Annoying creationists

[kleinman]

Annoying Creationists

When you question the intelligence or honesty of the opposing side, it is an inherently hostile and illogical argument. The only possible logical response to that is to say: "What you say about me may be true, but you have not addressed the merits of my argument."

Why don’t you do a simple count of how many times the word liar (or forms of the word) has been used in this thread and who has used it and report that result back to us.

I firmly believe that science can and will explain everything. If evolution is disproven, it will be disproven through scientific evidence such as you present. It will be highly interesting to me, but not salient to the question of God.

Really, science will explain everything? Science has come up with the theory of evolution by mutation and selection but the basic premise of the theory does not obey simple bookkeeping rules.

If evolution is disproven, it will be disproven through scientific evidence such as you present.

Here is where you are slightly mistaken. Kleinman has yet to offer anything that remotely approaches a notion that could even begin to be considered an inkling of a scientific argument.

I refer you to the kleinman FAQ, to his moving of goalposts, and to his overall lack of intellectual honesty.

Tojohndillionesq, when you do your count for the word liar, don’t forget to include terminology like “lack of intellectual honesty”. What I would say about joobz is that he is either ignorant or in denial of the mathematics of mutation and natural selection and the numerous real examples of this mathematics that I have presented.

 

[joobz]

Why don’t you do a simple count of how many times the word liar (or forms of the word) has been used in this thread and who has used it and report that result back to us.

Really, science will explain everything? Science has come up with the theory of evolution by mutation and selection but the basic premise of the theory does not obey simple bookkeeping rules.

Tojohndillionesq, when you do your count for the word liar, don’t forget to include terminology like “lack of intellectual honesty”. What I would say about joobz is that he is either ignorant or in denial of the mathematics of mutation and natural selection and the numerous real examples of this mathematics that I have presented.

If you don't want to be called a liar, then don't lie.

 

[Dr Adequate]

When you question the intelligence or honesty of the opposing side, it is an inherently hostile and illogical argument.

There is nothing "illogical" about pointing out that a stupid liar is a stupid liar.

As for "hostile", yes, certainly. I am hostile towards stupid liars.

The only possible logical response to that is to say: "What you say about me may be true, but you have not addressed the merits of my argument."

But if kleinman said that it would not be true. We've made mincemeat of his "argument", such as it was. And much of his "argument" consists of telling stupid lies, a fact hard to convey without at least hinting that he's a stupid liar.

 

[kleinman]

Annoying Creationists

Here are some more references that show that multiple selection pressures slow the evolution of resistance to those selection pressures.

The first example is from a paper on the treatment of Malaria that can be located at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1796884

The half-lives of the single drugs amodiaquine (7–21 days[18]) and mefloquine (14–21 days[19]) are in the range of the sensitivity analysis shown in Figure 2d, which shows their expected results are similar to those of sulfadoxine-pyrimethamine (bearing in mind the assumption that the same drug is used for IPT as for non-IPT therapy). However, when mutations in multiple unlinked genes are needed for resistance, breakdown of their association by recombination will undermine the impact of selection on the spread of resistance.

The following is another reference to combination therapy for HIV located at: 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]

The following is from a paper that addresses drug therapy for malaria in rodents and multiple selection pressures and is located at: 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.

Here is another paper that reference malaria treatment in humans and is located at: 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.

Here is another article that addresses combination selection pressures and the evolution of resistance in weeds and is located at: 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.

The following is a reference which discusses multiple selection pressures exhibited by a single drug on e coli. This article is interesting because it shows an example of a single selection pressure which when intensified acts like multiple selection pressures. This article is located at 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.

Multiple selection pressures slow evolution. This is what ev shows, this is what the Wikipedia reference to fitness landscape shows and this is what these real examples show. Do you evolutionists have any mathematical model or real examples that contradict this hypothesis? Otherwise, the evidence continues to pile up that the theory of evolution is mathematically impossible.

 

[joobz]

You understand that your plastic definition of SLOW and MULTIPLE are trite. All the references that you present say is that EVEN WITH multiple selection pressures, EVOLUTION STILL HAPPENS. ADAPTATION STILL HAPPENS. Please show more data of this kind, It just proves this point. And all of this in a timescale observable for a lab experiment.

You need to show that evolution will STOP with multiple selection pressures, and YOU need to show that this is the case for millions of years.

Sorry Kleinman, I know you thought you'd get away with bending definitions between slow and stop and few to multiple (which you still seem to not want to assign a real number to).


But again, thank you for presenting work that supports reality.

 

[Paul C. Anagnostopoulos]

Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies. This is a very active and precise process. Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures? Do you have any examples where this type of recombination occurs in the reproductive process? Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

Yes, those are the questions I asked you. Could you answer them?

~~ Paul

 

[Paul C. Anagnostopoulos]

Let's see what we can find ...

Recombinant allele composed of gene and pseudogene:

http://www.springerlink.com/content/2gqnd5bcgwaw0tqf/

Complex alleles from unequal crossover:

http://www.clinchem.org/cgi/content/full/51/11/2167


and, oh my, Gaucher disease:

http://www.journals.uchicago.edu/AJHG/journal/issues/v72n3/024533/024533.web.pdf

Oh look, and Fabry disease, too:

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=2539398&query_hl=9&itool=pubmed_DocSum

And:

http://www.ncbi.nlm.nih.gov/entrez/...t_uids=3195594&query_hl=9&itool=pubmed_DocSum

~~ Paul

 

[kleinman]

Annoying Creationists

You understand that your plastic definition of SLOW and MULTIPLE are trite. All the references that you present say is that EVEN WITH multiple selection pressures, EVOLUTION STILL HAPPENS. ADAPTATION STILL HAPPENS. Please show more data of this kind, It just proves this point. And all of this in a timescale observable for a lab experiment.

What’s the matter? All these examples are experiments that are done on observable timescales. They all demonstrate that single selection pressures evolve more rapidly than multiple selection pressures and that multiple selection pressures is the strategy to stop evolution of resistant strains of bacteria, parasites, pests, weeds, pests… If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage? So what is the selection pressure that evolves reptiles into birds or humans and chimpanzees from a primate precursor? You are still ignorant of or in denial of the mathematics of mutation and selection, perhaps both. You should study ev a little, you can get some education on this topic.

Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies. This is a very active and precise process. Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures? Do you have any examples where this type of recombination occurs in the reproductive process? Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

Yes, those are the questions I asked you. Could you answer them?

The recombination that occurs with production of antibodies occurs in somatic cells, not in gametes. If you think this is the mechanism which will counter the hypothesis that multiple selection pressures slow the evolutionary process, describe how this works explicitly and quote from your links to support your argument. The ultimate way of showing this would be to include this feature in ev and accelerate the profoundly slow acquisition of information on realistic length genomes. I do think that a mechanism of gene rearrangement that in half your links cause life threatening diseases doesn’t make for a very strong speculation for how the theory of evolution works, but if you can make a plausible explanation of how it works, I’m willing to listen.

 

[Dr Adequate]

Here are some more references that show that multiple selection pressures slow the evolution of resistance to those selection pressures.

The first example is from a paper on the treatment of Malaria that can be located at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1796884



The following is another reference to combination therapy for HIV located at: http://www.medscape.com/viewarticle/494361_3


The following is from a paper that addresses drug therapy for malaria in rodents and multiple selection pressures and is located at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract

and


Here is another paper that reference malaria treatment in humans and is located at: http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf

Here is another article that addresses combination selection pressures and the evolution of resistance in weeds and is located at: http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html

The following is a reference which discusses multiple selection pressures exhibited by a single drug on e coli. This article is interesting because it shows an example of a single selection pressure which when intensified acts like multiple selection pressures. This article is located at http://jac.oxfordjournals.org/cgi/content/full/49/6/925


Multiple selection pressures slow evolution. This is what ev shows, this is what the Wikipedia reference to fitness landscape shows and this is what these real examples show. Do you evolutionists have any mathematical model or real examples that contradict this hypothesis? Otherwise, the evidence continues to pile up that the theory of evolution is mathematically impossible.

So, you're still trying to prop up lies you can't justify by citing random paragraphs from articles you don't understand?

 

[kleinman]

Annoying Creationists

So, you're still trying to prop up lies you can't justify by citing random paragraphs from articles you don't understand?

Oh don’t be silly Adebz; it is random paragraphs and natural selection.

 

[Dr Adequate]

If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage?

Because reducing population size reduces the rate of evolution, as you've had explained to you half-a-dozen times, you stupid twat.

But "multiple selection pressures" in general do not "stop" evolution, what is why you can't quote a single one of these scientists saying so.

'Cos they're not retarded liars, you see.

 

[Dr Adequate]

Oh don’t be silly Adebz; it is random paragraphs and natural selection.

I suppose posting this gibberish was easier than finding an article which supports your lies in any way.

 

[joobz]

What’s the matter?

Your lies.

All these examples are experiments that are done on observable timescales.

yup

They all demonstrate that single selection pressures evolve more rapidly than multiple selection pressures and that multiple selection pressures is the strategy to stop evolution of resistant strains of bacteria, parasites, pests, weeds, pests…

No, they don't show this. They show simply that the can reduce the likelyhood of adaptation, this doesn't mean stop. I know in your head, you think it does, but that has no bearing on reality.

If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage?

Because they try to stave off resistance. Is that a hard concept to understand for you?

So what is the selection pressure that evolves reptiles into birds or humans and chimpanzees from a primate precursor?

You honestly think this is a valid argument? What's the exact mechanism of gravity?
We know it happened, the how is still not known (as far as I understand).
http://www.talkorigins.org/faqs/comdesc/section1.html#morphological_intermediates_ex1

You are still ignorant of or in denial of the mathematics of mutation and selection, perhaps both. You should study ev a little, you can get some education on this topic.

Yawn.

 

[kleinman]

Annoying Creationists

If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage?

Because they try to stave off resistance. Is that a hard concept to understand for you?

Of course it is not hard for me to understand, it is the entire premise of my argument. Multiple selection pressures stave off the ability of creatures to evolve resistance to those selection pressures. Understand rubberband?

 

[joobz]

Of course it is not hard for me to understand, it is the entire premise of my argument. Multiple selection pressures stave off the ability of creatures to evolve resistance to those selection pressures. Understand rubberband?

Oh thank you for the rubberband comment. I thought I had already addressed this point.

You understand that your plastic definition of SLOW and MULTIPLE are trite. All the references that you present say is that EVEN WITH multiple selection pressures, EVOLUTION STILL HAPPENS. ADAPTATION STILL HAPPENS. Please show more data of this kind, It just proves this point. And all of this in a timescale observable for a lab experiment.

You need to show that evolution will STOP with multiple selection pressures, and YOU need to show that this is the case for millions of years.

Sorry Kleinman, I know you thought you'd get away with bending definitions between slow and stop and few to multiple (which you still seem to not want to assign a real number to).


But again, thank you for presenting work that supports reality.

Yup, still true. YOU need to SHOW how evolution is STOPPED. you haven't done that.

 

[kleinman]

Annoying Creationists

Yup, still true. YOU need to SHOW how evolution is STOPPED. you haven't done that.

I don’t have to show that evolution is stopped; I only have to show that it is slowed down sufficiently that it is mathematically impossible to occur in the time available. You know that Paul said this and I agree with him:

You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.

Look what two or three selection pressures do to the evolution of viruses and bacteria. What do you think will happen with millions of selection pressures on much more complex creatures? If you studied ev a little, you would have some idea of the answer to this question. The mathematics of mutation and selection shows something completely different than what evolutionists allege.

 

[Taffer]

Is that an admission that recombination alone does not and can not create new genes? We are talking about mathematical precision in this discussion of mutation and selection, not the sloppy speculations that you evolutionists use to explain your theory.

Once you accept this point, then we can go on to your next misunderstanding of recombination and natural selection. That is that recombination and natural selection can cause the loss of alleles from the gene pool and thus the loss of information from the gene pool.

No, kleinman, stop your strawmen. It is possible for recombination to create new genes. But I never claimed that it does regularly, nor did I even use that as a part of my argument. I have given you a mathematical model for selection, and you said it was "recombination and selection", which is utter rubbish. Recombination creates variation. Mutations create variation. Reproduction creates variation. Gene flow creates variation. Selection only acts on variation, and it matters not how this variation arose.

So stop blathering on about "recombination and selection", and address my posts.

 

[Taffer]

You can have errors in the recombination process that can make new sequences of bases.

Yes. And you can also have recombination occuring inside of genes. It does not occur at specific locations, you realise.

Are you proposing this as the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

There are no deficiencies, only misconceptions on your part. Recombination creates variation. Mutation creates variation. Reproduction creates variation. Gene flow creates variation. Selection acts on this variation in the same way no matter whence that variation arose.

Ev only includes a single form of variation, which is why it does not model the entire phenomenon of evolution by natural selection.

 

[joobz]

I don’t have to show that evolution is stopped; I only have to show that it is slowed down sufficiently that it is mathematically impossible to occur in the time available.

And you are wrong. but what's new.

You know that Paul said this and I agree with him:

You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.

Look what two or three selection pressures do to the evolution of viruses and bacteria. What do you think will happen with millions of selection pressures on much more complex creatures? If you studied ev a little, you would have some idea of the answer to this question. The mathematics of mutation and selection shows something completely different than what evolutionists allege.

And Paul was making fun of you when he said that, unfortunately you were too foolish to realize. Let's see if I can explain this SLOWLY.
You have those MILLONS of selection pressures ALL THE TIME. Yet we still see adaptation.

 

[Taffer]

Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies.

This is a completely different type of recombination then that which happenes during meiosis.

This is a very active and precise process.

No, it isn't.

Somatic recombination, also known as V(D)J recombination, of immunoglobulins involves the random selection and combination of genes encoding each segment of the immunoglobulin variable region in a manner that generates a huge repertoire of antibodies with different paratopes.

Emphasis mine. Source.

Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures?

Recombination which occurs during meiosis is a completely different mechanism.

Do you have any examples where this type of recombination occurs in the reproductive process?

No, because it is a completely different mechanism.

Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

No, because it happens in somatic cells, and thus is not passed on to the next generation. I'm beginning to think you really don't know what recombination is.

Meiotic recombination can, and does, happen inside a gene. Not that it even matters. Your whole argument is pointless, because recombination creates variation, and it is variation which selection acts upon.