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If evolution is not valid science, somebody should tell the scientists.

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rmwilliamsll

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penicillin resistance is an interesting and somewhat complex topic.

a general article on the topic:
http://www.eff.org/Misc/Publications/Bruce_Sterling/FSF_columns/fsf.15

good review article:
http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=413858&pageindex=1

the fact is that the mutation to confer anything is always present before it is used. the option is to poof it into existence at the point in time that it is needed. not a scientific answer.

you only have 3 logically possible relationships in time between a mutation and when it is co opted to perform a particular function. the mutation existed before the function, the function and the mutation came into existence at the same time, or the mutation occurs after the function. only the first one is either logical or possible.
 
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Robert the Pilegrim

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nolidad said:
Well then we get down down to how mutation is defined,
You really need to go back the basics and learn something about biology.
for immuno support systems are inherent in most sentient creatures. They are part of the genome of the vcreature to protect it from the varied dieases that can inflict that species.
And the relevance of this is?
What exactly do you think the word "sentient" means?
Well I will accept the definition of evolutionists who define mutations as either neutral, harmful, or beneficial.
Fine, then the mutation for sickle cell anemia is either and/or both beneficial and harmful, depending on where you live.
I still want 10 variations that can be shown to have happened by mutation and preexisitng coding int he genome.
As I asked before, what will you accept as "shown"?
Did you understand what I wrote on the question?
or that radio decay is not constant
Pick a time any time, we have a nearly continuous record of atomic reactions and nuclear constants for the last 60,000 years in the form of light coming from stars within the Milky Way Galaxy.

If radioactive decay were not constant we would see changes in the light coming from stars.

If as one of the RATE papers you cited suggests 4 billion years of decay had been fit into a single day the natural reactor at the Oklo mine in Gabon and all the rock around it would have gone molten that day.
a simple question-- are you as hard on evolutionists that write and later are proven wrong or just YECers???
I frequently grind my teeth down to stubs when reading gradeschool and even high school presentations of history and science.

But that is producing predigested pap for students, YECers are claiming to Godly people defending the faith. And claiming to be "scientists".

In 1974 Morris wrote "Scientific Creationism" in which he made the moon dust argument based on a 1959 paper. The paper itself noted that its numbers were quite preliminary. There had been a number of papers and two full fledged conferences before 1970 that demonstrated that the conclusions of the 1959 paper were flawed.

In Evolution, The Fossils Say No by Duane T. Gish (1978)we find:

What do we find in rocks older than the Cambrian? Not a single, indisputable, multicellular fossil has ever been found in Precambrian rocks! Certainly it can be said without fear of contradiction that the evolutionary ancestors of the Cambrian fauna, if they ever existed, have never been found.​

Duane Gish received his Ph.D. in Biochemistry from the University of California at Berkeley in 1953. He was the Associate Director of the Institute for Creation Research (ICR) in 1975 and since at least 1996 he has been the Senior Vice President of ICR. He is the author of about 10% of the first 300 issues (1973-1998) of the ICR's Impact pamphlets.

The web page below then lists two citations from prominant publications:

Anderson, M. M. & Misra, S. B. 1968. Fossils found in the Pre-Cambrian Conception Group of South-eastern Newfoundland. Nature 220,681-681.

Glaessner, M. F. & Ward, M. 1966. The late Precambrian fossils from Ediacara, South Australia. Paleontology 9, 599-628.

I went to the library and quickly found two encyclopedias:

Grzimeks's Encyclopedia of Evolution, published by Van Nostrand Reinhold Company, copyright 1976.

Encyclopedia of Earth Sciences, Vol 7: Encyclopedia of Paleontology, published by Dowden, Hutchinson and Ross, copyright 1979

Both of which covered essentially the same ground; PreCambrian fossils of multicellular animals existed; PreCambrian trace fossils such as worm burrows had been found in comparitive abundance and significantly earlier than the animal fossils, those trace fossils could not be connected to the animal fossils; shells and skeletons had not yet evolved so only rarely occuring soft-body fossils are available to be found; the multicellular animal fossils that had been found were unlikely to be the ancestors of Cambrian life.

Encyclopedias are infamous for being behind the times so it can be taken as a given that the knowledge therein is common knowledge among those in the field. Yet a PhD, who should be familiar with the concept of doing literature searches, made two very strong statements of which contemporary encyclopedias show that one was patently false and the other unsurprising and, given the trace fossils, not provably true.

Is Gish, despite his PhD and lofty position and many publications within the YEC community, a lousy scientist? Does he, consciously or unconsiously, avoid too carefully examining the scientific literature for fear of finding that he is wrong?

Do you understand why running into this kind of thing again and again can wear on one's patience?

http://members.aol.com/dwise1/cre_ev/schimmrich/evaluate.html
 
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gluadys

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nolidad said:
I still want 10 variations that can be shown to have happened by mutation and preexisitng coding int he genome.

Its not hard to find these, but I don't have time to research a lot at once. You could start with this recent mutation of a hemoglobin gene in Burkina Faso.

http://www.genomenewsnetwork.org/articles/12_01/Malaria.shtml

It provides protection against malaria, but unlikethe more common HbS variant, it does not expose carriers to sickle-cell anemia.
 
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Willtor

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nolidad said:
. . .

a simple question-- are you as hard on evolutionists that write and later are proven wrong or just YECers???

I'm not hard on anyone who is proven wrong. I have quite a lot of respect for people who publish their hypotheses, even if they are shown wrong. I am never hard on Behe.

I am very hard on people who falsify data and publish with intent to deceive. It doesn't really matter to me what their background might be. If they are evolutionists, shame on them. If they are Christians, double-shame on them. Christians who try to spread the truth through deceit have no moral recourse when their falsehoods are uncovered.
 
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nolidad

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random guy writes:


I'm still confused by what you mean by sentient. For example, slugs and spiders have immuno response, as do plants. Are all these creatures sentient?

sentient Show phonetics
adjective FORMAL
able to experience physical and possibly emotional feelings:

You really need to go back the basics and learn something about biology

mutation: A change in genetic material that results from an error in replication of DNA. Mutations can be beneficial, harmful, or neutral.

So now I ask you, are the "mutations that produce insecticide resistence and resistence to malaria errors in replication or simply the immuno defensde systems acting as precoded? Especially inlight that some bacteria 100 years ago were already antibiotic resistant before they were even exposed to antibiotics???


If as one of the RATE papers you cited suggests 4 billion years of decay had been fit into a single day the natural reactor at the Oklo mine in Gabon and all the rock around it would have gone molten that day.

Well why don't you down load some of the condensed materials and see for yourself. instead of making presumptious nonfactual suppositions. It has already been proven that decay constantes can be alterred and it has been demonstrated.

As I asked before, what will you accept as "shown"?
Did you understand what I wrote on the question?

I guesss it would be shoe me new information plugged into the genetic code that was not there ( do not show me loss of code) show me a variant not there prior to it happening.

You continue to claim that Creationists would submit journals, but the evolutionists wouldn't even review it. Until you present evidence supporting this, I stand by my view that Creationists do no scientific research in Creationism as evidenced by the lack of peer reviewed papers in academic journals.

Well you are free to accept you rposition, but as you just said: scientists that control the universities, journals, revies boards etc. are all evolutionists. They reject creationism as non science or bad science-- so when papers used to be presenteds for review based on creation science they were rejected as bad sceince or unreviewed. I have doen about all the leg work I intend to do until you guys pony up tot he bar with the requests I have asked for.

Once again I want to see to proven "beneficial" mutations in species that happened without the coding already existing to produce the resistence (in this typoe o fmutation) you need to shoe tha immuno defensr systems di dnot have the capability until this mutation occurred.

Both of which covered essentially the same ground; PreCambrian fossils of multicellular animals existed; PreCambrian trace fossils such as worm burrows had been found in comparitive abundance and significantly earlier than the animal fossils, those trace fossils could not be connected to the animal fossils; shells and skeletons had not yet evolved so only rarely occuring soft-body fossils are available to be found; the multicellular animal fossils that had been found were unlikely to be the ancestors of Cambrian life.

Well two questions I would ask-- could these "worm burrows" been made by another method other than worms-- how did they rule out other methods of production?? Your article itself states the "burrows could not be connected to any animal fossils.

How were the ages determined? By radio dating?? It is too iniaccurate.
 
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random_guy

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Willtor said:
I'm not hard on anyone who is proven wrong. I have quite a lot of respect for people who publish their hypotheses, even if they are shown wrong. I am never hard on Behe.

I am very hard on people who falsify data and publish with intent to deceive. It doesn't really matter to me what their background might be. If they are evolutionists, shame on them. If they are Christians, double-shame on them. Christians who try to spread the truth through deceit have no moral recourse when their falsehoods are uncovered.

I am the same way. If someone is wrong, and is presented clear evidence of being wrong, but doesn't still accept it, then I am hard on them. However, I applaude any Creationist or Evolutionist that admits that they're wrong.

The problem is, the majority of cases where someone is proven wrong is usually Creationists, and they will almost never admit any error. For example, even AiG admits that Creationists shouldn't use flash frozen mammoths as evidence of a flood, there are no beneficial mutations, Paluxy tracks as evidence of human-dino cohabitation, etc... and yet, even if we point out to them that even AiG says not to use them, Creationists will still ignore us, or they will not accept it as wrong.
 
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Willtor

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random_guy said:
I am the same way. If someone is wrong, and is presented clear evidence of being wrong, but doesn't still accept it, then I am hard on them. However, I applaude any Creationist or Evolutionist that admits that they're wrong.

The problem is, the majority of cases where someone is proven wrong is usually Creationists, and they will almost never admit any error. For example, even AiG admits that Creationists shouldn't use flash frozen mammoths as evidence of a flood, there are no beneficial mutations, Paluxy tracks as evidence of human-dino cohabitation, etc... and yet, even if we point out to them that even AiG says not to use them, Creationists will still ignore us, or they will not accept it as wrong.

Let me qualify this, then. I think someone who continues to believe PRATT, even when the refutations of the PRATT are directed at him, is dishonest to himself. I think someone who actively works to invent and promote forgery and hoax is dishonest to the rest of us. The former is pitiable. The latter is contemptible. There really is no excuse for trying to "further the case of Christ" by perpetrating fraud. If, in fact, Christ is the truth (as I think he is), then the publication of deliberately dishonest research is as far from Christ as East is from West.

Thus, I differentiate the work of AiG from the work of Kent Hovind.
 
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Robert the Pilegrim

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nolidad said:
robert the pilegrim said:
If as one of the RATE papers you cited suggests [Edit]1.7[/Edit] billion years of decay had been fit into a single day the natural reactor at the Oklo mine in Gabon and all the rock around it would have gone molten that day.
Well why don't you down load some of the condensed materials and see for yourself.
instead of making presumptious nonfactual suppositions.
What condensed materials are you talking about?

What "presumptious nonfactual suppositions" are you claiming I am making?
It has already been proven that decay constantes can be alterred and it has been demonstrated.
First show that that is in the least bit relevant to what I wrote and then provide citations, preferably citations that state the magnitude of the effect.

It doesn't matter what the decay constant is, if the 1.7 billion years of decay that took place at natural uranium reactor had gone off in a single day it would have melted the rock around it. Actually I suspect that the uranium would probably would have heated to the extent of causing an explosion.

Oh, this is nuts, if the decay rate had been accelerated that much, the entire uranium ore layer would have gone critical.

Now back to the changes in decay rate.
The largest change suggested was 5% for a type of decay that has nothing to do with dating.

ICR.org decay article
search:

Matson's article on Hovind's (and others) claims about radioactive decay

for "decay constant"

Elsewhere on icr there is a claim about possible changes to the Fermi constant

http://prola.aps.org/abstract/PRD/v47/i10/p4774_1
shows that it has varied less than 5% for as far as we can observe and over times on the order of the lifetime of the universe.

Unless God has altered the physical evidence.
 
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Robert the Pilegrim

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nolidad said:
So now I ask you, are the "mutations that produce insecticide resistence and resistence to malaria errors in replication or simply the immuno defensde systems acting as precoded?
The evidence all points to the resistance to malaria being a mutation.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1676014&dopt=Abstract
see also:
http://unisci.com/stories/20012/0626011.htm

I can't find it... there is another mutation that confers resistance to malaria, it has no downside AFAICRemember. It's distribution suggested a much more recent origin. But no joy in trying to find it.
Especially inlight that some bacteria 100 years ago were already antibiotic resistant before they were even exposed to antibiotics???
Interesting, do you have a source for that?
 
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gluadys

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nolidad said:
So now I ask you, are the "mutations that produce insecticide resistence and resistence to malaria errors in replication or simply the immuno defensde systems acting as precoded? Especially inlight that some bacteria 100 years ago were already antibiotic resistant before they were even exposed to antibiotics???

This is why mutations are called "random". There is no necessary connection between the point in time that a beneficial mutation occurs and the time it becomes needed.

The presence of a toxin will not necessarily call forth a mutation that confers resistance to the toxin. (Although it apparently does speed up the rate of mutation, making it somewhat more likely that such a mutation will occur.) The absence of a toxin does not impede the occurrence of a mutation that confers resistance to it. In that case, the mutation will be inherited for a time as a neutral mutation. So there is nothing problematical about resistance showing up 100 years before it is needed.

And that is the problem with trying to discriminate between mutations and pre-existing code. How far do you need to go back to show that pre-existing code is not the consequence of a mutation which occurred before it was needed?


It has already been proven that decay constantes can be alterred and it has been demonstrated.

Has it also been shown that the conditions which can produce an alteration in decay rates exist or have existed on earth? And has it been shown that the alteration in decay rates would produce the amount of difference (4.5 billion vs. 6-10 thousand years) between old earth and young earth scenarios?


I guesss it would be shoe me new information plugged into the genetic code that was not there ( do not show me loss of code) show me a variant not there prior to it happening.

The most clear-cut example I know of is the nylon bug. Shernren gave the reference.
 
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nolidad

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gluadys writes:

And that is the problem with trying to discriminate between mutations and pre-existing code. How far do you need to go back to show that pre-existing code is not the consequence of a mutation which occurred before it was needed?

Well we need to get it back to where it was "inserted" into the code through random mutation--that is the heart of the debate here about mutations. Whethter they are preexisting variants within the code or actual true "new" info inserted intot he genome by random mutation.

Has it also been shown that the conditions which can produce an alteration in decay rates exist or have existed on earth? And has it been shown that the alteration in decay rates would produce the amount of difference (4.5 billion vs. 6-10 thousand years) between old earth and young earth scenarios?

And has it been proven other than mathematical formulas that decay occurs over millions and billions of years???

The most clear-cut example I know of is the nylon bug. Shernren gave the reference.

But again is this not simply an inherent ability to adapt diet or is it mutation??

robert the pilgrom writes:

I can't find it... there is another mutation that confers resistance to malaria, it has no downside AFAICRemember. It's distribution suggested a much more recent origin. But no joy in trying to find it.

I wish I remembered for I found it last night. Sickle cell anemia while it has a side effect of preventing maleria or helping africansd resist maleria is overall a deliterious mutation though not lethally so.

But the important thing to remember is that all this has done is to keep homo sapien sapien negroid still homo sapien sapien negroid. All it has done is help the species fight disease which is what immune systems were designed to do.

What "presumptious nonfactual suppositions" are you claiming I am making?

This:

If as one of the RATE papers you cited suggests [Edit]1.7[/Edit] billion years of decay had been fit into a single day the natural reactor at the Oklo mine in Gabon and all the rock around it would have gone molten that day.

Oh, this is nuts, if the decay rate had been accelerated that much, the entire uranium ore layer would have gone critical.

only you keep saying the decay constants are accelerated by that magnitude.

random guy writes:

The problem is, the majority of cases where someone is proven wrong is usually Creationists, and they will almost never admit any error. For example, even AiG admits that Creationists shouldn't use flash frozen mammoths as evidence of a flood, there are no beneficial mutations, Paluxy tracks as evidence of human-dino cohabitation, etc... and yet, even if we point out to them that even AiG says not to use them, Creationists will still ignore us, or they will not accept it as wrong.

Well it would appear that the only time you seek to applaud aig is when they bend to your side of the spectrum, but I am sure when they bend to the YEC side you would howl at them all over again.

I am an avid readwer of ICR articles and research data. I know of many things they presented as possible evidence for tings that upon further review by them--they alterred their positions. But they do take with greatr skepticism work by evolutionists without critically examining the rebut claims of them.
 
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rmwilliamsll

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Well we need to get it back to where it was "inserted" into the code through random mutation--that is the heart of the debate here about mutations. Whethter they are preexisting variants within the code or actual true "new" info inserted intot he genome by random mutation.

nylon bug is a frame shift mutation. wholely new protein is produced that the bug never produced before.

HERV-K is a coopted virus gene

on another thread was the evidence of inserting a random manmade piece of dna and having it mutate into a useful protein producing gene.

there is no debate. it is simply the inability to listen to the evidence that is in question.
about 1% of your genome is HERV's, they originate from RV infections in your ancestors. somewhere along the line that dna was not part of that organism's genome. then poof an infection of a germ line and here we are, another HERV added. It is happening today in those infected with HIV, they have cells with HIV genes newly integrated and if it is a germ line cell it can be passed on to their offspring.

qed.
new information.
period.
no debate. only lack of understanding or study.
 
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random_guy

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nolidad said:
random guy writes:

Well it would appear that the only time you seek to applaud aig is when they bend to your side of the spectrum, but I am sure when they bend to the YEC side you would howl at them all over again.

No where did I applaud them. I was pointing out that the argument was so bad, even a Creationist site won't even use it, and yet, Creationists still use the same arguments.
 
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nolidad

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This is why mutations are called "random". There is no necessary connection between the point in time that a beneficial mutation occurs and the time it becomes needed.

Before I forget--this wasn't a "mutation" discovered over a century ago--this was an already resistant species discovered a century ago-- we still do not havwe the mutation yet-- all we have is immune systems doing what they were designed to do and species with resistances already present. So find the true mutation.

from Robert the pilgrim:

What condensed materials are you talking about?

The condensed material is an at least 1mb download of info from the RATE research project.

No where did I applaud them. I was pointing out that the argument was so bad, even a Creationist site won't even use it, and yet, Creationists still use the same arguments.

Well unfortunately info delivery systems arenb't as efficient with millions of individuals versus a coordinated network between universitiesd so unfortunately many times when something that at first appeared to be "solid evidence" and is later found to be either equivocal or a false start can take many years to work its way out, this is notr only true of YEC/evo materials but many other issues as well.

rmwilliams pronounces:

there is no debate. it is simply the inability to listen to the evidence that is in question.
about 1% of your genome is HERV's, they originate from RV infections in your ancestors. somewhere along the line that dna was not part of that organism's genome. then poof an infection of a germ line and here we are, another HERV added. It is happening today in those infected with HIV, they have cells with HIV genes newly integrated and if it is a germ line cell it can be passed on to their offspring.

now show thisd to produce new species thayt became new genera. Once again we are not debating the existence of mutations, or even the existence of beneficial mutations for they do happen, but how do they advance life from one genera to another via speciation and natural selection. Bugs developing a new dietr make it the same bug with a different diet. Bacteria that are antibiotic resistant still are the same bacteria with a horizontal variant.
 
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random_guy

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nolidad said:
Well unfortunately info delivery systems arenb't as efficient with millions of individuals versus a coordinated network between universitiesd so unfortunately many times when something that at first appeared to be "solid evidence" and is later found to be either equivocal or a false start can take many years to work its way out, this is notr only true of YEC/evo materials but many other issues as well.

Even after we point it out that AiG says, "Don't do that"? That's the problem. Creationists refuse to listen to science, and when they use arguments so bad, that Creationist sites tell them not to use it, and we point it out, they'll still use it, defend it, or not retract the statement. In general, Creationists will never admit any fault, no matter how much evidence you give them.
 
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nolidad

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The problem is, the majority of cases where someone is proven wrong is usually Creationists, and they will almost never admit any error. For example, even AiG admits that Creationists shouldn't use flash frozen mammoths as evidence of a flood, there are no beneficial mutations, Paluxy tracks as evidence of human-dino cohabitation, etc... and yet, even if we point out to them that even AiG says not to use them, Creationists will still ignore us, or they will not accept it as wrong.

First off in response to this whole post--when did AiG ecome the premier creationist website? I kow of no hierarchy of orgs (though depsite the animosity towards them I hold ICR as one of the best).

Flash frozen mammals have been by ICR used as "possible" evidence of the advance of rapid ice age after the flood. It is still a plausible computer model based on data given in scripture.

I know of no creationist site that says there are no beneficial mutations. Most of the sites question the alleged quantity and how they produce the diversity in life forms.

As for Paluxy, I ahve seen the films and read the work of some creationists who swear they are man tracks, but I like ICR's 1986 article as the best report scientifically of the tracks.

The Paluxy River Mystery (#151)
by John Morris, Ph.D.

Abstract
Rarely has a single research project created as much interest and controversy as has the alleged discovery of human and dinosaur footprints together in the limestone beds of the Paluxy River, normally thought to be 120 million years old. As evolutionists Milne and Schafersman admit, "Such an occurrence, if verified, would seriously disrupt conventional interpretations of biological and geological history and would support the doctrines of creationism and catastrophism." 1 Consequently, anti-creationists have devoted an inordinate amount of attention to this project, often ignoring, ridiculing, and distorting the evidence as reported by creationists.
Rarely has a single research project created as much interest and controversy as has the alleged discovery of human and dinosaur footprints together in the limestone beds of the Paluxy River, normally thought to be 120 million years old. As evolutionists Milne and Schafersman admit, "Such an occurrence, if verified, would seriously disrupt conventional interpretations of biological and geological history and would support the doctrines of creationism and catastrophism." 1 Consequently, anti-creationists have devoted an inordinate amount of attention to this project, often ignoring, ridiculing, and distorting the evidence as reported by creationists. 1, 2, 3 However, little significant fieldwork was done at the site by the anti-creationists until 1982, when "The American Humanist Association . . . financed a team of four scientists to thoroughly investigate the claims first hand." 2 This team of four was comprised of Drs. Laurie Godfrey, John Cole, Steven Schafersman, and Ronnie Hastings, and with the exception of Hastings, has as yet done little fieldwork. On the other hand, the Paluxy project has been the site of numerous creationist field studies, since, while the creation model is not dependent on the Paluxy evidence, the claim has always provided an easily understood illustration of the creation model. The two most widely circulated and accepted sources were the 1973 film, "Footprints in Stone," 4 produced by the late Stan Taylor, of Films for Christ, Inc., and this author's 1980 book, Tracking Those Incredible Dinosaurs and the People Who Knew Them. 5
When Taylor and his film crew were drawn to the Paluxy in 1968 by a number of published and unpublished reports of human and dinosaur tracks together, he found many residents of the area who claimed to have seen many true human tracks in the bed of the river, the best of which had since been carried away by a flood, others badly eroded. Some of these long-time residents maintained that a number of tracks of both man and dinosaur had been removed from the river during the depression, and sold. These claims were given credence by the circular holes in the river bottom from which prints had been taken--in some cases with prints of approximately human appearance still leading into and away from the holes.
In an attempt to verify these claims and to find fresh evidence, the Taylor team excavated back into the riverbank in several areas. New human-like trails, as well as fresh prints in existing trails, were found, where there was no possibility of carving. Taylor never found perfect human footprints, but the prints found did have significant indications of a human foot and possessed no features incompatible with a human foot, so far as could be seen. No other animal was known which could have made these markings. It was concluded, therefore, that the weight of the evidence justified the interpretation that the tracks were most probably human, given the backdrop of "old timer" testimony.
Over the years, however, further erosion has dramatically changed the appearance of the prints. Creationist investigators have frequently clamed that only the freshly exposed evidence need be defended--not the eroded remnants of tracks. The controversy seemed forever deadlocked, since the original nature of the prints was available for study only in photos, movies, and casts. The only way creationist claims could be invalidated was for (1) features of the prints not visible beforehand to be exposed by erosion and (2) for the testimonies of the "old timers" to be discredited. As unlikely as this may seem, just such a scenario may be taking place today.
Due to an unknown cause, certain of the prints once labeled human are taking on a completely different character. The prints in the trail which I have called the "Taylor Trail," 5 consisting of numerous readily visible elongated impressions in a left-right sequence, have changed into what appear to be tridactyl (three-toed) prints, evidently of some unidentified dinosaur. The changes in the impressions themselves are mostly confined to lengthening in the downriver direction. The most significant change, however, is that surrounding the toe area. In almost each of the prints in the trail, three large "toes" have appeared, similar to nearby dinosaur tracks. These toes, typically, are coloration phenomena only, with no impressions, in most cases. Frequently the "mud push up" surrounding the original elongated track is crossed by this red coloration. The shape of the entire track, including both impression and coloration, is unlike any known dinosaur print.
A local resident had, in 1968, shown Taylor where he had removed a human track to sell during the 1930's. Three 9-1/2" long man-like tracks were found leading up to the hole, two of which showed the general outline of a human foot. Following this general direction, Taylor removed overlying strata for 200 feet downriver, and found what was later called the Taylor Trail. He made no claims that these prints contained unquestionable toes or other diagnostic features, but the bipedal stride and the general shape of the tracks were certainly compatible with what a human would make while walking in mud. In fact, the prints did possess features which were problematic, prompting creationist Berney Neufeld later to label them as shallow, eroded dinosaur tracks.6 The trail might not have been called human if not for the hole from which a "perfect" print had reportedly been taken some 50 feet away. (From a recent study of Taylor's field notes, it is fairly certain that the prints near the hole were not a part of the Taylor Trail, as previously thought.)
But what of the other trails at the same site, which have also been labeled "human?" The Turnage Trail, consisting of a trail of eight, with print numbers 2 and 5 missing, has also developed puzzling features in prints 3 and 4. Here a bluish coloration and minor impressions indicate a smaller but distinctly pointed tridactyl shape. The rest of the trail has not recently been exposed, and it is not known if those prints also show such features. In fact, prints 3 and 4 were always much different from the rest of the trail, and somewhat out of line, as well. In light of the new appearance, and the fact that new impressions have appeared in this part of the river in recent years, it would be worthwhile to reexamine the rest of the trail.
The "Giant Trail," consisting of six large prints, seemed like better evidence. The bank has collapsed over three of the six, but the three now visible show no dinosaurian features, even though the surface has been somewhat eroded. However, a trail of coloration features leading up to the Giant Trail do raise a question. Separating the first giant track (print number +1), and the closest possible coloration marking (now called print 0), is a distance of 90", and if both belong to the same trail, two prints are completely missing. That first coloration (print 0) is poorly formed, and not diagnostic. The toe area of the next in line (print 00) was stepped on by a clear dinosaur print, as was the next marking (print -1). Finally, the next farthest print (print -2) shows, in coloration only, claw features similar to the Taylor Trail. The association with the Giant Trail is tenuous, but the possibility that the entire trail might be dinosaurian cannot be ignored.
The Ryals Trail included a hole in the river from which "one of the best human footprints" (according to Jim Ryals and many others) was removed by Ryals over 50 years ago. The prints entering and leaving the cutout seemed (in 1968), at least compatible with a human foot. As with the other trails, these are now developing tridactyl colorations. If this trail is, in actuality, a dinosaur trail, the testimonies of the "old timers" must be questioned. Studies by a team of ICR scientists of cores taken through each of the claws of one print, in an effort to determine whether or not the coloration features are only surface stains, were inconclusive. The mottled rock material beneath the toes showed some evidence of infilling with a different material, but in other areas, showed only a thin veneer of slightly different material.
In view of these developments, none of the four trails at the Taylor site can today be regarded as unquestionably of human origin. The Taylor Trail appears, obviously, dinosaurian, as do two prints thought to be in the Turnage Trail. The Giant Trail has what appears to be dinosaur prints leading toward it, and some of the Ryals tracks seem to be developing claw features, also.
Trails and prints elsewhere along the Paluxy, while contributive to the original interpretation, may be insufficient to stand alone. Erosion has further deteriorated the once-interesting prints on the park ledge, but they are still recognizable. At the Dougherty site, no hints of the important Cherry Trail and Morris prints remain. The various controversial prints labeled as human by Carl Baugh in recent years are of uncertain origin, and at best are not comparable in quality to prints at the sites discussed above, thereby providing no support for the original position. Earlier prints which had been removed from the river before being documented, even if genuine, cannot be considered as compelling evidence, in view of their uncertain source.
The stain surrounding the prints has evidently increased over the past few years. It was first noted in 1982 by Mr. Glen Kuban, who since 1980 has been researching the area.7 At the invitation of Kuban, Paul Taylor, Marian Taylor, and Marvin Herrmann (all associated with the production of Footprints in Stone), Tom Henderson, early footprint investigator, and this author, returned to Paluxy in October 1985, to see the new evidence. Some of us have returned since to do additional fieldwork. With the exception of Kuban, who claims neutrality on the creation-evolution question, all share the conclusion that the recent reddish stain, so devastating to the original interpretation, is itself quite baffling as to source and meaning. The following additional mysterious points seem significant:​
  1. Fifteen years of erosion (contrary to the usual effects of erosion) seems to have "improved" the quality of the trackways. It is possible that a thin overlying layer is eroding, revealing an underlying print, but then why didn't the adjacent, deep dinosaur trail receive this infilling material, since it was evidently made first?
  2. Since the marl which filled in the deep dinosaur tracks was unconsolidated and easily removed by investigators, why did the Taylor tracks retain much of the material while providing a solid print bottom and flush toes?
  3. If the reddish stain is due to minerals in the river water, why did the Ryals Trail, which has been exposed at least 60 years, begin to stain at the same time as the more recently exposed prints?
  4. Applying a reddish stain to a rock surface can easily be accomplished by the application of certain readily available chemical agents.
  5. Is the Giant Trail extension valid? Likewise, are the tridactyl prints in the Turnage Trail really part of that trail? How could the "old timers" all be so wrong about the track removed from the Ryals Trail?
  6. Why do the cores not show unequivocal evidence of toe infilling if the red surface stain is indeed a chemical alteration of an infilling material?
Even though it would now be improper for creationists to continue to use the Paluxy data as evidence against evolution, in the light of these questions, there is still much that is not known about the tracks and continued research is in order. We stand committed to truth, and will gladly modify or abandon our previous interpretation of the Paluxy data as the facts dictate.
 
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Here is an interesting article from a molecular biologist on antibiotic resistence in bacteria.

The "Evolution" of Antibiotic Resistance (#378)
by Daniel Criswell, Ph.D
Download The "Evolution" of Antibiotic Resistance PDF
Abstract
Since World War II many more antibiotics isolated from fungi (molds) and bacteria have been used to treat a wide range of human and animal infections. One group of bacteria, the Streptomyces, produces most of the medically important antibiotics.
An increase in the frequency of antibiotic resistance in bacteria since the 1950s has been observed for all major classes of antibiotics used to treat a wide variety of respiratory illnesses, skin disorders, and sexually transmitted diseases. Is this resistance the result of bacteria evolving new genes in response to the presence of antibiotics, or are antibiotic-resistant bacteria selected for in the environment by possessing antibiotic resistance genes beforehand? To answer these questions a discussion of several factors involved in antibiotic resistance will show that resistance is a designed feature of pre-existing genes enabling bacteria to compete with the antibiotic producers in their environment.
A brief look at an example of penicillin resistance reveals the increase in the frequency of antibiotic-resistant organisms since the time when antibiotic use became common. Penicillin is an antibiotic produced by the common bread mold Penicillium that was discovered accidentally in 1929 by the British microbiologist, Alexander Fleming. By the 1940s, penicillin was available for medical use and was successfully used to treat infections in soldiers during World War II. Since then, penicillin has been commonly used to treat a wide range of infections. In 1967 the first penicillin-resistant Streptococcus pneumoniae was observed in Australia, and seven years later in the U.S. another case of penicillin-resistant S. pneumoniae was observed in a patient with pneumococcal meningitis.[1] In 1980 it was estimated that 3-5% of S. pneumoniae were penicillin-resistant and by 1998, 34% of the S. pneumoniae sampled were resistant to penicillin.1 Antibiotic resistance by other organisms reflects the same trend observed between S. pneumoniae and penicillin. Tetracycline resistance by normal human intestinal flora has exploded from 2% in the 1950s to 80% in the 1990s.[2] Kanamycin, an antibiotic used in the 1950s, has become clinically useless as a result of the prevalence of kanamycin-resistant bacteria. The increase in resistance among these organisms clearly indicates a change in the frequency of antibiotic resistance genes.
Since World War II many more antibiotics isolated from fungi (molds) and bacteria have been used to treat a wide range of human and animal infections. One group of bacteria, the Streptomyces, produces most of the medically important antibiotics.[3] Streptomyces release antibiotics into the soil in a sort of "biochemical warfare" scenario to eliminate competing organisms from their environment. These antibiotics are small molecules that attack different parts of an organism's cellular machinery. Streptomyces-produced quinolone and coumarin antibiotics, such as novobiocin, interfere with a protein called gyrase that assists in the normal separation of double-stranded DNA during replication of DNA or transcription of messenger RNA.[4] Failure of DNA to properly separate during these processes results in a bacterium not being able to divide normally or produce functional proteins. Ribosomes, the structures where protein synthesis is catalyzed, are the targets of many other Streptomyces antibiotics such as spectinomycin, tetracycline, and streptomycin. Spectinomycin and tetracycline prevent proteins from being assembled by the cell and streptomycin induces the assembly of the wrong amino acids into the translated protein.[5,6] Without proteins, which are necessary for normal cell function, the cell dies. The slight differences between human ribosomes which are not bound by these antibiotics and bacterial ribosomes make this type of antibiotic ideal for treating many illnesses. Other antibiotics, such as penicillin, block the assembly of the bacterial cell wall causing it to weaken and burst.[7] Penicillin is an effective antibiotic for human diseases because it interferes with a biological component in bacteria (cell wall) not found in human cells. The production of antibiotics by these organisms provides them with a competitive advantage over non-resistant bacteria in their environment. Just as large organisms such as plants and animals must compete for living space, food, and water, these microbes use antibiotics to eliminate competition with other microbes for these same resources.
However, not all bacteria are defenseless against the antibiotic producers. Many possess genes that encode proteins to neutralize the affects of antibiotics and prevent attacks on their cell machinery. Efflux pumps, located in the cell membrane, are one method of protection that many bacteria use against the influx of antibiotics.[6] The offensive antibiotic is pumped out of a cell that possesses these pumps before the antibiotic can cause harm to the cellular machinery. Although many efflux pumps may be specific for the substrate they pump out of the cell, they are not uncommon. Ribosomal protection proteins (RPP) are another source of resistance bacteria use to protect themselves from antibiotics. These proteins protect ribosomes by binding them and changing their shape or conformation. The change in the ribosome shape prevents an antibiotic from binding and interfering with protein synthesis.6 The RPP-bound ribosomes are able to function normally during protein synthesis, an important feature of this method of antibiotic resistance. Some bacteria produce enzymes that neutralize antibiotics by adding acetyl (COCH3) or phosphate (PO32-) groups to a specific site on the antibiotic.[8] This modification reduces the ability of the antibiotic to bind to ribosomes, rendering it harmless to the cell.[9] Interestingly, all three types of antibiotic-resistant genes that produce efflux pumps, ribosomal protection proteins, and modifying enzymes are found in Streptomyces species, the producers of many antibiotics. It appears this is the method Streptomyces uses to protect itself from its own antibiotics.
Is it possible to transfer these resistance genes to other bacteria? A unique bacterial characteristic that has not been demonstrated in plant and animal cells is the ability to transfer genes from one bacterium to another, a process called lateral gene transfer. Genes located on a circular strand of DNA called an R-plasmid may contain several antibiotic-resistant genes. Through a process called conjugation an antibiotic-resistant bacterium can transfer the antibiotic resistance genes from an R-plasmid to a non-resistant bacterium.[10] Ironically, several antibiotic resistance genes found in other pathogenic bacteria are very similar in DNA sequence to the genes found in Streptomyces species.[11] The efflux pumps that Streptomyces use to pump out antibiotics to eliminate their competitors are likely the same pumps that other species of bacteria are now using to pump out the offensive antibiotic delivered from Streptomyces! The antibiotic-resistant bacteria likely have acquired the genes for these efflux pumps through lateral gene transfer. The presence of ribosomal protection proteins and antibiotic modifying enzymes in resistant bacteria has also likely originated from Streptomyces or some other antibiotic-producing microbe.6 Bacteria don't appear to be evolving new genes; they are acquiring previously existing antibiotic resistance genes through lateral gene transfer. This allows a species of bacteria to possess enough genetic variability to adapt to a changing environment and to compete with its neighbors. (This method of defense is very similar to the genetic variability of mammalian antibody-producing B lymphocytes—a topic for another Impact article.) The bacterium that acquires the antibiotic resistance genes still has the physical and metabolic qualities that distinguish it from other bacteria kinds and associates it with its own kind of bacteria. The observed increase in the frequency of antibiotic-resistant bacteria has resulted from the increased use of antibiotics in medicine and agriculture, resulting in the reduction of organisms that do not possess antibiotic resistance genes.
Antibiotic resistance in bacteria can also be achieved when mutations in a ribosome or protein change the site where an antibiotic binds. For example, four of the antibiotics mentioned earlier, tetracycline, streptomycin, kanamycin, and spectinomycin, bind to a specific region of a ribosome and interfere with protein synthesis. Mutations may prevent an antibiotic from binding to the ribosome (kanamycin)[12] or allow the ribosome to function even while the antibiotic is bound (streptomycin and spectinomycin).[5] Although it appears these mutations are beneficial and provide an advantage to the bacterium possessing them, they all come with a cost. Ribosomal mutations, while providing antibiotic resistance for the organism, slow the process of protein synthesis, slow growth rates, and reduce the ability of the affected bacterium to compete in an environment devoid of a specific antibiotic.[13,14] Furthermore, a mutation that confers resistance to one antibiotic may make the bacterium more susceptible to other antibiotics.[15] These deleterious effects are what would be expected from a creationist model for mutations. The mutation may confer a benefit in a particular environment, but the overall fitness of the population of one kind of bacterium is decreased as a result of a reduced function of one of the components in its biological pathway. The accumulation of mutations doesn't lead to a new kind of bacterium—it leads to extinction.
References
  1. Doern, G.V. et al., 2001. Antimicrobial resistance among clinical isolates of Streptococcus pneumoniae in the United States during 1999_2000, including a comparison of resistance rates since 1994-1995. Antimicrobial Agents and Chemotherapy 45(6)1721-1729.
  2. Shoemaker, N.B. et al., 2001. Evidence for extensive resistance gene transfer among Bacteriodes spp. and among Bacteriodes of other genera in the human colon. Applied and Environmental Microbiology 67:561-568.
  3. Tanaka, Y., and S. Omura, 1990. Metabolism and products of actinomycetes: an introduction. Actinomycetologica 4:13-14.
  4. Contreras, A., and A. Maxwell, 1992. gyrB mutations which confer coumarin resistance also affect DNA supercoiling and ATP hydrolysis by Escherichia coli DNA gyrase. Molecular Microbiology 6(12):1617-1624.
  5. Carter, A.P. et al., 2000. Functional insights from the structure of the 30S ribosomal subunit and its interactions with antibiotics. Nature 407:340-348.
  6. Chopra, I., and M. Roberts, 2001. Tetracycline antibiotics: mode of action, applications, molecular biology, and epidemiology of bacterial resistance. Microbiology and Molecular Biology Reviews 65(2):232-260.
  7. Garrett, R.H., and C.M. Grisham, 1999. Biochemistry 2nd ed., Saunders College Publ., New York.
  8. Wright, G.D., 1999. Aminoglycoside-modifying enzymes. Current Opinion in Microbiology 2:499-503.
  9. Llano-Sotelo, B. et al., 2002. Aminoglycosides modified by resistance enzymes display diminished binding to the bacterial ribosomal aminoacyl-tRNA site. Chemistry and Biology 9:455-463.
  10. Campbell, N.A., and J.B. Reece, 2002. Biology 6th ed. Benjamin Cummings, Publ. San Francisco.
  11. Benveniste, R., and J. Davies, 1973. Aminoglycoside antibiotic-inactivation enzymes in actinomycetes similar to those present in clinical isolates of antibiotic-resistant bacteria. Proceedings of the National Academy of Sciences USA 172:3628-3632.
  12. Recht, M.I. et al., 1999. Basis for prokaryotic specificity of action of amino-glycoside antibiotics. EMBO Journal 18(11):3133-3138.
  13. Zengel, J.M. et al., 1977. Role of ribosomal protein S12 in peptide chain elongation: analysis of pleiotropic, streptomycin-resistant mutants of Escherichia coli. Journal of Bacteriology 129:1320-1329.
  14. Gregory, S.T. et al., 2001. Streptomycin-resistant and streptomycin-dependent mutants of the extreme thermophile Thermus thermophilus. Journal of Molecular Biology 309:333-338.
  15. Recht, M.I., and J.D. Puglisi, 2001. Aminoglycoside resistance with homogeneous and heterogeneous populations of antibiotic-resistant ribosomes. Antimicrobial Agents and Chemotherapy 45(9):2414-2419.
* Dr. Daniel Criswell has a Ph.D. in Molecular Biology and is a biology professor at the ICR Graduate School.
 
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