Annoying creationists

[Dr Adequate]

I’m sure you’re capable of understanding that simple distinction. Now what Adequate and rocketdodger are alleging is the exact opposite, that the greater the number of optimization conditions, the faster the sort occurs.

I have not, of course, said that, which is why you cannot quote me saying that.

No problem Adequate ...

Well, there is in fact a kind of teensy-tiny problem, which is that you have not, in fact quoted me "alleging" that "the greater the number of optimization conditions, the faster the sort occurs."

In fact, you have just quoted me as saying that:

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

You even highlighted it in red, so that no-one could possibly miss out on the difference between what I actually claim, and what you claim I claim.

 

[Dr Adequate]

Let's help kleinman out by putting it in one post.

He can even link to it, if he ever learns to use the forum controls.

(1) With simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

(2) More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

 

[kleinman]

Annoying Creationists

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve more rapidly than n selection pressures ...

What a silly lie. I claim no such thing.

Not only did you say this, you admitted contradicted yourself when you then said that your silly graph shows that more optimization takes more time. Then when asked to present a real example of this, you finally admitted that you had no real examples of you irrational and illogical conclusion. Let’s remind the readers of what you said:

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And then Adequate goes on to say this:

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?

And

So far as I know, no-one has done the experiment.

and

and too bad you don’t have any empirical examples of your silly graph ...

As I have explained to you, I produced the model because I've not heard of this precise experiment being done.

If physicians and scientists listen to your irrational and illogical thinking, it would lead to increases in premature death of people suffering from diseases subject to the mutation and selection phenomenon. Fortunately they don’t as this following citation reveals.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1636340

The presence of large numbers of random mutations within tumors could limit the efficacy of targeted therapies. By the time a tumor is clinically detected it contains ≈10^9 cancer cells. The average frequency of random mutations in tumor samples we analyzed was 2.2 × 10^−6 per base pair. Thus, each cell would contain more than a thousand random mutations, and the entire tumor could harbor as many as 10^12 different single-nucleotide substitutions. Many of these mutations would alter the properties of the encoded proteins, including mutations that confer resistance to radio-, chemo-, and/or immunotherapy (36). Thus, increased genetic variability in newly diagnosed cancers could encompass a reservoir of mutations available for immediate clonal expansion upon initiation of treatment with any given agent, leading to rapid emergence of resistance. This concept provides a molecular basis for the observed clinical efficacy of combination therapy, because any single cell would be unlikely to contain mutations that confer resistance to agents with different mechanisms of cytotoxicity. It can be hypothesized that tumors with fewer random mutations should be treated more conservatively, whereas tumors with a higher frequency of random mutations should be treated more aggressively and with combination therapies. Thus, mutation frequency could provide a new index for stratification of tumors. One possibility is that mutation frequency will exhibit an overall positive association with tumor stage and grade, but that there will be significant variability within defined stages and grades. This variability, which may contribute to differences in within-group outcome, could help to guide therapy for individual patients.

Adequate, you don’t have a clue how mutation and selection actually works. Your posts reveal this. What is your PhD in, perpleximatics?

Now you evolutionist have a good weekend, my hope for you is that you not be subjected to n+1 selection pressures. I’ll be back next week to present more citations which show that combination selection pressures profoundly slow the evolutionary process.

 

[Dr Adequate]

Adequate, the only problem I have with what you have said here is determining which is dumber, your silly graph where you claim that n+1 selection pressures evolve ...

Just for yucks and giggles, let's see if we can locate the only person on the entire Internet who has ever, ever, ever said that "selection pressures evolve".

By googling on the phrase "selection pressures evolve".

Oh look, it appears to be a chap who calls himself "kleinman". He seems to use the phrase quite a lot.

This guy "kleinman" seems to have a really radical take on biology. Specifically, he keeps getting it wrong at a very basic level.

 

[Dr Adequate]

Not only did you say this, you admitted contradicted yourself ...

What a silly lie. I admitted no such thing, which is why you cannot quote any such admission.

 

[Dr Adequate]

If physicians and scientists listen to your irrational and illogical thinking, it would lead to increases in premature death of people suffering from diseases subject to the mutation and selection phenomenon. Fortunately they don’t as this following citation reveals.

What a silly lie. We all know that combination therapy is effective and have explained to you why this is so.

 

[Dr Adequate]

Let’s remind the readers of what you said:

And then Adequate goes on to say this:

Of course. I said both of those things because they are true.

All the cartoon laughing dogs in the world won't make them contradict one another.

Perhaps, given your math block, you should spend some time figuring out why not.

Adequate, you don’t have a clue how mutation and selection actually works.

What a silly lie.

 

[Myriad]

I didn't think to look. It might be worth checking --- that looks like the sort of thing one might demonstrate directly from probability theory, without this fussing about with simulations.

I believe so. To be more specific, the total expected generations for n fixations should increase as the nth harmonic number (sum of the partial harmonic series 1 + 1/2 + 1/3 + ... + 1/n), which is approximated at large n by ln, though it doesn't actually converge on it (it converges on ln plus the Euler-Mascheroni constant). So, the expected rate would be close to ln/n.

This is assuming (I believe correctly, for your models) that as soon as any specific point mutation favored by a selection pressure occurs for the first time, it gets fixed in the population with a high degree of certainty. This would be the case provided that the chances of a favorable mutation being nullified by a simultaneous unfavorable one, and the chance of two simultaneous unfixed favorable mutations competing in the population, are negligible. (Which is the case if the mutation rate and/or the ratio of pressures to total genome length is sufficiently low.)

The rationale is that we're looking for the expected number of trials to get all of a specific set of n distinct "hits" in a random number generator that selects one of a superset of m possibilties. The expected time for the first hit is clearly m/n, after which the expected time for the second hit (with n-1 possible hit targets remaining) is m/(n-1), and so on until the nth hit which takes an expected m/1 = m trials. So the total expected time for n hits is m * (1/n + 1/(n-1) + ... + 1/2 + 1), which is m times the nth harmonic number.

Respectfully,
Myriad

ETA: It occurs to me that the conclusion remains the same even if the fixation probability is not close to one, as long as it's constant.

 

[Dr Adequate]

This is why I normally only post on this thread at weekends. The more often I explain precisely and carefully what I mean, the more opportunities kleinman has to tell mentally degenerate lies about what I mean. There's no helping him.

 

[Dr Adequate]

This is assuming (I believe correctly, for your models) that as soon as any specific point mutation favored by a selection pressure occurs for the first time, it gets fixed in the population with a high degree of certainty.

No, not really. It's a population model, it incorporates genetic drift.

I think you'll find that this doesn't make much difference to the maths, though. There is still a probability that any given mutation will go on to fixation.

 

[sol invictus]

Not only did you say this, you admitted contradicted yourself when you then said that your silly graph shows that more optimization takes more time. Then when asked to present a real example of this, you finally admitted that you had no real examples of you irrational and illogical conclusion. Let’s remind the readers of what you said:

Kleinman, one word:

RATE

RATE is not the same as TIME.

Mutation rate is the number of mutations divided by time. TIME AND RATE ARE NOT THE SAME THING.

Are you capable of understanding that?

Stop making yourself look like an utter fool.

 

[Dr Adequate]

I believe so. To be more specific, the total expected generations for n fixations should increase as the nth harmonic number (sum of the partial harmonic series 1 + 1/2 + 1/3 + ... + 1/n), which is approximated at large n by ln, though it doesn't actually converge on it (it converges on ln plus the Euler-Mascheroni constant). So, the expected rate would be close to ln/n.

The rationale is that we're looking for the expected number of trials to get all of a specific set of n distinct "hits" in a random number generator that selects one of a superset of m possibilties. The expected time for the first hit is clearly m/n, after which the expected time for the second hit (with n-1 possible hit targets remaining) is m/(n-1), and so on until the nth hit which takes an expected m/1 = m trials. So the total expected time for n hits is m * (1/n + 1/(n-1) + ... + 1/2 + 1), which is m times the nth harmonic number.

Respectfully,
Myriad

Ah, yes. Thanks.

To quote Huxley's remark on Darwinism: "How extraordinarily stupid of me not to have thought of that."

But can you explain it to kleinman?

 

[sol invictus]

I believe so. To be more specific, the total expected generations for n fixations should increase as the nth harmonic number (sum of the partial harmonic series 1 + 1/2 + 1/3 + ... + 1/n), which is approximated at large n by ln, though it doesn't actually converge on it (it converges on ln plus the Euler-Mascheroni constant). So, the expected rate would be close to ln/n.

This is assuming (I believe correctly, for your models) that as soon as any specific point mutation favored by a selection pressure occurs for the first time, it gets fixed in the population with a high degree of certainty. This would be the case provided that the chances of a favorable mutation being nullified by a simultaneous unfavorable one, and the chance of two simultaneous unfixed favorable mutations competing in the population, are negligible. (Which is the case if the mutation rate and/or the ratio of pressures to total genome length is sufficiently low.)

<snip for brevity>

ETA: It occurs to me that the conclusion remains the same even if the fixation probability is not close to one, as long as it's constant.

Right - what you describe was exactly my model. If you ask what is the number of generations you have to wait so that every individual in a fraction f of the population has undergone n mutations, each mutation with probability (per generation) p, the answer is

t = log/p - log(-log(f)) + order (1/n), valid for n>>1, p<<1.

So the RATE goes as p n/log, and increases with n.

 

[Dr Adequate]

Kleinman, one word:

RATE

RATE is not the same as TIME.

Mutation rate is the number of mutations divided by time. TIME AND RATE ARE NOT THE SAME THING.

Are you capable of understanding that?

Is he capable of understanding grade school mathematics?

Does he understand the difference between generations and fixations per generation?

Apparently not.

As I said, I usually only post here at weekends. You may slowly be realising why.

Stop making yourself look like an utter fool.

I believe that this point has also been explained to him.

This, too, went over his head.

If you haven't read this paper, you may find that it gives you some sort of insight into what it's like to be kleinman.

 

[Dr Adequate]

I think I'll try the highlighting thing too. It can't do any harm.

Hello, kleinman.

Are you listening carefully?

(1) With simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

(2) More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

---

I bet he still doesn't understand.

 

[cyborg]

I bet he still doesn't understand.

Understanding is dangerous: he'd have to give up his Lord.

 

[Dr Adequate]

Understanding is dangerous: he'd have to give up his Lord.

C'mon, we have plenty of Christians on the forum and they're not like this. He could understand grade-school math without abandoning his religion, lots of people do.

But in order to realise that there is something he needs to understand he'd have to give up something much more precious to him than his so-called religion --- his self-esteem.

Kleinman has shown no sign that he's ever had a glimpse of religious feeling. What kleinman apparently worships and exalts above all is the perfection and omniscience and glory of kleinman.

And now we want to explain to him the basic mathematics that he should have learned in grade school? Watch the cognitive dissonance set in.

 

[cyborg]

He could understand grade-school math without abandoning his religion, lots of people do.

No, he couldn't.

And now we want to explain to him the basic mathematics that he should have learned in grade school? Watch the cognitive dissonance set in.

Stop being nasty Dr A! Kleinman admitted he made a mistake when he said probabilities could be more than one.

(It is unfortunate for kleinman that it's a mistake any fourteen year old paying the minimal amount of attention to the very basics of probability would never make).

 

[rocketdodger]

If you haven't read this paper, you may find that it gives you some sort of insight into what it's like to be kleinman.

Much obliged for that link Adequate -- very enlightening.

The interesting thing about those results is that they almost seem to suggest a correlation between modesty and competence. If so ... well we all know what a veritable fountain of modesty Kleinman is...

 

[Kotatsu]

Kotatsu, why don’t you tell us how polyploid genes are transformed into new genes? Once you figure out it requires mutation and selection then you can study how mutation and selection actually works.

Nothing in polyploidisation implies that the genes in the diploid genome needs to evolve into new genes. Polyploidisation occurs without random point mutations, and results in double copies of the same chromosomes within the same nucleus. What happens after that is entirely irrelevant to the question of whether or not polyploidisation implies common descent or not (Note: it does).

Of course, after a polyploidisation event, evolution continues pretty much as before, with random point mutations and whatnot (supposing, of course, that the polyploid individual survives to reproduce). One of the copies is then also freer to evolve away from the pre-polyploidisation sequence as the resulting amino acid sequence will still be produced by the other copy.

Kleinman, I have studied polyploidisation for quite some time. I know much, much more about how it works and what it implies than you do. Being a smug parrot does not lead anywhere, so try to read what I write and understand it.

And your slowness "argument" --- or rather assertion --- is invalidated by the paper by Song et al. which I have referred to numerous times. The speed of evolution within five generations in that experiment was much higher than you seem to be able to imagine, and quiet sufficient for driving the evolution of any given character.