rocketdodger
Philosopher
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- Jun 22, 2005
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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 said: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?Belz… said:Just because you can't think of a third way doesn't mean there isn't one.
Kleinman said:Belz… said:
But that's besides the point, as anyone who's ever studied logic knows. You can't prove a theory by disproving another one.
Tell us of what evil that hasn’t gone un-judged?Belz… said:Funny, because lots of evil goes un-judged.Kleinman said:How do you know?Belz… said:Because to claim otherwise would be an argument from ignorance.
How do you know he doesn’t exist?Kleinman said:Do you think the fiend god gets away with evil?Belz… said:He doesn't, because he doesn't exist.
Adequate has posted a silly graph and you have posted the following:rocketdodger said: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.
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.rocketdodger said: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![]()
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?rocketdodger said: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.
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.rocketdodger said: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.
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:rocketdodger said: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.
So you got this wrong about the ev model and Dr Schneider said the following for how he intended to have ev used.Dr Schneider said:The weight matrix gene for an organism is translated and then every position of that organism's genome is evaluated by the matrix.
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.Dr Schneider said:Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
“Antibiotic interactions that select against resistance”Kleinman said:So here is an example where combination selection pressures not only slow the evolutionary process, it reverses the evolutionary process.rocketdodger said: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.
Abstract said: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 [size=+3]inversion of selection
[/SIZE]Abstract said: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.
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.
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.
lethal pressures, when combined, prevent populations from evolving resistance -- by killing them.
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:
The ev program only features 3 pressures, and they target 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.
Since simply color highlighting is not enough for rocketwhomissesthetarget, what do you think these authors mean by[size=+3]inversion of selection?[/SIZE]
.In that study they simply inverted the direction of a selective pressure.
]“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
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:Kleinman said:Adequate has posted a silly graph and you have posted the following:rocketdodger said: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.
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.rocketdodger said: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![]()
Kleinman said:Neither of you have done a systematic presentation of your models or given a real example of your models.rocketdodger said: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.
Kleinman said:rocketdodger said:
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 can’t help if you are so steeped in evolutionist dogma that you can’t recognize what the ev model shows.Kleinman said: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.rocketdodger said: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?
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.rocketdodger said: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![]()
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.Kleinman said: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?rocketdodger said: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.
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.Kleinman said: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.rocketdodger said:Which is why I said:rocketdodger quoting himself said:lethal pressures, when combined, prevent populations from evolving resistance -- by killing them.rocketdodger said:Tell me, Kleinman, if a population stops reproducing, how can it evolve?
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.Kleinman said: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.rocketdodger said: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?
Kleinman said:Antibiotic interactions that select against resistance”
Kleinman said:Remy Chait, Allison Craney, Roy Kishony. Nature. London: Apr 5, 2007. Vol. 446, Iss. 7136; pg. 668, 4 pgssol invictus said:Did you actually read that paper? It's pretty interesting, but it has no bearing on what you're trying to argue.sol invictus said:
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.
Giving Bacteria A One-Two Punch Drug combo stymies development of resistant bacteria said:Using the right combination of antibiotics could curtail the development of drug-resistant bacteria, a new study shows.
Giving Bacteria A One-Two Punch Drug combo stymies development of resistant bacteria said:
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.
All default settings except:kleinman said: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.
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:
is nothing more than rhetoric trash that is obvious to everyone.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![]()
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.
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?
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.
Sol, this article demonstrates exactly that combination selection pressures profoundly slow the evolution of resistance.
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.
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.
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 by[size=+3]inversion of selection?[/SIZE]
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
Sol, this article demonstrates exactly that combination selection pressures profoundly slow the evolution of resistance.
Why don’t you mention that the majority of the examples of aneuploidy are harmful.
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.
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.
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?
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...
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.
Kleinman said:You evolutionists do love you speculations and extrapolations.
Selfing ?
Self-pollination.