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Media Mum about Deranged Darwinist Gunman

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John West of the Discovery Institute Reports:

But when a gunman inspired by Darwinism takes hostages at the offices of the Discovery Channel, reporters seem curiously uninterested in fully disclosing the criminal’s own self-described motivations. Most of yesterday’s media reports about hostage-taker James Lee dutifully reported Lee’s eco-extremism and his pathological hatred for humanity. But they also suppressed any mention of Lee’s explicit appeals to Darwin and Malthus as the intellectual foundations for his views. At least, I could find no references to Lee’s Darwinian motivations in the accounts I read by the New York Times, the Los Angeles Times, the Washington Post, ABC, CNN, and MSNBC.

Major Media Spike Discovery

Comments
Now Now Indium, 'exploded' is such a real world term, let's put your 'evolutionary mechanism' glasses on see what happened, your IM probably had a random mutation that is right now at this very Instant (pun intended) being selected for a new higher level function in your computer's program! In fact in 'evolutionary mechanism land' you just got a free upgrade from Microsoft!!! 8)bornagain77
September 13, 2010
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There, you did it. My IM exploded. Was to be expected I guess.Indium
September 13, 2010
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Indium you state: "Since your tornado approach is a straw man (see above) and does not take into account evolutionary mechanisms it is not worth discussing." Let me fix this statement for you since you mis-wrote it: "Since your sure-footed approach is a valid example of reality (see above at your post) and does not take into account my imaginary evolutionary mechanisms that exist in my fantasy world it is not worth discussing." There you go Indium,, all better now! 8)bornagain77
September 13, 2010
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gpuccio: Oh, defensive mood? I did not want to ruin your day, my apologies! @151: Only when people want red herrings dragged across the track of truth and led out to hominem oil soaked strawmen ignited to cloud, choke, confuse, poison and polarise the atmosphere. (Cheers to kairosfocus, too!) @ba77: Since your tornado approach is a straw man (see above) and does not take into account evolutionary mechanisms it is not worth discussing.Indium
September 13, 2010
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Here is a direct reference for the e-coli quote: http://books.google.com/books?id=yNev8Y-xN8YC&pg=PA104&lpg=PA104&dq=a+one-celled+bacterium,+e.+coli,+is+estimated+to+contain+the+equivalent+of+100+million+pages+of+Encyclopedia+Britannica.+Expressed+in+information+in+science+jargon,+this+would+be+the+same+as+1012+bits&source=bl&ots=af595iZHH8&sig=uIFAYhd9WlHFybMNL4pyzYn4rn0&hl=en&ei=qjOOTJ7CNs_vngeeudWpCg&sa=X&oi=book_result&ct=result&resnum=2&ved=0CBgQ6AEwAQ#v=onepage&q=a%20one-celled%20bacterium%2C%20e.%20coli%2C%20is%20estimated%20to%20contain%20the%20equivalent%20of%20100%20million%20pages%20of%20Encyclopedia%20Britannica.%20Expressed%20in%20information%20in%20science%20jargon%2C%20this%20would%20be%20the%20same%20as%201012%20bits&f=falsebornagain77
September 13, 2010
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I don’t discuss things “in principle”.
Actually you do it all the time. You assert that evolution has been managed by design, that both mutations and selection have been influenced by design. You cannot cite any examples of this happening. No one has ever observed it happening. No one is willing to characterized the designer or the designer's methods or capabilities. So your argument boils down to saying that a process that can be observed and which can be subjected to controlled experimentation is less plausible that a process that has never been observed.Petrushka
September 13, 2010
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Well Indium you state my monkey's example is not 'how evolution works' but alas you provided zero evidence for evolution doing anything at all, besides your imaginative speculation for how it should work. Actually I felt my 'empirical test' of monkeys in a zoo was far closer to reality than any of the 'possible' speculations you have ever presented. Do you disagree that you are making the absurd claim that blind processes have produced more information than the library of congress? "Again, this is characteristic of all animal and plant cells. Each nucleus ... contains a digitally coded database larger, in information content, than all 30 volumes of the Encyclopaedia Britannica put together. And this figure is for each cell, not all the cells of a body put together. ... When you eat a steak, you are shredding the equivalent of more than 100 billion copies of the Encyclopaedia Britannica." (Dawkins R., "The Blind Watchmaker [1986], Penguin: London, 1991, reprint, pp.17-18. Emphasis in original) http://members.iinet.net.au/~sejones/PoE/pe08clml.html “a one-celled bacterium, e. coli, is estimated to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 1012 bits of information. In comparison, the total writings from classical Greek Civilization is only 109 bits, and the largest libraries in the world - The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library - have about 10 million volumes or 1012 bits.” - R. C. Wysong http://www.why-the-bible.com/origins.htm “an attempt to explain the formation of the genetic code from the chemical components of DNA… is comparable to the assumption that the text of a book originates from the paper molecules on which the sentences appear, and not from any external source of information.” Dr. Wilder-Smith Indium that you would argue about whether it is possible that protein could have perhaps. maybe. possibly, changed into another protein illustrates how completely disconnected you are from the real world for material processes have NEVER demonstrated the ability to produce ANY information, must less endless library shelfs full of information that exceeds man's ability to encode information: notes: The Coding Found In DNA Surpasses Man's Ability To Code - Stephen Meyer - video http://www.metacafe.com/watch/4050638 The Capabilities of Chaos and Complexity: David L. Abel - Null Hypothesis For Information Generation - 2009 To focus the scientific community’s attention on its own tendencies toward overzealous metaphysical imagination bordering on “wish-fulfillment,” we propose the following readily falsifiable null hypothesis, and invite rigorous experimental attempts to falsify it: "Physicodynamics cannot spontaneously traverse The Cybernetic Cut: physicodynamics alone cannot organize itself into formally functional systems requiring algorithmic optimization, computational halting, and circuit integration." A single exception of non trivial, unaided spontaneous optimization of formal function by truly natural process would falsify this null hypothesis. http://www.mdpi.com/1422-0067/10/1/247/pdf Can We Falsify Any Of The Following Null Hypothesis (For Information Generation) 1) Mathematical Logic 2) Algorithmic Optimization 3) Cybernetic Programming 4) Computational Halting 5) Integrated Circuits 6) Organization (e.g. homeostatic optimization far from equilibrium) 7) Material Symbol Systems (e.g. genetics) 8) Any Goal Oriented bona fide system 9) Language 10) Formal function of any kind 11) Utilitarian work http://mdpi.com/1422-0067/10/1/247/ag Stephen C. Meyer - The Scientific Basis For Intelligent Design - video http://www.metacafe.com/watch/4104651 The DNA Enigma - Where Did The Information Come From? - Stephen C. Meyer - video http://www.metacafe.com/watch/4125886 The Capabilities of Chaos and Complexity - David L. Abel - 2009 Excerpt: "A monstrous ravine runs through presumed objective reality. It is the great divide between physicality and formalism. On the one side of this Grand Canyon lies everything that can be explained by the chance and necessity of physicodynamics. On the other side lies those phenomena than can only be explained by formal choice contingency and decision theory—the ability to choose with intent what aspects of ontological being will be preferred, pursued, selected, rearranged, integrated, organized, preserved, and used. Physical dynamics includes spontaneous non linear phenomena, but not our formal applied-science called “non linear dynamics”(i.e. language,information). http://www.mdpi.com/1422-0067/10/1/247/pdf The DNA Code - Solid Scientific Proof Of Intelligent Design - Perry Marshall - video http://www.metacafe.com/watch/4060532 etc.. etc.. etc.. Indium it is completely ludicrous for you to pretend you are being reasonable by saying material processes can generate information when the fact is that you clearly dwell in a self-imposed fantasy land in which reality is never allowed to ruin your delusions.bornagain77
September 13, 2010
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Indium: As usual, you jump to conclusions. For my beers, I am more picky.gpuccio
September 13, 2010
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So, everybody is happy and we can finally have a beer together! Cheers!Indium
September 13, 2010
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Indium #149: Those are classical scenarios which have been used in discussions. And I agree tha "it is just not the way evolution works". Evolution (the darwinian type) simply does not work at all :) .gpuccio
September 13, 2010
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Indium: I am happy that you are happy of the exchange. You can remain with your happiness. I will remain with my well argued convictions. Lupas has shown a pathway? Would that be: "The similarity means that it is likely that the type I and type II phosphatases share a common ancestor. One possibility is that tandem duplication of an ancestral phosphatase domain and subsequent N- and C- terminal truncation lead to a permuted variant by a mechanism that has been well described elsewhere" Thanks God, you are not im my position and I am not in yours. So, each one of us can be happy, even if for very different motives. I wish you the best, my friend. After all, "in principle" you could even be right...gpuccio
September 13, 2010
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bs77: You are very fond of the tornado in the junkyard scenario (or monkey and typewriter). Sorry, nobody else is, since by definition it is just not the way evolution works.Indium
September 13, 2010
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Indium you state: "I have met your demand for a possible pathway from one group in the SCOP database to another" ,,,And its possible a infinite number of monkey's banging away at typewriters produced the entire library of congress, but can you empirically demonstrate it to be plausible: Monkey Theory Proven Wrong: Excerpt: A group of faculty and students in the university's media program left a computer in the monkey enclosure at Paignton Zoo in southwest England, home to six Sulawesi crested macaques. Then, they waited. At first, said researcher Mike Phillips, “the lead male got a stone and started bashing the hell out of it. “Another thing they were interested in was in defecating and urinating all over the keyboard,” added Phillips, who runs the university's Institute of Digital Arts and Technologies. Eventually, monkeys Elmo, Gum, Heather, Holly, Mistletoe and Rowan produced five pages of text, composed primarily of the letter S. Later, the letters A, J, L and M crept in — not quite literature. http://www.arn.org/docs2/news/monkeysandtypewriters051103.htm The Universal Plausibility Metric (UPM) & Principle (UPP) - Abel - Dec. 2009 Excerpt: Mere possibility is not an adequate basis for asserting scientific plausibility. A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, "Yes.",,, c?u = Universe = 10^13 reactions/sec X 10^17 secs X 10^78 atoms = 10^108 c?g = Galaxy = 10^13 X 10^17 X 10^66 atoms = 10^96 c?s = Solar System = 10^13 X 10^17 X 10^55 atoms = 10^85 c?e = Earth = 10^13 X 10^17 X 10^40 atoms = 10^70 http://www.tbiomed.com/content/6/1/27 Probability's Nature and Nature's Probability: A Call to Scientific Integrity - Donald E. Johnson Excerpt: "one should not be able to get away with stating “it is possible that life arose from non-life by ...” or “it’s possible that a different form of life exists elsewhere in the universe” without first demonstrating that it is indeed possible (non-zero probability) using known science. One could, of course, state “it may be speculated that ... ,” but such a statement wouldn’t have the believability that its author intends to convey by the pseudo-scientific pronouncement." http://www.amazon.com/Probabilitys-Nature-Natures-Probability-Scientific/dp/1439228620 Could Chance Arrange the Code for (Just) One Gene? "our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236)." http://www.creationsafaris.com/epoi_c10.htmbornagain77
September 13, 2010
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Lupas explains a rather simple evolutionary pathway between proteins which are in distinct groups in the SCOP database, exactly what you wanted. This is not a "mere logical deduction", it is a clear und relatively simple evolutionary pathway, demonstrating that there are indeed evolutionary bridges between the SCOP groups, exactly what you denied. I aggree that Lupas in other parts of the paper tries to speculate a bit, yes. So what? So far, I am very happy about this exchange: We have established that evolution can add information to genomes. We have seen that microevolutionary changes can lead to completely different changes in protein function and 3D structure, which makes microevolution extremely powerful, almost macroevolutionary... ;-) I have met your demand for a possible pathway from one group in the SCOP database to another, clearly demonstrating that the task for evolution can be much simpler than finding precise sequences of amino acids by random chance (which is basically the Axe-thesis). This is also why I am not convinced by the Axe paper: He doesn´t cite the relevant literature which demonstrates that nature does not have to search for new protein domains on an AA per AA basis. To be honest, if I were in your position now, I would not go the "This is not evidence!" and "Where you there?" way. I don´t think that you would be in a scientifically interesting position ones you go there...Indium
September 13, 2010
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Indium: how different folds in the SCOP database can in principle (which is what you deny!) be reached by evolutionary processes? I have never affirmed that one thing cannot happen "in principle". I don't discuss things "in principle". I have specified hundreds of times that my discussion is about empirical evidences, not logical deductions. So, you are mistaken. From my post #112 which answered your post #110: "3) “In principle”, stranger things are possible. ID is not about what is impossible “in principle” (ID theory is not a mathematical deduction). ID, and empirical science, is instead, about what is “empirically” impossible (or possible, or likely). If you are not interested in empirical science, it’s your option. Why do darwinists start imagining things when they have no more arguments? And I state again that IMO the paper you linked gives no convincing empirical argumantes. You are free to think differently. And I would be happy if you argued about the Axe paper for what it says, instead of criticizing the journal or invoking peer to peer censorship. I am for ideas, not for authority.gpuccio
September 13, 2010
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BTW, as a reviewer I wouldn´t have let Axe publish his paper without citing Lupas (cited over 100 times, which is a LOT in this field), Taylor etc. It is a mystery how this could happen. What kind of journal is this? It seems there are only two articles published in the whole history of Bio-Complexity!?Indium
September 13, 2010
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gpuccio, in which way does “Our inspection confirms a report that type I and type II phosphatases, partitioned into different folds in SCOP, are in fact related through a circular permutation (Fauman et al., 1998; Grishin, 2001b).” not constitue evidence for how different folds in the SCOP database can in principle (which is what you deny!) be reached by evolutionary processes? Is this now a kind of "Where you there?" argument?Indium
September 13, 2010
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Indium: the paper you link is pure wishful thinking. It proves absolutely nothing. It is a vague theory, with no evidence at all. It does not support any credible origin of protein domains, any more than all the paper about an RNA world demostrate that such a thing ever existed. Do you really believe that only because someone publishes a vague theory and supports it with vagut abstract considerations that theory is credible? The difficulties I have pointed to are objectively there, and unexplained by current models. "Arguments" such as: "One possibility is that tandem duplication of an ancestral phosphatase domain and subsequent N- and C- terminal truncation lead to a permuted variant by a mechanism that has been well described elsewhere" or: "The numerous instances of local sequence and structure similarities within different protein folds, together with evidence from proteins containing sequence and structure repeats, argues in favor of the evolution of modern single polypeptide domains from ancient short peptide ancestors (antecedent domain segments (ADSs)). In this model, ancient protein structures were formed by self-assembling aggregates of short polypeptides. Subsequently, and perhaps concomitantly with the evolution of higher fidelity DNA replication and repair systems, single polypeptide domains arose from the fusion of ADSs genes. Thus modern protein domains may have a polyphyletic origin." are the usual fairy tales to which we are unfortunately accustomed. The truth is: the Rna world, self-assembling aggregates of short polypeptides, and similar speculations are entities which have never been observed, and that, for all we know, have never existed and never will exist.gpuccio
September 13, 2010
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gpuccio, I hate to repeat myself but what you ask can be found in the aticles I linked to. For example: "Our inspection confirms a report that type I and type II phosphatases, partitioned into different folds in SCOP, are in fact related through a circular permutation (Fauman et al., 1998; Grishin, 2001b)." http://www.sdsc.edu/~shindyal/ejc020204.pdf I will have a look at the Axe paper again, thank you for the link.Indium
September 11, 2010
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Indium: I think you misunderstand what I say. Proteins are classified in fundamental separate 3D foldings. In SCOP classification, as I mentioned, the grouping according to "folds" includes at present 1195 different groups. My number of 6000, always derived from the SCOP classification, was based on a less than 10% homology between the groups. I believe that both criteria can point to isolated islands of functionality. For now, just for clarity, let's stick to the more restricitve one: folds according to the SCOP classification. My point is very simple, and I am surprised that you still don't fet it: when I speak of attaining a bew fold, I mean attaining a transition to a different fundamental group. If we use the "folds" classification, from one of the 1195 groups to another. If we use the 6000 sequence based classification, form one of the 6000 groups to another. Is that clear? Your examples are examples where the 3D fold changes a little, or a little more, but certainly does not deviate substantially from the initial fold, or if it does, it certainly does not achieve the functional fold in a new group, nor can at any level be considered "a step" in that direction. SAo, in no way your examples represent a transition, even partial, from one know functional fold grouping to another, unrelated one. Which was what I was requesting in my scenario. And why am I requesting that? It's simple: my argument is that we have many fundamental islands of functionality in the existing proteome. Those islands are those fundamental folds, or superfamilies, or unrelated families, according to the modality of grouping we choose. Always according to the grouping, the number of these fundamental functional units in the proteome is at present of about 1195 (folds) to 6000 (groups unrelated at primary sequence level). This is not an upper limit to anything: it is however the result of the search for functional structures in the 4 billion years of evolution, whatever the mechanism (darwinian or designed) by which those results were obtained. Moreover, there are many aspects of the modality of appearance of those functional units which suggest (at least IMO) that most of the functional structures useful in the biological context have probably been already found. That's an interesting aspect, and we can discuss it in more detail if you want. So, none of your examples is relevant to the discussion I have been doing with you (and that, it seems, you have not followed). I am not interested in evidence that mutations can change the folding of a protein: that's obvious. I state that simple random mutations cannot effect the transition from a folding functional group to another one. And anyway, just to understand better what I mean, why don't you read the paper by Axe, "The Case Against a Darwinian Origin of Protein Folds" which is exactly about this topic? Here is the link: http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.1gpuccio
September 11, 2010
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gpuccio, before I enjoy the rest of my weekend a quick reply, because there are a few things I don´t understand about your answers: In which way is the number of protein domains an upper limit to the number of possible fitness-positive changes to the genome of an organism? Secondly, in the examples discussed in the papers I linked to, all of the evolved proteins with a new folding have a function. Did you really read the papers? You can find exactly what you asked for: New folding domains combined with new functions and possible paths of evolution. And finally: You seem to think that evolution cannot achieve changes to the genome that enable it to generate a comletely new folding of a resulting protein. Therefore it is a bit of a mystery to me that you don´t see the relevance of my first example: Sometimes evolution doesn´t even have to evolve anything to generate a new protein folding! A few changes in solution parameters are enough. With these findings (and combined with the other papers) your position that the barriers between different protein foldings are uncrossable by evolution is untenable.Indium
September 11, 2010
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Yours is a gross representation...
The words I used are yours. There is no way to reconcile the published articles with your interpretation except to conclude that the authors are seriously wrong, or you mischaracterize them. The only difference between artificial and natural selection is that natural selection operates on all traits simultaneously, favoring the best balance for survival and reproduction. Artificial selection, as with animal and plant breeding, is often narrowly focused and produces individuals that would not survive without human assistance. I believe you suggested that the designer may tweak mutations as well as selection. I find this to be silly. No one has ever observed mutations that anticipate need, and plenty of researchers have looked. It would be an interesting research project for ID advocates, but I haven't seen any such research proposed.Petrushka
September 10, 2010
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Yours is a gross representation, not so much of ID, but certainly of the personal arguments which I have many times expressed to you.
Perhaps it is, but I think you misrepresent the papers you interpret. You essentially characterize Nobel Prize winners as either liars or incompetents. You characterize the people who publish research on protein evolution as either dishonest or unable to correctly interpret their own work. that's a pretty serious allegation.Petrushka
September 10, 2010
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Petrushka: Yours is a gross representation, not so much of ID, but certainly of the personal arguments which I have many times expressed to you. I have many times defined and discussed in detail the differences between natural selection and artificial selection, and it wwas not certainly the gross sillines that you state. And when I have said that a certain paper seemed to me abstract or inconclusive, it was because that was exactly my judgement about that specific paper. Good night to you.gpuccio
September 10, 2010
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It strikes me that the most cogent argument made so far for ID amounts to declaring that anything learned about mutation and selection in a laboratory setting is either abstract and inclusive, or an instance of design because the selection is artificial. It would seem that evolution is the first branch of science for which research is, by definition, impossible.Petrushka
September 10, 2010
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MathGrrl (#130). I agree with this post, with the following specifications: 1) I maintain that all empirical sciences are about what is empirically possible, and not about what is possible "in principle". 2) I maintain that the computation of the functional information of a protein is the only way to know how much functional information musty be created by the proposed models for its emergence, be they purely random, part chance and part necessity, or design based. What you call "the evolutionary history" of the protein must necessarily be part of the model, and explicitly. And the model, including the "evolutionary history", must be causally explanatory. That said, let's go to your #131: First, the reason for my use of scare quotes around “functional information”. While I’m getting a better feel for what you mean by this term, you have still not provided a mathematical definition that will allow me to calculate it on my own for a particular biological system. You’ve told me that it isn’t Shannon Information nor is it Kolmogorov Complexity, but you haven’t actually said what it is. I don't think that's true. I have said it many times, to you and others, and with various details. Briefly: a) I have never referred to CSI of a whole system. In my examples, I have always referred to CSI of single proteins, indeed of single protein domains. I have explained many times why. Essentially, it's easier and sufficient for our purposes. b) I use the specific subset of CSI which I call dFSCI: digital strings bearing information which is functionally specified. Genes and proteins are of that kind, so nothing is lost in the restriction. c) dFSCI is the non compressible (or scarcely compressible) information in the functionally specified string, computed as the ratio between the functional space and the search space. A practical method to approximate that ratio is to compute the uncertainty reduction in a protein family vs a random sequence, according to the Durston method, which computes the difference in Shannon's entropy H between the functional sequences in a family and a random sequence. Please see the Durston paper for the details. The method can also be applied to transitions. You say: Contributing to the definition problem is the ambiguity surrounding the “specification” issue. The amount of “functional information” in a system can vary greatly depending on how the function is specified. There seem to be no clear, unambiguous guidelines on what constitutes a valid specification. If the specification is subjective, CSI is useless as a scientific concept. I have discussed this point many times. Funtional specification is not subjective, but it can be recognized and defined only by a conscious intelligent observer. For the specification to be valid, it must however be defined objectively, and a method must be given to measure if it is present or not. If different specifications can be given for some object or system, the value of CSI will refer to the explicit specification which is given. There is nothing subjective in that: we measure a property in relation to another property. Anyway, for proteins usually the specification is absolutely obvious, if known, and corresponds to the biochemical function of the protein. Although the function of the single protein almost always is part of a higher level network of functions, for a primary analysis we must stick to the lower level function, the biochemical activity. In most cases, we can fix a conventional threshold of minimal activity, which can be measured in any lab. The definition of the function of many proteins can be easily found in protein databases. For the proteins we find in the proteome, the specification is not a problem at all: they are specified. We know their function, and we know that that function is necessary in their biological context. So, the only problem is to measure the functional complexity. Therfore, CSI is certainly not "useless as a scientific concept". A step-by-step rigorous calculation of CSI for a real world biological system would eliminate these questions and let us get to the next stage of actually testing your claims regarding CSI. A "real world biological system" is the existing proteome. We can calculate the CSI in the existing protein superfamilies. Durston has done that. And, we can calculate the CSI in any proposed transition in any explicit model for the emergence of any part of the proteome. Obviously, if darwinist do not give any explicit model for the emergence of a protein domain, we cannot calculate the CSI of a non defined transition. But for all proposed model of which we know enough detail, that can be done. It's a pity that the models darwinists propose explicitly are microevolutionary, and that their inherent functional information is always really low. Regarding the immune system and the proposed literature, I have begged for time, and I do that again. I have been rather busy here, as you can see, and my time resources are not infinite. But please believe that I am really interested to that subject, and that I have myself suggested many times some aspects of the immune system as very good examples of intelligentlòy designed algorithms. Regarding frameshift mutations, my point is very simple: the only frameshift mutation proposed in detail as a source of new functional information is, as far as I know, Ohno's model for nylonase. As it was detailed and explicit from the beginning (a great merit), it has been in time subjected to verification, and found false.gpuccio
September 10, 2010
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Arthur Hunt: I know well who you are, and I am honored that you are back here. I have great esteem of your competence, even if I may disagree with you on many points. Regarding what you say, you are obviously right, but I have probably expressed my thought without the due precision, confiding that the context of the discussion could make my point clear enough. I apologize if I have not been completely precise. I said: "A “transition between beta-strand and alpha-helical conformation” is not a change of folding, but just a change in local secondary structure." Obviously, I did not mean that a change in secondary structure does not affect tertiary structure at all. I have clarified that also in my further answer to Indium at #133. I should have said, more explicitly: "A “transition between beta-strand and alpha-helical conformation” is not a transition form one functional folding to another, unrelated folding, but just a change in local secondary structure which can affect, usually in a negative way, the existing functional folding." I had made very clear in all my discussion with Indium that what I was speaking of was the emergence of new fundamental functional folds or superfamilies in the proteome, and Indium countered that argument with links showing that single mutations could affect secondary structure. I was therefore stating that such a concept, while obvious, was in no way a response to my argument. As I have said many times, this is a blog, and we all write often in a hurry, confiding that the general context, often repeated many many times, will clarify our meaning. But I am happy that you have taken part again to our discussions. You are always welcome.gpuccio
September 10, 2010
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Indium: Have a nice weekend you too! And, if you want, reflect on the following: 1) Secondary structure is local and relatively simple to compute. 2) Tertiary structure and folding is all another matter. While secondary structure of the various parts of the sequence is certainly one of the components, protein folding is still a vastly non computable problem (with present resources). 3) There is no doubt that a change in local secondary structure in one place can influence the general folding. Sometimes it does, usually compromising more or less the existing function. Sometimes even a single aminoacid change can completely abolish the function through serious conformational deformations. Mendelian diseases are a well known example of that. 4) What you apparently don't understand is that all the above has nothing to do with finding a new functional folding starting from an existing, unrelated functional folding. Which is the problem I have posed, and that you still are ignoring. You can lose a functional folding through one or few appropriate mutations. But you cannot find a new, unrelated folding through one or few random mutations, which is what you seem not to understand. 5) It is clear that, under different environmental conditions, proteins fold differently. And so? 6) My number of 6000 is the number of protein groups unrelated at primary structure level which you get form the SCOP database. The same database gives also the following numbers for slightly different groupings: Folds: 1195 Superfamilies: 1962 Families: 3902 I have used the 6000 number to emphasize the separation at primary level. Therefore, IMO you have none of the things you say you have established. I agree only with one phrase: "There is good science being done on the origin of protein domains. " And nothing else.gpuccio
September 10, 2010
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As to the paper for solution changing 3D structures, this finding actually argues very forcefully against the molecular reductionist (materialist) model of neo-Darwinism as is clearly illustrated here: The Case Against Molecular Reductionism - Rupert Sheldrake and Bruce Lipton - video http://www.metacafe.com/watch/4899469 further notes against genetic reductionism: New Insights Into How (Adult) Stem Cells Determine What Tissue to Become - August 2010 Excerpt: Within 24 hours of culturing adult human stem cells on a new type of matrix, University of Michigan researchers were able to make predictions about how the cells would differentiate, or what type of tissue they would become.,,, "Our research confirms that mechanical factors are as important as the chemical factors regulating differentiation," Fu said. "The mechanical aspects have, until now, been largely ignored by stem cell biologists." http://www.sciencedaily.com/releases/2010/08/100801190257.htm Electricity Forms Your Heart - July 2010 Excerpt: “The direction of growth and orientation of various cell types in tissue culture can be influenced by externally applied electric fields.” They added, “Furthermore, endogenous [inside organism] electric currents exist in a variety of tissues and have been hypothesized to influence cell migration and shape.” http://www.creationsafaris.com/crev201007.htm#20100731a The Gene Myth, Part II - August 2010 Excerpt: So even with the same sequence a given protein can have different shapes and functions. Furthermore, many proteins have no intrinsic shape, taking on different roles in different molecular contexts. So even though genes specify protein sequences they have only a tenuous influence over their functions.,,, So, to reiterate, the genes do not uniquely determine what is in the cell, but what is in the cell determines how the genes get used.,,, Only if the pie were to rise up, take hold of the recipe book and rewrite the instructions for its own production, would this popular analogy for the role of genes be pertinent. http://darwins-god.blogspot.com/2010/08/gene-myth-part-ii.html Cortical Inheritance: The Crushing Critique Against Genetic Reductionism - Arthur Jones - video http://www.metacafe.com/watch/4187488 ,,,Thus Indium, please tell me exactly how these findings are not absolutely crushing against the required molecular reduction of neo-Darwinism. Are you completely impervious to this shattering disconnect in your theory?bornagain77
September 10, 2010
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gpuccio, Now, onward to hopefully reach further understanding and agreement! First, the reason for my use of scare quotes around "functional information". While I'm getting a better feel for what you mean by this term, you have still not provided a mathematical definition that will allow me to calculate it on my own for a particular biological system. You've told me that it isn't Shannon Information nor is it Kolmogorov Complexity, but you haven't actually said what it is. Contributing to the definition problem is the ambiguity surrounding the "specification" issue. The amount of "functional information" in a system can vary greatly depending on how the function is specified. There seem to be no clear, unambiguous guidelines on what constitutes a valid specification. If the specification is subjective, CSI is useless as a scientific concept. A step-by-step rigorous calculation of CSI for a real world biological system would eliminate these questions and let us get to the next stage of actually testing your claims regarding CSI. One particular area that I think would be interesting to test your claims on is the evolution of the immune system. From our earlier posts:
I have repeatedly suggestes a context which you have always refused to comment upon: the emergence of new protein domains, of new protein superfamilies, which we know has happened repeatedly in natural history.
This is an area of very active research, based on the predictions of modern evolutionary theory, in particular the nested hierarchy. Given your interest in ID, you may be familiar with this literature: http://www.nature.com/ni/journal/v7/n5/full/ni0506-433.html This link shows the literature on the evolution of the immune system (surely a specified function by your definition) presented to Behe at the Dover trial. This is only a small subset of the information available via Pubmed and other sources. Similar amounts of data are available on the evolution of other functional systems.
I cannot answer you about the immune system now, because I have not the time. I will try to get back on that later.
Another promising area for testing is that of frameshift mutations mentioned by Petrushka above. Those might show the creation of more "functional information" than simple point mutations. Let's get quantifiable!MathGrrl
September 10, 2010
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