DrREC, you see the GULO evidence as slam dunk evidence for common descent, I don't, in fact I think it is weak, pathetic, and grasping for straws, Thus once again I ask you to prove that neo-Darwinian evolution can actually do all that you claim; Perhaps passing the fitness test would not be too much to ask of you; For a broad outline of the 'Fitness test', required to be passed to show a violation of the principle of Genetic Entropy, please see the following video and articles: Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video http://www.metacafe.com/watch/3995248 Testing the Biological Fitness of Antibiotic Resistant Bacteria - 2008 http://www.answersingenesis.org/articles/aid/v2/n1/darwin-at-drugstore Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology Excerpt: it (an antibiotic resistant bacterium) reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution. http://www.evolutionnews.org/2010/03/thank_goodness_the_ncse_is_wro.html List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria: http://www.trueorigin.org/bacteria01.asp further note; Testing Evolution in the Lab With Biologic Institute's Ann Gauger - podcast with link to peer-reviewed paper Excerpt: Dr. Gauger experimentally tested two-step adaptive paths that should have been within easy reach for bacterial populations. Listen in and learn what Dr. Gauger was surprised to find as she discusses the implications of these experiments for Darwinian evolution. Dr. Gauger's paper, "Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,". http://intelligentdesign.podomatic.com/entry/2010-05-10T15_24_13-07_00 etc.. etc.. etc... bornagain77

So.....what data in the Truman and Borger Paper-JOURNAL OF CREATION 21(3) 2007 that you cited supports Dr. Dembski's claim regarding GULO? As Dr. Dembski says:”Its common defectiveness in humans and other primates, according to them, argues for its common ancestry apart from design (common defectiveness not being something readily explained by common design).” And it seems like the guinea pig defense is failing. Even the creation journal sees the error in the three way rat-human-guinea pig comparison, produces the correct phylogenies, and sees the primate genes sharing a stop codon, with no such common error shares with guinea pigs. DrREC

Once again DrREC, you insist that the GULO supports your, Collins and Giberson, contention that the evidence is overwhelming to supporting common descent. I find your contention very much less than impressive, and indeed I find it subject to much doubt. And furthermore, even though you dismiss their work because of their 'religious belief', the fact is that neo-Darwinism is as much, or more, of a blind dogmatic religious belief than I have ever seen come out of any Theistic religion, thus the same criticism you've leveled at them, of biased analysis of evidence, applies equally well to you! Thus, since I find much room for doubt of the GULO interpretation you insist is unbiased, I challenged you to empirically prove the vast claims you have laid at the feet of purely material processes to gradually create all the stunning diversity of life we see around us.; You can start by falsifying this null hypothesis so as to even get neo-Darwinism in the ballpark of empirical science, instead of the pseudo-scientific claptrap that it presently is; 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 The Law of Physicodynamic Insufficiency - Dr David L. Abel - November 2010 Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.” http://www.scitopics.com/The_Law_of_Physicodynamic_Insufficiency.html The GS (genetic selection) Principle – David L. Abel – 2009 Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.” http://www.bioscience.org/2009/v14/af/3426/3426.pdf http://www.us.net/life/index.htm Dr. Don Johnson explains the difference between Shannon Information and Prescriptive Information, as well as explaining 'the cybernetic cut', in this following Podcast: Programming of Life - Dr. Donald Johnson interviewed by Casey Luskin - audio podcast http://www.idthefuture.com/2010/11/programming_of_life.html bornagain77

"DrREC, do you simply ignore the Y chromosome study which described ‘large scale renovation??? " Is GULO on the Y-chromosome? No. "As to you false insistence that neo-Darwinists do not ignore large sections of DNA" Have I or any of my references ignored large sections of DNA in analyzing GULO? Let me be blunt. I have NO time for or interest in replying to your endless off-topic links. I wish to analyze the original claim by Dr. Dembski regarding GULO. As for the creationist paper you cite, they acknowledge the rat appears to be the outlier, the old analysis is flawed. The phylogenies in figure 2 and 3 refute the proposal that primates and guinea pigs share common defects. This is without even considering total gene structure, just exon 10. The primates analysed all contain a stop at position 97. Guinea pigs don't. The paper has no answer for this "The reasons why most Hominidae display a deletion at position 97 are not clear..." They get the data right (in a way that contradicts the claim that guinea pigs and humans share a common break, or mis-cluster phylogenetically). They then proceed to try to explain it away, favoring a model consistent with young earth creationism and Noah's flood. Maybe you should tell me what DATA in the paper supports Dr. Dembski's claim. Its funny you accuse me of being a bad scientist. i just look at the data, and I'm trying to analyse the claim Dr. Dembski made. Then you cite a paper which has the data right, but seeks to dismiss it because of religious belief. DrREC

DrREC perusing over the final GULO paper I cited, and particularly the conclusion, Why the shared mutations in the Hominidae exon X GULO pseudogene are not evidence for common descent Royal Truman and Peter Borger Conclusions We had originally intended to point out that identical mutations at the same location in guinea pigs, humans and various monkeys demonstrated that mutations could not have been neutral, but rather extraordinarily biased. This would reinforce the view that the same nucleotide deletion present in the human, chimpanzee, orangutan and macaque exon X pseudogene merely reflects a mutational hot spot. We are disturbed that for about 20 years authors, reviewers, publishers and readers of the GULO pseudogene literature were convinced the current neo-Darwinian theory had been established beyond question. An erroneous assumption, obvious to anyone who had enquired, has only now come to light. When examined in detail, the full pseudogene dataset we collected does not lend itself to a reasonable neo-Darwinian interpretation. Using standard bioinformatics tools and principles, we present alternative designs for at least the exon X portion of the GULO gene. These may be plausible due to nucleotide patterns being relevant as regulatory signals or the favouring of some codons for various possible reasons. We do accept that some mutations have occurred in this exon. But these novel proposals imply that the ancestors of the organisms studied may well never have had the exact same GULO sequence. The reasons why most Hominidae display a deletion at position 97 are not clear, but we argue that this fact should not be overrated. This position shows the characteristics of being a mutational hotspot, and during a period of high mutations and low populations many statistical coincidences can be generated. http://creation.com/images/pdfs/tj/j21_3/j21_3_118-127.pdf I don't find the evidence nearly as compelling as you do,, as to making, in my view, the radical claim that man evolved from some hypothetical ape-like ancestor. But since you think your data does support your radical claim and I adamantly hold that it does not, and is in fact a far cry from scientifically establishing all that you would like to lay claim to. Let's see if you can even establish, empirically, the plausibility of your scenario in the first place,,, Do you have any concrete examples of the gradualness that you can point to??? "Charles Darwin said (paraphrase), 'If anyone could find anything that could not be had through a number of slight, successive, modifications, my theory would absolutely break down.' Well that condition has been met time and time again. Basically every gene, every protein fold. There is nothing of significance that we can show that can be had in a gradualist way. It's a mirage. None of it happens that way. - Doug Axe PhD. Nothing In Molecular Biology Is Gradual - Doug Axe PhD. http://www.metacafe.com/watch/5347797/ Experimental Evolution in Fruit Flies - October 2010 Excerpt: "This research really upends the dominant paradigm about how species evolve".,,, as stated in regards to the 35 year experimental failure to fixate a single beneficial mutation within fruit flies. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies Waiting Longer for Two Mutations - Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’’ (Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘‘is 5 million times larger than the calculation we have just given’’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model. http://www.discovery.org/a/9461 Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Excerpt: Starting with a weakly functional sequence carrying this signature, clusters of ten side-chains within the fold are replaced randomly, within the boundaries of the signature, and tested for function. The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences. http://www.ncbi.nlm.nih.gov/pubmed/15321723 Evolution vs. Functional Proteins - Doug Axe - Video http://www.metacafe.com/watch/4018222 Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 This following video is a bit more clear for explaining exactly why mutations to the DNA do not control Body Plan morphogenesis, since the mutations are the ‘bottom rung of the ladder’ as far as the 'higher levels of the layered information’ of the cell are concerned: Stephen Meyer on Craig Venter, Complexity Of The Cell & Layered Information http://www.metacafe.com/watch/4798685 bornagain77

DrREC, do you simply ignore the Y chromosome study which described 'large scale renovation??? As to you false insistence that neo-Darwinists do not ignore large sections of DNA: DNA Comparisons between Humans and Chimps - Fazale Rana Excerpt: It is interesting that when evolutionary biologists discuss genetic comparisons between human and chimpanzee genomes, the fact that, again, as much as 25 percent of the two genomes won’t align receives no mention. Instead, the focus is only on the portions of the genome that display a high-degree of similarity. This distorted emphasis makes the case for the evolutionary connection between humans and chimps seem more compelling than it may actually be. http://www.reasons.org/dna-comparisons-between-humans-and-chimps-response-venema-critique-rtb-human-origins-model-part-2 Chimpanzee? 10-10-2008 - Dr Richard Buggs - research geneticist at the University of Florida ...Therefore the total similarity of the genomes could be below 70%. http://www.idnet.com.au/files/pdf/Chimpanzee.pdf Do you disagree with that point DrREC? And I noticed you ignored this previous point as well,,,, Chimps are not like humans - May 2004 Excerpt: the International Chimpanzee Chromosome 22 Consortium reports that 83% of chimpanzee chromosome 22 proteins are different from their human counterparts,,, The results reported this week showed that "83% of the genes have changed between the human and the chimpanzee—only 17% are identical—so that means that the impression that comes from the 1.2% [sequence] difference is [misleading]. In the case of protein structures, it has a big effect," Sakaki said. http://cmbi.bjmu.edu.cn/news/0405/119.htm Chimp chromosome creates puzzles - 2004 Excerpt: However, the researchers were in for a surprise. Because chimps and humans appear broadly similar, some have assumed that most of the differences would occur in the large regions of DNA that do not appear to have any obvious function. But that was not the case. The researchers report in 'Nature' that many of the differences were within genes, the regions of DNA that code for proteins. 83% of the 231 genes compared had differences that affected the amino acid sequence of the protein they encoded. And 20% showed "significant structural changes". In addition, there were nearly 68,000 regions that were either extra or missing between the two sequences, accounting for around 5% of the chromosome.,,, "we have seen a much higher percentage of change than people speculated." The researchers also carried out some experiments to look at when and how strongly the genes are switched on. 20% of the genes showed significant differences in their pattern of activity. http://www.nature.com/news/1998/040524/full/news040524-8.html Do you concede this point??? Is this how you practice science DrREC???, DO you insist on using only sequences that confirm your presupposed conclusion and ignore all other data??? VERY BAD SCIENCE DrDEC!!!!! Boy you sure want that GULO sequence since you ain't got nothing else, well let's see what else I have in that area,,,, Here is a detailed refutation of the Vitamin C (GULO) 'pseudogene' argument that is used by evolutionists to try to establish human/chimp common ancestry: Why the shared mutations in the Hominidae exon X GULO pseudogene are not evidence for common descent Excerpt; When examined in detail, the full pseudogene dataset we collected does not lend itself to a reasonable neo-Darwinian interpretation. http://creation.com/images/pdfs/tj/j21_3/j21_3_118-127.pdf bornagain77

Bornagain, The conclusion that the human GULO pseudogene is non-functional is not morphing a "conclusion into premise." It is based on the empirical data that the GULO pseudogene is non-transcribed. To make short proteins, regulatory RNAs, or microRNAs, transcripts would be necessary. Your references describe transcribed pseudogenes, which biologists have dug deep into the function of. But GULO isn't among these. See here: http://www.genecards.org/cgi-bin/carddisp.pl?gene=GULOP#exp_annot No transcripts detected. So your claim that I'm practicing "Very bad science DrRec!!!" is based on your non-engagement with the primary empirical data. I won't call this very bad science. Perhaps non-science. You do it again here: "it is fairly well known that large sections of dissimilar sequences are simply discarded because the conclusion does not match your predetermined conclusion." I apparently don't share this fairly common knowledge. Could you point me to an example? Perhaps you could look in this paper: A molecular phylogeny of living primates. PLoS Genet. 2011 Mar;7(3):e1001342. Epub 2011 Mar 17. http://www.ncbi.nlm.nih.gov/pubmed/21436896 I don't have the time to parse all your other off-topic links, although I'm sure they are interesting. I came here to ask if anyone could back up Dr. Dembski's claims on GULOP. As the page mentioning things I'm not supposed to talk about is approaching 15,000 words, staying on topic might be for the best, anyway. DrREC

further note; Pattern pluralism and the Tree of Life hypothesis - 2006 Excerpt: Hierarchical structure can always be imposed on or extracted from such data sets by algorithms designed to do so, but at its base the universal TOL rests on an unproven assumption about pattern that, given what we know about process, is unlikely to be broadly true. http://www.pnas.org/content/104/7/2043.abstract A Primer on the Tree of Life - Casey Luskin - 2009 Excerpt: The truth is that common ancestry is merely an assumption that governs interpretation of the data, not an undeniable conclusion, and whenever data contradicts expectations of common descent, evolutionists resort to a variety of different ad hoc rationalizations to save common descent from being falsified. http://www.discovery.org/a/10651 Do Molecular Clocks Run at All? A Critique of Molecular Systematics - Jeffrey H. Schwartz, Bruno Maresca Abstract: Although molecular systematists may use the terminology of cladism, claiming that the reconstruction of phylogenetic relationships is based on shared derived states (synapomorphies), the latter is not the case. Rather, molecular systematics is (largely) based on the assumption, first clearly articulated by Zuckerkandl and Pauling (1962), that degree of overall similarity reflects degree of relatedness. This assumption derives from interpreting molecular similarity (or dissimilarity) between taxa in the context of a Darwinian model of continual and gradual change. Review of the history of molecular systematics and its claims in the context of molecular biology reveals that there is no basis for the “molecular assumption.”.. For historians and philosophers of science the questions that arise are how belief in the infallibility of molecular data for reconstructing evolutionary relationships emerged, and how this belief became so central … http://www.mitpressjournals.org/doi/abs/10.1162/biot.2006.1.4.357 Why Darwin was wrong about the (genetic) tree of life: - 21 January 2009 Excerpt: Syvanen recently compared 2000 genes that are common to humans, frogs, sea squirts, sea urchins, fruit flies and nematodes. In theory, he should have been able to use the gene sequences to construct an evolutionary tree showing the relationships between the six animals. He failed. The problem was that different genes told contradictory evolutionary stories. This was especially true of sea-squirt genes. Conventionally, sea squirts - also known as tunicates - are lumped together with frogs, humans and other vertebrates in the phylum Chordata, but the genes were sending mixed signals. Some genes did indeed cluster within the chordates, but others indicated that tunicates should be placed with sea urchins, which aren't chordates. "Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another," Syvanen says. ."We've just annihilated the tree of life. It's not a tree any more, it's a different topology entirely," says Syvanen. "What would Darwin have made of that?" http://www.newscientist.com/article/mg20126921.600-why-darwin-was-wrong-about-the-tree-of-life.html I would like to point out that this, 'annihilation' of Darwin's genetic tree of life, article came out on the very day that Dr. Hillis, a self-proclaimed 'world leading expert' on the genetic tree of life, testified before the Texas State Board Of Education that the genetic tree of life overwhelmingly confirmed gradual Darwinian evolution. One could almost argue it was 'Intelligently Designed' for him to exposed as a fraud on that particular day of his testimony instead of just any other day of the year. Here is another paper, dealing with genes, that dealt a 'death blow' to Darwinian gradualism, at its very root, for ever coherently explaining multicellular organisms: More Questions for Evolutionists - August 2010 Excerpt: First of all, we have 65% of the gene number of humans in little old sponges—an organism that appears as far back as 635 million years ago, about as old as you can get [except for bacteria]. This kind of demolishes Darwin’s argument about what he called the pre-Silurian (pre-Cambrian). 635 mya predates both the Cambrian AND the Edicarian, which comes before the Cambrian (i.e., the pre-Cambrian) IOW, out of nowhere, 18,000 animal genes. Darwinian gradualism is dealt a death blow here (unless you’re a ‘true believer”!). Here’s a quote: “It means there was an elaborate machinery in place that already had some function. What I want to know now is what were all these genes doing prior to the advent of sponge.” (Charles Marshall, director of the University of California Museum of Paleontology in Berkeley.) I want to know, too! Here is another article, written by an evolutionist mind you, that states the true pattern found for life, from comparative genetic evidence, is not the tree pattern Darwin had envisioned: A New Model for Evolution: A Rhizome - May 2010 Excerpt: Thus we cannot currently identify a single common ancestor for the gene repertoire of any organism.,,, Overall, it is now thought that there are no two genes that have a similar history along the phylogenic tree.,,,Therefore the representation of the evolutionary pathway as a tree leading to a single common ancestor on the basis of the analysis of one or more genes provides an incorrect representation of the stability and hierarchy of evolution. Finally, genome analyses have revealed that a very high proportion of genes are likely to be newly created,,, and that some genes are only found in one organism (named ORFans). These genes do not belong to any phylogenic tree and represent new genetic creations. Since evolutionists continually misrepresent the true state of the evidence for molecular sequences, here are several more comments and articles, by leading experts, on the incongruence of molecular sequences to Darwin's theory: https://docs.google.com/document/pub?id=1S5wXsukzkauD5YQLkQYuIMGL25I4fJrOUzJhONvBXe4 this is particularly interesting; Kangaroo genes close to humans Excerpt: Australia's kangaroos are genetically similar to humans,,, "There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order," ,,,"We thought they'd be completely scrambled, but they're not. There is great chunks of the human genome which is sitting right there in the kangaroo genome," http://www.reuters.com/article/science%20News/idUSTRE4AH1P020081118 I don't know DrREC, you can pretend you are being fair in all this, but as I see it, you are merely building imaginary constructs from the 'Fit, DAMN YOU, FIT'!!!' method of science. Perhaps you should erase your chalkboard and start completely over with the correct model for all biological adaptations,, Genetic Entropy! The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net 'fitness gain' within a 'stressed' environment i.e. remove the stress from the environment and the parent strain is always more 'fit') http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Michael Behe talks about the preceding paper on this podcast: Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time - December 2010 http://intelligentdesign.podomatic.com/player/web/2010-12-23T11_53_46-08_00 Evolution Vs Genetic Entropy - Andy McIntosh - video http://www.metacafe.com/watch/4028086 bornagain77

But of more to the point with you DrREC, being a neo-Darwinists, how, in your materialistic worldview, do you possibly explain finding Quantum information on a massive scale in molecular biology??? notes; Quantum entanglement holds together life’s blueprint - 2010 Excerpt: “If you didn’t have entanglement, then DNA would have a simple flat structure, and you would never get the twist that seems to be important to the functioning of DNA,” says team member Vlatko Vedral of the University of Oxford. http://neshealthblog.wordpress.com/2010/09/15/quantum-entanglement-holds-together-lifes-blueprint/ Quantum Information/Entanglement In DNA & Protein Folding - short video http://www.metacafe.com/watch/5936605/ In the preceding video, 'Gretchen' asked if quantum entanglement/information could also somehow be measured in protein structures, besides just DNA, and it turns out that quantum entanglement/information has already been detected in protein structures. Here is one such measure; Proteins with cruise control provide new perspective: Excerpt: “A mathematical analysis of the experiments showed that the proteins themselves acted to correct any imbalance imposed on them through artificial mutations and restored the chain to working order.” http://www.princeton.edu/main/news/archive/S22/60/95O56/ The preceding is solid confirmation that far more complex information resides in life than meets the eye, for the calculus equations used for ‘cruise control’, that must somehow reside within the quantum information that is ‘constraining’ the entire protein structure to its ‘normal’ state, is anything but ‘simple information’. For a sample of the equations that must be dealt with, to ‘engineer’ even a simple process control loop like cruise control for a single protein, please see this following site: PID controller Excerpt: A proportional–integral–derivative controller (PID controller) is a generic control loop feedback mechanism (controller) widely used in industrial control systems. A PID controller attempts to correct the error between a measured process variable and a desired setpoint by calculating and then outputting a corrective action that can adjust the process accordingly and rapidly, to keep the error minimal. http://en.wikipedia.org/wiki/PID_controller It is very interesting to note that quantum entanglement, which conclusively demonstrates that ‘information’ in its pure 'quantum form' is completely transcendent of any time and space constraints, should be found in molecular biology on such a massive scale, for how can the quantum entanglement 'effect' in biology possibly be explained by a material (matter/energy) 'cause' when the quantum entanglement 'effect' falsified material particles as its own 'causation' in the first place? (A. Aspect) Appealing to the probability of various configurations of material particles, as Darwinism does, simply will not help since a timeless/spaceless cause must be supplied which is beyond the capacity of the material particles themselves to supply! To give a coherent explanation for an effect that is shown to be completely independent of any time and space constraints one is forced to appeal to a cause that is itself not limited to time and space! i.e. Put more simply, you cannot explain a effect by a cause that has been falsified by the very same effect you are seeking to explain! Improbability arguments of various 'special' configurations of material particles, which have been a staple of the arguments against neo-Darwinism, simply do not apply since the cause is not within the material particles in the first place! Yet it is also very interesting to note, in Darwinism's inability to explain this 'transcendent quantum effect' adequately, that Theism has always postulated a transcendent component to man that is not constrained by time and space. i.e. Theism has always postulated a 'eternal soul' for man that lives past the death of the body. Further notes: The Unbearable Wholeness of Beings - Steve Talbott Excerpt: Virtually the same collection of molecules exists in the canine cells during the moments immediately before and after death. But after the fateful transition no one will any longer think of genes as being regulated, nor will anyone refer to normal or proper chromosome functioning. No molecules will be said to guide other molecules to specific targets, and no molecules will be carrying signals, which is just as well because there will be no structures recognizing signals. Code, information, and communication, in their biological sense, will have disappeared from the scientist’s vocabulary. http://www.thenewatlantis.com/publications/the-unbearable-wholeness-of-beings The ‘Fourth Dimension’ Of Living Systems https://docs.google.com/document/pub?id=1Gs_qvlM8-7bFwl9rZUB9vS6SZgLH17eOZdT4UbPoy0Y Quantum no-hiding theorem experimentally confirmed for first time - March 2011 Excerpt: In the classical world, information can be copied and deleted at will. In the quantum world, however, the conservation of quantum information means that information cannot be created nor destroyed. http://www.physorg.com/news/2011-03-quantum-no-hiding-theorem-experimentally.html bornagain77

Moreover DrREC, you have no evidence whatsoever that evolution can accomplish body-plan morphogenesis,,, “Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find the information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing that there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype (Body Plan)." Michael John Denton page 172 of Uncommon Dissent This lack of beneficial morphological novelty also includes the highly touted four-winged fruit fly mutations: ...Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection." - Jonathan Wells http://www.evolutionnews.org/2008/08/inherit_the_spin_the_ncse_answ.html#footnote19 Darwin's Theory - Fruit Flies and Morphology - video http://www.youtube.com/watch?v=hZJTIwRY0bs Deep Genomics: In the Case of DNA, the Package Can Be as Important as Its Contents, New Work With Fruit Flies Reveals - January 2011 http://www.sciencedaily.com/releases/2011/01/110113102158.htm Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies Many times evolutionists will mention evo-devo (Evolutionary Developmental Biology) to try to support the Darwinian claim that minor changes/mutations to DNA can drive major morphological novelty, yet, in this following comment, from a 2005 Nature review article, evolutionary geneticist Jerry Coyne expressed strong skepticism at the proposed mechanism of 'gene switches' for evo-devo: "The evidence for the adaptive divergence of gene switches is still thin. The best case involves the loss of protective armor and spines in sticklebacks, both due to changes in regulatory elements. But these elements represent the loss of traits, rather than the origin of evolutionary novelties...We now know that Hox genes and other transcription factors have many roles besides inducing body pattern, and their overall function in development - let alone in evolution - remains murky." http://www.evolutionnews.org/2010/06/scott_f_gilbert_developmental035931.html Here is a more thorough critique of evo-devo: Nature's "Gems": Microevolution Meets Microevolution - Casey Luskin - August 2010 http://www.evolutionnews.org/2010/08/nature_gems_microevolution_mee037171.html#more bornagain77

DrREC, I find the fact that GULO psuedogenes are even presupposed by you, and other neo-Darwinists, to be functionless relics in the first place to be problematic. i.e. you have built your conclusion into premise, and you are operating as if any similarity you find confirms your conclusion all the while ignoring profound dissimilarities!!! Very bad science DrRec !!! Et tu, Pseudogenes? Another Type of "Junk" DNA Betrays Darwinian Predictions Excerpt: The paper reports that one study compared pseudogenes found in mice and humans and found conserved sequence, implying function: Interestingly, many of the pseudogenes examined were found to have very few mutations within the regulatory regions they shared with their parent genes, which might suggest that these regulatory regions are of importance to the pseudogene and that the pseudogene may be functional. The paper closes with a warning against assuming that pseudogenes are "nonfunctional relics" and acknowledges that they have been "overlooked in the quest to understand the biology of health and disease": Caution must be exercised when interpreting the results of functional experiments on pseudogenes. In some cases, what appears to be a nontranslated pseudogene can, in fact, code for truncated proteins (Kandouz et al. 2004; Zhang et al. 2006). Nevertheless, the evidence that some pseudogenes can exert regulatory effects on their protein-coding cousins is mounting. Such functions appear to be mediated by noncoding RNAs produced from active pseudogenes. While not all pseudogenes (or even all transcribed pseudogenes) will have biological functions, it is likely that, where an unexpected regulatory benefit results from the formation of a pseudogene, the effect will be conserved. For the large part, pseudogenes have been overlooked in the quest to understand the biology of health and disease, to the extent that pseudogene probes are often absent from commercially available microarrays. As evidence emerges that pseudogenes are deregulated in disease, and indeed that their deregulation can contribute to diseases such as diabetes and cancer, the prevalent attitude that they are nonfunctional relics is slowly changing. Perhaps the mindset of Dawkins, Giberson, and Collins is setting us up to miss important biological functions of pseudogenes. For a more complete discussion, see Jonathan Wells' new book The Myth of Junk DNA. http://www.evolutionnews.org/2011/04/et_tu_pseudogenes_another_type046121.html as to you appealing to molecular 'trees'; once again your conclusion is built into your premise and it is fairly well known that large sections of dissimilar sequences are simply discarded because the conclusion does not match your predetermined conclusion. notes: Moreover, when scientists did a actual Nucleotide by Nucleotide sequence comparison, to find the 'real world' difference between the genomes of chimps and Humans, they found the difference was even more profound than what Dr. Richard Buggs, or the statistical test, had estimated: Do Human and Chimpanzee DNA Indicate an Evolutionary Relationship? Excerpt: the authors found that only 48.6% of the whole human genome matched chimpanzee nucleotide sequences. [Only 4.8% of the human Y chromosome could be matched to chimpanzee sequences.] http://www.apologeticspress.org/articles/2070 Even this more recent evolution friendly article found the differences in the protein coding genes of the Y chromosome between chimps and Humans to 'differ radically': Recent Genetic Research Shows Chimps More Distant From Humans,,, - Jan. 2010 Excerpt: A Nature paper from January, 2010 titled, "Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content," found that Y chromosomes in humans and chimps "differ radically in sequence structure and gene content," showing "extraordinary divergence" where "wholesale renovation is the paramount theme.",,, “Even more striking than the gene loss is the rearrangement of large portions of the chromosome. More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome, and vice versa,,," http://www.evolutionnews.org/2010/04/recent_genetic_research_shows.html A False Trichotomy Excerpt: The common chimp (Pan troglodytes) and human Y chromosomes are “horrendously different from each other”, says David Page,,, “It looks like there’s been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages.” https://uncommondesc.wpengine.com/intelligent-design/a-false-trichotomy/ Chimp and human Y chromosomes evolving faster than expected - Jan. 2010 Excerpt: "The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content.,,, The chimp Y, for example, has lost one third to one half of the human Y chromosome genes. http://www.physorg.com/news182605704.html The evolutionary scientists of the preceding paper offered some evolutionary 'just so' stories of 'dramatically sped up evolution' for why there are such significant differences in the Y chromosomes of chimps and humans, yet when the Y chromosome is looked at for its rate of change we find there is hardly any evidence for any change at all, much less the massive changes the evolutionists are required to explain. CHROMOSOME STUDY STUNS EVOLUTIONISTS Excerpt: To their great surprise, Dorit and his associates found no nucleotide differences at all in the non-recombinant part of the Y chromosomes of the 38 men. This non-variation suggests no evolution has occurred in male ancestry. http://www.reasons.org/interpreting-genesis/adam-and-eve/chromosome-study-stuns-evolutionists bornagain77

"Do you agree with that this is among the most compelling pieces of evidence?" As Dr. Dembski says:"Its common defectiveness in humans and other primates, according to them, argues for its common ancestry apart from design (common defectiveness not being something readily explained by common design)." "If not what do you think is the most compelling piece of evidence of neo-Darwinian evolution of man from some hypothetical ape-like ancestor?" Perhaps another difficulty for design to explain are the robust phylogenies found in papers like this: A molecular phylogeny of living primates. PLoS Genet. 2011 Mar;7(3):e1001342. Epub 2011 Mar 17. http://www.ncbi.nlm.nih.gov/pubmed/21436896 The sequence data is freely available, and could be quite the opportunity for crafting a design hypothesis. I'm a bit puzzled by your reference on GULO. Higher primates lack all (of 12) but exons IV, VII, IX, X and XII. Guinea pigs lack I, V, and VI. These Danish pigs apparently lack exon VIII. Bats also have a broken GULO. What matters is that the primate GULOs are all broken in the same way-a common defect. Potentially a shared defect through ancestry. What I don't understand is lumping clearly different breakages in the same gene into some sort of phylogenetic argument against the primate conservation. Aren't these different defects in the same gene (which is unnecessary under a vitamin-C rich diet)? Humans lack more than 50% of the gene, and pigs lack one exon, and you call it the same defect? As for the 'four stop codons' the only reference (with very similar wording) is : http://www.answersingenesis.org/tj/v18/i3/mistakes.asp "Four same-site stop codons (3 TGA and 1 TAA) have been independently created in the guinea pig and human GULO pseudogenes, if all three overlapping ORFs (open reading frames) are considered." Of course, considering all three open reading frames is ludicrous. Only the frame matching unbroken GULO is necessary. In that frame, these residues could be anything, most likely coding amino acids. They aren't listed on that site, but if you name the codons, we could do an analysis. I bet they align with phylogeny. "For example, achondroplasia is a spontaneous mutation in humans in about 85% of the cases. In humans achondroplasia is due to mutations in the FGFR2 gene." No. That's FGFR3. Here's the gene card: http://ghr.nlm.nih.gov/gene/FGFR3 FGFR2 has no mention of achondroplasia. http://ghr.nlm.nih.gov/gene/FGFR2 "The short legs of the Dachshund are also due to the same mutation(s)." Achondroplastic dog breeds have no mutations in the transmembrane domain of the FGFR-3 gene. http://www.ncbi.nlm.nih.gov/pubmed/11041504 So I'm confused, and your reference has no link to the literature on this. Google has nothing either. Not saying this is total fiction, but I'm at a loss for anything to back it. I'll end there. The rest of the links are interesting, but beyond the scope of this discussion. DrREC

DrREC, it would appear in Dr. Collins/Giberson citing the GULO as part of the 'overwhelming' proof of neo-Darwinian evolution, of the few pieces of evidence that they dare cited, that they think this is among the most compelling pieces of evidence for neo-Darwinian evolution of man from some hypothetical ape-like ancestor. If this is what they think, and I see no reason to doubt it, Do you agree with that this is among the most compelling pieces of evidence? If not what do you think is the most compelling piece of evidence of neo-Darwinian evolution of man from some hypothetical ape-like ancestor? notes; Pseudogenes - Sean D. Pitman M.D. Excerpt: Why would both humans and guinea pigs share major deletions of exons I, V and VI as well as four stop codons if these mutations were truly random? In addition to this, a mutant group of Danish pigs have also been found to show a loss of GULO functionality. And, guess what, the key mutation in these pigs was a loss of a sizable portion of exon VIII. This loss also matches the loss of primate exon VIII. In addition, there is a frame shift in intron 8 which results in a loss of correct coding for exons 9-12. This also reflects a very similar loss in this region in primates (see Link). That's quite a few key similarities that were clearly not the result of common ancestry for the GULO region. This seems to be very good evidence that many if not all of the mutations of the GULO region are indeed the result of similar genetic instabilities and that are prone to similar mutations - especially in similar animals. As an aside, many other genetic mutations that result in functional losses are known to commonly affect the same genetic loci in the same or similar manner outside of common descent. For example, achondroplasia is a spontaneous mutation in humans in about 85% of the cases. In humans achondroplasia is due to mutations in the FGFR2 gene. A remarkable observation on the FGFR2 gene is that the major part of the mutations are introduced at the same two spots (755 C->G and 755-757 CGC->TCT) independent of common descent. The short legs of the Dachshund are also due to the same mutation(s). The same allelic mutation has occurred in sheep as well. http://naturalselection.0catch.com/Files/pseudogenes.html Further note; This following article, which has a direct bearing on the 98.8% genetic similarity myth, shows that over 1000 'ORFan' genes, that are completely unique to humans and not found in any other species, and that very well may directly code for proteins, were stripped from the 20,500 gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more circular and unfair example of practicing science! Human Gene Count Tumbles Again - 2008 Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes. Although this was strong evidence that the sequences were not true protein-coding genes, it was not quite convincing enough to justify their removal from the human gene catalogs. Two other scenarios could, in fact, explain their absence from other mammalian genomes. For instance, the genes could be unique among primates, new inventions that appeared after the divergence of mouse and dog ancestors from primate ancestors. Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes. http://www.sciencedaily.com/releases/2008/01/080113161406.htm The sheer, and blatant, shoddiness of the science of the preceding study should give everyone who reads it severe pause whenever, in the future, someone tells them that genetic studies have proven evolution to be true. This following site has a brief discussion on the biased methodology of the preceding study: https://uncommondesc.wpengine.com/intelligent-design/proteins-fold-as-darwin-crumbles/#comment-358505 If the authors of the preceding study were to have actually tried to see if the over 1000 unique ORFan genes of humans may actually encode for proteins, instead of just written them off because they were not found in in other supposedly 'related' species, they would have found that there is ample reason to believe that they may very well encode for biologically important proteins: A survey of orphan enzyme activities Abstract: We demonstrate that for ~80% of sampled orphans, the absence of sequence data is bona fide. Our analyses further substantiate the notion that many of these (orfan) enzyme activities play biologically important roles. http://www.biomedcentral.com/1471-2105/8/244 Dr. Howard Ochman - Dept. of Biochemistry at the University of Arizona Excerpt of Proposal: Although it has been hypothesized that ORFans might represent non-coding regions rather than actual genes, we have recently established that the vast majority that ORFans present in the E. coli genome are under selective constraints and encode functional proteins. https://uncommondesc.wpengine.com/intelligent-design/proteins-fold-as-darwin-crumbles/#comment-358868 In fact it turns out that the authors of the 'kick the ORFans out in the street' paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias: https://uncommondesc.wpengine.com/intelligent-design/proteins-fold-as-darwin-crumbles/#comment-358547 Moreover the 'anomaly' of unique ORFan genes is found in every new genome sequenced: Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references http://www.vimeo.com/17135166 As well, completely contrary to evolutionary thought, these 'new' ORFan genes are found to be just as essential as 'old' genes for maintaining life: Age doesn't matter: New genes are as essential as ancient ones - December 2010 Excerpt: "A new gene is as essential as any other gene; the importance of a gene is independent of its age," said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. "New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked." http://www.sciencedaily.com/releases/2010/12/101216142523.htm New genes in Drosophila quickly become essential. - December 2010 Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages. http://www.sciencemag.org/content/330/6011/1682.abstract etc.. etc.. etc.. bornagain77

bornagain77, Sorry for the slow reply-I hadn't noticed the post 'jumped' down the page. Thanks for the links-I may address your other questions at length, but out of respect for the original poster, I'll stick with the topic of GULO. Does anyone want to discuss it, specifically the claim that humans and guinea pigs share a ‘common defect’ and not different defects in the same gene? DrREC

Lots of good info there Born Again, thanks. QuestionMark

DrRec, not saying you believe in neo-Darwinian evolution, but just supposing you do; Why in the world is such shallow similarity between man and chimps given such weight while such profound dissimilarity is simply ignored??? Does this not strike you as extremely biased science??? notes; Chimps are not like humans - May 2004 Excerpt: the International Chimpanzee Chromosome 22 Consortium reports that 83% of chimpanzee chromosome 22 proteins are different from their human counterparts,,, The results reported this week showed that "83% of the genes have changed between the human and the chimpanzee—only 17% are identical—so that means that the impression that comes from the 1.2% [sequence] difference is [misleading]. In the case of protein structures, it has a big effect," Sakaki said. http://cmbi.bjmu.edu.cn/news/0405/119.htm Chimp chromosome creates puzzles - 2004 Excerpt: However, the researchers were in for a surprise. Because chimps and humans appear broadly similar, some have assumed that most of the differences would occur in the large regions of DNA that do not appear to have any obvious function. But that was not the case. The researchers report in 'Nature' that many of the differences were within genes, the regions of DNA that code for proteins. 83% of the 231 genes compared had differences that affected the amino acid sequence of the protein they encoded. And 20% showed "significant structural changes". In addition, there were nearly 68,000 regions that were either extra or missing between the two sequences, accounting for around 5% of the chromosome.,,, "we have seen a much higher percentage of change than people speculated." The researchers also carried out some experiments to look at when and how strongly the genes are switched on. 20% of the genes showed significant differences in their pattern of activity. http://www.nature.com/news/1998/040524/full/news040524-8.html Eighty percent of proteins are different between humans and chimpanzees; Gene; Volume 346, 14 February 2005: http://www.ncbi.nlm.nih.gov/pubmed/15716009 Yet neo-Darwinists cannot even account for the most trivial of changes in protein structure; When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://biologicinstitute.org/2011/04/16/when-theory-and-experiment-collide/ Dollo’s law, the symmetry of time, and the edge of evolution - Michael Behe - Oct 2009 Excerpt: Nature has recently published an interesting paper which places severe limits on Darwinian evolution.,,, A time-symmetric Dollo’s law turns the notion of “pre-adaptation” on its head. The law instead predicts something like “pre-sequestration”, where proteins that are currently being used for one complex purpose are very unlikely to be available for either reversion to past functions or future alternative uses. http://www.evolutionnews.org/2009/10/dollos_law_the_symmetry_of_tim.html etc.. etc.. etc.. bornagain77

Thanks Bornagain77-I guess that confirms my suspicion. An analysis of one exon of a gene/pseudogene between only three species led to Inai's mistake. Including additional animals makes it clear the changes from guinea pig to humans are conserved in other species. If you redo the analysis, it is clear that the rat has evolved significantly from the ancestral sequence. So, humans and guinea pigs didn't converge and the calculation is meaningless. Given the complete difference of the pseudogene structure between primates and guinea pigs, I still just can't understand calling it a 'shared error.' DrREC

DrRec hope this helps, Daniel Fairbanks Cherry Picks Data On Pseudogenes To Prop Up Common Descent - March 2011 Excerpt: What is particularly astonishing about Fairbanks’ citation is that the paper also documents the presence of shared deletions and substitutions in the GULO (Vitamin C) pseudogene of both humans and guinea pigs! Given that humans and guinea pigs are thought to have diverged at the time of the common ancestor with rodents, if the mutations are truly random, a mutational difference between the rat and guinea pig should not be shared by humans. But many mutational differences were shared by humans. Inai et al. argued that this was indicative of mutation hotspots where certain types of mutations occur with a greater frequency. The paper calculates the likelihood of these same substitutions in both humans and guinea pigs to be 1.87 x 10^-12. https://uncommondesc.wpengine.com/intelligent-design/daniel-fairbanks-cherry-picks-data-on-pseudogenes-to-prop-up-common-descent/ bornagain77

"In any case, Giberson and Collins scrupulously avoid getting into the details of evolutionary theory and deny that it is even questioned among mainstream biologists. That such questioning occurs, even in the mainstream, consider Susan Mazur's The Altenberg 16, subtitled An Exposé of the Evolution Industry. This book, by a secular journalist, shows how secular biologists are finding Darwinian theory so full of unresolved conceptual difficulties that they are conceding the field is in disarray and needs a new theoretical underpinning." Need we say more? mggarrison

Interesting Review. I am, however, puzzled by one claim: "But this same defect is also found in guinea pigs, which, on evolutionary grounds, are so far removed from humans that this common defect could not be attributed to a common ancestor but rather must be explained as some sort of evolutionary convergence. But in that case, the defective GULO gene hardly becomes compelling evidence for our common ancestry with primates—" My understanding is that higher primates have a common GULOP gene structure-with only about 5 of 12 exons left, while guinea pigs have 9 of the 12. Is there really evidence the defect is the same in humans or guinea pigs-a 'common defect'? If not, why is a different defect in the same gene evidence against the shared ancestry of the primate GULOP, which has the same defects in the same gene? Perhaps I missed a reference, or does this go back to Inai et al.? DrREC

Perhaps Collins, when he is done playing politics with 'consensus science', can get back to real science and show us ANY of the overwhelming evidence he has for evolution??? Perhaps he can show us the evolution of JUST ONE molecular machine??? "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject." James Shapiro - Molecular Biologist The following expert doesn't even hide his very unscientific preconceived philosophical bias against intelligent design,,, ‘We should reject, as a matter of principle, the substitution of intelligent design for the dialogue of chance and necessity,,, Yet at the same time the same expert readily admits that neo-Darwinism has ZERO evidence for the chance and necessity of material processes producing any cellular system whatsoever,,, ,,,we must concede that there are presently no detailed Darwinian accounts of the evolution of any biochemical or cellular system, only a variety of wishful speculations.’ Franklin M. Harold,* 2001. The way of the cell: molecules, organisms and the order of life, Oxford University Press, New York, p. 205. *Professor Emeritus of Biochemistry, Colorado State University, USA Michael Behe - No Scientific Literature For Evolution of Any Irreducibly Complex Molecular Machines http://www.metacafe.com/watch/5302950/ “The response I have received from repeating Behe's claim about the evolutionary literature, which simply brings out the point being made implicitly by many others, such as Chris Dutton and so on, is that I obviously have not read the right books. There are, I am sure, evolutionists who have described how the transitions in question could have occurred.” And he continues, “When I ask in which books I can find these discussions, however, I either get no answer or else some titles that, upon examination, do not, in fact, contain the promised accounts. That such accounts exist seems to be something that is widely known, but I have yet to encounter anyone who knows where they exist.” David Ray Griffin - retired professor of philosophy of religion and theology Michael Behe - Life Reeks Of Design - 2010 - video http://www.metacafe.com/watch/5066181 -------------- Articles and Videos on Molecular Motors/Machines http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMzlkNjYydmRkZw&hl=en bornagain77

Why do they always say its the best explanation? What does "best" mean? biological origins is a incredible subject and figuring it without having witnessed it is a incredible exercise in discovery. Is the quality and quantity of the evidence to draw the conclusions of mites to men incredible? It seems to me that this mutation to mutation to me is a line of reasoning that these authors would find reasonable without any thing else to back it up. Why is it reasonable the error on error created such complexity and such a biology? The greatest way to turn even more of the public against evolution is to tell them exactly what evolution is trying to persuade about biological origins. Most people, on any side, think that discovery has been made of actual processes for the great changes that evolution claims is the origin. Just dumb happanchance operations ideas would move more people to the good guys side. If mutations had not done any glory in biology how would this be known besides finding not enough evidence? How could evolution be falsified on the point of mutations having indeed created biology? How can one falsify zillions of reactions? Robert Byers

Excellent review Dr. Dembski. NZer

Wow. I personally didn't need it, but this is big-time evidence Collins has been given a gag order on origins issues by whoever put him in charge of the NIH. "But then we read in the preface that Francis Collins "fully completed his contribution in the spring of 2009" and "did no further work on this project after he assumed the directorship of the NIH." tragic mishap

...biological evolution, they contend, has come a long way since Darwin... No it hasn't. In fact, it (biological evolution, as understood as the Darwinian mechanism of random errors filtered by natural selection, which is obviously what they are talking about) has not only not "come a long way since Darwin," it has regressed even further into illogical darkness in light of the information age. GilDodgen

No theory is that good. Every theory admits anomalies. Every theory faces disconfirming evidence.

Evolution is not a theory. Modern evolutionary theory is in fact, a smorgasbord. Mung