Annoying creationists

[BPScooter]

Although I took this thread off of my regular updates, I did check and based on what I've just seen, here's a couple thoughts that should and could be easily dispelled by a resoundingly truthful-seeming mathematical explanation of something.

As I recall, dimensions are easily visualized up to about 3. Three axes, xyz, can be understood as up/down, back/forward, and right/left. By throwing an object straight up on a moving train, we introduce the 4th, which is time. The object appears to go up and down, but if we put it "in time" (view it from beside the train track) it then describes a curve where its position is described as something like "xyz at time T" and then "xyz at time T plus one millisecond" and the overall impression is a curve. Imagine that this moment-by-moment structure is done by many things on many parallel trains, at one moment, and you now get what Fourier was trying to think about in the 1700s. Can we capture complex periodic behavior in equations? Blasphemous and odd thought, that, but he was right. We can model acoustical phenomena in just the ways he imagined.

So I'm not at all put off by the idea that complex systems can be modeled with complex mathematics. The calculus allows us to even predict higher-order things, like "rates of change" (slope of curve) and relative maxima and minima.

You fill your tub of 30 gallons for a bath at 2 gallons per hour and the plug drains it at 1 gallon per hour, the hot water is 70 degrees C and you can account for turbulence in the water. Thermal loss is say anything, 5 degrees per hour. What is the temperature of the water in the bath after 7 hours? Has it overflowed? Is it too cold? Will you burn yourself? Now let's make an equation for all the bathtubs in the town.

OK, I admit I made this up but a decent model would give us a good equation for it to be, shall I say, "figure-out-able". And this doesn't bother me in the least.

I'm a simple non-mathematician. Without one accounting for Time (t) in terms of whether time is allowed to be approaching infinity (a limit) it seems like the elegances of calculus are not being approached.

Thanks for listening, I had to get that off my chest.

[kleinman]

Tomorrow, I’ll walk you through the generation of some tabular data (which could be plotted graphically but I’ll leave that to you) which describes this 6-dimensional surface using Dr Schneider’s ev computer simulation.I am sure your "walk through" will include the few sets of parameters you repeat over and over.
I’ve already asked what parameters you want to include. Include any parameters you want and produce the data that you think will support your irrational and illogical theory. What Dr Schneider’s model shows is that the more complex the selection conditions become the much, much slower the mutation and selection sorting/optimization process becomes. Now rocketdodger, if you think that you can find a set of parameters that will contradict this, produce the data. In the mean time I’ll show those who are interested how to analyze Dr Schneider’s model and why it shows the theory of evolution to be mathematically impossible.
As I recall, dimensions are easily visualized up to about 3. Three axes, xyz, can be understood as up/down, back/forward, and right/left. By throwing an object straight up on a moving train, we introduce the 4th, which is time. The object appears to go up and down, but if we put it "in time" (view it from beside the train track) it then describes a curve where its position is described as something like "xyz at time T" and then "xyz at time T plus one millisecond" and the overall impression is a curve. Imagine that this moment-by-moment structure is done by many things on many parallel trains, at one moment, and you now get what Fourier was trying to think about in the 1700s. Can we capture complex periodic behavior in equations? Blasphemous and odd thought, that, but he was right. We can model acoustical phenomena in just the ways he imagined.
It isn’t really that difficult to visualize systems with more than 3 or 4 dimensions, it just takes a little practice. Visualizing higher dimensional system simply requires multiple 2 dimensional images (or tabular data) to get an idea what these higher dimensional systems look like. You can think of it this way, a three dimensional object requires 3 2-dimensional blue prints to completely visualize the three dimensional object. A shape in a 4-dimensional space requires 4 3-dimensional projections to completely visualize the four dimensional shape and so on. Each of those three dimensional images can be described by a series of 2-dimensional images. You can think of it this way, the hyperbolic paraboloid can be visualized by looking at 2-dimensional projections (slices) done along each axis. Cuts along one axis looks like parabolas opening up, along another axis the slices look like parabolas opening down and along the third axis, the cuts look like lines or hyperbolas. You can think of this as views taken by a multidimensional CT or MRI scan.

So let’s get to how you describe the shape of the 6-dimensional surface generated by Dr Schneider’s computer simulation. We all know how impatient Belz is. This 6-dimensional surface is defined by the functional equation:

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

Where,

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

We will generate the data points using Dr Schneider’s ev computer simulation of random point mutations and natural selection. You can access the online version of this computer simulation (written by James Randi Educational Forum moderator Paul C. Anagnostopoulos) at http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/) . On this web page there is a hot spot that looks like this:
Click Here to Start the Evj Model (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html)

Note that you must have your browser Java enabled. If you don’t have Java for your browser, you can download the software free at http://www.java.com/en/ (http://www.java.com/en/) .

I will now assume you have been able to bring up the start-up screen for ev. Here is a brief description of this screen. At the top of the screen it says “Evj 2.37 Evolution of DNA binding sites, Java version”. Directly below this are four buttons, Restart, New, Help and about. Restart starts the model from the beginning. New brings up a window which allows the user to set parameters for the model at other values. Help is not implemented yet but you can let the mouse point linger over fields and get descriptions of their properties. About gives general information about the program. Below these buttons on the left are several user definable options and buttons. The Pause/Run button starts and stops the computation. The Step button allows the user to step through the computation one generation at the time. The speed spinner allows the user to set the rate at which the computer does the computation. I set this to the maximum value of 21 usually (this control does not affect the mathematical results obtained). Generation displays the number of generations computed. Cycles to run allow the user to set the maximum number of generations to be computed. To the right of this area is a display of the parameters used in the particular case being computed and a check box which tells the model whether to do selection or not. To the right of this area is some pretty graphics and to the right of this area is more display information and some check boxes which allow the user to determine when the program should stop executing. These check boxes include Pause on perfect creature, Pause on Rseq ≥ Rfreq and Pause on both. There is also a spin entry field which allows the user to change the rate at which the screen updates data. I tend to set this to a large value since it does not affect the computation and lots of screen updates slow the execution of the model. The bottom of the screen contains lots of pretty graphics.

If you left click on the New button you will see a window which allows you to set parameters in the model. In the left upper you will see a spin field that lets you set population, below that is Potential sites (this is G, the genome length), Binding sites (this is g, the number of binding sites), in the lower left are fields which allow you to set the binding site width and the weight width (the size of the array which determines if a selection condition is met) and a Placement field. In the upper right are fields for setting the mutation rate. One field allows the user to set the mutation rate per genome and the other field allow you to set the mutation rate per number of bases. Below these controls are check boxes that allow the user to stop execution for the two convergence conditions, perform selection and so on. The bottom two fields allow the user to set the maximum number of generations for the program to compute and to set the seed value for the random number generator. Below these fields are a row of buttons. The two important buttons are the OK button and the Advanced>> button. The OK button accepts the input parameters and returns the user to the start-up screen so you can run the computation. I will discuss the Advanced>> button later.

In order to get you started on running ev, go to the startup screen, without changing anything on the screen other than click the Pause on perfect creature check box and then click the Run button. You should see the colors and numbers on the screen change and the number of generations show 662 and the progress bar should be red and the words “perfect creature” should show in the progress bar.

Now click the New button and on the parameter screen, under mutation parameters, change “1” mutation(s) per genome to “2” and then click the OK button. Again click the Run button. In this case you should get 572 generations to evolve the “perfect creature”.

If you continue this process for 3 and 4 mutations per genome you will obtain a table of data which show for G=256, population=64, g=16, nsp=3 like this:
mr/gfc to perfect creature
1|662
2|572
3|12890
4|>1,000,000 did not converge

If you are so inclined to plot this data, it might appear paraboloid.

This data give our first glimpse at what the 6-dimensional surface looks like that is defined by Dr Schneider’s computer simulation of random point mutations and natural selection. What do you think will happen when we change the G value to a new value and then again vary the mutation rate?

[kjkent1]

I’ve already asked what parameters you want to include. Include any parameters you want and produce the data that you think will support your irrational and illogical theory. What Dr Schneider’s model shows is that the more complex the selection conditions become the much, much slower the mutation and selection sorting/optimization process becomes. Now rocketdodger, if you think that you can find a set of parameters that will contradict this, produce the data. In the mean time I’ll show those who are interested how to analyze Dr Schneider’s model and why it shows the theory of evolution to be mathematically impossible. (clip)Fascinating. Do go on, won't you?

[kleinman]

I’ve already asked what parameters you want to include. Include any parameters you want and produce the data that you think will support your irrational and illogical theory. What Dr Schneider’s model shows is that the more complex the selection conditions become the much, much slower the mutation and selection sorting/optimization process becomes. Now rocketdodger, if you think that you can find a set of parameters that will contradict this, produce the data. In the mean time I’ll show those who are interested how to analyze Dr Schneider’s model and why it shows the theory of evolution to be mathematically impossible. (clip)Fascinating. Do go on, won't you?
Of course I will, just for you, well, you and Dr Schneider and Paul, I think their work deserves to be recognized and understood. Aren’t you going to tell us what you think will happen when we change the G value to a new value and then again vary the mutation rate?

[rocketdodger]

...

[rocketdodger]

...

[kleinman]

I’ve already asked what parameters you want to include. Include any parameters you want and produce the data that you think will support your irrational and illogical theory. What Dr Schneider’s model shows is that the more complex the selection conditions become the much, much slower the mutation and selection sorting/optimization process becomes. Now rocketdodger, if you think that you can find a set of parameters that will contradict this, produce the data. In the mean time I’ll show those who are interested how to analyze Dr Schneider’s model and why it shows the theory of evolution to be mathematically impossible.I already did, you blind, stupid, ignorant, lying, fraudulent fool of a man. In fact, multiple people asked you to respond to my "data," which you of course are outright ignoring because it shows you to be plainly wrong.
Rocket who fizzles, is this the data you want me to respond to?
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
Sorry, I thought I responded to this. Let me respond again.
http://forums.randi.org/images/smilies/doglaugh.gif
In case you missed the post, here:What is Rfreq and Rseq?
You missed this post rocket that travels slower than a speeding snail: http://forums.randi.org/showpost.php?p=3323249&postcount=7732 (http://forums.randi.org/showpost.php?p=3323249&postcount=7732)
Of course I will, just for you, well, you and Dr Schneider and Paul, I think their work deserves to be recognized and understood. Aren’t you going to tell us what you think will happen when we change the G value to a new value and then again vary the mutation rate?
My guess is that the graph will shift to the right, I.E. the "optimal" mutation rate will increase.
Here’s the data for G=512, all other parameters the same for the G=256 base case the same, G=512, population=64, g=16, nsp=3 like this:
mr/gfc to perfect creature
1|2412
2|1251
3|973
4|13251
5|22790
6|>1,000,000 did not converge

Care to hazard a guess what the results will show for G=1024?

[kleinman]

I guess rocketdodger did not want to hazard a guess for the G=1024 series. For G=1024, population=64, g=16, nsp=3 like this:
mr/gfc to perfect creature
1|18030
2|9701
3|4679
4|2991
5|1299
6|1979
7|3782
8|7254
9|16243
10|>1,000,000 did not converge

These series which investigate the mutation rate all show a paraboloid appearance. Rocketdodger is the graph shifting to the right? I’ll post the data for G=2048 tomorrow and will see if rocketdodger’s guess is correct.

[kjkent1]

Of course I will, just for you, well, you and Dr Schneider and Paul, I think their work deserves to be recognized and understood. Aren’t you going to tell us what you think will happen when we change the G value to a new value and then again vary the mutation rate?Nope. I'm rather more interested in the behavior science experiment currently underway. It appears that failing to maintain combination selective pressure on the kleinman virus, even for one day, causes the kleinman virus to spread quickly to other forum threads.

Anyway, don't let me interrupt. Keep on telling us how evolution doesn't work. We're all a twitter!

[kleinman]

Of course I will, just for you, well, you and Dr Schneider and Paul, I think their work deserves to be recognized and understood. Aren’t you going to tell us what you think will happen when we change the G value to a new value and then again vary the mutation rate?Nope. I'm rather more interested in the behavior science experiment currently underway. It appears that failing to maintain combination selective pressure on the kleinman virus, even for one day, causes the kleinman virus to spread quickly to other forum threads.
The only problem you have is that you don’t have any selection pressures. For example, I just won my malpractice case that you so much enjoyed trying to discredit me with. It only took 6 years to win the case. Now you watch the web carefully because the Superior Court only posts their decisions for a week or so.
Anyway, don't let me interrupt. Keep on telling us how evolution doesn't work. We're all a twitter!
I do enjoy making evolutionists twitter.

[kjkent1]

The only problem you have is that you don’t have any selection pressures. For example, I just won my malpractice case that you so much enjoyed trying to discredit me with. It only took 6 years to win the case. Now you watch the web carefully because the Superior Court only posts their decisions for a week or so.

I do enjoy making evolutionists twitter.Good for you on your malpractice defense. There will be no living with you now.

Anyway, kindly get back to the thread topic. We're all waiting for you to prove evolution impossible.

[kleinman]

The only problem you have is that you don’t have any selection pressures. For example, I just won my malpractice case that you so much enjoyed trying to discredit me with. It only took 6 years to win the case. Now you watch the web carefully because the Superior Court only posts their decisions for a week or so.Good for you on your malpractice defense. There will be no living with you now.
Thank you and what makes you think that you could live with me before. Don’t you find it amazing that in all the years I have practiced medicine and the tens of thousands of people I have cared for, I have had only two malpractice cases, both which I have won with motions for summary judgment. I think it’s because when people tell me they smoke cigarettes, I tell them it’s good that they are doing this, they pay lots of taxes and keep us doctors busy.
Anyway, kindly get back to the thread topic. We're all waiting for you to prove evolution impossible.
Ok, ok, be patient, the wheels of science grind slowly but they do grind fine. However, I am not proving evolution impossible; I am proving the theory of evolution (common descent by mutation and selection) mathematically impossible. So where were we? Oh yes, we were mapping out the function:

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

Where,

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

And we were starting the mapping process by making a series of cuts in the 6-dimensional space in the mr, gfc planes and we have obtained the data from these planes for the following cases:

G=256, population=64, g=16, nsp=3:
mr|gfc to perfect creature
10^-7|95975841
10^-6|4278078
10^-5|1105535
10^-4|47279
10^-3|5029
1|662
2|572
3|12890
4|>1,000,000 did not converge

Note that I have included in this series a few more data points with more realistic mutation rates (1 mutation per 100,000 bases per generation down to 1 mutation per 10,000,000 bases per generation). Even this very simple series, the basis of which is the baseline case which Dr Schneider included in his publication shows that with a realistic mutation rate, it can take almost one hundred million generations to accomplish the sorting process for his three selection conditions. This series show that the maximum rate of sorting is around 2 mutations per genome per generation (2 mutations per 256 bases per generation) or about 1 mutation per 128 bases per generation.

G=512, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|2412
2|1251
3|973
4|13251
5|22790
6|>1,000,000 did not converge

This series show that the maximum rate of sorting is around 3 mutations per genome per generation (3 mutations per 512 bases per generation) or about 1 mutation per 170 bases per generation.

G=1024, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|18030
2|9701
3|4679
4|2991
5|1299
6|1979
7|3782
8|7254
9|16243
10|>1,000,000 did not converge

This series show that the maximum rate of sorting is around 5 mutations per genome per generation (5 mutations per 1024 bases per generation) or about 1 mutation per 205 bases per generation.

Here are a couple more series which show the effects of mutation rate on the generations for convergence to perfect creature.

G=2048, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|42641
2|36817
3|11480
4|6049
5|10364
6|9708
7|3634
8|5382
9|5089
10|6170
11|9851
12|3952
13|10880
14|38738
15|6145
16|105799
17|259469
18|>1,000,000 did not converge

This series show that the maximum rate of sorting is around 7-12 mutations per genome per generation (9 mutations per 2048 bases per generation) or about 1 mutation per 228 bases per generation.

G=4096, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|163722
2|48755
3|57212
4|30316
5|19675
6|23306
7|17689
8|21947
9|13328
10|8935
11|16043
12|10225
13|17029
14|16052
15|17186
16|7715
17|14761
18|8772
19|12152
20|8806
21|7647
22|6724
23|4959
24|4096
25|13463
26|8325
27|8067
28|17877
29|46876
30|1000000 did not converge

This series show that the maximum rate of sorting is around 24 mutations per genome per generation (24 mutations per 4096 bases per generation) or about 1 mutation per 170 bases per generation.

So, what can you say about the F(n,G,g,mr,nsp) = gfc 6-dimensional surface when you make a series of cuts through this surface with planes that are parallel to the mr, gfc coordinates. You can say that the surface has a paraboloid shape with the with the number of generations for convergence becoming extremely large to accomplish the sorting process when the mutation rate used is a realistic value or if the mutation rate used becomes unrealistically large.

The next coordinate we will consider will be g (the number of binding sites) and how it affects the gfc (generations for convergence).

I hope you all are enjoying the analysis of the mathematics of the mutation and selection sorting/optimization process.

[Mister Earl]

What weights are you using for the selection pressures? I note you left out that part. Also, when will you address Rocketdodger's results?

[kleinman]

What weights are you using for the selection pressures? I note you left out that part. Also, when will you address Rocketdodger's results?
All parameters not listed in the post were left at Dr Schneider’s baseline values. If I don’t mention a value for a particular parameter in the model, it is because they were not changed from the default values.

What results has rocketdodger presented? Rocketdodger spent an afternoon throwing together some code and then claims that n+1 selection pressures evolve more rapidly than n selection pressures. I’ll stick with Dr Schneider’s peer reviewed and published computer simulation that has been scrutinized for more than 20 years and for which Dr Schneider has published and posted extensive documentation, especially since the mathematical results from Dr Schneider’s model is reflected in real empirical examples of mutation and selection.

The weights for all the selection pressures were left at the default values of 1. Why don’t you study the effects of varying weights on the rate of convergence?

[kjkent1]

The weights for all the selection pressures were left at the default values of 1. Why don’t you study the effects of varying weights on the rate of convergence?I've already done that. Varying the weights creates a normal distribution centered around all three mistake weights set to the same number. The effect of the mistake weights are relative, not absolute, i.e., setting the weights all to 1 produces the same result as setting all the weights to 100.

The above is true unless you set a mistake weight to zero (0). When you do this, the "perfect creature" reported by the program is no longer actually perfect, because it contains missing and/or spurious bindings at the time perfection is reported. This is due to the fact that when the mistake weight is zero, the algorithm no longer detects the presence of that mistake.

Also, whenever a mistake weight is set to zero, Rseq never converges on Rfreq, clearly demonstrating that the genome being created does not model any known independently living life form, because all such life forms can be shown to have genomes where Rseq ~ Rfreq. I.e., ev without convergence, proves nothing about evolution.

Now, here's some questions that you can't answer without modifying the program:

1. The mistake weights can only be set from 1 to 100. There is no way to model what would occur were a mistake weight several magnitudes greater than some other.

2. How do we know that a creature with a small genome that is already generally perfect (Rseq ~ Rfreq) does not mutate by replication, for example, and then develop a new function without having to repeat a long iteration of fitness trials so as to cause the genome to converge again on perfection?

How do we know that the same cannot be said for a frame shift, a fusion, a deletion, a transposition, etc?

The early Earth had plenty of time to produce a small perfect creature, which could then act as a springboard for future and much faster evolutionary change.

Bottom line, kleinman, old boy, we only really need one self-replicator with a genome of any size wherein Rseq ~ Rfreq. As soon as this occurs, evolution is off and running.

And, while you can contend that the odds of this occurring are too remote to be possible, the fact is that we are here typing about it, and the evidence of common descent is overwhelming.

Therefore, that's what happened, unless you want to claim that God or some extraterrestrial set the ball rolling. Which you certainly can claim -- but the odds in favor of that are infinitely worse than random chance.

[kleinman]

The weights for all the selection pressures were left at the default values of 1. Why don’t you study the effects of varying weights on the rate of convergence?I've already done that. Varying the weights creates a normal distribution centered around all three mistake weights set to the same number. The effect of the mistake weights are relative, not absolute, i.e., setting the weights all to 1 produces the same result as setting all the weights to 100.
It should be obvious to you why setting all the mistake weights to the same number does not alter the sorting process of the algorithm.
The above is true unless you set a mistake weight to zero (0). When you do this, the "perfect creature" reported by the program is no longer actually perfect, because it contains missing and/or spurious bindings at the time perfection is reported. This is due to the fact that when the mistake weight is zero, the algorithm no longer detects the presence of that mistake.
Setting a mistake weight to zero reduces the number of selection conditions. A “perfect creature” is simply a creature that has satisfied the sorting conditions applied to the population.
Also, whenever a mistake weight is set to zero, Rseq never converges on Rfreq, clearly demonstrating that the genome being created does not model any known independently living life form, because all such life forms can be shown to have genomes where Rseq ~ Rfreq. I.e., ev without convergence, proves nothing about evolution.
Rseq ~ Rfreq is not a selection condition. Selection is based on mistakes identified by the selection conditions. I have many examples where Rseq ~ Rfreq yet you don’t have a “perfect creature” and visa versa. Kjkent1 is trying to make ev something which it isn’t. Ev is simply a sorting algorithm based on selection conditions and what ev shows is that it is far easier for the algorithm to sort based on a single selection condition than sorting on all three conditions simultaneously. This in fact is how mutation and selection works in reality.
Now, here's some questions that you can't answer without modifying the program:

1. The mistake weights can only be set from 1 to 100. There is no way to model what would occur were a mistake weight several magnitudes greater than some other.
Invite Paul to make such a change. It shouldn’t take much programming, perhaps changing a byte integer to a long integer and then increasing the limits on his entry field.
2. How do we know that a creature with a small genome that is already generally perfect (Rseq ~ Rfreq) does not mutate by replication, for example, and then develop a new function without having to repeat a long iteration of fitness trials so as to cause the genome to converge again on perfection?
Kjkent1, you are arguing that evolution does not take a series of small steps but somehow makes large step changes. That is you don’t need a series of microevolutionary steps to achieve a macroevolutionary change, you just get a macroevolutionary change in one fell swoop. There is no mathematical or empirical basis for such a concept. This is raw speculation.
How do we know that the same cannot be said for a frame shift, a fusion, a deletion, a transposition, etc?
We know that frame shifts occur with HIV and HBV yet combination selection pressures still profoundly slow the evolution of these viruses. It is not the type of mutations which dominates the mutation and selection sorting/optimization process; it is the number of selection conditions which dominates the process. The mutation and selection sorting/optimization process is mathematically predictable and empirically measurable and it simply does not work the way evolutionists allege.
The early Earth had plenty of time to produce a small perfect creature, which could then act as a springboard for future and much faster evolutionary change.
Once upon a time…
Bottom line, kleinman, old boy, we only really need one self-replicator with a genome of any size wherein Rseq ~ Rfreq. As soon as this occurs, evolution is off and running.
That explains why the world is filled with tribbles.
And, while you can contend that the odds of this occurring are too remote to be possible, the fact is that we are here typing about it, and the evidence of common descent is overwhelming.
A child of five would understand this -- send someone to fetch a child of five!
Therefore, that's what happened, unless you want to claim that God or some extraterrestrial set the ball rolling. Which you certainly can claim -- but the odds in favor of that are infinitely worse than random chance.
A mentsh tracht und Gott lacht.

While kjkent1 is dreaming of tribbles, let’s see what else we can learn from the mathematics of ev.

What happens if we make a cut in our 6-dimensional surface in the g, gfc plane?

G=4096, population=64, mr=1 mutation per genome per generation, nsp=3:
g|gfc to perfect creature
2|140441
3|55585
4|52475
5|65441
6|26551
7|56496
8|79879
9|32391
10|59240
11|10684
12|53572
13|30162
14|35564
15|54498
16|42641
17|61064
18|54802
19|31806
20|45631
40|24544
80|28916
160|34389
200|28826

It appears from this series that g has little effect on gfc, the generations for convergence. Any of you want to hazard a guess why? Tomorrow we will look at the effects of population on the rate of convergence of ev.

[kjkent1]

It should be obvious to you why setting all the mistake weights to the same number does not alter the sorting process of the algorithm.It's obvious to me, but it may not be obvious to other readers.

Setting a mistake weight to zero reduces the number of selection conditions. A “perfect creature” is simply a creature that has satisfied the sorting conditions applied to the population.

Rseq ~ Rfreq is not a selection condition. Selection is based on mistakes identified by the selection conditions. I have many examples where Rseq ~ Rfreq yet you don’t have a “perfect creature” and visa versa. Kjkent1 is trying to make ev something which it isn’t. Ev is simply a sorting algorithm based on selection conditions and what ev shows is that it is far easier for the algorithm to sort based on a single selection condition than sorting on all three conditions simultaneously. This in fact is how mutation and selection works in reality.kleinman doesn't know what he's talking about. The relationship between/convergence of Rseq ~ Rfreq is one of the most important components of "ev" and Schneider's paper. Kleinman doesn't like this particular fact because it wreaks his entire computational theory. But, I'll repeat it so it doesn't get lost: a genome where Rseq is not ~ Rfreq is likely not a living organism; therefore any result from ev that does not show this relationship has nothing to do with reality.

Kjkent1, you are arguing that evolution does not take a series of small steps but somehow makes large step changes. That is you don’t need a series of microevolutionary steps to achieve a macroevolutionary change, you just get a macroevolutionary change in one fell swoop. There is no mathematical or empirical basis for such a concept. This is raw speculation.It is? You need to get out more. Mutations with new functionality occur all the time. Most of them don't add any fitness benefit to the environment. But some do. Ask Daniel Tammet how he manages to memorize Pi to 24,000 places. Surely you wouldn't suggest that he's just got an extra good memory? And, what about the pesky 2p and 2q chromosomes found in non-human primates -- but fused into one chromosome in humans? I'd say that was a pretty gross macroevolutionary change, wouldn't you?

No, of course not. You would ignore it and say it's not even empirical data, because it messes with your theory. Well, you're theory is crap, Alan. It doesn't comport with reality.

We know that frame shifts occur with HIV and HBV yet combination selection pressures still profoundly slow the evolution of these viruses. It is not the type of mutations which dominates the mutation and selection sorting/optimization process; it is the number of selection conditions which dominates the process. The mutation and selection sorting/optimization process is mathematically predictable and empirically measurable and it simply does not work the way evolutionists allege.Now THAT was total speculation. I've previously posted a peer-reviewed paper that showed a frame shift which provided immunoprophylaxis escape for an HBV variant while under combination therapeutic pressure -- so you're statement above is absolutely falsified.

Once upon a time…...there was a physician in Clovis, Ca whose obsessive-compulsive behavior makes it impossible for him to maintain a relationship with anyone, because his low self-esteem prevents him from admitting that he could ever be in error about anything...the end.

[Mister Earl]

I'll repeat it so it doesn't get lost: a genome where Rseq is not ~ Rfreq is likely not a living organism; therefore any result from ev that does not show this relationship has nothing to do with reality.
Good luck. I've been barking up that tree for days. I pointed out that the paper he clings to also clearly states that it would have to factor in a great number of additional variables to accurately model realistic evolution. He ignores this part, of course. And every time I mention it, I get an immediate response from everyone's favorite nutbag, saying "But but but look at the MATH!", followed by a good number of posts containing no math whatsoever.

Bottom line, I don't think Kleinman is in any kind of mental state that would facilitate an opinion change. This latest thread direction is entirely for his own benefit. It is his intention that he sway our opinions. I think he's going to have to do a better job... so far I haven't seen him post anything that even gives me the shadow of a doubt that evolution doesn't happen they way present theory states. The arrogant tone doesn't exactly help, either...

[Mister Earl]

So just to summarize, Kleinman, I will no longer try to change your opinion, because I no longer believe that is possible. I will, however, patiently wait as you continue to present data and see if you can prove anything that'll sway me.

[rocketdodger]

What results has rocketdodger presented? Rocketdodger spent an afternoon throwing together some code and then claims that n+1 selection pressures evolve more rapidly than n selection pressures. I’ll stick with Dr Schneider’s peer reviewed and published computer simulation that has been scrutinized for more than 20 years and for which Dr Schneider has published and posted extensive documentation, especially since the mathematical results from Dr Schneider’s model is reflected in real empirical examples of mutation and selection.

He is talking about the post I made that shows how stupid you are when it comes to interpreting results from ev.

Tell us how these facts fit into your theory, Kleinman:

When the mistake weights are [1,0,0], [0,1,0], or [0,0,1] the simulation never stops on Rseq >= Rfreq (which, by definition, means these weights are invalid).

When the mistake weights are [0,1,0] or [0,0,1] the simulation evolves a perfect creature in one generation (which, by definition, is impossible -- thus these weights are invalid).

When the mistake weights are [100,100,100], convergence happens faster than [1,100,1] or [1,1,100] and convergence has a higher rate than [100,1,1].

[Mister Earl]

I wonder if Kleinman moved to a new thread, or if he's running additional simulations. It's out of character for him to not comment in this amount of time.

[sol invictus]

Some people in another thread requested to see my estimate of the scaling of the generations required for convergence to a perfect creature with the number of selection pressures.

Suppose we have a population of creatures, and we'll suppose for simplicity that they all start off with the same genes. They reproduce asexually, and each gives birth to one child per generation. So the population can be divided into a bunch of independent lines of descent, and we want to know how long we have to wait, on average, for a given line to mutate in N specific beneficial ways. To model selection pressure we can simply assume that once any of those beneficial mutations occurs in a particular line it is fixed from then on (so it never un-mutates). This reduces the problem to a rather trivial combinatorics exercise. (It's the same question as: if you buy tickets for N lotteries, all drawn simultaneously at regular intervals, how many rounds will you have to play on average before you've won all the lotteries at least once?)

Suppose for a moment we only cared about one gene, and the probability per generation that gene will mutate in the way we're interested in is p. Then the number of generations it takes for the mutation to occur is on average simply t_avg = 1/p.

Now suppose there are N mutations we want to keep track of, and for simplicity assume that each has that same probability p to occur in any given generation. It's true that the chance for them all to occur in a single generation is very small: p^N. But what's the average time it takes for all N mutations to occur?

That's slightly more complicated, but the answer is the following: the chance that after t generations a given mutation has not occurred is (1-p)^t. So that chance it has occurred is 1-(1-p)^t. Then the chance that all N have occurred is (1-(1-p)^t)^N. We can use that to compute the average time exactly, or make an estimate.

For N large, the answer is approximately t_avg ~ (1/p)(d + log[N]), where d is a number of order 1. So the time grows very slowly with N at large N, and the average time per mutation decreases at large N as log[N]/(pN). If p = 1/1,000,000 and N = 100, the average number of generations for all 100 mutations to occur is only 5.2 10^6, or 5.2/p.

So in this model, the rate of evolution per pressure INCREASES with the number of pressures as N/log(N), contrary to kleinman's repeated assertions that "evolution is profoundly slowed by multiple pressures". Furthermore this simple model seems to coincide with the results of at least two somewhat more sophisticated computer models, one being ev and the other being something rocketdodger coded a while back.

This type of scaling is the basic reason why so many mutations have occurred over the course of evolution, even though the chance of them all occurring in any one generation is vanishingly small.

[kjkent1]

When the mistake weights are [0,1,0] or [0,0,1] the simulation evolves a perfect creature in one generation (which, by definition, is impossible -- thus these weights are invalid).The funniest thing about this particular outcome is that if we were to accept it at face value, then ev proves that ANY arrangement of amino acids that accidentally occurs in nature will spontaneously bind together and start the cycle of organic life!

Thus, kleinman destroys his entire theory by conceding that ev proves abiogenesis.

I doubt that Schneider would agree with this ridiculous outcome from his algorithm, but hey, it's a "valid" ev result!

[Paul C. Anagnostopoulos]

I doubt that Schneider would agree with this ridiculous outcome from his algorithm, but hey, it's a "valid" ev result!
I guess this means that a person has to think about what is actually going on in Ev, in order to assign a valid interpretation to these fringe results. He can't just say "Oh look, viable creatures from only one selection pressure!"

~~ Paul

[m_huber]

I guess this means that a person has to think about what is actually going on in Ev, in order to assign a valid interpretation to these fringe results. He can't just say "Oh look, viable creatures from only one selection pressure!"

~~ Paul

Isn't that the point of this whole discussion?

[kleinman]

I apologize for not responding in a more timely manner but I'll back with you on Monday. You all enjoy your weekend.

[Mister Earl]

I hope you enjoyed yours. I spent mine getting bitten by a ravenous cockatiel in my sleep. Ended up cooking some spaghetti, just to placate the bird. Spaghetti > Birdseed apparently.

[kleinman]

Have any of you mathematically incompetent evolutionists learned anything about the mathematics of the mutation and selection sorting/optimization process yet? Let’s find out.

It should be obvious to you why setting all the mistake weights to the same number does not alter the sorting process of the algorithm.It's obvious to me, but it may not be obvious to other readers.
Well then, why don’t you explain it to the readers?
Setting a mistake weight to zero reduces the number of selection conditions. A “perfect creature” is simply a creature that has satisfied the sorting conditions applied to the population.

Rseq ~ Rfreq is not a selection condition. Selection is based on mistakes identified by the selection conditions. I have many examples where Rseq ~ Rfreq yet you don’t have a “perfect creature” and visa versa. Kjkent1 is trying to make ev something which it isn’t. Ev is simply a sorting algorithm based on selection conditions and what ev shows is that it is far easier for the algorithm to sort based on a single selection condition than sorting on all three conditions simultaneously. This in fact is how mutation and selection works in reality.kleinman doesn't know what he's talking about. The relationship between/convergence of Rseq ~ Rfreq is one of the most important components of "ev" and Schneider's paper. Kleinman doesn't like this particular fact because it wreaks his entire computational theory. But, I'll repeat it so it doesn't get lost: a genome where Rseq is not ~ Rfreq is likely not a living organism; therefore any result from ev that does not show this relationship has nothing to do with reality.
Really, legal beagle? Do you want to explain how to analyze and solve an implicit functional equation? Dr Schneider was surprised when his model showed the peculiar result that Rseq ~ Rfreq. Dr Schneider still hasn’t given a good explanation how this relates to the mutation and selection sorting/optimization process. Because Dr Schneider chose to focus on this peculiarity, he missed the obvious result that his model shows, that is that combination selection conditions profoundly slow evolution by the mutation and selection sorting/optimization process. If Dr Schneider had done the parametric study he called for in his publication, he would have discovered this result himself.
Kjkent1, you are arguing that evolution does not take a series of small steps but somehow makes large step changes. That is you don’t need a series of microevolutionary steps to achieve a macroevolutionary change, you just get a macroevolutionary change in one fell swoop. There is no mathematical or empirical basis for such a concept. This is raw speculation.It is? You need to get out more. Mutations with new functionality occur all the time. Most of them don't add any fitness benefit to the environment. But some do. Ask Daniel Tammet how he manages to memorize Pi to 24,000 places. Surely you wouldn't suggest that he's just got an extra good memory? And, what about the pesky 2p and 2q chromosomes found in non-human primates -- but fused into one chromosome in humans? I'd say that was a pretty gross macroevolutionary change, wouldn't you?
I don’t argue that polymerases can’t mutate so that they can cleave xeno-molecules like nylon, what I argue is that the evolutionists’ gross over-extrapolation of this microevolutionary process to the evolution of lizards to birds is irrational, illogical and mathematically impossible. The reason I make this argument is based on the mathematics of Dr Schneider’s ev simulation of random point mutations and natural selection which show that combination selection pressures profoundly slow the sorting/optimization process and hundreds of real examples of mutation and selection which demonstrates this same finding. You evolutionists have completely bungled the understanding of the mutation and selection sorting/optimization process.
No, of course not. You would ignore it and say it's not even empirical data, because it messes with your theory. Well, you're theory is crap, Alan. It doesn't comport with reality.
Really? You think the greater the number of selection conditions the faster the evolutionary process proceeds? Where are all you citations which show your contention?
We know that frame shifts occur with HIV and HBV yet combination selection pressures still profoundly slow the evolution of these viruses. It is not the type of mutations which dominates the mutation and selection sorting/optimization process; it is the number of selection conditions which dominates the process. The mutation and selection sorting/optimization process is mathematically predictable and empirically measurable and it simply does not work the way evolutionists allege.Now THAT was total speculation. I've previously posted a peer-reviewed paper that showed a frame shift which provided immunoprophylaxis escape for an HBV variant while under combination therapeutic pressure -- so you're statement above is absolutely falsified.
Are you contending that combination therapy should not be used on HBV? Are you contending that frame shifts overcomes the mathematical fact the Dr Schneider’s ev program demonstrates that combination selection pressures profoundly slow the mutation and selection sorting/optimization process?
Once upon a time…...there was a physician in Clovis, Ca whose obsessive-compulsive behavior makes it impossible for him to maintain a relationship with anyone, because his low self-esteem prevents him from admitting that he could ever be in error about anything...the end.
Why legal beagle, how many times have you said good bye on this thread and you keep coming back to this discussion? I think you are the one obsessed with this discussion. You can’t produce the mathematical or empirical data to support your irrational and illogical theory of evolution so you look for any way you can to discredit me. Do you want to talk more about my malpractice case which I won yet you tried to discredit me with that? It so typical of you evolutionists to jump to conclusions when you don’t have the facts to support your irrational and illogical thinking, lizards must evolve into birds because a polymerase can mutate so that it can cleave nylon, perhaps in one of your 10^500 alternative universes but not in this one.

Hey legal beagle, since you are such an expert on Dr Schneider’s ev model, why don’t you tell us why variations in g have such little effect on the generations for convergence?
I'll repeat it so it doesn't get lost: a genome where Rseq is not ~ Rfreq is likely not a living organism; therefore any result from ev that does not show this relationship has nothing to do with reality.Good luck. I've been barking up that tree for days. I pointed out that the paper he clings to also clearly states that it would have to factor in a great number of additional variables to accurately model realistic evolution. He ignores this part, of course. And every time I mention it, I get an immediate response from everyone's favorite nutbag, saying "But but but look at the MATH!", followed by a good number of posts containing no math whatsoever.
Mister Earl, what mathematical model of mutation and selection are you clinging to? Oh wait, you evolutionists don’t need any mathematical model to prove your irrational and illogical theory. You have your speculations and extrapolations to prove your point. Mister Earl, do you think that increasing the number of selection pressures will accelerate the mutation and selection sorting/optimization process?
Bottom line, I don't think Kleinman is in any kind of mental state that would facilitate an opinion change. This latest thread direction is entirely for his own benefit. It is his intention that he sway our opinions. I think he's going to have to do a better job... so far I haven't seen him post anything that even gives me the shadow of a doubt that evolution doesn't happen they way present theory states. The arrogant tone doesn't exactly help, either...
All you need to do Mister Earl is produce some mathematical or empirical evidence which show the combination selection pressures accelerates the mutation and selection sorting/optimization process. Sadly, you like other evolutionists are mathematically incompetent.
So just to summarize, Kleinman, I will no longer try to change your opinion, because I no longer believe that is possible. I will, however, patiently wait as you continue to present data and see if you can prove anything that'll sway me.
Mister Earl, you never had any mathematical or empirical evidence to change my opinion. You think irrational and illogical speculations and extrapolations constitute a scientific argument. I’ll continue to show the mathematical data from Dr Schneider’s peer reviewed and published mathematical model of mutation and selection which Dr Schneider believes represents the essential variables in this process (and so do I) and the empirical evidence which substantiates the results from Dr Schneider’s model.
What results has rocketdodger presented? Rocketdodger spent an afternoon throwing together some code and then claims that n+1 selection pressures evolve more rapidly than n selection pressures. I’ll stick with Dr Schneider’s peer reviewed and published computer simulation that has been scrutinized for more than 20 years and for which Dr Schneider has published and posted extensive documentation, especially since the mathematical results from Dr Schneider’s model is reflected in real empirical examples of mutation and selection.He is talking about the post I made that shows how stupid you are when it comes to interpreting results from ev.
Which post was that? Was it this one?
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
Or was it this one where you claim that all fitness landscapes are convex?
http://forums.randi.org/showpost.php?p=3170363&postcount=6644 (http://forums.randi.org/showpost.php?p=3170363&postcount=6644)
Do you even know what a fitness landscape looks like, Kleinman? Here is a hint for you -- regardless of the number of selective pressures, the landscape is always a convex shape. There is no such thing as local optima that the population can "get stuck on" or whatever nonsense it is that you assert.
Or perhaps it was this one where you claim that if you get enough selection conditions that the mutation and selection sorting/optimization process speeds up?
http://forums.randi.org/showpost.php?p=3126277&postcount=6348 (http://forums.randi.org/showpost.php?p=3126277&postcount=6348)
At first, it appeared as though Kleinman might be right -- adding selective pressures in low numbers really does slow the average rate of fixation way down. However, once a "critical mass" has been reached, adding pressures actually drives the rate back up. Eventually, with enough pressures, you get to a point where the average rate of fixation is equal to or faster than it is under only a single pressure.
Maybe it was this quote you made?
http://forums.randi.org/showpost.php?p=3127246&postcount=6359 (http://forums.randi.org/showpost.php?p=3127246&postcount=6359)
Actually, Adequate and I sort of are. My simulation shows that if you introduce enough strong pressures, and if you measure the rate of fixation on average, then fixation is just as fast (or even faster).
Rocketdodger, you claim that n+1 selection pressures evolve more rapidly than n selection pressures but you have no real examples of your ridiculous claims.
Tell us how these facts fit into your theory, Kleinman:

When the mistake weights are [1,0,0], [0,1,0], or [0,0,1] the simulation never stops on Rseq >= Rfreq (which, by definition, means these weights are invalid).
There is no selection pressure for Rseq >=Rfreq. This demonstrates a fundamental misunderstanding you have of Dr Schneider’s ev model and how his selection process works. The best documentation for how Dr Schneider’s selection process works was not written by Dr Schneider but by I.G.D. Strachan and is available at: http://www.iscid.org/papers/Strachan_EvEvaluation_062803.pdf (http://www.iscid.org/papers/Strachan_EvEvaluation_062803.pdf)

Here is a pertinent quote from the paper:
For the recognizer gene, Schneider uses a simple form of neural network, called a Perceptron, consisting of a numeric weight vector w, and a threshold value Ɵ. The recognition action is performed by computing the dot product of an input vector x with the weight vector, and subtracting the threshold from it. If the resultant value is greater than zero, then the system is considered to have \recognized" the input, and if it is below zero, then recognition is not deemed to have occurred. Hence the recognition criterion is:

w · x - Ɵ > 0 (2)

The numerical values of the weight vector and the threshold are encoded onto the recognizer gene, by using sequences of 5 bases for each number (as reported in the paper, but the number of bases can be specified in the input file to the program). By encoding A = 00; C = 01; G = 10 and T = 11 in binary, the five bases yield a 10-bit number that represents integers in the range -512 : : : +511.

The inputs to the perceptron are computed by assigning a 1-of-4 code to each of the six bases in the scanned potential site: A -> (1; 0; 0; 0); C -> (0; 1; 0; 0); G -> (0; 0; 1; 0) and T -> (0; 0; 0; 1). For a sequence of six bases, there are therefore 24 inputs to the perceptron, in six groups of 4. These are described in the paper as a “weight matrix”, reflecting the 6 x 4 grouping. Each of the six rows in the matrix can only have a single 1, and the rest are zeros. However, the linear algebra in equation (2) implies no matrix operation, only the vector operation of the dot product (taking the pairwise products of the two vectors and summing the result). Because the inputs to the perceptron in this simulation are always only 0 or 1, the equation reduces to summing the weight matrix row entries corresponding to the base found at each position. The operation is illustrated schematically in Figure 1.
The figure can be viewed by clicking the above link. This paper written by I.G.D. Strachan gives and excellent review of the mathematics which Dr Schneider employed in order to develop his selection scheme and mathematical model.
When the mistake weights are [0,1,0] or [0,0,1] the simulation evolves a perfect creature in one generation (which, by definition, is impossible -- thus these weights are invalid).
No it doesn’t rocketdodger, what this demonstrates is how easy it is for the weight matrix to find matches on the genome and how difficult it is for selection to remove improper matches to the weight matrix in one portion of the genome while maintaining matches in other portions of the genome. This demonstrates how difficult it is to sort multiple conditions simultaneously.
When the mistake weights are [100,100,100], convergence happens faster than [1,100,1] or [1,1,100] and convergence has a higher rate than [100,1,1].
Mistake weights of [100,100,100] give the same results as mistake weights of [1,1,1]. Changing the relative weights changes the shape of the fitness landscape. You remember what the fitness landscape is? That’s the surface you claim is always convex. Nothing affects the fitness landscape like setting two of the three selection conditions to zero. It becomes trivially easily to satisfy the remaining selection condition. Reduce the number of sorting conditions to one and that condition is extremely easy to sort for and satisfy.
Suppose…

Suppose…

So in this model, the rate of evolution per pressure INCREASES with the number of pressures as N/log(N), contrary to kleinman's repeated assertions that "evolution is profoundly slowed by multiple pressures". Furthermore this simple model seems to coincide with the results of at least two somewhat more sophisticated computer models, one being ev and the other being something rocketdodger coded a while back.
Sol, do you still want to lose $10,000? Ev shows nothing of the kind and rocketdodger shows nothing.
When the mistake weights are [0,1,0] or [0,0,1] the simulation evolves a perfect creature in one generation (which, by definition, is impossible -- thus these weights are invalid).The funniest thing about this particular outcome is that if we were to accept it at face value, then ev proves that ANY arrangement of amino acids that accidentally occurs in nature will spontaneously bind together and start the cycle of organic life!
What it proves by definition is that neither of you have any understanding of the mutation and selection sorting/optimization process which ev is modeling.
Thus, kleinman destroys his entire theory by conceding that ev proves abiogenesis.
Legal beagle, are you looking for another ambulance to chase?
I doubt that Schneider would agree with this ridiculous outcome from his algorithm, but hey, it's a "valid" ev result!
Who knows what Dr Schneider thinks of his algorithm anymore? Perhaps he has changed fields and now is a noodleologist?
I doubt that Schneider would agree with this ridiculous outcome from his algorithm, but hey, it's a "valid" ev result!I guess this means that a person has to think about what is actually going on in Ev, in order to assign a valid interpretation to these fringe results. He can't just say "Oh look, viable creatures from only one selection pressure!"
Well, well Mr RcaPaulcity, are you going to claim that evolution of resistance from single drug therapy does not give viable creatures. I have posted hundreds of real examples of mutation and selection which shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process and your own algorithm shows the same thing. What real example of Rcapcity have you shown?

Are you now going to claim that ev is evolving real viable creatures? Paul, you’ve earned this:
http://forums.randi.org/images/smilies/doglaugh.gif
I guess this means that a person has to think about what is actually going on in Ev, in order to assign a valid interpretation to these fringe results. He can't just say "Oh look, viable creatures from only one selection pressure!"Isn't that the point of this whole discussion?
M_huber, this is the point of this discussion. Ev does demonstrate something about the mathematics of the mutation and selection sorting/optimization process. Dr Schneider and other evolutionists missed the fundamental principles of the mathematical behavior on this phenomenon. Dr Schneider took a peculiar finding from his particular model and chose to focus on this and missed the fundamental nature of this sorting/optimization process. This is an example how the evolutionist bias has interfered and continues to interfere with the proper mathematical and empirical interpretation of the mutation and selection sorting/optimization process.
I hope you enjoyed yours. I spent mine getting bitten by a ravenous cockatiel in my sleep. Ended up cooking some spaghetti, just to placate the bird. Spaghetti > Birdseed apparently.
My weekend was better than Friday; I mixed up my hair spray and underarm deodorant spray. My hair smelled ok but I couldn’t lift my arms for a day.

Hey Mister Earl, isn’t it dangerous keeping a carnivorous cockatiel around the house?

Before I go on and give the data for varying population and it’s affect on the generations for convergence in ev, do any of you experts on ev want to explain why varying g has little affect on the generations for convergence in Dr Schneider’s model?

Do not use personal attacks to argue your point. This is your last warning before suspension.

[Mister Earl]

[Have any of you mathematically incompetent evolutionists learned anything about the mathematics of the mutation and selection sorting/optimization process yet? ... Really, legal beagle?
I was hoping your brief vacation would see you returning slightly more civil. I was wrong, I guess.
I don’t argue that polymerases can’t mutate so that they can cleave xeno-molecules like nylon, what I argue is that the evolutionists’ gross over-extrapolation of this microevolutionary process to the evolution of lizards to birds is irrational, illogical and mathematically impossible.
I suppose I could ask you to prove that it is mathematically impossible, but I'm pretty certain I'd just get the same rehashed statements from before.
The reason I make this argument is based on the mathematics of Dr Schneider’s ev simulation of random point mutations and natural selection which show that combination selection pressures profoundly slow the sorting/optimization process and hundreds of real examples of mutation and selection which demonstrates this same finding. You evolutionists have completely bungled the understanding of the mutation and selection sorting/optimization process.
I wonder what Dr. Schneider himself would think. I'm going to try to contact him via email, and bring him in on this discussion.

Really? You think the greater the number of selection conditions the faster the evolutionary process proceeds? Where are all you citations which show your contention?
Rocketdodger posted this point in a much more fluent way than I could. You may want to review his "Kleinman FAQ".

Are you contending that frame shifts overcomes the mathematical fact the Dr Schneider’s ev program demonstrates that combination selection pressures profoundly slow the mutation and selection sorting/optimization process?
Why is it your entire argument resides on "This is a mathematical fact" when you've never proven this? We've shown you why EV isn't a perfect simulator for biological evolution. I see no need to rehash this.

Why legal beagle, how many times have you said good bye on this thread and you keep coming back to this discussion? I think you are the one obsessed with this discussion. You can’t produce the mathematical or empirical data to support your irrational and illogical theory of evolution so you look for any way you can to discredit me. Do you want to talk more about my malpractice case which I won yet you tried to discredit me with that? It so typical of you evolutionists to jump to conclusions when you don’t have the facts to support your irrational and illogical thinking, lizards must evolve into birds because a polymerase can mutate so that it can cleave nylon, perhaps in one of your 10^500 alternative universes but not in this one.
Personal attacks prove nothing. Neither against you, Kleinman, or by you.

Hey legal beagle, since you are such an expert on Dr Schneider’s ev model, why don’t you tell us why variations in have such little effect on the generations for convergence?
Rocketdodgers model showed different results than yours.

Mister Earl, what mathematical model of mutation and selection are you clinging to? Oh wait, you evolutionists don’t need any mathematical model to prove your irrational and illogical theory. You have your speculations and extrapolations to prove your point. Mister Earl, do you think that increasing the number of selection pressures will accelerate the mutation and selection sorting/optimization process?
I've got a simulator at home called "Framsticks". It's pretty nice. I've run a multitude of simulations on it, where I've cranked up the selection pressures to obscene levels. One of two things happen: First, complete extinction. Second, a multitude of genomes with superior fitness levels. Unlike EV, you can configure framsticks to utilize population levels and multiple, varying, selection pressures. I've run the same simulation with only one selection pressure, and at a low level, and those genomes only reach about 15% of the fitness level of the previous test in the same number of generations. If you'd like, you can download Framsticks, and I can send you the files to replicate my tests. Would you like to do this? If not, why not?

All you need to do Mister Earl is produce some mathematical or empirical evidence which show the combination selection pressures accelerates the mutation and selection sorting/optimization process. Sadly, you like other evolutionists are mathematically incompetent.
More ad hominem attacks. Spare me your egotistical nonsense. Either give us definitive proof, or go cry somewhere else. Your pointless bluster doesn't cover up the fact that your argument has very little weight.

Mister Earl, you never had any mathematical or empirical evidence to change my opinion. You think irrational and illogical speculations and extrapolations constitute a scientific argument. I’ll continue to show the mathematical data from Dr Schneider’s peer reviewed and published mathematical model of mutation and selection which Dr Schneider believes represents the essential variables in this process (and so do I) and the empirical evidence which substantiates the results from Dr Schneider’s model.
Grab framsticks, and when I get home tonight I'll email you the two trial files. Then you can come back tomorrow and offer your point of view how my simulations aren't valid when you don't get the results you want.

Who knows what Dr Schneider thinks of his algorithm anymore? Perhaps he has changed fields and now is a noodleologist?
I'll email him and try to get him to join us.

My weekend was better than Friday; I mixed up my hair spray and underarm deodorant spray. My hair smelled ok but I couldn’t lift my arms for a day. Hey Mister Earl, isn’t it dangerous keeping a carnivorous cockatiel around the house?
Very much so. We've had him for fifteen years, so I think he's just getting old and ornery. When he's in a good mood, it offsets a great deal of the biting. I just take his actions into context. (Old, ornery bird).

[kjkent1]

Have any of you mathematically incompetent evolutionists learned anything about the mathematics of the mutation and selection sorting/optimization process yet? Let’s find out...(clip)kleinman, your reply to my posts and to others clearly demonstrates why you cannot successfully discuss your theory with anyone who doesn't already agree with you.

Your comments are entirely non-responsive in every instance. You don't address your opponents' arguments -- you ignore them and restate you own position -- or, you request that your opponent prove something which is completely irrelevant to the argument at the time that you raise the issue.

Thus, there's little point in my responding to each of your individual points.

I will say this: you concede that polymerases can "mutate so that they can cleave xeno-molecules like nylon," yet you dismiss as irrational that those same mutations cannot aggregate to create a morphologically distinct organism over time.

Well, there is a really long fossil record showing that what you say is irrational, actually occurred. Now you can moan all day long that it's mathematically impossible. But, if, as above, you concede that a gross mutational change can occur in the K172 bacteria, then you cannot avoid the evidence in the fossil record that such changes have actually occurred over the ages.

You can, of course, cling to the position that Schneider's math shows that creating a perfect creature is impossibly slow, but that's irrelevant, because you have long conceded that (1) Rseq ~ Rfreq is meaningless, and (2) that ev doesn't model any gross mutational behaviors. In the first case, without convergence, there is no means of measuring whether or not a creature has evolved, and no means of identifying a potential life form from a dead string of amino acids. I.e., how do you know that a creature filled with missing and/or spurious bindings cannot reproduce? Apparently, since you dismiss the relationship of Rseq and Rfreq, you cannot know anything about the target organisms, other than their slowness in removing mistakes.

In the second case, the target organism could spend a very long time without much substantive change, and then suddenly change quite rapidly, due to an unexpected and beneficial mutation. Now, you can certainly argue that this is contrary to some "gradualist" (point mutation) theory of evolution -- but, it's not contrary to the general theory of evolution by mutation and selection -- it fits just fine.

What this leaves you with is one argument: Schneider's algorithm doesn't demonstrate the entire process of evolution. Well, not even Schneider himself contends that to be true.

So, what ARE you arguing, kleinman? Of course, I already know the answer: Genesis 1:1.

But, the relevant issue is that you have yet to prove Genesis 1:1, and you will not do so by showing that evolution is not purely the product of point mutation.

[Mister Earl]

In the second case, the target organism could spend a very long time without much substantive change, and then suddenly change quite rapidly, due to an unexpected and beneficial mutation. Now, you can certainly argue that this is contrary to some "gradualist" (point mutation) theory of evolution -- but, it's not contrary to the general theory of evolution by mutation and selection -- it fits just fine.
I've seen this with the framsticks program. Say I'm sorting for speed, (The selection pressure). I might see fitness values like 0.80106... 0.80108... 0.80112... and suddenly see it jump to 1.2308... 1.4257... 1.7963. Whenever I see this, I slap on the "slow the simulation" button and take a close look at what happened. Usually it's some minor, random change that made the genome much more fit than its ancestors, and random variations that happened to build on that start a "Rush". Fitness values that had been pretty stagnant then begin a large climb, before eventually plateauing or creeping along again.

[tumnus]

So, what ARE you arguing, kleinman? Of course, I already know the answer: Genesis 1:1.

But, the relevant issue is that you have yet to prove Genesis 1:1, and you will not do so by showing that evolution is not purely the product of point mutation.

Ah, the million dollar question, that wont get answered. I get a bit distressed when I see such endless, convoluted, downright wierd arguments over extreme minutae, when slowly stuff is being dug up like intermediate fossils of where whales come from and the like. These people still go on the same warpath, with the conviction that if there is something at the very small and precise detail about evolution, it will automatically prove their belief system (Jeesus, Krishna, whatever) correct.

And that's just not the way it works.

As a side point, my ISP homepage ran a debate about god and evolution. I thought I'd wade in (its at http://boards.virginmedia.com/digital/soundbites/creationism.html?page=1 if I'm allowed for links yet, but its not important)

I was a bit saddened how the same questions get asked: "Why are they still monkeys if we evolved from monkeys?" "Why are there no transitory fossils?" (apart from the transitory fossils)

It ended up with accusations of mocking, and I am a fool for believing that the earth isn't young. I dont have biology training, but I found this stuff out by reading quite easily. I was quite shocked how little other adults are actually aware of this stuff. Education problems? (and this is in the UK, where I thought it wasnt so much of a problem)

[Belz...]

I will say this: you concede that polymerases can "mutate so that they can cleave xeno-molecules like nylon,"

He said that ?

Well, there is a really long fossil record showing that what you say is irrational, actually occurred. Now you can moan all day long that it's mathematically impossible.

If reality disagrees with your mathematics, then you're bad at maths! :p

Apparently, since you dismiss the relationship of Rseq and Rfreq, you cannot know anything about the target organisms, other than their slowness in removing mistakes.

Is that all ev is about ?

So, what ARE you arguing, kleinman? Of course, I already know the answer: Genesis 1:1.

Hey, I know how to disprove Genesis 1:1.

Genesis 2:1.

[kleinman]

[Have any of you mathematically incompetent evolutionists learned anything about the mathematics of the mutation and selection sorting/optimization process yet? ... Really, legal beagle?I was hoping your brief vacation would see you returning slightly more civil. I was wrong, I guess.
Now what are you whining about? I thought I was being more civil; after all, I could have called you evolutionists mathematically incompetent nutbags and I used to call kjkent1 lita’ gator which really annoyed him.
I don’t argue that polymerases can’t mutate so that they can cleave xeno-molecules like nylon, what I argue is that the evolutionists’ gross over-extrapolation of this microevolutionary process to the evolution of lizards to birds is irrational, illogical and mathematically impossible.I suppose I could ask you to prove that it is mathematically impossible, but I'm pretty certain I'd just get the same rehashed statements from before.
Correct, I will continue to rehash the mathematics of the mutation and selection sorting/optimization process and the empirical evidence which supports it, now if only you evolutionists had something to rehash besides your tired old speculations and gross extrapolations.
The reason I make this argument is based on the mathematics of Dr Schneider’s ev simulation of random point mutations and natural selection which show that combination selection pressures profoundly slow the sorting/optimization process and hundreds of real examples of mutation and selection which demonstrates this same finding. You evolutionists have completely bungled the understanding of the mutation and selection sorting/optimization process.I wonder what Dr. Schneider himself would think. I'm going to try to contact him via email, and bring him in on this discussion.
If you have trouble finding his email address, I’ll provide it to you, after all, I discussed Dr Schneider’s model with him for several months via email before going public. I think you are going to find it difficult to get him to discuss his model publicly anymore.
Really? You think the greater the number of selection conditions the faster the evolutionary process proceeds? Where are all you citations which show your contention?Rocketdodger posted this point in a much more fluent way than I could. You may want to review his "Kleinman FAQ".
Both rocketdodger and Adequate have proven to be complete incompetents in the mathematics of the mutation and selection sorting/optimization process. Adequate has show some intelligence by withdrawing from this thread because all he was able to do was show that he was ignorant and self contradictory, rocketdodger continues to be sophomoric. If you want to believe that the greater the number of selection pressures the faster the evolutionary process proceeds, remember this, it is this type of irrational and illogical evolutionist thinking that contributes to the premature death of millions of people with diseases subject to mutation and selection.
Are you contending that frame shifts overcomes the mathematical fact the Dr Schneider’s ev program demonstrates that combination selection pressures profoundly slow the mutation and selection sorting/optimization process?Why is it your entire argument resides on "This is a mathematical fact" when you've never proven this? We've shown you why EV isn't a perfect simulator for biological evolution. I see no need to rehash this.
Not only is it a mathematical fact demonstrated by ev but it is also an empirical fact demonstrated by hundreds of real examples of mutation and selection I have already posted but will continue to post. You mathematically incompetent evolutionists have demonstrated nothing other than you have no idea how the mutation and selection sorting/optimization process actually works. You have an excuse, you are not a mathematician. People like Adequate who claim to be mathematicians have no excuse. Adequate’s stupid and contradictory assertions about how mutation and selection works set a Guinness record for stupidity.
Hey legal beagle, since you are such an expert on Dr Schneider’s ev model, why don’t you tell us why variations in g have such little effect on the generations for convergence?Rocketdodgers model showed different results than yours.
Get your facts straight Mister Earl. It is Dr Schneider’s peer reviewed and published model, not mine and rocketdodger has shown nothing from his model other than assertions. Rocketdodger has presented no data from his model and no empirical examples which demonstrate his irrational and illogical claims.
Mister Earl, what mathematical model of mutation and selection are you clinging to? Oh wait, you evolutionists don’t need any mathematical model to prove your irrational and illogical theory. You have your speculations and extrapolations to prove your point. Mister Earl, do you think that increasing the number of selection pressures will accelerate the mutation and selection sorting/optimization process?I've got a simulator at home called "Framsticks". It's pretty nice. I've run a multitude of simulations on it, where I've cranked up the selection pressures to obscene levels. One of two things happen: First, complete extinction. Second, a multitude of genomes with superior fitness levels. Unlike EV, you can configure framsticks to utilize population levels and multiple, varying, selection pressures. I've run the same simulation with only one selection pressure, and at a low level, and those genomes only reach about 15% of the fitness level of the previous test in the same number of generations. If you'd like, you can download Framsticks, and I can send you the files to replicate my tests. Would you like to do this? If not, why not?
Why don’t you run a case with 3 billion sticks and see how long it takes to accomplish anything. You evolutionists like to take these trivial sorting/optimization algorithms and say this is the mathematical proof for your theory. This is what happens when you make irrational and illogical extrapolations. Oh, ev allows for varying populations, multiple and varying selection pressures, variable mutation rates and so on and it shows that the number of selection pressures dominates the mathematics of this process.
All you need to do Mister Earl is produce some mathematical or empirical evidence which show the combination selection pressures accelerates the mutation and selection sorting/optimization process. Sadly, you like other evolutionists are mathematically incompetent.More ad hominem attacks. Spare me your egotistical nonsense. Either give us definitive proof, or go cry somewhere else. Your pointless bluster doesn't cover up the fact that your argument has very little weight.
You evolutionists besides being mathematically incompetent are a collection of whining crybabies. The mathematical proof I have is from a peer reviewed and published mathematical model of random point mutations and natural selection and I have posted (and will continue to post) hundreds of real examples of mutation and selection which demonstrates exactly what ev is showing, that is combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.
Mister Earl, you never had any mathematical or empirical evidence to change my opinion. You think irrational and illogical speculations and extrapolations constitute a scientific argument. I’ll continue to show the mathematical data from Dr Schneider’s peer reviewed and published mathematical model of mutation and selection which Dr Schneider believes represents the essential variables in this process (and so do I) and the empirical evidence which substantiates the results from Dr Schneider’s model.Grab framsticks, and when I get home tonight I'll email you the two trial files. Then you can come back tomorrow and offer your point of view how my simulations aren't valid when you don't get the results you want.
If your framsticks algorithm properly models the mutation and selection sorting/optimization process, do the parametric study of varying the number of sticks, selection conditions, mutation rate and so on and see what the effects of varying these parameters are. In the meantime, I’ll continue to post the results of Dr Schneider’s model which was based on real biological data.
Who knows what Dr Schneider thinks of his algorithm anymore? Perhaps he has changed fields and now is a noodleologist?I'll email him and try to get him to join us.
I have asked him and he said he was busy with other things but that was more than a year ago.
My weekend was better than Friday; I mixed up my hair spray and underarm deodorant spray. My hair smelled ok but I couldn’t lift my arms for a day. Hey Mister Earl, isn’t it dangerous keeping a carnivorous cockatiel around the house?Very much so. We've had him for fifteen years, so I think he's just getting old and ornery. When he's in a good mood, it offsets a great deal of the biting. I just take his actions into context. (Old, ornery bird).
Maybe if you fed him a bit more he wouldn’t see you as a food source.
Have any of you mathematically incompetent evolutionists learned anything about the mathematics of the mutation and selection sorting/optimization process yet? Let’s find out...(clip)kleinman, your reply to my posts and to others clearly demonstrates why you cannot successfully discuss your theory with anyone who doesn't already agree with you.
You don’t even agree with the data that ev produces. Until you evolutionists comprehend that the more complex the selection conditions are, the much, much slower the mutation and selection sorting/optimization process proceeds, we will never be in agreement on this topic. I have mathematical and empirical evidence of my claim and you have 10^500 alternative universes.

[joobz]

Kleinman, I see you are attempting death by mod. I'm only happy to oblige.


Please note that in your entire 1+ years of posting in this thread, have you not ever approached anything resembling a reasoned logical statement. During this whole time, you've failed to provide any evidence to support your claims. To put it simply, your theory is wrong becuase your assumptions are wrong. You've never been able to refute this statement. All you are offering now are insults and derisions.

[rocketdodger]

For the record, fitness landscapes generated for pressures that only target a single base are convex, which is what I was talking about when I said it, which is why I retracted that statement later in the context of pressures in general.

And you are simply wrong about ev, Kleinman.

1) The whole purpose of ev is to investigate Rseq and Rfreq -- this is explicitly stated by Schneider. If the simulation never converges on Rseq >= Rfreq, it means nothing meaningful is happening.

2) The fact that a perfect creature evolves in one generation when weights [0,1,0] or [0,0,1] means only that there are no spurious binding sites in the genome -- BECAUSE NO BINDING SITES HAVE EVOLVED YET.

3) How can the simulation converge to a perfect creature in six generations, using weights [1,0,0], when it is mathematically impossible to mutate enough bases to get binding sites for every gene, never mind fix them, in that time? Think about it. How many genes are there in the genome? How many mutations per base? Even if every mutation was perfectly placed, could you generate binding sites for every gene in a mere 6 generations? Do the math, you fool.

[Mister Earl]

Now what are you whining about? I thought I was being more civil; after all, I could have called you evolutionists mathematically incompetent nutbags and I used to call kjkent1 lita’ gator which really annoyed him.
I suppose if you don't have evidence to back you up, you can always revert to the ad hominems and strawmen attacks. Gotta go with what is available to you, right?
Correct, I will continue to rehash the mathematics of the mutation and selection sorting/optimization process and the empirical evidence which supports it, now if only you evolutionists had something to rehash besides your tired old speculations and gross extrapolations.
You need to provide math that proves it first. You haven't gotten around to that yet.
If you have trouble finding his email address, I’ll provide it to you, after all, I discussed Dr Schneider’s model with him for several months via email before going public. I think you are going to find it difficult to get him to discuss his model publicly anymore.
Sure, let's see if you have a different one than I do.
Both rocketdodger and Adequate have proven to be complete incompetents in the mathematics of the mutation and selection sorting/optimization process. Adequate has show some intelligence by withdrawing from this thread because all he was able to do was show that he was ignorant and self contradictory, rocketdodger continues to be sophomoric. If you want to believe that the greater the number of selection pressures the faster the evolutionary process proceeds, remember this, it is this type of irrational and illogical evolutionist thinking that contributes to the premature death of millions of people with diseases subject to mutation and selection.
Baseless speculation. Please provide evidence.
Not only is it a mathematical fact demonstrated by ev but it is also an empirical fact demonstrated by hundreds of real examples of mutation and selection I have already posted but will continue to post. You mathematically incompetent evolutionists have demonstrated nothing other than you have no idea how the mutation and selection sorting/optimization process actually works. You have an excuse, you are not a mathematician. People like Adequate who claim to be mathematicians have no excuse. Adequate’s stupid and contradictory assertions about how mutation and selection works set a Guinness record for stupidity.
Baseless speculation. Please provide evidence.
Get your facts straight Mister Earl. It is Dr Schneider’s peer reviewed and published model, not mine and rocketdodger has shown nothing from his model other than assertions. Rocketdodger has presented no data from his model and no empirical examples which demonstrate his irrational and illogical claims.
Dr. Schneider's model also says it doesn't factor in a large number of parameters that would be required to simulate biological evolution. Of course, this makes your model look bad, so you ignore this part and try to distract us with pithy insults and strawmen.
Why don’t you run a case with 3 billion sticks and see how long it takes to accomplish anything. You evolutionists like to take these trivial sorting/optimization algorithms and say this is the mathematical proof for your theory. This is what happens when you make irrational and illogical extrapolations. Oh, ev allows for varying populations, multiple and varying selection pressures, variable mutation rates and so on and it shows that the number of selection pressures dominates the mathematics of this process.
Yet you ignore the part where it says in the study that population sizes weren't used, along with a large number of other parameters. You ignore this part, because cherry-picking data demands you ignore it.
You evolutionists besides being mathematically incompetent are a collection of whining crybabies. The mathematical proof I have is from a peer reviewed and published mathematical model of random point mutations and natural selection and I have posted (and will continue to post) hundreds of real examples of mutation and selection which demonstrates exactly what ev is showing, that is combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.
No, your interpretation proves it. In order to use your interpretation, we'd have to ignore the rest of the paper stating it didn't use a large number of parameters that would be required to simulate biological evolution.
If your framsticks algorithm properly models the mutation and selection sorting/optimization process, do the parametric study of varying the number of sticks, selection conditions, mutation rate and so on and see what the effects of varying these parameters are. In the meantime, I’ll continue to post the results of Dr Schneider’s model which was based on real biological data.
I've already done so, as noted in my previous post. The stronger the selection pressures I use, the faster I get higher fitness values. If I keep them high and don't vary them, like in your "model", then I still get a higher fitness value than when I use one selection pressure. If I vary them during the course of the simulation, as would be expected during realistic conditions, then I get even higher fitness values.
I have asked him and he said he was busy with other things but that was more than a year ago.
It's all good. I'll contact him and see what he has to offer, if anything.
Maybe if you fed him a bit more he wouldn’t see you as a food source.
Just like you, Kleinman. Making observations and declaring it fact when you don't have enough data available to you. He bites with the intention of getting my intention, not for consuming human flesh. He does the same when he wants a bath. He flies to the sink, and yaps until I open the tap for him.
You don’t even agree with the data that ev produces. Until you evolutionists comprehend that the more complex the selection conditions are, the much, much slower the mutation and selection sorting/optimization process proceeds, we will never be in agreement on this topic. I have mathematical and empirical evidence of my claim and you have 10^500 alternative universes.
Slight correction. I don't agree with your interpretation of your results. The point where we differ is where I note that the paper itself says that EV isn't a good model for evolution, because for THAT PAPER, it didn't use a large number of variables that would be needed to simulate biological evolution. You ignore this part and all contradicting evidence. You always will, and I accept that. I'll sit here and watch like I have been doing, in the likely-vain hope that you'll see the flaws in your theory and decide to either patch them up, or do other testing to account for that.

[sol invictus]

Sol, do you still want to lose $10,000? Ev shows nothing of the kind and rocketdodger shows nothing.

You already refused to bet on that, I suppose because even you don't believe your claims. That makes you a lying hypocrite, and I see no point in further dialog with you. In any case it appears you are trying to goad the moderator into suspending your account, in which case the point will be moot.

Have a nice day.

Keep in mind the Membership Agreement and do not use personal attacks or insults to argue your point.

[joobz]

Kleinman has been suspended for three days.

In the interest of full disclosure, I am the "whiny crybaby evolutionist" who reported him.

[m_huber]

Reality vs. Math.

When they fight, who wins?

Depends on which one serves your current agenda.

(Unless you are a scientist, and then reality wins every time.)

[rocketdodger]

Reality vs. Math.

When they fight, who wins?

Depends on which one serves your current agenda.

(Unless you are a scientist, and then reality wins every time.)

When reality and math fight, you have either your reality or your math wrong.

[m_huber]

When reality and math fight, you have either your reality or your math wrong.

That would be my point.

My example: Dr. Alan Kleinman.

[Belz...]

Suspended. Why am I not surprised ? Now he can go to answersingenesis and claim that we kicked him for being right.

[articulett]

Kleinman has been suspended for three days.

In the interest of full disclosure, I am the "whiny crybaby evolutionist" who reported him.

But you don't know if you are the only "whiny crybaby evolutionist" who reported him.

I kinda like to study him... the anosognosia... the way everything he reads and spews must be filtered through the "evolution is mathematically impossible" filter that allows him to keep his favorite delusion alive. He never has to put any alternate theory on the table-- just keep himself from accepting this one and the delusion stands-- he "wins". Every time he gets the last word he props up his belief in his rightness without ever having to put what it is he is right about on the table for examination.

Kleinman is the prototypical creationist woo--almost a caricature of the species.

They have a foundational premise built on a straw man that props up their delusion --and they do everything in their power to keep that straw man looking like a real life person to them. In Kleinman's case, it's more a Pinnochio than strawman, of course.

(Oh shoot... now he's going to ad hom me... I must remember "formosa's law"--I hope he doesn't start in with the font abuse!)

[Paul C. Anagnostopoulos]

Isn't that the point of this whole discussion?
You must be mistaking me for someone who is still taking this conversation seriously. :D

~~ Paul

[Belz...]

But you don't know if you are the only "whiny crybaby evolutionist" who reported him.

No, in fact I reported him several times in the past weeks. A few insults, I can take; in fact, as you know, I dish 'em out, myself. But Kleinman's tantrum was out of control.

ETA: But the Godwin part was hilarious.

I kinda like to study him... the anosognosia... the way everything he reads and spews must be filtered through the "evolution is mathematically impossible" filter that allows him to keep his favorite delusion alive.

I'm sure quite a few psychologists would love this thread.

They have a foundational premise built on a straw man that props up their delusion --and they do everything in their power to keep that straw man looking like a real life person to them.

"To them" are the key words, here. Why they are actually doing this on a web forum rather than by their lonesome at home is a mystery to me: there's no actual difference.

ETA: Kleinman's almost at the point where he really does have a conversation with himself. "Hey, look at those mathematically challenged evolutionists! - You said it, pal! They don't understand how multiple constant directional selection presures profoundly slow down the evolutionary process. Yes, indeed, evolution is mathematically and empirically impossible and we've proven it with the hundreds of real-life citations we've provided ! You're the man, Kleinman! Thanks, you too."

[articulett]

That's the way of the woo. They argue here because it props up their delusion that conclusions have been given careful scrutiny in the scientific community... and since no one could change their mind... they must be right.

It's sad. It's kind of schizophrenic. But some people would rather believe a delusion than understand that they've been fooling themselves. That's the nature of delusion-- sometimes it feels more real than reality... who needs evidence when you have faith...

[Bellatrix]

As for wanting to teach Creationism in public schools -- let them try. But give those kids an earlier start on Philosophy and Reason, especially when it comes to recognizing fallacious statements and unsubstantiated data.

You know; the "Scientific Method."

-

The only problem with the "Scientific Method" when dealing with some of these people is that if you read the home page of this group they feel that Rene Descartes is the beginning of the end for them. Because it is with his influence the scientific method came to be.
here's the url http://www.evolutionisdead.com/index.php

[joobz]

Suspended. Why am I not surprised ? Now he can go to answersingenesis and claim that we kicked him for being right.He can claim victory if he likes. You'll not stop a liar from lying.

But you don't know if you are the only "whiny crybaby evolutionist" who reported him.
True. I just assumed it because it would be easier if he could attack one cry baby instead of all posters.


This thread is purely a debate on citizen kane.
http://tubearoo.com/articles/91406/Kids_in_the_Hall_Citizen_Kane.html

[Dr Adequate]

The only problem with the "Scientific Method" when dealing with some of these people is that if you read the home page of this group they feel that Rene Descartes is the beginning of the end for them. Because it is with his influence the scientific method came to be.
here's the url http://www.evolutionisdead.com/index.php It's not often that a creationist comes up with a new lie, but that guy is actually equating natural selection with Lamarckian variation, isn't he?

As usual, it's hard to tell whether he's stupid, dishonest, or just off his nut.

[kleinman]

How could I let the weekend go by without posting more mathematical data and empirical evidence which shows that the theory of evolution is both mathematically and empirically impossible?

Let’s summarize where our discussion on the theory of evolution stands. The spokesman for your theory makes the following two claims.

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

2. The weather long ago transformed reptiles into birds. Can we put this concept into mathematical terms? Of course we can:

Lizards + Blizzards = Buzzards + Gizzards

Isn’t evolution a wizard? Now we don’t have weather anymore because lizards are still lizards and buzzards are still buzzards but someday, weather will return and blizzards will again turn lizards into buzzards with gizzards. An interesting speculation for the SciFi channel but no your spokesman has neither mathematical nor empirical evidence to back up this speculation either.

Enough of this illogical speculation of evolutionism and back to the mathematics of the mutation and selection sorting/optimization process and the empirical evidence which supports this mathematics. We have been looking at the peer reviewed and published mathematical model written by evolutionist Dr Tom Schneider and published in the evolutionist journal Nucleic Acids Research which mathematically models random point mutations and natural selection. This mathematical model maps out to an implicit multi-dimensional functional space given by the functional equation:

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

Where,

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

We have been mapping out the 6-dimensional surface described by this functional equation by taking series of cuts along planes through this 6-dimensional surface and generating the data points which describes this surface. The first series we looked at were through the mr, gfc planes and we obtained the following points on the functional surface:

G=256, population=64, g=16, nsp=3:
mr|gfc to perfect creature
10^-7|95975841
10^-6|4278078
10^-5|1105535
10^-4|47279
10^-3|5029
1|662
2|572
3|12890
4|>1,000,000 did not converge

G=512, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|2412
2|1251
3|973
4|13251
5|22790
6|>1,000,000 did not converge

G=1024, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|18030
2|9701
3|4679
4|2991
5|1299
6|1979
7|3782
8|7254
9|16243
10|>1,000,000 did not converge

G=2048, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|42641
2|36817
3|11480
4|6049
5|10364
6|9708
7|3634
8|5382
9|5089
10|6170
11|9851
12|3952
13|10880
14|38738
15|6145
16|105799
17|259469
18|>1,000,000 did not converge

G=4096, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|163722
2|48755
3|57212
4|30316
5|19675
6|23306
7|17689
8|21947
9|13328
10|8935
11|16043
12|10225
13|17029
14|16052
15|17186
16|7715
17|14761
18|8772
19|12152
20|8806
21|7647
22|6724
23|4959
24|4096
25|13463
26|8325
27|8067
28|17877
29|46876
30|1000000 did not converge

These series of cases done in mr, gfc plane demonstrate a paraboloid shape to the surface. With lower mutation rates, the sorting process takes more generations, after all if the mutation rate was zero, there would be nothing to sort and if the mutation rate is too high, the genome is being scrambled too much and the sorting conditions can not be satisfied. What do you evolutionists think would happen to a population subjected to a mutagen like radiation or a chemical mutagen?

Now what happened when we varied g? We got the following data:

G=4096, population=64, mr=1 mutation per genome per generation, nsp=3:
g|gfc to perfect creature
2|140441
3|55585
4|52475
5|65441
6|26551
7|56496
8|79879
9|32391
10|59240
11|10684
12|53572
13|30162
14|35564
15|54498
16|42641
17|61064
18|54802
19|31806
20|45631
40|24544
80|28916
160|34389
200|28826

None of you evolutionists dared to offer an explanation of why gamma just seems to oscillate around without giving any particular direction to this variable. So here is the explanation why the curve behaves like this. g is the number of binding sites which are simply the portions of the genome where if the weight matrix does not find a match, it is counted as a mistake in the algorithm. Varying g simply changes whether a match of the weight matrix gives a mistake or does not give a mistake in that portion of the genome. Sorting must still be done based on the selection conditions at each locus in the genome, varying gamma only changes whether the conditions must match or not match the weight matrix at those particular portions of the genome.

Now then, how does population affect Dr Schneider’s model? Let’s start with Dr Schneider’s published case.

G=256, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|662
128|741
256|569
512|492
1024|451
2048|296
4096|167
8192|154
16384|162
32768|186

Wait a minute; I thought you evolutionists said that increasing population accelerates evolution? What’s happening here? Dr Schneider’s model is showing that increasing population accelerates evolution slightly but then the curve flattens out? How could this be? Is Dr Schneider’s mathematics wrong? Let’s try Dr Schneider’s model with a mutation rate of mr=1 mutation per million bases per generation

G=256, mr=1 mutation/million bases-generation, g=16, nsp=3:
n|gfc to perfect creature
64|4278078
128|2587709
256|5968438
512|4429939
1024|4510187
2048|1638610
4096|685196
8192|694504
16384|917748
32768|380032

Anyone want to make a guess how large the lizard population was that you assert transformed into a bird population by mutation and selection?

Next week we’ll look at this further. While you are waiting for the next episode in the story of the mutation and selection sorting/optimization process, here are some more empirical examples of how mutation and selection actually works.

http://www.malariaandhealth.com/professional/abstracts.htm (http://www.malariaandhealth.com/professional/abstracts.htm)
The aim of this workshop was to issue updated practical recommendations for the rational use of the QingHaoSu (QHS) derivatives, (i.e. medicines really in use and not molecules still under development). 54 malariologists and other experts from Europe, Africa, Latin America and Asia were invited, from research centers, universities, national administrations, military research centers or hospitals, pharmaceutical companies, NGOs, etc., together with WHO and international agency observers. Thanks to working papers including the most recent available data, and particularly the Cochrane Center meta-analysis of clinical trials, several practical conclusions were agreed on by the participants (they are views of individuals and do not represent the opinions or recommendations of any official body or agency):

(1) In adults and children QHS derivatives are the most rapidly acting antimalarials against falciparum malaria, including multidrug resistant strains; (2) There has been no resistance identified so far, but this should not cause complacency in the use of QHS; (3) All the investigated QHS drugs have shown comparable efficacy. There is a serious practical risk associated with the appearance of substandard and inadequately labelled preparations on the international market; (4) QHS derivatives are well tolerated and there is no evidence so far of serious clinical toxicity in man. The neurotoxicity seen in animals after high doses of certain compounds has not been reported in man; (5) Whenever possible, these drugs should be used in combination with a second, longer-acting antimalarial to avoid or limit the risk of resistance; (6) QHS should not be used for chemoprophylaxis. It was agreed that for use in severe malaria IM artemether and probably IV or IM artesunate are at least as effective as quinine; rectal formulations of these drugs require further studies but seem very promising. Use in uncomplicated malaria or during pregnancy, pharmacokinetics, activity and tolerability, were also considered in detail.

The final conclusions were focused on GMP standards of quality, efficacy and safety and, in addition to their application to QHS derivatives and other antimalarials, they should be more generally employed to control all drugs used in Tropical Medicine.
And
Chlorproguanil-dapsone (Lapdap) is a novel antifolate combination which offers the potential for affordable treatment for Fansidar™-resistant falciparum malaria in Africa, and reduced selective pressure for drug resistance.

Laboratory work, which has underpinned the development of Lapdap, started in Kenya in the early 1980s. Chlorcycloguanil [CCG], the active metabolite of chlorproguanil [CPG], was shown to have high activity against both pyrimethamine-sensitive and -resistant parasites, and to act synergistically in combination with sulfonamides and sulphones. A pilot study of Lapdap at two sites in Kenya showed that parasitaemia was cleared by a single dose, although recrudescence was common. In 1987-88, the relationship between selective pressure for parasite resistance and elimination half-life was demonstrated at Kilifi, which established the potential advantage of a short half-life combination like Lapdap, and this was further supported by a comparison of the in vitro therapeutic indices of the available antifolate combination treatments, undertaken in Liverpool and Kenya in 1992. Current investigations aim to define the relationship between drug pharmacokinetics and susceptibility to antifolate action, of parasites with particular dhps and dhfr genotypes, and to define resistance to this class of drug at the molecular level.

To date, clinical trial work on Lapdap has been undertaken with scientific, rather than regulatory, aims in mind. The completed Kilifi trial compared Lapdap with pyrimethamine-sulfadoxine [PM/SD] in symptomatic childhood falciparum malaria. The trial studied both a single dose of Lapdap [1.2 mg kg-l and 2.4 mg kg-l of CPG and DDS respectively] and three doses at 24 hour intervals. A community control group was recruited to estimate the monthly incidence of new parasitaemia. Initial clinical response to Lapdap [both regimens] and PM/SD was similar. However, in comparison with the control group the relative risk of new parasitaemia was 2.10 [95%CI 1.66 to 2.65] after one dose of Lapdap, 1.31 [0.99, 1.73] after three doses and 0.63 [0.43, 0.93] after one dose of PM/SD. We interpret this trial to show that (a) one dose of this potent, but rapidly-eliminated, combination is inadequate, (b) three doses of Lapdap give an adequate response and (c) PM/SD provides a period of chemoprophylaxis with the disadvantage of high selection pressure for resistance. Pharmacokinetic work [done in parallel with this trial] suggested that, while the dose of DDS [2.4 mg kg- 1 daily] was probably satisfactory, the dose of CPG [1.2 mg kg- 1 daily] may have been too low, and rising dose tolerance studies subsequently established that a CPO dose of 2.0 mg kg-l was tolerable. Ongoing clinical trial work in Kenya, Malawi and Tanzania [using 2.0 and 2.5 mg kg-1 of CPG and DDS respectively, daily for 3 days] will study (a) whether the lack of chemoprophylaxis after Lapdap confers disadvantage to the individual patient in comparison with PM/SD, and (b) whether Lapdap is as effective a salvage therapy in patients with "PM/SD-failure", as in-vitro data would predict.
And
Antimalarial drug development depends on the clear recognition of the importance of the differential susceptibility both of different stages and species of Plasmodium to drugs and the genetic versatility of these protozoa. Unlike most antimicrobial agents, antimalarial drugs may be targeted against different life cycle stages. Most compounds have a limited range of stages against which they are effective. In antibacterial chemotherapy, especially against chronic infections such as tuberculosis, it has long been accepted that polytherapy is essential in order either to overcome or restrict the emergence of drug-resistant organisms. This principle, in spite of many warnings, has only just started to gain acceptance in the antimalarial field. Antimalarial combinations may (1) target different life cycle stages, (2) reinforce drug action against specific metabolic pathways, (3) block the emergence of genetic variants or (4) reverse the pharmacological sequelae resulting from the selection of drug-resistant mutants. The first principle which was originally proposed by Guttman and Ehrlich in 1891 has recently been resurrected with the use of the artemisinin family against drug-resistant falciparum malaria and is currently a novel focus of attention by WHO. It is also of major importance in the prevention and treatment of chloroquine-resistant P. vivax by, for example, etaquine. The second principle became of significance after Hurly showed in 1959 that pyrimethamine and sulphadiazine potentiate each other's action against P. falciparum. It is currently being pursued by such trials as that of dapsone plus chlorproguanil. The third principle is exemplified by laboratory studies of combinations containing novel endoperoxides and clinical trials of benflumetol with artemether. The fourth principle, which is of wide application in cancer chemotherapy, may shortly provide rational new ways to treat patients infected with multidrug-resistant parasites. The consistent reluctance of physicians and health authorities to deploy rationally designed antimalarial drug combinations must be abandoned.
And
Co-artemether is a fixed combination antimalarial containing the artemisinin derivative artemether and the aryl amino alcohol benflumetol (lumefantrine). The combination exploits the rapid actions of the artemisinins and the more prolonged actions of benflumetol. Artemether exerts its antimalarial actions via the generation of reactive free radical species within the parasite's digestive food vacuole. These species are produced by the iron-dependent catalytic breakdown of the unusual peroxide bridge in this molecule. Benflumetol shares structural and physicochemical characteristics with other so called '"Class II blood schizontocides" such as mefloquine. As such, it is assumed that these drugs interact with some component of the haemoglobin degradation pathway characteristic of intra-erythrocytic parasites. The central importance of this pathway to benflumetol action has been established using a specific inhibitor of the initial haemoglobin cleavage event. The use of the combination has additional advantages in that the drugs have been shown to interact synergistically both in vitro against P. falciparum and in vivo against P. berghei and the use of drug combinations should reduce the rate of resistance development. The artemisinins are rapidly eliminated in man with elimination half-lives in the order of hours, whereas benflumetol shows variable bioavailability and a long elimination half-life. These pharmacokinetic differences between the two drugs will limit the importance of the synergy between the two drugs and may have an influence on the rate of resistance development.
And
Benflumetol (lumefantrine) and artemether are two new antimalarials developed in China. Both have good therapeutic effects against chloroquine-resistant Falciparum malaria. Benflumetol is a fluoremethanol, and is an active schizonticidal drug. It is formulated for oral administration as a solution in linoleic acid in the form of capsules. In China it has cure rates of above 95% against P. falciparum infections, but its onset of action is slow. It has low toxicity. Artemether is a derivative of artemisinin. It is characterised by its rapid onset of schizonticidal action, but has a relatively high rate of recrudescence.

A combination of the two drugs was developed in China in order to maintain their strong points while averting their shortcomings. This combination of artemether and benflumetol is synergistic. The synergistic indices were more than 5 and 6, calculated from ED50 and ED90 respectively, when tested against P. berghei in mice. The combination delayed the emergence of drug resistance and reduced the resistance level.

A regimen for clinical use was established. A fixed combination tablet comprising one part of artemether (20 mg) and six parts of benflumetol (120 mg) is in use. Four doses of four tablets taken at 0, 8, 24 and 48 hours had a satisfactory effect in patients with Falciparum malaria infections.

The treatment combines the benefits of both drugs, with a relatively short therapeutic course, rapid onset of action and high cure rate. It has low toxicity and is a well-tolerated drug for the treatment of malarial infections.
And
Antimalarial drug resistance is increasing throughout the tropical world. In some parts of Southeast Asia and South America there is complete resistance of P. falciparum to chloroquine and the combination of sulphadoxine-pyrimethamine. There is also partial resistance to quinine and mefloquine in some areas. Resistance to artemisinin and its derivatives has not been reported, although when used alone, these compounds are associated with high recrudescence rates, particularly if used in courses of less than 5 days. In 1994, the combination of mefloquine plus artesunate was introduced on the western border of Thailand and since then it has retained excellent efficacy. In vitro tests have confirmed that there has been no further decline in P. falciparum sensitivity to mefloquine.

Drug resistance arises as a result of genetic mutation(s), which are selected under drug pressure and then transmitted from one host to another. Combining unrelated drugs reduces the chance that a resistant mutant will be selected by (i.e. survive) drug treatment. The artemisinin derivatives are the most active antimalarials available and will reduce the infecting parasite biomass by 10,000-fold each cycle (2 days).

There is evidence from laboratory and field studies that the rate of gametocyte carriage increases with declining antimalarial efficacy. A recrudescent (i.e. resistant) infection is more likely to present with patent gametocytaemia, and as a consequence more drug-resistant strains are more likely to be transmitted. The artemisinin derivatives markedly reduce gametocyte carriage. Combination treatment regimens that include artemisinin derivatives reduce the emergence of resistance, the transmission, and thus the spread of, drug-resistant strains of P. falciparum.
The empirical evidence is clear and in the coming weeks, the mathematical evidence will become clear to you as well as we continue to investigate the mathematical behavior of Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

Dr Schneider, I continue to support your model and the results it gives despite the fact that your fellow evolutionists continue to discredit your model. Dr Schneider, your model shows mathematically what has been observe empirically about the mutation and selection sorting/optimization process for more than 50 years.

Hopefully we can avert another generation from being confused on how this process works and it will not take 5 years to figure out that combination therapy should be used for diseases like HIV and other diseases subject to the mutation and selection sorting/optimization process and that we can prevent evolutionists from propagating the erroneous, illogical and irrational teaching of how the mutation and selection process works and their contribution to the premature death of millions of people with diseases subject to mutation and selection. All you evolutionists need to do is use some 21st century mathematics to bring your 19th century theory up to date. Of course when you do that, you would realize that it is mathematically impossible to transform a lizard into a bird by the mutation and selection sorting/optimization process no matter what the weather is like.

You all have a good weekend pondering these facts of how the mutation and selection sorting/optimization process actually works.

[Belz...]

Have you spoken about this obsession of yours to your local psychologist, Kleinman ? I'm sure he'd be very interested.

This is getting a little cheesy. Let's keep the armchair psychoanalysis to a minimum.

[kjkent1]

How could I let the weekend go by without posting more mathematical data and empirical evidence which shows that the theory of evolution is both mathematically and empirically impossible?Well, for starters, you could actually post some evidence supporting your position.

What would life be without at least a daily dose of kleinmania?

[m_huber]

Alan, the human body is not the best environment to model evolution. But if that is what you choose, then at least look at what the good doctors are trying to do. They are adding something to the environment that would not otherwise be there in an attempt to slow the evolution of an organism. Without an intelligent design, evolution runs rampant. Only when an intelligence acts on the system does it completely (and quite unnaturally) stabilize.

Even if lack of evolution was a reasonable conclusion to reach from the data that you have been looking at, it does not speak at all about organisms larger than bacteria (and perhaps not even that large). Life behaves somewhat differently on different scales. If you show evolution not to work in a specific case on a micro scale, you have not defeated evolution.

[Dr Adequate]

How could I let the weekend go by without posting more mathematical data and empirical evidence which shows that the theory of evolution is both mathematically and empirically impossible?

Let’s summarize where our discussion on the theory of evolution stands. The spokesman for your theory makes the following two claims.

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

2. The weather long ago transformed reptiles into birds. Can we put this concept into mathematical terms? Of course we can:

Lizards + Blizzards = Buzzards + Gizzards

Isn’t evolution a wizard? Now we don’t have weather anymore because lizards are still lizards and buzzards are still buzzards but someday, weather will return and blizzards will again turn lizards into buzzards with gizzards. An interesting speculation for the SciFi channel but no your spokesman has neither mathematical nor empirical evidence to back up this speculation either.

Enough of this illogical speculation of evolutionism and back to the mathematics of the mutation and selection sorting/optimization process and the empirical evidence which supports this mathematics. We have been looking at the peer reviewed and published mathematical model written by evolutionist Dr Tom Schneider and published in the evolutionist journal Nucleic Acids Research which mathematically models random point mutations and natural selection. This mathematical model maps out to an implicit multi-dimensional functional space given by the functional equation:

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

Where,

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

We have been mapping out the 6-dimensional surface described by this functional equation by taking series of cuts along planes through this 6-dimensional surface and generating the data points which describes this surface. The first series we looked at were through the mr, gfc planes and we obtained the following points on the functional surface:

G=256, population=64, g=16, nsp=3:
mr|gfc to perfect creature
10^-7|95975841
10^-6|4278078
10^-5|1105535
10^-4|47279
10^-3|5029
1|662
2|572
3|12890
4|>1,000,000 did not converge

G=512, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|2412
2|1251
3|973
4|13251
5|22790
6|>1,000,000 did not converge

G=1024, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|18030
2|9701
3|4679
4|2991
5|1299
6|1979
7|3782
8|7254
9|16243
10|>1,000,000 did not converge

G=2048, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|42641
2|36817
3|11480
4|6049
5|10364
6|9708
7|3634
8|5382
9|5089
10|6170
11|9851
12|3952
13|10880
14|38738
15|6145
16|105799
17|259469
18|>1,000,000 did not converge

G=4096, population=64, g=16, nsp=3:
mr|gfc to perfect creature
1|163722
2|48755
3|57212
4|30316
5|19675
6|23306
7|17689
8|21947
9|13328
10|8935
11|16043
12|10225
13|17029
14|16052
15|17186
16|7715
17|14761
18|8772
19|12152
20|8806
21|7647
22|6724
23|4959
24|4096
25|13463
26|8325
27|8067
28|17877
29|46876
30|1000000 did not converge

These series of cases done in mr, gfc plane demonstrate a paraboloid shape to the surface. With lower mutation rates, the sorting process takes more generations, after all if the mutation rate was zero, there would be nothing to sort and if the mutation rate is too high, the genome is being scrambled too much and the sorting conditions can not be satisfied. What do you evolutionists think would happen to a population subjected to a mutagen like radiation or a chemical mutagen?

Now what happened when we varied g? We got the following data:

G=4096, population=64, mr=1 mutation per genome per generation, nsp=3:
g|gfc to perfect creature
2|140441
3|55585
4|52475
5|65441
6|26551
7|56496
8|79879
9|32391
10|59240
11|10684
12|53572
13|30162
14|35564
15|54498
16|42641
17|61064
18|54802
19|31806
20|45631
40|24544
80|28916
160|34389
200|28826

None of you evolutionists dared to offer an explanation of why gamma just seems to oscillate around without giving any particular direction to this variable. So here is the explanation why the curve behaves like this. g is the number of binding sites which are simply the portions of the genome where if the weight matrix does not find a match, it is counted as a mistake in the algorithm. Varying g simply changes whether a match of the weight matrix gives a mistake or does not give a mistake in that portion of the genome. Sorting must still be done based on the selection conditions at each locus in the genome, varying gamma only changes whether the conditions must match or not match the weight matrix at those particular portions of the genome.

Now then, how does population affect Dr Schneider’s model? Let’s start with Dr Schneider’s published case.

G=256, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|662
128|741
256|569
512|492
1024|451
2048|296
4096|167
8192|154
16384|162
32768|186

Wait a minute; I thought you evolutionists said that increasing population accelerates evolution? What’s happening here? Dr Schneider’s model is showing that increasing population accelerates evolution slightly but then the curve flattens out? How could this be? Is Dr Schneider’s mathematics wrong? Let’s try Dr Schneider’s model with a mutation rate of mr=1 mutation per million bases per generation

G=256, mr=1 mutation/million bases-generation, g=16, nsp=3:
n|gfc to perfect creature
64|4278078
128|2587709
256|5968438
512|4429939
1024|4510187
2048|1638610
4096|685196
8192|694504
16384|917748
32768|380032

Anyone want to make a guess how large the lizard population was that you assert transformed into a bird population by mutation and selection?

Next week we’ll look at this further. While you are waiting for the next episode in the story of the mutation and selection sorting/optimization process, here are some more empirical examples of how mutation and selection actually works.

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

And

And

And

And

And

The empirical evidence is clear and in the coming weeks, the mathematical evidence will become clear to you as well as we continue to investigate the mathematical behavior of Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

Dr Schneider, I continue to support your model and the results it gives despite the fact that your fellow evolutionists continue to discredit your model. Dr Schneider, your model shows mathematically what has been observe empirically about the mutation and selection sorting/optimization process for more than 50 years.

Hopefully we can avert another generation from being confused on how this process works and it will not take 5 years to figure out that combination therapy should be used for diseases like HIV and other diseases subject to the mutation and selection sorting/optimization process and that we can prevent evolutionists from propagating the erroneous, illogical and irrational teaching of how the mutation and selection process works and their contribution to the premature death of millions of people with diseases subject to mutation and selection. All you evolutionists need to do is use some 21st century mathematics to bring your 19th century theory up to date. Of course when you do that, you would realize that it is mathematically impossible to transform a lizard into a bird by the mutation and selection sorting/optimization process no matter what the weather is like.

You all have a good weekend pondering these facts of how the mutation and selection sorting/optimization process actually works. So ... you're still posting the same old crap?

I notice that you still haven't succeeded in deceiving anyone.

Have you noticed that?

[jimbob]

This cross forum post from Ambrielle at badscience could go here for some light relief:

There are two websites I check every day: Bad Science Forums and fstdt.com. Says it all really. :D
That first quote is probably my favourite, along with:
One of the most basic laws in the universe is the Second Law of Thermodynamics. This states that as time goes by, entropy in an environment will increase. Evolution argues differently against a law that is accepted EVERYWHERE BY EVERYONE. Evolution says that we started out simple, and over time became more complex. That just isn't possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it. [emphasis added]
Although this one has the advantage of being pithy:
I can sum it all up in three words: Evolution is a lie

[Zeuzzz]

One of the most basic laws in the universe is the Second Law of Thermodynamics. This states that as time goes by, entropy in an environment will increase.

Correct.

Evolution argues differently against a law that is accepted EVERYWHERE BY EVERYONE. Evolution says that we started out simple, and over time became more complex.

Correct. The effects of intention and consious thought can change the law of entropy, see Maxwell's demon. http://en.wikipedia.org/wiki/Maxwell's_demon
In other words, Maxwell imagines two containers, A and B. The containers are filled with the same gas at equal temperatures and placed next to each other. Observing the molecules on both sides, a little "demon" guards a trapdoor between the two containers. When a faster-than-average molecule from A flies towards the trapdoor, the demon opens it, and the molecule will fly from A to B. The average speed of the molecules in B will have increased while in A they will have slowed down on average. However, since average molecular speed corresponds to temperature, the temperature will have decreased in A and increased in B; this is contrary to the second law of thermodynamics.

That is just about the only time you will ever see that law broken, when conscious thought is input on a system to intentionally change it. Infact a lot of people define life as the reverse of entropy.


That just isn't possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it. [emphasis added]


Incorrect, and quite frankly, obsurd.


I can sum it all up in three words: Evolution is a lie

well, if thats true, you shoudn't exist then. I love self debunking crackpots :)

[jimbob]

Quote:
That just isn't possible: UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it. [emphasis added]
Incorrect, and quite frankly, obsurd.

Quote:
I can sum it all up in three words: Evolution is a lie
well, if thats true, you shoudn't exist then. I love self debunking crackpots

er Zeuzzz...

FSDT.com, and Ambrielle were pointing out that the Sun is a "giant outside source of energy", a source of which, is needed for local entropy to decrease, though global entropy has to increase. If local entropy couldn't decrease, then fridges wouldn't work.

Ambrielle was also noting how many words there were in the phrase "evolution is a lie"

[Zeuzzz]

er Zeuzzz...

FSDT.com, and Ambrielle were pointing out that the Sun is a "giant outside source of energy", a source of which, is needed for local entropy to decrease, though global entropy has to increase. If local entropy couldn't decrease, then fridges wouldn't work.

Ambrielle was also noting how many words there were in the phrase "evolution is a lie"

Ah. Whoops. :rolleyes:

Pardon me, I haven't had my weetabix yet today.

[jimbob]

Ah. Whoops. :rolleyes:

Pardon me, I haven't had my weetabix yet today.

No dammit, this is the annoying creationists thread, it makes the train wrecks I have been more active in, seem exemplars of rationality and civility*. ;-)

Ah well...


* I don't tend to hang out on the CT subforum...

[Paul C. Anagnostopoulos]

Correct. The effects of intention and consious thought can change the law of entropy, see Maxwell's demon.
What does that have to do with evolution?

~~ Paul

[Dr Adequate]

Correct. The effects of intention and consious thought can change the law of entropy ... No they can't.

[jimbob]

Originally Posted by Zeuzzz
Correct. The effects of intention and consious thought can change the law of entropy ...
No they can't.

My favourite answer to the original statment by creationists is that local entropy can decrease in a fridge. But global entropy can only increase.

Local entropy can be only lowered by increasing global entropy.

I do wonder if the original quoted by FSDT was actually a parody...

"UNLESS there is a giant outside source of energy supplying the Earth with huge amounts of energy. If there were such a source, scientists would certainly know about it."

It almost seems too stupid even for a ctreationist...

[m_huber]

It almost seems too stupid even for a creationist...

Nah.

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

[Belz...]

Correct. The effects of intention and consious thought can change the law of entropy, see Maxwell's demon.

Nuh-huh.

[jimbob]

In case anyone was wondering: Here (http://badscience.net/forum/viewtopic.php?t=4201) ie the thead where I got this quote from.

There are some gems...

[kleinman]

Any of you evolutionists figure out how the mutation and selection sorting/optimization process works either mathematically or empirically? Of course not, because if you had, you would understand why five years of monotherapy was wasted on the treatment of HIV introducing huge numbers of resistant viruses into the gene pool despite a Nobel Laureate speech thirty years previous explained exactly what was needed and how years of sequential use of monotherapies produced MRSA, multidrug resistant gonorrhea and numerous other multidrug resistant microbes. You evolutionists have done an incredibly poor job of describing how the mutation and selection sorting/optimization process actually works and this has and will continue to contribute to the premature deaths of millions of people with diseases subject to the principles of mutation and selection. But I must admit, you have done an incredibly good job destroying the field of biology. So let’s see if we can reverse some of the massive damage you have done with your irrational and illogical speculations that have no place in the study of science.

We have been looking at the analytical geometric surface generated by the functional equation:

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

Where,

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

And we have been examining the shape of this surface in the n, gfc plane. We have the following data so far:

G=256, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|662
128|741
256|569
512|492
1024|451
2048|296
4096|167
8192|154
16384|162
32768|186

And

G=256, mr=1 mutation/million bases-generation, g=16, nsp=3:
n|gfc to perfect creature
64|4278078
128|2587709
256|5968438
512|4429939
1024|4510187
2048|1638610
4096|685196
8192|694504
16384|917748
32768|380032

These cases do not show a rapid drop in the gfc. Let’s examine another series of case:

G=512, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|2412
128|1863
256|1836
512|1300
1024|1022
2048|632
4096|694
8192|610
16384|534

G=1024, mr=1 mutation/genome-generation, g=16, nsp=3:
n|gfc to perfect creature
64|18030
128|4446
256|4000
512|3896
1024|2710
2048|1793
4096|1140
8192|1182

G=1000, mr=1 mutation per 1000 bases per generation, g=16, nsp=3:
n|gfc to perfect creature
2 | failed to converge
4 | 66547
8 | 15916
16 | 17257
32 | 16416
64 | 9082
128 | 9378
256 | 4078
512 | 3685
1024 | 2793
2048 | 2080
4096 | 2565
6000 | 1541
8192 | 1798
16384 | 1001
32768 | 743
65536 | 633
131072 | 483
262144 | 702
524288 | 642
1048576 | 438

It is clear that large populations do not have a huge affect on the generations for convergence. This is one of the many speculations evolutionists assert for your mathematically illogical and irrational theory. Any of you evolutionists want to explain why continually doubling populations does not continually halve the generations for convergence?

Next, we will look at the affect of G, the genome length on the gfc. Any of you evolutionists want to speculate how this will affect the mutation and selection sorting/optimization process? While you are pondering this, here are some more empirical examples of how the mutation and selection sorting/optimization process actually works.

http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf)
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
http://en.wikipedia.org/wiki/Pesticide (http://en.wikipedia.org/wiki/Pesticide)
Tankmixing pesticides is the combination of two or more pesticides with different modes of action. This practice may improve individual pesticide application results in addition to the benefit of delaying the onset of or mitigating existing pest resistance.
http://www.weeds.iastate.edu/mgmt/2004/combination.shtml (http://www.weeds.iastate.edu/mgmt/2004/combination.shtml)
The evolution of herbicide resistance within a weed population is based on selection pressure. The more frequently a herbicide is used, the more pressure placed on a weed population, and the sooner resistance will appear at a troublesome level in the population. Using alternative modes of action can reduce the potential for selecting resistant weeds by placing different selection pressures on weed populations. In a system relying only on glyphosate, a weed possessing a trait allowing it to survive glyphosate will rapidly increase in frequency. But if a second herbicide is used with glyphosate, this alternative herbicide may kill the weed with the glyphosate resistant trait and prevent it from increasing within the weed population. Theoretically this approach is sound and can reduce the potential for herbicide resistance.
http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us (http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us)
Coumatetralyl (Racumin ) has been known since 1957 as a multiple dose anticoagulant and has been used successfully over many decades. In the seventies and especially the eighties, rats developed an increased resistance to anticoagulants in certain regions of Central Europe. Also, the addition of vitamin K to animal feed (especially to chicken feed) has reduced the efficacy against rats and mice in farm buildings. Combinations of anticoagulants with different types of vitamin D are generally described to increase the efficacy of action against rodents. It was found that especially the combination of coumatetralyl with cholecalciferol (vitamin D3) could overcome the above mentioned problems. Cholecalciferol causes hypercalcemia and, therefore, has a different mode of action compared to anticoagulants. The combination of these active ingredients leads to an obvious increase in efficacy against rodents, even under difficult conditions. The formulation with optimal rodenticidal efficacy contains 0.04 % coumatetralyl and 0.025 % cholecalciferol mixed in rolled oats.
How can this be? I thought you evolutionists said that increasing the number of selection pressures accelerates evolution. Something just doesn’t add up in your theory. We’ll continue studying the mathematics of ev and find out what it is. Of course, if you evolutionists want to give us an example of multiple selection pressures accelerating the mutation and selection sorting/optimization process, that would be interesting, but as one of you evolutionists has said that experiment just hasn’t been done. How many decades will it take for you evolutionists to figure out that mutationandselectiondidn’tdoit?

[kjkent1]

How can this be? I thought you evolutionists said that increasing the number of selection pressures accelerates evolution. Something just doesn’t add up in your theory. We’ll continue studying the mathematics of ev and find out what it is. Of course, if you evolutionists want to give us an example of multiple selection pressures accelerating the mutation and selection sorting/optimization process, that would be interesting, but as one of you evolutionists has said that experiment just hasn’t been done. How many decades will it take for you evolutionists to figure out that mutationandselectiondidn’tdoit?First, kleinman sets up a strawman: evolutionists say that increasing the number of selection pressures accelerates evolution. I don't believe anyone who understands evolution will flatly claim that an organism beseiged by combinations of toxins will easily survive so as to have the opportunity to reproduce and evolve. So, kleinman's strawmen and his empirical examples are not an attempt to model anything close to the natural conditions under which organisms evolve. Instead, kleinman presents the scenario of: what happens when you conduct an intellitgent extermination of a species?

Answer: it dies.

Brilliant conclusion, kleinamn...brilliant.

What is somewhat more interesting, however, is that there are peer-reviewed studies showing that DESPITE the hostility of an all out toxic attact on an organism, the organism can sometimes manage to evolve so as to escape the intelligently designed deathtrap. This shows just how vital the process of evoluion really is.

In sum, we begin another week of watching repeated kleinman self immolations. It's a great spectacle, the first few times it's observed. But, then, it gets sooooooooooo booooooooooriiiiiiiiiiig.

Everybody...yawn.

[m_huber]

Any of you evolutionists figure out how the mutation and selection sorting/optimization process works either mathematically or empirically? Of course not, because if you had, you would understand why five years of monotherapy was wasted on the treatment of HIV introducing huge numbers of resistant viruses into the gene pool despite a Nobel Laureate speech thirty years previous explained exactly what was needed and how years of sequential use of monotherapies produced MRSA, multidrug resistant gonorrhea and numerous other multidrug resistant microbes.

Alan, you do realize that you are citing numerous examples of evolution taking place, don't you?

Before the State of the Union address tonight, I saw the Simpson's episode where Lisa opposes Creation Science in the classroom. What a great show. Too bad they didn't use hyperbole.

[Myriad]

In sum, we begin another week of watching repeated kleinman self immolations. It's a great spectacle, the first few times it's observed. But, then, it gets sooooooooooo booooooooooriiiiiiiiiiig.


Yes, but now there's a difference.

Last week, he was suspended, and came back after three days.

So now, he has a lot more in common with Jesus.

Respectfully,
Myriad

[Shalamar]

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

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

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

[jimbob]

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

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

Indeed. Behe did manage to get a pHd.

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

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

Stupid ideas from someone who might otherwise seem clever.

[kleinman]

Now, here’s the specific proof that evolutionists are incompetent in either understanding or teaching how the mutation and selection sorting/optimization process actually works.
http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html (http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html)
In microbiology the roles of mutation and selection in evolution are coming to be better understood through the use of bacterial cultures of mutant strains. In more immediately practical ways, mutation has proven of primary importance in the improvement of yields of important antibiotics - such as in the classic example of penicillin, the yield of which has gone up from around 40 units per ml of culture shortly after its discovery by Fleming to approximately 4,000, as the result of a long series of successive experimentally produced mutational steps. On the other side of the coin, the mutational origin of antibiotic-resistant micro-organisms is of definite medical significance. The therapeutic use of massive doses of antibiotics to reduce the numbers of bacteria which by mutation could develop resistance, is a direct consequence of the application of genetic concepts. Similarly, so is the increasing use of combined antibiotic therapy, resistance to both of which would require the simultaneous mutation of two independent characters.

As an important example of the application of these same concepts of microbial genetics to mammalian cells, we may cite the probable mutational origin of resistance to chemotherapeutic agents in leukemic cells 44, and the increasing and effective simultaneous use of two or more chemotherapeutic agents in the treatment of this disease.
And
http://www.pbs.org/wgbh/pages/frontline/aids/interviews/ho.html (http://www.pbs.org/wgbh/pages/frontline/aids/interviews/ho.html)
In 1994, Dr. David Ho discovered that what was then thought of as a latency phase -- when a person was infected with HIV but not experiencing any symptoms -- was in fact a period of continuous onslaught, in which the virus and the immune system are engaged in a pitched battle. Once he was able to measure the amount of virus in the blood, he learned that in fact billions of HIV particles were being produced every day. This breakthrough allowed Ho and his collaborators to come up with the idea for combination therapy -- treating a person with several drugs at once to suppress the virus down to undetectable levels. Patients near death rebounded dramatically after beginning what was called "triple cocktail" therapy, and Ho was named Time magazine's "Man of the Year" in 1996 for his work. In this wide-ranging interview, Ho recounts his breakthrough discoveries and his battles against the virus over the years. He also talks about the implications of combination therapy on the future of the epidemic and the importance of prevention efforts. "We have to bear in mind that during the years where this concerted treatment effort took place, approximately 2 million were treated. But during those years, another 15 million or so got newly infected." Currently Ho is executive director of the Aaron Diamond AIDS Research Center, where he is working on potential vaccine approaches, which he also discusses here. This transcript is drawn from four interviews conducted in New York and China in April and June 2005, and March 2006.
and
The consequence of that obviously is central to thinking about how HIV destroys the immune system, but also it has great ramifications for therapy, because HIV is an error-prone virus. As it replicates it makes mistakes. Now, that may not be all bad, because mistakes allow HIV to generate new variants, some of which will allow it to survive in the presence of drugs, survive in the presence of immune attack, so that's actually an advantage to HIV. When we know how much virus replication is going on and we know the error rate with which the virus makes mistakes, then we could begin to calculate what HIV would do if we applied drug pressure, and from those type of calculations came to the conclusion that it's inevitable for HIV to develop drug resistance if you give it one drug at a time. However, if you start to combine the drugs and try to force the virus into a corner using multiple drugs, it is exceedingly difficult or statistically improbable for HIV to become resistant to all the drugs simultaneously. That for us formed the foundation of thinking about combination therapy.
Edward Tatum in 1958 explained the essential principle of the mutation and selection sorting/optimization process, that is combination selection pressures profoundly slow the process. David Ho and his collaborators took years to come up with the concept of combination therapy even though Edward Tatum had taught this concept decades earlier. The failure of evolutionists to understand and teach this basic principle of the mutation and selection sorting/optimization process has contributed and continues to contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection and selection. This is the contribution that evolutionism has made to the field of biology, that is the confusion and obfuscation of the mutation and selection sorting/optimization process.

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

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

Now the gross extrapolation and speculation of the mutation and selection sorting/optimization process does not form the foundation for a scientific theory. It requires mathematical and empirical correlation. One of the common speculations that evolutionists make is that huge populations markedly accelerate evolution by the mutation and selection sorting/optimization process but Dr Schneider’s mathematical model shows otherwise. Why doesn’t doubling the population halve the generations for convergence? This is best explained by Myriad which he posted on the Evolutionisdead forum. Unfortunately the text has been deleted from the forum but I have a copy of Myriad’s explanation.
In this particular instance, the probability of the mutation not occurring in an individual obeys the multiplicative rule over the members of the population. The probability that the mutation will not occur in any individual is the product of the probabilities that the mutation will not occur in each individual, because for the mutation to not occur in any individual the event "the mutation does not occur in this individual" must occur, independently, for every individual.

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

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

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

This is exactly analogous to the miscalculation that leads to the wrong conclusion that the probability of not rolling any 1s in a roll of four dice equals 1/3. You're applying the additive rule to events that are independent rather than mutually exclusive.
What Myriad has shown is that the probability that a particular mutation occurring at a particular locus does not obey the addition rule of probabilities. Doubling population does not double the probability that a particular mutation will occur at a particular locus. Continued doubling of population does increase the probability of a particular mutation occurring at a particular locus but that probability very quickly approaches a probability of one and then further increases in population have very little affect on increasing this probability. Dr Schneider’s computer simulation demonstrates this effect very nicely. This is why huge populations do not markedly accelerate evolution by the mutation and selection sorting/optimization process.

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

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

Where,

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

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

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

Let’s remind you evolutionists what Dr Schneider said about his simulation:
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/truman/
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.

There’s nothing like some empirical evidence to finish off a post. So here are some more citations which show how the mutation and selection sorting/optimization process actually works.
http://www.medscape.com/viewarticle/494361_3 (http://www.medscape.com/viewarticle/494361_3)
There may be several reasons for the favored emergence of L74V after M184V during selection by abacavir: the extent of resistance conferred may be greater (hence selection favors it), the mutation may be more prevalent in quasispecies at baseline, or this mutation pair may have greater fitness than M184V plus K65R (or M184 plus Y115F). Coadministration of abacavir with a thymidine analogue prevents or dramatically reduces the frequency with which L74V, K65R, and Y115F are observed.[21]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract)
The influence of combinations containing the blood schizontocides chloroquine (CQ) or mefloquine (MEF), together with the 8-aminoquinolines (8AQ) primaquine (PQ) or the new, long-acting compound, tafenoquine (TAF), on the rate of selection of resistance to the individual compounds was examined using the asexual, intra-erythrocytic stages in rodent malaria models.
and
It is concluded that, whereas use of an 8AQ alone carries a high risk of selecting resistance, combinations containing 8AQ may have a place in the protection of blood schizontocides that are to be deployed in endemic areas.
http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf (http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf)
The hope is that combined drug therapies can be implemented more widely in affected areas. Like the AIDS “cocktail” that has transformed that illness from an automatic death sentence to something that can be aggressively managed, at least in industrialized countries, the new malaria combination therapies are believed to be more effective at delaying the emergence of resistance when compared to single drugs used as stand-alone treatments, which are rapidly losing their effectiveness.
http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html (http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html)
Mixtures or sequences of herbicides with differing modes of action are important especially to prevent or overcome resistance based on target site differences. To be effective the herbicides used in mixtures or sequences must have similar efficacy against the target weed. If the resistance is based on enhanced metabolism, this technique may also be useful, as the metabolic processes may be specific to certain types of molecule, but an empirical approach is needed to determine the best herbicide combinations.
These citations show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. We’ll continue with the mathematical study of Dr Schneider’s ev simulation of random point mutation and natural selection and show that his mathematical model shows the same thing and that the theory of evolution is mathematically and empirically impossible.

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

[kjkent1]

These citations show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.No, the citations show that if you build a dam in a river, the water will back up behind the dam. Eventually the water will either overflow or the river will dry up -- one or the other. But, it's a nice strawman that you create for any creationist who wants to know why "God did it."

We’ll continue with the mathematical study of Dr Schneider’s ev simulation of random point mutation and natural selection and show that his mathematical model shows the same thing and that the theory of evolution is mathematically and empirically impossible.All Schneider's program shows is that information gain from a random start is possible. Up until ev was created, the contrary position was a linchpin of creationist dogma. Schneider falsified that position. Now, kleinman takes this out of context and attempts to construct Hoover Dam. Quite a spectacle when you first see it. But, if you work there for a couple of years, it gets pretty dull.

Now why don’t you evolutionists post all your fossil Rorschach tests and prove that the mathematical and empirical evidence of the mutation and selection sorting/optimization process is wrong.Pretty arrogant of you to contend that the fossil and geological record, which has been so exquisitely and carefully investigated, is nothing but an inkblot test. Also, pretty boring.

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

[Mr. Scott]

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

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

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

However, you seem to frame it like this:

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

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

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

I await your refutation.

[X]

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




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

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

[Mr. Scott]

;3382931'] I have a quick question: Is this Kleinman fellow serious?

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

;3382931']Anybody else find that line coming from a (presumed) creationist to be a tad ironic?

Kleinman's ironyrama is endlessly amusing. Read Dr. Adequate's Kleinman FAQ (http://forums.randi.org/showthread.php?p=2533858#post2533858) list for some of Kleiman's best work from last year.

[X]

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

Kleinman's ironyrama is endlessly amusing. Read Dr. Adequate's Kleinman FAQ (http://forums.randi.org/showthread.php?p=2533858#post2533858) list for some of Kleiman's best work from last year.

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

[kleinman]

So here is the functional equation:

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

Where,

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

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

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

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

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

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

http://jac.oxfordjournals.org/cgi/content/full/49/6/925 (http://jac.oxfordjournals.org/cgi/content/full/49/6/925)
In E. coli, fluoroquinolones, including ciprofloxacin, primarily inhibit DNA gyrase (GyrA) with topoisomerase IV (ParC) as a secondary target.19 Single-site mutations at codon 83 or 87 of the gyrA QRDR are sufficient to confer low-level ciprofloxacin resistance, whereas higher levels of resistance either require double (codons 83 and 87) mutations in gyrA, or gyrA mutations in combination with parC or marA mutations, the latter enhancing drug efflux via the AcrAB–TolC system and reducing influx by suppressing expression of the outer membrane protein OmpF.20,21 Thus, at low concentrations ciprofloxacin has a high endogenous resistance potential, but at higher selective concentrations there is a requirement to generate simultaneous mutations in two or more loci4 and the agent consequently displays low endogenous resistance potential.
http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)
Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations. The latter mutation has not been associated with famciclovir resistance.
And
HBV resistance to lamivudine monotherapy
is associated with a complex mixture of variants that limit the efficacy of second-line nucleoside-analogue therapy. First-line potent combination therapy may reduce the emergence of HBV drug resistance.
http://en.wikipedia.org/wiki/Antiretroviral_drug (http://en.wikipedia.org/wiki/Antiretroviral_drug)
Combinations of antiretrovirals create multiple obstacles to HIV replication to keep the number of offspring low and reduce the possibility of a superior mutation. If a mutation arises that conveys resistance to one of the drugs being taken, the other drugs continue to suppress reproduction of that mutation. With rare exceptions, no individual antiretroviral drug has been demonstrated to suppress an HIV infection for long; these agents must be taken in combinations in order to have a lasting effect. As a result the standard of care is to use combinations of antiretroviral drugs. Combinations usually comprise two nucleoside-analogue RTIs and one non-nucleoside-analogue RTI or protease inhibitor.[2]
http://www.ajtmh.org/cgi/reprint/68/5/608.pdf (http://www.ajtmh.org/cgi/reprint/68/5/608.pdf)
Based on the results of this study and with the objective of slowing the development of resistance, the Peruvian Ministry of Health has decided to revise its malaria treatment policy and recommend combination therapy with MQ-AS as the new first-line treatment of uncomplicated P. falciparum malaria in the Amazon region.
There are no selection pressures that cooperate to move a population on the fitness landscape. Selection pressures interfere with each other in the evolution of a population. This is a mathematical and empirical fact of life demonstrated by Dr Schneider’s ev program and these real examples of mutation and selection. Mutation and selection is nothing more than a sorting process which is profoundly slowed when you have more than a single selection pressure targeting a single gene. Edward Tatum understood this 50 years ago, David Ho rediscovered this 15 years ago and Dr Schneider’s computer model demonstrates this same fact. Now, teaching naïve school children that blizzards transforms lizards into buzzards with gizzards is training them to be ignorant of how the mutation and selection sorting/optimization process actually works. Of course you will continue to be contributing to the premature deaths of millions of people suffering from diseases subject to the mutation and selection phenomenon.

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

[sol invictus]

So here is the functional equation:

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


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

Oh, the irony...

[delphi_ote]

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

2. The weather long ago transformed reptiles into birds. Can we put this concept into mathematical terms? Of course we can:
Lizards + Blizzards = Buzzards + Gizzards
Those poor, poor strawmen. You attack them as soon as you create them. They barely have a chance to say, "Hello" to the world around them before you start tearing them down.

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

[joobz]

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

Really, kleinman. We're the ones you want. Leave your defenseless creations out of this!
I think he used the three days to train with Edge (see sig).

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

[delphi_ote]

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

Current kleinman status: repeating discounted arguments. Nothing to see here.
This is a serious issue, dammit!

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

[kjkent1]

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

What happens when the environment changes?

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

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

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

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

Duh.

[Oroborus]

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

[Mr. Scott]

So here is the functional equation:

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

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

Oh, the irony...

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

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

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

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

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

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

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

[kleinman]

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

“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”
Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111
Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable.
In this case, only 5 point mutations are needed to confer high resistance but not only do these 5 point mutations need to occur at the proper loci, they must occur in a sequence in which each mutation gives greater fitness to that member of the population. Considering that Penicillin was initially mass produced in 1943 and Penicillin resistant Staphylococcus aureus appeared in 1947 and Methicillin resistance appeared in 1961, how quick is the mutation and selection sorting/optimization process? What is the population of Staphylococcus aureus? 10^15? 10^20? And what is the generation time for Staphylococcus aureus? 20 minutes under ideal circumstances, how many generations do you think you will get in 4 years? This huge population and thousands of generations, perhaps tens of thousands of generations to evolve 5 loci, then you evolutionists make the irrational and illogical extrapolation that millions of loci can evolve in tiny populations in a small number of generations. You can’t even describe the selection pressures that would do this. So how does the mutation and selection sorting/optimization process actually work? The sorting process works well with single selection pressures targeting single genes. Here is how Dr Schneider’s model reveals this.

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

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

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

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

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

http://www-lmmb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html (http://www-lmmb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html) :
If you had a reasonable sized genome would you find that there won't be an information gain? No. Don't be lazy, go try it yourself! But notice that it will take a lot more computation, and the runs may take some years unless you write a version that uses parallel processors.

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

http://faculty.ucr.edu/~walton/bacteria.htm (http://faculty.ucr.edu/~walton/bacteria.htm)
Two Bacillus are currently used for mosquito control in California; however, because Bacillus thuringiensis subsp. israelensis (Bti) is comparatively less effective against mosquitoes inhabiting the organically enriched waters of treatment wetlands, Bacillus sphaericus currently offers a viable alternative for microbial control of mosquitoes in organically-enriched treatment wetlands (Walton et al. 1998). Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae. Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309). In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602)
The effective treatment of HCV infection will likely require multiple antiviral drugs with different resistance profiles to delay the emergence of resistance, as has been shown in human immunodeficiency virus (35). In the present study, treatment with either a thumb or a palm inhibitor alone rendered large numbers of resistant replicon colonies in vitro, a potential indication of the likely rapid emergence of HCV-resistant variants upon initiation of monotherapy. Importantly, by combining two inhibitors binding to the thumb and to the palm sites of the HCV polymerase we observed a greater-than-additive inhibitory effect of replicon RNA replication.
http://www.ajtmh.org/cgi/content/full/72/2/163 (http://www.ajtmh.org/cgi/content/full/72/2/163)
The goal of combination therapy (CT) is to delay the emergence and spread of drug resistance. The strategy is supported empirically by the success of CT in treating tuberculosis and human immunodeficiency virus infections, and by mathematical models.1 The rationale for CT is simple. If two drugs have independent mechanisms of action, mutations that confer resistance to each drug will only rarely co-exist in the same parasite. By this logic, drug combinations should both improve treatment cure rate, and delay the emergence of drug resistance.2
http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml (http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml) .
Plutella xylostella[/I] (Linnaeus)"]It is very essential to address resistance problem in diamondback moth. In most instances, development of resistance is directly related to the intense selective pressure due to excessive use of a specific insecticide. This selection pressure will be reduced by rotating insecticides of various classes in the management program of diamondback moth.
and
Frequent use of any insecticides for controlling beet armyworm will be reduced by rotating multiple insecticides in the proposed management program. Bt based insecticides will be applied to control early development stages of beet armyworm. Conventional chemical insecticides will be applied to control late stage larvae after every two applications of Bt based insecticides. This practice will significantly delay development of resistance in beet armyworms against any insecticides.
http://ipm.ncsu.edu/apple/chptr4.html (http://ipm.ncsu.edu/apple/chptr4.html) .
To avoid development of resistance to the DMI fungicides, apply these fungicides only in combination with a broad spectrum, protectant fungicide such as captan or the EBDC fungicides (metiram or mancozeb).
Now I know you evolutionists believe that blizzards transform lizards into buzzards with gizzards and that is the perfect formula for causing the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. This is why you evolutionists are useless for teaching or understanding how the mutation and selection sorting/optimization process actually works. You are stuck in your science fiction world. Oh yes, if you think that intensity of selection pressures makes a big difference in the mathematics of the mutation and selection sorting/optimization process, prove it, it is your dumb theory. Wait a minute that means you evolutionists would have to do some mathematics.

[Mister Earl]

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

[kleinman]

I like how evolutionists like to speculate that changing the number and intensities of selection pressures is how blizzards transform lizards into buzzards with gizzards. You are overwhelming me with all your zero of your citations and all zero of your mathematics. On the other hand, I have poor Dr Schneider’s peer reviewed and published mathematical model which has now been discredited by evolutionists from all alternative universes and my few measly hundreds of citations which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.
http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm (http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm) Mix or alternate fungicides with different modes of action.
and
Triazole fungicides should be used in mixtures with non cross-resistant partner fungicides in order to reduce the risk of resistance developing in the target pathogens.
http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf (http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf)
Repeat herbicide applications with the same site of action to the same or different crops.
and
Herbicides used without other weed control options (e.g. cultivation) and are considered "stand alone" weed control programs.
http://www.niaid.nih.gov/factsheets/treat-hiv.htm (http://www.niaid.nih.gov/factsheets/treat-hiv.htm) .
As HIV reproduces itself, different strains of the virus emerge, some that are resistant to antiretroviral drugs. Therefore, doctors recommend patients infected with HIV take a combination of antiretroviral drugs known as HAART. This strategy, which typically combines drugs from at least two different classes of antiretroviral drugs, has been shown to effectively suppress the virus when used properly. Developed by NIAID-supported researchers, HAART has revolutionalized how we treat people infected with HIV by successfully suppressing the virus and decreasing the rate of opportunistic infections.
Perhaps you evolutionists should post your Rorschach fossil data? Or perhaps you should post your stick model data? Or perhaps you found out that your stick model becomes very slow when you use 3 billion sticks?

[Mr. Scott]

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

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

[joobz]

I like how evolutionists like to speculate that changing the number and intensities of selection pressures is how blizzards transform lizards into buzzards with gizzards. Did you think of the rhyme while dressed as a wizard, eating lunch with Eddie Izzard, after your date fun with Miss. Herd while thinking of a fizz word?

[kleinman]

Combination selection pressures profoundly slow the mutation and selection sorting/optimization process. That is what Dr Schneider’s peer reviewed and published mathematical model shows and that is what the empirical evidence shows.
http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)
The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.
http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html)
Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens1, 2, 3. On a broader scale, such combinations are also important in understanding microbial ecology and evolution4, 5. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations1, 6, 7. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population1. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract)
Monotherapy does not give long-term suppression of viral replication and evolution, and combination therapy is viewed as a potentially more effective long-term approach based on increased and more durable suppression of HIV replication.
http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html (http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html)
Many manufacturers of systemic, single-site fungicides are now marketing them formulated as combinations with multi-site fungicides, with the intent of "preventing" the evolution of resistance to the systemic fungicides. Similarly, alternate applications of fungicides with different modes of action or "cocktails" of two or more fungicides applied in the same spray or have been used as a means of combating fungicide resistance. The often-stated rationale for these fungicide combinations is that they prevent the buildup of resistance because the multi-site fungicide in the spray program kills any mutants resistant to the single-site fungicide.

This explanation of the effectiveness of fungicide combinations is not entirely correct, since a multi-site fungicide such as captan is no more effective against a benomyl-resistant Venturia population than it is against the wild-type population. However, even partial suppression of the resistant population will reduce the rate of selection of fungicide resistance and give the grower time to react before there is a catastrophic crop failure. Fungicide combinations, therefore, are a good tactic, not because they prevent resistance, but because they slow down the selection of resistance and thus can prevent crop loss.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)
Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins. For example, when populations of C. quinquefasciatus were selected against a strain producing only Cry11Aa at a concentration that killed 95% (LC95) of the larvae, the level of resistance was 1,000-fold after 28 generations (9). When the same species was selected at the same level with a strain of B. thuringiensis subsp. israelensis that produced Cry11Aa, Cry4Aa, and Cry4Ba, resistance was 217-fold after the same number of generations (9). Interestingly, the level of resistance was only 3.3-fold when C. quinquefasciatus was selected with wild-type B. thuringiensis subsp. israelensis which, in addition to the Cry endotoxins, produces Cyt1Aa (9). The implication of these results is that combinations of Cry endotoxins, and especially combinations of Cry endotoxins and Cyt1Aa, are responsible for delaying resistance.
Now you evolutionists have asserted that variations in the weather are what drive evolution. In other words, blizzards transform lizards into buzzards with gizzards!
http://forums.randi.org/images/smilies/doglaugh.gif
That’s almost as funny as chemicals cooperating to spontaneously form life.

I looked out the window the other day and it was snowing, I thought I saw a lizard turning into a buzzard but it actually was chemicals cooperating to spontaneously make life. You evolutionists really know how to explain mutation and selection.
http://forums.randi.org/images/smilies/doglaugh.gif

[Mr. Scott]

Now you evolutionists have asserted that variations in the weather are what drive evolution. In other words, blizzards transform lizards into buzzards with gizzards!

No evolutionist said anything like that. Preference to attack straw men instead of real evolution theory illustrates you are aware of the fatal weakness of your thesis.

Even your supporters would appreciate it if you stopped evading and specifically refuted the importance of variability in selective pressures.

[kleinman]

You evolutionists continue to have a problem understanding how variation in intensity and number of selection pressures affects the mutation and selection sorting/optimization process. This citation which I just posted explains exactly how variation in selection pressures works.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)
Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins. For example, when populations of C. quinquefasciatus were selected against a strain producing only Cry11Aa at a concentration that killed 95% (LC95) of the larvae, the level of resistance was 1,000-fold after 28 generations (9). When the same species was selected at the same level with a strain of B. thuringiensis subsp. israelensis that produced Cry11Aa, Cry4Aa, and Cry4Ba, resistance was 217-fold after the same number of generations (9). Interestingly, the level of resistance was only 3.3-fold when C. quinquefasciatus was selected with wild-type B. thuringiensis subsp. israelensis which, in addition to the Cry endotoxins, produces Cyt1Aa (9). The implication of these results is that combinations of Cry endotoxins, and especially combinations of Cry endotoxins and Cyt1Aa, are responsible for delaying resistance.
This empirical example shows exactly how variation in the number of selection pressures accelerates the evolutionary process. This citation shows that if you reduce the number of selection pressures it accelerates the ability of the population to evolve against the remaining selection pressures. Dr Schneider’s computer simulation shows this same effect mathematically.

This following citation which was so kindly posted by an evolutionist shows what happens if you subject a population to single selection pressures sequentially.

http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes.

What this citation shows is the recipe for producing multi-drug resistant microbes. Treat microbes with monotherapy and then when the population evolves resistance to this monotherapy change to a new monotherapy and when the population evolves resistance to that drug change to a new monotherapy… That is the recipe for producing superbugs. This citation shows what you need in order to accelerate evolution. You evolutionists have been so good at describing how the mutation and selection sorting/optimization process works; we all thank you for giving us MRSA.

[kjkent1]

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

“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”, Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111
"Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable. "I think that this cite by kleinman is worth responding to, lest someone be mislead to believe that the scientific community is drawing a consensus that evolution is impossible.

The above-quoted cite is an experiment intended to reveal the possible outcomes of "point mutation." The article specifically states: "Seen as an analysis of clinical cefotaxime resistance evolution, our treatment makes several simplifying assumptions about the mutational and selective processes. For example, we have disregarded horizontal gene transfer and have limited attention to only five mutations. Furthermore we have assumed that selection acts only to increase resistance to cefotaxime, whereas microbes are exposed to a spatial and temporal diversity of antibiotic compounds in nature as well as in clinical settings."

The point is that kleinman has seemingly intentionally limited the scope and use of this article so as to bolster his position that evolution is impossible, while the article itself states that the experiment is only intended to analyze clinical cefotaxime resistance by examining a specific five mutations. That is, the experiment is deliberately limited and in no way is an attempt to deal with the unlimited real-world potential of non-point mutation mechanisms, such as "horizontal gene transfer."

Another day, another self immolation -- courtesy of Dr. Alan Kleinman.

[Paul C. Anagnostopoulos]

nsp = number of selection pressures
gfc = generations for convergence.

That's confusing. In math, juxtaposition of letters indicates multiplication. This is not economics.

~~ Paul

[m_huber]

Well, Alan, you've made nice, long posts about how evolution can't possibly work.

Let's imagine a world in which evolution doesn't occur.

For this to be the case, all forms of life currently on the planet must have been on the Earth from either the beginning of time or the "seeding" of the planet by some being(s). Since fossils are abundant at ages of greater than 600 million years, it is reasonable to think that this "seeding" occurred around that time. Of course, stromatolites and other simple plants are dated much older than that, but we will assume that these were "early experiments." Life continues until the Permian, roughly 350 million years later, at which time 90% of all fossil species go extinct. Life then continues for roughly 300 million years, at which time 65% of all fossil species go extinct (including the dinosaurs). Then, over the next 65 million years, almost all large mammals go extinct. That brings us to today, when humans are a major factor in driving animals to extinction.

The question, then, is how does life survive in steady state? Large objects hit the earth. These wipe out large numbers of life forms. The climate of the planet changes significantly. This effects what niches are available. Swings in earth's temperature may be in the order of 40ºC, which is not a small number! how do you propose that life, in steady state, has dealt with all of these extinctions and changes in the planet?

Evolution alleviates this problem. The mechanisms may be simple or complex. What you are looking at does not answer the question of mechanism.

[kleinman]

There are some evolutionists who think that if you really scramble a genome it accelerates evolution and that it somehow overcomes the mathematical and empirical fact that combination selection pressures profoundly slow the evolutionary process. HBV does frame shifts but combination therapy still profoundly slows the evolution of this virus.
http://www.emedicine.com/med/topic3180.htm (http://www.emedicine.com/med/topic3180.htm)
Increasingly, combination therapy with more than one nucleoside or nucleotide analog is contemplated for patients with chronic hepatitis B. Combination therapy may be more effective than monotherapy in patients who have exhibited drug resistance. It remains to be determined whether combination therapy is appropriate for patients with chronic hepatitis B who are drug naive.
And
http://www.cirquemeded.com/AGA/FCU2006/Kwo.pdf (http://www.cirquemeded.com/AGA/FCU2006/Kwo.pdf)
221649: Evolution of Multi-Drug Resistant HBV: Implications on Rescue Therapy. Hyung Joon Yim, Munira Hussain, Stephen Wong, Ying Liu, Scott K Fung, Anna S Lok
Background: Multi-drug resistant HBV have been reported in patients who received sequential treatment with nucleoside monotherapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine (LAM) and adefovir (ADV) have marked reduction in sensitivity to combination of LAM+ADV, while constructs with mutations resistant to either drug remain sensitive to the other drug. Aims: To determine if mutations conferring resistance to multiple antiviral agents are present on the same HBV genome in vivo and to describe the evolution of these mutations. Methods: Sera from 6 patients found to have dual-resistant HBV mutations on direct sequencing were cloned after nested PCR, 18-20 clones from each sample were sequenced. Results: Mutations to both therapies were present on the same genome in 163/195 (84%) clones from 10 samples with dual-resistant mutations to LAM+ADV, LAM+HBIG, or LAM+entecavir (ETV) on direct sequencing, 32 (16%) clones had mutations to one drug. Evolution of mutations was examined in 3 patients. Patient 1 received LAM+ETV after LAM breakthrough, all 18 clones had L180M and M204V/I at month 0 (start of ETV), clonal analysis first detected ETV-resistant mutation (T184L) at month 20, 6 months earlier than direct sequencing. Both treatments were stopped at month 34 (T184L: 20/20 clones); 6 months later, T184L was detected in 12/20 clones while L180M and M204V/I remained detectable in 19/20 clones. Patient 2 was switched to ETV monotherapy after LAM breakthrough, all 20 clones had L180M+M204V at month 0. At month 36, ETV-resistant mutation I169T was detected in 15 and S202G in 4 clones. At month 41, S202G was present in 17 clones and I169T in 4 clones, LAM-resistant mutations remained detectable in all 20 clones. Patient 3 developed HBV recurrence after transplant despite receiving LAM+HBIG. All 18 clones had M204I and sG145R when HBV recurrence was diagnosed. ADV was added and LAM stopped 7 months later. ADV breakthrough occurred after 41 months of ADV when all 18 clones had ADV-resistant N236T. Four months after reintroduction of LAM, all 20 clones had L180M+M204V, 12 clones had additional V173L change. However, N236T was replaced by a different ADV-resistant mutation P237H. Conclusions: Our study showed that mutations conferring resistance to multiple antiviral agents are present on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing dual-resistant HBV. Sequential antiviral therapy leads to selection of multi-resistant HBV; mutations evolve during continued treatment resulting in mutants with increased replication fitness.

And here is an example of a deletion with HIV and we all know that combination therapy works for HIV.
http://jvi.asm.org/cgi/content/full/81/9/4713 (http://jvi.asm.org/cgi/content/full/81/9/4713)
Deletions, insertions, and amino acid substitutions in the ß3-ß4 hairpin loop-coding region of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) have been associated with resistance to nucleoside RT inhibitors when appearing in combination with other mutations in the RT-coding region. In this work, we have measured the in vivo fitness of HIV-1 variants containing a deletion of 3 nucleotides affecting codon 69 ( 69) of the viral RT as well as the replication capacity (RC) ex vivo of a series of recombinant HIV-1 variants carrying an RT bearing the 69 deletion or the T69A mutation in a multidrug-resistant (MDR) sequence background, including the Q151M complex and substitutions M184V, K103N, Y181C, and G190A. Patient-derived viral clones having RTs with 69 together with S163I showed increased RCs under drug pressure. These data were consistent with the viral population dynamics observed in a long-term-treated HIV-1-infected patient. In the absence of drugs, viral clones containing T69A replicated more efficiently than those having 69, but only when patient-derived sequences corresponding to RT residues 248 to 527 were present. These effects could be attributed to a functional interaction between the C-terminal domain of the p66 subunit (RNase H domain) and the DNA polymerase domain of the RT. Finally, recombinant HIV-1 clones bearing RTs with MDR-associated mutations, including deletions at codon 69, showed increased susceptibilities to protease inhibitors in phenotypic assays. These effects correlated with impaired Gag cleavage and could be attributed to delayed maturation and decreased production of active protease in those variants.
And we also know that HIV does recombination, as does Malaria and numerous other microbes yet combination selection pressures slow the evolution of all these life forms. It is not the type of mutation which dominates the mutation and selection sorting/optimization process; it is the number of selection pressures applied to the population which determines the rate of evolution. If you evolutionists taught this to naïve school children instead of blizzards transform lizards into buzzards with gizzards, it may not have taken David Ho years to figure out that combination therapy was what was needed to treat HIV. Thank you evolutionists for teaching children to be completely ignorant of the mutation and selection sorting/optimization process, of course you did this by teaching these children everything you know about mutation and selection.

[kjkent1]

There are some evolutionists who think that if you really scramble a genome it accelerates evolution and that it somehow overcomes the mathematical and empirical fact that combination selection pressures profoundly slow the evolutionary process. HBV does frame shifts but combination therapy still profoundly slows the evolution of this virus.
http://www.emedicine.com/med/topic3180.htm (http://www.emedicine.com/med/topic3180.htm)

And
http://www.cirquemeded.com/AGA/FCU2006/Kwo.pdf (http://www.cirquemeded.com/AGA/FCU2006/Kwo.pdf)


And here is an example of a deletion with HIV and we all know that combination therapy works for HIV.
http://jvi.asm.org/cgi/content/full/81/9/4713 (http://jvi.asm.org/cgi/content/full/81/9/4713)

And we also know that HIV does recombination, as does Malaria and numerous other microbes yet combination selection pressures slow the evolution of all these life forms. It is not the type of mutation which dominates the mutation and selection sorting/optimization process; it is the number of selection pressures applied to the population which determines the rate of evolution. If you evolutionists taught this to naïve school children instead of blizzards transform lizards into buzzards with gizzards, it may not have taken David Ho years to figure out that combination therapy was what was needed to treat HIV. Thank you evolutionists for teaching children to be completely ignorant of the mutation and selection sorting/optimization process, of course you did this by teaching these children everything you know about mutation and selection.Another complete self immolation by Alan Kleinman, above.

In his first two cites, kleinman argues that frame shifts are irrelevant against HVB and combination therapies. Unfortunately, neither of the citations say word one about frame shifts -- thus the articles are totally irrelevant and don't support kleinman's position at all. Whereas the citation I posted a few weeks back showing that HVB with a frame shift actually escaped despite combination therapy, directly falsifies kleinman's position on this point.

In kleinman's third citation, the article states: "In summary, the 3-nucleotide deletion (69) along with S163I in the context of an MDR RT genotype favored the ex vivo Replication Capacity under drug pressure, in agreement with its in vivo emergence and evolution in a long-term-treated HIV-1-infected patient."

This statement shows that the experiment actually demonstrated the exact opposite of what kleinman hoped to show. The deletion provided more resistance to combination therapy.

I love the smell of naplam in the morning. In this case, there's no strawman to burn -- just a total error on kleinman's part. He really ought to read his articles before he posts them.

[kleinman]

Over the past year, evolutionists have argued that recombination, frame shifts, huge populations, the weather, you name it makes the theory of evolution mathematically possible. Unfortunately for you evolutionists, you have neither the mathematics nor the empirical evidence to counter the mathematically and empirically proven fact that combination selection pressures profoundly slow the evolutionary process. Dr Schneider’s peer reviewed and published model of random point mutations and natural selection shows how mutation rates, genome length, population all affect the generations for convergence. Even though Dr Schneider’s model does not include the above named mechanisms of gene transformation, the empirical evidence fills that gap. There are no measurable, repeatable examples of mutation and selection which show that combination selection pressures don’t profoundly slow the mutation and selection sorting/optimization process. It doesn’t matter whether there are frame shifts, recombination or blizzards, combination selection pressures profoundly slow the mutation and selection sorting/optimization process. It should be obvious to everyone that making the sorting conditions more complex profoundly slows the ability of a population to sort beneficial and detrimental mutations. If this were understood and taught by evolutionists, we may have been able to avoid MRSA, multi-drug resistant gonorrhea, years in delay in understanding that HIV required combination therapy and the numerous other examples of poly-resistant microbes, weeds, cancers and other diseases subject to the principles of mutation and selection phenomenon. Mutation and selection doesn’t give common descent but it does cause many problems in fighting disease. You evolutionists interfere in this fight and contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. You evolutionists don’t understand the mathematics but here are some more empirical examples which may penetrate your evolutionist programmed minds.

http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2 (http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2)
Pyrethroid-treated nets are an efficient tool for reducing malaria transmission and morbidity. The recent evolution of pyrethroid resistance in several Anopheles species represents a major threat for the future success of roll back malaria in Africa. The possible use of nonpyrethroid insecticides, such as carbamates, on nets is a promising alternative solution because these insecticides are effective against susceptible and pyrethroid-resistant populations of Anopheles and Culex mosquitoes. Unfortunately, carbamate resistance as a result of insensitive acetylcholinesterase has recently been detected in Anopheles gambiae s.s. populations from Côte d’Ivoire. Using biochemical assays on surviving Anopheles mosquitoes from an experimental hut trial, we showed evidence for selection for an insensitive acetylcholinesterase mechanism by carbamate impregnated bednets. However, no such selection has been found with nets treated with pyrethroid alone or pyrethroid/carbamate “two-in-one”-treated nets. Because pyrethroid-impregnated nets were suspected to select for the Kdr mutation in An. gambiae, we propose that use of two-in-one nets could be a promising alternative strategy for the management of insecticide resistance in malaria vectors.
http://www.journals.uchicago.edu/JID/journal/issues/v192n7/34874/34874.html (http://www.journals.uchicago.edu/JID/journal/issues/v192n7/34874/34874.html)
There is consensus that combination therapy in general and ACT in particular is the way forward in antimalarial chemotherapy. Maybe the optimal future combination will be a 3-drug ACT including 2 intersynergistic quinoline drugs with similar, relatively long half-lives, protecting each others' efficacies after the fast elimination of the artemisinine derivative. Additionally, the expected complex multigenic mechanism needed for quinolone-based antimalarial resistance would be expected to slow down the emergence of this resistance to these drugs.
http://www.bact.wisc.edu/themicrobialworld/bactresanti.html (http://www.bact.wisc.edu/themicrobialworld/bactresanti.html)
• Patients should be give combinations of antibiotics, when necessary, to minimize the development of resistance to a single antibiotic
• Patients need to be given another antibiotic or combination of antibiotics if the first is not working
http://content.healthaffairs.org/cgi/content/abstract/25/2/325 (http://content.healthaffairs.org/cgi/content/abstract/25/2/325)
Artemisinin-based combination treatments (ACTs) are seen as an important tool in the global effort to roll back malaria. With parasite resistance to chloroquine increasing rapidly in many parts of the world, there is greater recognition of the need for a globally coordinated strategy to ensure that artemisinins are not used as monotherapy, which has the potential to cut short their useful therapeutic life. We find that even a partial subsidy could delay the emergence of resistance and that a delay in implementing a subsidy for ACTs could facilitate the emergence of resistance and lower the economic value of ACTs.
Where are all your evolutionist citations? Where is all your evolutionist mathematics? You have a peer reviewed and published evolutionist mathematical model which when it shows what you don’t want to hear, you discredit the model. Well, Dr Schneider’s mathematical model is correct, it does capture the essentials of the mutation and selection sorting/optimization process. Dr Schneider said it well when he posted this on the internet:
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
Well done model Dr Schneider, and Paul, you did a very nice job producing the online java version of the program.

[m_huber]

Selection pressures are not what we need evidence of. To demonstrate that evolution is false, you need some form of test that would show that, for example, reptiles and birds are not related. Instead, when we test them genetically, they come up as similar. When we observe the fossil lineage, we find that dinosaurs provide a common ancestor. We find that some reptiles can reproduce asexually; in some cases, (1 in 100, I am told), a chicken can reproduce asexually. So, morphological similarities aside (Ever look at a chicken's foot?), there are numerous logical pathways that can be used to arrive at the conclusion that reptiles and birds are related. This has been guessed since the early 1800's, and evidence backs it up. When we look at steady-state ideas, which were largely disposed of in the 1800's, we find that there is no evidence to suggest that things remain constant over history. While there are periods of stasis, eventually, the only thing that stays the same is that everything changes. In other words, evolution happens.

Alan, I would love to see you expand your worldview. Even if you don't accept evolution, it would be nice to see you talk about something other than a computer program.

[kleinman]

Some evolutionist draw the erroneous conclusion that just because things look alike they evolved from each other. With that type of thinking, a cloud, a watermelon and a jellyfish must have evolved from each other because they are all mostly water. It is this type of nonsensical speculation that forms the basis for the theory of evolution. The fundamental principle that forms the basis of the theory of evolution is the mutation and selection sorting/optimization process and it simply does not work the way evolutionists allege. In fact evolutionists have failed to properly elucidate how this phenomenon actually works and it has hurt millions of people with diseases subject to mutation and selection in the process. Diseases like HIV have force people to come to grips with how the mutation and selection sorting/optimization process actually works and this process doesn’t use blizzards to turn lizards into buzzards with gizzards. Here are more empirical examples of how the mutation and selection sorting/optimization process actually works.
http://jac.oxfordjournals.org/cgi/content/full/52/1/11 (http://jac.oxfordjournals.org/cgi/content/full/52/1/11)
Since many bacterial species have two intracellular targets for the fluoroquinolones (DNA gyrase and DNA topoisomerase IV), these agents have been investigated for dual targeting.58 Several new compounds (moxifloxacin, gatifloxacin, gemifloxacin and clinafloxacin) approach the dual target situation with S. pneumoniae, as judged (i) by very low mutation frequencies,59 (ii) by decreased susceptibility of both gyrA and parC resistance mutants (clinafloxacin),59 and (iii) by a diminished plateau (inflection point) in plots of mutant recovery versus fluoroquinolone concentration (moxifloxacin).24 Thus dual targeting appears to be a good approach for refining compounds to restrict resistance.
And
According to these ideas, restricting the development of resistance requires that antimicrobial concentrations at the site of infection be kept above MPC. If that cannot be done for a given agent–pathogen combination, the agent should be used as part of a combination therapy involving agents with different targets. Such an approach is likely to be required for plasmid-borne resistance.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594)
Single agent therapy is unlikely to be successful for very long because the emergence of resistant strains of tumor cells is almost the rule in such circumstances. Only combination therapy using different types of drugs that attack a target at different sites on a molecule or attack other key molecules can prevent resistance in most cases.
http://jcm.asm.org/cgi/content/full/43/1/208 (http://jcm.asm.org/cgi/content/full/43/1/208)
Infection with cytomegalovirus (CMV) remains a significant cause of morbidity and mortality among hematopoietic cell transplant (HCT) recipients. We describe two pediatric HCT recipients who developed persistent and severe drug-resistant CMV infections. CMV resistance to foscarnet and ganciclovir was detected after only 6 and 11 weeks of therapy, respectively. Viral pol mutations associated with drug resistance in these patients included T838A (a novel mutation) and D588N, which were shown by marker transfer to confer foscarnet and multidrug resistance, respectively. Each of these mutations significantly reduced in vitro replication of CMV, suggesting that they may decrease viral fitness. This finding was further supported by the disappearance of mutations upon withdrawal of antiviral pressure in one patient. Novel antivirals or combination therapy may be required for the treatment of drug-resistant CMV in HCT recipients and perhaps in other severely immunocompromised patients.
http://www.malariajournal.com/content/3/1/2 (http://www.malariajournal.com/content/3/1/2)
The effect is extremely dependent on the size of infection. As an example, if a human is inoculated with a drug-sensitive clone and there are 10^11 parasites in the host and the mutation rate to the drug resistant form is 10^-8, then there will be a sub-population of 10^3 resistant parasites. Following drug treatment, the sensitive forms will be eliminated and the sub-population of 10^3 resistant forms will expand to dominate the infection. Needless to say, if the mutation rate to resistance is 10^-8, then infection sizes of less than ten thousand would rarely contain the appropriate mutation. Current antimalarial drug deployment strategies utilise this effect by using drugs in combination. If mutation rates to resistance are 10^-8 for each drug in a two-drug mixture, then even an infection of 10^12 individual malaria parasites is highly unlikely (a probability of 0.0001) to simultaneous contain a spontaneous drug-resistant mutation in each gene.

[tsig]

This is a serious issue, dammit!

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

Not yet I still need more straw to mulch my garden.

[kleinman]

Oh no, an evolutionist has used the all powerful strawman argument. I guess that’s what you evolutionists do when you don’t have any mathematical or empirical data. Since I have both, why don’t I give you some more empirical examples of how the mutation and selection sorting/optimization process works, which is combination selection pressures profoundly slow the process.
http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf (http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf)
The main objective of antiretroviral drug resistance testing in clinical practice is to improve the outcome of therapy by helping to choose the most effective combination regimens.
and
Other factors related to the evolution of drug resistance concerned or associated with antiretroviral therapy, such as inadequate drug prescription, drug–drug interactions, previous sequential monotherapy or pre-existing resistance.
http://www.malariajournal.com/content/5/1/48 (http://www.malariajournal.com/content/5/1/48)
This improved understanding of the evolution of drug resistance has come from a relatively simple situation. Until recently, the number of antimalaria drugs in common use was small: chloroquine and sulfadoxine-pyrimethamine in Africa and the Americas, with mefloquine and more recently, mefloquine-artesunate in Southeast Asia[13]. As chloroquine and sulfadoxine-pyrimethamine have lost their efficacy, combination drugs have been strongly endorsed as the most effective next step [14].
http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html (http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html)
Despite the emergence of multidrug-resistant strains of hepatitis B virus (HBV) and previous success with combination therapy for other chronic viral infections, we are still using sequential monotherapy for chronic HBV infection.
http://www.dissectmedicine.com/resistance (http://www.dissectmedicine.com/resistance)
"Long-term endocrine therapy with either aromatase inhibitors (AIs) or tamoxifen may lead to endocrine resistance and disease progression. Recent years have seen advances in our understanding of the complex biological mechanisms associated with resistance. Growth factor signaling pathways appear to be upregulated in hormone-resistant tumours and interact with oestrogen-receptor (ER) signaling, which remains functional even after long-term endocrine deprivation. Signaling through the human epidermal and insulin-like growth-factor receptor (HER and IGFR, respectively) pathways may promote ligand-independent ER gene transcription and stimulate growth factor signaling. Therapeutic agents that inhibit these signal transduction pathways, when combined with AIs, may offer breast cancer patients new hope for more robust, longer-term remissions. Preliminary data from phase II studies of combination therapies are encouraging. There is a large programme of ongoing randomised, controlled trials, the results of which should pave the way for integrating combination therapies into clinical practice. To identify which patients will respond best to particular combinations of treatments, biomarkers and gene expression profiles are being investigated as predictors of sensitivity or resistance. In time, breast cancer treatment will become truly individualised because physicians will be able to match patients with a variety of disease phenotypes to optimal combination therapies." British Journal of Cancer (2006) 95, 661-666.

[kjkent1]

Oh no, an evolutionist has used the all powerful strawman argument. I guess that’s what you evolutionists do when you don’t have any mathematical or empirical data. Since I have both, why don’t I give you some more empirical examples of how the mutation and selection sorting/optimization process works, which is combination selection pressures profoundly slow the process.You have both? Hmmm...I wonder why you've never provided any for us, then?

Curiouser and curiouser. :p

[kleinman]

Some evolutionists are having a hard time seeing the mathematical and empirical evidence that evolutionbymutationandselectiondidn’tdoit. So let’s post some more empirical citations for those myopic evolutionists who forgot their glasses.
http://www.mitpressjournals.org/doi/abs/10.1162/106454698568431 (http://www.mitpressjournals.org/doi/abs/10.1162/106454698568431)
An understanding of antiviral drug resistance is important in the design of effective drugs. Comprehensive features of the interaction between drug designs and resistance mutations are difficult to study experimentally because of the very large numbers of drugs and mutants involved. We describe a computational framework for studying antiviral drug resistance. Data on HIV-1 protease are used to derive an approximate model that predicts interaction of a wide range of mutant forms of the protease with a broad class of protease inhibitors. An algorithm based on competitive coevolution is used to find highly resistant mutant forms of the protease, and effective inhibitors against such mutants, in the context of the model. We use this method to characterize general features of inhibitors that are effective in overcoming resistance, and to study related issues of selection pathways, cross-resistance, and combination therapies.
http://www.imbim.uu.se/forskning/swedbergresearch.html (http://www.imbim.uu.se/forskning/swedbergresearch.html)
Several antimalarial drugs act on the folate metabolism affecting synthesis of DNA precursors, especially dTTP. Examples are Fansidar, which is a combination of pyrimethamine and sulfadoxine, and LapDap, which is a combination of chlorproguanil and dapsone. We still do not know exactly how these compounds interfere with the folate pathways, which include both de novo synthesis and salvage of folates from the host. To be an efficient antimalarial, a drug or drug combination should act on both pathways.
http://www.cropscience.org.au/icsc2004/symposia/2/5/1401_powles.htm (http://www.cropscience.org.au/icsc2004/symposia/2/5/1401_powles.htm)
It is clear that herbicides remain the most efficient technology for large-scale weed control, worldwide. However, the continued increase in evolved herbicide resistance in prominent weed species must lead to change in the way herbicides are used. As there is a paucity of new herbicide modes of action being commercialised there is an imperative to maximize the longevity of the available herbicide resource. To do this requires more pro-active herbicide usage than has been the case until now. Herbicide resistance management strategies need to be implemented that aim to maximise herbicide longevity in farming systems. Maximising the diversity of crops and weed control tools employed is essential for sustainable crop weed management. In the future, bio-economic and population genetics simulation models will assist more sustainable herbicide usage. Careful crop and herbicide rotation together with herbicide sequences and mixtures will be required. Equally, non-herbicide agronomic and biological techniques will be employed to reduce herbicide reliance thereby helping to ensure greater longevity of the precious herbicide resource.
http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf (http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf)
In some cases it is the combination of multiple stressors that lead to the decline of species or groups of species; e.g., amphibians by nematodes (Johnson et al., 1999), increased UV radiation and pollutants (Hatch and Blaustein, 2003; Beebee and Griffiths, 2005), and disease (Collins and Storfer, 2003; Daszak et al., 2003). Conserving endangered species and facilitating their recovery is one the main environmental challenges of the 21st century. Unfortunately, history has shown that in most cases permanent removal of stressors has not been possible and species often need to be
managed indefinitely to ensure their persistence; of the 1263 species listed under the Endangered Species Act of the United States less than 2% have been de-listed (US Fish and Wildlfe Service, 2004).
Now if I only had some fossil Rorschach tests.

[Shalamar]

You have both? Hmmm...I wonder why you've never provided any for us, then?

Curiouser and curiouser. :p

I think he knows he has no evidence or proof for his claims, but if he says it often enough, people will stat to believe him.

'Creationism, apply directly to the buttocks...'

[delphi_ote]

I'm just wanted to stop by and continue my protest of kleinman's unethical treatment of straw men/women. I don't care if they're made of straw or wood or even bricks, forcing these fragile people to take insane positions and then torturing them with terrible arguments is wrong!

Strawpeople are people, too!

[joobz]

I'm just wanted to stop by and continue my protest of kleinman's unethical treatment of straw men/women. I don't care if they're made of straw or wood or even bricks, forcing these fragile people to take insane positions and then torturing them with terrible arguments is wrong!

Strawpeople are people, too!
He also believes in torturing these poor poor strawindividuals with terrible rhymes.

[Ottis]

Just one question. Do these strawpeople wear watches that were designed spontaneously? or did the watch design EVOLVE over thousands of years from hour-glasses and sun-dials???
Just wondering....

[joobz]

Just one question. Do these strawpeople wear watches that were designed spontaneously? or did the watch design EVOLVE over thousands of years from hour-glasses and sun-dials???
Just wondering....
That's an excellent question. From what I understand, these strawpeople love using the evolved watches. They also prefer flying airplanes built by tornadoes in a junk yard.

[m_huber]

Some evolutionist draw the erroneous conclusion that just because things look alike they evolved from each other. With that type of thinking, a cloud, a watermelon and a jellyfish must have evolved from each other because they are all mostly water. It is this type of nonsensical speculation that forms the basis for the theory of evolution.

Not exactly sure how you come up with this..

Look back at my last post. I said "morphological similarities aside." Yes, we can infer from the simple fact that every single mammal, bird, reptile, amphibian, and dinosaur either has 4 limbs, a head, two eyes, a mouth, and an anus (etc) or has bone structure that corresponds to having 4 limbs, etc (such as a snake). We could also look at, say, the progression of different types of finches on islands off of South America and conclude that the best finches to survive would be the ones with beaks that best reach into the plants that they eat from. We could say that finches could actually change over time as different beak shapes allow for easier eating. But if we say this, we need the ability to back it up with other data. Genetic data would do. Fossils located in the right places would do. Guess what? We have both.

To say, "In time, breast cancer treatment will become truly individualised because physicians will be able to match patients with a variety of disease phenotypes to optimal combination therapies," is effectively to say that different phenotypes of cancer exist within each individual. Did God specially create each phenotype, or is this just a subtle evidence of evolution?

[jimbob]

I know this has been addressed before, but Kleinman,

When cocktails of drugs are used to treat e.g. a viral infection, should any viruses survive, haven't they already demonstrated adequate resistance to the cocktail in the doses that they have been exposed to?

The survivors are the only ones that reproduce. If an organism reproduces, it is obviously sufficiently adapted to its environment to reproduce. Any mathematical modelling will not change that basic fact.

If you wipe out the entire population, then there will be no evolution in that population. Should some part survive and reproduce, then these are already adapted enough to reproduce; some of their offspring are likely to be better adapted, and some worse adapted than their parents.

[kjkent1]

He also believes in torturing these poor poor strawindividuals with terrible rhymes.As long as we're discussing strawmen, I think that we ought to read the thoughts of the most famous strawman of all time. It's truly prophetic in light of the present continuing insanity by our favorite annoying creationist. My hat's off to lyricist "Yip" Harburg:

I could while away the hours
Conferrin' with the flowers
Consultin' with the rain
And my head, I'd be scratchin'
While my thoughts were busy hatchin'
If I only had a brain.

I'd unravel ev'ry riddle
For any individ'le
In trouble or in pain
With the thoughts you'd be thinkin'
You could be another Lincoln,
If you only had a brain.

Oh, I could tell you why
The ocean's near the shore,
I could think of things I never thunk before
And then I'd sit and think some more.

I would not be just a nuffin'
My head all full of stuffin'
My heart all full of pain.
I would dance and be merry
Life would be a ding-a-derry
If I only had a brain--Whoa!

[BPScooter]

I've always found it interesting that we all are, well, Interested in this topic. That would make us all fellow seekers toward increased knowledge, right?

The poster known as Kleinman appears to divide the world into "evolutionists" and say things like "you evolutionists" or some such thing. A binary system that contains no nuances. He does the same with math, and says things like You Evolutionists that Don't Understand Math. Proceeds to denigrate, taunt, and use other very non-scientific techniques to make a point.

If I'm right, Kleinman is attempting a semantic revolution. "Evolutionist" is a bad word, my enemy, my feared-most opponent. When he says "you evolutionists" he is saying "you my enemies" and in doing so attempts to diminish or extinguish the importance of these points of view. Many on this thread have noticed this. A contrary and humorous response is not capable of registering.

It would be fun to translate a typical Kleinman statement into opposite terms. Let me try:

From about 5 posts up, Kleinman said
"Some evolutionists are having a hard time seeing the mathematical and empirical evidence that evolutionbymutationandselectiondidn’tdoit."

Translation"
"Some [creationists] are having a hard time seeing the cultural and epistemological evidence that godintheskywithnoexplanationdidn'tdoit"

Does Kleinman really claim to represent "all creationists"? I certainly don't claim to represent "evolutionists." My personal decision process, which has resulted in my current belief system, is Socratic (in that I know the limits of my knowledge) and Baconian (in giving weight to observed evidence). A sort of faith, but not what we'd think to be Faith Based. Faith in evidence, I'll grant.

[kleinman]

It seems you evolutionists are having difficulty with the fundamentals of the mutation and selection sorting/optimization process. So I think it worthwhile to discuss the fundamentals of this process.

You evolutionists seem surprised that selection pressures kill members of a population. But that is what selection pressures do to a population. Selection pressures impair the fitness of members of a population. If you recall, fitness is the measure of the ability to reproduce. This impairment of the fitness of members of the population can be caused by selection pressures by killing off the less fit members of the population as is seen with bacteriocidal antibiotics or simply by impairing the ability of members of the population to reproduce as is seen with antiviral agents that interfere with the enzymes viruses use to reproduce. These antiviral agents do not kill the virus. This is how the mutation and selection sorting/optimization process works.

Now consider this; do selection pressures increase the diversity of a population or do selection pressures reduce the diversity of a population? Let’s see if any of you evolutionists can answer this fundamental question about the mutation and selection sorting/optimization process. While you are pondering this, here are some more empirical examples of how the mutation and selection sorting/optimization process actually works and what these examples demonstrate is the fundamental principle that the greater the number of selection conditions, the much, much slower the process proceeds.
http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423 (http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423)
The Global Program for the Elimination of Lymphatic Filariasis (GPELF) intends to achieve its aims through yearly mass treatments with albendazole (ABZ) combined with ivermectin (IVM) or diethylcarbamazine (DEC). The use of ABZ and IVM separately to combat parasites of veterinary importance has, on many occasions, resulted in widespread drug resistance. In order to help predict the spread of potential ABZ resistance alleles through a population of Wuchereria bancrofti, we have developed a mathematical model that incorporates population genetics into EPIFIL, a model which examines the transmission dynamics of the parasite. Our model considers the effect of the combined treatments on the frequency of a recessive allele, which confers ABZ resistance. The model predicts that after 10 yearly treatments with ALB and DEC, 85% coverage and an initial resistance allele frequency of 5%, the frequency of the resistance genotype will increase from 0·25 to 12·7%. If non-random mating is assumed, the initial genotype frequency will be 2·34% and will increase to 62·7%. ABZ and IVM combination treatment may lead to weaker selection for this genotype. Treatment coverage, initial allele frequencies and number of treatments also affect the rate of selection.
http://evonet.sdsc.edu/evoscisociety/eb_meeting_societal_needs.htm (http://evonet.sdsc.edu/evoscisociety/eb_meeting_societal_needs.htm)
Agricultural entomologists trained in evolutionary genetics 31, 53 are contributing to efforts to delay or prevent the evolution of resistance, such as rotational use of different control measures and judicious combination of chemical with nonchemical controls.
http://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck (http://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck)
The use of combinations of antiretroviral drugs has proven remarkably effective in controlling the progression of human immunodeficiency virus (HIV) disease and prolonging survival,1 but these benefits can be compromised by the development of drug resistance.2,3 Resistance is the consequence of mutations that emerge in the viral proteins targeted by antiretroviral agents.
More real, repeatable, measurable empirical examples which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process; this is also demonstrated mathematically by Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection.

Now I don’t want you evolutionists to worry, I’ll be patient with you and show you how the fundamentals of the mutation and selection sorting/optimization process really works. We all want to understand how your confused misinterpretation of the process has led to MRSA and other multidrug resistant microbes and delayed the usage of combination therapy for HIV and other diseases subject to the mutation and selection process. We don’t want to keep making this evolutionist blunder. Of course you will then realize that common descent by this process is utter nonsense but do feel free to post all your fossil Rorschach tests and show us how blizzards turn lizards into buzzards with gizzards.

[Shalamar]

Dear gods. Does Mr. Klienman ignore everything that people post here, unless it proves the Theory of Evolution wrong?

No-one is surprised that 'selection pressures' can kill off members of a population. In fact, that is one of the major concepts of the Theory of Evolution. The survivors reproduce, proving themselves fit enough for their environment. Should the environment change, then those survivors may no longer be fit enough to survive.

However, He continues to say he has mathematical proof of the impossibility of evolution, he STILL has no math to post. Just something that on first glance looks like an equation, but still falls sort of being, well, you know.. math.

I still hold to my hypothesis that he NEED evolution to be false with every fiber of his being. To the point where he will grasp at straws, and ignore science. ALL science.

[kleinman]

Wait a minute, we have an evolutionist who realizes that selection pressures kill off (or at least impair the ability to reproduce) members of the population. Does this evolutionist want to speculate on whether selection pressures increase the diversity or decrease the diversity of a population? Let’s see if we can drag this evolutionist out of the intellectual mire he is stuck in.

[Shalamar]

*sigh*

No-one has EVER said that selection pressures cannot kill off a population, or limit its ability to reproduce. However, this does not mean that it stops or prevents evolution. Those members of the population that survive due to being fit enough, will certainly reproduce starting the whole chain starting up again.

Mr. Kleinmans purposely limited statement that since selection pressures can kill off members of a population, thus proving evolution mathematically impossible, is wrong. Creatures die ALL the time for one reason or another. Those that can adapt to what is causing this are more likely to pass on these traits to future generations, thus slowing down the die off, and ensuring a future for the species. It doesn't matter if there is one pressure, two pressures, or a thousand. If enough of a population survives, they WILL reproduce, and they WILL adapt to survive.

His belief that slow=stop, and that multiple pressures ONLY kill off each and every member of a given population is wrong. And you have been shown this over, and over and over again. Mr Klienman simply chooses to ignore this, because he feels that evolution is morally wrong, because he feels that creationism is true (It is full of lies).

If one looks at the science, and can learn to understand it, then a greater world will be open to you. If one chooses dogmatic and fundamentalist belief, then your eyes will be forever closed to the world around you, no matter how much you scream and stamp your feet for the claim that it isn't true. Reality shows us what is there. Science helps us to understand the process. A shame there are so many that refuse to accept science.

[kjkent1]

Wait a minute, we have an evolutionist who realizes that selection pressures kill off (or at least impair the ability to reproduce) members of the population. Does this evolutionist want to speculate on whether selection pressures increase the diversity or decrease the diversity of a population? Let’s see if we can drag this evolutionist out of the intellectual mire he is stuck in.Look who's talking about being in an intellectual mire!

In his recent cite to the parasite infestation and combination therapy study at: http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423 (http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423), Dr. Kleinman frivolously suggests that because the study shows a decrease in resistance to combination anti-parasitic therapies from 0.25% to 62.7% during a 10 year period, that this somehow falsifies the theory of evolution.

One wonders what the other 37.3% of the population of parasites which remained resistant to the combination therapy would say about this were they capable of being polled on the issue.:rolleyes:

Another day at the self-Burning Man festival, with Dr. Alan Kleinman, M.D., Ph.D., M.E.

[Shalamar]

Look who's talking about being in an intellectual mire!

In his recent cite to the parasite infestation and combination therapy study at: http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423 (http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423), Dr. Kleinman frivolously suggests that because the study shows a decrease in resistance to combination anti-parasitic therapies from 0.25% to 62.7% during a 10 year period, that this somehow falsifies the theory of evolution.

One wonders what the other 37.3% of the population of parasites which remained resistant to the combination therapy would say about this were they capable of being polled on the issue.:rolleyes:

Another day at the self-Burning Man festival, with Dr. Alan Kleinman, M.D., Ph.D., M.E.


Maybe he's a cherry picker for his night job?

[m_huber]

Kleinman, I see, I understand! I think I get what you are talking about!

Evolution must not happen. Selection pressures prevent it!

[kleinman]

You evolutionists still are having trouble with the fundamental mathematical and empirical facts of how the mutation and selection sorting/optimization process actually works. Combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process and you complain that they don’t cause extinction. Do you think that additional selection pressures will speed up the process?

So let’s see if any of you evolutionists can answer this fundamental question about the mutation and selection sorting/optimization process. Do selection pressures increase the diversity or decrease the diversity of a population? I’ll give you a hint, the answer is in one of the recently posted citations.

[Shalamar]

Too bad Mr. Kleinman still has no evidence of this math of his. What he has posted as an 'equation' is more of his creationist lies.

[kleinman]

Are you evolutionists having trouble figuring out whether selection pressures increase or decrease the diversity of a population? Why don’t you post some fossil Rorschach tests then? You evolutionists really have a hard time understanding the basic science and the mathematics of the mutation and selection sorting/optimization process but you have an excuse for this, you were taught by an evolutionist not by a scientist.

[Belz...]

It seems you evolutionists are having difficulty with the fundamentals of the mutation and selection sorting/optimization process. So I think it worthwhile to discuss the fundamentals of this process.

"I am a broken record..."

you were taught by an evolutionist not by a scientist.

So I guess no scientist is a real scientist, eh, kleinbot ?

[Shalamar]

It seems that he's failed the turing test.

[kleinman]

Are any of you evolutionists going to answer the question whether selection pressures increase or decrease the diversity of a population? Or is all that you have for your theory is a tiny collection of fossil Rorschach tests? Since none of you evolutionists seem to have any idea of the basic science or mathematics of the mutation and selection sorting/optimization process, I’ll go back to posting more citations which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process and that is why the theory of evolution is mathematically and empirically impossible. (You know, Dr Schneider’s peer reviewed and published computer simulation of random point mutations shows this!)
http://www.stanford.edu/~siegelr/philhsu.htm (http://www.stanford.edu/~siegelr/philhsu.htm)
Protease inhibitors are the latest addition to the arsenal of drugs designed to combat the HIV virus. Preliminary studies show that combination therapy with reverse transcriptase inhibitors have resulted in decrease of viral load to undetectable levels.1 The FDA, encouraged by these early studies, approved protease inhibitors in late 1995 after an accelerated approval process.2 The popular media has portrayed protease inhibitors as the cure for HIV infection and AIDS. However, the medical community remains reservedly optimistic about protease inhibitors because studies have also shown that despite early potent antiviral effects, HIV eventually develops resistance to protease inhibitors.1 This review will attempt to explain the mechanism by which HIV gains resistance and the potential limits to HIV's mutability as elucidated by recent scientific literature.
And
Protease inhibitor therapy has been shown to decrease viral load substantially, but in the long run, it has not been shown to maintain its antiviral potency. However, this does not mean that protease inhibitor therapy is a lost cause. Recent research suggests that HIV gains resistance at substantial cost to protease functionality and that increased selective pressure from more protease inhibitors may lead to less virulent strains of HIV. Therefore, more funding should be given to new and more potent protease inhibitor development.

In addition, the appearance of cleavage site mutations and the possibility that these mutations might be a rate limiting step in the evolution of resistance give hope that HIV has only a limited amount of options left for resistance mutation. Research should focus on ways to inhibit the mutated cleavage sites. If cleavage site mutations are a rate limiting step in resistance development, simultaneous inhibition of cleavage site and protease could be very effective; HIV would have to mutate at both the protease and the cleavage site simultaneously to develop resistance.
http://www.medscape.com/viewarticle/512015_4 (http://www.medscape.com/viewarticle/512015_4)
Predicting the degree of resistance and its clinical relevance of any set of mutations to a specific antiretroviral agent, or combination therapy, is complicated by several factors, including the potential for interactions within and between drug classes.[8,26,27] Therefore we augmented our analyses of antiretroviral susceptibility based on a genotypic rule-based algorithm, with predicted phenotypic results. Because the degree of reduced susceptibility correlated with diminished clinical response is not well defined for most antiretroviral agents, we assessed several available cut-offs.[28] In all cases our analyses were consistent with the genotype rule-based results.

Current treatment guidelines recommend switching patients to at least 2 active antiretroviral agents at the earliest evidence of detectable viremia related to decreased drug susceptibility.[1,5] This approach is appealing if a new regimen is available, well tolerated, and succeeds in limiting HIV replication to undetectable levels, thereby minimizing the probability of acquiring additional resistance. The aggressiveness with which to approach virologic failure, however, must be balanced by the risks associated with exposing patients to additional antiretroviral agents. Our findings demonstrate a relatively slow rate of resistance evolution in patients with HIV-1 subtype B, especially among individuals with multiple mutations, who have stable HIV RNA levels in plasma over time, and who maintain HIV RNA levels <1000 copies/mL. These data suggest that maintaining specific patients on a failing regimen results in relatively slow resistance evolution with limited reduction in antiretroviral drug susceptibility. However, this must be tempered by the specific regimen and prior resistance profile of the patient, because acquiring even a single mutation may cause resistance to all NNRTIs and the M184V mutation leads to resistance to lamivudine and emtricitabine.

Many patients maintained on an incompletely suppressive regimen continue to derive immunologic, virologic, and clinical benefit, possibly due to the reduced replication capacity of mutant HIV variants, enhanced HIV-specific immune responses, and residual drug activity.[3,6,29,30] Therefore, delaying switching of suboptimal regimens may be indicated in some patients. However, patients with HIV-1, with limited resistance, especially those with plasma HIV RNA >1000 copies/mL, are at risk for emergence of increasingly resistant virus. Further studies monitoring resistance evolution over time are needed, and combined analyses across observational clinical cohorts would strengthen our initial observations.
Of course, we know that blizzards transform lizards into buzzards with gizzards, which happened after chemicals cooperated to spontaneously form life.
http://forums.randi.org/images/smilies/doglaugh.gif

[Shalamar]

Now Mr. Kleinman believes that Fossils are fake. So now he claims that biology is false, he's added Geology into the irrational and false sciences.

I await to see what else he can pull out of his buttocks.

[Shalamar]

Of course, we know that blizzards transform lizards into buzzards with gizzards, which happened after chemicals cooperated to spontaneously form life.

This one statement, for all the lurkers out there, shows how Mr. Kleinman fails. He fails to understand science. And he fails to understand what is the Theory of Evolution.

Evolution does not say 'blizzards turned lizards into buzzards with gizzards'. Nowhere. I've looked. This came from the limited Mr. Kleinman.

His second statement is in regards to Abiogenesis. Evolution says nothing about the creation of life. That is a separate science.

Mr. Kleinmans strawman statements are an failed attempt to belittle people who trust in the evidence of the Theory of Evolution. But all they do is make him look small, and show his limited understanding of the world around him.

That dog isn't laughing with him. It laughs at him.

[m_huber]

Are you evolutionists having trouble figuring out whether selection pressures increase or decrease the diversity of a population?

The real question would be which selection pressures you are talking about. For example, if the selection pressure were related to the climate becoming substantially warmer, you would expect that many of the organisms affected would have to migrate, go extinct, or evolve. Diversity would decrease as animals go extinct, then increase as new animals fill the niches that are newly opened. The evidence of this is how well suited to their environments modern animals are. Given that the climate does change, animals must also change in order to stay fit within a given geographic area.

If the selection pressure were, instead, some type of predator, then you would find that diversity would not change so much as the prey would simply adapt unidirectionally to the best version of itself that could evade the predator.

You could also have selection pressures associated with disease, albedo, humidity, ocean levels, mountain ranges forming or being destroyed, rivers meandering, geographic boundaries being formed or destroyed in general, allowing populations to mix, or a whole host of other possibilities. One that generally doesn't effect non-microscopic animals is antibodies. We big animals are generally able to either spot poison, or figure out that when Bob ate it, he died. Perhaps this is an intelligence selection..

[kleinman]

What’s the matter, can’t you evolutionists figure out this simple question? Do selection pressures increase or decrease the diversity of a population? I’ll give you another hint, it either increases or decreases the diversity of the population. Just pretend you are taking one of your evolutionists true/false tests, (you know those tests, the ones without any mathematics) and flip a coin, you have 50-50 chance of getting the right answer.

If you don’t feel this is your lucky day, just post some fossil Rorschach tests.

[kleinman]

Wait a minute, we have an evolutionist who is trying to make this into a multiple choice test and is choosing c), none of the above. He even tries to make a rational to support this answer and of course, this evolutionist rational is half right and half wrong. Now which part is right and which part is wrong?

[kjkent1]

Are any of you evolutionists going to answer the question whether selection pressures increase or decrease the diversity of a population? Or is all that you have for your theory is a tiny collection of fossil Rorschach tests? A tiny collection?

Fossil evidence of the morphological changes leading to the modern elephant and horse are fabulously well documented. But, for certain: no matter how many transitional fossils are found for any particular evolutionary lineage, there will never be enough to satisfy Alan Kleinman, M.D., Ph.D, M.E., because God made Noah's Ark big enough to hold every creature that has ever existed.

Which causes me to ask: how long would it take for every creature that ever existed to board the Ark? Seems like it would be a really long line. Do the math for us Alan.


Tickets, please...

[kleinman]

Now we have an evolutionist who is claiming that he has a huge number of fossil Rorschach tests. You evolutionist must enjoy looking at the clouds and seeing all kinds of things in this collection of water vapor. Now it is just too bad that the mathematics and empirical evidence of the mutation and selection sorting/optimization process does not support what you see in the clouds.

So aren’t any of you evolutionists going to tell us whether selection pressures increase or decrease the diversity of a population? We’ve had one guess and he said the coin has landed on its edge with a half right and half wrong explanation for his conclusion. Any other takers?

[Shalamar]

Hmm.. What is a fossil rorschach test? Were these made by ancient psychiatrists, which then fossilized to see if creationists could see their mother in them?

At least Mr. Kleinman has stopped claiming that Wookies are real, and he's started to admit that weather just might be a real phenomenon.

But he still thinks that biology is not science, and that Geology is not science. He sure does change his mind a lot!

[kjkent1]

Now we have an evolutionist who is claiming that he has a huge number of fossil Rorschach tests. You evolutionist must enjoy looking at the clouds and seeing all kinds of things in this collection of water vapor. Now it is just too bad that the mathematics and empirical evidence of the mutation and selection sorting/optimization process does not support what you see in the clouds.

So aren’t any of you evolutionists going to tell us whether selection pressures increase or decrease the diversity of a population? We’ve had one guess and he said the coin has landed on its edge with a half right and half wrong explanation for his conclusion. Any other takers?I'll answer your question, just as soon as you show us the math describing how long it took to load every living thing on Noah's Ark! :cool:

Come on, that should be easy for a genius such as yourself. Just try not to light yourself on fire again in the process.

[kleinman]

Still no evolutionists will tell us whether selection pressures increase or decrease the diversity of a population. I wonder why? Didn’t any evolutionists teach you the answer to this question? Didn’t any evolutionist teach you how the mutation and selection sorting/optimization process actually works? Of course not because if evolutionists had taught this, we wouldn’t have MRSA and numerous other multidrug resistant microbes and it wouldn’t have taken years to figure out that treatment of HIV require combination therapy. Well lets post some more citations which demonstrate exactly how the mutation and selection sorting/optimization process actually works, that is combination selection pressures profoundly slow evolution by this process.
http://www.journals.royalsoc.ac.uk/content/kljr3bmug6kxqppu/ (http://www.journals.royalsoc.ac.uk/content/kljr3bmug6kxqppu/)
Antimarial drug resistance develops when spontaneously occurring parasite mutants with reduced susceptibility are selected, and are then transmitted. Drugs for which a single point mutation confers a marked reduction in susceptibility are particularly vulnerable. Low clearance and a shallow concentration–effect relationship increase the chance of selection. Use of combinations of antimalarials that do not share the same resistance mechanisms will reduce the chance of selection because the chance of a resistant mutant surviving is the product of the per parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. Artemisinin derivatives are particularly effective combination partners because (i) they are very active antimalarials, producing up to 10 000-fold reductions in parasite biomass per asexual cycle; (ii) they reduce malaria transmissibility; and (iii) no resistance to these drugs has been reported yet. There are good arguments for no longer using antimalarial drugs alone in treatment, and instead always using a combination with artemisinin or one of its derivatives.
http://www.annals.org/cgi/content/short/128/11/951 (http://www.annals.org/cgi/content/short/128/11/951)
First, using drugs that require the virus to undergo multiple mutations to achieve high-level resistance maximizes the efficacy of the drug for the existing viral population and minimizes the probability of breakthrough. In this respect, a drug to which resistance develops after only a single amino acid substitution is expected to be more vulnerable to resistance than an equipotent drug that requires the virus to undergo multiple mutations to achieve the same degree of resistance.

Second, the need for multiple mutations can be increased further by combining different drugs that inhibit independent targets. Three distinct therapeutic classes of drugs with nonoverlapping sets of resistance determinants exist: protease inhibitors, nucleoside inhibitors, and non-nucleoside reverse transcriptase inhibitors. There is no evidence that mutations compromising the effects of members of one class will reduce the utility of members of any other class. This is one of the most important benefits of divergent combination therapy: When many simultaneous mutations are required, the probability of preexisting resistance in a therapy-naive patient becomes negligible and the effect of the drug combination is maximized.
I’ll take hard mathematical and measurable, repeatable empirical evidence any day over fossil Rorschach tests and claims that blizzards turn lizards into buzzards with gizzards. But I do understand why you evolutionists would rather talk about your fossil Rorschach tests than the mathematics of the mutation and selection sorting/optimization process because it proves the theory of evolution to be mathematically impossible.

[kjkent1]

I’ll take hard mathematical and measurable, repeatable empirical evidence any day over fossil Rorschach tests and claims that blizzards turn lizards into buzzards with gizzards. But I do understand why you evolutionists would rather talk about your fossil Rorschach tests than the mathematics of the mutation and selection sorting/optimization process because it proves the theory of evolution to be mathematically impossible.The difference, of course, is that your "hard" evidence fails to support the impossibility of evolution, because each and every test that you post proves that evolution actually occurs. Whereas the fossil evidence is directly relevant, and supports the proof that evolution has occurred and caused morphological change over the eons.

It's really all about the "quantity" of evidence, not the "quality." You have exactly zero on your side of the scale, so it really doesn't matter how much evidence we have. If we have any -- you lose.

And, you do lose, Alan Kleinman, M.D., Ph.D., M.E. Completely and utterly -- you lose.

[kleinman]

Are there no evolutionists willing to tell us whether selection pressures increase or decrease the diversity of a population? If you won’t do that will you at least post the fossil Rorschach tests that show that blizzards turn lizards into buzzards with gizzards? Of course we know it took eons so there must be lots of fossil Rorschach tests to show us.
http://forums.randi.org/images/smilies/doglaugh.gif

[Belz...]

Kleinman is obsessed with the word "evolutionist". Not a single post of his in the last few weeks doesn't start with a sentence that includes the work.

I have no idea what it means. I'm a realist. You're a fundie.

[kjkent1]

Even your little laughing icon has a fossil history: http://www.hyaenidae.org/ancient-hyaenas.html.

I tell ya, Alan, didn't your mother tell you not to play with matches or you'll get burned. It's a wonder you have any skin left to set ablaze with your nonsensical rhetoric.

[kleinman]

Still there are no evolutionists who are willing to tell us whether selection pressures increase or decrease the diversity of a population. And the answer to this question is not “in some cases yes and in some cases no”. How many hints do you need?

Now I would like to see some of your fossil Rorschach tests. I have always been a fan of science fiction.

[kjkent1]

I like science fiction as well. Unfortunately, Noah's Ark and the Antediluvian Age is more like fantasy -- sort of like your belief that evolution is impossible.

[kleinman]

This is such a simple question. Do selection pressures increase or decrease the diversity of a population? Come on now, there must be an evolutionist out there that knows the answer to this question. While you are thinking about this question, here are some more citations which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization phenomenon, after all, that’s what Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection shows.
http://www.bentham.org/cdt/contabs/cdt3-4.htm (http://www.bentham.org/cdt/contabs/cdt3-4.htm)
Recent preclinical and clinical studies have addressed the resistance problem by using combinations of different drugs that target TS, or by combining TS-targeting and non-TS-targeting drugs.
And
Distinctive cellular responses to targeting of specific TS mRNA regions provide exciting therapeutic opportunities. Antisense ODN treatment to modulate TS activity, in combination with TS-targeting chemotherapeutic drugs, has the potential to be an effective anti-tumor therapy.
and
Protozoan parasites are responsible for important diseases that threaten the lives of nearly one-quarter of the human population world-wide. Among them, leishmaniasis has become the second cause of death, mainly due to the emergence of parasite resistance to conventional drugs. P-glycoprotein (Pgp)-like transporters overexpression is a very efficient mechanism to reduce the intracellular accumulation of many drugs in cancer cells and parasitic protozoans including Plasmodium and Leishmania, thus conferring a multidrug resistance (MDR) phenotype. Therefore, there is a great clinical interest in developing inhibitors of these transporters to overcome such a resistance. Pgps are active pumps belonging to the ATPbinding cassette (ABC) superfamily of proteins, and consist of two homologous halves, each containing a transmembrane domain (TMD) involved in drug efflux, and a cytosolic nucleotide-binding domain (NBD) responsible for ATP binding and hydrolysis. Most conventional cancer MDR modulators interact with the drug-binding sites on the TMDs of Pgps, but they are also usually transported and the required concentrations for a permanent inhibition produce subsequent side effects that hamper their clinical use. Besides, they only poorly modulate the resistance in protozoan parasites. We review here a rational strategy developed to overcome the MDR phenotype in Leishmania, consisting in: i) the selection of an MDR Leishmania tropica line that overexpresses a Pgp-like transporter; ii) the use of their cytosolic NBDs as new pharmacological targets; iii) the search of new natural compounds that revert the MDR phenotype in Leishmania by binding to the TMDs; iv) the combination of subdoses of the above selected modulators directed to both targets in the transporter, NBDs and TMDs, to accumulate their reversal effects while diminishing their toxicity. In this way, we have reverted the MDR phenotype in Leishmania, including the resistance to the most promising new antileishmania agents, the alkyl-lysophospholipids. This approach might be extrapolated to be used in other eukaryotic cells.
http://www.k-state.edu/pdecology/MundtGarrett2002.pdf (http://www.k-state.edu/pdecology/MundtGarrett2002.pdf) .
Integration of practices often provided better disease control than using either practice singly. In two of three cases, the effect of combining management practices was greater than that predicted by a multiplicative relationship. Clearly, it is possible to attain substantial epidemiological synergism by combining disease practices.
It sure is difficult finding examples of combination selection pressures profoundly slowing evolution by the mutation and selection sorting/optimization process. I’m still looking for that citation which shows blizzards transform lizards into buzzards with gizzards.

Since you evolutionists are having difficulty answering the question whether selection pressures increase or decrease the diversity of a population, would you please post some of your fossil Rorschach tests?

[joobz]

Still there are no evolutionists who are willing to tell us whether selection pressures increase or decrease the diversity of a population. And the answer to this question is not “in some cases yes and in some cases no”.That's the best answer that can be given to your horribly silly question.
Now I would like to see some of your fossil Rorschach tests. I have always been a fan of science fiction.
I see you've decided to attack a new strawman. Perhaps you'd like to try your hand at more substantial enemies.


To discount evolution, you'll have to come up with an alternative, self-consistent, rational explanation for the following observations:
Start with
1.) the fossil record
2.) molecular biology describing the fundemental mechanism of evolution
3.) the phylogenetic tree
4.) How the fact that how an evaluation of variation in sequence of each protein that presists between species matches what would be predicted by the phylogenic tree.
5.) ERVs
6.) human chromosome fusion
7.) multi drug resistent bacteria
8.) existence of RNAi
9.) Mitochondrial DNA
10.) Success of Directed evolution techniques
11.) vestigal organs
12.) prions
13.) protein multifunctionality
14.) protein polymorphisms
15.) symbiosis
16.) interspecies viable offspring
17.) nylon-eating bacteria
18.) Persistence of Sickle Cell

Remember, sticking fingers in your ear shouting "la la la, I can't hear you" doesn't count as a rational argument.

[kleinman]

Somebody has written a shopping list:

1.) the fossil Rorschach record
2.) molecular biology describing the fundamental mechanism of evolution, the mutation and selection sorting/optimization process is far too slow because combination selection pressures can not be sorted quickly and any way you don’t have the selection pressures to transform lizards into birds, well you do have blizzards that transform lizard into buzzards with gizzards.
3.) the phylogenetic tree is an imaginary relationship that evolutionist like to group things that exists between different species, it only works for occasional genes. If phylogenic trees were representative of reality, thousands of genes would give identical phylogenic trees.
4.) How the fact that how an evaluation of variation in sequence of each protein that persists between species matches what would be predicted by the phylogenic tree, except despite the fact that humans and chimpanzees have identical insulin molecules the preproinsulin molecules are different.
5.) ERVs, energy efficient recreational vehicles?
6.) human chromosome fusion-like Robertsonian translocations which leads to Down’s syndrome.
7.) multi drug resistant bacteria-thank you evolutionists for your fine job in explaining how the mutation and selection sorting/optimization process works, you evolutionists have given us MRSA, and numerous other multidrug resistant microbes because of your failure to properly explain how the process works. Oh yes, thank you for the multiple year delay in the understanding of how to treat HIV. If you evolutionists had properly explained how the mutation and selection sorting/optimization process actually works, it would have been obvious that combination therapy had to be used. Oh yes, blizzards do transform lizards to buzzards with gizzards though.
8.) existence of RNAi-you evolutionists can’t even explain how to form ribose nonenzymatically and if you could, the ribose molecule is unstable and would break down very quickly. Ribose can barely last a couple years, so much for billions of years for abiogenesis.
9.) Mitochondrial DNA-you call that proof of evolution?
10.) Success of Directed evolution techniques-don’t tell me you believe in Intelligent Design?
11.) vestigal organs-just because you don’t know what an organ does you claim it evolved, fits in good with your gap theory of evolution.
12.) prions-Oh, are these the missing link?
13.) protein multifunctionality-that explains why we only have 20,000 or so genes
14.) protein polymorphisms-variations in enzymes gives common descent?
15.) symbiosis-just because two life forms have a symbiotic relationship that is proof of evolution?
16.) interspecies viable offspring-you had better reexamine your definition for species.
17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?
18.) Persistence of Sickle Cell-Sickle cell only persists in Malaria endemic areas, having Hgb-S in a region without Malaria is not beneficial; of course you never were involved in the care of someone with Sickle-cell disease because then you would know this.

Oh, the author of blizzards transform lizards into buzzards with gizzards is wrong about whether selection pressures sometimes increasing and sometimes decreasing diversity in a population. He would understand this if he had some knowledge of how the mutation and selection sorting/optimization process works. This misinterpretation is understandable since evolution is not his field. His field is chemical engineering and he claims that chemicals cooperated to form life billions of years ago. The only problem for this individual is to explain why chemicals are not cooperating any more. Don’t we have enough energy around for chemicals to cooperate and form life now?
http://forums.randi.org/images/smilies/doglaugh.gif

Enough of evolutionist speculations; let’s get back to presenting real measurable and repeatable empirical examples of how the mutation and selection sorting/optimization process actually works.
http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf (http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf) .
2.4. Drug Combinations: Computer modelling has shown that the best way to inhibit the development of drug resistance is by the simultaneous applications of drugs (i.e. the use of combinations or mixtures) [3,12].
You mean that Dr Schneider’s computer model is not the only mathematical model which show that combination selection pressures profoundly slow the evolutionary process?
http://jama.ama-assn.org/cgi/content/abstract/286/2/196 (http://jama.ama-assn.org/cgi/content/abstract/286/2/196)
Based on the samples that could be amplified, low-level viremia in children and adults receiving HAART with prolonged suppression of viremia to less than 50 copies/mL of HIV-1 RNA may result primarily from archival, pre-HAART virus, reflecting earlier treatment conditions, and does not appear to require development of new, HAART-selected mutations reflecting partial resistance to therapy. Low-level viremia below 50 copies/mL may represent less of a concern regarding impending drug failure of current HAART regimens. However, the archival drug-resistant virus may be relevant regarding future treatment strategies.
Pretreatment conditions, they are talking about years of monotherapy for the treatment of HIV which introduced drug resistant strains into the gene pool. Thank you very much evolutionists for your incompetent and irrational explanation of how mutation and selection works.
http://jvi.asm.org/cgi/content/abstract/74/19/9328 (http://jvi.asm.org/cgi/content/abstract/74/19/9328)
We studied the combined anti-human immunodeficiency virus type 1 (HIV-1) effects of a derivative of stroma-derived factor 1 (SDF-1), Met-SDF-1, and a modified form of RANTES, aminooxypentane (AOP)-RANTES. The antiviral agents were tested singly or in combination at 95 and 99% virus inhibitory concentrations. Clinical R5 and X4 HIV-1 isolates were used. AOP-RANTES inhibited R5 but not X4 viruses, whereas Met-SDF-1 had the opposite effect. Combinations of these compounds inhibited mixed infections with R5 and X4 viruses (95 to 99%), whereas single drugs were less inhibitory (32 to 61%). Combinations of R5 and X4 inhibitors are promising and deserve further evaluation.
Combination selection pressures profoundly slow the mutation and selection sorting/optimization process. That is what the mathematics shows and that is what the empirical data shows.

Now I know you evolutionists believe that chemicals cooperated and spontaneously formed life and that blizzards transforms lizards into buzzards with gizzards in fact I think I saw a buzzard sitting in a phylogenic tree.
http://forums.randi.org/images/smilies/doglaugh.gif
But the mathematical and empirical data shows that evolutionbymutationandselectiondidn’tdoit. The mutation and selection sorting/optimization process simply doesn’t work that way. You evolutionists can cling to your irrational and illogical view of the mutation and selection sorting/optimization process and you will continue to contribute to the premature death of millions of people suffering from diseases subject to mutation and selection.

Now, I ask you evolutionists once again if selection pressures increase diversity or decrease diversity in a population. So far we have gotten two wrong answers of sometimes yes and sometimes no. Any of you evolutionists want to flip a coin and see if you get the right answer? Next week I’ll give you the correct answer and explain to you why. In the meantime, you all have a good weekend and I’ll see you next week with more empirical examples of how the mutation and selection sorting/optimization process actually works.

[delphi_ote]

More strawmen up in flames... we barely knew them. :cry1

[Ottis]

Wait a minute, we have an evolutionist who realizes that selection pressures kill off (or at least impair the ability to reproduce) members of the population. Does this evolutionist want to speculate on whether selection pressures increase the diversity or decrease the diversity of a population? Let’s see if we can drag this evolutionist out of the intellectual mire he is stuck in.

What part of "survival of the fittest" cant /wont you understand??? (Hint; the unfit don't survive to reproduce... get it? hu? hu?)
I'm prob the least educated (formally) member of this board and I understood this as a child. Diversity results from how many different "niches" are available in any given environment, eg, harsh environments like the north pole, (you know, where Santa lives, I'm sure you believe in him also) have less diversity then say, a tropical rain forest..... Get it??? Something is week or dumb, it gets ate, something is strong or smart, it lives to reproduce.......

[joobz]

Somebody has written a shopping list:
And someone responded with stupidity. Good job, you!
1.) the fossil Rorschach recordthat's a stupid thing to say.

2.) molecular biology describing the fundamental mechanism of evolution, the mutation and selection sorting/optimization process is far too slow because combination selection pressures can not be sorted quickly and any way you don’t have the selection pressures to transform lizards into birds, well you do have blizzards that transform lizard into buzzards with gizzards.
That's a stupid and boring thing to say.
3.) the phylogenetic tree is an imaginary relationship that evolutionist like to group things that exists between different species, it only works for occasional genes. If phylogenic trees were representative of reality, thousands of genes would give identical phylogenic trees.
that's also stupid and horribly uniformed. Give examples of the genes that don't fit.
4.) How the fact that how an evaluation of variation in sequence of each protein that persists between species matches what would be predicted by the phylogenic tree, except despite the fact that humans and chimpanzees have identical insulin molecules the preproinsulin molecules are different.You've said this before and it's a still stupid observation. explain why they wouldn't be same.
5.) ERVs, energy efficient recreational vehicles?I know you don't like this topic. it's scary for you.
6.) human chromosome fusion-like Robertsonian translocations which leads to Down’s syndrome.that's not just a stupid thing to mention, but it helps further support evolution. Good job!
7.) multi drug resistant bacteria-thank you evolutionists for your fine job in explaining how the mutation and selection sorting/optimization process works, you evolutionists have given us MRSA, and numerous other multidrug resistant microbes because of your failure to properly explain how the process works. Oh yes, thank you for the multiple year delay in the understanding of how to treat HIV. If you evolutionists had properly explained how the mutation and selection sorting/optimization process actually works, it would have been obvious that combination therapy had to be used. Oh yes, blizzards do transform lizards to buzzards with gizzards though.
I see you are again going for the stupid statement of the year award.
8.) existence of RNAi-you evolutionists can’t even explain how to form ribose nonenzymatically and if you could, the ribose molecule is unstable and would break down very quickly. Ribose can barely last a couple years, so much for billions of years for abiogenesis.
dumb dumb dumb.
9.) Mitochondrial DNA-you call that proof of evolution?
It's supported by evolutionary theory.
10.) Success of Directed evolution techniques-don’t tell me you believe in Intelligent Design?
How can something that doesn't exist be used to do something? Do you believe in magic...oh wait.
11.) vestigal organs-just because you don’t know what an organ does you claim it evolved, fits in good with your gap theory of evolution.
male nipples.
12.) prions-Oh, are these the missing link?No, they are just another nail in your logic coffin.
13.) protein multifunctionality-that explains why we only have 20,000 or so genes
wastenot want not. That's what evolution says.
14.) protein polymorphisms-variations in enzymes gives common descent?chicken...egg...
15.) symbiosis-just because two life forms have a symbiotic relationship that is proof of evolution?
got a better idea...oh wait... Have any idea?
16.) interspecies viable offspring-you had better reexamine your definition for species.
I define species as impossible, therefore god did it. You're not doing very good.

17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?
bwa ha ha ha ha!!! Something that doesn't exist evolves something that exists and that doesn't prove evolution?!??! Yeah, we have the new stupid statement.
18.) Persistence of Sickle Cell-Sickle cell only persists in Malaria endemic areas, having Hgb-S in a region without Malaria is not beneficial; of course you never were involved in the care of someone with Sickle-cell disease because then you would know this.
natural selection at work. thanks for playing.



I noticed you failed to provide any counter theory that explains all of those observations.

[Olowkow]

I'm taking bets that this thread will not hit 8000 posts.:hypnotize

http://forums.randi.org/imagehosting/2087847a285b3c47f1.gif (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10496)

[m_huber]

Alan, I'm almost convinced that you're really an award-winning novelist, working on a new novel about your experience baiting scientists into defending evolution against ridiculous arguments.

Nevertheless, you do have one point.
http://forums.randi.org/imagehosting/thum_2104647a2915a1b4fc.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=10498)

This doesn't look anything like a fossil horse. (name: Equus simplicidens)

As for selection pressures, they can go both ways. The amount of available food is a selection pressure. If there is too little, diversity will decrease as species go extinct and fill specific niches. If there is too much, diversity will increase as a wider variety of morphologies will survive to reproduce. This really isn't either hard or necessarily mathematical. What's your problem here?

I would like to know something specific, though. You obviously have an emotional attachment to evolution being wrong. When people come here and are not emotional about a subject, they say "yeah, whatever" and back off. You have persisted for some time. What is your reason for wanting evolution to be wrong? How does it benefit you? Do you think the Genesis account is the ultimate correct answer, or do you discount it?

Just wondering.

[Belz...]

the fossil Rorschach record

Yeah. Sure. Those aren't wings and teeths and a tail...

http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=8609)

[joobz]

I need to repeat this, becuase it's a new funny that kleinman made.

When asked how he explains nylon-eating bacteria evolving.

17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?
So his explanation that evolution doesn't occur is by admitting that bacteria evolves and evolves new functionality that it didn't not have before.

This is a clear admission to evolution occuring. and it is a macroscopic change. The ability for a bacteria to digest a food source that it previously couldn't can't possibly be labelled as "microscopic evolution". If it is, it renders the definitions meaningless.

[Belz...]

17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?

Did he just say it "evolves" ? I thought that was mathematically and empirically impossible !

[Shalamar]

Its almost sad that someone could fight so hard against something supported by evidence, just because their faith tells them it can't be true.

And its the lack of ANY evidence for creationism that makes creationists evil. They want to pollute and twist the minds of our children by telling them that science is wrong and evil. They don't see the damage that they're doing, or the results on how the rest of the world sees Americans these days.

And all Mr. Kleinman can do is yell 'Ha Ha. Evolution is stupid. You stupid evolutionists, look! I have no math to prove its mathematically impossible! Ha Ha!'

I weep for humanity.

[joobz]

Did he just say it "evolves" ? I thought that was mathematically and empirically impossible !
Yeah, I hope Dr. A gets a load of that one.

I'm sure kleinman will explain it as "microevolution", but that would simply be denying reality. This is a new gene that arose from a gene that did something completely different. And it used a frameshift mutation to do it.

[kjkent1]

Did he just say it "evolves" ? I thought that was mathematically and empirically impossible !Kleinman is merely operating as a troll at this point, using the tried and true method of maintaining a debate without any substantive argument:

1. State an inflammatory proposition;
2. Ignore or ridicule opposing arguments;
3. Go to 1.

I wish forum moderators would prevent contributors from engaging in this behavior. It's such a waste of resources.

[Belz...]

Yes, but there is no rule against being stubborn, obtuse or stupid.

[m_huber]

What I find interesting is that Kleinman seems to treat us like enemies. We could easily agree to disagree and have a civil conversation. Even if we were to continue throwing jabs at each other, we could still learn something from one another.

I guess I don't always mind when someone has a false belief. What bothers me is when someone tries to either 1) force me to believe it or 2) use that belief for illegitimate personal gain. Kleinman has been unwilling to back down, choosing instead to come here and mock us and post segments of papers that talk about evolution. As a doctor, I'm sure that he knows both a tremendous amount of medical knowledge and a large number of interesting anecdotal stories. We will probably never know, as all we will ever see from him is his anti-evolution mode, which does neither him nor us any good.

[CriticalThanking]

I know I am going to regret posting in this thread. And no, I have not read all 7900 (and counting) posts in it. My apoligies if this has already been discussed. How could it not be after this many posts? :rolleyes:

If I recall some of this thread and understood the arguments, one of Kleinman's arguments is that multiple selection pressures cause would cause evolution to slow such that what we observe today could not have evolved in the time given. My musings:

1) There was a recent article noting that fishery policies of catch size restrictions (size of the individual fish, not the size/volume of total catch) have caused an observed accelleration of fish evolution. Specifically, the species are coming to sexual maturity faster and not growing as large. A new selection pressure (size selection during "predation") has resulted in an observable accelleration.

2) When is there ever only one selection pressure? Just thinking about the fish example, there are always many pressures. Preators that eat eggs, predators that eat fry, predators that eat large fish, predators that pick a specific size of fish (see #1), availability/seasonailty of food, changes in food types, bacteria, virii, changes in water temperature/sailnity/clarity/pollutants/depth/availability, AND CONSTANT CHANGES TO THE INTENSITY OF EACH OF THESE PRESSURES. And yet we observe evolutionary changes. It took me less than a minute to think of all items in this list. There must be more.

We now return you to your strawman burning already in progress.

CT

[Mr. Scott]

I know I am going to regret posting in this thread. And no, I have not read all 7900 (and counting) posts in it. My apoligies if this has already been discussed. How could it not be after this many posts? :rolleyes:

I know exactly how those nitwit creationist loonies will answer.

If I recall some of this thread and understood the arguments, one of Kleinman's arguments is that multiple selection pressures cause would cause evolution to slow such that what we observe today could not have evolved in the time given.

Multiple selection pressures confound the process of evolution by mutation and natural selection. It's a sorting/optimization problem that becomes profoundly slowed by multiple sorting conditions.


1) There was a recent article noting that fishery policies of catch size restrictions (size of the individual fish, not the size/volume of total catch) have caused an observed accelleration of fish evolution. Specifically, the species are coming to sexual maturity faster and not growing as large. A new selection pressure (size selection during "predation") has resulted in an observable accelleration.

They're still fish, aren't they?


2) When is there ever only one selection pressure? Just thinking about the fish example, there are always many pressures. Preators that eat eggs, predators that eat fry, predators that eat large fish, predators that pick a specific size of fish (see #1), availability/seasonailty of food, changes in food types, bacteria, virii, changes in water temperature/sailnity/clarity/pollutants/depth/availability, AND CONSTANT CHANGES TO THE INTENSITY OF EACH OF THESE PRESSURES. And yet we observe evolutionary changes.

The intensity of the selection pressure has no effect on the sorting/optimisation problem. The more pressures, the longer it takes.

It took me less than a minute to think of all items in this list. There must be more.

It took me less than a minute to guess how the nut cases would respond.

We now return you to your strawman burning already in progress.

CT

Ah, the all-powerful strawman argument. Have you evolutionists figured out the mathematics and empirical facts about mutation and natural selection, or are you still responsible for the deaths of millions with your monotherapies based on the evolution fairy tale?[/mockery]

[Dr Adequate]

I think it worthwhile ...

<1500 words of kleinmania deleted for pointlessness> Yes, you do find it worthwhile.

No-one knows why.

It's not as if you've deceived anyone, ever, during the course of the last fifteen months.

I wouldn't find fifteen months of failure at anything to be "worthwhile", least alone failure at something so stupid and pointless as lying to people about basic biology, but then we are two very different people.

[kleinman]

Some evolutionists think that I view them as enemies. On the contrary, I view of you evolutionists as very confused and wrong about how the mutation and selection sorting/optimization process actually works both mathematically and empirically. Instead, you substitute illogical and irrational speculations that obfuscate how this process works in reality and as a consequence millions of people have and will continue to die prematurely from diseases subject to the mutation and selection sorting/optimization process. For example, several evolutionists on this thread have speculated that in some cases selection pressures increase the diversity of populations and in other cases selection pressures decrease the diversity of populations.

In all cases, selection pressures decrease the diversity of populations. This can be shown mathematically with Dr Schneider’s ev computer simulation of random point mutations and natural selection as well as empirically with as many examples as you like. First let’s look at how Dr Schneider’s computer model demonstrates that natural selection reduces the diversity of a population.

Dr Schneider’s computer model starts with an initial condition of a population of randomly distributed genomes. This is the most diverse condition you can have and represents an initial condition of maximum disorder. When the algorithm is initiated, the selection conditions reduces the disorder of the sequences of genomes (increase the information content) in the population. This decrease in disorder (increase in information) is demonstrated by the following graph from Dr Schneider’s web site:
http://www.ccrnp.ncifcrf.gov/~toms/icons/ev-fig2b.gif
Note that with the removal of the selection conditions, any information accumulated by the mutation and selection sorting/optimization process is lost until the genome returns to random sequences.

In real cases of the mutation and selection sorting/optimization process, selection pressures eliminate phenodeviants (members of the population who can only survive to reproduce in an environment without those selection pressures). This is clearly seen when an antimicrobials is used on a population sensitive to that antimicrobial, when cancer cells are subjected to anti-cancer therapy, when weeds are subjected to herbicides and so on.

Diversity of populations occurs when you remove selection pressures. The reason why the Madagascar rain forest has such diverse populations is the low selection pressures (abundant water, mild temperatures without extremes, abundant food), while environments like deserts have far fewer diverse forms of life because of the lack of water, much greater temperature extremes and lack of food. If you tamper with the rainforest, these diverse life forms are quickly killed off. On the other hand, put a house up in the desert and the rattlesnakes and scorpions are much more likely to survive this intrusion. Selection pressures reduce the diversity of the populations subjected to these selection pressures. A citation which demonstrates this empirically is:

http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf (http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf)
In some cases it is the combination of multiple stressors that lead to the decline of species or groups of species; e.g., amphibians by nematodes (Johnson et al., 1999), increased UV radiation and pollutants (Hatch and Blaustein, 2003; Beebee and Griffiths, 2005), and disease (Collins and Storfer, 2003; Daszak et al., 2003). Conserving endangered species and facilitating their recovery is one the main environmental challenges of the 21st century. Unfortunately, history has shown that in most cases permanent removal of stressors has not been possible and species often need to be
managed indefinitely to ensure their persistence; of the 1263 species listed under the Endangered Species Act of the United States less than 2% have been de-listed (US Fish and Wildlfe Service, 2004).
Manage indefinitely means remove selection pressures.

Now I note that you evolutionists have posted some fossil Rorschach. Don’t just post your images; tell us what your imaginations give you.

I also note that the author of blizzards turns lizards into buzzards with gizzards and the author of the n+1 selection pressures evolve more rapidly than n selection pressures but he doesn’t have any reality to back up his mythematics. We all enjoy your blizzdom.
http://forums.randi.org/images/smilies/doglaugh.gif

[m_huber]

Do you even read other people's posts?

[Mr. Scott]

Do you [Kleinman] even read other people's posts?

The evolutionists who post on this thread are mere props in Kleinman's act, the objective of which is to google-bomb his nitwit ideas. To him we are cardboard cutout targets for him to knock down in the hope of future fame. Quite a pathetic spectacle.

[kleinman]

Some evolutionists don’t think that I read their posts, such as those evolutionists who think that variations in the weather is what turns lizards into buzzards or that n+1 selection pressures sort more rapidly than n selection pressures. Sure you evolutionists have lots of speculations, but your mathematical and empirical evidence is simply not there. Here are some more empirical evidence that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://homepages.ed.ac.uk/eang09/research.html (http://homepages.ed.ac.uk/eang09/research.html)
The development of combination antiretroviral therapy was an immense breakthrough in HIV treatment, turning a previously lethal infection into a chronic treatable condition. In the absence of a vaccine, combination therapy is the only way HIV infection can be controlled, but there are two major problems, side effects due to toxicity and the development of resistance. Almost all drug failure is associated with antiretroviral resistance, which for some drugs (eg 3TC monotherapy) can arise within days (Frost et al. 2000). Combination therapy extends the period of efficacy greatly, but resistance still appears in a majority of patients.
http://www.ajtmh.org/cgi/content/full/71/2_suppl/179 (http://www.ajtmh.org/cgi/content/full/71/2_suppl/179)
Increasing resistance of Plasmodium falciparum malaria to antimalarial drugs is posing a major threat to the global effort to "Roll Back Malaria". Chloroquine and sulfadoxine-pyrimethamine (SP) are being rendered increasingly ineffective, resulting in increasing morbidity, mortality, and economic and social costs. One strategy advocated for delaying the development of resistance to the remaining armory of effective drugs is the wide-scale deployment of artemisinin-based combination therapy. However, the cost of these combinations are higher than most of the currently used monotherapies and alternative non-artemisinin-based combinations.
How about this citation? You evolutionists think that recombination is the super mechanism which somehow transforms one species into another.
http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html (http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html)
The immune deficiency syndrome, AIDS is a huge health problem worldwide – and will remain so for some time to come. One reason lies in the HI-viruses' ability to become resistant to specific drugs. Until now, scientists have supposed that the recombination of different viruses plays an important role here. But researchers at ETH now show that the recombination can in fact slow down the build-up of resistance and that it advances it under certain specific conditions. This throws light on the question of why sexuality exists.
and
So what are the possible consequences of this model for the ETH research team? Sebastian Bonhoeffer points to two aspects, the first of which is medical. If gene variants that are antagonistic to one another exist, then the build-up of resistance to a combination of drugs that favours such genes would be slowed down by recombination. What is missing from the picture is information on how strongly certain mutations in the HIV genome act synergistically or antagonistically on one another. Bonhoeffer now wants to turn his attention to this question using HI-virus data sequences, which he has in abundance.

However, such an analysis is not only relevant from a medical point of view. Bonhoeffer comes to his second point. It is highly possible that the results of such an investigation could also deliver insights into a far more fundamental question; why on earth does recombination exist? Because, as Bonhoeffer's model shows, in many cases this process has unfavourable consequences for HI-viruses. From an evolutionary point of view, it must be presumed that, under certain circumstances, the acquisition of recombination is advantageous. If these circumstances can be identified in the case of the HI-viruses then conclusions might be drawn on the reason – or reasons – for recombination in higher-order beings. Even though sexual reproduction and concomitant recombination is widespread, the advantages of sex as a means of reproduction is still one of biology's better kept secrets – despite numerous theories.
Could it be that recombination slows evolution? That can’t be, it doesn’t fit ridiculous evolutionists speculations. Who cares if millions of people die prematurely from diseases subject to the mutation and selection sorting/optimization process? The irrational and illogical theory of evolution is much more important than premature death of millions of people.

[m_huber]

You know, using the "Quote" button and responding to specific claims would make your case against "evolutionists" much more intelligible. Instead, you post large blocks of scientific articles that are moderately difficult to read, which you then claim support the belief that evolution doesn't happen. Instead, when those have been broken down, they only show that extinction prevents evolution. In other cases, evolution has been demonstrated at the bacterial and viral level, but instead of saying "oh, wow, reality exists!" you say, "But you don't have a mathematical proof!"

Math is trumped by reality. Always. Newton predicted that the world would end in 2060. (http://en.wikipedia.org/wiki/Isaac_Newton's_religious_views#2060_A.D.)

[kleinman]

I’m not sure why evolutionists are having a hard time reading scientific articles. I thought the theory of evolution was based on science. Could it be that evolutionists have gotten so used to irrational and illogical speculations that when they are confronted with the mathematical and empirical evidence that multiple selection pressures profoundly slow the mutation and selection sorting/optimization process it confuses them? I have shown with Dr Schneider’s computer simulation that multiple selection conditions profoundly slow the sorting process in his algorithm. And now I am posting the empirical evidence which demonstrates the same effect when multiple selection pressures are applied to a population. Here are some more real example which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://www.annalsnyas.org/cgi/content/abstract/918/1/9 (http://www.annalsnyas.org/cgi/content/abstract/918/1/9)
Large-cohort studies in North America, Europe, and Thailand have shown that zidovudine/azidothymidine (AZT) monotherapy, given at the late stages of pregnancy, is of proven benefit in reducing mother-to-infant HIV transmission by 51% to 68%. AZT monotherapy will not be of long-term benefit for mothers because no single drug can counteract viral infection; benefits to babies will be short-lived if HIV-1 is acquired through breastfeeding after birth. Unfortunately, ongoing mutation of HIV under conditions of drug pressure allows for the evolution and selection of AZT-resistant viruses. Emergence of AZT-resistant variants in pregnant mothers (7-29%) and their infected offspring (5-21%) has been described in several studies. Drug resistance arises more frequently in those mothers who received AZT therapy before pregnancy. Recent advances in combination chemotherapy may provide alternative strategies in prevention of vertical transmission and drug resistance. Genotypic screening of the HIV-1 isolated from pregnant mothers may provide rational modifications in antiretroviral (ARV) strategies to circumvent vertical HIV transmission. This may be of advantage for resource-rich nations but not for underdeveloped nations with limited access to ARVs. Public health programs are vital to have an impact on the tragic pandemic of pediatric AIDS.
http://www.who.int/infectious-disease-report/2000/ch5.htm (http://www.who.int/infectious-disease-report/2000/ch5.htm)
Drug combinations have long been recognised as critical in combating multi drug-resistant malaria.
And
It wasn't until the 1950s that effective treatment for leprosy was introduced into vulnerable populations. By the 70s, the organism had launched a major counter-offensive and had effectively disarmed and rendered obsolete the sulpha drug dapsone. By the 1980s, two drugs – rifampicin and clofazamine – cleared the way for viable treatment alternatives. The organism developed resistance to all three drugs when prescribed singly but in combination with dapsone, these new medications effectively trounced the leprosy bacilli and led the way to cure and – researchers hope – elimination by 2005. Wiser for the experience, scientists are holding back three alternative drugs in the event that resistance recurs. The only outstanding issue however is cost. Fortunately, a solution involving the private and public sectors working in tandem with corporate interests means patients need wait no longer. Blister packs containing multi-drug therapies are now being distributed to patients free of charge. Thanks to WHO-sponsored research grants, Nippon Foundation funds, and donations of medication from the Swiss pharmaceutical Novartis, leprosy is on the way out.
http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103 (http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103)
"In the history of malaria disease, we lost all the single drugs by drug resistance."
and
For example, the best current treatments for malaria are clearly artemisinin-based combination therapies, or ACTs, which were develop in the early 1990s. These drugs exploit the effectiveness of artemisinin, to which resistance has not yet developed, but combine it with older antibiotics to sustain this effectiveness.
Now I know that there are evolutionists out there who have the ridiculous belief that variations in the weather like blizzards turn lizards into buzzards with gizzards and there are evolutionist mythematicians who believe that n+1 selection pressures cause a population to evolve more quickly than n selection pressures and this is good stuff for the SciFi channel but they simply do not have mathematical or empirical evidence of these ridiculous speculations. While on the other hand, we have posted and will continue to post the empirical evidence which substantiates the mathematics which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

[kleinman]

You evolutionists continue to have difficulty understanding the mathematics of the mutation and selection sorting/optimization process. Let’s give a brief review how Dr Schneider (head of computational molecular biology at the National Cancer Institute) did his mathematical model and how accurately his mathematical model simulates the real behavior of the mutation and selection sorting/optimization process. Dr Schneider’s mathematical model is based on the following which is from his web site at http://www.lecb.ncifcrf.gov/~toms/paper/ev/evj/evj-guide.html (http://www.lecb.ncifcrf.gov/~toms/paper/ev/evj/evj-guide.html) :
http://www.lecb.ncifcrf.gov/~toms/paper/ev/evj/penta/penta.jpg
Mutate each creature by changing its genome randomly. For example, the program might change the letter at position 82 from an A to a T. Mutation happens everywhere in the genome, both in the gene, in the binding sites, and in the spaces between. The location is random and the change is random.
Then
Evaluate each creature: count the number of mistakes each one makes.
This is the first step of selection.
Then
Sort the creatures by their mistakes.
This is the second step of selection.
then
Kill half of the creatures, the ones that make the most mistakes.
This is the final step of selection.
Then
Replicate (make another copy of) the creatures that make the least mistakes.
Then
The cycle is repeated every 'generation'.
Now, Dr Schneider has suggested the following in his publication on ev in Nucleic Acids Research http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (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). However, this could be caused by mutation rates, and/or it could be the result of some kind(s) of evolutionary pressure that we don’t understand, so how one implements the skew may well affect or bias the results.
When you actually do the bookkeeping associated with the mutation and selection sorting/optimization process that Dr Schneider has mathematically modeled, it shows that increasing population sizes have only a small affect on the rate of information accumulation, increasing genome length markedly slow the rate of information accumulation, number of sites has only a minimal affect on the rate of information accumulation, mutation rate has an approximately linear affect on the rate of information accumulation (for realistic mutation rates) however, the number of selection pressures has a profound affect on the rate of information accumulation. A single selection condition can be sorted for very rapidly by Dr Schneider’s sorting algorithm while all three selection conditions can only be sorted for rapidly only on extremely tiny unrealistic length genomes. This mathematical behavior that Dr Schneider’s mathematical model demonstrates is reflected in reality as demonstrated by more of these real examples of the mutation and selection sorting/optimization process.
http://www.ctu.mrc.ac.uk/penta/abcpath.pdf (http://www.ctu.mrc.ac.uk/penta/abcpath.pdf)
Abacavir (ABC) selects for four mutations (K65R, L74V, Y115F and M184V) in HIV-1 reverse transcriptase (RT), both in vitro and during monotherapy in vivo. The aim of this analysis was to compare the selection of these and other nucleoside reverse transcriptase inhibitor (NRTI)-associated mutations by ABC-containing therapies in the presence and absence of concurrent lamivudine (3TC) and/or zidovudine (ZDV) and to assess the effect of these mutations on phenotypic susceptibility to the NRTIs.
and
The results of this study demonstrate that ZDV is useful as a resistance modulator, at least in combination with ABC, effectively reducing the incidence of selection forK65R and L74V. This may increase the likelihood that agents such as ddI, TDF and others affected by these two mutations will remain efficacious in second-line regimens. The relevance of these findings to combinations including NRTIs other than ABC, 3TC and ZDV remains to be elucidated.
http://cancerres.aacrjournals.org/cgi/reprint/22/11_Part_1/1290.pdf (http://cancerres.aacrjournals.org/cgi/reprint/22/11_Part_1/1290.pdf)
The possible application to chemotherapy of factors affecting the regulatory systems of cells has been considered. The extensive coordinate changes in intracellular enzyme concentrations which result from exposure to compounds interfering with the normal regulatory mechanisms suggest the possibility of combination therapy based upon the selective induction of quantitative changes in enzymatic activities. Such approaches would appear to be useful in circumventing two major problems of chemotherapy: finding sufficient metabolic differences between host and parasite to provide targets for selective drug toxicity, and preventing the eventual development of drug resistance.

It is concluded that a combination of two compounds affecting the same metabolic pathway, one producing feedback inhibition and the other effective through lethal synthesis, will show an enhanced differential toxicity greater than that from either drug alone. Similarly, pairs of compounds in which one member produces enzyme repression and the other is active through lethal synthesis should produce collateral sensitivity and thus prevent the development of drug-resistant populations.
The failure of evolutionists to understand and acknowledge this mathematical and empirical fact of life that combination selection pressures profoundly slow the mutation and selection sorting/optimization process contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon. This was sadly demonstrated by the many year delay in understanding that HIV requires combination therapy to slow the evolution of this virus despite the fact that this was known decades earlier. You evolutionists have blundered in your description of the mutation and selection sorting/optimization process because the basic science and mathematics of this process does not fit with your irrational and illogical world view.

[Mr. Scott]

A single selection condition can be sorted for very rapidly by Dr Schneider’s sorting algorithm while all three selection conditions can only be sorted for rapidly only on extremely tiny unrealistic length genomes. This mathematical behavior that Dr Schneider’s mathematical model demonstrates is reflected in reality as demonstrated by more of these real examples of the mutation and selection sorting/optimization process.

Dr. Kleinman, I’m glad you brought this up because I am prepared to drive a silver spike through the heart of that argument.

Your error has to do with your equation of model execution time with the virtual time that it is modeling.

Nature does not execute a sort algorithm. The time it takes to sort a population in a computer in no way models the time needed to sort a population in nature. Organisms in a natural colony sort themselves instantaneously, whereas a computer model, by the nature of the usual computer program implementation, must execute an algorithm sequentially, and necessarily needs more CPU time as the number of items or selection conditions increases.

A computer program has to execute one instruction at a time, with a single CPU sequentially going through a sort algorithm step by step, item by item, and condition by condition. In nature, though, each organism has, in a sense, it’s own CPU, so a sort happens with massive parallelism. A colony of a trillion microbes has, in effect, a trillion processors running a trillion sorts all at the same time, and the number of conditions (selection pressures) would have no effect on the real time sort speed.

I’ll give you an example of how this works. Suppose a photographer needs one hundred students to line up for a photograph sorted by height. If the photographer were to make each comparison himself and order each swap himself and wait for each swap to occur before making the next comparison, it would take a very long time indeed for the hundred students to be sorted. Alternatively, the photographer could give the students the following instruction: “everyone please position yourself so that you have a taller person to your right and a shorter person to your left” and the students would sort themselves very, very quickly.

The first example is how Ev sorts -- laboriously, one comparison and swap at a time. The second example is how nature sorts -- every organism sorts itself, by reproducing or not reproducing according to how competition plays out, and the count of sort conditions would have no affect on the speed of that sort -- some die, some don't. No sort time is required.

In summary, though a condition (selection pressure) count may have a detrimental effect on computation time of a model like Ev, the time it takes for organisms to be selected or not because of multiple selection conditions in nature would not be similarly affected.

Now, Dr. Kleinman, if you were a real scientist and my argument were shown to be true, then you would thank me for advancing your knowledge in computer science and evolution. If you show me I’m wrong, I will thank you.

I await your refutation.

[kleinman]

Once again, we have an evolutionist who thinks there is something unique about the mutation and selection sorting/optimization process. Somehow, evolutionists think that the sorting occurring with biological systems behaves differently from other sorting problems (or for that matter iteration problems or optimization problems) found in non-biological systems. All these mathematical problems are markedly slowed for more complex sorting conditions (or for iteration or optimization conditions). The computer model execution time and virtual time are directly correlated with real time. This is how Dr Schneider responded to this argument on his ev blog site, http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html)
13) Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!
and
Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world.1. The simulation was of phenomena in the "real" world.
2. Dr. Jones is invited yet again to do an experiment.
Dr Schneider is correct here. His sorting algorithm is exactly analogous to what happens in nature. Just because Dr Schneider’s algorithm can do generation cycles is some cases millions of times faster in the computer than could be done in real life, his model still properly models the mutation and selection sorting/optimization process.

Now the notion that there are trillions of sorting processes going on simultaneously is simply a fantasy that evolutionists try to use to justify their theory. Unfortunately for you evolutionists, there is no mathematical or empirical basis for this claim. In fact these types of claims obfuscate how the mutation and selection sorting/optimization process actually works as demonstrated by Dr Schneider’s mathematical computer simulation and the hundreds of real examples of mutation and selection which substantiates Dr Schneider’s simulation. Here are more examples which substantiate the result that Dr Schneider’s model demonstrates, which is that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://pathmicro.med.sc.edu/lecture/hiv14a.htm (http://pathmicro.med.sc.edu/lecture/hiv14a.htm)
These drugs are non-competitive reverse transcriptase inhibitors, that is they bind elsewhere than the active site of the enzyme.

Because of the problems with AZT and the other nucleoside analogs in the treatment of HIV, interest grew in another approach to inhibiting the same enzyme, reverse transcriptase. Alternative drugs might be useful in combination therapy since there is a limit to the number of mutations that reverse transcriptase can bear without losing function. Clearly, mutations resistant to a non-nucleoside non-competitive inhibitor of reverse transcriptase would be at a different site in the enzyme from the mutation that makes the enzyme resistant to a competitive nucleoside analog.
http://www.absw.org.uk/Briefings/insecticide_resistance.htm (http://www.absw.org.uk/Briefings/insecticide_resistance.htm)
Using high doses of insecticide should maximise kill of heterozygotes and this strategy was popular among theorists in the 1970s. But to be really effective, the dose was too high to be acceptable on either environmental or cost grounds. Another drawback was that uniform coverage of the crop was not assured. The high dose strategy could be revived though with transgenic plants if it is possible to maintain a high level of expression of the toxin gene. The other strategy is pyramiding which involves creating trangenic plants with genes for two different toxins. Insects resistant to one will be killed by the other, and vice versa. This provides a double hit strategy for seeing off heterozygotes and discouraging the spread of resistance genes. It also parallels the successful use of combination drug therapy in leprosy, TB and HIV/AIDS.
http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resi stance&hl=en&ct=clnk&cd=297&gl=us (http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resi stance&hl=en&ct=clnk&cd=297&gl=us)
With its high mutation rate, small genome, and large population size, HIV is highly likely to generate resistance mutations (as we’ve seen with 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
http://www.ann-clinmicrob.com/content/5/1/25 (http://www.ann-clinmicrob.com/content/5/1/25)
in this study the checkerboard analysis showed that amikacin in combination with cephalothin or dicloxacillin was synergistic against most of the resistant strains of S. aureus and coagulase-negative Staphylococcus. Vancomycin in combination with a beta-lactam (cephalothin or imipenem) showed additivity. An indifferent effect predominated for the combination vancomycin plus amikacin. Even though a synergistic effect is expected when using a beta-lactam plus amikacin combination, it is possible that the effect cannot be clinically achievable. Careful selection of antimicrobial combinations and initial MICs are mandatory for future evaluations.
Now if you evolutionists think there are trillions of sorting process going on simultaneously, present the mathematical and empirical basis for such a claim. Otherwise, all you do with such irrational and illogical claims is to contribute to the premature death of millions of people with diseases subject to mutation and selection. That includes stepfathers who die from cancer.

[kjkent1]

kleinman, scientific discovery marches on, despite your protestations to the contrary. You may want to check this link: http://www.livescience.com/health/080124-dna-telepathy.html. It discusses a weird, but empirically verifiable property of DNA, which may help explain how evolutionary processes get past your claims of statistical impossibility.

What is clear from the cited article is that we still don't know exactly how evolution works. We do, however, observe that it does work. As always, you are free to attribute the unexplained to God, while the scientist will attribute the unexplained to a lack of verifiable evidence.

In the end, it's still primarily a philosophy argument "in the gaps."

[kleinman]

Now that’s a good one, DNA demonstrates telepathy. I guess you evolutionists forgot that there are electromagnetic fields around molecules. You evolutionists go further and further into the paranormal and have no idea about the basic science and mathematics of the mutation and selection sorting/optimization process. You go even further by indoctrinating naïve school children with this type of nonsense so they have no idea or foundation how to deal with diseases subject to the mutation and selection process. This is how evolutionist nonsense contributes to the premature death of millions of people suffering from disease subject to the mutation and selection sorting/optimization process. The theory of evolution is not only nonsense; it has and will continue to hurt millions of people.

[Belz...]

DNA demonstrates telepathy.

Yeah, like God. :rolleyes:

[kleinman]

You evolutionists can’t even explain how the mutation and selection sorting/optimization process works. What makes you think that you know how God works?

Here are more citations which show how the mutation and selection sorting/optimization work empirically. And it works the same as Dr Schneider’s ev model, which is that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://www.bmj.com/cgi/content/full/325/7374/1221?etoc (http://www.bmj.com/cgi/content/full/325/7374/1221?etoc)
Artemisin combinations may delay and possibly reverse the development of drug resistance through a variety of mechanisms.
http://journal.paho.org/?a_ID=335 (http://journal.paho.org/?a_ID=335)
Suboptimal treatment regimens, such as monotherapy or dual therapy, treatment with poor-quality antiretroviral drugs, suboptimal dosing, and poor absorption, may increase the rate at which viral resistance evolves among treated individuals
http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html (http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html)
The genetic instability of tumor cells renders them the ability to rapidly become resistant to many chemotherapies. As a result, there is great interest in selecting combination chemotherapeutic regimens that will overcome resistance and exert synergistic therapeutic activity.
Now since you evolutionists have no idea how the mutation and selection sorting/optimization process works, why don’t you speculate on how God works. Perhaps you can figure it out from your fossil Rorschach tests?

[rocketdodger]

Dr. Kleinman, I’m glad you brought this up because I am prepared to drive a silver spike through the heart of that argument.

Your error has to do with your equation of model execution time with the virtual time that it is modeling.

Nature does not execute a sort algorithm. The time it takes to sort a population in a computer in no way models the time needed to sort a population in nature. Organisms in a natural colony sort themselves instantaneously, whereas a computer model, by the nature of the usual computer program implementation, must execute an algorithm sequentially, and necessarily needs more CPU time as the number of items or selection conditions increases.

A computer program has to execute one instruction at a time, with a single CPU sequentially going through a sort algorithm step by step, item by item, and condition by condition. In nature, though, each organism has, in a sense, it’s own CPU, so a sort happens with massive parallelism. A colony of a trillion microbes has, in effect, a trillion processors running a trillion sorts all at the same time, and the number of conditions (selection pressures) would have no effect on the real time sort speed.

I’ll give you an example of how this works. Suppose a photographer needs one hundred students to line up for a photograph sorted by height. If the photographer were to make each comparison himself and order each swap himself and wait for each swap to occur before making the next comparison, it would take a very long time indeed for the hundred students to be sorted. Alternatively, the photographer could give the students the following instruction: “everyone please position yourself so that you have a taller person to your right and a shorter person to your left” and the students would sort themselves very, very quickly.

The first example is how Ev sorts -- laboriously, one comparison and swap at a time. The second example is how nature sorts -- every organism sorts itself, by reproducing or not reproducing according to how competition plays out, and the count of sort conditions would have no affect on the speed of that sort -- some die, some don't. No sort time is required.

In summary, though a condition (selection pressure) count may have a detrimental effect on computation time of a model like Ev, the time it takes for organisms to be selected or not because of multiple selection conditions in nature would not be similarly affected.

Now, Dr. Kleinman, if you were a real scientist and my argument were shown to be true, then you would thank me for advancing your knowledge in computer science and evolution. If you show me I’m wrong, I will thank you.

I await your refutation.

This is why in computer models we measure rates according to the number of generations, or virtual time, that it takes something to happen -- it removes any processing considerations from the experiment and allows us to focus only on the algorithm. It also allows us to emulate parallel processes, like evolution, on serial machines, like computers.

Kleinman is incapable of understanding this (among other things), and thats why he doesn't have a clue what he is talking about when it comes to either ev or his hundreds of empirical examples. If a computer takes more real time to sort, kleinman interprets this as "the sorting being confounded," which is of course utter nonsense.

It doesn't matter, nobody cares about this thread anymore. Kleinman is old news.

[hamelekim]

Isn't the title of this thread a little redundant?

[kleinman]

I enjoy annoying evolutionists with the mathematical and empirical facts of how the mutation and selection sorting/optimization process actually works. Now, you evolutionists have completely bungled the basic science and mathematics of the mutation and selection sorting/optimization process and in the meantime are still trying to figure out what “random” means. Your irrational and illogical concepts of abiogenesis and the theory of evolution have made a framework for your speculations but do not fit the mathematical and observed evidence. You may have successfully institutionalized these ideas into the field of biology but they are totally useless concepts in the explanation of how the basic science and mathematics of the mutation and selection process actually works. Perhaps a few more examples of how the mutation and selection process actually works will clarify the mathematical and empirical fact of life that combination selection pressures profoundly slow evolution by this process.
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract)
Even patients with extensive resistance to the failing regimen were still receiving benefit from treatment.
http://agfacts.tamu.edu/~jbenedic/TRANS.htm (http://agfacts.tamu.edu/~jbenedic/TRANS.htm)
On these bases transgenic insect-resistant crops are a new tool for insect pest management of crop plants. This new tool is complimentary to many existing pest management tactics, and when used in combination, these tactics may provide superior pest management compared to any single tactic.
and
Other strategies to use in combination with the refuge are: (1) stacking two or more insecticide producing genes in the same transgenic plant; (2) low dose producing transgenic plants that act in concert with natural enemies to decrease target pest populations; (3) tissue-, time-, or signal-dependent expression of toxins; (4) rotation over time (years) of insecticidal toxins with different modes of action; and (5) deploying different toxins in different crop varieties in the same year and production system.
http://www.annclinlabsci.org/cgi/content/abstract/32/4/406 (http://www.annclinlabsci.org/cgi/content/abstract/32/4/406)
In recent years, resistance testing has become an important tool in optimizing the combination therapy for treating HIV infected individuals. The identification of resistance mutations has allowed physicians to select the antiviral agents with maximum therapeutic benefic and minimum toxic side effects.
http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml (http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml)
There is a need to develop broadleaf combinations or mixtures to control glyphosate and multiple HT volunteers pre-seed. For example, 2,4-D, MCPA, bromoxynil and a low residual sulfonylurea like tribenuron methyl in combination with glyphosate would provide broad-spectrum pre-seed weed control including volunteer glyphosate HT canola. In some situations amitrole and paraquat could provide effective pre-seed control and resistance management for volunteer HT canola.
And
Herbicide mixtures to manage volunteers and reduce selection pressure could be a requirement for future HT crop releases.
Trillions of sorting process occurring simultaneously, chemicals “cooperating” to form life by abiogenesis, variations in the weather causing blizzards to turn lizards into buzzards with gizzards, n+1 selection pressures evolving more rapidly than n selection pressures even though you don’t have a single empirical example of this nonsense? These would all be very amusing if it were not a fact that these ridiculous assertions contribute to the premature death of millions of people with diseases subject to mutation and selection. We all thank you evolutionists for MRSA, delay in the understanding that diseases like HIV and cancer require combination therapy and your diligent work of indoctrinating naïve school children with irrational speculations and calling it science.

[Shalamar]

Too bad Kleinman has no facts. And still has no math.

He's just a parrot, repeating only what he is allowed to understand.

[Nogbad]

Nearly at page 200 I see and yet...:)

[kleinman]

You evolutionists are so correct when you say I have no mathematics to back up my argument except you continue to forget one thing, I have Dr Schneider’s peer reviewed and published mathematical model of random point mutations and natural selection and I have only a few hundred measly empirical citations which demonstrates what Dr Schneider’s mathematical model shows, that is combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. Why don’t I post a few more just to annoy some irrational and illogical evolutionists.
http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf (http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf)
Combining drugs from different classes can slow down the emergence of resistant variants substantially, because mutants that are resistant to all components are unlikely to pre-exist, and new variants need to generate several escape mutations while retaining the ability of effective replication.
http://www.ecologyandsociety.org/vol3/iss2/art12/ (http://www.ecologyandsociety.org/vol3/iss2/art12/)
Protease inhibitors of HIV prevent infected cells from producing infectious virus. The overall dynamics are very similar to the case of reverse transcriptase inhibitors, because the infectious virus particles present initially decay very rapidly. Combination of reverse transcriptase and protease inhibitors has led to tremendous success in HIV therapy.

Essentially, all of these drugs, if used as single antiviral therapy, lead to the emergence of resistant virus mutants. The pattern is often similar. Initially, there is a decay in virus abundance, but after some time, the virus resurges. The decisive treatment breakthrough was to combine several drugs at once. For about 2 years, this combination therapy has proved to be a tremendous success. In many patients, virus abundance in the blood decays below detection limit within weeks of treatment and can remain undetectable for years.
http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf (http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf)
Antimicrobial exposure inevitably exerts a selection pressure on the pathogen being actively treated, as well as commensal organisms, 80% to 90% of which are currently non-culturable (Wilson & Blitchington, 1996; Langendijk et al 1995). Therefore, its potential to act as a reservoir for antimicrobial resistance genes may be immense. As the “normal” commensal flora acts to inhibit the attachment and multiplication of pathogenic micro-organisms by various mechanisms, its disturbance may also facilitate colonization with exogenously acquired pathogens. Consequently, the aim of antimicrobial therapy must be to destroy the pathogen rapidly and efficiently, while producing the least amount of “collateral” damage. This can be achieved by giving careful consideration to the agent employed, its spectrum of activity, method of administration, penetration to the site of infection, magnitude of dose, frequency of administration, duration of therapy, and the use of agents in combination, such as in TB and HIV therapy.
Come on now, won’t you evolutionists post some more of your fossil Rorschach tests and then tell us what your imagination shows?

[Shalamar]

Remember folks: Mr. Kleinman isn't allowed to accept the evidence behind the Theory of Evolution.

So he has to make things up using misinterpreted data.

[kleinman]

I understand that I have to be patient with you evolutionists. After all you have been programmed for years with irrational and illogical speculations. Evolutionist propaganda has always avoided describing the basic science and mathematics of the mutation and selection sorting/optimization process. Is it any wonder that Dr Schneider has not published the results of the parametric study that he recommends in his original publication on ev? If he had, he would have a lot of explaining to do about how his model contradicts the theory of evolution. After all, his mathematical model shows that the dominant parameter is the number of selection conditions. One selection condition in his model takes trivially small number of generations to evolve that condition while all three selection conditions simultaneously takes huge number of generations to satisfy all three selection conditions (except on the tiniest, unrealistic length genomes). I’ll just keep posting real examples of this and perhaps in a few years some of you evolutionist devotees will understand how the mutation and selection sorting/optimization process actually works. Here are a few more examples for you to consider.
http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html (http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html)
In this paper we discuss the case of the evolution in weed species of resistance to glyphosate, a valuable and widely used broad-spectrum non-selective herbicide first developed by Monsanto in the early 1970s.
and
The authors conclude that “The use of glyphosate in combination with other low risk herbicides for weed control with RR cotton provides an opportunity to significantly reduce the risk of off-site herbicide contamination in Australian cotton production”
http://www.aegis.com/factshts/tpc/guide/ (http://www.aegis.com/factshts/tpc/guide/)
Based on what is known about HIV's error-prone replication process (see above), we can assume that all patients have at least a few subpopulations of HIV that are resistant to individual drugs. However, these strains are often too limited in number and strength to compete with wild-type virus, and they stand a good chance of being killed off by initiating combination antiretroviral therapy. After all, the purpose of combination therapy is to serve as a multipronged attack on such strains.
http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)
The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.
Isn’t that interesting, the empirical evidence agrees with Dr Schneider’s mathematical model which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. That is why the theory of evolution is mathematically and empirically impossible.

Now you all have a good weekend and if you can’t find a fossil Rorschach test to fuel your imaginations, just look at the clouds. We’ll be back next week to again correct the bungled evolutionist explanation of how the mutation and selection sorting/optimization process actually works.

[Paul C. Anagnostopoulos]

You evolutionists can’t even explain how the mutation and selection sorting/optimization process works. What makes you think that you know how God works?
And with this remark we understand that you will never, ever again bring up god in relation to the origin of species.

~~ Paul

[sol invictus]

Kleinman is incapable of understanding this (among other things), and thats why he doesn't have a clue what he is talking about when it comes to either ev or his hundreds of empirical examples. If a computer takes more real time to sort, kleinman interprets this as "the sorting being confounded," which is of course utter nonsense.

Are you serious? I didn't realize he was that idiotic.

So if I port ev to my iphone and it runs slowly, does that mean evolution is profoundly slowed by the existence of iphones?

[m_huber]

If anyone who is reading this thread has a headache fueled by reading repetitive ignorance, try a nice cold glass of actual science:

http://www-personal.umich.edu/~gingeric/PDFfiles/PDG132_JGeolEdu.pdf

[Belz...]

I enjoy annoying evolutionists

Troll, troll, troll.

[Mr. Scott]

Dr. Kleinman, I know you are away for the weekend, but when you come back, would you tell us what sorting algorithm nature uses during micro-evolution? Different sort algorithms would profoundly affect the speed of any sorting/optimization, so I'd really like to know which sort nature uses. Does it use Quick Sort (http://en.wikipedia.org/wiki/Quicksort)? Bubble Sort (http://en.wikipedia.org/wiki/Bubble_sort)? Selection Sort (http://en.wikipedia.org/wiki/Selection_sort)? Insertion Sort (http://en.wikipedia.org/wiki/Insertion_sort)? Shell Sort (http://en.wikipedia.org/wiki/Shell_sort)? Merge Sort (http://en.wikipedia.org/wiki/Merge_sort)? Heap Sort (http://en.wikipedia.org/wiki/Heapsort)? Bucket Sort (http://en.wikipedia.org/wiki/Bucket_sort)? Radix Sort (http://en.wikipedia.org/wiki/Radix_sort)?

[rocketdodger]

The closest analog is probably bucket sort, I would say.

[Mr. Scott]

The closest analog is probably bucket sort, I would say.

rocketdodger, it was a question for Kleinman, doggone it!

Why the bucket sort?

Explain please. For example, if you have a colony of HIV and you apply three intiviral medications at once, where does the bucket sort enter into the picture?

[joobz]

Are you serious? I didn't realize he was that idiotic.

So if I port ev to my iphone and it runs slowly, does that mean evolution is profoundly slowed by the existence of iphones?
I've been down this road before with Kleinman back in April of last year.

I'm still waiting for a good reason why
model takes too long= evolution does not exist.

A MD simulation of 1 ml of water would take an extremely long time to acheive equilibrium (a thermodynamic equivilent to your perfect creature), does this mean that water doesn't exist?

I feel the universe arround us beginning to unravel.:rolleyes:

Doesn't matter. fact and truth doesn't matter to kleinman.

truly, I suggest just dropping him.

Sure he's said new stupid things.
like
17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?
but it's just not even interesting anymore.
I mean, when he claims that evolution doesn't prove evolution..... Do we really bother with him?

[badnewsBH]

rocketdodger, it was a question for Kleinman, doggone it!

Why the bucket sort?

Explain please. For example, if you have a colony of HIV and you apply three intiviral medications at once, where does the bucket sort enter into the picture?




In the bucket there's a blizzard that evolves buzzards with gizzards!



Sorry, it had to be done. :p

[coops]

hi Kleinman.

heres a good article for you to read and discuss.

http://sciencenow.sciencemag.org/cgi/content/full/2008/204/2 (if someone can fix the link for me that would be great)

it discusses a team of French and Spanish scientists discovery of humans accelerated evolutionary change due to "strong positive selection pressures".

they have identified specific genes with specific functions that have evolved differently in different populations over the last 60,000 years.

if you could give us your scientific rebuttal of this work without resorting to petty remarks, lame quips, or other dodges that would be super.

[Olowkow]

http://sciencenow.sciencemag.org/cgi/content/full/2008/204/2

Looks interesting, and welcome to the madness. :)

[rocketdodger]

rocketdodger, it was a question for Kleinman, doggone it!

Why the bucket sort?

Explain please. For example, if you have a colony of HIV and you apply three intiviral medications at once, where does the bucket sort enter into the picture?

Well when organisms reproduce, they don't all globally sort themselves and then choose the absolute highest fitness partner. They just look around in their local environment and choose the best option at the time. So the "buckets" in the sort would be the local environment of whichever organisms we are looking at.

Furthermore, they don't sort themselves fully before reproduction, they just kind of sort little by little as they reproduce. Again, buckets approximate this behavior better than the other sorting algorithms.

As to the three medications, well ... there is nothing about bucket sort that makes it more suited to sort on multiple conditions better than any other algorithm. If you want the best analog to the sorting going on in evolution under multiple pressures, that would be radix sort. In fact radix sort works by essentially breaking a larger condition down into multiple smaller ones, so it is naturally suited to that kind of task.

Keep in mind that the actual sorting going on in nature is very different than any of the algorithms humans use on computers, because in nature the sorting happens in parallel. If you want to think of it as a bucket sort, it would be a bucket sort where all the buckets are sorted at the same time as one another on each pass.

[Mr. Scott]

Keep in mind that the actual sorting going on in nature is very different than any of the algorithms humans use on computers, because in nature the sorting happens in parallel.

Yes, that's my point. Kleinman thinks that the time a Java program takes to do a sort on multiple conditions is somehow relevant to the time nature would have required to evolve higher life forms. That's essentially one leg of his argument. The other leg, relating to triple therapy we've also completely debunked. Kleinman is revealing profound ignorance of computer models. Odd, since IIRC he has claimed he taught computer modeling. Did he lie about his credentials?

Kleinman experiences some kind of amnesia after his 3-day doctor's weekend, and by Monday morning (sometimes Sunday night) he comes right back on the attack as if the previous 7000 posts and refutations never happened. Perhaps he's trying to make his mark before dimentia completely disables his faculties. (Hmmm...could that be why he didn't follow up on Powell's MRI?)

Creationists -- a bunch of pathetic whining losers.

[cyborg]

Kleinman is incapable of understanding this (among other things), and thats why he doesn't have a clue what he is talking about when it comes to either ev or his hundreds of empirical examples. If a computer takes more real time to sort, kleinman interprets this as "the sorting being confounded," which is of course utter nonsense.

Yeah, I think it was shown some 150 pages ago that kleinman didn't grasp the difference between the time taken to compute something and a model of time as in a computation.

I couldn't believe he could be that dumb - well, I sorta could since the whole "probabilities greater than 1," incident.

Well, that is what happens when your entire ability to argue a case is based on cutting & pasting the thoughts of others with no understanding of how to correctly interpret them.

So for all the newcomers to this thread remember: kleinman gets the basics wrong with regularity. Don't be surprised if he says something monumentally stupid with authority.

[rocketdodger]

To be fair, Kleinman is mainly concerned with the damping effect pressures have on each other under certain conditions. It does take more generations for genomic anomalies (by which I mean mutations, transpositions, insertions, deletions, fusions, whatever can happen to DNA on chromosomes) to fixate if many of them are active at the same time.

Intuitively, this makes sense. Say you have two anomalies, A and B, that confer the same relative fitness to their carriers. Normally, if only A or B was present, then carrying one or the other would make an organism more fit than its peers. With both active, the presence of one negates the lack of presence of the other, which makes fixation take more generations.

Of course, carriers of both, AB, are the most fit, and with just 2 anomalies having both would confer as much of an advantage over just A or B as A or B alone would over nothing. But suppose there were 3 anomalies, A, B, and C. Then you end up with AB, BC, and AC carriers -- they have 2/3 the fitness of ABC carriers. As you add anomalies, the fitness bonus for the top tier converges to equality, which means it would take a large number of generations indeed before all the anomalies are fixed.

As the computer simulations that Adequate and I wrote show, however, the time saved by sorting/optimizing another anomaly simultaneously, I.E. in parallel with all the others, outweighs the above described effect.

[cyborg]

As the computer simulations that Adequate and I wrote show, however, the time saved by sorting/optimizing another anomaly simultaneously, I.E. in parallel with all the others, outweighs the above described effect.

Exponents are bigger than polynomials in other words.

[kleinman]

Well, I think it is time to start making my closing arguments. (Now don’t get excited Delphi, that only means that I am half way through and there will be at least a couple hundred more pages to this thread.) Since we are only half way through this discussion, it is time for the evolutionist midterm report card. Here are your midterm results:

Irrational and Illogical Speculations: A+
Imaginative Interpretations of Fossil Rorschach Tests: C
Baseless Extrapolations of Microevolutionary Processes: A+
Mathematics of the Mutation and Selection Sorting/optimization Process: F-

Now there is hope that we can raise that last grade before your final report card. We finally have some evolutionists almost asking the correct question. We have an evolutionist asking which sorting algorithm nature is using to accomplish microevolutionary processes. Mutation and selection is not simply a sorting process, it is a sorting/optimization process. Each selection condition is also an optimization condition. Let’s go over the citation so kindly provided by the author of the concept that blizzards transform lizards into buzzards with gizzards.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes.

This example of the mutation and selection sorting/optimization process demonstrates very nicely how the mathematics works. Attaining two goals (optimums) simultaneously based on two different selection conditions would require the population to attain two different sets of mutations for each goal simultaneously. The simple case where each goal requires only a single mutation with each mutation having a probability of 10^-6 would give a probability of any descendent having both mutations simultaneously of 10^-12.

Now the authors of this article show that reducing the mutation and selection sorting/optimization process to the sequential application of single selection conditions does speed up the evolutionary process and there are real examples of this mathematical phenomenon. Some of these real examples include MRSA, multi-drug resistant Gonorrhea, and so on. The sequential use of drugs on microbes such as S. Aureus, starting with Penicillin, then switching to a different monotherapy when the this bacteria evolved resistance to Penicillin is the optimal way to apply selection pressures to a population in order to achieve multi-drug resistant microbes.

Mutation and selection is not simply a sorting process, it is an optimization process where the optima are defined by the selection conditions. Now, how would you evolutionists describe the sorting process used in nature to achieve these optima?

[Shalamar]

Do you have any of the math to actually show us?

Then again, Its nothing like a good start to the week when an annoying creationist with no understanding of science or math, tells the entire scientific community that they're wrong.

[rocketdodger]

The bottom image shows the trajectory the population takes to achieve both goals sequentially .

Wrong. The bottom image is the "effective" trajectory taken when they apply the pressures singly back and forth in an alternating fashion. Kind of like it says in the caption...


This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes.

Wrong. As I explained in my last post, and as I have been explaining for six months, the slowdown caused by pressures interfering with each other is more than made up for by the solutions to the pressures being found in parallel.


This example of the mutation and selection sorting/optimization process demonstrates very nicely how the mathematics works. Attaining two goals (optimums) simultaneously based on two different selection conditions would require the population to attain two different sets of mutations for each goal simultaneously. The simple case where each goal requires only a single mutation with each mutation having a probability of 10^-6 would give a probability of any descendent having both mutations simultaneously of 10^-12.

So what? Why does the population need to attain both goals simultaneously? Why do any descendents need to have both mutations simultaneously? If you think they need to, then you really have a serious misunderstanding of the mechanisms of evolution and it is no wonder you come up with these crazy theories.

Now the authors of this article show that reducing the mutation and selection sorting/optimization process to the sequential application of single selection conditions does speed up the evolutionary process and there are real examples of this mathematical phenomenon.

Wrong, you liar. They show that applying single pressures in an alternating fashion can speed up the process compared to single pressures being applied sequentially. So if anything you have it totally backwards.

Furthermore, the reason this happens has nothing to do with multiple pressures confounding each other -- it has to do with alternating pressures drawing the population out of local maxima that they would otherwise get stuck in for long periods of time.

We have been over all of this before. Have you forgotten so soon? Do you think we have forgotten so soon?

When will you stop lying and present an argument that doesn't fall apart immediately?

[Belz...]

Is that chatbot still functioning ?

[m_huber]

Is this what Creation Science classes would be like?

[Cardelitre]

Do you have any of the math to actually show us?
Wow. Last time I checked this maddening thread some 50 pages ago, this question was already obstinately ignored by the bot. That's almost frightening to see a "discussion" so stuck.

[kleinman]

Evolutionists have a hard time understanding that achieving both goals sequentially is the same as applying selection pressures singly back and forth in an alternating fashion. However, evolutionists continually claim that selection pressures are evolved in some type of parallel fashion. I guess that means while blizzards evolve lizards into buzzards with gizzards in location, hail turns snails into whales with tails. It’s amazing what that parallel processing will do. I can’t wait to see what fog will make dogs into and what kind of weather will turn bats into cats? You’d better keep that one under your hat!
http://forums.randi.org/images/smilies/doglaugh.gif
So are you evolutionists abandoning your n+1 selection pressures evolving faster than n selection pressure nonsense and now going to assert that evolution occurs with parallel processing nonsense? The weather sure does wonders for evolution.
So back to real measurable examples of the mutation and selection sorting/optimization process, examples which demonstrate what Dr Schneider’s model shows, that is simultaneous selection pressures profoundly slow evolution by mutation and selection.
http://www.mdlinx.com/IDLinx/news.cfm?subspec_id=125 (http://www.mdlinx.com/IDLinx/news.cfm?subspec_id=125)
Conclusions: Resistant HCV isolates are selected rapidly during therapy with the highly active protease inhibitor telaprevir. Combination therapy with pegylated interferon-alfa or other direct antiviral drugs seem mandatory to avoid developing resistance.
http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html)
Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens 1, 2, 3. On a broader scale, such combinations are also important in understanding microbial ecology and evolution 4, 5. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations 1, 6, 7. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population1. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.
http://www.natap.org/2006/AASLD/AASLD_17.htm (http://www.natap.org/2006/AASLD/AASLD_17.htm)
Brief Summary: Tara Keiffer from Vertex presented an oral talk at AASLD on VX-950 drug resistance and how to prevent resistance. She presented an analysis of patients who received VX950 in a 14-day study. The goal of this sub-study analysis was to identify VX950 resistant variants (mutations) and the kinetics of their emergence (selection) in patients dosed with VX950 or VX950+Pegasys. They used a highly sensitive clonal method to characterize the mutations (viral variants), and they also did a phenotypic analysis. VX-950 has demonstrated a rapid & profound viral load reduction; drug resistance mutations can emerge when VX950 is given alone (as monotherapy), as sequence changes (mutations) in the HCV genome occur spontaneously & frequently as a natural result of the high levels of replication of the HCV virus-pre-existing mutations are likely present at a low level prior to drug treatment; but, resistant HIV and wild-type HCV (non-resistant virus) were suppressed & became undetectable with Pegasys added in combination therapy. With continued use of Pegasys+Ribavirin, after VX950 was stopped in the short-term study of VX950, wild-type & resistant HCV were suppressed & became or remained undetectable.

Telaprevir, also known as VX-950, is an oral HCV protease inhibitor, which has been previously shown in study to reduce HCV RNA by 4.4 logs as monotherapy and by 5.5 logs in combination with peginterferon in patients with HCV genotype 1.

In early studies there has been some patients whose viral load rebounded on VX950 monotherapy. I have reported from EASL in the Spring 2006 where Vertex reported this information on the development of resistance mutations: low-level resistance (< 25-fold increase in 50% inhibitory concentration): V36M/A, T54A, R155K/T, A156S; high-level resistance (> 50-fold increase in 50% inhibitory concentration): A156V/T, V36M/A + R155K/T, V36M/A + A156V/T

Tara Keiffer from Vertex, reported on a sub-study at AASLD an analysis to display the emergence & kinetics of VX950 HCV protease mutations when dosed with VX950 alone or in combination with Pegasys. Using sensitive methods to identify & characterize resistant variants she showed that although VX-950 produces dramatic HCV RNA suppression over 14-day course of treatment either alone or in combination with peginterferon alfa-2a, viruses with VX950 resistance mutations emerged as wild-type virus was cleared. Keiffer, however, reported that subsequent peginterferon alfa-2a/ribavirin therapy suppressed VX950 resistant virus to undetectable levels.
http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)
We suggest that the risk of emergence of nucleoside-analogue resistance will be reduced by initial use of potent drug combinations, rather than sequential therapy, as has been illustrated for human immunodeficiency virus–infected patients. [15]
You evolutionists seem to be missing citations which show that evolution is occurring in parallel. Maybe it is happening in one of those 10^500 alternative “parallel” universes?
http://forums.randi.org/images/smilies/doglaugh.gif

[cyborg]

You evolutionists seem to be missing citations which show that evolution is occurring in parallel.

He's right of course - the bacteria in my gut absolutely don't get a chance to be selected until they can join the bacteria in his gut, get arranged in a big line and ordered from "least fit" to "most fit" at which point the former half is eliminated.

This is how ev works.

[kleinman]

Ok, now we have the author of the cruft theory of evolution who makes a valid point. One population is subjected to a single selection pressure and a second population is subjected to a different single selection pressure and then these populations are mixed. Why isn’t that the very reason that HIV is so difficult to treat today? The use of monotherapy for years has created many strains of HIV that are resistant to one or more drugs and these strains are in the gene pool. So how does this example of parallel evolution explain the evolution of birds into lizards? What are your individual single selection pressures and what are your target genes? There is no selection pressures that target hundreds, perhaps thousands of genes needed to be transformed to accomplish the transformation of lizards into birds. It is a mathematical impossibility, the mutation and selection sorting/optimization process simply does not work that way. However, you can parallel process the mutation and selection sorting/optimization process by imposing single targeted selection pressures on multiple different populations simultaneously and contribute to the premature death of millions of people suffering from diseases subject to the mutation and selection phenomenon.

[coops]

hi Kleinman.

heres a good article for you to read and discuss.

sciencenow (dot) sciencemag (dot) org/cgi/content/full/2008/204/2 (if someone can fix the link for me that would be great)

it discusses a team of French and Spanish scientists discovery of humans accelerated evolutionary change due to "strong positive selection pressures".

they have identified specific genes with specific functions that have evolved differently in different populations over the last 60,000 years.

if you could give us your scientific rebuttal of this work without resorting to petty remarks, lame quips, or other dodges that would be super.


bumped for Kleinman.

you keep asking for documentation of specific genes evolving, well here is an example for you.

[kleinman]

Once again evolutionists assume that I don’t believe that evolution occurs. Once again I state that microevolution occurs but there is no mechanism that takes these microevolutionary processes and combines them to achieve macroevolutionary changes. If you want an example of what a macroevolutionary change, it would be a blizzard transforming lizards into buzzards with gizzards. Certainly genes evolve but it is an irrational and illogical extrapolation to say that lizards can be transformed into buzzards by the mutation and selection sorting/optimization process. Mutation and selection does not work that way. It is a mathematical and empirical impossibility.

It has been a while since I asked you evolutionists this question and so far none have answered it. Tell us what the selection pressure is that would evolve a gene de novo and describe the process to us.

[cyborg]

Tell us what the selection pressure is that would evolve a gene de novo and describe the process to us.

Any.

Evolution.

[coops]

[SIZE=3]Once again evolutionists assume that I don’t believe that evolution occurs. Once again I state that microevolution occurs but there is no mechanism that takes these microevolutionary processes and combines them to achieve macroevolutionary changes. SIZE]

So Kleinman, can you please explain at what SPECIFIC point micro evolution turns into macro evolution and hence becomes impossible.

If you could give a scientific definition that we could test that would be super.

Just a hint, 'lizards into buzzards with gizzards' is not generally considered a scientific definition.

[kleinman]

I guess we have another evolutionist who is not going to tell us how a gene evolves de novo. You can’t explain how genes initially appear, you can’t explain how life arose from inorganic molecules and you don’t understand how the mutation and selection sorting/optimization process actually works, yet you claim your irrational and illogical theory of evolution is true. Why don’t you post some more of your fossil Rorschach tests?

Evolutionists take the mutation and selection sorting/optimization process and claim that all life evolved by this mechanism. I have and will continue to show both mathematically and empirically that the mutation and selection sorting/optimization process can only evolve a tiny number of selection conditions targeting only a tiny number of genes simultaneously. Once you have more than two or three genes evolving simultaneously, the trajectory on the fitness landscape becomes extremely difficult for any population to traverse to the multiple local optima simultaneously. Combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. The concept that thousands of genes can evolve simultaneously by this process is mathematically and empirically impossible. This is shown mathematically with Dr Schneider’s ev computer model and here are more citations which show this empirically.
http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml (http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml)
Combining two different antibiotics has long been used as a way to prevent resistance.
http://www.genetics.org/cgi/reprint/163/4/1237.pdf (http://www.genetics.org/cgi/reprint/163/4/1237.pdf)
In addition to predicting the ways in which specific enzymes can evolve the ability to confer resistance to different antibiotics, pharmaceutical companies could also use this method to test the effectiveness of using different antibiotic combinations to inhibit the evolution of resistance. For example, while it is clear that selection for resistance to cefepime indirectly selects TEM alleles that confer high levels of resistance to aztreonam and ceftazadime, it is possible that the TEM enzymes are not capable of conferring high levels of resistance to cefepime and cefotaxime at the same time. Combination of those two antibiotics may increase the time required for resistance to those antibiotics to evolve.
The failure of evolutionists to comprehend and properly teach the basic science and mathematics of the mutation and selection sorting/optimization process actually works contributes to the premature death of millions of people suffering from diseases subject to mutation and selection.

[coops]

So Kleinman, can you please explain at what SPECIFIC point micro evolution turns into macro evolution and hence becomes impossible.

If you could give a scientific definition that we could test that would be super.

Just a hint, 'lizards into buzzards with gizzards' is not generally considered a scientific definition.

Bump for Kleinman, i think you must have forgotten to answer my simple question in your last post.

[Paul C. Anagnostopoulos]

Once you have more than two or three genes evolving simultaneously, the trajectory on the fitness landscape becomes extremely difficult for any population to traverse to the multiple local optima simultaneously.
Then that would pretty much do it for microevolution, too. So you don't actually believe in any kind of evolution. Unless perhaps you believe in the microevolution of nongenes.

~~ Paul

[kleinman]

I’m not sure if you evolutionists are unable to comprehend this because of your biases or you simply don’t pay attention. Microevolutionary processes do occur. The mutation and selection sorting/optimization process can transform a single gene fairly easily when a population is subjected to a single targeted selection pressure. Once you add additional simultaneous selection pressures, the sorting/optimization process is profoundly slowed. This is why combination therapy is effective for HIV, TB, HBV, HCV, cancer, weeds… So the mutation and selection sorting/optimization process otherwise is an extremely slow process for doing any kind of genetic transformation, far too slow to make common descent a mathematical possibility (in addition, you don’t have the selection conditions which would explain common descent). On the other hand, the recombination and selection microevolutionary process is a very rapid mechanism for transformation of a population. We see this in the large number of breeds of dogs, cats, cattle, horses,… You can obtain striking differences in the morphology of members of a population but genetically, dogs remain dogs, cats remain cats,…

The mutation and selection sorting/optimization process is a very limited process. This is demonstrated by Dr Schneider’s peer reviewed and published ev model which show the combination selection pressures profoundly slow the sorting/optimization process and real measurable and repeatable examples of mutation and selection show the same thing. Here are more empirical examples which demonstrate how the mutation and selection sorting/optimization process actually works.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=95155&ProduktNr=224031 (http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=95155&ProduktNr=224031)
Objective: Ribavirin and interferon combination therapy is more effective than interferon monotherapy in patients with chronic hepatitis C virus (HCV) infection. To test the hypothesis that ribavirin induces nucleotide substitutions in the viral genome and reduces viral load by forcing it into error catastrophe in the combination therapy, we investigated the molecular evolution of HCV quasispecies in 3 patients who received combination therapy and 2 patients who received interferon monotherapy. Methods: The quasispecies were analyzed before and after therapy by sequencing at least 8 clones in five regions of the HCV genome; 5' untranslated region, EI, E2, NS5A and NS5B. Results: Marked genetic drift was observed in the NS5A and NS5B regions in patients treated with combination therapy. However, genetic distances between clones obtained after therapy were closer than those obtained before therapy. Conclusion: Our results suggest that the combination therapy modified HCV quasispecies, but that this did not reflect the induction of error catastrophe by ribavirin. Modification of quasispecies by this therapy requires further investigation in a larger number of patients to elucidate the possible mechanism of viral resistance against the combination therapy.
http://jcm.asm.org/cgi/reprint/43/1/208.pdf (http://jcm.asm.org/cgi/reprint/43/1/208.pdf)
The clinical settings in which combination anti-CMV therapy should be used remain to be established. The observation of attenuated growth in viruses with resistant genotypes (such as the T838A and D588N pol mutations seen here) may help to explain the reported superior clinical efficacy of combination therapy compared with single-agent anti-CMV therapy (21), even when one of the agents appears to have lost its activity against CMV (29). Maintaining therapy with the drug to which resistance has developed could be beneficial if the drug selects for growth-impaired genotypes.
Perhaps in the evolutionist fantasy world, combination selection pressures evolve thousands of genes simultaneously but in Dr Schneider’s mathematical model it doesn’t work that way and in the measurable real world, it doesn’t work that way. The theory of evolution is mathematically and empirically impossible and the failure of evolutionists to properly describe and teach how the mutation and selection sorting/optimization process actually works contributes to the premature death of millions of people suffering from diseases subject to the mutation and selection process.

[coops]

So Kleinman, can you please explain at what SPECIFIC point micro evolution turns into macro evolution and hence becomes impossible.

If you could give a scientific definition that we could test that would be super.

Just a hint, 'lizards into buzzards with gizzards' is not generally considered a scientific definition.

Bumped again for Kleinman.

You should probably be able to answer this question within 2 sentences max i would imagine.

It should be a lot faster for you to answer this simple question than your continued evasion of it.

[Shalamar]

I’m not sure if you creationists are unable to comprehend this because of your biases or you simply don’t pay attention.

Looks like both for Creationists. Remember the mantra for creationism: State that Evolution is false. THEN try to find any straw men you can grasp to that you can lie about evolution being false.

Remember folks, Mr. Klienman says that biology, geology, and astronomy are false!

[articulett]

I’m not sure if you creationists are unable to comprehend this because of your biases or you simply don’t pay attention.

Looks like both for Creationists. Remember the mantra for creationism: State that Evolution is false. THEN try to find any straw men you can grasp to that you can lie about evolution being false.

Remember folks, Mr. Klienman says that biology, geology, and astronomy are false!

And he believes he has the equation that proves it.


Jesus, however is true. No math needed per Kleinman.

[kleinman]

If you evolutionists didn’t have so much difficulty with the mathematics of the mutation and selection sorting/optimization process, you would realize that microevolution never becomes macroevolution. You don’t have the selection conditions that would transform lizards into birds and if you did, the mutation and selection sorting/optimization process is far too slow. The reason why the mutation and selection sorting/optimization process is so slow is that combination selection pressures interfere with each other as the population tries to find a trajectory on the fitness landscape to these multiple optima. Now if you evolutionists think that multiple selection conditions evolve more quickly than single selection conditions, present the mathematics and empirical examples to prove it. On the other hand, I have and will continue to present hundreds of citations which show that multiple selection pressures profoundly slow evolution by mutation and selection. Here are a few more examples.
http://www.medscape.com/viewarticle/424503_6 (http://www.medscape.com/viewarticle/424503_6)
While we await the results of studies that will help define the best time to alter therapy, the guiding principle for selecting a new combination remains to switch as many drugs as possible, preferably including new drugs from two or more different classes of agents. Dr. Lawrence illustrated this point by discussing ACTG 364, a rollover study for patients who participated in ACTG 175 (the study that compared zidovudine monotherapy versus ddI monotherapy and ZDV + ddI and ZDV + ddC) then received a second nucleoside RTI regimen in ACTG 302/303 (a rollover study of ACTG 175)[12]. Thus, patients in ACTG 364 had experience with at least two nucleoside reverse transcriptase inhibitors, but were NNRTI and PI naive. Patients were assigned to efavirenz (600 mg qd), nelfinavir (750 mg q8h), or a combination of the two drugs, in combination with two nucleoside RTIs (ideally those ones that the patient had not experienced). After 24 weeks of study, a greater proportion of patients on the four drug combination had viral loads less than 500 copies/mL than patients receiving triple therapy with either efavirenz or nelfinavir.
https://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html (https://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html)
Despite the emergence of multidrug-resistant strains of hepatitis B virus (HBV) and previous success with combination therapy for other chronic viral infections, we are still using sequential monotherapy for chronic HBV infection.
and
Studies of combination therapy to date have used traditional endpoints — short-term reduction of HBV DNA levels and HBeAg seroconversion — rather than evolution of resistance.
and
There is now an emerging body of data suggesting that combination therapy can decrease antiviral resistance in HBV infection, the endpoint likely to be of greatest long-term importance, and, rather than adding or replacing an antiviral agent after resistance develops, it is likely to be more effective in treatment-naïve patients.
You evolutionists have plenty of irrational and illogical speculations and extrapolations to support you nonsensical theory, now where are your empirical examples? You evolutionists continue to teach your irrational nonsense of how the mutation and selection sorting/optimization process works and this contributes to the premature death of millions of people suffering from diseases subject to the mutation and selection process.

[Shalamar]

Have any evidence for your claims, Mr. Kleinman?

Too bad your citations all show strong evidence in favor of evolution.

So sorry. you fail. Go back and take remedial biology, m'kay?

[coops]

Kleinman,
I hate to keep repeating myself, perhaps you have me on ignore and can't see my posts, but you STILL haven't answered my simple question.

You stated before that micro-evolution is possible but macro-evolution isn't.

Could you please give a clear, concise definition of each term and explain the specific point at which micro-evolution becomes marco-evolution and hence is no longer possible.

[kleinman]

Perhaps you evolutionists don’t get it, the mutation and selection sorting/optimization process is profoundly slowed when you have combination selection pressures. This is what Dr Schneider’s computer simulation of random point mutations and natural selection shows and this is what real examples of mutation and selection shows. Let’s see if I have more empirical examples of this mathematical fact of life? Why yes I do and here they are.
http://www.malariajournal.com/content/5/1/48 (http://www.malariajournal.com/content/5/1/48)
Whenever drug treatment is required to control a pathogen, selection of drug resistance is inevitable [1]. The huge size of pathogen populations and their short generation times guarantee the outcome. Plasmodium falciparum is a prime example. In humans, an acute infection can produce a population as high as 10^11 haploid parasites, so that mutations have ample scope to occur [2]. In the obligate sexual cycle, reassortment and recombination can "reshuffle the deck" for rapid evolution of new resistant genotypes in each generation. Thus, favoured combinations of genes can arise fairly quickly, even if more than one mutant gene is required for resistance. These sets of genes can, of course, also be separated during the sexual cycle but under the strong selection that drugs can exert, even a multigenic, resistant genotype may become fixed in a population.

The impact of this strong selection has been revealed at many different levels. Most important, as the use of chloroquine increased, drug resistance evolved in parasite populations and childhood mortality from malaria increased, even as all-cause mortality in children decreased [3-5]. The sequence of the P. falciparum genome has recently been published [6] and this has made it possible to trace the ancestry of highly drug-resistant parasites. These studies show that parasites resistant to chloroquine and sulfadoxine-pyrimethamine have arisen relatively rarely, but they have spread widely from a few initial foci in "selective sweeps" of the parasite population [7-11]. This new view affects many of the assumptions that underlie models of the speed at which resistance evolves [12] and inform practical decisions about changes in drug policy. Parasites without borders make it absolutely essential that the emergence of drug resistant populations be "tracked" worldwide; a resistant parasite that arises in Southeast Asia may travel rapidly to East Africa.

This improved understanding of the evolution of drug resistance has come from a relatively simple situation. Until recently, the number of antimalaria drugs in common use was small: chloroquine and sulfadoxine-pyrimethamine in Africa and the Americas, with mefloquine and more recently, mefloquine-artesunate in Southeast Asia[13]. As chloroquine and sulfadoxine-pyrimethamine have lost their efficacy, combination drugs have been strongly endorsed as the most effective next step [14]. In response to this emphasis, many different combination drugs, most containing an artemisinin derivative are being used in various countries, especially in East Africa (Figure 1. Many of these combinations have shown excellent initial efficacy in drug trials [13], but only mefloquine/artesunate has a long enough history to allow a strong prediction of the useful therapeutic life of these combinations [15]. It is particularly important to establish a baseline for effectiveness of new drugs and combinations so that any subsequent changes can be seen. This complex situation underlines the importance of regional surveillance of drug use, efficacy and effectiveness as these new combinations are tried in a variety of demographic and ecological settings. What has worked well for a long time in Thailand may not be so long lived in Tanzania [16]!

Appropriately, the gold standard for drug efficacy has been the outcome of clinical treatment. When patients are treated with the drug, do they recover? The substantial expense and logistical difficulty to change the recommended drug treatment have led most countries to rely on a large increase in clinical treatment failure before initiating a change [17]. Systematic studies have shown repeatedly that assessment in vitro of drug efficacy in local parasite isolates can give an early warning of rising drug resistance in vivo [18-20]. In addition, when molecular correlates of drug resistance are known, the prevalence of resistant alleles can also give early warning of evolving resistance in the parasite population [21-23]. In all three approaches, the temporal and geographic patterns of resistance are most informative. When the in vitro tolerance of parasites to a drug is rising or when the prevalence or the geographic range of resistant alleles is increasing, clinical drug failure is likely to increase as well. Figure 2 shows a small example of the linkage among the three parameters. In this data set, the increase in the in vitro IC50 values and the increased prevalence of the triple mutant allele of P. falciparum dhfr preceded by several years the increase in sulfadoxine-pyrimethamine treatment failure among young children in Coastal Kenya. Similar studies will be needed to determine whether the lags between these parameters observed in Kilifi will be similar in other sites or for other drugs, but it is clear that the in vitro increase in IC50 values and the increase in the molecular marker can provide an early warning of the onset of clinical treatment failure. The community will need similar data sets in many different settings for all of the drugs in use to manage effectively the current drugs and any novel drugs that are introduced in the future.
http://www.retroconference.org/2007/Abstracts/30238.htm (http://www.retroconference.org/2007/Abstracts/30238.htm)
Background: HIV drug resistance is thought to have at least 2 origins: pre-existing resistant mutants at a low frequency that are selected by therapy; and suboptimal therapy that permits replication, evolution, and selection of resistant mutants. Studying the mechanisms and anatomic origins of HIV drug resistance in humans is constrained by limited blood or tissue sampling and ethical restrictions on therapy. Here we examined the impact of short-course efavirenz (EFV) monotherapy on the evolution of drug resistance in a macaque model of ART.
and
Conclusions: Combination therapy with TDF+FTC+EFV was effective in suppressing RT-SHIV replication in macaques. Brief exposure to EFV monotherapy resulted in selection of NNRTI-resistant variants in 2 of 3 animals and early failure of triple drug therapy in 1 of 3 animals. The effect of interruption and re-initiation of therapy on the selection of resistance is being determined. This new animal model of ART has the flexibility to address many key questions about the selection, tissue origins and persistence of drug resistance that cannot be answered in human studies.
Only in your evolutionist dreams do multiple selection pressures evolve more quickly than single selection pressures. The mathematical and empirical fact of life is that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. And the failure of you evolutionists to comprehend the basic science and mathematics of the mutation and selection sorting/optimization process contributes to the premature death of millions of people suffering from diseases subject to the mutation and selection sorting/optimization process.

[coops]

Is there a specific reason why your refusing to answer my question Kleinman?

If there is i'd love to know it.

[Shalamar]

The mathematical and empirical fact of life is that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.


Have any evidence or math to back up your claim, Mr. Kleinman?

No?

[kleinman]

You evolutionist really don’t get it. You have been programmed for so long with evolutionist dogma that when you are presented with the mathematical and empirical evidence which shows that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process and that when you have more than a single selection pressure targeting a single gene, it profoundly slows the ability of the population to evolve against these multiple selection pressures. It is not when hundreds of genes are targeted by selection conditions or even dozens of genes targeted by selection pressures; it is when more than a single gene is targeted by selection pressures that the sorting/optimization process is profoundly slowed.

Perhaps if we looked at it from the other perspective, what are the selection conditions required and the genes targeted that would transform a lizard population into a bird population? How do you take a sorting/optimization process which can transform only at most only a two or three genes at a time and get a sequence of microevolutionary processes that would turn a lizard population into a bird population. There is no answer to this because there are no sequence of selection pressures that would transform a lizard population into a bird population by the mutation and selection sorting/optimization process. Even if you could envision a real sequence of selection conditions (and you can’t) that would cause such a transformation, it would be so profoundly slow that you simply do not have sufficient generations to carry out such a transformation. The concept of common descent is mathematically and empirically irrational. You do not have the selection conditions and you do not have sufficient number of generations to carry out these massive transformations required to transform a lizard population into a bird population.

I encourage you to study Dr Schneider’s ev computer model of random point mutations and natural selection so that you would get some understanding how the mutation and selection sorting/optimization process actually works. Then you would realize how nonsensical and irrational the evolutionist speculations are. These irrational speculations contribute to the premature death of millions of people suffering from diseases subject to mutation and selection.

[coops]

[SIZE=3]when you have more than a single selection pressure targeting a single gene, it profoundly slows the ability of the population to evolve against these multiple selection pressures. SIZE]

So is this your definition of micro-evolution Kleinman?

Do you state that micro-evolution is when a single gene evolves in response to a single selection pressure?

Are you also then stating that anything other than this is macro-evolution and hence impossible?

Would you agree with the following statement ' 'it is impossible for more than a single gene to simultaneously evolve in any organism as this would constitute macro-evolution.'

[Shalamar]

And its been shown that the ev model doesn't actually show what Mr. Kleinman thinks it does.

And the chatbot can't answer questions to which it knows would prove its premises false.

Evolution is strong verifiable, and falsifiable science. But fundies like Mr. Kleinman can only accept what they are told by their religious leaders.

[tsig]

You evolutionist really don’t get it. You have been programmed for so long with evolutionist dogma that when you are presented with the mathematical and empirical evidence which shows that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process and that when you have more than a single selection pressure targeting a single gene, it profoundly slows the ability of the population to evolve against these multiple selection pressures. It is not when hundreds of genes are targeted by selection conditions or even dozens of genes targeted by selection pressures; it is when more than a single gene is targeted by selection pressures that the sorting/optimization process is profoundly slowed.

Perhaps if we looked at it from the other perspective, what are the selection conditions required and the genes targeted that would transform a lizard population into a bird population? How do you take a sorting/optimization process which can transform only at most only a two or three genes at a time and get a sequence of microevolutionary processes that would turn a lizard population into a bird population. There is no answer to this because there are no sequence of selection pressures that would transform a lizard population into a bird population by the mutation and selection sorting/optimization process. Even if you could envision a real sequence of selection conditions (and you can’t) that would cause such a transformation, it would be so profoundly slow that you simply do not have sufficient generations to carry out such a transformation. The concept of common descent is mathematically and empirically irrational. You do not have the selection conditions and you do not have sufficient number of generations to carry out these massive transformations required to transform a lizard population into a bird population.

I encourage you to study Dr Schneider’s ev computer model of random point mutations and natural selection so that you would get some understanding how the mutation and selection sorting/optimization process actually works. Then you would realize how nonsensical and irrational the evolutionist speculations are. These irrational speculations contribute to the premature death of millions of people suffering from diseases subject to mutation and selection.

We fully intended this to happen. How else can our evil experiment work?

Oh Kleinman don't take in any stray cats.

[kleinman]

Perhaps if I post this reference so kindly given by Delphi then you might understand why mutation and selection can not do what you assert.
http://en.wikipedia.org/wiki/Fitness_landscape (http://en.wikipedia.org/wiki/Fitness_landscape)
Apart from the field of evolutionary biology, the concept of a fitness landscape has also gained importance in evolutionary optimization methods such as genetic algorithms or evolutionary strategies. In evolutionary optimization, one tries to solve real-world problems (e.g., engineering or logistics problems) by imitating the dynamics of biological evolution. For example, a delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time. In order to use evolutionary optimization, one has to define for every possible solution s to the problem of interest (i.e., every possible route in the case of the delivery truck) how 'good' it is. This is done by introducing a scalar-valued function f(s) (scalar valued means that f(s) is a simple number, such as 0.3, while s can be a more complicated object, for example a list of destination addresses in the case of the delivery truck), which is called the fitness function or fitness landscape. A high f(s) implies that s is a good solution. In the case of the delivery truck, f(s) could be the number of deliveries per hour on route s. The best, or at least a very good, solution is then found in the following way. Initially, a population of random solutions is created. Then, the solutions are mutated and selected for those with higher fitness, until a satisfying solution has been found.

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).

The concept of a scalar valued fitness function f(s) also corresponds to the concept of a potential or energy function in physics. The two concepts only differ in that physicists traditionally think in terms of minimizing the potential function, while biologists prefer the notion that fitness is being maximized. Therefore, multiplying a potential function by -1 turns it into a fitness function, and vice versa.
You are trying to assert that hundreds, perhaps thousands of genes can be transformed in order to evolve a lizard population into a bird population. There is no mathematical or empirical basis for this type of speculation. Mutation and selection can only transform a tiny number of genes subject to selection conditions. This is why three drug therapy combination works for the treatment of HIV despite the fact that HIV is a very rapidly reproducing virus with huge populations and high mutation rates. Despite this, effective three drug combination therapy profoundly slow the ability of this virus to find a trajectory on the fitness landscape to optimize fitness against three selection conditions. If you were to use the same three drugs sequentially, the population could easily evolve to these selection conditions in weeks.

When you try to extrapolate this mathematical behavior to a slowly reproducing lizard population with much small population size than HIV and much smaller mutation rates, you can not transform these huge lizard genomes into bird genomes. It is mathematically impossible. The mutation and selection sorting/optimization process simply does not work this way. The concept of common descent is mathematically and empirically irrational and the persistent evolutionist assertion that mutation and selection does to this contributes to the premature death of millions of people with diseases subject to mutation and selection. Here is another example of how the mutation and selection sorting/optimization process actually works. http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15766932 (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15766932)
The 2362 strain of Bacillus sphaericus (Bs) Neide is a highly mosquitocidal bacterium used in commercial bacterial larvicides primarily to control mosquitoes of the genus Culex. Unfortunately, Bs is at high risk for selecting resistance in mosquito populations, because its binary toxin apparently only binds to a single receptor type on midgut microvilli. A potential key strategy for delaying resistance to insecticidal proteins is to use mixtures of toxins that act at different targets within the insect, especially mixtures that interact synergistically. We tested this hypothesis for delaying the phenotypic expression of resistance by exposing Culex quinquefasciatus Say larvae to Bs alone or in combination with Cyt1A from Bacillus thuringiensis subsp. israelensis. Two laboratory lines of Cx. quinquefasciatus, one sensitive to Bs and the other containing Bs resistance alleles, were subjected to intensive selection pressure for 20 generations with either Bs 2362 or a 3:1 mixture of Bs 2362+Cyt1A. At the end of the study, the sensitive line had evolved >1000-fold resistance when selected with Bs alone, whereas the parallel line selected with Bs+Cyt1A exhibited only low resistance toward this mixture (RR95, 1.4). Similar results were observed in the lines containing Bs resistance alleles. Both lines selected with Bs+Cyt1A exhibited substantial resistance to Bs in the absence of Cyt1A. Although selection with Bs+Cyt1A did not prevent the underlying evolution of resistance to Bs, these results suggest that a mixture of Bs with other endotoxins, particularly one like Bs+Cyt1A in which the components interact synergistically, will provide longer lasting and more effective mosquito control than Bs alone.
Examples like this demonstrate empirically what Dr Schneider’s model shows mathematically and what the Wikipedia reference to fitness landscape are describing with single versus multiple conditions and the ability of a population to find a trajectory on the fitness landscape and to find an optima. It is the number of selection conditions and the number of genes targeted which dominates the mathematical and empirical behavior of the mutation and selection sorting/optimization process.

[X]

Forgive me if I haven't read every post, but it seems to me that Klienman keeps repeating nonsense about how his math is superior to ours, coupled with random quotes from various sources (several of which seem to support evilution) instead of actuall responding to questions.

Come to think of it, does he even have an argument besides "You evolutionists just don't get it."?

[Shalamar]

;3425572']Forgive me if I haven't read every post, but it seems to me that Klienman keeps repeating nonsense about how his math is superior to ours, coupled with random quotes from various sources (several of which seem to support evilution) instead of actuall responding to questions.

Come to think of it, does he even have an argument besides "You evolutionists just don't get it."?

Nope. He doesn't get it. At least he's stopped calling people names because they trust in science. Mr. Kleinman doesn't like science. Makes people think!

[coops]

So is this your definition of micro-evolution Kleinman?

Do you state that micro-evolution is when a single gene evolves in response to a single selection pressure?

Are you also then stating that anything other than this is macro-evolution and hence impossible?

Would you agree with the following statement ' 'it is impossible for more than a single gene to simultaneously evolve in any organism as this would constitute macro-evolution.'

Yet another bump for Kleinman.

Kleinman, if you have no intention of ever answering my questions please just let me know. Just a simple 'Coops, i have no interest in discussing specifics with you.' and i'll stop bugging you to explain yourself.

Or better yet, you could answer my question.

Up to you really.


PS - perhaps someone could re-post my message. maybe Kleinman has put me on ignore by accident and can't see my question. Thats the only logical reason that i can think of for his continued refusal to answer.

Thanks

[coops]

double post

[kleinman]

I don’t have anyone on ignore and it is not my mathematical model. It is Dr Schneider (head of computational molecular biology at the National Cancer Institute) peer reviewed and published mathematical model of random point mutations and natural selection. The online version of the model was written by Paul C. Anagnostopoulos, a moderator on this forum. What Dr Schneider’s mathematical model demonstrates is the fundamental behavior of the mutation and selection sorting/optimization process. What Dr Schneider’s model shows is that the number of selection conditions dominates the rate at which selection conditions can be satisfied. Dr Schneider’s model which has three selection conditions is profoundly slow at evolving all three conditions on all but the tiniest genomes. On the other hand, setting any two of the three selection conditions in Dr Schneider’s model to zero, the remaining selection condition evolves in a trivially small number of generations. This mathematical behavior is reflected in the real behavior of mutation and selection as demonstrated by the hundreds of real examples I have posted and will continue to post. The mutation and selection sorting/optimization process can only rapidly evolve a tiny number of selection conditions simultaneously. This is the mathematical and empirical fact of life you evolutionists just can not fathom. This is why the theory of evolution is mathematically impossible. Because you evolutionists dominate the field of biology with your mathematically irrational and illogical concept of the mutation and selection sorting/optimization process; you mislead virtually everyone who must deal with real problems of mutation and selection. It is this obfuscation of the mutation and selection sorting/optimization process that contributes to the death of millions of people suffering from disease subject to mutation and selection. Rather than properly teaching the basic science and mathematics of the mutation and selection sorting/optimization process, you mislead naïve school children and virtually everyone else with your irrational and illogical speculations and assertions. The mutation and selection sorting/optimization process does not work the way you assert. It is mathematically and empirically impossible.

[coops]

I don’t have anyone on ignore ....

If you don't have me on ignore could you please answer my question Kleinman?

I've already posted it enough times today I don't think it necessary to add it to the post as well.

If you can't or won't answer my simple question in a direct manner could you at least explain WHY you can't or won't?

[kleinman]

The answer to your question is that the mutation and selection sorting/optimization process is dominated mathematically and empirically by the number of selection (optimization) conditions and genes targeted by these selection conditions. If you have a single selection pressure targeting a single gene, this sorting/optimization process can be done fairly quickly as seen when monotherapy was tried with HIV and the fairly rapid evolution of resistance to bacteria when single drug therapy is used with these microbes. As soon as you add a second selection pressure, the mutation and selection sorting/optimization process is profoundly slowed. Each additional selection pressure slows the evolutionary process much, much, much more. That is how the mutation and selection sorting/optimization process works mathematically and that is how it works empirically. You can not transform entire genomes by the mutation and selection sorting/optimization process. It is mathematically and empirically irrational to think that you can. Here are more empirical examples of how the mutation and selection sorting/optimization process actually works.
http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0 (http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0)
The following possible methods of minimising the risks of resistance are considered: (a) adjustment of the dosage and frequency of spraying so that resistance genes are effectively recessive; (b) detection and eradication of new foci of resistance before they have a chance to spread; (c) spraying a mosaic of unrelated insecticides with the intention that immigrants from one sector of the mosaic to another will dilute the frequency of resistance genes; (d) re-introduction of susceptibility genes into the progeny of wild females by the release of heterozygous males with resistance genes translocated on to their Y chromosome so that they are protected from insecticidal killing but will pass susceptibility to their female progeny; (e) replacement of a resistant by a susceptible population by means of a negatively heterotic system such as bidirectional cytoplasmic incompatibility. A plausible case can be made for each of these methods based on theoretical models and appropriate assumptions. However, an assessment of whether any of them will really beof any value depends on the answers to certain questions in the field. Therefore field projects have been initiated on Anopheles culicifacies in Sri Lanka and Pakistan, Culex quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The results so far are summarized.
http://www.dcp2.org/pubs/DCP/55/Section/8167 (http://www.dcp2.org/pubs/DCP/55/Section/8167)
Some interventions, such as the use of drug combinations, reduce the likelihood that resistance will emerge, whereas other interventions, such as improvements in drug prescribing and patient compliance with dosing, reduce the likelihood that a resistant pathogen will survive and proliferate.
and
The appropriate choice of drug treatment is an important step in delaying the evolution of drug resistance. Drug combinations that include drugs with different targets were first used in the treatment of tuberculosis and have now become routine practice in the treatment of cancer and HIV/AIDS. Combinations of artemisinin and its derivatives with other antimalarials, notably mefloquine, have accelerated recoveries, increased cure rates, and reduced transmissibility. In the refugee camps on the western border of Thailand, where most of the recent studies with artemisinin combinations have been conducted, the use of combinations delayed the development of resistance and reduced the incidence of disease (Nosten and others 2000). The rationale behind drug combinations is that, if resistance results from spontaneous genetic mutations, the chance that a parasite will emerge that is simultaneously resistant to two drugs with unrelated modes of action (that is, drug targets) is the mathematical product of the individual parasite mutation frequencies multiplied by the total number of parasites exposed to the drugs (White 1998, 1999). Combinations, therefore, reduce enormously the probability that a resistant mutant will arise. Sequential deployment of the drugs is much less effective, because it does not exploit the multiplicative reduction in selection risk.
and
In the context of antibiotics, combinations have typically been used to broaden the spectrum of antimicrobial coverage rather than to reduce the likelihood of the emergence of resistance. With the development of new penicillins and cephalosporins with broader spectra of activity a decade ago, most serious infections have been treated with monotherapy. The use of combination therapy to preserve new classes of antibiotics from the emergence of resistance at a societal level may be rational, but it has not been implemented because of cost concerns and the potential for enhanced toxicity associated with the use of more agents than necessary to effect a cure in an individual patient.
There are no empirical examples of the mutation and selection sorting/optimization process which shows that it works any other way. Combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. The failure of evolutionists to understand and teach the basic science and mathematics of this process properly contributes to the premature death of millions of people suffering from diseases subject to mutation and selection. The simple answer to your question is that you can not evolve entire genomes by the mutation and selection sorting/optimization process. You do not have the selection conditions and if you did, you can barely evolve a population of HIV to three selection conditions despite its huge population, rapid reproductive rate and high mutation rate. You evolutionists need to learn the basic science and mathematics of the mutation and selection sorting/optimization process. Study Dr Schneider’s peer reviewed and published mathematical model of the process, then you will realize why your theory is mathematically and empirically irrational and illogical.

[coops]

So is this your definition of micro-evolution Kleinman?

Do you state that micro-evolution is when a single gene evolves in response to a single selection pressure?

Are you also then stating that anything other than this is macro-evolution and hence impossible?

Would you agree with the following statement ' 'it is impossible for more than a single gene to simultaneously evolve in any organism as this would constitute macro-evolution.'

Kleinman, does this earlier post of mine accurately summarise your views on what is and is not possible within evolution?

I'm not sure if its intentional or not, but your previous post didn't specifically answer my question.

If my summary of your position is wrong in any way could you please let me know the specifics of where i have misinterpreted you?

Thanks

[kleinman]

The answer to your question is that the mutation and selection sorting/optimization process is dominated mathematically and empirically by the number of selection (optimization) conditions and genes targeted by these selection conditions. If you have a single selection pressure targeting a single gene, this sorting/optimization process can be done fairly quickly as seen when monotherapy was tried with HIV and the fairly rapid evolution of resistance to bacteria when single drug therapy is used with these microbes. As soon as you add a second selection pressure, the mutation and selection sorting/optimization process is profoundly slowed. Each additional selection pressure slows the evolutionary process much, much, much more. That is how the mutation and selection sorting/optimization process works mathematically and that is how it works empirically. You can not transform entire genomes by the mutation and selection sorting/optimization process. It is mathematically and empirically irrational to think that you can. Here are more empirical examples of how the mutation and selection sorting/optimization process actually works.
http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0 (http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0)
The following possible methods of minimising the risks of resistance are considered: (a) adjustment of the dosage and frequency of spraying so that resistance genes are effectively recessive; (b) detection and eradication of new foci of resistance before they have a chance to spread; (c) spraying a mosaic of unrelated insecticides with the intention that immigrants from one sector of the mosaic to another will dilute the frequency of resistance genes; (d) re-introduction of susceptibility genes into the progeny of wild females by the release of heterozygous males with resistance genes translocated on to their Y chromosome so that they are protected from insecticidal killing but will pass susceptibility to their female progeny; (e) replacement of a resistant by a susceptible population by means of a negatively heterotic system such as bidirectional cytoplasmic incompatibility. A plausible case can be made for each of these methods based on theoretical models and appropriate assumptions. However, an assessment of whether any of them will really beof any value depends on the answers to certain questions in the field. Therefore field projects have been initiated on Anopheles culicifacies in Sri Lanka and Pakistan, Culex quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The results so far are summarized.
http://www.dcp2.org/pubs/DCP/55/Section/8167 (http://www.dcp2.org/pubs/DCP/55/Section/8167)
Some interventions, such as the use of drug combinations, reduce the likelihood that resistance will emerge, whereas other interventions, such as improvements in drug prescribing and patient compliance with dosing, reduce the likelihood that a resistant pathogen will survive and proliferate.
and
The appropriate choice of drug treatment is an important step in delaying the evolution of drug resistance. Drug combinations that include drugs with different targets were first used in the treatment of tuberculosis and have now become routine practice in the treatment of cancer and HIV/AIDS. Combinations of artemisinin and its derivatives with other antimalarials, notably mefloquine, have accelerated recoveries, increased cure rates, and reduced transmissibility. In the refugee camps on the western border of Thailand, where most of the recent studies with artemisinin combinations have been conducted, the use of combinations delayed the development of resistance and reduced the incidence of disease (Nosten and others 2000). The rationale behind drug combinations is that, if resistance results from spontaneous genetic mutations, the chance that a parasite will emerge that is simultaneously resistant to two drugs with unrelated modes of action (that is, drug targets) is the mathematical product of the individual parasite mutation frequencies multiplied by the total number of parasites exposed to the drugs (White 1998, 1999). Combinations, therefore, reduce enormously the probability that a resistant mutant will arise. Sequential deployment of the drugs is much less effective, because it does not exploit the multiplicative reduction in selection risk.
and
In the context of antibiotics, combinations have typically been used to broaden the spectrum of antimicrobial coverage rather than to reduce the likelihood of the emergence of resistance. With the development of new penicillins and cephalosporins with broader spectra of activity a decade ago, most serious infections have been treated with monotherapy. The use of combination therapy to preserve new classes of antibiotics from the emergence of resistance at a societal level may be rational, but it has not been implemented because of cost concerns and the potential for enhanced toxicity associated with the use of more agents than necessary to effect a cure in an individual patient.
There are no empirical examples of the mutation and selection sorting/optimization process which shows that it works any other way. Combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process. The failure of evolutionists to understand and teach the basic science and mathematics of this process properly contributes to the premature death of millions of people suffering from diseases subject to mutation and selection. The simple answer to your question is that you can not evolve entire genomes by the mutation and selection sorting/optimization process. You do not have the selection conditions and if you did, you can barely evolve a population of HIV to three selection conditions despite its huge population, rapid reproductive rate and high mutation rate. You evolutionists need to learn the basic science and mathematics of the mutation and selection sorting/optimization process. Study Dr Schneider’s peer reviewed and published mathematical model of the process, then you will realize why your theory is mathematically and empirically irrational and illogical.

[coops]

The answer to your question is >deleted as duplicate post<.

Can you give a yes or no answer to my question Kleinman?

I gave a summary of my understanding of your position. Can you respond by simply stating either -
a) yes, your summary is correct.
b) no, your summary is incorrect.

If the answer is b then please feel free to correct my statement accordingly.

Your above duplicate post really doesnt make it clear to me where you specifically draw the line between micro-evolution and macro-evolution.

[rocketdodger]

I really think this man is insane.

[Belz...]

Evolutionists have a hard time understanding

Creationists have a hard time breathing, let alone thinking.

If you evolutionists didn’t have so much difficulty with the mathematics of the mutation and selection sorting/optimization process, you would realize that microevolution never becomes macroevolution.

That's not even logical.

Hey, Klein. When did you decide to stop answering posts and instead focus on spamming this thread ?

[Mr. Scott]

Dr. Kleinman, why do you believe the time it takes for a computer program to sort one generation of genomes in Ev corresponds with the time it takes nature to "sort" genomes in a generation by natural selection?

[CurtC]

I really think this man is insane.

I just popped into this thread for the first time in a long time, and I'm not convinced it's a real person. It's like a spambot.

[CurtC]

I really think this man is insane.

I just popped into this thread for the first time in a long time, and I'm not convinced it's a real person. It's like a spambot.

[Nogbad]

I don't think the Doc is a spambot but I am considering the posibility he has written a programme so he can type mutation and selection sorting/optimization by depressing just two keys.

[Belz...]

Actually, he's probably got entire paragraphs pre-programmed into macros...

[m_huber]

So this man, who denies that fossils are valid evidence of evolution, who believes that entering an invalid set of numbers into a computer program modeling the interior of a human body debunks evolution, who thinks that microevolution and macroevolution are separate enough entities to claim that only one happens, but not the other, who answers no specific refutations of his arguments, who chooses to laugh at anyone who disagrees with him (ignoring any opportunity to learn from them), this man is a medical doctor?

[joobz]

Remember kleinman said that the evolution of nylon eating bacteria isn't proof of evolution because
17.) nylon-eating bacteria-a polymerase evolves into a polymerase, what’s your point?
Yes, his argument is that it doesn't count because an enzyme evolves into another enzyme.