Evolving New Information

traderdrew responds to me:

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Proteins have specific complex shapes and their overall structures are not assembled or conform to standard Euclidean mathematics.

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"Geometry." The word you are looking for is "geometry."And where is your evidence that protein folding is non-Euclidean? Do you even know what that word means? Are you saying in the world of a protein molecule, there is something up with the parallel postulate?

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Common sense says throwing the amino acids together randomly is highly unlikely to generate functional coherence.

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And since when is chemistry "random"? When I take two moles of hydrogen gas and a mole of oxygen gas, mix them at STP, and spark the mixture, why is it that the most dominant compound that results is water and not hydrogen peroxide?As we're finding out by the examination of space, organic molecules are outrageously abundant. You can't get away from them.But even if we go along with your highly unjustifiable premise that chemical reactions happen in a "random" method, you are ignoring the sheer vastness of the universe.Let's test your math: Suppose I have darts and a dartboard. For the sake of this experiment, the probability of me hitting the dartboard is inversely proportional to the number of darts I have to begin with. That is, if I have n darts, then each dart has only a 1/n chance of hitting the dartboard.As the number of darts increases, the chances of hitting the dartboard with any given dart become quite small. Indeed, as the number of darts approaches infinity, the chance of hitting the dartboard with any given dart approaches 0.But suppose I throw them all. Given an infinite number of darts, each with an infinitesimal chance of hitting the dartboard, what is the probability that I have hit the dartboard at least once?Given a universe as large as it is, as packed to the brim with organic molecules as it is, where does this idea come from that it is extremely unlikely to have happened? Quite the opposite is true.

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How many articles do proponents of ID need?

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Well, currently they don't have any. I think the first goal is to get one. For once they manage to get that first one, other scientists can get to work in examining it, seeing how the results might relate to other phenomena, and develop a coherent theory about what ID actually does.But so far, there hasn't been a single paper produced that has ever survived review.

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There is also the subject of resistance or pressure organizations may apply against articles that support ID.

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Oh...I see. It's a grand conspiracy. Nevermind that overturning the dominant paradigm of a field would win you the Nobel Prize and have every university and laboratory in the world come banging on your door begging you to join their staff. No, the world of science of full of evil atheists who have a deep-seated, visceral, one might even say pathological hatred of "intelligent design" and would sell their own parents and children into sexual slavery in order to keep the Truth from being presented.

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I might get rhrain or (whatever he posts as)

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Um, are you in second grade? Is your argument so pathetic that the only way you can continue is to play stupid games with my name?(*le sigh*)

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If I saw him in person I would put my hand up to interrupt him and say, "All you have to do is show me or direct me to a model of how one of them evolved with a step by step Darwinian fashion."

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Already done. You have read the relevant journal articles, haven't you?-----The evolution of adaptive immunity.Pancer Z, Cooper MD.Center of Marine Biotechnology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21202, USA. pancer@comb.umbi.umd.eduApproximately 500 mya two types of recombinatorial adaptive immune systems appeared in vertebrates. Jawed vertebrates generate a diverse repertoire of B and T cell antigen receptors through the rearrangement of immunoglobulin V, D, and J gene fragments, whereas jawless fish assemble their variable lymphocyte receptors through recombinatorial usage of leucine-rich repeat (LRR) modular units. Invariant germ line-encoded, LRR-containing proteins are pivotal mediators of microbial recognition throughout the plant and animal kingdoms. Whereas the genomes of plants and deuterostome and chordate invertebrates harbor large arsenals of recognition receptors primarily encoding LRR-containing proteins, relatively few innate pattern recognition receptors suffice for survival of pathogen-infected nematodes, insects, and vertebrates. The appearance of a lymphocyte-based recombinatorial system of anticipatory immunity in the vertebrates may have been driven by a need to facilitate developmental and morphological plasticity in addition to the advantage conferred by the ability to recognize a larger portion of the antigenic world.PMID: 16551257 [PubMed - indexed for MEDLINE]-----The evolution of adaptive immune systems.Cooper MD, Alder MN.Division of Developmental and Clinical Immunology, Departments of Medicine, Microbiology, Pediatrics, and Pathology, University of Alabama at Birmingham, Birmingham, AL 35294, USA. max.cooper@ccc.uab.eduA clonally diverse anticipatory repertoire in which each lymphocyte bears a unique antigen receptor is the central feature of the adaptive immune system that evolved in our vertebrate ancestors. The survival advantage gained through adding this type of adaptive immune system to a pre-existing innate immune system led to the evolution of alternative ways for lymphocytes to generate diverse antigen receptors for use in recognizing and repelling pathogen invaders. All jawed vertebrates assemble their antigen-receptor genes through recombinatorial rearrangement of different immunoglobulin or T cell receptor gene segments. The surviving jawless vertebrates, lampreys and hagfish, instead solved the receptor diversification problem by the recombinatorial assembly of leucine-rich-repeat genetic modules to encode variable lymphocyte receptors. The convergent evolution of these remarkably different adaptive immune systems involved innovative genetic modification of innate-immune-system components.PMID: 16497590 [PubMed - indexed for MEDLINE]-----Reconstructing immune phylogeny: new perspectives.Litman GW, Cannon JP, Dishaw LJ.Department of Pediatrics, University of South Florida College of Medicine, All Children's Hospital Children's Research Institute, 830 First Street South, Saint Petersburg, Florida 33701, USA. litmang@allkids.orgNumerous studies of the mammalian immune system have begun to uncover profound interrelationships, as well as fundamental differences, between the adaptive and innate systems of immune recognition. Coincident with these investigations, the increasing experimental accessibility of non-mammalian jawed vertebrates, jawless vertebrates, protochordates and invertebrates has provided intriguing new information regarding the likely patterns of emergence of immune-related molecules during metazoan phylogeny, as well as the evolution of alternative mechanisms for receptor diversification. Such findings blur traditional distinctions between adaptive and innate immunity and emphasize that, throughout evolution, the immune system has used a remarkably extensive variety of solutions to meet fundamentally similar requirements for host protection.PMID: 16261174 [PubMed - indexed for MEDLINE]-----On the origins of the adaptive immune system: novel insights from invertebrates and cold-blooded vertebrates.Kasahara M, Suzuki T, Pasquier LD.Department of Biosystems Science, School of Advanced Sciences, The Graduate University for Advanced Studies (Sokendai), Shonan Village, Hayama 240-0193, Japan. kasahara@soken.ac.jpWhen and how adaptive immunity emerged is one of the fundamental questions in immunology. Accumulated evidence suggests that the key components of adaptive immunity, rearranging receptor genes and the MHC, are unique to jawed vertebrates. Recent studies in protochordates, in particular, the draft genome sequence of the ascidian Ciona intestinalis, are providing important clues for understanding the origin of antigen receptors and the MHC. We discuss a group of newly identified protochordate genes along with some cold-blooded vertebrate genes, the ancestors of which might have provided key elements of antigen receptors. The organization of the proto-MHCs in protochordates provides convincing evidence that the MHC regions of jawed vertebrates emerged as a result of two rounds of chromosomal duplication.PMID: 15102370 [PubMed - indexed for MEDLINE]-----New insights into the genomic organization and origin of the major histocompatibility complex: role of chromosomal (genome) duplication in the emergence of the adaptive immune system.Kasahara M.Department of Biochemistry, Hokkaido University School of Medicine, Sapporo, Japan. kasahara@hucc.hokudai.ac.jpRecently, it became clear that the human and mouse genomes contain at least three regions paralogous to the major histocompatibility complex (MHC) region. This observation led us to the proposal that the MHC region emerged as a result of chromosomal duplication that took place at an early stage of vertebrate evolution. Here I briefly review this proposal. Accumulating evidence indicates that (a) genome-wide duplication(s) took place close to the origins of vertebrates. Taking this and others into account, I suggest that the duplication(s) involving the MHC region probably took place as a part of the genome-wide duplication(s). The human T cell receptor (TCR) and immunoglobulin (Ig) genes also appear to be located on paralogous chromosomal segments. These findings raise the possibility that the genome-wide duplication provided a major impetus not only to the emergence of the full-fledged MHC system, but also to the appearance of other key molecules of the adaptive immune system such as TCR and Ig.PMID: 9420471 [PubMed - indexed for MEDLINE]-----Mechanisms of antigen receptor evolution.Eason DD, Cannon JP, Haire RN, Rast JP, Ostrov DA, Litman GW.Department of Pediatrics, Children's Research Institute, University of South Florida College of Medicine, 830 First Street South, St. Petersburg, FL 33701, USA.The adaptive immune system, which utilizes RAG-mediated recombination to diversify immune receptors, arose in ancestors of the jawed vertebrates approximately 500 million years ago. Homologs of immunoglobulins (Igs), T cell antigen receptors (TCRs), major histocompatibility complex (MHC) I and II, and the recombination activating genes (RAGs) have been identified in all extant classes of jawed vertebrates; however, no definitive ortholog of any of these genes has been identified in jawless vertebrates or invertebrates. Although the identity of the "primoridal" receptor that likely was interrupted by the recombination mechanism in the common ancestor of jawed vertebrates may never be established, many different families of genes that exhibit predicted characteristics of such a receptor have been described both within and outside the jawed vertebrates. Various model systems point toward a range of immune receptor diversity, encompassing many different families of recognition molecules, including non-diversified and diversified Ig-type variable (V) regions, as well as diversified VJ domains, whose functions are integrated in an organism's response to pathogenic invasion. The transition from the primordial antigen receptor to the monomeric Ig-/TCR-like domain and subsequent antigen-specific heterodimer likely involved progressive refinement of unique intermolecular associations in parallel with the acquisition of combinatorial diversity and antigen-specific recognition through somatic modification of the V region. RAG-mediated recombination and associated junctional diversification of both Ig and TCR genes occurs in all jawed vertebrates. In the case of Igs, somatic variation is expanded further through class switching, gene conversion, and somatic hypermutation. Various approaches, including both genomic and protein functional analyses, currently are being applied in jawless vertebrates, protochordates and other invertebrate deuterostome model systems in order to examine both RAG-mediated and alternative forms of antigen receptor diversification. Such studies have uncovered previously unknown mechanisms of generating receptor diversity.PMID: 15522620 [PubMed - indexed for MEDLINE]----And that was without even trying. When are you going to start doing your homework?Basically, your argument comes down to: "Because we don't know everything, that means we know nothing."

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Rrhain

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Thank you for your submission to Science. Your paper was reviewed by a jury of seventh graders so that they could look for balance and to allow them to make up their own minds. We are sorry to say that they found your paper "bogus," specifically describing the section on the laboratory work "boring." We regret that we will be unable to publish your work at this time.

Here we agree. Yes, you really shouldn't - it's not been defined even by the people bandying it about, or has been successfully refuted... d'oh! Oh, carry on... shown to be false. irreducibly complex? Shown to be false by far more competent people than I. damn right it doesn't, that has nothing to do with genetics. well, information theory shouldn't tell you how a cell evolved. Understandably, really.And you may want to add that evolution and natural selection (and please remember this) do not tell us how abiogenesis occured. It was never meant to. It doesn't. It only, merely, explains how we get from there to here.The next few paragraphs I won't comment on, as there's little substance to it - it's mainly bluster and indignation, sorry. Look, religious people feeling indignant about the beauty of Darwin's theory have been calling it "morally bankrupt" and "a passing fad" and many other epithets for 150 years and the evidence FOR it only gets stronger and stronger.It's not a theory in crisis, it's not contraversial (except with IDiots who get ruffled feathers and apoplexy every time it's mentioned) and it is a solid, firmly confirmed fully accepted scientific theory. no it isn't. There isn't one single credible paper on ID or creationism. ohhhhh yes you do. the very existence of this board (and thousands of others) tells me that's a baldfaced lie. to be frank, there's only one cause for many things. You can't have "intelligent falling" and "gravity" both existing at the same time unless you believe in pantheistic solipsism, in which case... I think you missed some words or a sentence or something, but if you mean we can't reconstruct history...I think you're wrong. We've done a marvellous job on proving evolution as a theory over 150 years, we've got solid theories explaining the facts over such things as the age of the earth, where our ancestors came from, how the universe started and what it was like when it began, and more.Sadly, you won't accept any of these fact-based theories because of your reliance on a book written two thousand years ago or more by a collection of people including bronze-age shepheds.Edited by greyseal, : No reason given.

Of course it would. However, one reason why I am here is to learn more about the subject matter. The debate helps me gain understanding. Your 30% substitution rate in the third position of each codon wasn't a guess? I wonder what are the chances of a series of random mutations hitting only the third position in a chain of amino acids.You know that I really do not understand the language of DNA. This doesn't say that others don't understand it better than me. Your point doesn't say the code isn't specified. I think it is specified enough. Here are some quotes.Some have also argued that alterations in sequencing would likely result in loss of protein function before fundamentally new function could arise (Eden 1967, Denton 1986).Maybe we study Eden's and Denton's work we will get to understand it better. Somehow I doubt they are creationists.Too many processes in the cell depend upon particular proteins having just the right shape and sequence of amino acids to leave the assembly of these molecules to chance. "Signature in the Cell"Recently, experiments in molecular biology have shed light on these questions. A variety of mutagenesis techniques have shown that proteins (and thus the genes that produce them) are indeed highly specified relative to biological function (Bowie & Sauer 1989, Reidhaar-Olson & Sauer 1990, Taylor et al. 2001).In particular, Axe (2000) has shown that multiple as opposed to single position amino acid substitutions inevitably result in loss of protein function, even when these changes occur at sites that allow variation when altered in isolation. Cumulatively, these constraints imply that proteins are highly sensitive to functional loss as a result of alterations in sequencing, and that functional proteins represent highly isolated and improbable arrangements of amino acids -arrangements that are far more improbable, in fact, than would be likely to arise by chance alone in the time available (Reidhaar-Olson & Sauer 1990; Behe 1992; Kauffman 1995:44; Dembski 1998:175-223; Axe 2000, 2004). I'm not whining. The article Meyer wrote that was published in Proceedings of the Biological Society of Washington (volume 117, no. 2, pp. 213-239). I believe the man who had PhDs who authorized it had his keys taken away and was transferred to a hostile supervisor. Most everyone would fear negative reprocussions for publishing an ID article in a journal like that one.

I'm contemplating your post. Does science ever declare it has the truth? Can it declare it has the truth in all cases? People infer the truth from it but I think subtle aspects that make up our psychology get in the way. You mean there's no controversy if scientists don't infer the existence of a designer or the lack of one? I seem to remember Kenneth Miller reported that scientists almost broke out in a fist fight at a meeting when they were arguing about categorizing certain prehistoric animals. It seems to me the lack of a designer hinges on Darwinism being correct.

I don't know what planet you are on. Let's see, Rrhain has made 4,878 posts here on the evcforum and going and still clueless. Here is information leading to a famous one.On August 4th, 2004 an extensive review essay by Dr. Stephen C. Meyer, Director of Discovery Institute's Center for Science & Culture appeared in the Proceedings of the Biological Society of Washington (volume 117, no. 2, pp. 213-239). The Proceedings is a peer-reviewed biology journal published at the National Museum of Natural History at the Smithsonian Institution in Washington D.C.In the article, entitled The Origin of Biological Information and the Higher Taxonomic Categories, Dr. Meyer argues that no current materialistic theory of evolution can account for the origin of the information necessary to build novel animal forms. He proposes intelligent design as an alternative explanation for the origin of biological information and the higher taxa.It is about time you posted some meaty information. I see it is about the immune system. I don't have a dog in that complex fight although I know Behe wrote about it. This thread is about information anyway. I wasn't referring to that. Try explaining functional coherence of protein binding sites.Edited by traderdrew, : No reason given.Edited by traderdrew, : No reason given.Edited by traderdrew, : No reason given.

It has been defined as CSI. Successfully refuted? You must have read it and able to articulate it. So if Shannon information has nothing to do with it, then what kind of information does? How else are the mutations expressed other than expressing themselves other than the As, Cs, Gs, Ts and Us? It doesn't convince me. See message #390 in Expelled thread in "links and information". Rehtorical talk. I don't speak for others. If there isn't any evidence for a world wide flood then I won't support it. ID supports something based on evidence. Creationism shoehorns evidence into a biblical framework. That is dogma. Contrary to what Theodoric wrote, I have criticized creationism before and I just did it again here. Read the section on Elliott Sober in "Signature in the Cell". Better yet, read the whole chapter.I have had about enough with debating you Darwinists for now. 4 to 1 ratio against me is enough. If I don't stop I will be thinking and debating it ad infidium ad nauseum.Edited by traderdrew, : No reason given.

trader. Yes, it's simply a rehash of "it's-so-complicated-it-couldn't-have-evolved" argument hidden behind a few sciency sounding words in am attempt to give the old argument from incredulity some credulity.Sorry, but it's still an argument from incredulity. It just tries to make incredulity "evidence" when it is no such thing.MarkEdited by mark24, : No reason given.Edited by mark24, : No reason given.Edited by mark24, : No reason given.Edited by mark24, : No reason given.

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There are 10 kinds of people in this world; those that understand binary, & those that don't

No, of course it wasn't. It is a natural consequence of the degenerate nature of the genetic code. If you accept that third base wobble exists then it naturally follows that you can change up to 30% of most protein coding sequences without changing their primary amino acid sequence. How can you not understand this? If you have evidence contradicting the commonly understood mappings between codons and amino acids then that is pretty exciting news, care to tell us what it is? Yes I do know. You also don't seem to understand the language of biology or information theory, and yet this hasn't stopped you from making numerous assertions about all of these things.I'm not sure what you are doing for the rest of your post. If those are quotes then surely they are from one paper rather than several. If they aren't quotes then what was the point in italicising them.It looks like all of your quotes are actually from the Meyer paper. I am hardly won over by the fact that Meyer agrees with you.I have to say though that this ... Is not really born out by Axe's paper. At least not until you reach a substantial number of substitutions. In fact he replaces 1/5th of all the external sites, even an enzyme with 30 amino acid substitutions still has some functionality. It is idiotically obvious that if you just keep on replacing amino acids you will eventually compromise function. Bear in mind that if you can change 20% of amino acids without affecting function, which also isn't what the paper shows but for argument's sake, then that, in addition to our 30% divergence in the DNA without producing any amino acid substitutions, means that you could change more than 50% of the DNA sequence in some cases and maintain some functionality. I think that if you work the maths out properly it might even be higher. I'm sure you do believe it, the same way you apparently uncritically believe everything you read on ID propaganda sites.TTFN,WKEdited by Wounded King, : No reason given.Edited by Wounded King, : No reason given.

There is a 'great debates' forum for one to one debates. If the dogpiling is a bit too much, and I can see how it would be, that is a more evenly paced alternative to consider.TTFN,WK

I know I said that I will leave for now. I lied. With posts like the one Mark24 posted, I can't believe how Darwinists could think that I am not objective and they are objective like minded scientists. I just got the below off the net. You see, I am willing to go into hostile territory and read what they say. I think you people don't want to do that. I think it would cause to much pain in you. So much for objectivity.The nucleus is the final organelle that I want to discuss. Although the nucleus contains the chromosomes whose DNA encodes most of the cell’s proteins, and though the DNA is copied into RNA in the nucleus, the nuclear proteins are made in the cytoplasm. The nucleus contains a large number of proteins, none of which is synthesized there. Can you give me some idea of the kinds of proteins that you'd expect to find in the nucleus? Answers could be: DNA replication enzymes, histones, RNA transcription and processing enzymes, gene regulatory proteins, and the like. Since ribosomes are assembled in the nucleus (nucleolus) ribosomal proteins are also present in nucleus.How many codons are required in all of these proteins? And that is just for the proteins in DNA replication. How many codons would be required to generate the first living replicating cell?I'm sure the information can mutate. Some of those sequences can handle frameshift mutations and that could be what they were designed to do (or evolved giving you the benefit of the doubt as a casual explanation.) I personally think natural genetic engineering is a plausible hypothesis in some instances.Is this information not specified? The proteins have specific functions do they not? How do you generate proteins with specific functions if the information that is involved in transcription wasn't specified? Is this information not complex? Does the information not have start and stop codons? Are the codons not arranged in specific sequences? If the proteins have to interact in coherent ways, in other words they were designed or evolved to function together, is this not another form of specificity besides other protein functions? Does all of this mean there is no specified information in the cell?Edited by traderdrew, : No reason given.

I'll explain it the way I see it: IDists and creationists are saying that evolution can't possibly generate "more information" naturally.Unfortunately, "more information" hasn't been successfully defined, or if you believe it has, then examples from nature have been given that fulfill these requirements. Shannon's work explains the transmission of information. That is all. It doesn't say evolution can or can't happen. It doesn't say that transcription errors and mutations can or can't happen. It doesn't say whether mutations are going to be deleterious or positive. It doesn't say how cells divide, it doesn't say how DNA or RNA repairs itself. It doesn't say anything about the mechanics of genetics, since it is not about genetics! information theory doesn't tell you how a cell evolved. It can tell you what would be necessary for it to successfully divide (PURELY in terms of information), it can tell you plenty about how resilient the cell is to damage and how well it could repair itself, but based on factors which, to the best of my knowledge, have never been quantified.However, how it could happen (esoteric theory lacking mechanics) and how it DID happen (physical reality) are two different things. I'm not surprised. I'll hunt around to see if I can find the post that showed me how long this anti-darwin crusade has been going. It was a real eye-opener.The thing about ID is that it's religion. It's creationism in sheep's clothing. It has produced nothing of substance in the whole time since it was dreamt up and that's because it can't.

traderdrew, It doesn't matter one iota whether you, Dembski or anyone else slaps a label on the phenomenon, it still boils down to an argument from incredulity.Basically the CSI argument is "it's complex & has function & there's information involved (well, possibly, but since you conveniently won't define it we can't even be sure of that), therefore can't have evolved". Once you have demonstrated that no CSI structure can possibly evolve, then CSI means something. But since no-one has demonstrated any such thing it's a gimmick to fool gullible creationists/Ider's that they have science on their side rather than the same old argument dressed up in the Emperor's new clothes. A baseless argument from incredulity isn't objectively derived evidence, that's how. You're kidding yourself.Mark

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There are 10 kinds of people in this world; those that understand binary, & those that don't

Science is tentative. It never declares it has the once and for all final truth. Science seeks what is most likely true about the universe we live in through empirical research, but it is tentative and will always change in light of new evidence and/or improved insights.What IDists must do to influence accepted scientific theories is take their evidence and arguments to scientists, not the general public as Dembski does. If scientists find his evidence and arguments persuasive then theory will change. I mean scientists are not arguing about whether a designer is responsible for the diversity of life on earth. Science class teaches science, and therefore science class would be the proper venue to teach about scientific controversies, as opposed to history or English class. But there's no controversy within science pitting those who accept evolution against those who accept design. There's only a social controversy affecting the schools that pits conservative Christians who see science as a threat to faith against school boards who have been mandated with teaching currently accepted scientific views to students.It would be a lie to teach students that there is a scientific controversy over evolution and design, for the simple reason that no such controversy exists.It would equally be a lie to teach students ID as accepted science, for the simple reason that it is not.The ID insistence that new information cannot be created has to demonstrated through research before it can be taught as accepted science.--Percy

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I know I said that I will leave for now. I lied. With posts like the one Mark24 posted, I can't believe how Darwinists could think that I am not objective and they are objective like minded scientists

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I don't know exactly what you object to in Mark's post but the problem seems to be that you don't understand how CSI has been defined.The most important issue here is that CSI - as defined by Dembski - requires that you calculate the probability of a feature evolving. Nobody has managed to produce a valid calculation, and there are simply no known examples of that sort of CSI in biology.So I would say that Mark's comment is largely correct. Certainly you haven't offered any valid counter examples - just guesses.On the other hand you claimed that ID had "done better" than publishing the occasional math/informatics paper that sank without trace - but all you offered was a review paper sneaked into a journal by an unethical editor - that also sank without a trace. That doesn't sound a lot better (it sounds worse to me).
And how does one paper published years ago show that ID is "on the up" ?(And I have to say that if you consider this site to be hostile territory you haven't been looking at the ID blogs).

traderdrew writes:

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I wonder what are the chances of a series of random mutations hitting only the third position in a chain of amino acids.

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Actually, it's quite high. The mechanisms the cell has for mutation detection and repair tend to be not nearly as picky about the third codon.Now, before you go on a "See! Design!" hyperventilation, ask yourself: Why does the cell need mechanisms for detecting and repairing mutation?Now, please note that Signature in the Cell is a popular press book, not an actual journal article. Take its protestations with massive amounts of salt.

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The article Meyer wrote that was published in Proceedings of the Biological Society of Washington (volume 117, no. 2, pp. 213-239). I believe the man who had PhDs who authorized it had his keys taken away and was transferred to a hostile supervisor.

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Incorrect. First, you're thinking of Richard Sternberg, the managing editor of the journal that published the Meyer article.Second, there was no persecution of Sternberg. He put an article in the journal that not only hadn't been peer reviewed, it was completely outside the scope of the journal: The journal is about taxonomy but the paper is about the Cambrian explosion. This is not the journal to publish it in.Sternberg then claims discrimination from the Smithsonian, but all of his claims are false. First, he held an unpaid position as a research associate. He wasn't fired as he wasn't an employee, but beyond that he certainly wasn't dismissed, either. In fact, he had resigned from the position of editor six months before the edition was published (lead time). But not only did he remain in his position as research associate, the Smithsonian actually extended it to the end of 2006. However, he never showed up.His actual job at the NIH was never in jeopardy, his pay did not change, and he wasn't fired over it.Regarding the claim that he "had his keys taken away," that simply isn't true. Instead, there was a reorganization of the entire office space: 17 people and 20 offices were adjusted. He knew about the reorg long before the article was published: He has lied about the report from the Office of Special Council.

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Most everyone would fear negative reprocussions for publishing an ID article in a journal like that one.

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You mean somebody said something not so nice but he wasn't affected in his life in any way? That's sufficient to cause IDers to run screaming into the hills?

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Rrhain

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Thank you for your submission to Science. Your paper was reviewed by a jury of seventh graders so that they could look for balance and to allow them to make up their own minds. We are sorry to say that they found your paper "bogus," specifically describing the section on the laboratory work "boring." We regret that we will be unable to publish your work at this time.