Summations Only

You are getting confused again. It's up to you, as the claimant, to provide evidence for your claim. It's not our job to disprove your claim until after that.But I'll humor you. Fluvial response to foreland basin overfilling; the Late Permian Rangal Coal Measures in the Bowen Basin, Queensland, Australia is about fluvial deposition. Percy has already pointed out that geologists can tell the difference between fluvial and flood deposits.Your turn. Sigh. You've already been chastised about Googling up a few terms without any attempt at understanding. Your reference discusses the magnetic field in the mid-Cretaceous. Not the Permian. Not even close. Reference please, and try to make sure that it's relevant this time. Sigh again. You haven't taken any thermo, have you. Or maybe you just reject it. The amount of water vapor in the atmosphere is essentially zero relative to the amount in the oceans. From Where is Earth's water located?: There's a reason for this. Much more water and we'd all be dead. More water in the atmosphere means more pressure and higher temperature at the surface. For this and otehr reasons all variations on a vapor canopy have been dead for many decades. For examp, YECs Vardiman and Bousselot produced Sensitivity Studies on Vapor Canopy Temperature Profiles in which they concluded that if everything were carefully optimized one just might be able to squeeze enough water into the atmosphere to cover a perfectly flat Earth with two meters of water. Certainly not enough to cover the Permian Appalachians! And there's always the significant heat produced by condensing that vapor, and in some scenarios significant heat produced by converting the potential energy of the vapor at altitude to heat when brining it down to the surface. As Homer would say: "Mmmmmmmm! Pressure-cooked people!".{ETA}: You've seen mine, and you've done an exceptionally poor job of responding. "the bible confirms further DNA injections after the flood"… do you really think that the phrase "and also after that" confirms DNA injections after the fludde? And the many more questions you've ducked.Edited by JonF, : No reason given.Edited by JonF, : No reason given.

Ah. So, no evidence. You spoke of "confirmed injection of DNA". So your interpretation of a Bible verse, with no explanation of how these many thousands of others survived the fludde or could mate with humans, is "confirmed injection".We do have Bible forums; this is a science forum. Interpret the Bible in a Bible forum, present evidence in a science forum. If you have no evidence (which you don't), admit it and hie thee out of the scientific arena. 14 to 18 alleles of a highly conserved gene is not necessarily a bottleneck. You need much more information to conclude a bottleneck. Sad that you can't remember what was said a week or two ago.How many alleles do humans have for blood type?I see you still haven't figured out what an allele is.And you are way off on the mutation rate.

... Except, of course, when you don't have any evidence for your claims.Edited by JonF, : Bad tags

You have no evidence other than your interpretation of the Bible. Believe whatever you want to believe for whatever reasons make sense to you, but if you want to convince anyone that your views have some relationship with reality you'll need evidence. Your interpretation of a vague reference to some unspecified time period is not meaningful evidence.I see you are ducking questions like mad. You claimed that "... the bible confirms further DNA injections after the flood". The appropriate definition of "confirm" is:

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to give new assurance of the validity of : remove doubt about by authoritative act or indisputable fac

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{emphasis added}For confirmation you need at least two sources, one confirming the other. You have only one source. Therefore your claim of confirmation is wrong.Plus the Bible does not explicitly say any such thing, it requires a particularly strained and question-raising interpretation to get to "DNA injections after the flood".Your opinion of what the Bible says is not evidence. The scientific consensus is that a Noachic fludde would require bottlenecks in all animal including humans, and we know there was no human bottleneck, and we have no evidence of bottlenecks in any but a very few animal species. If you want to claim there's some way that humans avoided a bottleneck, in a scientific forum, you need real evidence. Not your personal satisfaction with your interpretation of a very vague phrase. OK. You started with: Which I and Dr. Adequate pointed out is gobbledygook. You responded: As I've pointed out before, any change in a base pair is an allele. Alleles always, not often, differ if only one base pair differs. Plus it's not particularly easy to "analyze the entire allele and see if there are significant differences".I see that you've ignored a rather important question: I'll tell you. Three. Therefore, since you claim that "14 and 18 alleles is a bottleneck" certainly you are claiming that three alleles is a bottleneck and therefore humans experienced a bottleneck. But this contradicts your claim that humans did not experience a bottleneck. The obvious reason for this contradiction is that you haven't a clue how to diagnose a bottleneck. You cannot diagnose a bottleneck on the basis of one gene, two genes, or a few genes. You need to analyze lots and lots of genes. In lots and lots of individuals from the bottlenecked and related species.Here's an extended quote from Genetic Basis for Species Vulnerability in the Cheetah (1985) which indicates how one could establish a bottleneck:

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In the past 15 years approximately 250 species have been examined for the extent and character of biochemical genetic variation in natural populations (18). Electrophoretic analysis of isozyme and soluble protein variation has revealed abundant genetic variation, with frequencies of polymorphic loci ranging from 0.15 to 0.60 and average heterozygosity estimates from 0.0 to 0.26. In an earlier study of 55 cheetahs from two separate South African populations (15), we found a total absence of genetic polymorphism in 47 allozyme (allelic isozyme) loci and a low frequency of polymorphism of proteins (polymorphic loci, 3.2 percent; heterozygosity, 0.013) by two-dimensional gel electrophoresis. The allozyme survey of the cheetah population has been extended here to include carbonic anhydrase-2, catalase, phosphoglyceromutase, pyruvate kinase, and transferrin (19). All five of these new loci were monomorphic in the sampled cheetahs, including transferrin (Fig. 2), a protein with a high degree of polymorphism in domestic cats, man, and several other mammalian species (18, 20). Monomorphism for transferrin in the cheetah extends to 19, the number of "polymorphic cluster Loci'' (those that tend to be polymorphic in mammals) that are nonetheless monomorphic in the cheetah (15, 21).

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It was possible that the cheetah's low genetic variation is characteristic of wild species of felids and that the cheetah is only one of several highly monomorphic species. This possibility prompted an examination of genetic variation in other species of the Felidae. A survey of seven cat species was undertaken in which the same 50 allozyme loci that had been examined in the cheetahs were sampled. The species included the leopard, lion, serval, and caracal, which overlap the cheetah's range in Africa. The results are summarized in Table 2 (22). All species showed moderate to high levels of genetic variation, further emphasizing the absence of genetic variability in the cheetah.

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Isogenidty of the Cheetah at Its Major Histocompatibility Complex

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The most polymorphic Locus in vetebrates is the major histocompatibility complex (MHC), designated HLA in man, H-2 in the mouse, DLA in the dog, and so forth (23). The MHC, ubiquitous among vertebrates, encodes a group of cell surface antigens responsible for strong cell-mediated rejection of allogeneic tissue grafts (23, 24). The MHC has been the object of intensive molecular and immunological study in recent years and has been shown to consist of a group of tightly linked loci encoding at least three classes of gene products: class I, serologically defined transplantation antigens expressed on the surface of most types of mammalian cells; class II, cell surface proteins (l region-associated antigens) found on B and some T lymphocytes, which participate in the induction of antibody production; and class III, several components of the complement system (24, 25). The MHC system in all species studied to date encodes multiple alleles for class I phenotypes as defined by graft rejection and cytotoxicity reactions with allogeneic antisera. In human populations the variation is so great at the HLA locus that the most common h.aplotype (combination of alLeles of the subloci linked on a single chromosome) has a frequency of Less than 1 percent, so that occurrence of the most common phenotype is 10-⁴ (23). Variation of the cheetah MHC was monitored by measuring the trming of allograft rejection between unrelated cheetahs. In man the average survival time of skin grafts between unrelated individuals is 10.5 days (23).

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Rejection of grafts between inbred mouse strains of different H-2 haplotypes occurs between 10 and 12 days (23, 26). Similarly, unrelated domestrc cats reject skin grafts between 7 and 13 days after grafting (27). Rejections at this time occur suddenly, progress rapidly, and are accompanied by the production of cytotoxic alloanti sera against donor Lymphocytes. Occasionally, and often when grafts are exchanged between related individuals, slower progression and usually much later rejections are observed in these species. Rapid rejections are interpreted as resulting from a difference at the MHC locus, while slow rejections are the result of allelic differences at one or more "minor histocompatibility loci" in the face of identity at the MHC (23, 25, 27). Reciprocal skin grafts were surgically performed on 14 South African cheetahs- four at the De Wildt Cheetah Breeding and Research Center, South Africa, two at the Johannesburg Zoo, and eight at Wildlife Safari, Winston, Oregon. The pedigrees of the cheetahs used in this analysis are presented in Fig. 3. Six graft pairs were between unrelated animals and one pair was between sibLings. The cheetahs were immobilized at approximately 5-day intervals and the grafts were monitored for signs of immunological rejection and for gross differences between allograft and autograft. The characteristics of rejection anticipated from rapid rejections in domestic cats and other species (23, 26, 27) include darkening and discoloration, changes in skin pliability, absence of hair growth, and induration, scabbing, and sloughing of skin.

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The fate of 14 reciprocal split-thickness grafts are summarized in Table 3 and illustrated in Fig. 4. None of the 14 cheetahs showed rapid graft rejection, and clear evidence of slow rejection was observed in only three animals (Rhett, Mkia, and Blondii). A photographic chronology of the progress of two grafting experiments (Molly and Kali) is presented in Fig. 4. In every case the allograft and autograft were virtually indistinguishable 2 weeks after surgery. The De Wildt and Johannesburg studies were terminated early (day 23), but none of the six animals showed evidence of rejection of allografts, which were similar to control autografts in hair growth, texture, pliability, and appearance. Since all the allografts were apparently accepted through the rapid rejection stage, the possibility existed that cheetahs were immunologically incapable of rejecting an allograft. To control for this alternative, skin from a domestic cat also was grafted to two of the Oregon cheetahs, Tamu and Kali (Fig. 4). These xenografts were rapidly rejected (after 10 to 14 days) by both animals, while the autografts and allografts survived and were apparently accepted (Table 3). Surgical biopsies of the autograft, allograft, and xenograft of Kali taken on day 14 revealed that the xenograft was heavily infiltrated with mononuclear inflammatory cells, characteristic of a cell-mediated immune reaction, while the allograft and autograft were not. We conclude that 14 of 14 reciprocal skin grafts (12 of which were between unrelated animals) were accepted beyond the rapid rejection stage, suggesting identity of donor and recipient at the cheetahs' MHC locus.

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Of course, today we'd rely a lot more on sequencing data. But my point is made. Yup. Got any evidence (other than your personal opinion) that this is a problem? (and I'm not sure that Wikipedia is correct in that claim)I also don't know about Taq's number, but I suspect you've garbled it. You need to be very careful to use the appropriate units and be sure you're looking at germ-line mutations (i.e. eggs and sperm) From the Wikipedia article you quoted:

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... these rates are considered to be significantly higher than rates of human genomic mutation at ~2.510⁻⁸ per base per generation.[3] Using data available from whole genome sequencing, the human genome mutation rate is similarly estimated to be ~1.110⁻⁸ per site per generation

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Also from Rate, molecular spectrum, and consequences of human mutation:

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Although the estimated base-substitutional mutation rate derived in this study, 12.8 (2.0) 10^-9 per site per generation, is approximately 25% lower than an earlier estimate of 17.0 (0.2) 10^-9 derived by Kondrashov (8), it is nevertheless higher than the rate for any other well studied species. A recent pedigree-based estimate derived from highthroughput sequencing of Y chromosomes separated by 13 generations (4) yields a base-substitutional mutation rate estimate of 17.3 (8.6) 10^-9 when scaled across the sexes under the assumption of a 6.5-fold inflation in males (see Methods), which is compatible with both previous estimates.

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There are several potential explanations for the deviation of the current results from Kondrashov (8). First, the set of genes employed here extends beyond that used by Kondrashov (8), as a number of relevant data sets became available in the intervening period. Second, with new information on the incidences of disorders and the fractions of affected individuals as a result of de novo mutations, the estimated per-locus mutation rates to defective alleles are in some cases substantially different between our two studies. Third, because of data judged to be inadequate, three loci employed by Kondrashov (8) were discarded (ABCD1, AR, and EMD), and when these are excluded, Kondrashov’s estimate declines to 16.0 (0.2) 10^-9, which is statistically compatible with the estimate provided here. Fourth, whereas the Kondrashov study (8) was confined to mutations to nonsense codons, the current investigation integrated over a wider range of contextual sequence space by incorporating both nonsense and missense mutations.

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I see several estimates there that are very close, and none of which are compatible with "its normally a few base pairs per generation per individual across the entire genome".#8722;8sup

Yes it does. Eight. You are making stuff up in a vain attempt to justify your preconceptions. Did Noye decide to toss in a few hundred Elohim even though God hadn't told him to? Did he genetically screen them to make sure of preserving the maximum number of alleles?

That's your opinion. It's not, as you claimed "confirmed". Nor is your opinion particularly meaningful in a scientific forum.I see you are giving up claiming that there's a been a bottleneck any any but a very few species in which we would see a bottleneck if there had been a fludde. Case closed. Again.

I've already pointed out, twice, that the information presented in this thread does not look like a bottleneck. Your only reason for believing in a bottleneck is that you want it to be so.You ignored the data I posted on jaguars. Here's the bottomline:

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Electrophoretic analysis of isozyme and soluble protein variation has revealed abundant genetic variation, with frequencies of polymorphic loci ranging from 0.15 to 0.60 and average heterozygosity estimates from 0.0 to 0.26. In an earlier study of 55 cheetahs from two separate South African populations (15), we found a total absence of genetic polymorphism in 47 allozyme (allelic isozyme) loci and a low frequency of polymorphism of proteins (polymorphic loci, 3.2 percent; heterozygosity, 0.013) by two-dimensional gel electrophoresis.

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47 genes with only one allele. The remainder of genes studied well below the average of other species, and of other similar animals in similar environments. And more. That's a bottleneck.16-18 alleles of one gene in one animal indicates, if anything, no bottleneck. You haven't presented anywhere near enough data to claim a bottleneck.Edited by JonF, : No reason given.

Define "significantly unique".I already pointed you to the IPD-MHC Database, which lists 60 BoLA-DQ1 alleles, 130 BoLA-DRB3 alleles, 82 BoLA-DQB alleles, and 60 BoLA-DQA alleles in cattle. Please show your calculations of how this is consistent with your hypothesis. No hand-waving of "high mutation rate", let's see the numbers.

The correct word is "belabor". It's a natural reaction to creationists ducking significant issues. E.g.: So I've pointed out exactly why your made-up "criterion" for a bottleneck is wrong, in several different ways. Yet you are still looking for more than 14 alleles, and hand-waving away the examples I've given of many more, and ignoring the fact that your "criterion" requires claiming a bottleneck in humans. I'm pointing out that your interpretation of the Bible is very poor evidence at best in a scientific setting. I'm also pointing out that your claim of confirmation is flat-out wrong. OK, you're wrong. Why is it that you (and so many other creationists) are so in love with Making Stuff Up rather than Finding Things Out, and then presenting your Made Up Stuff as established fact?(In looking back I see you saying "only one base pair differs (very recent mutation) ", which is yet another error; single base pair variations are not necessarily recent). Well, 35-40 sure doesn't sound like a few to me, but "few" is an imprecise term.So, calculate how many different alleles should have arisen and fixed in any particular population for which we have data in your time frame.

He did originally say "I acknowledge recent mutations, its normally a few base pairs per generation per individual across the entire genome.". So he was not talking about within the population, he was talking about per person.

Show your calculations.

In that message, yes. By Making Stuff Up I was referring to your oft-repeated claim that a number of alleles of one gene in the teens indicates a bottleneck. You Made That Up.Stop doing that.

The vast majority do correlate. That's done extremely rarely, and when it's done it's clear that the calibrated date is not independent of the "calibrator". None of Razd's correlation are of this type. Of course it's available to the public, and even fairly easy to find. You are Making Stuff Up again. E.g. Call for an improved set of decay constants for geochronological use, THE URANIUM HALF-LIVES: A CRITICAL REVIEW, Precision Measurement of Half-Lives and Specific Activities of 235U and 238U.MIT's Barton Library will send any paper to you as a PDF for $15.

100% "accumulation" (which I presume is what a geneticist would call fixation) is not realistic. Yes some genes mutate more and some mutate less.So you think that two new alleles could have arisen since the fludde. How many alleles did the average mamal set on the Ark carry?

His message was a little incoherent, but seemed to be focusing on the determination of radioactive decay rates. I interpreted that sentence as a reference to calibrating one isotope's decay rate by another's (238U), from a rock dated by both isotopes. It's tempting to do that since the decay constant for 238U is known to significantly better precision than others (bombs and reactors tend to generate lots of research). I considered the possibility that he just made it up, as he makes so much stuff up, and just happened to stumble on something that is done occasionally. Be that as it may, in Call for an improved set of decay constants for geochronological use Bergman et al include a very good introduction to the methods of measuring decay constants, including:

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3. Geological comparison. This approach entails multichronometric dating of a rock and cross-calibration of different radioisotopic age systems by adjusting the decay constant of one system so as to force agreement with the age obtained via another dating system. In essence, because the half-life of 238U is the most accurately known of all relevant radionuclides, this amounts to expressing ages in units of the half-life of 238U.

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This procedure is less than ideal, however.The different radioisotopic dating systems were developed, and as a rule are being utilized, because different parent/daughter element pairs are affected in different ways by different geological processes. Thus, employing a variety of element pairs often allows to distinguish chemical, thermal, mechanical, or other processes capable of fractionating or homogenizing the chemical signature of its minerals during a rock’s history. It is the sequence of such events that one wants to learn about.This, in turn, implies that there is the practical problem of selecting a sample where the initial event starting the radioisotopic clock was so short and simple as to be truly point-like in time, and whose subsequent perturbations were totally nonexistent.

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As illustrated by the case of early comparisons between Rb-Sr and K-Ar ages, or K-Ar and U-Pb ages, on non-retentive materials like micas, feldspars, and uraninites in plutonic rocks, simple concepts about ideal samples that were considered valid a quarter of a century ago have not withstood the test of time. Our present perception of isotopic closure has been changed as a result of improved understanding of mineralogy and isotope systematics; consequently, now the definition of a point-like event is more restrictive than that implicitly assumed by the studies that influenced Steiger and Jager (1977). The obvious requirements are that the two isotopic systems being compared are exactly coherent due to simple thermal, chemical, and mechanical histories. In addition to selecting a sample which was rapidly quenched from a magmatic stage, it is of vital importance to ascertain that the sample escaped any retrogressive change of mineralogy and especially any exchange with fluids, and was spared any later disturbance, chemical and/or thermal. This can be investigated by detailed microchemistry of major and trace elements. Vagaries and problems potentially encountered with the standard Pb-Pband U-Pb ages used for this kind of calibration have most recently been discussed by Tera and Carlson (1999).

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