Annoying creationists

[Shalamar]

I see that Mr. Kleinman has posted some sort of vague equation. He talks about 6th dimensional maths and the like, while still smugly declaring that he has found evolution impossible, while using evolution to prove its own impossibility.

Looks like he still doesn't have anything. Doesn't appear to be actual math, just a bunch of claims which can only back his own deluded position.

Is he still ignoring all evidence for the opposite of what he claims?

 

[jimbob]

Originally Posted by jimbob
It almost seems too stupid even for a creationist...

Nah.

Seriously, we talk about creationists being stupid, but they are really better described as "deluded." They think they have reality figured out, and when someone points out that facts disagree with their view of reality, it puts them in a position of having to either dismiss their old version of reality or their new version of reality. The ones who come here generally have their minds made up already, and they reject any new version of reality, but there are many who are riding the fence, and just need to see evidence. It is instructive to those people to point out the lengths that creationists have to go to support their positions (such as arguing that the sun doesn't exist).

Indeed. Behe did manage to get a pH_d.

I know at least one creationist who is highly clever (misplaced and with very compartmentalised interests, "railway-track" thinker) but he is highly qualified, in a technical subject, and yet fails to apply his critical faculties to his beliefs. "The sign of a first-class intellect is the ability to hold two mutually contridictory opinions at the same time".

Highly clever, very detail-orientated, very compartmentalised interests, and fanatical in those interests. Also very good at almost the "theology" of technical work. Doesn't really believe in "messy" experimental data.

Stupid ideas from someone who might otherwise seem clever.

 

[kleinman]

Annoying Creationists

Now, here’s the specific proof that evolutionists are incompetent in either understanding or teaching how the mutation and selection sorting/optimization process actually works.
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.

And
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.

Edward Tatum in 1958 explained the essential principle of the mutation and selection sorting/optimization process, that is combination selection pressures profoundly slow the process. David Ho and his collaborators took years to come up with the concept of combination therapy even though Edward Tatum had taught this concept decades earlier. The failure of evolutionists to understand and teach this basic principle of the mutation and selection sorting/optimization process has contributed and continues to contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection and selection. This is the contribution that evolutionism has made to the field of biology, that is the confusion and obfuscation of the mutation and selection sorting/optimization process.

Now it appears that some evolutionists are confused about what selection pressures do. What selection pressures do is impair the fitness of part or all of a population to reproduce. These selection pressures can kill part or all of the population or as in the case of drugs used to treat viral infections, they only impair the ability of members of the population to reproduce. Somehow in the indoctrination of evolutionists, they have gotten the idea that selection pressures do something different like blizzards turning lizards into buzzards with gizzards.

And some confused evolutionist thinks that this thread is “sooooooooooo booooooooooriiiiiiiiiiig”. Once again an evolutionist is wrong. At the time of writing this post, the Science, Mathematics, Medicine, and Technology Forum has Threads=10,353 and Posts=322,011. Posts on this thread=7,819 Views on this thread=141,428. The next closest thread with number of views is 41,247 and the next closed thread with number of posts is 2,832. The nearest thread on this forum has less than 1/3 the views and about the same fraction of posts. Now it is probably the interest in learning how blizzards turn lizards into buzzards with gizzards which attracts everyone to this discussion. It has nothing to do with understanding how the mutation and selection sorting/optimization process actually works and why the incompetent teachings of evolutionism contributes to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. So while you evolutionists look to the Simpsons to support your theory of evolution, let’s look at what the mathematical and empirical evidence has to show.

Now the gross extrapolation and speculation of the mutation and selection sorting/optimization process does not form the foundation for a scientific theory. It requires mathematical and empirical correlation. One of the common speculations that evolutionists make is that huge populations markedly accelerate evolution by the mutation and selection sorting/optimization process but Dr Schneider’s mathematical model shows otherwise. Why doesn’t doubling the population halve the generations for convergence? This is best explained by Myriad which he posted on the Evolutionisdead forum. Unfortunately the text has been deleted from the forum but I have a copy of Myriad’s explanation.

In this particular instance, the probability of the mutation not occurring in an individual obeys the multiplicative rule over the members of the population. The probability that the mutation will not occur in any individual is the product of the probabilities that the mutation will not occur in each individual, because for the mutation to not occur in any individual the event "the mutation does not occur in this individual" must occur, independently, for every individual.

Get a bunch of fair six-sided dice each representing one individual. Say that any time a die rolls a 1, the specific mutation in question has occurred in that individual. The probability of the mutation not occurring for one die is 5/6. The probability of the mutation not occurring anywhere in a roll of four dice is (5/6)^4, or .482253, pretty close to .5.

It might appear correct to instead apply the additive rule to the complement events, like this: "The probability of a die rolling a 1 is 1/6. Therefore the probability of rolling at least one 1 in a roll of four dice is 1/6+1/6+1/6+1/6 = 2/3 (additive rule), and therefore the probability of not rolling any 1s in a roll of four dice is 1/3." But it's not. Try it. (One hint that that reasoning is incorrect is, suppose you're rolling 7 dice. Is the probability of rolling at least one 1 then 1/6+1/6+1/6+1/6+1/6+1/6+1/6 = 7/6? Having a probability come out less than zero or greater than one is a sure sign of incorrect application of the rules.) The additive rule only applies if the individual events are mutually exclusive -- and rolling a 1 on one die is not mutually exclusive with rolling a 1 on a different die.

An example of the correct use of the additive rule is: the probability of rolling any specific number on a die is 1/6. Therefore the probability of rolling a number that's 4 or less -- that is, rolling a 1, rolling a 2, rolling a 3, or rolling a 4 -- is 1/6+1/6+1/6+1/6 = 2/3. It works correctly in this case because on a single die, rolling a 1 is obviously mutually exclusive with rolling a 2, rolling a 3, etc.

This is exactly analogous to the miscalculation that leads to the wrong conclusion that the probability of not rolling any 1s in a roll of four dice equals 1/3. You're applying the additive rule to events that are independent rather than mutually exclusive.

What Myriad has shown is that the probability that a particular mutation occurring at a particular locus does not obey the addition rule of probabilities. Doubling population does not double the probability that a particular mutation will occur at a particular locus. Continued doubling of population does increase the probability of a particular mutation occurring at a particular locus but that probability very quickly approaches a probability of one and then further increases in population have very little affect on increasing this probability. Dr Schneider’s computer simulation demonstrates this effect very nicely. This is why huge populations do not markedly accelerate evolution by the mutation and selection sorting/optimization process.

So, what does genome length, G, have on the function equation:

F(n,G,g,mr,nsp) = gfc

Where,

n = population size
G = genome length
g = number of sites
mr = mutation rate
nsp = number of selection pressures
gfc = generations for convergence.

Let’s look at a particular series. G is varied, mr=1 mutation per 16,384 bases per generation, g=16, nsp=3, n=64:
G|gfc to perfect creature
256 | 68,266
512 | 207,590
1024 | 213,611
2048 | 688,439
4096 | 340,048
8192 | 875,420
16384 | 6,894,433

My, my, doesn’t the generation for convergence go up quickly as you increase G. I wonder why it does this?

Let’s remind you evolutionists what Dr Schneider said about his simulation:
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/truman/

A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

There’s nothing like some empirical evidence to finish off a post. So here are some more citations which show how the mutation and selection sorting/optimization process actually works.
http://www.medscape.com/viewarticle/494361_3

There may be several reasons for the favored emergence of L74V after M184V during selection by abacavir: the extent of resistance conferred may be greater (hence selection favors it), the mutation may be more prevalent in quasispecies at baseline, or this mutation pair may have greater fitness than M184V plus K65R (or M184 plus Y115F). Coadministration of abacavir with a thymidine analogue prevents or dramatically reduces the frequency with which L74V, K65R, and Y115F are observed.[21]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract

The influence of combinations containing the blood schizontocides chloroquine (CQ) or mefloquine (MEF), together with the 8-aminoquinolines (8AQ) primaquine (PQ) or the new, long-acting compound, tafenoquine (TAF), on the rate of selection of resistance to the individual compounds was examined using the asexual, intra-erythrocytic stages in rodent malaria models.

and

It is concluded that, whereas use of an 8AQ alone carries a high risk of selecting resistance, combinations containing 8AQ may have a place in the protection of blood schizontocides that are to be deployed in endemic areas.

http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf

The hope is that combined drug therapies can be implemented more widely in affected areas. Like the AIDS “cocktail” that has transformed that illness from an automatic death sentence to something that can be aggressively managed, at least in industrialized countries, the new malaria combination therapies are believed to be more effective at delaying the emergence of resistance when compared to single drugs used as stand-alone treatments, which are rapidly losing their effectiveness.

http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html

Mixtures or sequences of herbicides with differing modes of action are important especially to prevent or overcome resistance based on target site differences. To be effective the herbicides used in mixtures or sequences must have similar efficacy against the target weed. If the resistance is based on enhanced metabolism, this technique may also be useful, as the metabolic processes may be specific to certain types of molecule, but an empirical approach is needed to determine the best herbicide combinations.

These citations show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. We’ll continue with the mathematical study of Dr Schneider’s ev simulation of random point mutation and natural selection and show that his mathematical model shows the same thing and that the theory of evolution is mathematically and empirically impossible.

Now why don’t you evolutionists post all your fossil Rorschach tests and prove that the mathematical and empirical evidence of the mutation and selection sorting/optimization process is wrong. Let’s see what kind of weird stories you can cook up such as blizzards turning lizards into buzzards with gizzards. In the meantime, know that your irrational and illogical misconceptions of the mutation and selection sorting/optimization process is contributing to the premature death of millions of people with diseases subject to the principles of mutation and selection.

 

[kjkent1]

These citations show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.

No, the citations show that if you build a dam in a river, the water will back up behind the dam. Eventually the water will either overflow or the river will dry up -- one or the other. But, it's a nice strawman that you create for any creationist who wants to know why "God did it."

We’ll continue with the mathematical study of Dr Schneider’s ev simulation of random point mutation and natural selection and show that his mathematical model shows the same thing and that the theory of evolution is mathematically and empirically impossible.

All Schneider's program shows is that information gain from a random start is possible. Up until ev was created, the contrary position was a linchpin of creationist dogma. Schneider falsified that position. Now, kleinman takes this out of context and attempts to construct Hoover Dam. Quite a spectacle when you first see it. But, if you work there for a couple of years, it gets pretty dull.

Now why don’t you evolutionists post all your fossil Rorschach tests and prove that the mathematical and empirical evidence of the mutation and selection sorting/optimization process is wrong.

Pretty arrogant of you to contend that the fossil and geological record, which has been so exquisitely and carefully investigated, is nothing but an inkblot test. Also, pretty boring.

Let’s see what kind of weird stories you can cook up such as blizzards turning lizards into buzzards with gizzards. In the meantime, know that your irrational and illogical misconceptions of the mutation and selection sorting/optimization process is contributing to the premature death of millions of people with diseases subject to the principles of mutation and selection.

Generalized ad hominems are the stuff of despots and dictators. Are you running for President?

 

[Mr. Scott]

Continued doubling of population does increase the probability of a particular mutation occurring at a particular locus but that probability very quickly approaches a probability of one and then further increases in population have very little affect on increasing this probability.

Kleinman, you seem to be again supplying arguments that refute your own thesis.

We are discussing extremely miniscule probabilities when we discuss whether or not evolution is "mathematically possible." You seem to be arguing that when the populations become very great, the probability of extremely unlikely events, like those needed for speciation, approaches one. This sounds to me like you are conceding that extremely improbable evolutionary events are inevitable in huge populations.

However, you seem to frame it like this:

Given that unlikely evolutionary events are nearly inevitable when populations are huge, when these populations are increased still further the probability is not significantly increased. Therefore, huge populations are of little benefit to the progress of evolution, and evolution is thereby refuted.

My counter-argument is that the less likely the evolutionary event, the more its odds are benefitted by enormous increases in already enormous populations. Therefore, the incredibly unlikely events needed for speciation are most helped by vast populations that happen to be of little benefit to more probable events.

My claim:
The lower the probability of a mutation, the more it benefits from collosal population size.

I await your refutation.

 

[X]

I have a quick question: Is this Kleinman fellow serious?

But I must admit, you have done an incredibly good job destroying the field of biology. So let’s see if we can reverse some of the massive damage you have done with your irrational and illogical speculations that have no place in the study of science.

Emphasis mine.
Anybody else find that line coming from a (presumed) creationist to be a tad ironic?

 

[Mr. Scott]

I have a quick question: Is this Kleinman fellow serious?

The quick answer is yes, he is completely serious. His modus operandi is that if science asserts anything that disagrees with his interpretation of the bible, the science is in error. He won't budge from that position.

Anybody else find that line coming from a (presumed) creationist to be a tad ironic?

Kleinman's ironyrama is endlessly amusing. Read Dr. Adequate's Kleinman FAQ list for some of Kleiman's best work from last year.

 

[X]

The quick answer is yes, he is completely serious. His modus operandi is that if science asserts anything that disagrees with his interpretation of the bible, the science is in error. He won't budge from that position.

Kleinman's ironyrama is endlessly amusing. Read Dr. Adequate's Kleinman FAQ list for some of Kleiman's best work from last year.

Thanks for the reply.
I didn't want to have to read nearly 8-thousand posts to figure out where the thread sits.

 

[kleinman]

Annoying Creationists

So here is the functional equation:

F(n,G,g,mr,nsp) = gfc

Where,

n = population size
G = genome length
g = number of sites
mr = mutation rate
nsp = number of selection pressures
gfc = generations for convergence.

Variations in population give a hyperboloid shape curve with extremely large generations for convergence with tiny populations and as population increases, the generations for convergence approaches an asymptote very rapidly.

Variations in g give little change in the generations for convergence, only oscillation around a constant value.

Variations in mutation rates gives a paraboloid curve with a maximum evolutionary rate at mutation rates much, much higher than seen in reality. For all practical purposes, the mutation rate affects generations for convergence in approximately linear fashion.

Variations in G appear to affect the generations for convergence in an exponential fashion in ev.

Now, some of you evolutionists are having a problem understanding what happens when populations become huge and why it doesn’t markedly accelerate the evolutionary process. With huge populations, the probability is virtually 1 and as such you will get a proper mutation at a particular locus but what happens if you need two mutations at two different loci in order to achieve a local optimum on the fitness landscape. If each mutation has a probability of 10^-6, then the probability of getting both mutations on one descendent is 10^-12. The greater the number of loci which must have beneficial mutations in order to evolve to the selection pressures the much, much less likely that any particular descendent will have all the needed beneficial mutations. You will have the mutations somewhere in the population but no single descendent will have all the needed mutations. This is why combination therapy works. In addition, when you have selection pressures that target multiple genes, the ability of the population to find a trajectory on the fitness landscape is confounded. Each selection condition is driving the population on its own particular trajectory interfering with any single selection pressure from achieving a local optimum for its selection pressure. Tomorrow I’ll post the data from ev which shows this. In the meantime, here are some more citations which show this fact empirically.

http://jac.oxfordjournals.org/cgi/content/full/49/6/925

In E. coli, fluoroquinolones, including ciprofloxacin, primarily inhibit DNA gyrase (GyrA) with topoisomerase IV (ParC) as a secondary target.19 Single-site mutations at codon 83 or 87 of the gyrA QRDR are sufficient to confer low-level ciprofloxacin resistance, whereas higher levels of resistance either require double (codons 83 and 87) mutations in gyrA, or gyrA mutations in combination with parC or marA mutations, the latter enhancing drug efflux via the AcrAB–TolC system and reducing influx by suppressing expression of the outer membrane protein OmpF.20,21 Thus, at low concentrations ciprofloxacin has a high endogenous resistance potential, but at higher selective concentrations there is a requirement to generate simultaneous mutations in two or more loci4 and the agent consequently displays low endogenous resistance potential.

http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF

Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations. The latter mutation has not been associated with famciclovir resistance.

And

HBV resistance to lamivudine monotherapy

is associated with a complex mixture of variants that limit the efficacy of second-line nucleoside-analogue therapy. First-line potent combination therapy may reduce the emergence of HBV drug resistance.

http://en.wikipedia.org/wiki/Antiretroviral_drug

Combinations of antiretrovirals create multiple obstacles to HIV replication to keep the number of offspring low and reduce the possibility of a superior mutation. If a mutation arises that conveys resistance to one of the drugs being taken, the other drugs continue to suppress reproduction of that mutation. With rare exceptions, no individual antiretroviral drug has been demonstrated to suppress an HIV infection for long; these agents must be taken in combinations in order to have a lasting effect. As a result the standard of care is to use combinations of antiretroviral drugs. Combinations usually comprise two nucleoside-analogue RTIs and one non-nucleoside-analogue RTI or protease inhibitor.[2]

http://www.ajtmh.org/cgi/reprint/68/5/608.pdf

Based on the results of this study and with the objective of slowing the development of resistance, the Peruvian Ministry of Health has decided to revise its malaria treatment policy and recommend combination therapy with MQ-AS as the new first-line treatment of uncomplicated P. falciparum malaria in the Amazon region.

There are no selection pressures that cooperate to move a population on the fitness landscape. Selection pressures interfere with each other in the evolution of a population. This is a mathematical and empirical fact of life demonstrated by Dr Schneider’s ev program and these real examples of mutation and selection. Mutation and selection is nothing more than a sorting process which is profoundly slowed when you have more than a single selection pressure targeting a single gene. Edward Tatum understood this 50 years ago, David Ho rediscovered this 15 years ago and Dr Schneider’s computer model demonstrates this same fact. Now, teaching naïve school children that blizzards transforms lizards into buzzards with gizzards is training them to be ignorant of how the mutation and selection sorting/optimization process actually works. Of course you will continue to be contributing to the premature deaths of millions of people suffering from diseases subject to the mutation and selection phenomenon.

I guess none of you evolutionists who claim there are all these fossil Rorschach tests which prove your theory are going to post your evidence. Why don’t you post all your experimental evidence that chemicals cooperate to spontaneously form life? So much speculation and no evidence, we’ll continue to post the mathematical and empirical evidence that shows the theory of evolution only has a place on the SciFi channel.

 

[sol invictus]

So here is the functional equation:

F(n,G,g,mr,nsp) = gfc

This is such a totally meaningless equation... and the best part is, you're the only one reading this thread that doesn't know that.

Oh, the irony...

 

[delphi_ote]

1. Inorganic chemicals cooperate to form life spontaneously. Now this happened billions of years ago because chemicals no longer cooperate these days. Why can’t these chemicals just get along these days and form life spontaneously again? We must not have enough energy around anymore. This spokesman has neither mathematical nor empirical evidence for this speculation.

2. The weather long ago transformed reptiles into birds. Can we put this concept into mathematical terms? Of course we can:
Lizards + Blizzards = Buzzards + Gizzards

Those poor, poor strawmen. You attack them as soon as you create them. They barely have a chance to say, "Hello" to the world around them before you start tearing them down.

Really, kleinman. We're the ones you want. Leave your defenseless creations out of this!

 

[joobz]

Those poor, poor strawmen. You attack them as soon as you create them. They barely have a chance to say, "Hello" to the world around them before you start tearing them down.

Really, kleinman. We're the ones you want. Leave your defenseless creations out of this!

I think he used the three days to train with Edge (see sig).

Current kleinman status: repeating discounted arguments. Nothing to see here.

 

[delphi_ote]

I think he used the three days to train with Edge (see sig).

Current kleinman status: repeating discounted arguments. Nothing to see here.

This is a serious issue, dammit!

Straw men have constantly been subject to torture and abuse in this thread, and it just needs to stop. Enough is enough. This cruelty will not stand!

 

[kjkent1]

With huge populations, the probability is virtually 1 and as such you will get a proper mutation at a particular locus but what happens if you need two mutations at two different loci in order to achieve a local optimum on the fitness landscape. If each mutation has a probability of 10^-6, then the probability of getting both mutations on one descendent is 10^-12. The greater the number of loci which must have beneficial mutations in order to evolve to the selection pressures the much, much less likely that any particular descendent will have all the needed beneficial mutations. You will have the mutations somewhere in the population but no single descendent will have all the needed mutations. This is why combination therapy works. In addition, when you have selection pressures that target multiple genes, the ability of the population to find a trajectory on the fitness landscape is confounded. Each selection condition is driving the population on its own particular trajectory interfering with any single selection pressure from achieving a local optimum for its selection pressure.

Yawn...

What happens when the environment changes?

What happens when the genome changes size or composition via frame shift, addition, fusion, deletion, duplication, etc?

I wonder if any of that would mess with your fitness landscape or trajectories?

I wonder what happens when a creature with many competing fitness trajectories, nevertheless happens to be the most fit for the external environment?

I wonder if maybe that creature would simply be analyzed as subject to one selective pressure in aggregate, rather than many in competition?

Duh.

 

[Oroborus]

Pretty good strategy there. Straife the issues/rebuttlals, shotgun blast approach to data, spread enough of it and you're sure to kill em!

 

[Mr. Scott]

So here is the functional equation:

F(n,G,g,mr,nsp) = gfc

This is such a totally meaningless equation... and the best part is, you're the only one reading this thread that doesn't know that.

Oh, the irony...

Yes, not only is it meaningless, it leaves out at least one parameter that is clearly decisive.

For example, there is no place to parameterize the intensity of a selection pressure. An intense pressure, like an antibiotic used against a bacterial infection, would have a very high intensity, say 99% of the colony killed per generation. Other selection pressure may be affecting the colony simultaneously, of lesser intensity, each killing, for example, only 1% of the colony per generation.

Now, in triple therapy, all three pressures are ordinarily at near-extinction levels, so the population would be so severely reduced that the probability of mutations to resist these pressures becomes very low (Dr. Kleinman himself has made the point that it's in small populations that population size most affects the probability of adaptive mutation). This is why triple therapy works: the poulation is kept low enough to make the emergence of resistance profoundly unlikely. The affect of intensities of multiple therapies could be tested easily by subjecting bacterial colonies to multiple but very faint selection pressures to see if triple resistance emerges faster than in colonies where the same pressures are applied intensely enough to reduce the populations near extinction.

The other factor not in Dr. Kleinman's formula is variable intensity and presence of selection pressures. I recall that when I once had a bacterial infection, I was advised to continue taking a single antibiotic for two weeks after symptoms disappeared. If I stopped taking the med right after symptoms subsided, or missed doses, there was a significant chance that the infection would not only return, but return with resistance to the med. (The monotherapy worked very well, thank you.)

It's perfectly obvious that this phenomenon must occur frequently in nature. For example, a colony of plants may lack resistance to sub-freezing temperatures. During a cold snap, 99% of the population may be killed, the other 1% surviving because of local variations in temperature. Between cold snaps, the colony recovers, reaching populations again large enough to allow a mutation that endows plants with resistance. Each time such a mutation occurs, even if offering only a very slight advantage, more plants with that mutation will survive, and the colony can develop, in time, robust resistance through a succession of accumulative mutations.

So, both intensity and regularity of selection pressures profoundly affect the probability of macro-evolution. However, Dr. Kleinman's formula does not include this critical factor.

I await Dr. Kleinman's detailed, specific, non-evasive rebuttal.

 

[kleinman]

Annoying Creationists

I think it worthwhile to explain in more detail why huge populations have only a small effect on the rate of evolution when compared to the number of selection pressures. The following example concerns the evolution of resistance to Beta-lactam drugs (Penicillin class antibiotics).

“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”
Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111

Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable.

In this case, only 5 point mutations are needed to confer high resistance but not only do these 5 point mutations need to occur at the proper loci, they must occur in a sequence in which each mutation gives greater fitness to that member of the population. Considering that Penicillin was initially mass produced in 1943 and Penicillin resistant Staphylococcus aureus appeared in 1947 and Methicillin resistance appeared in 1961, how quick is the mutation and selection sorting/optimization process? What is the population of Staphylococcus aureus? 10^15? 10^20? And what is the generation time for Staphylococcus aureus? 20 minutes under ideal circumstances, how many generations do you think you will get in 4 years? This huge population and thousands of generations, perhaps tens of thousands of generations to evolve 5 loci, then you evolutionists make the irrational and illogical extrapolation that millions of loci can evolve in tiny populations in a small number of generations. You can’t even describe the selection pressures that would do this. So how does the mutation and selection sorting/optimization process actually work? The sorting process works well with single selection pressures targeting single genes. Here is how Dr Schneider’s model reveals this.

This data was generated based on a G=16,384, all other parameters were left at the base line values Dr Schneider used in his published case. The generations required to satisfy all three selection conditions simultaneously was 6,894,433 generations. Now if you take this case and remove any two of the three selection conditions, you get the following data.

missed site | spurious binding within gene | spurious binding outside gene
1 | 223 | 223
In order to satisfy all three selection conditions simultaneously it takes almost 7 million generations while satisfying any single selection condition takes at most 223 generations.

If you look at the case where G=32,768, you get the following data.
missed site | spurious binding within gene | spurious binding outside gene
1 | 115 | 403

If you look at the case where G=65,536, you get the following data.
missed site | spurious binding within gene | spurious binding outside gene
1 | 788 | 1026

You evolutionists can run these last two cases with all three selection conditions enabled and you will understand why Dr Schneider said this:

http://www-lmmb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html :

If you had a reasonable sized genome would you find that there won't be an information gain? No. Don't be lazy, go try it yourself! But notice that it will take a lot more computation, and the runs may take some years unless you write a version that uses parallel processors.

The more complex your selection conditions, the much, much slower the mutation and selection sorting/optimization process becomes. But let’s not just take Dr Schneider’s mathematical model as proof of this, let’s look at a few more empirical examples of the mutation and selection sorting/optimization process.

http://faculty.ucr.edu/~walton/bacteria.htm

Two Bacillus are currently used for mosquito control in California; however, because Bacillus thuringiensis subsp. israelensis (Bti) is comparatively less effective against mosquitoes inhabiting the organically enriched waters of treatment wetlands, Bacillus sphaericus currently offers a viable alternative for microbial control of mosquitoes in organically-enriched treatment wetlands (Walton et al. 1998). Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae. Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309). In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602

The effective treatment of HCV infection will likely require multiple antiviral drugs with different resistance profiles to delay the emergence of resistance, as has been shown in human immunodeficiency virus (35). In the present study, treatment with either a thumb or a palm inhibitor alone rendered large numbers of resistant replicon colonies in vitro, a potential indication of the likely rapid emergence of HCV-resistant variants upon initiation of monotherapy. Importantly, by combining two inhibitors binding to the thumb and to the palm sites of the HCV polymerase we observed a greater-than-additive inhibitory effect of replicon RNA replication.

http://www.ajtmh.org/cgi/content/full/72/2/163

The goal of combination therapy (CT) is to delay the emergence and spread of drug resistance. The strategy is supported empirically by the success of CT in treating tuberculosis and human immunodeficiency virus infections, and by mathematical models.1 The rationale for CT is simple. If two drugs have independent mechanisms of action, mutations that confer resistance to each drug will only rarely co-exist in the same parasite. By this logic, drug combinations should both improve treatment cure rate, and delay the emergence of drug resistance.2

http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml .

It is very essential to address resistance problem in diamondback moth. In most instances, development of resistance is directly related to the intense selective pressure due to excessive use of a specific insecticide. This selection pressure will be reduced by rotating insecticides of various classes in the management program of diamondback moth.

and

Frequent use of any insecticides for controlling beet armyworm will be reduced by rotating multiple insecticides in the proposed management program. Bt based insecticides will be applied to control early development stages of beet armyworm. Conventional chemical insecticides will be applied to control late stage larvae after every two applications of Bt based insecticides. This practice will significantly delay development of resistance in beet armyworms against any insecticides.

http://ipm.ncsu.edu/apple/chptr4.html .

To avoid development of resistance to the DMI fungicides, apply these fungicides only in combination with a broad spectrum, protectant fungicide such as captan or the EBDC fungicides (metiram or mancozeb).

Now I know you evolutionists believe that blizzards transform lizards into buzzards with gizzards and that is the perfect formula for causing the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. This is why you evolutionists are useless for teaching or understanding how the mutation and selection sorting/optimization process actually works. You are stuck in your science fiction world. Oh yes, if you think that intensity of selection pressures makes a big difference in the mathematics of the mutation and selection sorting/optimization process, prove it, it is your dumb theory. Wait a minute that means you evolutionists would have to do some mathematics.

 

[Mister Earl]

I like how obvious it is that Kleinman will mention selection pressures, but goes so far out of his way to ignore that they change in number and very in strength. His whole theory falls to pieces the second this is taken into consideration. As far as his post above goes, it's more of the same thing he's been saying for months. More telling is what he isn't saying.

 

[kleinman]

Annoying Creationists

I like how evolutionists like to speculate that changing the number and intensities of selection pressures is how blizzards transform lizards into buzzards with gizzards. You are overwhelming me with all your zero of your citations and all zero of your mathematics. On the other hand, I have poor Dr Schneider’s peer reviewed and published mathematical model which has now been discredited by evolutionists from all alternative universes and my few measly hundreds of citations which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.
http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm

Mix or alternate fungicides with different modes of action.

and

Triazole fungicides should be used in mixtures with non cross-resistant partner fungicides in order to reduce the risk of resistance developing in the target pathogens.

http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf

Repeat herbicide applications with the same site of action to the same or different crops.

and

Herbicides used without other weed control options (e.g. cultivation) and are considered "stand alone" weed control programs.

http://www.niaid.nih.gov/factsheets/treat-hiv.htm .

As HIV reproduces itself, different strains of the virus emerge, some that are resistant to antiretroviral drugs. Therefore, doctors recommend patients infected with HIV take a combination of antiretroviral drugs known as HAART. This strategy, which typically combines drugs from at least two different classes of antiretroviral drugs, has been shown to effectively suppress the virus when used properly. Developed by NIAID-supported researchers, HAART has revolutionalized how we treat people infected with HIV by successfully suppressing the virus and decreasing the rate of opportunistic infections.

Perhaps you evolutionists should post your Rorschach fossil data? Or perhaps you should post your stick model data? Or perhaps you found out that your stick model becomes very slow when you use 3 billion sticks?

 

[Mr. Scott]

Or perhaps you should post your stick model data? Or perhaps you found out that your stick model becomes very slow when you use 3 billion sticks?

What is this "stick model" you are referring to?