Vestiges

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Originally posted by octipice:

Of course the definition of vestigial is biased in favor of evolution. The reason is that the concept of "vestigial" is based on evolution. Why would God create useless organs?... But the idea behind the relationship of vestiges and evolution is that these useless parts are gradually disappearing from the species. The idea of something truly "vestigial" just doesn't fit with Creationism.

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Welcome OctipiceYou’ve spoken fairly well for the faith/biases we all have. I do concede things appear more redundant and vestigial-like since the observed entropic ‘curse’ (a creationist term) upon all things we observe. I have referred to them as ‘vestigiloid’, to take away some of the ‘implied’ evolutionary effects (which may or may not be true).Please continue your discussion; I apologize if I don’t answer promptlyPhilip T

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Originally posted by Dr_Tazimus_maximus:
OK Philip, first there are three sources of antibiotic resistence of bacterial: 1) Plasmid transfer, 2) mutations within the transcriptional/translational machinery of the bacteria and, 3) lateral gene transfer between bacterial species (non-plasmid transfer of genetic material). If you doubt these statements go to PubMed and input the search terms yourself. I worked in the same group as a guy in the NIH who did work on how the Multi Drug Resistence Protein in bacteria worked (search term MDRP and/or tagging radiolabeled iodine) so I do know a little bit about this one. Second, you avoided the rest of the comments. For example, malaria and flu, the comment was pertaining to "hot spots" of coat proteins to alter the antigenic properties and fool the bodies defense system. Having been in a process development/manufacturing environment for vaccines I know what a bitch that this one is. Mutations within coat proteins within so called "hot spots" within the genome change the antigenic presentation of the infections particles presenting a serious challenge to the host response and preventing good herd immunity. This fits a competition evolution model based on Neo-Darwinian principles, please describe to us how it fits a creation model.

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#1) Plasmids, I quoted already.
#2) Transcription (DNA->RNA) is not DNA-mutation. Merely a sophisticated ‘pre-coded’ defense mechanism ‘built’ into the pre-existing chromosome and/or extra-chromosomal plasmid ‘slaves’. Translation (RNA->AAs) are even more remote (not DNA-mutations at all).
#3) Lateral gene transfer of other extra-chromosomal material (so-called ‘supernumery’ chromosomes) does not exist in prokaryotes (to the best of my knowledge). But if you are stating mere ‘INTRA-species transfer of DNA’ that would again have to follow a sophisticated ‘PRE-coded’ defense mechanism, i.e., ‘built’ into the pre-existing chromosome of those bacteria. What appears mutational (mutationaloid) is a mere pre-existing defense mechanism and is not DNA-mutation within the ‘master’-chromosomes.As to the rest of the comments; I will hit on some shortly. Mutations within coat proteins may follow #1, #2, and/or #3 above. Malaria I must read up on a little.Again, I detect serious ‘begging of the question’ reasoning within your model(s). They are completely invalid and unrelated to the ‘mutational’ model, being merely ‘variations’ coded into the master-DNA. Please don’t use it on me again (or on anyone else in this forum) until you demonstrate to us a ‘chance’ CHROMOSOMAL mutation in these bacteria.The creation model you just gave me is too obvious:
Extremely sophisticated extrachromosomal (self-replicating) plasmids whose survival is dependent on host genomes, and appear to have no function in bacterial speciation whatsoever (ouch). Where did these ‘cursed’ ‘weapons’ come from? The other 2 examples also appear as ‘cursed’ defense weapons (from a physician’s perspective)? An ‘angry’ designer appears as a culprit at least, they are ‘fearfully and wonderfully made. This follows the biblical design argument.

GENE (thanks for the reply)
I may be wrong, but am willing to concede, a great deal of ‘practical’ studies are done by physicians. As a podiatrist, I NEVER refer to the animal literature on surgery, but the podiatric journals, etc. The same with medicine and biomechanics. While the PDR cites animal studies, most studies are from human experiments (referring to the various percentages of complications within the physiological systems). Perhaps we are both barking an arbitrary tree in this matter.

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Your claim that all antibiotic resistance is conferred by plasmids has a serious problem. For resistance/virulence factors to be introduced to a laboratory culture, the pathogens present must be living in the same culture as a strain already carrying the virulence plasmid and the recipient pathogen must be competant for the transfer.

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(1) "Plasmids are preprogrammed..." -- Fallacy: begging the question

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(2) "{Plasmids are} in the genes..." -- Wrong, genes may be "in the plasmids" but plasmids are not contained "in" genes.

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(3) "{Plasmids are} NOT mutations." Correct. But they contain genes and those genes may contain mutations.

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Gene, what exactly are you throwing at me. True, I’m an over-educated idiot like everyone else here. Things other than plasmids (see my discussion on Dr. Taz) do exist, but are equivalent to plasmids in their arbitrary effects upon mutational ‘speciation’ and other supposed ‘mutational’ models you’ve concocted. What you call mutations are not mutations of any mutational model that invokes speciation.
Now who is ‘begging the question’?

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I'm a bit confused why you are asking me for examples of a principle of biology so basic that it can be taught in high school biology labs, but here is one example of spontaneous microbial mutations that convey antibiotic resistance.

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(Where is your example, Gene? Did you forget it? Or, is that is below?) High school biology labs? Stop the doting, Gene!

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You have another problem. Antibiotic resistance (even MDR) occurs in pathogens that do not contain plasmids. (Example: Mycobacterium tuberculosis)

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I confess I have never heard of MDR. No matter. That this bacteria is like Dr. Taz’s examples is rebutted above.

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Originally posted by Philip:
GENE (thanks for the reply)
I may be wrong, but am willing to concede, a great deal of ‘practical’ studies are done by physicians. As a podiatrist, I NEVER refer to the animal literature on surgery, but the podiatric journals, etc. The same with medicine and biomechanics.

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I've been watching too much Seinfeld.Elaine: You sure you don’t mind?
Doctor (name?): No of course not. People ask me medical questions all the time.
Elaine: Well the question isn’t even for me it’s for a friend.
Doctor: Elaine, I’m used to it. I’m a doctor.
Elaine: Well podiatrist.
Doctor: Huh?
Elaine: No no, I’m just saying you didn’t really go to medical school, you went to podiatry school. Which I’m sure is very grueling in it’s own way.
Doctor: I went to podiatry school because I like feet. I chose to work with feet.

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[This message has been edited by Mister Pamboli, 04-29-2002]

Mr. Pamboli and Darwin, can’t you condense your discussion a bit? I’m already swamped responding to others. If you don’t like non-evolutionist terms (like ‘excellent’, ‘IC’, etc.), that’s your problem don’t you think?DARWIN: Allow me to focus on specifics that I choose for now, else be more specific, please. Also, regarding your own English, please consider your own questionable rhetorical skills and oversimplified drawings. We’re all puffed up pseudo-educated idiots on this post. I’m just a meager podiatrist with a few other degrees, (a mere masters in biomedical science). If you don’t want to discuss with me, fine. I don’t wish to indulge in doting, excess jesting, etc.Vestigiality is primarily a ‘mutationalist’ term, I think we agree. THE BIBLICAL CREATIONIST WOULD JUSTIFY ‘VESTIGILOID’ CHARACTERISTICS AS REFLECTING A ‘CURSED’ CREATION BECAUSE OF SIN (I shout this because you didn’t seem to pick it up in my other discussions). This is the scheme I follow, ‘hope it helps. I use the term ‘vestigiloid’ (vestigial-like) to help myself against biased ‘dictionary’ terms.Your view of the coccyx I believe is ‘out-on-the-limb’, I would consult the orthopedic literature but don’t have time (forgive me). You stated: morphological features which are irrelevant to its functioning purely as a muscle-fixer (what about ligamentous attachments to the pelvis?), and which only make sense if it used to be something else too. A pelvic nob is not better biomechanically because ligamentous flexibility is lost in the lower anatomy therein. Suffice it to say, I won’t comment on it here as being vestigiloid as I believe its not even that. It would be better for you to focus on the ‘foot’ or lower extremities, before my limited ‘podiatric’ expertise becomes increasingly valid so you infer what you may here. But I should speculate at least: if the coccyx has ‘irrelevant’ morphology, how would one really design it more ‘excellent’/’fitting’? And consider a creator’s idea of ‘excellent’/’fitting’ (harmonious, with symmetries and/or proportions), not your own, merely?The same biomechanical attributes holds true for the other examples you give. The appendix ‘design’/homology/morphology may seem reminiscent of a ‘mutationalistic’ mechanism to you but not to me. A ‘biblical creationist’ might respond, however,
1) It was cursed awaiting some sort of restoration in the Day of redemption by the Christ
2) Surgeons botched it up in the past, they’re botching up the immune system with lack of knowledge again, they like to get paid for ‘simple’ operations
3) The appendix is fearfully and wonderfully made, who can know it thoroughly?
4) The appendix devolved via detrimental mutations (consistent with the curse of God).
That the appendix is an ‘frail’ organ as you stated is common knowledge and fully supports a ‘cursed creation’. (a surgeon calling it a mere ‘relic’ is grounds for medical malpractice, trust me, Darwin)How would you ‘curse’ a creation filled with sin, Darwin?‘Wiggling the ears’ and/or other facial stretchings seems to allow necessary exercise and focus during communication; that some people can and can’t is begging the question (to me)Numerous other examples you mentioned fit easily under my creationist model/scheme and won’t be discussed unless you specifically request them. The snake underwent an extreme curse as mentioned in Genesis 3.15, etc.Numerous other detrimental mutations took place and continue to take place, making many of your examples appear vestigiloid, when they have in fact devolved from a more ‘fitting’ state, i.e., from accruing detrimental chromosomal mutations and/or being suddenly ‘cursed’ (i.e., with severely mutated chromosomes and/or protein factors). Your bird example, like so many other examples you give, are ideal candidates for your scheme or mine. ‘Chromosomes do metastasize when you force them to’ still means detrimental (vs. beneficial) mutations.The laryngeal nerve, perhaps not perfect at present, is extremely complex in humans (let alone giraffes) and requires more study on your part before you call it stupid design. Consider, its association with the sympathetics, reflex and trigger points, and other neural pathways, many that are yet undiscovered. Consider its intricate connections with the viscera before you call it mere nerve cabling. Have you considered its complex rami distribution whose modality is motor, general sensory, visceral afferent, and parasympathetic, too? Who or what ‘scientist’ would dare call it mere nerve cabling.Nonetheless, Darwin, your examples do demonstrate very curious genetic flux(es) to a great extent. Yet, you’ve managed to only support my scheme (which seems to be entirely biblical). At present I detect that your scheme is forcing the question of vestiges, and that because you’ve given no evidence of beneficial mutations, is strongly delusional as well. (Forgive my bluntness as I, too, am ‘full of it’)Please don’t push me further with your ‘tarsal’ scheme. An ABPMS board certified foot surgeon, I will declare that every human tarsal is a peculiar ‘fixed’ complexity: that, from a gross biomechanical perspective, is exceedingly ‘fitted’, exact and precise, for each individual. If, I alter a non-pathological tarsal bone surgically to make it more ‘fitting’, I will lose the lawsuit! These pedal complexities are essentially non-reducible, and are fixed irreducible complexities (ICs). No vestigiloid characteristics here, Darwin. There are, however numerous other peculiarities (somewhat like those you’ve mentioned), which do appear vestigiloid somewhat, yet excellently designed in this ‘cursed creation’ that we abide in.Again, I hope, this helps.Philip

Hi PhilipSince you insist on viewing all questions through the rather odd filter of the Fall and the Curse of Adam, perhaps you could use this viewpoint to explain the success of many lineages in establishing themselves in numerous different niches and adaptive zones? Even more interesting, how do you explain the failures of different lineages to adapt to zones where they haven't been successful (there are only 200 species of birds, out of 9800, who can be considered aquatic, but none can live entirely in water, nor have any succeeded fully in becoming leaf eaters), no amphibians have adapted to salt water, etc.?WRT the Fall, how is it possible for a negative curse to create fully adapted flightless birds, salamanders with gills, fish with rudimentary lungs, etc? How does the Fall explain endosymbiosis? Mitochondrial DNA? Chloroplasts? Endothermy? Complex central nervous system? The change from C3 to C4 grasses in North America that successfully wiped out almost all grazing horse lineages (a positive adaptation for grass)? Parasite/host, predator/prey, or plant/pollinator coevolution? (And just to keep in sync with the topic of this thread) How does original sin explain the disappearing molars in adult Desmodus rotundus - a species that can't chew?Your biblical apologetics fail miserably to explain anything we actually observe in the natural world. In addition, it fails utterly when attempting to apply it to real-world problems. How does sin allow one to develop antibiotics to combat disease? If one wishes to reintroduce a species into a recovering ecosystem, how does the Curse of Adam allow us to predict how many individuals make up a viable population? If we're trying to preserve an endangered ecosystem, how does reference to a biblical Fall permit us to determine keystone species for conservation?

[QUOTE][b]As a podiatrist, I NEVER refer to the animal literature on surgery, but the podiatric journals, etc. The same with medicine and biomechanics.[/QUOTE][/b]Of course, I hadn't stopped to consider it before but humans being bipeds, human feet would have few animal analogues. Now I see your position. [QUOTE][b]While the PDR cites animal studies, most studies are from human experiments[/QUOTE][/b]Human experiments are the end product of most pharmaceutical research, but the starting point is in animals. [QUOTE][b]Things other than plasmids (see my discussion on Dr. Taz) do exist, but are equivalent to plasmids in their arbitrary effects upon mutational ‘speciation’ and other supposed ‘mutational’ models you’ve concocted. What you call mutations are not mutations of any mutational model that invokes speciation.[/QUOTE][/b]A plasmid is a carrier of genetic material, not the ultimate cause of a change in a microbial population. The mutation in the genetic material that composes the plasma is the ultimate cause of resistance or virulence factors.Plasmids can distribute a survival function across species but for the transfer to occur you have to *already* have that survival function existing inside a population which is coexisting with the recipient microbe. In a monoculture where did that plasmid come from? If a new function occurs in a culture, there are two possible origins: (1) Mutation (2) Horizontal gene transfer. Asepsis eliminates (2). Is there a third possibility here?In short, if all plasmids are preprogrammed and no new functions are appearing, how are those plasmids getting into the lab and even bacteria that don't have plasmids? [QUOTE][b](Where is your example, Gene? Did you forget it?[/QUOTE][/b]I provided a lab exercise that demonstrates mutation-driven antibiotic resistance in asepsis. I also provided a reference to the survivability of influenza mutants in human subjects being treated with an antiviral and an example of a selected mutation in a human genetic disorder. I think I can find more examples as well. [QUOTE][b]I confess I have never heard of MDR.[/QUOTE][/b]Multiple drug resistance. Very bad bugs. [QUOTE][b]No matter. That this bacteria is like Dr. Taz’s examples is rebutted above.[/QUOTE][/b]Perhaps you would like to elaborate further?Meanwhile I found something else of interesting. Mechanisms of resistance to fluoroquinolones. http://www.cdc.gov/ncidod/eid/vol7no2/pdfs/hooper.pdfChoice quotes from the paper:Page one:"These alterations arise from spontaneous mutations in the genes encoding the enzyme subunits and thus can exist in small numbers (1 in 10⁶ to 1 in 10⁹ cells)""One of the common resistance mutations in GyrA, which causes a change from serine at position 83 to tryptophan, causes reduced binding of norfloxacin to the gyrase-DNA complex."
The following internal cite associated with the above quote:Willmott, CJ; Maxwell, A. A single point mutation in the DNA gyrase A
protein greatly reduces binding of fluoroquinolones to the gyrase-DNA complex. Antimicrob Agents Chemother 1993; 37:126-27While we're on the importance of "mutational evolution" to microbiology, are you familiar with the Ames test?

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[This message has been edited by gene90, 04-29-2002]

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Originally posted by Philip:

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#2) Transcription (DNA->RNA) is not DNA-mutation. Merely a sophisticated ‘pre-coded’ defense mechanism ‘built’ into the pre-existing chromosome and/or extra-chromosomal plasmid ‘slaves’. Translation (RNA->AAs) are even more remote (not DNA-mutations at all).

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You either have no clue as to what I said or are missing it on purpose. Mutations to the DNA which code for various spects of the transcriptional/translational machinery are known. Resistence to rifampicin and chloremphenicol are two examples. Oh, and as you seem to wish to be pissy, transcription is DNA to mRNA and translation is mRNA to protein with the help of rRNA and tRNA.

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#3) Lateral gene transfer of other extra-chromosomal material (so-called ‘supernumery’ chromosomes) does not exist in prokaryotes (to the best of my knowledge).

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The best of your knowledge is not very good here.

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But if you are stating mere ‘INTRA-species transfer of DNA’ that would again have to follow a sophisticated ‘PRE-coded’ defense mechanism, i.e., ‘built’ into the pre-existing chromosome of those bacteria. What appears mutational (mutationaloid) is a mere pre-existing defense mechanism and is not DNA-mutation within the ‘master’-chromosomes.

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again, you really do not know what you are talking about. Here are a few links to educate you.
http://statgen.ncsu.edu/dahlia/journclub/nrg528.pdf[/URL][/URL]
http://www.life.umd.edu/CBMG/faculty/diruggiero/lectures/lecture5handout.pdf
http://www.tigr.org/~salzberg/ScienceLateralTransfer.pdf
http://www.yvm.net/vme/hgt/AnnuRevGenVol28pp237-261yr1994.PDF
lateral gene transfer is rather common it seems, and between related and not so related species.

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Again, I detect serious ‘begging of the question’ reasoning within your model(s). They are completely invalid and unrelated to the ‘mutational’ model, being merely ‘variations’ coded into the master-DNA. Please don’t use it on me again (or on anyone else in this forum) until you demonstrate to us a ‘chance’ CHROMOSOMAL mutation in these bacteria.

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My, you are rather arrogant aren't you. First, there is no master DNA, that is like a comment that a creationist told me in a debate concerning proteins and activity. He said that info could not be gained from a mutation and when I gave him some mutational examples he said that it merely made the protein closer to what it was supposed to be. Idiotic Aristotelian BS.
Here are some examples for you of hypervariable and other MUTATIONAL spots withn the chromosomes (and other areas within the overall genetic makeup).
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list _uids=10773319&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8162410&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8525637&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8892902&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=1696640&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=8874497&dopt=Abstract
By the way, your choice of the term "chance" is somewhat disingenuous. Chance in this area means merely that it can not be completely predetermined. Ie we can give a probability of an event within a population but we can not give the exact sequence and the exact gene and the exact individual. [QUOTE] The other 2 examples also appear as ‘cursed’ defense weapons (from a physician’s perspective)? An ‘angry’ designer appears as a culprit at least, they are ‘fearfully and wonderfully made. This follows the biblical design argument.[/B][/QUOTE]These only appear cursed from a superstitions perspective from someone who really does not understand molecular biology. And the data follows the model that I mentioned earlier, ie evolution.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

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[This message has been edited by Dr_Tazimus_maximus, 04-29-2002]

To Dr_Tazimus_maximus
--Might you agree with me on post #26?------------------

Dr. Taz, Gene, Quetzel, Darwin:I will respond to what I perceive your most appropriate SELECT arguments, that seem scientifically relevant as they supposedly violate the creationist "Curse" model, which I admit needs development. I do not have time nor energy tonight to satisfy my consciences nor yours. Suffice to say my rebuttals should demonstrate in part (at least) some creationist and scientific truth that is if you wish to continue; i.e.,1) Mutational (i.e., even chromosomal) events in life-forms must be essentially ‘pre-programmed’ from ‘powerful’ gene pools that ‘allow’ changes only and not arise as metastasis changes that are mere ‘chance’ phenomenon. The original (i.e., ‘designed’) gene pools merely ‘allow’ changes. All other supposed ‘beneficial’ mutational events appear delusional.
2) The Adamic-Curse model/Christ-crucified-risen model: is a viable scientific hypothesis/theory (as suggested biblically: Rom 8.19-22, KJV/ASV).Again, as my hasty English is poor, perhaps you can correct it, i.e., replace a word with one that is more ‘coherent’ if you dare help me. By doing so, we both may advance in truth. So lend your ‘enemy’ a helping hand if possible so communication at least becomes viable. Most pioneering efforts are crude attempts by non-geniuses like yourselves and myself. Note my limited credentials (I won’t ever argue global flood dynamics nor geology):Real name: Philip M. Traynor (look me up in Albertville, AL)
BA Psychology 1975 (w/minor in art and philos)
Marine Corps Jet Pilot (FLUNKED out in Meridian Naval Air Station 1981)
Assoc. Applied Sci. Elect Eng Tech (computers) (1986)
M.S. Biomedical Sci. (Barry Univ., Miami) 1989
Doctor of Podiatric Medicine (Barry Univ.) 1992
ABPMSB board certification in Podiatric Medicine and Surgery: 1999 to present.I mention these only to give you my current ‘scientific’ perspective(s) so we can communicate better. Some of you are way beyond me in genetics, but not in biomedicine per se. You already know my exceedingly stubborn faith/biases, convictions, etc. Perhaps we might discuss more ‘scientifically’ and rationally to avoid profane and vain babblings, and oppositions of science falsely so called. You see my flaws; I see yours. IQ-wise we are all about the same level, (though my English is lower). Tell me your current ‘scientific’ and/or academic specialties/expertise, too, so I know I’m debating with a chemist, physicist, geneticist (as per Darwin_T), biochemist, aspiring student, or what have you.Darwin_T, I can’t digest all your references? ‘Tis your MODEL I so lovingly attack (#1)... Love that word 'hypervariability', so true and yet so arbitrary to your model. I know I’m attacking your model in ‘crude’ oversimplified unpublishable language from your overly-sophisticated genetics perspective to cut-to-the-chase points (#1 and #2) above. I’ve posted #2 (my ‘crude’ abbreviated model which needs work) on this forum for Mr. Pamboli under DESTINY/FREE WILL.

Philip: Although I don't see the relevance of "credentials" to this discussion, I'll give you a brief synopsis to establish a baseline since you seem to think it important for some reason.My educational background is in environmental science and management science (two degrees). My field work has been primarily in the neotropics in the areas of ecology and conservation biology. My two most intensive and rewarding areas of fieldwork were in sea turtle conservation and reclamation/re-foresting/preservation of a montane rainforest wildlife preserve. I am co-founder and senior partner in an environmental consulting firm based in Central America specializing in environmental impact assessments and baseline studies for neotropical development programs, with a significant emphasis on national park development and management. The company has a second business area in ecotourism management consulting and development. I am currently working "out of my field" on a long-term economic development project funded by the US government. I have four years experience studying and working in the neotropics, and 16 years of program management experience.Gee, I guess you "out-credential" me. Does that mean you'll no longer take my posts seriously? Especially the one's you're unable to answer?

Philip: There is one other statement in your post that demands comment.

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2) The Adamic-Curse model/Christ-crucified-risen model: is a viable scientific hypothesis/theory (as suggested biblically: Rom 8.19-22, KJV/ASV).

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I read your, hmmm, "model" on the other thread. I find it very difficult to believe that you actually consider that verbiage to represent anything remotely "scientific". From what I was able to parse amid the odd non-sequiturs and stream-of-consciousness maunderings, it sounds like a simple "argument from personal incredulity". To wit, since you - Philip - don't understand why something happens, it must mean there is some teleological plan. If that's your belief, fine. However, I would say you should refrain from calling it "scientific" as your "model" is anything but...

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Originally posted by Philip:

1)Mutational (i.e., even chromosomal) events in life-forms must be essentially ‘pre-programmed’ from ‘powerful’ gene pools that ‘allow’ changes only and not arise as metastasis changes that are mere ‘chance’ phenomenon. The original (i.e., ‘designed’) gene pools merely ‘allow’ changes. All other supposed ‘beneficial’ mutational events appear delusional.

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This, as far as I can tell, is just an assertion. I admit that my knowledge in this regard is limited, however, I have yet to see you offer any evidence of this. Someone points out a mutation and you say 'pre-programmed' or something similar without giving any evidence.How can people like myself chose anything but evolution when the creationist side gives no supporting evidence?------------------
compmage

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Originally posted by Philip:
1) Mutational (i.e., even chromosomal) events in life-forms must be essentially ‘pre-programmed’ from ‘powerful’ gene pools that ‘allow’ changes only and not arise as metastasis changes that are mere ‘chance’ phenomenon. The original (i.e., ‘designed’) gene pools merely ‘allow’ changes. All other supposed ‘beneficial’ mutational events appear delusional.

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I am going to respond a little out of order here. later in you post you mentioned that you were not attacking my sites but rather the model. What you apparently fail to grasp is that a model without supporting data is no model at all, at least in the scientific sense. My sites were meant to generate information concerning both you erroneous statemetns concerning genetics and to provide information in support of evolution (the observation of change over time) through or partially through neo-darwinian selection (the theory or model as you call it). The data is there for all to see as to which "model" is best suported.

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2) The Adamic-Curse model/Christ-crucified-risen model: is a viable scientific hypothesis/theory (as suggested biblically: Rom 8.19-22, KJV/ASV).

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Can you please tell me where I can find this model and supporting data. I rather think that it is a rewrite of the "Fallen earth" model where genetic systems, lifeforms and teh earth are in a state of degredation since the "fall of mankind". If that is the case there is no supporting data and, as I indicated in my last post there is a great deal of data against it.

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Note my limited credentials (I won’t ever argue global flood dynamics nor geology):

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I mention these only to give you my current ‘scientific’ perspective(s) so we can communicate better. Some of you are way beyond me in genetics, but not in biomedicine per se.

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OK, I will post my credential but not my name. The reason is that my wife, who is also a scientist, is an active member in her church and there are some narrow minded @$$holes in her church who, if they are on this board, would give her a great deal of grief over my views. They never do to MY face though.
BS (actually a dual BS) General Biology and Biochemistry, 1994, University of Illinois
Ph.D. Biochemistry and Cellular Biology, 1990, Rice University
Postdoctoral Awards and Fellowships at the NIH including grants from the Foundation for Bio-Medical Research and Education
I have been working in the biotech industry for the last 8 years in areas ranging from process development and manufacturing to research. My main areas of speciality are physical biochemistry and cell biology although I do some molecular biology.

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Darwin_T, I can’t digest all your references?

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are you refering to Darwins Terrier or to me? Or are you refering to both. Anyway, they provide info concerning data supporting evolution.

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‘Tis your MODEL I so lovingly attack (#1)...

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Please see my statement above concerning models and supporting data.

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Love that word 'hypervariability', so true and yet so arbitrary to your model.

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Sorry, your last part is completely wrong. Hypervariability is a standard term pertaining to areas of increased mutational probability within a genome and is a well defined and described phenomina. [QUOTE] I’ve posted #2 (my ‘crude’ abbreviated model which needs work) on this forum for Mr. Pamboli under DESTINY/FREE WILL.[/B][/QUOTE]I will try to take a look at it later but have to leave town on business.------------------
"Chance favors the prepared mind." L. Pasteur
Taz

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Originally posted by Philip:

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Note my limited credentials (I won’t ever argue global flood dynamics nor geology)

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Fair enough. So why do you think you know enough about evolution to attack it? Not being a podiatrist, I would not have the arrogance to argue with you about the tendons associated with the third metatarsal or whatever, at least without a hell of a lot of checking. Yet you, by challenging a scientific fact (common descent) and the theories which explain it (random mutation plus natural selection, genetic drift, etc) are claiming that all working zoologists, botanists, palaeontologists, microbiologists, parasitologists, anthropologists, geneticists, biogeographers, comparative anatomists, ecologists, population geneticists, geologists, geophysicists, and the rest, are incompetent fools. How come? This is not an argument from authority, btw, simply that the sensible baseline to start from is that, just maybe, these folks know what they’re talking about.

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Real name: Philip M. Traynor (look me up in Albertville, AL)
BA Psychology 1975 (w/minor in art and philos)
Marine Corps Jet Pilot (FLUNKED out in Meridian Naval Air Station 1981)
Assoc. Applied Sci. Elect Eng Tech (computers) (1986)
M.S. Biomedical Sci. (Barry Univ., Miami) 1989
Doctor of Podiatric Medicine (Barry Univ.) 1992
ABPMSB board certification in Podiatric Medicine and Surgery: 1999 to present.

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Good for you. None of which is relevant for this discussion, any more than my BA (hons) Classical Studies from the University of Wales, Lampeter (1989) is. Can you actually define evolution? Do you know what cladistics is? What’s the difference between homologous and analogous structures? And a crucial one: can you define ‘species’... and how does it relate to the ‘kind’ which you think is immutable? Can you define the latter?

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Tell me your current ‘scientific’ and/or academic specialties/expertise, too, so I know I’m debating with a chemist, physicist, geneticist (as per Darwin_T)

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I wish! Do you mean Dr T M?

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biochemist, aspiring student, or what have you.

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I guess I come under the heading of aspiring student. I read. And I chase references, back to the originals if necessary. Specialities/expertise... seeing illogicalities and nonsense in creationist arguments, I guess. Interests: evolutionary biology and all its ramifications, especially palaeoanthropology, palaeontology, parasitism, ethology, and some genetics. Aim: not to argue for the sake of it, but to explain why creationists are wrong, in the forlorn hope that some of them might be open-minded enough to see the truth if you hit 'em with enough evidence.All clear now? TTFN, Darwin’s Terrier