Annoying creationists

[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.

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?

[kleinman]

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

[/kleinman]

Sorry, it had to be done.

 

[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]

Annoying Creationists

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

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]

Annoying Creationists

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!

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

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

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

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

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?

 

[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]

Annoying Creationists

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.