Annoying creationists

[kleinman]

Annoying Creationists

You are as poor at doing your literature searches as you are in the mathematics of mutation and selection. You don’t know who my thesis advisor was and who wasn’t. You are simply a big mouth coward; everyone here is capable of reading and understanding this point.

You have 2 publications listed on web of science, which typically ignores conference proceedings/abstracts. Why do you get so angry with me, when it was you who raised this issue in the first place. If you are embarrassed by your track record, why do you mention it?

You would save yourself much frustration and humiliation if you simply stuck to the topic at hand. I've asked 3 times now, what are your justifications for your model assumption?

You have never answered this question. Indeed, you failed to answer any question that clearly demonstrates your poorly conceived theory for what it is.

You are the one who brought up my PhD thesis and you claimed you could find irregularities in it. So find the irregularities. Why do you continue to attribute Dr Schneider’s computer model to me? Can’t you even get that fact straight?

That’s a fitting “backstory” for the theory of evolution since ev converges to a local optimum, it just doesn’t happen to be a “perfect creature” local optimum for longer genomes.

It's not simply "longer genomes," now is it? We can run one experiment with a longish genome that converges, and another with the same length genome that does not. Therefore, obviously, there is another factor at work.

That isn’t a profoundly longish genome is it? Paul, there is a way to determine what this factor is. You have to map out the fitness landscape. You do this by computing the mistakes in 4^G combinations of genomes. I’ll let you do the arithmetic on that one. What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

 

[joobz]

You are the one who brought up my PhD thesis and you claimed you could find irregularities in it. So find the irregularities. Why do you continue to attribute Dr Schneider’s computer model to me? Can’t you even get that fact straight?

So again, you wish to make yourself look foolish by repeating the same missinterpretation of my statements? Such actions only help to confirm Dr. Adequate's assessment of your mental health. Is that your goal?

Why do you try so hard to avoid answering my question? What are your justifications for your model? I've given you a list of nine assumptions that are required to make your analysis valid. Any one of them would being wrong would destroy your theory. Is this your way of finally admitting you've been wrong this whole time?

 

[rocketdodger]

Wrong rocketdodger, adding selection pressures slows down the mutation and selection process, removing selection pressures speed up the mutation and selection process.

Oh, so removing the penicillin selective pressure will speed up the evolution of penicillin resistance? Now I understand. So according to your theory, as long as we keep removing pressures, evolution will get faster and faster, until we get to zero pressures, at which point species must just pop into existence.

How could you argue about the results from ev. You don’t understand the model and you’ve never run a case.

I understand the model, and I ran the cases you told me to, which led to results different than yours, go figure.

With respects to your model, you have yet to post a systematic study of your model. There is nothing to argue about your model.

And you have yet to post a systematic study of ev. Who the hell cares? I told you already that every conceivable set of parameters you can give my simulation leads to the same conclusion -- for some n != 0, the rate of fixation under n+1 pressures is greater than the rate of fixation under n pressures. If you want the actual numbers from actual runs, fine. I will run the simulation a few times tonight on a wide variety of possible inputs and give you the results.

Will it matter? No, because you are full of sh--. Regardless of what I show you, you will cry about some other nonexistent problem and whine about how it must be throwing off my results. All of this, of course, without giving us a single mathematical explanation for why the results should be off, except the generic Kleinman cop-out that we all know so well -- "the mathematical and empirical evidence shows otherwise." Suuuuure.

Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is
1 – (1.0 x 10^-999999999) ≈ 1

Hahahahah. Nice creationist math there, genius. Try treating the two as independent events and see where that gets you. You do know about independent events in probability theory, right, grad-student?

You just won’t accept the mathematical and empirical facts.

I will accept any mathematical facts that you can show, Kleinman, using a mathematical proof, to actually be a mathematical fact. It is clear that you are a fraud and never wrote a thesis, because if you had, you would understand the concept of proof and how to construct a coherent argument.

I will also accept any empirical facts that you can show to actually be facts. That is why we have consistently asked you to prove to us why your theory is correct. Curiously, your only method of "proof" has been to regurgitate an assertion that your theory is correct.

That’s why you can’t find a single real example of n+1 selection pressures evolving more rapidly than n selection pressures. It just doesn’t happen.

Except in every single study you have cited, of course.

 

[rocketdodger]

What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

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.

If you think otherwise, please tell us all, what combination of mutations represent a local optima?

 

[kleinman]

Annoying Creationists

Wrong rocketdodger, adding selection pressures slows down the mutation and selection process, removing selection pressures speed up the mutation and selection process.

Oh, so removing the penicillin selective pressure will speed up the evolution of penicillin resistance? Now I understand. So according to your theory, as long as we keep removing pressures, evolution will get faster and faster, until we get to zero pressures, at which point species must just pop into existence.

No rocketdodger, you are attributing a property to mutation and selection that has no mathematical or empirical basis. Adding penicillin does not speed up the evolution of weak selection pressures. The evolution of resistance on the background of weak selection pressures slows the evolution of penicillin resistance. That is why you answered correctly when I asked you under what circumstances does penicillin resistance evolve more quickly, in vivo when there is an immune response against the bacteria or in vitro when there is no immune response. That’s the point rocketdodger; things don’t just pop into existence. There is a cause and effect relationship.

How could you argue about the results from ev. You don’t understand the model and you’ve never run a case.

I understand the model, and I ran the cases you told me to, which led to results different than yours, go figure.

You are not doing something correctly with the model. A given set of input parameters always give identical output from the model. Those input parameters include the seed value for the random number generator.

With respects to your model, you have yet to post a systematic study of your model. There is nothing to argue about your model.

And you have yet to post a systematic study of ev. Who the hell cares? I told you already that every conceivable set of parameters you can give my simulation leads to the same conclusion -- for some n != 0, the rate of fixation under n+1 pressures is greater than the rate of fixation under n pressures. If you want the actual numbers from actual runs, fine. I will run the simulation a few times tonight on a wide variety of possible inputs and give you the results.

Rocketdodger, that data from ev is on this thread. All you have posted is this:

I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

This is your idea of a parametric study. This is the kind of sloppy analysis you evolutionists like to call science. Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

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.

Like I said, Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

 

[Paul C. Anagnostopoulos]

That isn’t a profoundly longish genome is it?

I'm not sure why it matters. Do you want to amend your statement to "That’s a fitting “backstory” for the theory of evolution since ev converges to a local optimum, it just doesn’t happen to be a “perfect creature” local optimum for really extra long genomes of extra big size."?

Paul, there is a way to determine what this factor is. You have to map out the fitness landscape. You do this by computing the mistakes in 4^G combinations of genomes. I’ll let you do the arithmetic on that one. What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

I agree completely, Alan. It's a complicated landscape. What do you suppose creates those hills and valleys? You appear to think it's magic.

~~ Paul

 

[Paul C. Anagnostopoulos]

Adding penicillin does not speed up the evolution of weak selection pressures.

Please stop saying this. Selection pressures do not evolve. Please say what you actually mean, so at least we have a chance.

~~ Paul

 

[rocketdodger]

No rocketdodger, you are attributing a property to mutation and selection that has no mathematical or empirical basis. Adding penicillin does not speed up the evolution of weak selection pressures. The evolution of resistance on the background of weak selection pressures slows the evolution of penicillin resistance.

Will introducing penicillin to a population speed up the evolution of penicillin resistance, Kleinman? YES or NO?

This is your idea of a parametric study. This is the kind of sloppy analysis you evolutionists like to call science. Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

Can you show anyone here why the algorithms used by Dr. Adequate and myself are not sorting algorithms? YES or NO?

Like I said, Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

Can you show anyone here what distribution of mutations in a population might correspond to a local optima in the fitness landscape for that population? YES or NO? To make it simple for you Kleinman, lets suppose only two selective pressures of equal magnitude (A and B) are affecting the population.

 

[Paul C. Anagnostopoulos]

I ran two experiments with the standard model but a genome size of 4096:

weight width 7, site width 8 (Rcapacity >> Rfrequency): 124,827 generation to perfect creature

weight width 6, site width 7 (Rcapacity > Rfrequency): 131,375 generation to perfect creaure

weight width 5, site width 6 (Rcapacity > Rfrequency): 163,722 generations to perfect creature

weight width 4, site width 5 (Rcapacity > Rfrequency): 198,279 generations to perfect creature

weight width 3, site width 4 (Rcapacity = Rfrequency): still 16 mistakes after 1,000,000 generations

weight width 2, site width 3 (Rcapacity < Rfrequency): still 16 mistakes after 1,000,000 generations


~~ Paul

 

[UnrepentantSinner]

Klein, I think something broke in your mind around post 6614. I'm with Adequate. Get help.

I think you're being overly magnaimous since his is clearly a pre-existing condition. I can't even read Kleinmann's posts, but then again, I could never wade through the Unibomber's manifesto either. Dr. A's diagnosis is spot on.

 

[Mr. Scott]

Before I looked at Dr Schneider’s and Paul’s model, I didn’t understand how mutation and selection

worked.

(snip)

I have always been skeptical of the interpretation of the evidence presented by evolutionists but this is the first time I

have done my own analysis of the evidence and it shows that evolutionists have the concept of mutation and selection

backwards.

Precisely why were you skeptical of the interpretation of the evidence presented by evolutionarians before you looked at Dr. Schneider's and Paul's model?

 

[Kotatsu]

Common descent is a myth.

While what you say is usually nonsense, I am still waiting for you to comment on the discussion Delphi_ote and I had of random point mutation independent ways which implies common descent, such as gene order and polyploidisation events. Also, I have been waiting for some time to get an explanation for what exactly it is we see when we construct a phylogenetic tree based on gene data. Does the exact method we use to construct the phylogenies make any difference?

 

[Kotatsu]

Wow, one of you must have really pushed one of his buttons. He doesn't seem at all as comparatively cheery as he used to, and he doesn't even seem to put as much effort into his insults and lies. Or is it just the combined weight of the responses that's wearing him down?

That'd make sense, really. The more pressure he's under, the slower he thinks.

 

[Belz...]

Just because you have an interest in mutation and selection doesn’t mean you have any understanding of the process. You have admitted that.

Gosh, if you wanted to prove that you forgot what the context of Joobz' post was, you succeeded quite eloquently.

 

[Belz...]

Now that we know how mutation and selection actually works, probability theory alone is useless.

Fascinating. And how did you come to the conclusion that it was impossible ? Theory.

Why don’t you tell us what the selection pressure was that evolved the first gene de novo?

You understand nothing of evolution if you think that makes any sense at all.

Tell us what the probability is for a 500 base gene to form by random additions of bases?

Random ? Who said anything about random ?

You may have forgotten the "selection" part. You know, the part that ISN'T part of the definition of "beggaminases" that you so conveniently forgot ?

 

[Belz...]

Sure I do, you evolutionists have no idea how mutation and selection actually works. This is why you can’t find a single citation which show that n+1 selection pressures evolve more quickly than n selection pressures.

Of course we can. In fact, you keep finding those examples for us.

 

[Belz...]

Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is
1 – (1.0 x 10^-999999999) ≈ 1

False dichotomy.

 

[Belz...]

Wow, one of you must have really pushed one of his buttons. He doesn't seem at all as comparatively cheery as he used to, and he doesn't even seem to put as much effort into his insults and lies. Or is it just the combined weight of the responses that's wearing him down?

Check post 6614. Something definitely happened, there.

 

[kjkent1]

The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.

Heck, that's easy, and I'm not even a mathematician:

Let math = The scientific study of the measurement, relationships, and properties of quantities and sets, using numbers and symbols.

Let God = an entity which cannot be measured scientifically.

Therefore, if the creator is God, and God is unmeasurable, then the creator is mathematically impossible.

OK, kleinman, it's your turn -- let's see your math for impossible evolution.

 

[kleinman]

Annoying Creationists

What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

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.

Rocketdodger, you haven’t paid much attention to the citations posted so I’ll repeat one that show some graphics of a very simple fitness landscape for two selection conditions. I have to thank joobz for this citation though he thought varying environments had to do with the weather in this paper.
http://www.pnas.org/cgi/content/full/104/34/13711

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.

That isn’t a profoundly longish genome is it?

I'm not sure why it matters. Do you want to amend your statement to "That’s a fitting “backstory” for the theory of evolution since ev converges to a local optimum, it just doesn’t happen to be a “perfect creature” local optimum for really extra long genomes of extra big size."?

Paul, I’m just pulling your leg for using the term “longish”. No, I am not going to amend the above statement. Are you claiming that ev does not converge to a local optimum, even when Rfrequency exceeds your Rcapacity value?

Paul, there is a way to determine what this factor is. You have to map out the fitness landscape. You do this by computing the mistakes in 4^G combinations of genomes. I’ll let you do the arithmetic on that one. What I think you will find is there are lots of hills and valleys on the landscape which prevent the population from finding a perfect creature local optimum.

I agree completely, Alan. It's a complicated landscape. What do you suppose creates those hills and valleys? You appear to think it's magic.

Of course I don’t think it is magic. Ev’s complicated fitness landscape is caused by the same thing that causes complicated fitness landscapes in real cases of mutation and selection. There are more potential detrimental mutations at more loci than beneficial mutations at their relatively small number of loci, especially when you have combined selection pressures. You evolutionists like to ignore the detrimental affect of mutations but it is these detrimental mutations which confound the mutation and selection process.

Adding penicillin does not speed up the evolution of weak selection pressures.

Please stop saying this. Selection pressures do not evolve. Please say what you actually mean, so at least we have a chance.

Each selection pressure imposes its own sorting condition on the mutation and selection process. Imposing a strong selection pressure on a population does not speed up the sorting process for the weak selection pressures. What the weak selection pressures give is a noisy background that slows the sorting process for the strong selection pressure. Certainly selection pressures do not evolve; they cause a population to evolve by sorting beneficial and detrimental mutations. I’ll try to better with my phraseology. If you are looking for a chance that mutation and selection can give common descent, you don’t have a chance. We now know how the mutation and selection sorting/optimization process works. This sorting/optimization process can barely sort beneficial and detrimental mutations for two targeted genes let alone the thousands of genes which would need to be transformed to evolve reptiles into birds.

I ran two experiments with the standard model but a genome size of 4096:

weight width 7, site width 8 (Rcapacity >> Rfrequency): 124,827 generation to perfect creature

weight width 6, site width 7 (Rcapacity > Rfrequency): 131,375 generation to perfect creaure

weight width 5, site width 6 (Rcapacity > Rfrequency): 163,722 generations to perfect creature

weight width 4, site width 5 (Rcapacity > Rfrequency): 198,279 generations to perfect creature

weight width 3, site width 4 (Rcapacity = Rfrequency): still 16 mistakes after 1,000,000 generations

weight width 2, site width 3 (Rcapacity < Rfrequency): still 16 mistakes after 1,000,000 generations

Your last two cases converge to a local optimum with 16 mistakes rather than a zero mistake local optimum. In order for the population to evolve to a perfect creature in these cases, the population must traverse a reduced fitness trough but the selection conditions prevent this. Take a look at the figures of fitness landscapes I reposted above. That should help you understand why ev behaves as it does. I think you look at this problem in the wrong way. Ev is really showing how few cases will actually converge to a perfect creature, most cases will not.

No rocketdodger, you are attributing a property to mutation and selection that has no mathematical or empirical basis. Adding penicillin does not speed up the evolution of weak selection pressures. The evolution of resistance on the background of weak selection pressures slows the evolution of penicillin resistance.

Will introducing penicillin to a population speed up the evolution of penicillin resistance, Kleinman? YES or NO?

You don’t get a yes or no answer to this question. Sometimes you can introduce penicillin to a population and it wipes out the population. Sometimes you can introduce penicillin to a population for which it exerts no selection pressure and therefore does nothing to the population. If you want the fastest evolution of resistance to penicillin for population which is subject to the toxic effects of this drug, you subject the population to a sub-lethal concentration of penicillin while minimizing all other selection pressures and slowly increase the concentration of penicillin. That’s how mutation and selection actually works.

This is your idea of a parametric study. This is the kind of sloppy analysis you evolutionists like to call science. Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

Can you show anyone here why the algorithms used by Dr. Adequate and myself are not sorting algorithms? YES or NO?

It’s up to you two to show that your algorithms actually represent mutation and selection. You definitely haven’t shown that n+1 selection pressures evolve more rapidly than n selection pressures when you say this:

I also found a set of parameters that brought it down to be lower than for a singly applied pressure but I forgot what it was.

Like I said, Rocketwhomissesthetarget, you have a way to go to understand how the mutation and selection sorting/optimization process works.

Can you show anyone here what distribution of mutations in a population might correspond to a local optima in the fitness landscape for that population? YES or NO? To make it simple for you Kleinman, lets suppose only two selective pressures of equal magnitude (A and B) are affecting the population.

This one you get a yes answer. See the citation and figures at the beginning of the post. I don’t think you appreciate how complex a real fitness landscape can be but there is an example of a simple fitness landscape for two selection pressures of equal magnitude for a computer simulation.

Precisely why were you skeptical of the interpretation of the evidence presented by evolutionarians before you looked at Dr. Schneider's and Paul's model?

My first real skepticism of abiogenesis and the theory of evolution occurred when I took courses in organic chemistry. In the laboratory we were required to synthesize a variety of more complex molecules from simpler molecules. In order to get a side group to bond to a particular site often required activating catalysts and shielding groups to prevent reactions at other sites. Often times the reactions would have to take place in strongly acidic then strongly basic solutions and visa versa. The idea that the complex organic molecules that form life can occur in some fanciful primordial soup is as joobz puts it, speculation.

Common descent is a myth.

While what you say is usually nonsense, I am still waiting for you to comment on the discussion Delphi_ote and I had of random point mutation independent ways which implies common descent, such as gene order and polyploidisation events. Also, I have been waiting for some time to get an explanation for what exactly it is we see when we construct a phylogenetic tree based on gene data. Does the exact method we use to construct the phylogenies make any difference?

Oh, I thought I addressed this, several times, but I’ll address it again for you. So you have polyploidy, how do you transform those duplicated genes to a new form? Why Kotatsu, it requires mutation and selection and as we have seen over and over, transforming more than a single gene at a time profoundly slows the evolutionary process.

You can construct phylogenic trees based on similarities of genes. All that it shows is that living things can have some similarity in chemical structure. In order to use these phylogenic trees as evidence of common descent, you need to show how mutation and selection can accomplish the transformation from one form to another. The mathematical and empirical evidence of mutation and selection shows that it can not make the transformations.

Wow, one of you must have really pushed one of his buttons. He doesn't seem at all as comparatively cheery as he used to, and he doesn't even seem to put as much effort into his insults and lies. Or is it just the combined weight of the responses that's wearing him down?

That'd make sense, really. The more pressure he's under, the slower he thinks.

The only button you have pushed is the laughter button. Are you talking about the combined weight of the citations which show that n+1 selection pressures evolve more rapidly than n selection pressures? I don’t know how I can bear all zero of your citations.

Since there are only two possibilities how we got here, either abiogenesis and evolution or we were created, the probability that we were created is

1 – (1.0 x 10^-999999999) ≈ 1

False dichotomy.

Now wait a minute Belz, rocketwhomissesthetarget gave the probability that evolution is true (1.0 x 10^-999999999) and the only other probability that we got here is that we were created. Since you evolutionists have shown that the sum of all probabilities is 1, it is a simple mathematical fact that probability that we were created based on rocketwhomissesthetarget’s own number is ≈ 1. Now you could change this if you can come up with an alternative explanation of how we got here. Wait a minute, you have, we have beggaminased.

The theory of evolution is mathematically impossible, let’s see you prove creationism mathematically impossible.

Heck, that's easy, and I'm not even a mathematician:

Let math = The scientific study of the measurement, relationships, and properties of quantities and sets, using numbers and symbols.

Let God = an entity which cannot be measured scientifically.

Therefore, if the creator is God, and God is unmeasurable, then the creator is mathematically impossible.

OK, kleinman, it's your turn -- let's see your math for impossible evolution.

Kjkent1, you are not able to measure God but you can measure the creation.

Now, it is not my math which shows the theory of evolution to be mathematically impossible, it is Dr Schneider’s mathematical model of mutation and selection which show how mutation and selection works. What Dr Schneider’s model shows is that combination selection pressures profoundly slow the mutation and selection process and that what real examples of mutation and selection shows. Here are a couple more real examples of mutation and selection which show that combination selection pressures profoundly slow the sorting of beneficial and detrimental mutations.
http://aac.asm.org/cgi/reprint/48/11/4226.pdf

Whether or not resistant mutants will be present before the start of antibiotic treatment of an initially susceptible population of bacteria depends on the size of the infecting population, the rate of mutation to resistance, and the amount of time that the population has been maintained. In the present investigation, we argue that for the treatment of chronic infections caused by hypermutable Pseudomonas aeruginosa of the sort frequently found in cystic fibrosis patients, mutants resistant to all single antipseudomonal drugs will almost invariably be present in a high proportion at the onset of treatment, and consequently, these strains should be considered resistant to all agents when they are used as monotherapy. Using a construct of P. aeruginosa strain PAO1 with a mutS deletion (strain PAO▲mutS), we show that when in vitro populations of less than 5 x 10^4 seemingly susceptible hypermutable bacteria are confronted with any of 11 antipseudomonal agents, mutants for which the MICs and the minimum bactericidal concentrations are in the range of clinical resistance will almost invariably ascend to dominance within 24 to 36 h. This does not occur for PAO1 without the mutS deletion. The results of our detailed analysis of this evolution of acquired resistance to two of these antibiotics, imipenem and ciprofloxacin, indicate that although the rates of mutation to resistance in PAO▲mutS are on the order of 1 x 10^6 per generation, resistant mutants are very likely to either be present in cultures of between 2 x 10^4 and 4 x 10^4 bacteria or arise after the bacterial populations are confronted with antibiotics. We also demonstrate with in vitro experiments that the problem of acquired resistance to treatment with single antibiotics can be thwarted by combination therapy with pairs of antibiotics of different classes with synergistic activities. We discuss the clinical implications of our analysis of these observations.

This following citation is for rocketwhomissesthetarget who thinks that weak selection pressures do not slow the evolutionary process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90521

Understanding the mechanisms of the emergence of drug resistance and the factors that affect it will aid in the design of improved preventive strategies. This will occur by several means. Experimental data will help refine the mathematical models of the emergence of resistance and also provide a basis for predicting the probability of the development of resistance to new agents (10). Furthermore, the results of the drug combination experiments suggest that susceptibility results may not be a good indicator of the utility of antimicrobials for prevention of the emergence of resistance to other agents. Thus, drugs that are not considered highly active may still have a role in reducing or preventing resistance. The screening of antibiotics for the ability to reduce the level of resistance has been proposed by others (4, 10), and the results presented here lend support to that approach. However, the problem may be how to assess the emergence of resistance in a straightforward, reproducible, and clinically relevant manner (10).

Drugs which have weak selective affect still slow the evolution of resistance to strong selection pressures. That’s how the mutation and selection sorting/optimization process works mathematically and that’s how the process works empirically.