Annoying creationists

[joobz]

I don't think its quite fair that only Kleinman is getting censored.

I have been calling him a f---ing moron, or something along those lines, for awhile now, and none of my posts get cut.

If we are going to start enforcing the "attack the argument not the one making it" rule we should enforce it across the board. Just my opinion.

Kleinman is an idiot but that doesn't mean he should be treated unfairly.

actually, others have been censored and kept in check.
There hasn't been any bias by any mod.


Check the context of the exchange:
1. Kleinman makes argument claiming evolutionists are responsible for millions of AIDS deaths.
2. Dr.A challenges this argument by stating if this is true, why do you waste time in the forum instead of saving millions.
3. Kleinman refuses to respond
4. Dr. A asks again
5. Kleinman rebuffs by asking Dr.A's reasons for posting
6. Dr. A answers and asks his question again.
7. Kleinman responds with a direct insult with still no answer to the question.
8. Dr. A ignores this and reasks the question.

 

[Mr. Scott]

we can talk about endogenous retroviruses. Let’s start with you explaining to us what the selection pressures these viruses cause and the target genes for these selection pressures.

Sorry, Alan, that's changing the subject again. You claimed that the endogenous retrovirus evidence that humans and chimps are related was misinterpreted. Please explain, specifically, precisely how. Elaborate. Why is evolutionist's interpretation incorrect? What is the correct interpretation?

 

[rocketdodger]

Hmmm...

If you are saying that using improper debate tactics plays a part in being censored, then I agree. So if I insult someone as part of an informative reply, its OK, but if its part of a nonsense post, its not? I kind of like that system, actually... its more along the lines of a real life debate moderator.

 

[Belz...]

Allright, then. Dodger, I think the colour of your lightsaber is stupid.

There. Censor me.

 

[joobz]

Hmmm...

If you are saying that using improper debate tactics plays a part in being censored, then I agree. So if I insult someone as part of an informative reply, its OK, but if its part of a nonsense post, its not? I kind of like that system, actually... its more along the lines of a real life debate moderator.

Partly, yes. It's ok to insult the argument, but not the arguer.

So to say,
"Good job! that's the stupidest thing I have ever read."-would be ok.
But to say,
"Good job! You are now the stupidest thing alive."-not ok.


His insult was entirely meant to provoke and avoid the debate. It had nothing to do with the argument at all. Much like most of Kleinman's pet names for everyone.

 

[Foster Zygote]

Allright, then. Dodger, I think the colour of your lightsaber is stupid.

There. Censor me.

But it's a Hooloovoo.

 

[Paul C. Anagnostopoulos]

Strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman, strawman!!!!

And don't forget strawman!

~~ Paul

 

[Myriad]

Could I have mine with strawman instead of the baked beans?

Respectfully,
Myriad

 

[kleinman]

Annoying Creationists

If what you claim is true, you do have the choice.

If what he claimed were true, he would be able to provide us with the state he is certified as both an engineer and doctor, so we can look him up and make sure he is who he says he is. Of course, he refuses, so...

The information is on the thread, others have been able to verify this. Anyway, what difference does that make? You can read the citations that show that combination selection pressures profoundly slow evolution and you can run Dr Schneider’s ev program which shows the same thing. It doesn’t matter what my credentials are, it doesn’t change the mathematical and empirical fact of how mutation and selection actually works.

Evolution is not deterministic, Alan. Two trials of an experiment using identical selection pressures will not necessarily produce the same evolutionary outcome,..

Uh oh, expect droves of Disagreeers/Hecklers. Well, that's what I always get anyway when I state the obvious.

Hang on a mo. You're not seriously suggesting that our disagreement with your sig line has been one of deterministic vs. random, are you? No one has ever suggested that evolution is deterministic.

Paul, I think there is evidence that evolution by mutation and selection is deterministic. Once a selection condition is specified, there are only a limited number of genetic sequences that can satisfy that selection condition. It is this result that forms the basis of genetic sequencing of viruses, etc. for resistance to particular drugs. In addition, ev always converges on the same value when a given set of input parameters are specified. Once a fitness landscape is defined, the trajectory to the next local optimum is defined.

Hey, I saw that movie. I wonder what will replace us when they make the next “meteor hits” movie.

You have no interest in an honest debate.

You ask for an example. I provide such an example, and you act like a child. How fitting for a theist.

This debate ended long ago once it was clear that combination selection pressures profoundly slow the evolutionary process. This is clear both mathematically and empirically. I just keep posting real examples of combination selection pressures profoundly slowing evolution like a meteor shower falling on the heads of you evolutionists.

I don't think its quite fair that only Kleinman is getting censored.

I have been calling him a f---ing moron, or something along those lines, for awhile now, and none of my posts get cut.

If we are going to start enforcing the "attack the argument not the one making it" rule we should enforce it across the board. Just my opinion.

Kleinman is an idiot but that doesn't mean he should be treated unfairly.

How touching! Now rocketdodger, if I am an idiot for believing that combination selection pressures profoundly slow evolution and have a peer reviewed and published computer simulation of the process which shows this and hundreds of empirical examples which show the same thing and you have a computer program which you spent 4 hours writing which has random selection pressures (whatever that is) where you claim n+1 selection pressures evolve faster than n selection pressures and zero empirical examples of your computer program, it makes an interesting contrast.

Now I want you to rest easy, I have put up with you whining thin skinned cry baby evolutionists for over a year now. Nothing got censured in my last post. I think that there is just too much hard edged truth for evolutionists like Adequate when I suggest that evolutionist doctrine has slowed the understanding of how mutation and selection actually works and has led to inappropriate use of monotherapy for treatment of rapidly evolving systems which in turn has led to premature deaths of many people and complicating the therapy for diseases like HIV.

we can talk about endogenous retroviruses. Let’s start with you explaining to us what the selection pressures these viruses cause and the target genes for these selection pressures.

Sorry, Alan, that's changing the subject again. You claimed that the endogenous retrovirus evidence that humans and chimps are related was misinterpreted. Please explain, specifically, precisely how. Elaborate. Why is evolutionist's interpretation incorrect? What is the correct interpretation?

I tell you what Mr Scott, once we finish hammering in the nail about combination selection pressures profoundly slowing evolution, we’ll address your question. Except for one thing, you have to tell us why you think of your parents as liars. You really need to get this off your chest.

Could I have mine with strawman instead of the baked beans?

Hey Myriad, do you recall that thread you started a while back on the Evolutionisdead Forum on complex behavior? What I find interesting is that once you realize that evolution by mutation and selection is simply a sorting/optimization problem, it is much easier to understand the complex behavior of such systems. You were going to try to accelerate the evolutionary process in ev by introducing noise into the weight matrix. You might be able to get ev to converge to a different local optimum by doing this if the noise were sufficient to get the population to traverse a trough on the fitness landscape. The only problem with the concept is there is no analog in reality.

Now Myriad, here is how an Ecologist at an Arizona University describes how this sorting/optimization process works:
http://72.14.253.104/search?q=cache:ZJ8EaeJZZEMJ:www.eebweb.arizona.edu/Courses/Ecol409_509/2006_lectures/lecture18.ppt+mutation+selection+evolution+%E2%80%9Ccombination+therapy%E2%80%9D+resistance&hl=en&ct=clnk&cd=399&gl=us

Natural selection quickly breeds for resistance to AZT

What was needed was a way to increase the number of mutations that must arise in a virion’s genome to render it resistant to the drug

The key breakthrough was to use combination therapy, cocktails of multiple drugs acting together which are not only very effective, but which delay evolution of resistance

And here is how the sorting/optimization process works with HBV.
http://jac.oxfordjournals.org/cgi/content/full/55/5/608

Owing to the persistence of hepatitis B virus (HBV) and the selection of drug-resistant mutants, a new concept of antiviral therapy for chronic hepatitis B relies on the combination of nucleoside analogues. In experimental models of HBV infection, several key points concerning these combinations were addressed. (i) Is it possible to achieve a synergic antiviral effect with polymerase inhibitors? (ii) Is it possible to impact on intracellular viral covalently closed circular DNA? (iii) What is the impact of the cross-resistance patterns of the different nucleoside analogues? (iv) What is the effect of viral load suppression on the restoration of specific antiviral cellular responses? The clinical impact of these key issues is discussed in the perspective of new clinical trials.

And

It is important to note that most of the nucleoside analogues administered in monotherapy may select for drug-resistant mutants, as this was shown with HIV.23 The profile of cross-resistance of these mutants has been studied in vitro after transfection of the mutants in hepatoma cell lines and the study of their susceptibility to other drugs.2 It was shown that lamivudine and emtricitabine share the same cross-resistance profile with the selection of the M204V or M204I polymerase mutants that are susceptible to adefovir. To date, telbivudine is associated with the emergence of the M204I mutant, which is resistant to lamivudine and emtricitabine. Adefovir selects for the A181V and N236T mutants, which are susceptible to lamivudine. Entecavir is less active against lamivudine-resistant strains and selects for specific resistance mutations on a genetic background of lamivudine resistance mutations. Clevudine is not active against the lamivudine-resistant strains and was shown to select for the same resistant mutants in woodchucks chronically infected with WHV.24 It also exhibits some antiviral activity against the adefovir-resistant strains in vitro. Elvucitabine is not active against the lamivudine-resistant mutants but is active against the adefovir-resistant strains. Tenofovir shows a good antiviral efficacy against the lamivudine-resistant strains and slightly decreased activity against the adefovir-resistant mutants. A tenofovir-resistant mutant was also recently described. Given the cross-resistance profile of these drugs, the rationale is to combine the drugs that would inhibit the emergence of drug-resistant strains to one or the other drug. This may lead to an improved management of antiviral therapy of chronic HBV infection in the long term.

And

The current understanding of chronic HBV infection and its treatment suggest that the patients who are more likely to seroconvert anti-HBeAg antibodies should first receive a course of pegylated interferon-.30 In this setting, pegylated interferon therapy may be the best option because of the possibility of short-term therapy and the absence of selection of resistant mutants. On the other hand, the majority of patients who are non-seroconverters or are infected with a pre-core mutant will require long-term maintenance therapy to control viral replication and liver disease. In this view, the development of clevudine and emtricitabine opens new avenues in the management of these patients. Clevudine, with its unusual antiviral activity profile, may be the first nucleoside analogue to be used as a relative short-term treatment and to achieve sustained control of viral replication even after treatment withdrawal. On the other hand, emtricitabine, as well as other drugs in development, offers a new option for combination of nucleoside analogues that do not share the same cross-resistance profile. For instance, it may be used in combination with adefovir or tenofovir. The evaluation of such combination strategies will need to rely on accurate endpoints and timing for such analysis.

And Myriad, that’s how Dr Schneider’s model behaves with his three selection conditions. It is the combination selection pressures which profoundly slow the evolutionary process. Any of you evolutionists have a real example which shows otherwise?

 

[rocketdodger]

Why should I even waste my time trying to refute your computer program?

You don't have to -- since I know you are a fraud, and that you know nothing about mathetmatics, I gave you a simple version of my algorithm that even a bible school kiddie can understand, which I will repeat right here:

1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

If you can provide one real example of your model then I’ll spend some time trying to understand your algorithm.

If it takes you time to understand the above algorithm, Kleinman, then you genuinely are a fraudulent moron. There is just no way someone could get a doctorate, even from the worst night school in Mexico, and not be able to easily grasp exactly what is done in the above algorithm. It is only four steps. Four simple, easy to understand, uncomplicated steps.

Can you show anyone here why the above algorithm is not a sorting/optimization algorithm?

NUMBER OF TIMES KLEINMAN HAS FAILED TO RESPOND TO THIS POST: 2

 

[kleinman]

Annoying Creationists

Why should I even waste my time trying to refute your computer program?

You don't have to -- since I know you are a fraud, and that you know nothing about mathetmatics, I gave you a simple version of my algorithm that even a bible school kiddie can understand, which I will repeat right here:

1) Randomly mutate x number of bases in each creature's genome.
2) Determine the fitness of each creature according to the pressures exerted on the population.
3) Reproduce, such that creatures with higher fitness have more offspring.
4) Go back to 1, stopping when the targeted mutations of all pressures have achieved 80% or more fixation in the population.

Ok rocketdodger, let’s reward your persistent whining and let’s talk about your algorithm. So you randomly mutate x number of bases in each creature’s genome, that’s ok. Then you determine the fitness of each creature according to the pressures exerted on the population. What are these so called random selection pressures? And how do you determine the fitness? Dr Schneider uses a weight matrix and depending on whether there are matches or not, he counts these as mistakes.

If you can provide one real example of your model then I’ll spend some time trying to understand your algorithm.

If it takes you time to understand the above algorithm, Kleinman, then you genuinely are a fraudulent moron. There is just no way someone could get a doctorate, even from the worst night school in Mexico, and not be able to easily grasp exactly what is done in the above algorithm. It is only four steps. Four simple, easy to understand, uncomplicated steps.

Can you show anyone here why the above algorithm is not a sorting/optimization algorithm?

NUMBER OF TIMES KLEINMAN HAS FAILED TO RESPOND TO THIS POST: 2

Aside from being a whining cry baby, do you also have to be a bigot? Have you been taking lessons from Adequate?

So quit whining and explain your algorithm before you cure everyone’s insomnia.

 

[sol invictus]

Ok rocketdodger, let’s reward your persistent whining and let’s talk about your algorithm. So you randomly mutate x number of bases in each creature’s genome, that’s ok. Then you determine the fitness of each creature according to the pressures exerted on the population. What are these so called random selection pressures? And how do you determine the fitness? Dr Schneider uses a weight matrix and depending on whether there are matches or not, he counts these as mistakes.

Why are you still posting on this subject? You recently admitted you don't understand probability.

In fact you even admitted that multiple selection pressures increase the rate of evolution, in the sense that the time required per pressure decreases as you increase the number of pressures (if you don't recall admitting that, I'm happy to quote the post where you did).

And now you're saying the opposite - so you're flipflopping yet again? Why post on a subject you don't understand? It only makes you look foolish.

I recommend you go away for a while and try to learn some math.

 

[rocketdodger]

Ok rocketdodger, let’s reward your persistent whining and let’s talk about your algorithm. So you randomly mutate x number of bases in each creature’s genome, that’s ok. Then you determine the fitness of each creature according to the pressures exerted on the population. What are these so called random selection pressures?

They are randomly generated at initialization and then they remain constant. Each of them has a target "base" in the "genome" and a desired match, undesired match, and two neutral match values. These are also choosen randomly at initialization as well.

The idea is that if an individual exhibits the desired match at that base, the pressure is satisfied. If it exhibits an undesired match, not only is the pressure still unsatisfied, but the organism f---ed up and will probably not be able to produce some important protein or what have you. If it exhibits a neutral match, the pressure is not satisfied but the organism still functions normally.

And how do you determine the fitness?

If an individual exhibits the desired value at a pressure's target base in the genome, a given amount is added to that individual's fitness score. If it exhibits the undesired value, a much higher amount is subtracted from it's fitness score. If it exhibits either of the two neutral values, nothing happens to its fitness score. This is repeated for every pressure and on every individual.

Dr Schneider uses a weight matrix and depending on whether there are matches or not, he counts these as mistakes.

Basically the same thing I do, except I only use 3 discrete values (bad, neutral, good) per match.

 

[kleinman]

Annoying Creationists

Ok rocketdodger, let’s reward your persistent whining and let’s talk about your algorithm. So you randomly mutate x number of bases in each creature’s genome, that’s ok. Then you determine the fitness of each creature according to the pressures exerted on the population. What are these so called random selection pressures?

They are randomly generated at initialization and then they remain constant. Each of them has a target "base" in the "genome" and a desired match, undesired match, and two neutral match values. These are also choosen randomly at initialization as well.

The idea is that if an individual exhibits the desired match at that base, the pressure is satisfied. If it exhibits an undesired match, not only is the pressure still unsatisfied, but the organism f---ed up and will probably not be able to produce some important protein or what have you. If it exhibits a neutral match, the pressure is not satisfied but the organism still functions normally.

So, each selection condition is for only a single locus in the genome. Are the genomes random sequences as well at initialization? And you are only testing for errors at those loci which have selection conditions? How do you account for the affect of mutations at other positions on the genome?

And how do you determine the fitness?

If an individual exhibits the desired value at a pressure's target base in the genome, a given amount is added to that individual's fitness score. If it exhibits the undesired value, a much higher amount is subtracted from it's fitness score. If it exhibits either of the two neutral values, nothing happens to its fitness score. This is repeated for every pressure and on every individual.

Ok, you are still sorting.

Dr Schneider uses a weight matrix and depending on whether there are matches or not, he counts these as mistakes.

Basically the same thing I do, except I only use 3 discrete values (bad, neutral, good) per match.

And that’s ok as well, it may not be realistic, but you are still doing a sort.

The big question I have for you is how you account for mutations on the non-selection loci. This was something that Paul had difficulty understanding for a while. If you set the mutation rate as fixed per number of bases rather than per genome, he couldn’t understand why the generations for convergence were going up so rapidly as you lengthened the genome in ev. What is happening is the mutations away from the binding site region were affecting the selection and slowing the evolutionary process (affecting the trajectory on the fitness landscape). The genome length is a strong parameter affecting convergence (but not as strong as the number of selection pressures). The genome length increases the search space for a local optimum by 4^G. If you are not considering the affect of mutations at non-selection sites, you are ignoring a very important condition. Dr Schneider took this affect into account by counting weight matrix matches in the non-binding site region as mistakes which affects the evolutionary process.

 

[Mr. Scott]

It is not my job to refute every misinterpretation that you evolutionists come up with.

But it is your job to back up claims you made, Alan. You claimed the endogenous retrovirus evidence of common ancestry between humans and chimps was "misinterpreted." Why do you believe this?

 

[delphi_ote]

What I am saying is that evolutionbymutationandselectiondidn’tdoit. The mathematical and empirical evidence shows what mutation and selection can do and it doesn’t do what you allege.

Okay. Let me ask one more time to make sure we're clear. You agree that the species we observe on earth all descended from a common ancestor over the course of millions of years? You disagree only on the mechanism?

 

[kleinman]

Annoying Creationists

It is not my job to refute every misinterpretation that you evolutionists come up with.

But it is your job to back up claims you made, Alan. You claimed the endogenous retrovirus evidence of common ancestry between humans and chimps was "misinterpreted." Why do you believe this?

Now that we know how mutation and selection actually works, that is combination selection pressures profoundly slow the evolutionary process (and this has been shown numerous times both mathematically and empirically). And mutation and selection is the foundation mechanism for the theory of evolution. Since the foundation mechanism can not accomplish what is required for the theory of evolution to be plausible, every interpretation that evolutionists make of the evidence is called into question. This not only includes endogenous retroviruses, fossil record and phylogenic trees but any evidence which is extrapolated, speculated or imagined to fit into the evolutionist belief system. The mathematics of mutation and selection and the vast amount of accurately measured examples of mutation and selection provide hard measurable and repeatable evidence that mutation and selection can not accomplish what is required for the theory of evolution to be true. If that is not enough, the theory of evolution requires abiogenesis which is nothing short of fanciful thinking when considering the complexity of the simplest life forms.

What I am saying is that evolutionbymutationandselectiondidn’tdoit. The mathematical and empirical evidence shows what mutation and selection can do and it doesn’t do what you allege.

Okay. Let me ask one more time to make sure we're clear. You agree that the species we observe on earth all descended from a common ancestor over the course of millions of years? You disagree only on the mechanism?

Delphi, the whole concept of common descent by mutation and selection is nonsense. There is no mechanism that can do what you evolutionists allege.

 

[Shalamar]

Delphi, the whole concept of common descent by mutation and selection is nonsense. There is no mechanism that can do what you evolutionists allege.[/FONT][/SIZE]

So then Kleinman, if you allege that common descent is 'nonsense', then please tell us how all the species on earth came to be as we see them today. And provide your proofs for this.

 

[rocketdodger]

The big question I have for you is how you account for mutations on the non-selection loci.

The genome length is a strong parameter affecting convergence (but not as strong as the number of selection pressures). The genome length increases the search space for a local optimum by 4^G.

If you are not considering the affect of mutations at non-selection sites, you are ignoring a very important condition. Dr Schneider took this affect into account by counting weight matrix matches in the non-binding site region as mistakes which affects the evolutionary process.

I started to respond seriously, Kleinman, but then I remembered what you will do when that happens. Thus, lets cut to the chase, shall we?

1) You agree that my algorithm is a sorting algorithm.
2) My algorithm always exhibits a higher rate of sorting under n + 1 conditions than n conditions, for some value of n != 0.
3) Therefore you agree that your claim of sorting/optimization algorithms always being confounded by additional sorting conditions is wrong.

 

[kleinman]

Annoying Creationists

Delphi, the whole concept of common descent by mutation and selection is nonsense. There is no mechanism that can do what you evolutionists allege.

So then Kleinman, if you allege that common descent is 'nonsense', then please tell us how all the species on earth came to be as we see them today. And provide your proofs for this.

Don’t you know what the name of this thread is Shalamar? Here is how the proof goes. There are only two possible ways we got here. We were either created or we came about by abiogenesis and evolution. Panspermia just puts the creation or abiogenesis to another location. If you can prove either of the two propositions to be impossible, the other proposition is true by process of elimination. Abiogenesis and the theory of evolution have been eliminated. Shalamar, you were created and you should seek to know your Creator.