Annoying creationists

[kjkent1]

What is Rfreq and Rseq?
(clip)

This post is a brilliant summary. Nominated.

Some brave moderator should spare us further punishment and close the thread.

 

[kleinman]

Annoying Creationists

Good thing then that Evolution doesn't really talk about Survival of the Fittest.

Shalamar, you should take a university-entrance exam in England, you would pass with flying colors.

What is Rfreq and Rseq?

(clip)

This post is a brilliant summary. Nominated.

Tell us kjkent1, what is Rfreq and Rseq? You are an expert on ev and claim to know what ev shows and doesn’t show.

Some brave moderator should spare us further punishment and close the thread.

You find the mathematical and empirical evidence of how the mutation and selection sorting/optimization process actually works punishing? I thought it was only annoying. I pray for God’s forgiveness that I enjoy the thought that showing how the mutation and selection sorting/optimization process is punishing for a legal beagle. Well, that’s a legal beagle whose only argument for his theory is to censor those who don’t believe his irrational and illogical theory.

 

[Shalamar]

Rocketdodger, thaty post was actually quite enlightening, and explains Kleinmans problems. His sole source of 'evidence' is ev for the most part, and the writers of ev have said that it doesn't work the way Kleinman thinks (Or prays) it does.

And oh? Kleinman? Survival of the Fittest is a largely Darwinian term. The ToE shows that it is not just the fittest that survive. Just the 'Fit enough'. Or not the least fit.

 

[Henners]

It didn’t take very long for the English Empire to evaporate...

"English Empire"

!

I see that your competence in Biology and Mathematics is easily matched by your knowledge of History.

Where's the shaggy dog gone, and who's going to clean your carpet?

___________________________

My point was that you were describing creeping creationism rather than evolution - and this illustrates a fundamental lack of command of your subject.

In fact, a detailed description of your whole approach may be found here:
http://en.wikipedia.org/wiki/Wedge_strategy

 

[kleinman]

Annoying Creationists

And oh? Kleinman? Survival of the Fittest is a largely Darwinian term. The ToE shows that it is not just the fittest that survive. Just the 'Fit enough'. Or not the least fit.

Show us your mathematics.

 

[Henners]

Show us your mathematics

Show us your carpet.

Come on, you've only every done one thing around here, and we know what it is.

 

[Shalamar]

Show us your mathematics.

I asked you first. A long time ago, in fact.

 

[Mr. Scott]

I'll repeat this essential question you ignored, Dr. Kleinman. Perhaps there's a problem with your browser:

You've stated that population size doesn't matter in the progress of evolution. I'm not trying to straw man, that's just what I recall. This seems to me to be quite unintuitive. If, for example, there's a one in a billion chance of a specific adaptive mutation happening in a bacterium in a day, the a population of a billion would be expected to achieve this mutation, on the everage, once a day. Double the population, and you expect to see a similar mutation twice a day. Seems obvious to me. The vast populations even in something like a serious HIV infection would seem to be beyond the scope of a limited program like Ev.

So please convince me of your claim that population size has no bearing on the progress of evolution. I'm willing to listen.

 

[kleinman]

Annoying Creationists

Show us your mathematics

Show us your carpet.

Come on, you've only every done one thing around here, and we know what it is.

You are correct; I’m pulling the rug from under your theory. And that rug is woven from mathematical and empirical evidence. I hope you find that annoying but not too punishing unless you are a legal beagle.

 

[Shalamar]

Kleinman, Why don't you address Rocketdodgers points on ev?

Or are you unable to do so? I notice you are flat out ignoring it, and making strange rug comments instead.

 

[Henners]

You are correct; I’m pulling the rug from under your theory. And that rug is woven from mathematical and empirical evidence. I hope you find that annoying but not too punishing unless you are a legal beagle.

My theory?

Perhaps I didn't make myself clear.

Edited by Cuddles: 

Edited out personal attack.

 

[kleinman]

Annoying Creationists

I'll repeat this essential question you ignored, Dr. Kleinman. Perhaps there's a problem with your browser:

You've stated that population size doesn't matter in the progress of evolution. I'm not trying to straw man, that's just what I recall. This seems to me to be quite unintuitive. If, for example, there's a one in a billion chance of a specific adaptive mutation happening in a bacterium in a day, the a population of a billion would be expected to achieve this mutation, on the everage, once a day. Double the population, and you expect to see a similar mutation twice a day. Seems obvious to me. The vast populations even in something like a serious HIV infection would seem to be beyond the scope of a limited program like Ev.

So please convince me of your claim that population size has no bearing on the progress of evolution. I'm willing to listen.

I’ve never said that population size has no bearing on the mutation and selection sorting/optimization process. What I have said is that huge populations do not accelerate evolution in the way evolutionists allege. If you read back in this thread you will see that I have done extensive studies with ev which investigates the effects of population on the rate of sorting in ev. That data has been posted previously and I will post it again if you wish. What that data shows is that increasing population size very quickly approaches an asymptote for the rate of convergence of the model as you use larger populations in the model. Initially this didn’t make sense to me since I erroneously thought that the effect of population size on the probability of a proper beneficial mutation would occur at a particular locus was additive with population. Myriad corrected my error and I acknowledged this. Myriad showed that the effect of population on a beneficial mutation occurring at a proper locus is less than additive and this is reflected in the population data you obtain from ev. Interestingly, when you set two of the three selection conditions to zero in ev, the remaining selection condition evolves very quickly, even with tiny populations. This finding is reflected in reality. For example, treating HIV with monotherapy can drive down viral loads to very small numbers for a short period of time but the remaining relatively small population can still easily evolve resistance to the single selection pressure.

By the way, ev (Pascal version) is not limited by population size used other than the memory capacity of the computer you are using to do the calculation.

Kleinman, Why don't you address Rocketdodgers points on ev?

Oh, you want me to explain to you what Rfreq and Rseq are? Why don’t you read Dr Schneider’s web site.
For the definition of Rfrequency, click here http://www.ccrnp.ncifcrf.gov/~toms/glossary.html#Rfrequency

For the definition of Rsequence, click here http://www.ccrnp.ncifcrf.gov/~toms/glossary.html#Rsequence

Now be careful Shalamar, you may run into some mathematics.

Perhaps I didn't make myself clear.

You are as clear as a London fog, fitting for someone who believes in a theory that only exists in a fog. But don’t worry, we have Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection and hundreds of real examples of mutation and selection to clear away that fog.

 

[Henners]

You are as clear as a London fog, fitting for someone who believes in a theory that only exists in a fog.

The theory only exists in a fog?

Rubbish.

I've seen all the pictures you posted, you disgusting little pup.

 

[kleinman]

Annoying Creationists

If you like to screw stuff made of mathematics, well, who am I to judge?

If you were an evolutionist with any competence in the mathematics of mutation and selection sorting/optimization process, you could judge but since evolutionists get their degrees from Mathishard University, it makes it quite difficult for you to judge.

You are as clear as a London fog, fitting for someone who believes in a theory that only exists in a fog.

The theory only exists in a fog?

Rubbish.

That correct, rubbish can exist in fog, don’t you remember the black fog in London?

I've seen all the pictures you posted, you disgusting little pup.

Wait a minute; are you discrediting the picture I posted of a Wookie? Don’t you know that joobz, the Wookie Weatherman has shown that the weather evolves Wookies, it was probably in a London black fog. Now Henners, since you like my pictures so much, let me post a word picture which shows how the mutation and selection sorting/optimization process actually works and it doesn’t work anything like you evolutionists allege. Bow wow.
http://drugs.adisonline.com/pt/re/drugs/abstract.00003495-200060030-00001.htm;jsessionid=HGBJRkCysz1w6fbCHL9G4Z5Qx11c7W5h22VD6W54HQSghlTFlhPL!-1297386286!181195629!8091!-1

Hepatitis B virus (HBV) was identified as a cause of viral hepatitis more than 30 years ago and hepatitis B vaccines have been available for almost 20 years, but HBV infection continues to be a global health problem, responsible for about 1.2 million deaths annually. By the end of this year, almost 400 million people - about 5% of the world's population and more than ten times the number infected with human immunodeficiency virus (HIV) - will be infected with HBV. Chemotherapy remains the only treatment option for controlling chronic HBV infection once acquired, but none of the many different chemotherapeutic strategies used in the past has proven consistently successful. Prospects for successful treatment of HBV have improved dramatically during the past decade due to the development of new, well tolerated and efficacious anti-HBV drugs, and to advances in our understanding of HBV replication and pathogenesis. The newer anti-HBV drugs are capable of reducing viral loads very rapidly, but the initial response is invariably followed by very much slower elimination of residual virus. As more effective anti-HBV drugs become available, the emergence of drug resistance during the slower phase of HBV elimination will probably become the most significant obstacle in the way of eventual control of HBV infection. Experience with HIV indicates that combination chemotherapy may suppress or eliminate drug resistance and methods for pre-clinical and clinical assessment of anti-HBV drug combinations are being developed. Basic research into mechanisms of drug action and interaction should assist in the design and optimisation of combination chemotherapy for HBV infection, for which additional new anti-HBV drugs will undoubtedly be required in future.

Hey kjkent1, this word picture is for you to. You had better contact these authors and tell them that HBV does frame shifts and therefore combination therapy will not work.

 

[Henners]

If you were an evolutionist with any competence in the mathematics of mutation and selection sorting/optimization process, you could judge but since evolutionists get their degrees from Mathishard University, it makes it quite difficult for you to judge.

My, where to start...

How about here:

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

or here, also from Wikipedia...

"...excessive seeking for attention, criticism of others, overly dutiful obedience, and worry."

Sound familiar?

Do your best.

 

[Shalamar]

SO the answer is 'no'. Kleinman will not address Rocketdodgers post, and he still won't show any evidence for his claim.

 

[kleinman]

Annoying Creationists

"...excessive seeking for attention, criticism of others, overly dutiful obedience, and worry."

What’s the matter Henners, do you have your evolutionary shorts in a mathematical wedgie?

 

[kleinman]

Annoying Creationists

So another week goes by trying to teach evolutionists the mathematics of the mutation and selection sorting/optimization process. This week has been dominated by claims of conspiracy by you evolutionists. You think that I believe there is a conspiracy on the part of evolutionists to contribute to the premature deaths of millions of people suffering from diseases subject to the principles of mutation and selection. If there is a conspiracy on the part of evolutionists it is simple a conspiracy of ignorance. Then we have Henners belief that I’m conspiring with the Discovery Institute, his evidence for this is that he has his evolutionist shorts in a mathematical wedgie. And then we have had numerous calls to try to censor anyone who doesn’t hold to the evolutionist dogma, especially when they annoy evolutionists with the mathematical and empirical evidence which shows that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. It just doesn’t register with evolutionists that this is a mathematical and empirical fact of life. Well, what we have here is the Titanic theory of evolution running into a mathematical iceberg and this unsinkable theory is now sitting down at the bottom of the primordial sea, millions of self replicators swimming in an out of the portholes. Perhaps sometime we can organize a tour of this wreck of a theory and look for arti-culett-facts. In the meantime, here are a couple more citations which show how the mutation and selection sorting/optimization process actually works which is combination selection pressures profoundly slow evolution by this process.

http://www.malariaandhealth.com/professional/abstracts.htm

The rationale for combining drugs with independent modes of action to prevent the emergence of resistance was developed first in antituberculous chemotherapy. It has subsequently been adopted in the treatment of cancer and, more recently, AIDS. These infections are now never treated with a single drug. The same should apply to the treatment of malaria. The principle is simple. Resistance arises from one or more mutations. These will be selected when exposed to concentrations of antimalarial drug which kill susceptible parasites but not those with the mutation(s). When two unrelated drugs are used together, a parasite with mutations conferring resistance to one drug will be killed by the other drug, and vice versa. The chance that a mutant will emerge that is simultaneously resistant to both the drugs is the product of the individual mutation frequencies, and will be many orders of magnitude lower than that for the drugs individually. Thus, compared with sequential use of single drugs (current policy), combinations will considerably retard the development of resistance. Artemisinin and its derivatives (artesunate, artemether, dihydroartemisinin) are the most potent and rapidly acting of antimalarials, reducing the infecting parasite biomass by approximately 10,000-fold per asexual (two day) life cycle compared to 100 to 1,000-fold for other antimalarial drugs. They are remarkably well tolerated and no significant resistance has been reported either in clinical isolates or in laboratory experiments. Combinations of artemisinin, or one of its derivatives, and mefloquine or lumefantrine (benflumetol) have proved highly effective even against multi-drug resistant P. falciparum. On the North-Western border of Thailand, which harbours the most resistant P. falciparum in the world, the use of combination chemotherapy has halted the progression of mefloquine resistance. This is attributed to two factors. First, combinations ensure high cure rates because the residuum of parasites remaining after treatment with an artemisinin derivative for three or more days is exposed to maximum concentrations of the more slowly eliminated mefloquine. This residuum (a maximum of 105 parasites or 0.000001% of the asexual parasites present initially) is all that is exposed to mefloquine alone, thus the selective pressure for the emergence of mutants with reduced mefloquine sensitivity is lessened considerably. Second, the artemisinin derivatives reduce gametocyte carriage by approximately 90%. Recrudescent (i.e. resistant) infections are associated with increased gametocyte carriage rates which provide a powerful selection pressure to the spread of resistance. This is prevented by the artemisinin derivatives. Combination therapy makes therapeutic sense, and there are good arguments for combining an artemisinin derivative with all antimalarial drugs.

And

The combination of artesunate and mefloquine is now the standard treatment for uncomplicated falciparum malaria in the displaced populations living on the Thai-Burmese border. The use of the combination was made necessary because P. falciparum had developed high-grade resistance to all antimalarials, including mefloquine and halofantrine. Since 1994, all patients with uncomplicated falciparum infections have received artesunate (4 mg/kg/day for 3 days) combined with mefloquine (25 mg/kg) as first-line therapy. The in vivo efficacy, prospectively monitored in over 3000 patients, has remained high and stable (95%). This stabilisation of mefloquine efficacy for the 4th consecutive year, following the rapid decline that we witnessed between 1986 and 1994, was confirmed by in vitro sensitivity monitoring. This coincides with a rapid decline in the incidence of falciparum (but not vivax) malaria incidence in the populations where the combination is used, but not in the surrounding communities. Concomitantly, entomological surveillance indicates that the mosquito vector abundance remains unchanged but that only vivax (and not falciparum) sporozoites can be detected in the salivary glands of the anophelene captures. Clinical studies indicate that the rate of gametocyte carriage in the population increased with the decline in mefloquine efficacy when the drug was used alone. However, we described how artemisinin derivatives reduce the gametocyte carriage rate by 90% following treatment of an acute episode. The rapid effect (and elimination) of artesunate on sexual and asexual stages of the parasite reduces the selective drug pressure of the slowly eliminated mefloquine (i.e. artesunate protects mefloquine and vice versa), prevents the spread of resistant strains, and selectively reduces falciparum transmission. The same impact on transmissibility of falciparum malaria was observed with another highly effective combination: artemether-benflumetol. All patients with P. falciparum infection should be treated with a combination of drugs that includes an artemisinin derivative.

Now you all have a good weekend and I’ll be back next week to annoy you with more citations which show how the mutation and selection sorting/optimization process actually works. If you are a legal beagle it does a little more than annoy you, God forgive me for enjoying that.

 

[kleinman]

Annoying Creationists

Well this is a little change of pace. No evolutionists have responded this weekend. Have I bored you? Or have I convinced you with the empirical evidence of how the mutation and selection sorting/optimization process actually works? Have you read Dr Schneider’s web site and learned how mutation and selection works? Do you all understand Dr Schneider’s mathematics? I think I’ll change gears and stop posting empirical examples and show you how you to study the mathematics of mutation and selection sorting/optimization process. In order to study the mathematics of mutation and selection you need to understand two advanced topics of mathematics, analytic geometry and functional analysis. I’m going to assume that you evolutionists understand basic algebra and will start the discussion from this point. We’ll start with the basics on analytic geometry. Do you recall the following equation?

y = f(x) = mx + b

For the moment, ignore the f(x) term and you should recognize the above equation as the algebraic representation of a straight line. What analytic geometry does is to take the algebraic representation of a function and expresses that algebraic representation as a shape (sometimes as a line or point). The analytic geometric representation of the above equation would look like this (From the Math Forum @ Drexel) http://mathforum.org/cgraph/cslope/mxplusb.html

y = 1/3 x + 4

Now consider the much more interesting function:

(x/a)^2 – (y/b)^2 – z = 0 = f(x,y,z)

The analytic geometric representation of this function from Wikipedia looks like this:

This interesting shape which looks something like a saddle gives a good example how you can use analytic geometry to study the shape of a function. For example if you make a cut through this shape along a plane where y held constant, you get a section with a parabola opening upward. If you make a cut through this shape with x held constant, you get a section with a parabola opening downward. If you make cuts along the z axis, you can get a section with straight lines at z = 0 or hyperbolas if z ≠ 0.

Now, if you would consider the terms y = f(x) and f(x,y,z) = 0. These are examples of the implicit mathematical notation for a functional equation. The first example is read as “y” is a function of “x”, or the value of “y” depends on the value of “x”. The second example is read as, there are certain values of “x”, “y” and “z” that when plugged into f(x,y,x) will give a value of zero. An explicit example of the function f(x,y,z) is given above with the algebraic equation for the hyperbolic paraboloid. There are many other examples of explicit functions which mathematicians use all the time, the trigonometric functions sin(x), cos(x) etc., logarithmic functions log(x), ln(x) and so on. These explicit functions are relatively easy to understand, tabulate and plot geometrically. Now the question for you to consider is how do you understand, tabulate and plot geometrically an implicit function f(x,y,z) that you can not express algebraically because many scientific problems can not be expressed explicitly in simple algebraic terms. The example we are considering on this thread is the mathematics of the mutation and selection sorting/optimization process. How do you even write out the mathematics of this process? How do you tabulate and plot such a phenomenon. The problem that most biologists have is that they don’t study and understand analytic geometry and functional analysis. Engineers study these topics in upper division applied mathematics courses and regularly use these principles to analyze and solve functional equation which you can not write down algebraically. Let’s see if you evolutionists can understand how this is done.

Let finish this post by expressing the mathematics of the mutation and selection sorting/optimization process in functional notation, Dr Schneider’s publication on ev gives guidance on writing this functional equation:
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794

Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution. Another use of the program may include understanding the sources and effects of skewed genomic composition (4,7,30,31).

Here are some of the variables in this functional relationship:

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

The functional expression for these variables can be written:

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

The analysis of this function requires the mapping of a surface in a six dimensional space. Any of you want to suggest how to map this six dimensional surface? Any of you want to suggest other variables for this function? In my next post, I’ll show you how to map this functional equation in a six dimensional space. Oh, one last point, this is not the same surface that we talk about when we speak of the fitness landscape.

 

[Belz...]

Well this is a little change of pace. No evolutionists have responded this weekend. Have I bored you?

No, it's just that watching paint dry is a more enjoyable experience.

Or have I convinced you with the empirical evidence of how the mutation and selection sorting/optimization process actually works? Have you read Dr Schneider’s web site and learned how mutation and selection works? Do you all understand Dr Schneider’s mathematics? I think I’ll change gears and stop posting empirical examples and show you how you to study the mathematics of mutation and selection sorting/optimization process. In order to study the mathematics of mutation and selection you need to understand two advanced topics of mathematics, analytic geometry and functional analysis. I’m going to assume that you evolutionists understand basic algebra and will start the discussion from this point. We’ll start with the basics on analytic geometry. Do you recall the following equation?

That's what I mean.