. The second example is how nature sorts -- every organism sorts itself, by reproducing or not reproducing according to how competition plays out, and the count of sort conditions would have no affect on the speed of that sort -- some die, some don't. No sort time is required.

In summary, though a condition (selection pressure) count may have a detrimental effect on computation time of a model like Ev, the time it takes for organisms to be selected or not because of multiple selection conditions in nature would not be similarly affected.

Now, Dr. Kleinman, if you were a real scientist and my argument were shown to be true, then you would thank me for advancing your knowledge in computer science and evolution. If you show me I’m wrong, I will thank you.

I await your refutation.

This is why in computer models we measure rates according to the number of generations, or virtual time, that it takes something to happen -- it removes any processing considerations from the experiment and allows us to focus only on the algorithm. It also allows us to emulate parallel processes, like evolution, on serial machines, like computers.

Kleinman is incapable of understanding this (among other things), and thats why he doesn't have a clue what he is talking about when it comes to either ev or his hundreds of empirical examples. If a computer takes more real time to sort, kleinman interprets this as "the sorting being confounded," which is of course utter nonsense.

It doesn't matter, nobody cares about this thread anymore. Kleinman is old news.

 

[hamelekim]

Isn't the title of this thread a little redundant?

 

[kleinman]

Annoying Creationists

I enjoy annoying evolutionists with the mathematical and empirical facts of how the mutation and selection sorting/optimization process actually works. Now, you evolutionists have completely bungled the basic science and mathematics of the mutation and selection sorting/optimization process and in the meantime are still trying to figure out what “random” means. Your irrational and illogical concepts of abiogenesis and the theory of evolution have made a framework for your speculations but do not fit the mathematical and observed evidence. You may have successfully institutionalized these ideas into the field of biology but they are totally useless concepts in the explanation of how the basic science and mathematics of the mutation and selection process actually works. Perhaps a few more examples of how the mutation and selection process actually works will clarify the mathematical and empirical fact of life that combination selection pressures profoundly slow evolution by this process.
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract

Even patients with extensive resistance to the failing regimen were still receiving benefit from treatment.

http://agfacts.tamu.edu/~jbenedic/TRANS.htm

On these bases transgenic insect-resistant crops are a new tool for insect pest management of crop plants. This new tool is complimentary to many existing pest management tactics, and when used in combination, these tactics may provide superior pest management compared to any single tactic.

and

Other strategies to use in combination with the refuge are: (1) stacking two or more insecticide producing genes in the same transgenic plant; (2) low dose producing transgenic plants that act in concert with natural enemies to decrease target pest populations; (3) tissue-, time-, or signal-dependent expression of toxins; (4) rotation over time (years) of insecticidal toxins with different modes of action; and (5) deploying different toxins in different crop varieties in the same year and production system.

http://www.annclinlabsci.org/cgi/content/abstract/32/4/406

In recent years, resistance testing has become an important tool in optimizing the combination therapy for treating HIV infected individuals. The identification of resistance mutations has allowed physicians to select the antiviral agents with maximum therapeutic benefic and minimum toxic side effects.

http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml

There is a need to develop broadleaf combinations or mixtures to control glyphosate and multiple HT volunteers pre-seed. For example, 2,4-D, MCPA, bromoxynil and a low residual sulfonylurea like tribenuron methyl in combination with glyphosate would provide broad-spectrum pre-seed weed control including volunteer glyphosate HT canola. In some situations amitrole and paraquat could provide effective pre-seed control and resistance management for volunteer HT canola.

And

Herbicide mixtures to manage volunteers and reduce selection pressure could be a requirement for future HT crop releases.

Trillions of sorting process occurring simultaneously, chemicals “cooperating” to form life by abiogenesis, variations in the weather causing blizzards to turn lizards into buzzards with gizzards, n+1 selection pressures evolving more rapidly than n selection pressures even though you don’t have a single empirical example of this nonsense? These would all be very amusing if it were not a fact that these ridiculous assertions contribute to the premature death of millions of people with diseases subject to mutation and selection. We all thank you evolutionists for MRSA, delay in the understanding that diseases like HIV and cancer require combination therapy and your diligent work of indoctrinating naïve school children with irrational speculations and calling it science.

 

[Shalamar]

Too bad Kleinman has no facts. And still has no math.

He's just a parrot, repeating only what he is allowed to understand.

 

[Nogbad]

Nearly at page 200 I see and yet...

 

[kleinman]

Annoying Creationists

You evolutionists are so correct when you say I have no mathematics to back up my argument except you continue to forget one thing, I have Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection and I have only a few hundred measly empirical citations which demonstrates what Dr Schneider’s mathematical model shows, that is combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. Why don’t I post a few more just to annoy some irrational and illogical evolutionists.
http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf

Combining drugs from different classes can slow down the emergence of resistant variants substantially, because mutants that are resistant to all components are unlikely to pre-exist, and new variants need to generate several escape mutations while retaining the ability of effective replication.

http://www.ecologyandsociety.org/vol3/iss2/art12/

Protease inhibitors of HIV prevent infected cells from producing infectious virus. The overall dynamics are very similar to the case of reverse transcriptase inhibitors, because the infectious virus particles present initially decay very rapidly. Combination of reverse transcriptase and protease inhibitors has led to tremendous success in HIV therapy.

Essentially, all of these drugs, if used as single antiviral therapy, lead to the emergence of resistant virus mutants. The pattern is often similar. Initially, there is a decay in virus abundance, but after some time, the virus resurges. The decisive treatment breakthrough was to combine several drugs at once. For about 2 years, this combination therapy has proved to be a tremendous success. In many patients, virus abundance in the blood decays below detection limit within weeks of treatment and can remain undetectable for years.

http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf

Antimicrobial exposure inevitably exerts a selection pressure on the pathogen being actively treated, as well as commensal organisms, 80% to 90% of which are currently non-culturable (Wilson & Blitchington, 1996; Langendijk et al 1995). Therefore, its potential to act as a reservoir for antimicrobial resistance genes may be immense. As the “normal” commensal flora acts to inhibit the attachment and multiplication of pathogenic micro-organisms by various mechanisms, its disturbance may also facilitate colonization with exogenously acquired pathogens. Consequently, the aim of antimicrobial therapy must be to destroy the pathogen rapidly and efficiently, while producing the least amount of “collateral” damage. This can be achieved by giving careful consideration to the agent employed, its spectrum of activity, method of administration, penetration to the site of infection, magnitude of dose, frequency of administration, duration of therapy, and the use of agents in combination, such as in TB and HIV therapy.

Come on now, won’t you evolutionists post some more of your fossil Rorschach tests and then tell us what your imagination shows?

 

[Shalamar]

Remember folks: Mr. Kleinman isn't allowed to accept the evidence behind the Theory of Evolution.

So he has to make things up using misinterpreted data.

 

[kleinman]

Annoying Creationists

I understand that I have to be patient with you evolutionists. After all you have been programmed for years with irrational and illogical speculations. Evolutionist propaganda has always avoided describing the basic science and mathematics of the mutation and selection sorting/optimization process. Is it any wonder that Dr Schneider has not published the results of the parametric study that he recommends in his original publication on ev? If he had, he would have a lot of explaining to do about how his model contradicts the theory of evolution. After all, his mathematical model shows that the dominant parameter is the number of selection conditions. One selection condition in his model takes trivially small number of generations to evolve that condition while all three selection conditions simultaneously takes huge number of generations to satisfy all three selection conditions (except on the tiniest, unrealistic length genomes). I’ll just keep posting real examples of this and perhaps in a few years some of you evolutionist devotees will understand how the mutation and selection sorting/optimization process actually works. Here are a few more examples for you to consider.
http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html

In this paper we discuss the case of the evolution in weed species of resistance to glyphosate, a valuable and widely used broad-spectrum non-selective herbicide first developed by Monsanto in the early 1970s.

and

The authors conclude that “The use of glyphosate in combination with other low risk herbicides for weed control with RR cotton provides an opportunity to significantly reduce the risk of off-site herbicide contamination in Australian cotton production”

http://www.aegis.com/factshts/tpc/guide/

Based on what is known about HIV's error-prone replication process (see above), we can assume that all patients have at least a few subpopulations of HIV that are resistant to individual drugs. However, these strains are often too limited in number and strength to compete with wild-type virus, and they stand a good chance of being killed off by initiating combination antiretroviral therapy. After all, the purpose of combination therapy is to serve as a multipronged attack on such strains.

http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html

The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.

Isn’t that interesting, the empirical evidence agrees with Dr Schneider’s mathematical model which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. That is why the theory of evolution is mathematically and empirically impossible.

Now you all have a good weekend and if you can’t find a fossil Rorschach test to fuel your imaginations, just look at the clouds. We’ll be back next week to again correct the bungled evolutionist explanation of how the mutation and selection sorting/optimization process actually works.

 

[Paul C. Anagnostopoulos]

You evolutionists can’t even explain how the mutation and selection sorting/optimization process works. What makes you think that you know how God works?

And with this remark we understand that you will never, ever again bring up god in relation to the origin of species.

~~ Paul

 

[sol invictus]

Kleinman is incapable of understanding this (among other things), and thats why he doesn't have a clue what he is talking about when it comes to either ev or his hundreds of empirical examples. If a computer takes more real time to sort, kleinman interprets this as "the sorting being confounded," which is of course utter nonsense.

Are you serious? I didn't realize he was that idiotic.

So if I port ev to my iphone and it runs slowly, does that mean evolution is profoundly slowed by the existence of iphones?

 

[m_huber]

If anyone who is reading this thread has a headache fueled by reading repetitive ignorance, try a nice cold glass of actual science:

http://www-personal.umich.edu/~gingeric/PDFfiles/PDG132_JGeolEdu.pdf

 

[Belz...]

I enjoy annoying evolutionists

Troll, troll, troll.

 

[Mr. Scott]

Dr. Kleinman, I know you are away for the weekend, but when you come back, would you tell us what sorting algorithm nature uses during micro-evolution? Different sort algorithms would profoundly affect the speed of any sorting/optimization, so I'd really like to know which sort nature uses. Does it use Quick Sort? Bubble Sort? Selection Sort? Insertion Sort? Shell Sort? Merge Sort? Heap Sort? Bucket Sort? Radix Sort?

 

[rocketdodger]

The closest analog is probably bucket sort, I would say.