Annoying creationists

[kjkent1]

The mathematical data from Dr Schneider’s peer reviewed and published mathematical model gives important clues to how this process actually works. Once you identify that it is the number of selection conditions which cause his model to take huge number of generations to sort and optimize the selection conditions on anything other than a trivially small genome then it should be obvious why the empirical data show the same thing.

You evolutionists have taken for granted that just because you can shut off any other viewpoint in the field of biology that your theory must be correct. In fact, the mathematical and empirical behavior of the mutation and selection sorting/optimization process does not support the theory of evolution. Here are more empirical examples which show why the theory of evolution is mathematically impossible.

Blitheringly stupid logic, kleinman.

Does a selection pressure that favors webbed feet (swim faster) profoundly slow the selection of feathers (weight advantage)? Or do each of these traits provide advantages which would improve the probability of the successful fixation of the other.

Your theory is based on so many false premises: that all selection pressures are of equal intensity; that they all act against one another; that they are all toxically hostile before reproduction occurs; that they are all invariable.

You went to school to learn so much about science -- only to turn around and accept the absolute nonsense that is the Christian Bible on faith.

Blitheringly stupid -- nothing less.

 

[m_huber]

It's obvious here that Kleinman has stopped attempting to engage in actual debate/discussion. I can only assume that this is because he is incapable of actually defending his position.

I simply wonder how long Kleinman can continue to repeat his argument/quotes to various articles and statements before it is considered spamming/flooding.


It is useless for anyone to continue engaging in this thread.

I'm pretty close to being done here. Kleinman has made his point. He is not interested in discussion, but rather insists on insulting those of us that have answers to his argument. I would love him to come up with a real solution to the history of life that is different than evolution, but all indications are that this isn't going to happen. I would also love him to admit that he doesn't have answers (assuming that he doesn't), but this doesn't look very likely either. So he continues to say the exact same thing over and over again. I wonder why he does this.

 

[Mr. Scott]

So he continues to say the exact same thing over and over again. I wonder why he does this.

In his own words:

The first thing I did was discuss this directly with Dr Schneider and Paul Anagnostopoulos who is Dr Schneider’s java programmer for ev. Paul is the one who started this thread. I then asked Dr Schneider if he was willing to discuss this publicly because he had in the past but said no to my request, however Paul was willing to take up the banner. Dr Schneider had started a thread on the Evolutionisdead web site so I went ahead and started a discussion there. That went on for several months and there were a couple of evolutionists (including Paul) who were willing to debate this issue but they ran out of ideas on how to counter the data that was coming out of the model. Paul’s argument has gone from saying that ev simulates reality to it simulates a small portion of the rich evolutionary landscape. I also contacted the editors of Nucleic Acids Research who originally published Dr Schneider’s results based on unrealistic parameters in his model. I hoped to submit a letter to the editor. I told them that when realistic parameters are used in his model that it predicts that random point mutation and natural selection is too slow to account for macroevolution. They gave the usual evolutionist argument and said I was setting up a strawman, in addition they don’t take letters to the editor and to publish in their journal costs over $1000. So here we are James Randi educational forum.

 

[Nogbad]

The question of how the mutation and selection sorting/optimization process actually works is more than just of academic interest. It directly relates to many societal issues, not just in the field of medicine but agriculture, pest control and other fields as well.

The mathematical data from Dr Schneider’s peer reviewed and published mathematical model gives important clues to how this process actually works. Once you identify that it is the number of selection conditions which cause his model to take huge number of generations to sort and optimize the selection conditions on anything other than a trivially small genome then it should be obvious why the empirical data show the same thing.

You evolutionists have taken for granted that just because you can shut off any other viewpoint in the field of biology that your theory must be correct. In fact, the mathematical and empirical behavior of the mutation and selection sorting/optimization process does not support the theory of evolution. Here are more empirical examples which show why the theory of evolution is mathematically impossible.
http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt

http://www.ajtmh.org/cgi/reprint/71/2_suppl/187.pdf

http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010015

These examples illustrate how the mutation and selection sorting/optimization process works in reality. There are no imaginary selection pressures acting in parallel turning lizard populations into bird populations but there are real societal problems associated with the mutation and selection process and evolutionists have failed in describing how this process works.

When you discuss influenza, consider that Tamiflu, one of the most effective anti-influenza drugs available has already started selecting for resistant strains. When the next big influenza epidemic hits and the available anti-influenza drugs have been dissipated because they were used as monotherapies, who gets the credit for the millions of deaths? Will Time Magazine make someone else “Man of the Year” when he rediscovers again that combination therapy for influenza slow the evolution of resistance strains of the influenza virus?

The key determining factors in treatments applied, particularly in third world countries, are access to health care and economics. Drug resistent strains are stimulated when poor people stop taking their medication because they feel a bit better and wish to avoid further cost. This has sweet very little to do with biological theories reagrding the origins of species. Yes, I agree that the old adage "that which does not kill us makes us stronger" applies to bugs just as much as anything else and I seriously doubt any biologist regardless of stripe would disagree with this. Therapies that do not prevent the mutation and stengthen bugs are clearly not in our long term interest and what passes for health care in poor countries could impact on us all in the longer term and it is enlightened self interest to ensure that they can afford to implement therapies properly (mono or combo). However, these are economic, social and political issues and are not driven by some Darwinian misunderstanding of mutation.

So I beg to differ - I do not see the debate over evolution vs ID informing politicians as whether they should spend money or not.

 

[m_huber]

In his own words:

I see. Am I to understand, then, that all of this thread amounts to "real scientists wouldn't listen to me/I wouldn't listen to them, so I came here in hopes that I would have a more receptive audience"?

 

[Belz...]

It's obvious here that Kleinman has stopped attempting to engage in actual debate/discussion.

When did he actually start ?

 

[joobz]

When did he actually start ?

Well, true. But at least before, he pretended to answer you while lobbing insults and derisions. Now that he's been told that any future rule violation will result in his banning, he can't risk attacks. All his argument has ever been is illogical false premises mixed with insults. So to avoid making personal attacks, he posts the same illogical false premises addressed to the indistinct "evolutionists". It's a rather transparent ploy and simply exposes the shallowness of his argument and shows that his hibitual avoidance of arguments and reposting of the same claptrap is nothing more than forum flooding.

 

[kleinman]

Annoying Creationists

Let’s see, you evolutionists appear to have abandoned the ridiculous notion that n+1 selection conditions evolve more rapidly than n selection conditions for the mutation and selection sorting/optimization process. When did sorting/optimization accelerate when you make the sorting/optimization conditions more complex? This is utter illogical nonsense, but of course, that is the foundation for the theory of evolution. So now you claim that common descent occurs by parallel evolution. This little bit of illogical and irrational thinking is based on the extrapolation of the parallel use of monotherapy for the treatment of HIV. This blunder introduced resistant viruses in the gene pool and makes finding effective three drug combination therapy much more difficult to obtain. However this does not stop evolutionists from making the ridiculous extrapolation and speculation that a particular population of lizards evolved beaks, another population of lizards evolved feathers, and a third population of lizards evolved gizzards then all the populations got together to make birds. Of course your description of these processes is done with evolutionist precision.

You evolutionists really need to stick with your fossil Rorschach tests; you can claim anything you want. Forget the discussion about the mathematics of mutation and selection because that one sinks the Titanic theory of evolution. The mathematics and the empirical evidence completely contradict the theory of evolution. And what the mathematics shows is that combination selection pressures profoundly slow the mutation and selection sorting/optimization process. And the empirical evidence show the same thing. Here are some more examples.
The following two quotes are found at http://www.chemweb.com/journals?type=issue&jid=09298673&iid=14002

Possible Effects of Early Treatments of Hsp90 Inhibitors on Preventing the Evolution of Drug Resistance to Other Anti-Cancer Drugs by Li Xiao, Parsa Rasouli, Douglas Ruden (pp. 223-232).

Hsp90 is a chaperone that is critically important for both cancer progression and tumor survival. Hsp90 is an exciting target for anti-cancer drugs because most of the proteins that interact with Hsp90 are known to be in the cell cycle, signaling and chromatin-remodeling pathways. Recent work in fungi has shown that reduction of Hsp90 activity dramatically increases the efficacy of many fungicides. Furthermore, in studies on the evolution of drug resistance in fungi, it has been shown that high levels of Hsp90 increase the rate of the development of fungicide resistance, whereby low levels of Hsp90 decrease the rate of fungicide resistance. Similarly, in humans and mammalian models, Hsp90 inhibitors have been shown to act additively or synergistically with many other cancer therapies for killing both solid tumors and leukemias. Also, several recent studies have shown that Hsp90 inhibitors potentiate the activity of drugs in cancer cells lines that are otherwise resistant to the drug. However, during the evolution of drug resistance in cancer cells, it has not yet been determined whether early exposure to Hsp90 inhibitors slows the rate of developing resistance to other anti-cancer drugs, as would be expected from the fungal studies. In this review, we summarize the effects of the Hsp90 inhibitors geldanamycin and its derivatives with other anti-cancer drugs on killing cancer cells. We also discuss other basic science and clinical studies that need to be done to determine the optimum exposure regimens for Hsp90 inhibitor treatments to maximize its cancer-killing activities, and to minimize the evolution of resistance to other anti-cancer drugs.

Virostatics: A New Class of Anti-HIV Drugs by F. Lori, A. Foli, L.M. Kelly, J. Lisziewicz (pp. 233-241).

In this review we discuss the features of a new class of antiretroviral combinations, namely “Virostatics”. Virostatics are characterized by the combination of a drug directly inhibiting virus production (viro), and another drug indirectly inhibiting the virus by reducing cellular proliferation (static). In particular, we will focus on the combination of hydroxyurea and didanosine against HIV-1. Hydroxyurea and didanosine synergize to control viral replication and present with a favorable resistance profile, suppressing several resistant quasi-species. Because virostatics target essential cellular proteins, they exert an immune modulating activity and reduce viral targets (CD4 T cells), possibly with limited immunosuppressive effects. Importantly, a dose-finding clinical study has shown that decreasing the dose of hydroxyurea not only diminishes toxicity but also increases antiviral potency. Therefore, the combination of hydroxyurea and didanosine strikes a balance between viral suppression, drug-related toxicity and viral escape, and could have a role both in induction and maintenance therapy. In this review we would like to appraise what is known about hydroxyurea and didanosine and specifically address the major advantages, i.e. novel mechanism of action leading to a new class of drugs and resistance profile providing durability, as well as the major criticisms of this combination, i.e. toxicity and reasons for prescribing a perceived immune suppressant to immune compromised patients.

http://www6.lexisnexis.com/publisher/EndUser?Action=UserDisplayFullDocument&orgId=1809&topicId=26923&docId=l:623811163&start=23

To avoid the selection of these genetic variants by exposure to the drug during therapy, it is vital that a combination of different TB drugs is administered together since the odds of a single bacterium simultaneously carrying mutations that are able to confer resistance to two or more drugs are extremely slim (much less than one in a trillion).

So the basic science and mathematics of the mutation and selection sorting/optimization process show that combination selection conditions profoundly slow evolution and in addition, selection pressures reduce genetic diversity in populations.

Now if you evolutionists want to believe that beaks evolved in one lizard population and feathers evolved on another lizard population and that gizzards evolved on a third lizard population, could you give us a concise description how this occurred?

 

[Shalamar]

So Mr. Kleinman. Still saying that the sciences of Biology, Geology, and Astronomy are all wrong? Why not publish your findings. If they are all indeed true, and you have all this math, and evidence, you'd be able to set Science on its ear.

Oh? You mean you're just making it all up as you go? You have no evidence? Ok then.

Oh. Hey! Kleinman posted yet more lies!

However this does not stop evolutionists from making the ridiculous extrapolation and speculation that a particular population of lizards evolved beaks, another population of lizards evolved feathers, and a third population of lizards evolved gizzards then all the populations got together to make birds. Of course your description of these processes is done with evolutionist precision.

Nope. No scientists or biologist have ever said these things. Please stop lying, Mr. Kleinman.

 

[kleinman]

Annoying Creationists

Evolutionist claim that evolution occurs in parallel, which it can as seen with the use of monotherapy on different populations of HIV; this in turn accelerated the evolution of resistant strains of viruses in the gene pool. Now evolutionists assert that parallel evolution is how common descent has occurred. When are you evolutionists ever going to give us a concise description how this occurred? Perhaps you evolutionists can fool naïve laymen with your mush of mythology but the mathematical and empirical evidence is clear, the mutation and selection sorting/optimization process only works for extremely simple sorting conditions and the process is confounded when multiple selection conditions are applied to a population. Here are more examples of how mutation and selection works.
http://doctor.medscape.com/viewarticle/420664

Dr. Daniel Kuritzkes of the University of Colorado began his plenary presentation[1] by commenting on the incremental benefits we have seen over the evolution of antiretroviral therapy, from modest survival improvements with monotherapy to the current era of combination therapy. Success is now measured by the proportions of patients achieving plasma viral load suppression and by the number of years to viral rebound. This has been accompanied by dramatic falls in the number of clinical events amongst people with established HIV infection and declines in vertical transmission. However, these advances have not been without costs in terms of toxicity, regimen complexity, resistance, quality of life, and financial burdens on society. Clearly, there is still a need for new drugs to help manage these problems. Many questions remain, including when to start, what to start, the role of resistance testing, definitions of drug failure, and the management of metabolic and fat redistribution problems. As many of these subjects have been addressed during the conference, Dr Kuritzkes chose to discuss three other issues: viral reservoirs, treatment interruptions, and discordant CD4+/viral load responses.

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. Traditional analysis of drug combination effects on cells is based on a number of assumptions and idealizations. A more rational mechanistic modeling approach may accelerate the search for effective drug combinations that are tailored to individual responses. The chemotherapeutic drugs, carmustine and etoposide, each nominally induces G2 phase arrest and, secondarily, apoptosis. Despite this similarity in mechanism, we found that the pharmacodynamic responses to these agents is dramatically different on human glioma cell lines. We have developed a cell cycle structured model of chemotherapeutic activity based on the dynamic transitions of cells along the phases of the cell cycle. We show that our mathematical model is able to explain the shapes of the dose response curves of multiple cell lines to these agents. We are able to predict with the model the effects of drug combinations, taking into account variable dose and timing regimens, to determine the most effective strategy. Using this model, we are able to explain several non-intuitive experimental observations involving combinations of chemotherapeutic drugs on glioma-derived cell lines.

The mathematics and empirical evidence of the mutation and selection sorting/optimization process is clear, combination selection pressures profoundly slow the process and common descent is a mathematical impossibility. Perhaps naïve laymen believe otherwise but the mathematical and empirical evidence is clear, the theory of evolution is mathematically impossible.

 

[Shalamar]

*yawn*

Have anything new? Or are you going to continue to lie, and ignore questions poisted by people?

Still no math? Then you have nothing.

This is proof, however, that a person can be poorly educated, and still be a Doctor. Or, at least, claim to be one. No doctor could be this stupid.

 

[kleinman]

Annoying Creationists

For those evolutionists who are having difficulty understanding the mathematics of the mutation and selection sorting/optimization process, read this citation again.
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. Traditional analysis of drug combination effects on cells is based on a number of assumptions and idealizations. A more rational mechanistic modeling approach may accelerate the search for effective drug combinations that are tailored to individual responses. The chemotherapeutic drugs, carmustine and etoposide, each nominally induces G2 phase arrest and, secondarily, apoptosis. Despite this similarity in mechanism, we found that the pharmacodynamic responses to these agents is dramatically different on human glioma cell lines. We have developed a cell cycle structured model of chemotherapeutic activity based on the dynamic transitions of cells along the phases of the cell cycle. We show that our mathematical model is able to explain the shapes of the dose response curves of multiple cell lines to these agents. We are able to predict with the model the effects of drug combinations, taking into account variable dose and timing regimens, to determine the most effective strategy. Using this model, we are able to explain several non-intuitive experimental observations involving combinations of chemotherapeutic drugs on glioma-derived cell lines.

The reason why Dr Schneider constructed his mathematical model and the scientists at Rutgers constructed their mathematical model is to help explain non-intuitive experimental observation. Mathematical models like these enforce rigorous relationships between variables in order to examine the behavior under a variety of different conditions. For example, evolutionists believe and teach that the mutation and selection sorting/optimization process transforms entire genomes such as lizards populations turn into bird populations. This is a mathematically and empirically irrational misconception. This misconception may fit their belief system but it does not fit the mathematical and empirical evidence. The concept of common descent is mathematically and empirically irrational. The mutation and selection sorting/optimization process is confounded when you have more than a very simple set of selection conditions.

The failure of evolutionists to properly describe the basic science and mathematics of the mutation and selection sorting/optimization process contributes to the premature death of millions of people suffering from diseases subject to mutation and selection. The theory of evolution is not only wrong, it is harmful to people.

 

[m_huber]

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.

Do you have a model that is based on an organism that is genetically stable?

Note again (if you are, in fact, interested in reading anything I write) that the purpose of chemotherapy is to kill the tumor. This is different from a natural system, as there is no underlying maniacal purpose in normal planetary processes. Floods/earthquakes/fires/volcanoes can kill organisms, but they are relatively rare events, they do not have intention to kill organisms, and they can often be avoided. So, you probably need a different mathematical model. If you have one that applies to a real ecological system, I would be interested in seeing it.

 

[kleinman]

Annoying Creationists

You evolutionists are very confused about how the mutation and selection sorting/optimization process actually works. Genetic instability and then selection (sorting/optimization) is the basis of the process. If genes were completely stable, there would be no mutation and selection process. You evolutionists have failed to give a proper description of the basic science and mathematics of the process. You have assumed, speculated and grossly extrapolated how the process actually works. Now Dr Schneider’s computer simulation shows that extremely high mutation rates actually slow the rate of information acquisition while at the other extreme, extremely low mutation rates also slow the rate of information acquisition for the mutation and selection sorting/optimization process. Too high a mutation rate scrambles genomes and is incompatible with life, a zero mutation rate gives no mutation and selection sorting/optimization process.

And once again, evolutionists fail to recognize that selection pressures impair the fitness of a population to reproduce. This can occur by killing off members of a population or by impairing the ability of members of the population to reproduce as is done with antiviral therapy. Strong selection pressures which impair the reproduction of many members of a population require that the remaining population evolve rapidly to these strong selection pressures or otherwise the population goes extinct. On the other hand, weak selection pressures have little effect on the frequency of particular sequences of bases and cause little if any evolutionary change per generation.

The single strong selection pressures that are used with antimicrobial and cancer therapies give the most rapid examples of the mutation and selection sorting/optimization process and the most rapid transformation of particular genes. However when two or more strong selection pressures are applied to a population, you don’t get more rapid evolution, the mutation and selection sorting/optimization process is profoundly slowed. That is the empirical basis for combination therapy to stop the evolutionary process and this empirical strategy is confirmed by Dr Schneider’s mathematical model of random point mutations and natural selection.

Here are more empirical examples which demonstrate what Dr Schneider’s mathematical model shows, that is combination selection conditions profoundly slow evolution by the mutation and selection sorting/optimization process.
http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010039

Drug combinations have the potential to protect the two partner drugs against selection of resistant strains, thus delaying the emergence of drug-resistant organisms. Combinations may allow dosage reduction of each drug in the combination, reduce the overall toxicity while maintaining good efficacy. Combinations may also allow for a simpler administration, improving the feasibility of treatment in Africa's isolated health facilities, most of which have logistic and staffing limitations.

http://pubs.ama-assn.org/media/2007j/0403.dtl

“The report by Hatakeyama et al raises more questions than it answers, including questions about viral evolution, biological fitness, and transmissibility. But some facts are strikingly clear. Influenza B mutants with reduced sensitivity to neuraminidase inhibitors are circulating, and these viruses can cause infections with no difference in duration of symptoms, level of viral shedding, or clinical outcome. Contrary to what had been hoped until now, some resistant variants are vigorous pathogens. Whether these viruses arise by spontaneous mutation or through drug selection, or whether they are transmitted within families or acquired from the community, the resistant variants may be here to stay. In light of the recent observation that oseltamivir may be less effective against influenza B than against influenza A, an important concern is whether suboptimal dosing for these viruses will lead to increased selection of viruses with high-level resistance.”

“Influenza viruses evolve rapidly and nimbly, which compels ongoing investigation of antiviral therapies that use alternative mechanisms of action and target different points in the viral life cycle. The emergence of drug-resistant influenza B should draw attention to the importance of continual monitoring of strains over time and to the need for frequent rethinking of policies for use of antiviral drugs. While the news about resistance is not good and certainly calls into question some of the current assumptions about drug-resistant viruses, an effective response to this news can help contend with the new challenges of influenza.”

http://mct.aacrjournals.org/cgi/content/abstract/6/2/655

Chronic myelogenous leukemia is caused by the Bcr-Abl hybrid gene that encodes the p210Bcr-Abl chimeric oncoprotein. Although it reduces the total body burden of leukemia cells, the use of imatinib mesylate as a single agent may be accompanied by the evolution of resistance due mainly to the acquisition of point mutations. Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have reduced but not completely eliminated the rate at which point mutations are acquired in the p210Bcr-Abl kinase. Thus, it is important to identify additional new inhibitors of the p210Bcr-Abl kinase. One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action. To identify such a new class of inhibitors that could suppress the growth of chronic myelogenous leukemia cells and prevent the evolution of cells that are resistant to imatinib, we screened two low-complexity libraries of compounds based on planar and linear scaffolds. These libraries were screened using a cell-based assay for molecules that suppress p210Bcr-Abl–dependent cell growth. The application of this method resulted in the isolation of two new classes of drugs, both of which inhibited imatinib-resistant cells in the low micromolar range. Some of these drugs were potent inhibitors not only of Abl tyrosine kinase but also of the Src, Lyn, and Fyn tyrosine kinases. [Mol Cancer Ther 2007;6(2):655–66]

 

[Belz...]

Rinse. Repeat.

 

[articulett]

The more you repeat it, the more true it becomes (in your head.)

Ah, the power of affirmation! You, too, can believe anything if only you repeat that you believe it enough. Praise "belief"! --The key to eternal salvation (and impenetrable) thought processes.)

 

[kleinman]

Annoying Creationists

Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
Lizards evolve into birds
.
.
.
Nope, I tried repeating it and it doesn’t make it true. Let’s try this one.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
.
.
.
Hey, wait a minute, that one might be working. Let’s try it again.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Beggaminases is how evolution works.
Yeah, that one works.

Well, we just have to content ourselves with the mathematical and empirical evidence which shows how the mutation and selection sorting/optimization process actually works. Dr Schneider’s mathematical model very nicely shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process, let see if we can find some more empirical examples which demonstrate the same thing.
http://www.fghp.org/monitor/pdf/HTM070416.pdf

“The rapid evolution of bacterial drug resistance and the alarming slowdown in development of new antibiotics is spurring attention towards multidrug treatments, ”say Remy Chait and colleagues of Harvard Medical School in an article published in Nature this week. But mixing drugs can have odd effects: the combinations can be synergistic, additive, or antagonistic. In certain ‘hyper-antagonistic’ cases, the mixture can prove even less effective than either drug alone; this is called suppression. In general, resistance to one of the drugs in a combination gives the resistant bacteria an advantage, so they outgrow those that are sensitive to the drug. But, Chait et al. theorised that in suppressive cases, resistance to one of the drugs might actually be a disadvantage to bacteria. Although resistance would diminish the effects of one of the medicines, it might also remove the suppression, making the drug combination more effective against resistant bacteria than sensitive ones.

http://cohesion.rice.edu/Engineering/bioe/emplibrary/Physics_Today_Jan07.pdf

At the molecular level, what are the likely escape mutants that lead to new viral strains or new antibiotic-resistant bacteria? To be specific, I’ll consider viruses. The immune system recognizes regions of viral proteins, and it develops the ability to clear the virus from the body based on that recognition. If not completely eradicated from the human(and possibly animal) population, the surviving virus will tend to accumulate mutations in the region of the genetic sequence that codes for those recognizable protein pieces and thus avoid immune recognition. Predicting which mutations are likely in the surviving virus could allow vaccination against potential future strains—the escape mutants—and more effective control of the virus in the population. Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.

http://www.haematologica.org/eha10/edu/pdf/08.2.pdf

Thus, if a cell-based approach is used, known resistance mechanisms can be studied in detail and novel mechanisms of resistance can be identified for different targets using investigational compounds and clinically used drugs. This or similar screening approaches will provide data that can be translated into combination and sequential treatment strategies for a variety of rational drug targets in hematology and oncology. Specific patterns of resistance mutations can be predicted prior to their identification in patients, and critical serum concentrations can be defined that must be achieved in the clinic in order to minimize the emergence of resistance.

http://www.annalsnyas.org/cgi/content/abstract/918/1/9?ck=nck

Large-cohort studies in North America, Europe, and Thailand have shown that zidovudine/azidothymidine (AZT) monotherapy, given at the late stages of pregnancy, is of proven benefit in reducing mother-to-infant HIV transmission by 51% to 68%. AZT monotherapy will not be of long-term benefit for mothers because no single drug can counteract viral infection; benefits to babies will be short-lived if HIV-1 is acquired through breastfeeding after birth. Unfortunately, ongoing mutation of HIV under conditions of drug pressure allows for the evolution and selection of AZT-resistant viruses. Emergence of AZT-resistant variants in pregnant mothers (7-29%) and their infected offspring (5-21%) has been described in several studies. Drug resistance arises more frequently in those mothers who received AZT therapy before pregnancy. Recent advances in combination chemotherapy may provide alternative strategies in prevention of vertical transmission and drug resistance.Genotypic screening of the HIV-1 isolated from pregnant mothers may provide rational modifications in antiretroviral (ARV) strategies to circumvent vertical HIV transmission. This may be of advantage for resource-rich nations but not for underdeveloped nations with limited access to ARVs. Public health programs are vital to have an impact on the tragic pandemic of pediatric AIDS.

http://www.thebody.com/content/art39095.html

This year's Resistance Workshop featured three oral presentations on the activity and mechanisms of drug resistance associated with anti-HCV polymerase inhibitors. Investigators from Merck & Co. presented an important proof of concept study, which showed that two chimpanzees receiving the novel nucleoside polymerase inhibitor MK-0608 had 2- to 3-log reductions in virus levels after a single intravenous dose, and up to a 5-log reduction after seven days of therapy [Abstract 5].24 Whether or not this compound will be found to be useful for treating human HCV infection will not be known for a few years. Several days following the discontinuation of MK-0608, investigators detected a mixture of wild-type and mutant virus at a position in the enzyme associated with HCV resistance. Nonetheless, this study suggests that we may soon be seeing more potent polymerase inhibitors with activity rivaling that of the HCV protease inhibitors.

Isabel Najera (Roche Pharmaceuticals) and Akhter Molla (Abbott Laboratories) [Abstracts 3 and 4, respectively]25,26 each described data on the in vitro activity and in vitro selection of mutations associated with resistance to nonnucleoside polymerase activity. Najera described the activity of two nonnucleoside polymerase inhibitors -- one that binds to the polymerase thumb region and the other to the palm region. During in vitro passage with each drug alone, mutations developed in the region of the molecule that was targeted by the inhibitor, as well as secondary mutations for the palm site inhibitor. During in vitro passage with both inhibitors, both thumb and palm site mutations emerged allowing the virus to develop resistance to both drugs. Molla described a new highly active polymerase inhibitor to which virus resistance developed rapidly during in vitro passage but which was highly synergistic when used in combination with interferon (IFN).

Taken together, these and previous studies of new small molecule inhibitors of HCV suggest that although some inhibitors will be highly potent, most will have a low genetic barrier to resistance. If these drugs are used as monotherapy agents, the rapid development of resistance appears to be inevitable. This resistance may be more rapid than that observed for HIV-1, as it is estimated that HCV is replicating at a level that is 2 to 3 logs higher than HIV-1 (i.e., the production of about 1 trillion virions per day), and because it appears that even within tissue culture there may be more heterogeneous genotypes than observed with HIV-1.

So there it is, more empirical citations which substantiates what Dr Schneider’s peer reviewed and published computer simulation of random point mutations and natural selection shows. And what his model shows is that the more complex selection conditions are, the much, much, much slower the mutation and selection sorting/optimization process proceeds, even when you have 1 trillion virions produced per day. Now you evolutionists chant the following:
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
The theory of evolution doesn’t need a mathematical basis
.
.
.
And I’ll be back next week to chant:
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
The theory of evolution is mathematically and empirically impossible.
.
.
.
So you all have a good weekend until then.

 

[tsig]

Evolutionists seem to think that I don’t understand their reasoning. This is not the case. I have studied biology for decades and listened to evolutionist lectures and arguments many, many times. The evolutionist hypothesis is actually quite simple. The evolutionist hypothesis states that life started with some simple forms billions of years ago and by the process of mutation and selection transformed these initial simple life forms into the myriad of complex life forms that we see today.

Rather than investigating the basic science and mathematics of the mutation and selection sorting/optimization process; evolutionists have developed an industry around the interpretation of the fossil record and the so called mapping of genetic similarities between different species and then calling it evidence for their theory. The real question is whether mutation and selection can accumulate the massive amount of information contained in even the simplest life forms.

It is clear from Dr Schneider’s mathematical model of random point mutations and natural selection that the answer is no. The next question is whether Dr Schneider’s model is a valid simulation of the mutation and selection process. Dr Schneider says yes, the peer reviewers at Nucleic Acids Research say yes and I say yes. Are there real examples of what Dr Schneider’s model demonstrates? The answer to that question is yes! There are hundreds of real examples of what Dr Schneider’s model demonstrates and it shows exactly how the mutation and selection sorting/optimization process actually works. What Dr Schneider’s model shows is that the mutation and selection sorting/optimization process is very strongly dependent on the complexity of the selection conditions. Simple single selection conditions evolve very quickly while complex multiple selection conditions evolve much, much more slowly. So what does this do to the theory of evolution; life started with some simple forms billions of years ago and by the process of mutation and selection transformed these initial simple life forms into the myriad of complex life forms that we see today? The answer to this question is that the evolutionist hypothesis is wrong. The mutation and selection process is far too slow and the selection conditions don’t exist to evolve genes de novo or to do the radical transformations required to turn amoebas into humans or even lizards into birds.

The failure of evolutionists to properly elucidate the basic science and mathematics of the mutation and selection sorting/optimization process has harmed society. It delayed the treatment of HIV with combination therapy for years; the improper use of antimicrobial monotherapy has led to MRSA, Gonorrhea super bugs and many other multi-drug resistant pathogens. It is this failure on the part of evolutionists to explain the basic science and mathematics of the mutation and selection sorting/optimization process that contributes to the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. This includes stepfathers who die from cancer.

Accusing members of this forum of contributing to the deaths of millions is getting tiring.

 

[coops]

Well, true. But at least before, he pretended to answer you while lobbing insults and derisions. Now that he's been told that any future rule violation will result in his banning, he can't risk attacks. All his argument has ever been is illogical false premises mixed with insults. So to avoid making personal attacks, he posts the same illogical false premises addressed to the indistinct "evolutionists". It's a rather transparent ploy and simply exposes the shallowness of his argument and shows that his hibitual avoidance of arguments and reposting of the same claptrap is nothing more than forum flooding.

So true.

I have to wonder what Kleinman feels he is accomplishing in this thread. By refusing to answer direct questions and engage in any meaningful 2-way discussion he is merely talking to himself in front of an audience.

The chances of anybody reading this thread and agreeing with Kleinman's position is as good as zero due to his childish behaviour.

I guess now the thread has turned into a game of patience. Kleinman is hoping that he can post longer than everyone else so that he can have the last word, and hence 'win' the debate. Thats the only reason I can think of for Kleinman's current behaviour.

 

[godless dave]

You evolutionists are very confused about how the mutation and selection sorting/optimization process actually works. Genetic instability and then selection (sorting/optimization) is the basis of the process. If genes were completely stable, there would be no mutation and selection process. You evolutionists have failed to give a proper description of the basic science and mathematics of the process. You have assumed, speculated and grossly extrapolated how the process actually works. Now Dr Schneider’s computer simulation shows that extremely high mutation rates actually slow the rate of information acquisition while at the other extreme, extremely low mutation rates also slow the rate of information acquisition for the mutation and selection sorting/optimization process. Too high a mutation rate scrambles genomes and is incompatible with life, a zero mutation rate gives no mutation and selection sorting/optimization process.

So what?

You're doing one of my favorite creationist tactics: repeat some basic fact about biology, but frame it as a problem for evolution that stumps the experts.

Yes, an extremely high mutation rate or an extremely low mutation rate can cause extinction. I believe this observation can be found in most introductory biology textbooks.

So what?