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Genes switching rows of teeth = Efficient ID Design?

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The “Msx1, a feedback activator of Bmp4 expression” with the Osr2 control gene has been discovered to switch between single vs multiple sets of teeth. E.g. distinguishing between humans and sharks. This efficient compact control mechanism appears to fit well within an ID Design paradigm. The serious cleft pallet defects caused by errors further suggest an irreducibly complex system.

What evidence might there be for random mutation and “selection” to form such a complex yet elegant control system so “early” in evolution?

Finding genes that make teeth grow all in a row By LAURAN NEERGAARD, AP Thursday, February 26, 2009

Ever wonder why sharks get several rows of teeth and people only get one? . . .A single gene appears to be in charge, preventing additional tooth formation in species destined for a limited set. When the scientists bred mice that lacked that gene, the rodents developed extra teeth next to their first molars _ backups like sharks and other non-mammals grow, University of Rochester scientists reported Thursday. . . .Also intriguing: All the mice born without this gene, called Osr2, had cleft palates severe enough to kill. So better understanding of this gene might play a role in efforts to prevent that birth defect, the Rochester team reported in the journal Science.

Teeth may not be visible until long after birth, but they start to form early in embryo development. Teeth ultimately erupt from a thickened band of tissue along the jaw line called the dental lamina, a band that forms in a top layer of the gum called the epithelium.
. . . All the action takes place instead in a deeper cell layer called the mesenchyme.

Think of the Osr2 gene as a control switch, a kind of gene that turns on and off the downstream actions of other genes and proteins. In that mesenchymal tissue, the Osr2 gene works in concert with two other genes to make sure budding teeth form in the right spot, said lead researcher Dr. Rulang Jiang, a geneticist at Rochester’s Center for Oral Biology.

See: full article.

Antagonistic Actions of Msx1 and Osr2 Pattern Mammalian Teeth into a Single Row
Zunyi Zhang, Yu Lan, Yang Chai, Rulang Jiang
Science 27 February 2009: Vol. 323. no. 5918, pp. 1232 – 1234;
DOI: 10.1126/science.1167418

Mammals have single-rowed dentitions, whereas many nonmammalian vertebrates have teeth in multiple rows. Neither the molecular mechanism regulating iterative tooth initiation nor that restricting mammalian tooth development in one row is known. We found that mice lacking the transcription factor odd-skipped related-2 (Osr2) develop supernumerary teeth lingual to their molars because of expansion of the odontogenic field. Osr2 was expressed in a lingual-to-buccal gradient and restricted expression of bone morphogenetic protein 4 (Bmp4), an essential odontogenic signal, in the developing tooth mesenchyme. Expansion of odontogenic field in Osr2-deficient mice required Msx1, a feedback activator of Bmp4 expression. These findings suggest that the Bmp4-Msx1 pathway propagates mesenchymal activation for sequential tooth induction and that spatial modulation of this pathway provides a mechanism for patterning vertebrate dentition.

Comments
Pertinent to the issue is the recent post: But remember there isn't a debate over Darwinism Note Behe's Blog Waiting Longer for Two Mutations, Part 4 In particular:
Furthermore, I “assumed” nothing. I merely cited empirical results from the literature. The figure of 1 in 10^20 is a citation from the literature on chloroquine resistance of malaria. Unlike their model, it is not a calculation on my part.
eintown's
That “10^20? rubbish has been so thoroughly debunked!
misses the issue that this probability is based on experimental fact, not models.DLH
March 17, 2009
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From this gene controlling multiple teeth example, ID gives the fruitful insights: Search for genes that control switching between multiple options, based on compact design coding of controls.DLH
March 16, 2009
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You and Joseph both emphasized the merits of recognizing design. And so studying a subject in that light. Neither has shown how the leads to anything fruitful.
Until it is ALLOWED to ID won't be able to do much of anything. Again ID would lead us to understand that living organisms are NOT reducible to matter and energy. And that alone would tell us quite a bit. For example it would tell us to stop looking for a reducible solution and instead focus on a design solution.Joseph
March 16, 2009
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"Appeal to your own authority with no evidence or reference does not stand any chance in debate" If you’d care to read the posts, you would see where I gave info about that. No appeal to my authority required. Yes I didn’t reference the source. I should have – I concede (see we evilutionsist concede when wrong). "Ad hominen" I wrote up a summary of a couple of things that were requested. Prior to that post, I there were numerous posts per day requesting it. After the post, people fell silent for practically the entire day (save 1 poster). You and Joseph both emphasized the merits of recognizing design. And so studying a subject in that light. Neither has shown how the leads to anything fruitful. I was asked how an evolutionary view would prompt hypothesis etc, and I listed some. What would ID lead to?eintown
March 16, 2009
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eintown
That “10^20? rubbish has been so thoroughly debunked!
Appeal to your own authority with no evidence or reference does not stand any chance in debate.
"And its funny how the creationist have now fallen silent"
Ad hominem attacks also get you nowhere. By the way, you might wake up to the reality that UD focus on Intelligent Design, not creation science. Your efforts to equate the two evidence very little study and recognition of the issues involved. I recommend you begin by taking a course in logic. Study how to avoid logical fallacies. e.g. The Fallacy Files ad hominem attacks. After that you should learn what qualifies as objective evidence, proper citation and serious scientific and engineering evaluation.
ID? Gosh god made a machine. Now what?
To start with, can you recognize evidence of human design when you see it? e.g. the computer and browser you are using. Do you recognize that as having coming from an intelligent cause? You still give no evidence you have read or comprehended Behe, let alone distinguishing systems caused by stochastic effects from those that were designed. We await your maturing sufficiently to enter into serious discussion.DLH
March 15, 2009
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Well from that hypopthesis a scientist can do the following:
What hypothesis?
1 - See if those precursor structures exist.
How can one tell if it is a "precursor" as opposed to a devolved form? Or for that matter a form of common design?
2- If they dont exist, can one induce them through mutation.
No one has been able to show that any amount of mutational accumulation can give a flagellum where one never existed. As a matter of fact there isn't anything that demonstrates cumulative selection is real- ie exists in the real world.
3- Once produced are they functional.
None produced. And when the ribosome was synthesized, it didn't function. <blockquoteID? Gosh god made a machine. Now what? Wrong again, as usual. ID doesn't require "God". ID says that the structure in question is designed now let's study it in that light. I have already gone over this and you seem to wish to remain ignorant. Oh well...Joseph
March 14, 2009
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Well from that hypopthesis a scientist can do the following: 1 - See if those precursor structures exist. 2- If they dont exist, can one induce them through mutation. 3- Once produced are they functional. 4 - Do they increase the fitness of the organism. ID? Gosh god made a machine. Now what?eintown
March 14, 2009
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Not all mutations are deleterious. Some can be neutral- perhaps even the bulk may be neutral. Some may covey some benefit- benefit being a relative word. And then there are those mutations which lead to death and disease. But anyways eintown, please answer the following: How the heck can one test the premise that the flagellum arose via an accumulation of genetic acidents? What is the hypothesis for such a premise?Joseph
March 14, 2009
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"Oh, what science do you study and what year?" Biology. Last year. "So now the story changes, not all the mutations are deleterious." It has not changed. This has been my position. I was speaking for myself and others may disagree. "E.g One mutation leads to drug resistance, but decreases replicative ability. Another different mutation then arises in response and increases the fitness. You dont see the accessory mutations alone. SO your statement actually doesnt hold." Yes it does, when I said co-dependent I was referring to functionally co-dependent protiens I am surprised you didn't realize that as much as you have posted here already.Lord Timothy
March 13, 2009
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Oh, what science do you study and what year? So now the story changes, not all the mutations are deleterious. So again lets look at HIV, how does drug resistance develop with such ease? After a single dose of an antiretroviral, drug resistance develops. Not just one mutation but a handful. And not isolated mutations, some work together. E.g One mutation leads to drug resistance, but decreases replicative ability. Another different mutation then arises in response and increases the fitness. You dont see the accessory mutations alone. SO your statement "Especially when you are trying to mutate genes which code for co-dependent protiens" actually doesnt hold. If those co-dependent mutations dont arise, scientists are suprised.eintown
March 13, 2009
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"Plagiarize? No fellows, I did the experiments myself!!" Now exactly what experiments are these? "Obviously I took the info from othersites. Its plagirism when you pass the info as your own original work." Correct, when an individual posts something, it is presumed to be that poster's own work unless he or she notes otherwise. "The response I got when I referenced a couple of papers was “read it yourself”. SO i post a summary and I get accused of plagirism." If you would have noted anywhere that it was not your own work, or if you had provided a link as reference, then it would not be an issue. In fact you went as far as to say it was something you "wrote out" and never did you note or imply that it was a summary of another argument. "So cute. Attack me rather than the data." I would actually rather not. I am a forgiving guy, but for future reference cite your source. As for your "data" or should I say Matzke's, I provided the specific rebuttle in which it was addressed, and it seems to have been shot down again in my absence. "And please, PLEASE can the people who are in their “20s, in college, and working on degrees in science” identify themselves!"" You are speaking to one. "Again if thats true why is life around? Why doesnt every organism just fall apart." Why would every organism just fall apart? "So all mutations are deleterious? ALL?" No, not all, just most of them. Especially when you are trying to mutate genes which code for co-dependent protiens.Lord Timothy
March 13, 2009
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Again if thats true why is life around? Why doesnt every organism just fall apart. Must I really ask again: So all mutations are deleterious? ALL? Then why has life been going along happily for billions of years. For eg: Viruses, like HIV exhibit EVERY possible mutation within each population. But, why pray tell, is HIV or any highly mutable RNA retrovirus in existence. Surely they would just ‘degrade’ into extinction. Why do so many random mutations in HIV lead to beneficial properties like drug resistance?eintown
March 13, 2009
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eintown:
That “10^20? rubbish has been so thoroughly debunked!
Perhaps you should read what Dr Behe says about that: Waiting Longer for two mutations parts 1-3
That number only comes about when the events have to happen simultaneously.
No it doesn't. IOW it does not pertain to simultaneous events. Read what Behe says and also read the paper that tries, but failed, to refute his "Edge of Evolution".Joseph
March 13, 2009
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it shows that the majority of the genes controlling flagellum development are closely related. ie. they had a common origin, diverged, which lead to flagellum development.
It may show they are closely related but how? Via common descent or common design? Common descent is assumed. Convergence can also explain similarities. IOW there are other explanations for similarity other than common descent.
Whats more, a “speculation based on the assumption” leads to testable, falsifiable hypothesis
How the heck can one test the premise that the flagellum arose via an accumulation of genetic acidents? What is the hypothesis for such a premise?Joseph
March 13, 2009
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What does ID say about the flagellum? It is designed so let's study it in that light. Ya see experience has taught us that in order to truly understand something you have to study it in the proper light. For example Stonehenge- Do you think we could have the knowledge we now have had we studied it as a naturally occurring formation?Joseph
March 13, 2009
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For example the flagelllum with its approx. 40 proteins requires differing amounts of these proteins. IOW it isn't that the flagellum is made up of just 40 proteins. You not only need those 40 proteins but in the correct amount, at the correct time and brought to the right place for assembly. Some, if not most, of the proteins require a chaperone so that they will not react with other molecules already present in the organism. All of that requires meta-information. The point being is even if all 40 proteins are in one organism a flagellum will not form unless all thta meta-information is already present and functioning. 1- the filament requires 20,000 subunits of the flagellin protein FliC 2- The 3 ring proteins- about 26 subunits each (Flgh, I & F) 3- the distal rod requires 25 subunits 4- The hook contains about 130 subunits of FlgE And that is just the basics but you should get the point. Next is the assembly. That is not so easy because of cross-reactions thta would occur unless proteins are chaperoned to the correct spot. So the organism requires the meta-information for the chaperone as well as the info that tells the chaperone where to bring the protein it carries. The we have the issue of "homologs". Homology is assumed. Homoplasy also explains similarities without having to conjure up some unknown common ancestor.Joseph
March 13, 2009
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it shows that the majority of the genes controlling flagellum development are closely related. ie. they had a common origin, diverged, which lead to flagellum development. SO you can trace the history through the genetic changes. Whats more, a "speculation based on the assumption" leads to testable, falsifiable hypothesis. What does ID have to say about the flagellum? Gosh, way too complex, gosh, must be god. Which is science?eintown
March 13, 2009
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eintown, There isn't any scientific data which demonstrates that a flagellum or an immune system can evolve via an accumulation of genetic accidents from a population that didn't have one- a flagellum of an immune system. You should read the papers you found that allegedly show that each can evolve. Do that and you will see it is all speculation based on the assumption.Joseph
March 13, 2009
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[38] take the time to read what I wrote and you'll see the Demski's arguement hinges on "For a number of the proteins that make up the flagellum, there simply are no known homologues". [38] shows that the numbers are rubbish.eintown
March 13, 2009
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Plagiarize? No fellows, I did the experiments myself!! Obviously I took the info from othersites. Its plagirism when you pass the info as your own original work. The response I got when I referenced a couple of papers was "read it yourself". SO i post a summary and I get accused of plagirism. So cute. Attack me rather than the data. And please, PLEASE can the people who are in their "20s, in college, and working on degrees in science" identify themselves!eintown
March 12, 2009
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"And its funny how the creationist have now fallen silent after I took the time to write up that stuff which they were whining for!" Yes, I am sure it took you plenty of time to plagiarize Matzke. *eyeroll*Lord Timothy
March 12, 2009
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jerry, "We should just thank Eintown for his performance here. It is people like him who are our best advertisments for ID." I most certainly agree with you. He seems to clearly demonstrate the utter vacuity of the rhetoric among some of these critics. eintown, "Because I have nothing better to do than fight with middle aged creationists." What about those in their 20s, in college, and working on degrees in science? Oh also, about your origin of the flagellum, paraphrasing without citing a source is also called plagiarism. Especially when you use soo many of the same words. http://www.talkdesign.org/faqs/flagellum.html Your text compared with Matzke's: "begin(s) with a passive, (somewhat general inner) membrane pore 1 Begin with a passive membrane pore (1a) that is converted to a more substrate-specific pore - (1b) Interaction of an F1F0-ATP synthetase 2 Pore becomes substrate specific - couples with a synthetase. (1c). Addition of a secretin which associates with the cytoplasmic ring 4 . Associate with secretin, has secretory function. (3a) Oligomerization of the adhesin produces a pentameric ring, allowing more surface adhesins without blocking other secretion substrate 5. Oligomerization allows more surface adhesins without blocking other secretion substrates. (3b). Polymerization of this ring produces a tube, a primitive type III pilus 6. Polymerization leads to primitive pilus. (4a)Oligomerization of a pilin produces the cap, increasing assembly speed and efficiency 7. Further oligomerization and duplication increases the efficiency and strength This has already been adequately addressed. http://www.arn.org/docs/dembski/wd_biologusubjunctive.htm "But now that I have raised some technical points, the reaction is going to be predictable: “Behe/Demski/Luskin have eloquently responded to those objections”. “While the majority of the genes/parts are explained SOME are not”. So again, I’ll ask, what is the point of bringing that up??" You also misunderstand the argument completely, it is about the plausibility of transitioning between each step. Not about manufacturing a narrative. Matzke's and your responses are an adventure in missing the point.Lord Timothy
March 12, 2009
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And DLH your post which references my post 31, had NOTHING to do with it. And its funny how the creationist have now fallen silent after I took the time to write up that stuff which they were whining for!eintown
March 12, 2009
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That "10^20" rubbish has been so thoroughly debunked! That number only comes about when the events have to happen simultaneously. Which they dont!eintown
March 12, 2009
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What the hell does “hand waving” actually mean, and why do creationists think its some super smart argumentative technique?? 1) Why introduce ‘bits’ into the discussion, why do you even justify the ‘2.1’. 2) Wow, big numbers always seem to scare creationists. Do you know that once a day something with a probability of 1 in 6 billion/day happens more than 6 times??? 3) So all mutations are deleterious? ALL? Then why has life been going along happily for billions of years. For eg: Viruses, like HIV exhibit EVERY possible mutation within each population. But, why pray tell, is HIV or any highly mutable RNA retrovirus in existence. Surely they would just ‘degrade’ into extinction. Why do so many random mutations in HIV lead to beneficial properties like drug resistance?eintown
March 12, 2009
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George L Farquhar at 32
I think you’ll find that not all of “DNA space” is searched. Only the parts adjacent to where the organism already is can be searched. This removes the “DNA space is too large to search in a random manner” . . .
Try explaining that one to any mathematics prof., statistician, or actuarian. Casino's would love to have your play at their tables. "Only searching adjacent space" only shows how much more difficult and slow is the process.
How slow is this “degrading” that it’s unnoticiable? When would we expect to see the first effects?
Start with OMIM ® - Online Mendelian Inheritance in Man ® It currently has some 19,319 entries. As of November 26, 2008, Hamosh & Sutland noted: "Total # of mutations catalogued in OMIM >16,667" You are a walking example of some of them. (No beneficial mutations yet that I know of.) Perhaps you should read Sanford. You might find him enlightening and informative. The implications of the Mathematics of Evolution are fascinating once you pull together the major theories and apply them with practical numbers. PS Sanford invented the Gene Gun. Whether I personally believe any of that is irrelevant to the challenge of showing how abiogenesis and neo-Darwinian evolution to present complexity are but "Just so stories". (PS I really enjoyed reading Kipling growing up. Darwin's stories are equally laughable. I especially like Darwin's How the whale learned to swim.
"In North America the black bear was seen . . . swimming for hours with widely open mouth, thus catching, like a whale, insects in the water. Even in so extreme a case as this, if the supply of insects were constant, and if better adapted competitors did not already exist in the country, I can see no difficulty in a race of bears being rendered . . . more and more aquatic in their structure and habits, with larger and larger mouths, till a creature was produced as monstrous as a whale"
Storyteller: Charles Darwin, Origin of Species, First edition (Not in the 6th edition)DLH
March 12, 2009
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eintown at 31 1) Take your 20 proteins, calculate the number of nucleotides, then calculate the probabilities of arriving at a particular configuration de novo. Average gene length in Chromosome 1 ~ 2510 bp. e.g., 20 genes * 2500 ~ 50,000 bp. or 16,667 codons. For argument's sake conservatively assume only 2.1 bits/amino acid site for just known residues/codon. See: Yockey Information Theory, Evolution, and the Origin of Life, 92005) Table 6.3 (Compare Yockey's calculation of 3.38 bits for all residues. Table 6.3) PS. I highly recommend Yockey for your edification in matters biochemical and problematic. 16,667 codons * 2.1 bits ~ 35,000 bits. Time from formation of oceans to origin of life ~ 2*10*8 years or 6.3*10^15 seconds. Yockey p 95. When you get tired of hand waving, perhaps you could explain how you obtain 50,000 bp de novo or 35,000 bits in 6.3*10^15 seconds. You might start by converting that to powers of 10. Note Behe's review that empirical fact of the difficulty of coming up with just 2 necessary mutations is about 10^20. Compare that challenge with the maximum probabilities of taking all particles times all time at the fastest rate possible. i.e. < 10^120. Even if I have have made gross mistakes, I am all ears to hear how you show any rational probability of arriving at your hypothesized method using stochastic processes. ps some risk their $ on races with probabilities down to 1 in 100. ~10^2. Some on Powerballs: The probability of matching 5 white balls and one powerball is 195,249,054 or ~2*10^8.DLH
March 12, 2009
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DLH
You don’t understand the time/space probability demands of randomly searching through DNA space for the hundreds of necessary mutations.
I think you'll find that not all of "DNA space" is searched. Only the parts adjacent to where the organism already is can be searched. This removes the "DNA space is too large to search in a random manner" objection so often used on this board.
Sanford cites the population models developed by ardent evolutionists to show that “natural mutation” overwhelms any “selection”, resulting in steadily degrading genomes.
And yet bacteria, who have many many generations in a year are still around. How slow is this "degrading" that it's unnoticiable? When would we expect to see the first effects? Did the bacteria that gained the ability to digest Citrate in the Lenski study "degrage"? And if everything is "degrading" that must mean it started from a more ordered or perfect state. Tell me DLH, do you believe in a literal garden of Eden, and the fall of man etc? Did meat eating animals eat flowers before the fall? Do you believe all that?George L Farquhar
March 11, 2009
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Because I have nothing better to do than fight with middle aged creationists. 1. Begin with a passive membrane pore. 2. Pore becomes substrate specific - couples with a synthetase. 4. Associate with secretin, has secretory function. 5. Oligomerization allows more surface adhesins without blocking other secretion substrates. 6. Polymerization leads to primitive pilus. 7. Further oligomerization and duplication increases the efficiency and strength. 8. Further duplication produce the axial proteins. 9. Structural instability increases rotation. 10. Couple more steps I’ve missed and you end up with the good ‘ol flagellum. ID claims: “The TTSS (secretory system) is after all much simpler than the flagellum. The TTSS contains ten or so proteins that are homologous to proteins in the flagellum. The flagellum requires an additional thirty or forty proteins, which are unique” This means say the IDists the flagellum could not have evolved stepwise. Too many parts are unique. BUT. One then glances over the research done on flagella (indecently conducted by evil evolutionists) and we see that there are 42 proteins, with only 15 (35%) being unique! Which is FAR less that the 80% claimed. So stepwise evolution is possible. And how did the genes come about? BLASTing (look it up) has show significant homology between more than 20 of the genes, suggesting a common ancestor. However lateral gene transfer may have played a large role. Also IDist claim 40 proteins are required for the flagellum to function. The number is however at 20. So there are very few unique genes as the majority arose through duplication and then divergence. The number of essential and required parts is far lower than IDist claim. So it appears as if the flagellum did not did arise out of nowhere but slowly evolved piece by piece, with the majority of the genes traced together and clearly linked. But now that I have raised some technical points, the reaction is going to be predictable: “Behe/Demski/Luskin have eloquently responded to those objections”. “While the majority of the genes/parts are explained SOME are not”. So again, I’ll ask, what is the point of bringing that up??eintown
March 11, 2009
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Lord Timothy, Don't try to refute Eintown. He is a typical anti ID person. So he is playing his part perfectly. None have any information so they have to bluff it somehow. We should just thank Eintown for his performance here. It is people like him who are our best advertisments for ID.jerry
March 11, 2009
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