Annoying creationists

[Mr. Scott]

Oh wait, you evolutionists claim that evolution occurs in parallel. One lizard population is evolving beaks, another lizard population is evolving feathers and a third lizard population is evolving gizzards and then all these populations get together to make a bird. Those lizards are an intelligent lot.

So, you've never heard of hybrid vigor?

 

[Belz...]

It appears you evolutionists still haven’t figured out how the mutation and selection sorting/optimization process works either mathematically or empirically.

Well, one thing's for sure, Klein. YOU don't evolve.

 

[Belz...]

When was the last time an evolutionist made a concise statement?

Evolution works. There.

fossil Rorschach tests

 

[kleinman]

Annoying Creationists

Well, well, well, the author of the concisely described concepts of cooperative chemistry for abiogenesis and variations in weather give blizzards which transform lizards into buzzards with gizzards is going to give us a concise description of the de novo evolution of the 20,000 or so genes in humans and the 20,000 different selection pressures that 20,000 different populations were in parallel evolving these 20,000 genes. Then he is going to give us a concise description of the parallel transfer of these genes that assembled themselves spontaneously to make humans. You evolutionists don’t understand the basic science and mathematics of the mutation and selection sorting/optimization process yet you make these irrational and illogical speculations.

Now, we have an evolutionist who is starting to post his fossil Rorschach test. He takes a couple of images and speculates from these images that everything evolved. Well how did everything evolve? There are two basic mechanisms for things to evolve. You have recombination and selection and mutation and selection.

Recombination and selection can give large morphological changes to a population. We see this effect with dog breeding. In a few thousand years, wild dogs have been selectively bred and you see such great variations such as Chihuahuas to Great Danes. There are tremendous variations in dogs but genetically they are all homologous despite these huge morphological differences. You see the same thing with horses. Selective breeding can give miniature horses the size of a large dog or Belgian draft horses but they retain genetic homology. Recombination and selection can not create new species but you can get very rapid changes to the morphology of a population.

Then we have mutation and selection. What can mutation and selection do? Mutation and selection can not create a gene de novo. There is no selection for something that does not exist. What mutations do is give variants of existing genes. If these variants give some fitness benefit, then these variants are passed to the next generation. What selection does is eliminate variants which do not have sufficient fitness to pass their phenotype to the next generation. Selection reduces the diversity of a population. So how does this process work mathematically and empirically?

Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection demonstrates several important principles of this phenomenon. First, it is clear from Dr Schneider’s model that more complex selection conditions are the much, much, much slower the sorting/optimization process is. Second, it is clear from Dr Schneider’s model that increasing the genome length increases the search space for the mutation and selection sorting/optimization process and have a profound slowing on his sorting/optimization algorithm (that is it takes many more generations to satisfy the selection conditions). Third, it is clear from Dr Schneider’s model that increasing population increases the sorting/optimization rate but with decreasing effectiveness with increasing population. The effect of increasing population is clearly less than linear on the rate of sorting/optimization in his algorithm.

So let’s give some more empirical examples which demonstrate the principle mathematical behavior of Dr Schneider’s model which is the more complex the selection conditions, the much, much slower the mutation and selection sorting/optimization process becomes.
http://www.malariaconsortium.org/data/files/pages/act_6.pdf

Antifolate drug resistance (i. e. pyrimethamine means that new combinations are urgently needed particularly because addition of a single drug to an already failing regimen is rarely effective for very long.

http://jama.ama-assn.org/cgi/content/abstract/286/2/196

Based on the samples that could be amplified, low-level viremia in children and adults receiving HAART with prolonged suppression of viremia to less than 50 copies/mL of HIV-1 RNA may result primarily from archival, pre-HAART virus, reflecting earlier treatment conditions, and does not appear to require development of new, HAART-selected mutations reflecting partial resistance to therapy. Low-level viremia below 50 copies/mL may represent less of a concern regarding impending drug failure of current HAART regimens. However, the archival drug-resistant virus may be relevant regarding future treatment strategies.

http://jvi.asm.org/cgi/content/abstract/74/19/9328

We studied the combined anti-human immunodeficiency virus type 1 (HIV-1) effects of a derivative of stroma-derived factor 1

(SDF-1), Met-SDF-1, and a modified form of RANTES, aminooxypentane (AOP)-RANTES. The antiviral agents were tested singly or in combination at 95 and 99% virus inhibitory concentrations. Clinical R5 and X4 HIV-1 isolates were used. AOP-RANTES inhibited R5 but not X4 viruses, whereas Met-SDF-1had the opposite effect. Combinations of these compounds inhibited mixed infections with R5 and X4 viruses (95 to 99%), whereas single drugs were less inhibitory (32 to 61%). Combinations of R5 and X4 inhibitors are promising and deserve further evaluation.

So when you evolutionist post your fossil Rorschach tests and claim these show that blizzards transform lizards into buzzards with gizzards, remember this, evolutionbymutationandselectiondidn’tdoit. The mutation and selection sorting/optimization process simply does not work the way you evolutionists allege and teaching naïve school children your mathematically and empirically irrational concepts contributes to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection phenomenon.

 

[Belz...]

While (1 == 1)
Execute "RandomPostString.exe"
End

 

[Mr. Scott]

Dr. Kleinman, why do you believe the time it takes for a computer program to sort one generation of genomes in Ev corresponds with the time it takes nature to "sort" genomes in a generation by natural selection?

Did you lie about your computer science credentials?

 

[kleinman]

Annoying Creationists

You evolutionists really have a problem with this concept of generations versus cpu time to converge a mutation and selection sorting algorithm. Perhaps if you see how Dr Schneider puts it for his own algorithm.
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!

It is the number of generations necessary to sort and optimize that is the important dependent variable in the mutation and selection sorting/optimization process. You can correlate cpu time with the generations for convergence with the clock rate as your proportionality constant. And as you can see, nature has neither a fast enough clock rate nor the selection conditions to accomplish common descent. Of course, you can teach naïve school children that nature does have these properties but then you would be contributing to the premature death of millions of people suffering from diseases subject to the principles of the mutation and selection phenomenon.

 

[m_huber]

Now, we have an evolutionist who is starting to post his fossil Rorschach test. He takes a couple of images and speculates from these images that everything evolved. Well how did everything evolve? There are two basic mechanisms for things to evolve. You have recombination and selection and mutation and selection.

Read it again. I did not speculate from those images that everything evolved. I posted the reasoning behind why we can go from fossils to evolution. I understand that you have a lot to do, just as all of us do, but please do me the courtesy of actually reading my post instead of just looking at the pictures and claiming that my argument is bogus.

To go back to the high points, however, the mechanism doesn't matter. We do not understand why things fall. We can observe it, test it, and quantify it. It does not matter if a graviton particle actually exists. We interpret the mechanisms from the observations. The interpretations may be wrong, but the observations are not.

Fossils qualify as observations. Many are absolutely identical in form to modern animals, so it is safe to say that they represent once-living creatures. Most of the morphologies that we have from fossils have no living analogue. Therefore, most morphologies that have existed have gone extinct. Since the earth is not capable of supporting all of the species that have been observed from the fossil and modern record at the same time, they must have lived at different times; therefore, there must have been periods when new organisms appeared on the planet. Since fossil records are continuous through strata, we can determine that life has been continuously on this planet, and was not re-seeded at different points in history. Therefore, existing species must have somehow been altered to form new species through some mechanism. We call this process "evolution."

 

[Mr. Scott]

Dr. Kleinman Please Answer My Question

You can correlate cpu time with the generations for convergence with the clock rate as your proportionality constant. And as you can see, nature has neither a fast enough clock rate nor the selection conditions to accomplish common descent.

Did you lie about your computer science credentials?

 

[cyborg]

Did you lie about your computer science credentials?

I am reminded of the time Dr Adequate posted a Pascal program and then kleinman complained it wouldn't run: a constant was not defined - even though Dr A specifically told him he had to define a constant for it to do so.

 

[kleinman]

Annoying Creationists

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.

 

[rocketdodger]

Did you lie about your computer science credentials?

I don't recall him posting any CS credentials at all.

Certainly the fact that he is unable to comprehend even the basic idea of "parallel," which most children find easy to grasp, speaks volumes about both his education and mental capability.

 

[kleinman]

Annoying Creationists

Evolutionists make all kinds of claims such as n+1 selection pressures evolve more rapidly than n selection pressures and now the latest claim is that somehow that species evolve in parallel. Now it is true that if you subject one population to a single selection pressure and that population evolves to that selection pressure and then subject another population to a different single selection and that second population evolves to that different selection pressure and then mix the two populations, you will have population gene pool which has made the adaptation to those two selection pressures. This is precisely the blunder that was made when HIV treatment was initiated and monotherapy was used. It introduced large numbers of resistant viruses into the gene pool. In fact here is a citation which shows this happens with Malaria.
http://asmcourse.ivic.ve/articulos/Hastings-2004.pdf

The main consequence is that anti-malarial drug policy must be considered on an inter-national, rather than a national, basis. A sophisticated and expensive national policy designed to suppress the emergence and spread of resistance can be easily negated by mutations originating and spreading from neighbouring countries. This does not necessarily mean that all countries in a region should have the same policy, simply that their policies should not undermine each other. For example, suppose a country deploys drug A and drug B as a CT. A neighbouring country deploying drug C as a monotherapy would not undermine this policy (providing the mechanism of resistance to C is independent to that of A or B), but a neighbouring country deploying either drug A or B as a monotherapy is likely to pose a significant threat.

Now evolutionists want to make the irrational and illogical extrapolation that this is how common descent works. Now one population of lizards is subjected to a particular targeted selection pressure and these lizards evolve beaks. Then another lizard population is subjected to a different targeted selection pressure and this population evolves feathers and then a third lizard population is subjected to yet another targeted selection pressure and it evolves gizzards. Then all these populations gather together, share their genes and make birds.

It is this kind of evolutionist nonsense that contributes to the premature death of millions of people suffering from diseases subject to the principles of the mutation and selection phenomenon.

 

[m_huber]

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.

Dr. Kleinman, this is the most coherent thing I have seen you post in a long time. Kind of makes me glad. It does get frustrating when you repeat the exact same thing for pages on end.

Anyway, to get back to the discussion:
As a point of history, the principle of faunal succession was established well before the Origin of Species was published. Fossils were being interpreted to represent former life before anyone had any idea of how old the earth was and before anyone had any real notion of evolution. As it stands now, evolution explains the fossil record quite well. If you are proposing that evolution does not exist, then you need to also propose some alternative that would also explain the fossil record. Otherwise, there is no reason to abandon the theory. At best, one could say "Evolution doesn't work mathematically, but it does explain all of the data." For that reason, it would continue to be taught and used in scientific circles.

There is no conspiracy of evolution. As I have said elsewhere in this forum, I was raised as a Young Earth Creationist. I went to college to become a geologist because I wanted to prove that evolution was not true. (Please don't assume that I am trying to pad my personal history. My second career choice would have been preacher.) What I found was a robust theory that deals quite effectively with tangible, physical evidence. I accept that evolution is true because I see a valid argument for its existence. I have not seen valid evidence for any other theory that would explain where species came from.

I'm not sure if you realize this or not, but the marketing of evolution is not an incredibly profitable venture. There is no industry of evolution; nobody stands to gain from it.

The general thrust of your argument appears to be similar to the "Evolution can't add information to the genome" argument, which has been thoroughly dealt with in numerous places.

I also fail to see how acceptance of evolution has caused any harm to society. If anyone had recognized a better way to cure HIV, I am quite confident that they would have done so, if for no other reason than the money they would make from it (not to mention the humanitarian benefit). Your arguments seem to hinge on the idea that, if evolutionary theory were no taught, science would advance faster. In fact, the reason we know the cause of the problems is because of long-term experimentation, which would have happened in the presence of the disease evolutionary theory or no. Doctors tried what they knew before, then found it didn't work, then figured out why, then figured out what to do about it. Because of this, you think that evolution is harmful? It seems to be a non-sequitur...

 

[kleinman]

Annoying Creationists

The failure of evolutionists to properly elucidate the basic science and mathematics of the mutation and selection sorting/optimization process certainly has hurt people who suffer from diseases subject to the mutation and selection phenomenon. In 1958 Nobel Prize winner Edward Tatum properly described the dominant property of the mutation and selection sorting/optimization process.
http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html

In microbiology the roles of mutation and selection in evolution are coming to be better understood through the use of bacterial cultures of mutant strains. In more immediately practical ways, mutation has proven of primary importance in the improvement of yields of important antibiotics - such as in the classic example of penicillin, the yield of which has gone up from around 40 units per ml of culture shortly after its discovery by Fleming to approximately 4,000, as the result of a long series of successive experimentally produced mutational steps. On the other side of the coin, the mutational origin of antibiotic-resistant micro-organisms is of definite medical significance. The therapeutic use of massive doses of antibiotics to reduce the numbers of bacteria which by mutation could develop resistance, is a direct consequence of the application of genetic concepts. Similarly, so is the increasing use of combined antibiotic therapy, resistance to both of which would require the simultaneous mutation of two independent characters.

As an important example of the application of these same concepts of microbial genetics to mammalian cells, we may cite the probable mutational origin of resistance to chemotherapeutic agents in leukemic cells 44, and the increasing and effective simultaneous use of two or more chemotherapeutic agents in the treatment of this disease.

If this concept was a regular part of the instruction on how the mutation and selection sorting/optimization process actually works, it would not have taken scientists and physician years to figure out that combination therapy was required for the treatment of HIV.
http://www.pbs.org/wgbh/pages/frontline/aids/interviews/ho.html

In 1994, Dr. David Ho discovered that what was then thought of as a latency phase -- when a person was infected with HIV but not experiencing any symptoms -- was in fact a period of continuous onslaught, in which the virus and the immune system are engaged in a pitched battle. Once he was able to measure the amount of virus in the blood, he learned that in fact billions of HIV particles were being produced every day. This breakthrough allowed Ho and his collaborators to come up with the idea for combination therapy -- treating a person with several drugs at once to suppress the virus down to undetectable levels. Patients near death rebounded dramatically after beginning what was called "triple cocktail" therapy, and Ho was named Time magazine's "Man of the Year" in 1996 for his work. In this wide-ranging interview, Ho recounts his breakthrough discoveries and his battles against the virus over the years. He also talks about the implications of combination therapy on the future of the epidemic and the importance of prevention efforts. "We have to bear in mind that during the years where this concerted treatment effort took place, approximately 2 million were treated. But during those years, another 15 million or so got newly infected." Currently Ho is executive director of the Aaron Diamond AIDS Research Center, where he is working on potential vaccine approaches, which he also discusses here. This transcript is drawn from four interviews conducted in New York and China in April and June 2005, and March 2006.

and

The consequence of that obviously is central to thinking about how HIV destroys the immune system, but also it has great ramifications for therapy, because HIV is an error-prone virus. As it replicates it makes mistakes. Now, that may not be all bad, because mistakes allow HIV to generate new variants, some of which will allow it to survive in the presence of drugs, survive in the presence of immune attack, so that's actually an advantage to HIV. When we know how much virus replication is going on and we know the error rate with which the virus makes mistakes, then we could begin to calculate what HIV would do if we applied drug pressure, and from those type of calculations came to the conclusion that it's inevitable for HIV to develop drug resistance if you give it one drug at a time. However, if you start to combine the drugs and try to force the virus into a corner using multiple drugs, it is exceedingly difficult or statistically improbable for HIV to become resistant to all the drugs simultaneously. That for us formed the foundation of thinking about combination therapy.

David Ho was made Time Magazine “Man of the Year” for rediscovering what Edward Tatum said more than thirty years earlier. The failure of evolutionists to properly teach how the mutation and selection sorting process actually works has and continues to contribute to the premature death of millions of people suffering from diseases subject to mutation and selection phenomenon. Evolutionists are in complete denial of how the mutation and selection sorting/optimization process actually works and their dominance in the field of biology prevents the proper teaching of the basic science and mathematics of this phenomenon. Instead, evolutionists would rather indoctrinate naïve school children with irrational and illogical speculations.

 

[Nogbad]

The argument regarding whether the evolutionary process occurs as currently understood is rightly a matter for debate and it is for the good Doc to demonstrate that his understanding of the process is the correct one.

What I fail to see is the connection between treatment of illness and evolution. Far from hindering the fight against viruses surely an appreciation that such things can evolve is an advantage not a disadvantage? Who has said that combination therapy should not be used against HIV because it does not fit with Darwin's views on natural selection? Combination therapy has been used since the early 50s on TB patients - without which a great many would still be dying from a serious and dangerous disease. I am sure the Doc mentioned Spanish Flu at some point too in his general rail against evolutionists which surprised me somewhat as that was back in 1918-20 before we even had a proper understanding of the influenza virus.

 

[kleinman]

Annoying Creationists

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

Summary: Artemisinin-based combination treatments (ACTs) are seen as an important tool in the global effort to roll back malaria. With rapidly increasing parasite resistance to chloroquine in many parts of the world, there is greater international recognition of the need for both a different antimalarial and a coordinated malaria treatment strategy to ensure that resistance does not needlessly cut short the useful therapeutic life of any successor drug to chloroquine. The effectiveness of antimalarial drugs is a global public good, of particular value in malarious regions that also are among the most economically impoverished parts of the world. Inappropriate drug use in neighboring countries reduces

the incentive of any given country to deploy drug regimens that may be rapidly undermined by resistance originating outside their borders. Therefore, a case can be made for globally coordinated action to protect the effectiveness of these valuable drugs. Translating this case to one for a global subsidy is not straightforward. On the one hand, in the absence of such a subsidy to ensure that ACTs are comparably priced to monotherapies, increasing monotherapy of artemisinin and other antimalarials that would
be used along with artemisinin in ACT will hasten the demise of this drug. On the other hand, a global subsidy would greatly increase the use and potential misuse of ACTs and could result in resistance emerging at a more rapid rate.

This study finds that a subsidy to ACTs is likely to slow the rate of emergence of resistance to artemisinin and partner drugs, even if such a subsidy were to increase the use of ACTs significantly. This conclusion is robust to alternative assumptions regarding the responsiveness of demand to the lower price for ACTs and a wide range of epidemiological and economic parameters. However, the simulation results show that a subsidy for two or more ACT combinations is likely to be much more cost-effective than a subsidy to a single ACT. The only consideration is that the drugs used as partners to artemisinin be unrelated to each other and to artemisinin in mechanism of action and in genetic bases of resistance, so that a single mutation cannot encode resistance to both components. Such a subsidy program for ACTs, administered globally, that reduces reliance on any single combination, and discourages monotherapy, not only of artemisinin but of any effective antimalarial that could potentially be used as partner drug with artemisinin, is likely to be effective (and cost-effective) both in buying time for ACTs and in saving lives.

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

There are other considerations that play an important role in the selection of the most appropriate antimalarial treatment strategy. First, an important parameter that determines the evolution of resistance to ACTs is the starting frequency of resistance, not just to artemisinin, but also to the partner drug in the combination. With the widespread availability of all antimalarials from private drug sellers in Africa, it may be difficult to control the emergence of resistance to the companion drug, which in turn would expedite the emergence of resistance to the combination. Our model shows that the economic advantages of introducing ACTs immediately are generally lower for higher starting frequencies of resistance to either drug in the combination, although this result depends on the impact of effective treatment on retarding the acquisition of immunity. Second, SP involves a one-day treatment dose, which is much easier to comply with than the five-day treatment of ACTs. To the extent that reduced compliance, which is more likely in the case of ACTs, will significantly expedite the evolution of resistance, our analysis errs on the side of overstating the economic advantages of immediate introduction of ACTs.

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

The widespread occurrence of drug-resistant parasites in malaria endemic regions has led to rapid changes in antimalarial treatment policies in many countries. In some parts of Southeast Asia, multidrug-resistant parasites are prevalent and have greatly reduced the efficacy of the majority of monotherapy regimens. This has led to the implementation of combination therapies, including artemisinin-based treatment throughout the region [1]. In sub-Saharan Africa, monotherapies such as chloroquine (CQ) and the antifolate fixed combination sulphadoxine-pyrimethamine (SP) have continued to be widely used. Parasites resistant to CQ are common and known to contribute to excess severe malaria cases [2], and SP-resistant genotypes have spread widely across the continent from a few focal origins [3]. Thus, despite there being few studies of multidrug-resistant Plasmodium falciparum in Africa, it is likely that parasites harbouring mutations conferring resistance to both CQ and SP circulate in many areas. Policy changes towards the implementation of artemisinin-containing combination therapies (ACTs) are now occurring in many countries [4].

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?

 

[joobz]

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.

 

[coops]

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.
QUOTE]


I have to agree.

I have asked Kleinman 17 times now to define the difference between micro evolution and macro evolution. It seems to me that since he is saying one is possible and the other one impossible he should be able to define the terms so that everyone can understand his position better.

Not once has Kleinman answered my question directly.

He has posted plenty of long posts mocking 'evolutionists' and repeating himself but has so far refused to actually give a direct answer to a question about his beliefs.

It really does come across as though you are simply spamming the thread now Kleinman.

 

[Mr. Scott]

Dr. Kleinman Please Answer

I don't recall him posting any CS credentials at all.

Certainly the fact that he is unable to comprehend even the basic idea of "parallel," which most children find easy to grasp, speaks volumes about both his education and mental capability.

Because of my engineering background and training with the development and application of large scale computer simulations, I simply put those skills to use on Dr Schneider’s model.

Dr. Kleinman, please supply verifiable evidence of your statement, above, that you have "training with the development and application of large scale computer simulations."