Annoying creationists

[Shalamar]

I had a thought. Imagine of People who practiced Medicine, Doctors, treated patients the same way that creationists did science?

A patient would come in, and say he wasn't felling ill. The Doctor would immediately announce that the illness was 'X', and then would look for any symptoms that would confirm his limited 'diagnosis' while ignoring any symptoms that didn't point to declared illness. If the patient didn't get better, the doctor would say it was the patients fault for not believing him. And the patient may well die of a different illness, because the doctor would not diagnose AFTER looking at the symptoms.

[kleinman]

It appears you evolutionists still haven’t figured out how the mutation and selection sorting/optimization process works either mathematically or empirically. You evolutionists fantasize that the small evolutionary changes due to identifiable selection conditions targeted at specific genes can be extrapolated to imaginary selection pressures targeting entire genomes such that lizards turn into birds. This is a mathematically and empirically irrational and illogical extrapolation that you evolutionists like to call science. It is clear that when you have identifiable selection pressures which target specific genes, the greater the number of selection conditions and corresponding genes targeted, the much, much, much slower the mutation and selection sorting/optimization process works. These real examples of mutation and selection don’t create new genes with new functions, these examples show that modification of genes and their corresponding enzymes by mutation and selection only change the conformation of enzymes so that the chemicals targeting them no longer bind to interfere with the enzymes.

Now you evolutionists irrationally speculate that mutation and selection will create thousands of genes with new functions when it has shown both mathematically and empirically that transforming the conformation of two or three genes and their corresponding enzymes to a new conformation (but still with the same function) due to two or three different selection pressures is profoundly slowed when compared to the evolution of a single gene and enzyme to a single targeted selection pressure. None of you evolutionists are willing to describe how the mutation and selection sorting/optimization process will evolve a gene de novo. It wouldn’t have anything to do with you have no idea how such a thing could happen?

Now don’t get confused with cpu time and number of generations necessary to accomplish a mutation and selection sorting/optimization process. For example, running Dr Schneider’s model on a computer with a clock rate of 1GHz would take twice as much cpu time as a different computer with a clock rate of 2GHz. However, the number of generations to run Dr Schneider’s sorting/optimization algorithm to converge this case on either computer would be the same. Even Dr Schneider’s simple selection conditions take huge number of generations to do the sort/optimization when the search space is 4^17,000. I think the largest genome Paul has been able to converge in ev with the three selection conditions is only about G=100,000. This is still a factor of 5 smaller than the smallest genome for any free living creature. On the other hand, it takes a trivially small number of generations to sort and optimize any single selection condition in Dr Schneider’s model. So when we talk about generation time, it can be minutes for microbes and weeks, months or years for animals. Take the example of the evolutionist claim that lizards evolved into birds. What do you want to use for the generation time, 6 months, a year? How many years to you want for the transformation, 500,000,000 million? So you claim that a gigabase lizard genome is transformed into a gigabase bird genome in 500,000,000 or 1,000,000,000 generations? All those new genes to produce feathers, beaks, gizzards evolving de novo yet you have no selection pressures that would do this and the mutation and selection sorting/optimization process is far to slow to do this when it is clearly seen mathematically and empirically that transform existing genes to adapt to multiple selection pressures is profoundly slow and in these cases, new function is not being evolved. 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.

Well, you evolutionists think your fossil Rorschach tests override the mathematical and empirical evidence of how the mutation and selection sorting/optimization process actually works. Post your fossil Rorschach tests and tell us what your imagination shows us. In the meantime, I’ll continue to post the real, measurable and repeatable evidence of how the mutation and selection sorting/optimization process actually works and it works just like Dr Schneider’s peer reviewed and published mathematical model works and that is combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. Here are a few more examples.
http://newsarchive.asm.org/jan01/feature3.asp (http://newsarchive.asm.org/jan01/feature3.asp)
Conceptually, a combination treatment regimen containing two or more drugs of different classes should require at least two resistance mutations for the pathogen to grow. Because the simultaneous development of two such mutations could be expected only in a bacterial population of much greater size than is normally present within any individual, combination therapy with two distinct antibiotic types provides a way to reduce mutant selection using moderate concentrations of compounds that may individually have very high MPCs.

The best examples of combination therapy are found with tuberculosis. Because the standard agents used for treating patients with this disease cannot be dosed at concentrations that exceed the respective MPCs of these drugs, resistance readily arises when any of the agents is used in monotherapy. Dual-drug and often multidrug therapies thus are used routinely to reduce the number of treatment failures. Currently cases of drug resistance developing among tuberculosis patients are generally associated with the failure of patients to comply fully with therapy regimens. In effect, sporadic compliance creates the equivalent of repeated monotherapy punctuated by periods of bacterial population expansion. To assure patient compliance, a major effort has been placed on directly observed therapy (DOT), which significantly lowers the incidence of resistance-associated treatment failure.
http://www.3dgenoscience.com/molecular_modeling/halfon_aucopy2.pdf (http://www.3dgenoscience.com/molecular_modeling/halfon_aucopy2.pdf)
Development of hepatitis B virus (HBV)-resistant strains following nucleos(t)ide analogue treatment is a major concern. The A181V mutation within the reverse transcriptase (RT) of HBV has been shown to be associated with HBV resistance to adefovir dipivoxil (ADV), and its level of sensitivity to other nucleos(t)ide analogues is an important issue. This article reports two cases of chronically HBV infected patients who developed rtA181V HBV mutants following lamivudine (LAM) monotherapy. This was subsequently associated with virological breakthrough under LAM monotherapy or LAM/ADV bi-therapy, which were rescued by tenofovir disoproxil fumarate treatment. These observations suggest that rtA181V mutation may unusually emerge under LAM monotherapy, and may be associated with cross resistance to LAM and ADV, but remains sensitive to tenofovir disoproxil fumarate. Moreover, they highlight that HBV sequence analysis is an essential tool to optimize therapeutic management of HBV chronic infection in clinical practice in order to choose the appropriate nucleos(t)ide analogues.
These examples once again demonstrate how the mutation and selection sorting/optimization process actually works. The greater the number of selection pressures, the much, much slower the evolutionary process proceeds, much too slow for common descent to be mathematically possible (that is if you had the selection conditions which would accomplish such a process and you don’t). It is this gross misinterpretation of the basic science and mathematics of the mutation and selection sorting/optimization process which evolutionists assert and teach which contributes to the premature death of millions of people with diseases subject to the principles of the mutation and selection phenomenon.

[articulett]

Yep... they have the "truth" they want... and they just jam facts, words, semantics, math, whatever can fit inside and ignore all the good filler like EVIDENCE.

They'd rather believe that have the truth than find out they've been wrong.

[Cardelitre]

I really think this man is insane.
And I'm beginning to think this is not even a man. It really looks like an out of control internet bot experiment... Not the slightest answer to any specific question, ever. Repeated mantra with few variations but not significantly different, with a selection of random quotes most of the time irrelevant and often clearly in support of evolution mecanisms.

No living man, even deeply insane, would be able to produce this crazy thing for so long. I just can't accept this idea.

[Shalamar]

Nah. Not a bit, Mr. Kleinman has made a point to mention the speed of the computer.

But, he still fails remedial science. If this is what medical schools are putting out, I fear for our health.

[Shalamar]

I also want to know where anywhere at alkl, Evolution says 'lizards turned into buzzards with gizzards'. Because of the Theory of Evolution says this anywhere, then Mr. Kleinman is lying.

But Mr. Kleinman lying is normal around here.

[joobz]

I'm still hoping for a repeat explanation on how proof of a newly evolved enzyme with wholly new function doesn't prove evolution.

[kleinman]

You evolutionists seem to be having a little problem understanding how the mutation and selection sorting/optimization process actually works. So let me answer a few questions for you. First of all, blizzards don’t turn lizards into buzzards with gizzards, neither does hail turn fish with scales into snails with mail nor does fog turn logs into frogs in bogs. And unless the primordial soup was alphabet soup, you don’t get life spontaneously popping up just because the sun is shining on it. However, you can make sun tea.

So, how does the mutation and selection sorting/optimization process work in nature? It works exactly like Dr Schneider’s peer reviewed and published mathematical model works. Combination selection conditions profoundly slow the sorting/optimization process. Can we find a real example of what Dr Schneider’s model shows? Let’s take a look.

Why yes indeed, we can find a real example which demonstrates that combination selection pressures profoundly slow the evolutionary process. Here’s one specifically for you evolutionists.
These reduced-risk insecticides offer a wide range of pest management options available to vegetable growers and should be used wisely or in rotation with one another to minimize selection for resistance to any one given material.
http://www.malariajournal.com/content/6/1/9 (http://www.malariajournal.com/content/6/1/9)
Combination therapy would also be advantageous if the required set of mutations was initially absent in the population, so that selection could not start to act.
I apologize, I said I was going to present one citation for you evolutionists but I inadvertently presented two. Will you forgive me and show us one of you fossil Rorschach tests instead? Or perhaps you would tell us how a gene evolves de novo by mutation and selection? Or perhaps one of you evolutionists could tell us how selection would transform inorganic chemicals into living creatures? Oh, wait, you did answer that one; you said chemicals cooperate; all they need is free energy.
http://forums.randi.org/images/smilies/doglaugh.gif

[coops]

Can you give a yes or no answer to my question Kleinman?

I gave a summary of my understanding of your position. Can you respond by simply stating either -
a) yes, your summary is correct.
b) no, your summary is incorrect.

If the answer is b then please feel free to correct my statement accordingly.

Your above duplicate post really doesnt make it clear to me where you specifically draw the line between micro-evolution and macro-evolution.


And yet again, another bump for Kleinman.

Your last post seemed to indicate that my summary was correct but you seem determined not to answer me directly.

Why is that Kleinman? Why are you refusing to give a definate answer to a specific question?

[joobz]

http://forums.randi.org/images/smilies/doglaugh.gif
So you won't make up any new stupid statements, but repeat the same old stupid statements?
Oh well.

[coops]

double post

[Shalamar]

You evolutionists seem to be having a little problem understanding how the mutation and selection sorting/optimization process actually works. So let me answer a few questions for you. First of all, blizzards don’t turn lizards into buzzards with gizzards, neither does hail turn fish with scales into snails with mail nor does fog turn logs into frogs in bogs. And unless the primordial soup was alphabet soup, you don’t get life spontaneously popping up just because the sun is shining on it. However, you can make sun tea.

Ok. Mr. Kleinman has gone stark raving mad.

Kleinman.. do you seriously think that this is what The Theory of Evolution, a well established aspect of science SAYS? If so, you are among the most ill educated, and overtly indoctrinated people I know.

Also. to repeat, even though I know you will ignore it, the Theory of Evolution SAYS NOTHING. Absolutely NOTHING about the creation of life! THAT is called abiogensis.


For the love of god, open up a frakking biology textbook, and READ.

[kleinman]

In answer to your question; none of you evolutionists have properly summarized my statements. What I am showing you is how the basic science and mathematics of the mutation and selection sorting/optimization process works. The ability of a population to evolve to more than a single selection condition targeting a single gene is markedly impaired. This is a mathematical and empirical fact of life. Selection conditions that target an entire genome have a huge search space fitness landscape (4^G) in order to traverse to a new local optimum. The path this population must take must always be of increasing fitness. There are no selection conditions or mathematically plausible way for a population to make such a huge transformation. The mutation and selection sorting/optimization process is simply far to slow and the selection conditions do not exist. The theory of evolution is mathematically and empirically impossible.

Now did I say something stupid such as chemicals cooperate to make life spontaneously occur or that variation in weather cause blizzards to transform lizards into buzzards with gizzards?
http://forums.randi.org/images/smilies/doglaugh.gif
What I have been saying is that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. If you evolutionists understood this mathematical and empirical fact, HIV would not have been treated using monotherapy for years introducing huge numbers of resistant viruses into the gene pool. Let’s see if we can find a citation which shows this. Oh yes, here is one.
https://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck (https://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck)
The use of combinations of antiretroviral drugs has proven remarkably effective in controlling the progression of human immunodeficiency virus (HIV) disease and prolonging survival, 1 but these benefits can be compromised by the development of drug resistance. 2,3 Resistance is the consequence of mutations that emerge in the viral proteins targeted by antiretroviral agents. In the United States, as many as 50 percent of patients receiving antiretroviral therapy are infected with viruses that express resistance to at least one of the available antiretroviral drugs. 4 Consequently, the transmission of drug-resistant strains is also a growing concern. 5,6,7
The failure of evolutionists to properly elucidate how the mutation and selection sorting/optimization process actually works has and will continue to contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection sorting/optimization process, this includes people suffering from HIV. Despite the fact that Edward Tatum pointed out in his 1958 Nobel laureate speech how mutation and selection actually works, evolutionists are still in denial of how this phenomenon behaves either mathematically or empirically.

[Shalamar]

What I am showing you is how the basic science and mathematics of the mutation and selection sorting/optimization process works.

You have NEVER shown the math you claim to have.

Show your math. Put up, or shut up.


The theory of evolution is mathematically and empirically impossible.

Show your evidence for this. Which you have never shown.


Now did I say something stupid such as chemicals cooperate to make life spontaneously occur or that variation in weather cause blizzards to transform lizards into buzzards with gizzards?

The first statement has nothing to do with Evolution. A fact which eludes your deluded mind. The second is the raving of a religiously indoctrinated idiot.

[coops]

[SIZE=3]In answer to your question; none of you evolutionists have properly summarized my statements. SIZE]

THANKYOU!!

Seriously, thankyou Kleinman for finally answering my question.

So if my summary was wrong could you please answer my original question to correct me.

Q - At what EXACT point does micro evolution become macro evolution and hence becomes impossible.

No need for a multiple paragraph answer Kleinman. One or two concise sentences should be able to summarise your answer without to much trouble.

[kleinman]

An evolutionist wants a concise statement. That’s hilarious. When was the last time an evolutionist made a concise statement? So let’s see if we can bracket the value when a microevolutionary process becomes a macroevolutionary process. In the human genome there are about 20,000 genes. So in the mutation and selection sorting/optimization process for humans, there are somewhere between 1 and 20,000 genes which have to be sorted and optimized. Do any of you evolutionists want to make a concise estimate for the number of genes which can evolve simultaneously by the mutation and selection sorting/optimization process before a microevolutionary process becomes a macroevolutionary process?

While you are thinking about that, here is a citation which talks about how many genes can evolve simultaneously in the malaria parasite.
http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt (http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt)
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.
These authors seem to think that targeting two genes with two different selection pressures will profoundly slow the mutation and selection sorting/optimization process and that it will save lives. I wonder what would happen if three genes were targeted simultaneously?

[joobz]

An evolutionist wants a concise statement. That’s hilarious. When was the last time an evolutionist made a concise statement? So let’s see if we can bracket the value when a microevolutionary process becomes a macroevolutionary process. In the human genome there are about 20,000 genes. So in the mutation and selection sorting/optimization process for humans, there are somewhere between 1 and 20,000 genes which have to be sorted and optimized. Do any of you evolutionists want to make a concise estimate for the number of genes which can evolve simultaneously by the mutation and selection sorting/optimization process before a microevolutionary process becomes a macroevolutionary process?

And you know full well that evolution doesn't claim the formation of 20,000 gene simultaneously.

[coops]

[SIZE=3]Do any of you evolutionists want to make a concise estimate for the number of genes which can evolve simultaneously by the mutation and selection sorting/optimization process before a microevolutionary process becomes a macroevolutionary process?SIZE]

I see you repeated my question but you didn't answer it Kleinman.

If you have no intention of answering a direct question I would prefer it if you just admitted it to me.

So what is YOUR opinion on the above question Kleinman?

Where do YOU draw the line EXACTLY between micro-evolution and macro-evolution?

[X]

He's starting to sound like Dr. Seuss.

In the end, however, it all seems like much sound and fury, signifying nothing.

[m_huber]

[FONT=Times New Roman][SIZE=3]Well, you evolutionists think your fossil Rorschach tests override the mathematical and empirical evidence of how the mutation and selection sorting/optimization process actually works. Post your fossil Rorschach tests and tell us what your imagination shows us.

As you wish.

But first, a Rorschach test:

http://forums.randi.org/imagehosting/thum_2104647b283774484e.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10782)

I think it kind of looks like a cat. Understand what a Rorschach test is: In the strictest sense, the Rorschach Inkblot Test is a test or assessment of perception. It is designed to evaluate how someone approaches their environment, In other words, it asks the question, "How does someone view and organize the world around them?"

Through analyzing what someone sees, where they see it, and what about the blot makes what they saw look like whatever they saw, the psychologist is able to make various hypotheses about how that person views and organizes the world. Furthermore, the psychologist can compare the person's perceptions to a clinical or normative sample. From this analysis, the psychologist then makes inferences about the person's approach to the world (which is largely stable and described often as character or personality), insofar as, one's feelings, thoughts, stress tolerance, relationships, and self-perception shapes and influences how that person views and organizes their world. (Source (http://www.rorschach.org/faqs.htm))

So, this test takes an abstract image and asks how someone makes it concrete. What about fossils? What are they? Do they qualify as Rorschach tests? Well, no. Fossils are not abstract images. If you think that they are, then you probably haven't seen many fossils. An example:

http://forums.randi.org/imagehosting/thum_2104647b2850cee6fb.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10783)
(Source (http://www.curiogrove.com/shrimp/smp002.htm))

Can you guess what that is? Does it look something like this:

http://forums.randi.org/imagehosting/thum_2104647b286435dd6a.gif (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10784)(Source (http://webs.lander.edu/rsfox/rsfoximages3/shrimp11L_x550_x_377x.gif))

While fossils are not always so clear cut or complete as this shrimp, there is always a coherent argument for what various fossils represent. For instance, whale fossils are often identified by the tooth structure (which is unique amongst whales) and the inner ear structure (which is also unique). Because of this, only a small portion of the skull is needed for positive whale identification. Further, by analyzing the types of sediments around a fossil, we can learn about the type of environment the organism lived in. Sometimes, we don't even get a hard part:

http://forums.randi.org/imagehosting/thum_2104647b287b3c05f7.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10785) (Source (http://roadsofstone.com/category/environment/))

This is still considered a fossil, as it is completely enclosed in the rock. These are footprints, very similar to bird footprints found in mud on beaches, streams, or after a heavy rainstorm.

None of this says anything about evolution. All I have demonstrated is that fossils are not Rorschach tests. They can be definitely tied to very tangible organisms that are still alive today. A fossil bird is no more a Rorschach test than a modern bird.

When fossils start to tell us about evolution is when we find the organisms that cannot be tied to anything modern.

http://forums.randi.org/imagehosting/thum_2104647b288e51edb0.gif (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10786)

This fossil, named Hallucigenia, bears no resemblance to any modern living thing that we know of. There are not many fossils of it, but what we have is preserved well enough to show that this organism does not have anything that we can recognize as either a mouth or an anus.

This is only one example of an organism that is known from fossils but not from modern observation. There are tens of thousands of clear examples. The question, then, is, "where did they go?"

If fossils are in fact the preserved remains of once-living organisms, as they have every indication of being, then one is left to conclude that the majority of the life that has inhabited Earth has gone extinct. Without going further into what is observed in and around fossils, we can begin to ask significant questions. Did all of these organisms inhabit the Earth at the same time? Could all of these organisms coexist? What made some of these organisms go extinct, while others survived?

When we find fossils, we find them in clusters. Each cluster consists of a set of fossils that are always found together in the rocks. This proved to be consistent enough that, well before Darwin wrote the "Origin of Species", was used to make geologic maps of much of Europe and subsequently codified into the geologic time scale. This answers the first and second question: The organisms did not overlap in time because we never find fossils in the wrong cluster. Trilobites, for example, are not ever found after the Permian-Triassic (P-T) boundary.

So what made them go extinct? We have found numerous mechanisms that cause extinction. Major impacts (represented by a strong body of evidence for both the impactor and the fallout from the impact; we can discuss this further if you like), possibly plate convergence in the example of the P-T Boundary, and possibly major volcanic eruptions have been associated with the major extinctions in the geologic record. However, these are recognized as major extinctions against a "background" extinction level.

This can be displayed graphically:
http://forums.randi.org/imagehosting/thum_2104647b28bfe490ad.png (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10787)(Source (http://www.answers.com/topic/extinction-event?cat=technology))
(Notice the large "End P" spike)

There has been a near-continual extinction level (represented by the yellow line). The curious thing is that there are always organisms that replace those that go extinct. These are not limited to a handful of organisms, but instead are represented by organisms that range from large and exciting (like the dinosaurs and mammoths) to various marine worms.

Where do these organisms come from? Late 1800's theologians proposed that God had destroyed the Earth and rebuilt it numerous times, and the great Deluge of Noah was only the most recent event. However, the continual background extinction level and strong correlation of major extinction events to discernible major geologic upheavals strongly suggests that, in fact, the history of life is a continuum. The fossils seem to represent (even in the absence of "transitional forms" or well-defined evolutionary progression within a single species) the development of life. This happens in 3 basic stages: 1) extinction; 2) diversification and radiation of remaining organisms; 3) establishment of species and subsequent stasis until the next extinction event.

This argument is built on the basis of tangible evidence. Anyone can look at rocks and make interpretations about them, but through the three hundred years of detailed analysis, the geologic community has come to this consensus. There is much still debated in paleontological circles; what is not debated is the information I just presented.

Mathematics is a useful tool for understanding the world. It has shown us how the planets move, has been used to build impressive buildings, and generally has allowed our modern world to exist. However, mathematics must be viewed only within the realm that it effects. Newton's theory of Gravity does not say that things fall; rather, it says that a certain attraction exists between all bodies. So it is no surprise that things "float" in space. Similarly, the modern theory of Evolution says that organisms change; it is not particularly surprising or difficult that targeted drug therapy can eliminate viruses in a human body.

[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 (http://en.wikipedia.org/wiki/Heterosis)?

[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

http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=8609)

[kleinman]

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 (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 (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 (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]

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 (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]

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]

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]

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 (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.
http://forums.randi.org/images/smilies/doglaugh.gif

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 (http://www.talkorigins.org/indexcc/CB/CB102.html).

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]

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 (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 (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]

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-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 (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 (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]

[QUOTE=joobz;3432236]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]

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."

[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-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://www.ajtmh.org/cgi/reprint/71/2_suppl/187.pdf)

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

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.
http://forums.randi.org/images/smilies/doglaugh.gif
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 (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 (http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0009C.SGM) 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 (http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0010C.SGM) 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 (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?
http://forums.randi.org/images/smilies/doglaugh.gif

[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]

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 (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 (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]

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 (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]

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 (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 (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 (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]

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.
http://forums.randi.org/images/smilies/doglaugh.gif
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 (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 (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 (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 (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 (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?

[joobz]

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.
I had originally thought that. But one weekend, no one responded to him, and he felt the need to enter another thread perpetuating the same nonsense.

I got the distinct impression that he wants the attention. If we really want to get his goat, we just stop posting.

I would love to see this post be the last in the thread.:)

[Belz...]

Beggaminases is how evolution works.

And that's the last thing he ever said.

Suicide by mod. Gotta love it.

Now he can whine to his creationist friends (and, unfortunately but probably, to his patients), about how badly he was treated by those mathematically challenged evolutionists who didn't understand how evolution by mutation and selection really worked mathematically and empirically and how multiple directional selection pressures profoundly slowed the evolution process.

How am I doing, so far ?

[Nogbad]

And that's the last thing he ever said.

Suicide by mod. Gotta love it.

Now he can whine to his creationist friends (and, unfortunately but probably, to his patients), about how badly he was treated by those mathematically challenged evolutionists who didn't understand how evolution by mutation and selection really worked mathematically and empirically and how multiple directional selection pressures profoundly slowed the evolution process.

How am I doing, so far ?

Spooky - like he is still here :eek:

[Shalamar]

Well, I'm glad he's gone, but yeah, he'll still spread his lies about the evils of Science.

I worry about the damage he could spread to his patients as he is in a position of authority.

[tsig]

Well, I'm glad he's gone, but yeah, he'll still spread his lies about the evils of Science.

I worry about the damage he could spread to his patients as he is in a position of authority.

Just call it evolution in action.

[Foster Zygote]

So he fell on his plastic sword...

[coops]

ummmm, so i know the guy was really annoying and all (hence the thread title)

But what was the reason for him getting banned?

He didnt appear to be any more rude, evasive, or dishonest than usual in his last post so i'm just curious as to what was the final straw.

[Olowkow]

Double post. sorry.

[Olowkow]

Active Warning
Breach of Rule 6: You will not "spam" or "flood" the Forum. Expires
Never Left By
Darat
03:18 AM 15th February 2008

[Mr. Scott]

But what was the reason for him getting banned?

He didnt appear to be any more rude, evasive, or dishonest than usual in his last post so i'm just curious as to what was the final straw.

Kleinman received a warning for the repetitive post below (see the yellow icon at its end), which probably qualified as some kind of flooding:

Lizards evolve into birds
Lizards evolve into birds
[etc]

It was really, really obnoxious, which was, I'd think, reason enough, but it became painfully obvious that he didn't want a civil discussion about evolution. Kleinman outed himself as, essentially, spamming the forum to publish his "letter to the editor" he wanted to publish but couldn't in Nucleic Acids Research.

Of course, he'll report to his chums that he was banned because the evolutionists "ran out of" arguments against his thesis, which would be a lie because we were still coming up with novel refutations virtually to the last day. Reminds me of the Black Night in Monty Python and the Holy Grail who, after losing both arms and legs to his opponent, offered to call the duel a draw, although Kleinman is no doubt still judging himself the winner.

[Olowkow]

I'm taking bets that this thread will not hit 8000 posts.:hypnotize


Good thing no one took me up on my bet! :D

[coops]

Kleinman received a warning for the repetitive post below (see the yellow icon at its end), which probably qualified as some kind of flooding.

Fair enough. I'm just amazed it took 8000 posts and over a year before it happened.

The mods here must be a lot more forgiving then i would imagine most other forum moderators would be.

wonder how long it will be before kleinman mk2 appears.

[Apathia]

Reminds me of the Black Night in Monty Python and the Holy Grail who, after losing both arms and legs to his opponent, offered to call the duel a draw, although Kleinman is no doubt still judging himself the winner.

:lol2:

I predict he'll publish a book that many Christians will point to on their bookshelves (though they've never read it) and say, "See, that's the book by the guy that disproved evolution." Whenever doubt arises, they'll take it down and hold it in their hands as if it were holy scripture.
Well, as far as scriptural content goes, I suppose it could be.

[m_huber]

:lol2:

I predict he'll publish a book that many Christians will point to on their bookshelves (though they've never read it) and say, "See, that's the book by the guy that disproved evolution." Whenever doubt arises, they'll take it down and hold it in their hands as if it were holy scripture.
Well, as far as scriptural content goes, I suppose it could be.

I have a couple of creationist books on my shelf right now (from my pre-skeptic days). I actually read them when I was a Christian. There are certainly some christians who do not read their materials, but it might surprise you how many actually do. The problem is that the arguments sound good, unless you know a bit of real science. Alan's argument is that evolution is not mathematically possible, and that is the same basic argument as Behe and many others. On YEC forums, many times they will fall back on that basic argument. If you have no knowledge of why science actually thinks that evolution happens, it sounds like a reasonable problem. For instance, perpetual motion machines are not possible theoretically, so whenever we see someone claim to invent one, we dismiss it. I have a certain pity for creationists. Ones like Alan make the whole batch look bad, but many are friendly and otherwise quite intelligent people. Some of my family members have changed to acceptance of evolution since I learned what real science is. So, while Alan is a hopeless case, he is not representative of all creationists.

[rocketdodger]

ummmm, so i know the guy was really annoying and all (hence the thread title)

But what was the reason for him getting banned?

He didnt appear to be any more rude, evasive, or dishonest than usual in his last post so i'm just curious as to what was the final straw.

He should have been banned long ago.

I don't care about personal attacks or spamming the thread. I do, however, strongly disapprove of (the word hate is more appropriate I think) the way Kleinman consistently avoided ever addressing the issues we brought up and acted like a debate bully in the process.

If this was an arbitrated debate instead of a forum he would not have lasted a single page before breaking the rules. That makes him the worst of the worst in my book. I have zero tolerance for people that attempt to argue using misquotes, misrepresentations, and misinformation.

[Dr Adequate]

So, the final tally.

Number of posts by kleinman: 1538

Number of words in kleinman's posts (estimated from a sample of his weekly tallies) ~ 750,000

Number of posts by kleinman including the word "mathematics": 300.

Number of posts by kleinman containing mathematics: 0.

Number of posts by kleinman including the word "cheese": 166.

Number of posts made by kleinman in which he uses the phrase "selection pressures evolve": 71. (That's the trouble with automating the lying process.)

Number of people deceived by kleinman: 0.

Ladies and gentlemen, we may have just witnessed the single greatest act of human pointlessness since the reign of King Olaf the Pointless.

[Olowkow]

Ummm...how many laughing dogs? Just asking...:)

greatest act of human pointlessness

Funny, the first time I read this, I saw "politeness"!

My question is: Who will be the final poster on this thread? It would have been fitting that Dr Adequate be the one, but I just had to add my .01 quid.

[Dr Adequate]

The Last Word

In search of lasting fame, he raised
himself a monument: a crazed
and ostentatious folly, built
of marble, laced about with gilt
for ornament, designed in mock-
Egyptian mixed with late Baroque,
with Grecian porticos, and sets
of neo-Gothic minarets:
a thing that would have quite digraced
a magpie's sense of proper taste;
with lots of statues, all of him
enthroned among the cherubim,
and busts and portraits by the ton;
and, when the gaudy thing was done,
he carved upon its massive base:

Here Lies, Beneath This Hallowed Place,
A Man Whose Lofty, Noble Mind
Reflected Glory On Mankind;
A Peerless, Wise, And Saintly Sage;
The Very Wonder Of His Age,
With All The Gifts That Heaven Sends;
Who, Now His Mortal Jouney Ends,
Lays Down His Burden, And With Great
Humility (His Leading Trait)
Accepts His Heavenly Reward
As What Is Owed Him By The Lord..

Today, his tomb, as you might guess
(what's left of it) does not impress:
for, since he'd chosen to reject
advice from every architect,
and botched his grandiose design
in each distorted, crooked line,
and built upon the shifting sand,
his mausoleum didn't stand
for quite so long as he had planned;

and Time, that loves the final laugh,
has edited his epitaph.
A word's sufficient to the wise.
One word remains, and that is: Lies.

[delphi_ote]

But it wasn't a dream. It was a place, and you and you and you... and you were there!

But you couldn't have been, could you? No, Aunt Em. This is a real, truly live place. And I remember that some of it wasn't very nice. But most of it was beautiful. But just the same, all I kept saying to everybody was, 'I want to go home.' And they sent me home.

Oh, but anyway, Toto, we're home! Home! And this is my room - and you're all here! And I'm not gonna leave here ever, ever again because I love you all! - And oh, Auntie Em, there's no place like home. There's no place like home.

[tsig]

But it wasn't a dream. It was a place, and you and you and you... and you were there!

But you couldn't have been, could you? No, Aunt Em. This is a real, truly live place. And I remember that some of it wasn't very nice. But most of it was beautiful. But just the same, all I kept saying to everybody was, 'I want to go home.' And they sent me home.

Oh, but anyway, Toto, we're home! Home! And this is my room - and you're all here! And I'm not gonna leave here ever, ever again because I love you all! - And oh, Auntie Em, there's no place like home. There's no place like home.


And don't let the blizzard turn your lizzard into a wizzard.

[Belz...]

I think Kleinman was more like a buzzard.

Well, he DID think he was the evolutionists' worst predator.

[m_huber]

I think Kleinman was more like a buzzard.

Well, he DID think he was the evolutionists' worst predator.

He may have been the worst..

[Kotatsu]

Number of posts by kleinman including the word "mathematics": 300.

Number of posts by kleinman containing mathematics: 0.

Number of posts by kleinman including the word "cheese": 166.

It seems this tally can't be very final, as it doesn't include even an estimate of how many of his posts actually contained cheese. Don't biased towards mathematics!

[zeusbheld]

He may have been the worst..

well if he was the worst predator, i predict the extinction of 'evolutionists' ...

next major comet strike.

[Paul C. Anagnostopoulos]

Hey, Kleinman is banned!

It's amazing what you miss when you're lying on the beach ...

~~ Paul

[Mr. Scott]

Hey, Kleinman is banned!

It's amazing what you miss when you're lying on the beach ...

~~ Paul

The headline was: "Creationist Repeatedly Pwned by Skeptics Commits Suicide by Mods"

[kjkent1]

FYI: Kleinman has returned to whence he came:

http://www.evolutionisdead.com/forum/viewtopic.php?t=587

I strongly suggest that he be left alone to rant. At the moment, there are nine posts in the new thread on his brand of information theory -- every one of them by kleinman.

Res ipsa locquitur

[Paul C. Anagnostopoulos]

Well, all I can say is it's the end of an errah.

~~ Paul

[Paul C. Anagnostopoulos]

Kleinman is now hassling Tom Schneider (and me) directly. Here is the final paragraph from his latest email:

If you don't have time to correct your misinterpretations then please send me the email address of your supervisor so that we can correct this and that children can learn properly how the mutation and selection sorting/optimization process works.

~~ Paul

[cyborg]

Grade A kook.

[biomorph]

Kleinman is now hassling Tom Schneider (and me) directly. Here is the final paragraph from his latest email:


~~ Paul
<spamfilter>
I'm guessing you are reading those mails in your "deleted items" or "junk" folders again?:p
</spamfilter>

[delphi_ote]

Kleinman is now hassling Tom Schneider (and me) directly. Here is the final paragraph from his latest email:


~~ Paul
Poor Kleinman...
http://i71.photobucket.com/albums/i133/delphi_ote/n1704710_32372253_5550.jpg

[Dr Adequate]

Oh, I found out that the search function only goes up to 300 posts. In fact, that was only the number of times he'd made a post with the word "mathematics" in it since August.

What a strange little man he was.