Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
1 online now:
Newest Member: popoi
Post Volume: Total: 915,818 Year: 3,075/9,624 Month: 920/1,588 Week: 103/223 Day: 1/13 Hour: 0/1


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   evidence that intelligent design can't explain
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 31 of 50 (14552)
07-31-2002 7:37 AM
Reply to: Message 30 by mark24
07-30-2002 5:11 AM


Bumping points 1-3 on message 21.........
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 30 by mark24, posted 07-30-2002 5:11 AM mark24 has replied

Replies to this message:
 Message 32 by mark24, posted 08-08-2002 8:45 PM mark24 has not replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 32 of 50 (15046)
08-08-2002 8:45 PM
Reply to: Message 31 by mark24
07-31-2002 7:37 AM


& again.....
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 31 by mark24, posted 07-31-2002 7:37 AM mark24 has not replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 33 of 50 (15050)
08-08-2002 9:22 PM
Reply to: Message 28 by Peter
07-29-2002 3:25 AM


Dear Peter,
You state:
"Random in the sense of ToE means we don't know when it will
happen. It is not a direct response to the environment, but
a happy circumstance if it's a benefit."
I say:
'When' and 'where' are completely different questions. I say that a mechanism introduces the mutations observed in the 1G5 gene (and maybe also in other genes). It maybe in response to the environment (this answers the when question).
For instance.
Q: WHEN do antibody genes start to mutate to improve affinity?
A: When the immune cells (B cells) that produce the immunoglobulins encounter antigen that can be bound by the antibody.
Elucidating the underlying mechanism will answer the WHERE question. But at present it is certain that it is protein mediated and therefor cannot be at random.
Peter

This message is a reply to:
 Message 28 by Peter, posted 07-29-2002 3:25 AM Peter has replied

Replies to this message:
 Message 46 by Peter, posted 08-12-2002 6:55 AM peter borger has not replied

  
peter borger
Member (Idle past 7666 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 34 of 50 (15052)
08-08-2002 10:33 PM
Reply to: Message 21 by mark24
07-25-2002 6:44 AM


dear Mark,
You say:
"Good grief, this isn’t in dispute!!!"
If mutations can be non-randomly introduced how can the NDT still be around? Once more, how do you conceive hot-spots in the DNA? Is a mechanism involved, or not? If not, how do you conceive hot-spots in the DNA? I am really interested in your opinion.
And:
"1/ That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab."
First of all, the GLO gene is an inactive gene since it has been interupted at several sites. The sequence shown in the paper is the sequence of exon X. It is of interest since it demonstrates a non-sense mutation (introduction of a stop codon). Since the protein is not expressed at all, all positions in the DNA are completely neutral. This means that natural selection does not act on the sequence since the protein is not expressed. So, mutations should be introduced completely at random according to NDT (and according to Kimura with a neutral rate). If not, than a hot-spot is present in the DNA. It tells me that a mechanism drives the mutations. Since we presently do not know the mechanism we cannot say where exactly the mutations will occur.
For the 1G5 gene there are much more data than the GLO gene and the hotspots are pretty clear. One may even be able to predict future mutations in the gene of Drosophila melanogaster. If you have a close look at the figure in Schmidt and Tautz article you will notice that some nucleotides change in different subpopluations at the same spot in the DNA, idependent from selection. Since we do not yet have such extended data for subpopulations of primates it is too early to say something about it. However, there are such data for human subpopulations, but these are not yet thoroughly scrutinised.
I am sure we will find the mechanism of non-random mutation.
And you state:
"Common descent & genetic drift remains the best explanation for non-vit c synthesis in primates, particularly given that the two prosimian primates that can synthesise vit c, fit in nicely at the bottom of the primate phylogeny, where they would be expected if evolution & common descent were responsible. That is, that vit c gene wrecking occurred after the prosimian divergence, leaving them unnaffected. A remarkable coincidence, don’t you think?"
You are free to believe that common descent and genetic drift are the best naturalistic explanations. However, if mutations are non-random these conclusion cannot be drawn. As observed in the 1G5 gene of D. simulans even indel-mutations may be non-random. As long as we do not know this, your conlusion is unwarranted. I can imagine that you -- as an evolutionist-- are eager to take the GLO gene as proof for common descent. However, then I could take all genes that violate the species tree as evidence against common descent. So, it doesn't proof anything. Common descent is merely a believe.
And:
"2/ That you are able to attribute the existence of hot spots to design, when the cause of hot spots is UNKNOWN. God-Of-The-Gaps."
I (and others) have already explained that if the information is already present in the genome it makes it hard not to believe in design. Maybe you know a naturalistic explanation. I am very curious to hear about it.
3/ That non-random means directed, or pre-programmed in the sense of design, with regard to spontaneous mutations. If you think it does, rather than not-an-equal-chance-of-mutation-at-each-site, then you need to back this up. Remember, you have already told me you aren’t conflating the statistical & colloquial definitions of random/non-random."
At present the only well presented gene in subspieces of an organism is the 1G5 gene of D. mel. I invite you to study the sequences of the 13 subspecies extensively and have a careful look at the site of the mutations, and the type of substitutions. (Please do, since I am becoming a bit tired of repeating myself.)
And, what exactly did I tell you about conflating the statistical and colloquial definitions of random/non-random?
Best wishes,
Peter

This message is a reply to:
 Message 21 by mark24, posted 07-25-2002 6:44 AM mark24 has replied

Replies to this message:
 Message 38 by mark24, posted 08-09-2002 1:55 PM peter borger has not replied

  
William E. Harris
Inactive Member


Message 35 of 50 (15074)
08-09-2002 3:50 AM
Reply to: Message 1 by monkenstick
07-23-2002 1:23 AM


I believe in a pre-earth life in which we learned about creation and genetic engineering and in fact were the ones who created the evolutionary steps under God's supervision. God pronounced what was accomplished as "good", not perfect. Perhaps some unimportant imperfections were allowed.
If you claim to be an anthiestic evolutionist, why do you live by faith in assuming that speciation eventually leads to new Genera, Orders etc. while you can give no evidence for it?
William

This message is a reply to:
 Message 1 by monkenstick, posted 07-23-2002 1:23 AM monkenstick has not replied

  
monkenstick
Inactive Member


Message 36 of 50 (15083)
08-09-2002 7:48 AM


if you are going to allow for "unimportant imperfections" what use is ID as a scientific theory?
if it only describes part of the genome, how are we to distinguish between sequences which are designed and which have evolved?

Replies to this message:
 Message 37 by John, posted 08-09-2002 9:39 AM monkenstick has not replied
 Message 41 by William E. Harris, posted 08-10-2002 12:19 PM monkenstick has not replied

  
John
Inactive Member


Message 37 of 50 (15088)
08-09-2002 9:39 AM
Reply to: Message 36 by monkenstick
08-09-2002 7:48 AM


quote:
Originally posted by monkenstick:
if you are going to allow for "unimportant imperfections" what use is ID as a scientific theory?
That's a good point. It makes determining designed from not-designed much more difficult. And casts some question on the 'intelligence' part of the equation.
quote:
if it only describes part of the genome, how are we to distinguish between sequences which are designed and which have evolved?
I really wish someone would answer this question. I have asked several people here to do so, and so far without result.
------------------
http://www.hells-handmaiden.com

This message is a reply to:
 Message 36 by monkenstick, posted 08-09-2002 7:48 AM monkenstick has not replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 38 of 50 (15101)
08-09-2002 1:55 PM
Reply to: Message 34 by peter borger
08-08-2002 10:33 PM


quote:
Originally posted by peter borger:
dear Mark,
You say:
"Good grief, this isn’t in dispute!!!"
If mutations can be non-randomly introduced how can the NDT still be around? Once more, how do you conceive hot-spots in the DNA? Is a mechanism involved, or not? If not, how do you conceive hot-spots in the DNA? I am really interested in your opinion.

The NDT is around because it uses a different definition of random to you, you are putting words in peoples mouths in order to make your strawman.
http://EvC Forum: molecular genetic proof against random mutation (1) -->EvC Forum: molecular genetic proof against random mutation (1)
Is a mechanism involved in hot spots? Yup, no problem with that, in the same way the GC rich sequences in some way provide a mechanism for chiasmata to occur. I think you’re leaping ahead & assuming mechanism is analogous with design. After all, evaporation & condensation/precipitation is mechanistic. Plate tectonics is mechanistic. Solar eclipses are mechanistic, ad infinitum.
If mechanisms occur naturally, & you are unable to tell the difference between natural & non-natural mechanisms, then it’s the same old ID argument again.
[QUOTE]Originally posted by peter borger:
[B]
And:
"1/ That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab."
First of all, the GLO gene is an inactive gene since it has been interupted at several sites. [/QUOTE]
[/b]
If I can interrupt you (pun unintended) right there. Non-transcribed DNA has been shown to have function. So interruption to transcription does not equate to non-function. Regulatory sequences etc.
[QUOTE]Originally posted by peter borger:
[B]
The sequence shown in the paper is the sequence of exon X. It is of interest since it demonstrates a non-sense mutation (introduction of a stop codon). Since the protein is not expressed at all, all positions in the DNA are completely neutral. [/QUOTE]
[/b]
There ARE non-transcribing DNA elements that have function. Do you think transposons are transcribed, the ones that are functional & not bang in the middle of genes, that is? So, you can’t equate lack of expression/transcription to lack of function.
Furthermore, it is possible for transcription sequences to be greatly shortened by non-sense mutations, yet still be transcribed (everything after the stop codon doesn’t get transcribed, unless, of course a new start codon appears further downstream the gene sequence..). Protein functions are then unknown, & not proven functionless.
[QUOTE]Originally posted by peter borger:
[B]
This means that natural selection does not act on the sequence since the protein is not expressed. [/QUOTE]
[/b]
Natural selection may well act upon the sequence, you haven’t shown total lack of function, see above.
[QUOTE]Originally posted by peter borger:
[B]
So, mutations should be introduced completely at random according to NDT (and according to Kimura with a neutral rate). [/QUOTE]
[/b]
They are completely at random, I’ve shown you the intended definition elsewhere. I don’t see what you hope to gain by mis-representing THE INTENDED MEANING of random as it pertains to random mutation.
Oh, my mistake, I do!
[QUOTE]Originally posted by peter borger:
[B]
Since the protein is not expressed at all, all positions in the DNA are completely neutral. This means that natural selection does not act on the sequence since the protein is not expressed. So, mutations should be introduced completely at random according to NDT (and according to Kimura with a neutral rate). If not, than a hot-spot is present in the DNA. It tells me that a mechanism drives the mutations. Since we presently do not know the mechanism we cannot say where exactly the mutations will occur. [/QUOTE]
[/b]
Taking this passage as a whole;
You still haven’t told me how you identify a hot spot in an ancestral sequence? A site can mutate once or a thousand times, how can you tell from a substitution from A to C,T, or G that it is a hotspot?
How can you tell that more mutations have occurred at a locus than at the neutral rate? It’s A,C,G or T?
More below.
[QUOTE]Originally posted by peter borger:
[B]
For the 1G5 gene there are much more data than the GLO gene and the hotspots are pretty clear. One may even be able to predict future mutations in the gene of Drosophila melanogaster. If you have a close look at the figure in Schmidt and Tautz article you will notice that some nucleotides change in different subpopluations at the same spot in the DNA, idependent from selection. Since we do not yet have such extended data for subpopulations of primates it is too early to say something about it. However, there are such data for human subpopulations, but these are not yet thoroughly scrutinised. [/QUOTE]
[/b]
I’m not talking about the 1G5 gene, but your claim that the GLO pseudogene was wrecked by hotspots & not conventional random mutation. I’d still like to know how you can tell a random substitution from a non-random one in ancestral DNA.
[QUOTE]Originally posted by peter borger:
[B]
I am sure we will find the mechanism of non-random mutation. [/QUOTE]
[/b]
Me too. I’m also sure it will be entirely natural, but that you will still call it evidence of design.
[QUOTE]Originally posted by peter borger:
[B]
And you state:
"Common descent & genetic drift remains the best explanation for non-vit c synthesis in primates, particularly given that the two prosimian primates that can synthesise vit c, fit in nicely at the bottom of the primate phylogeny, where they would be expected if evolution & common descent were responsible. That is, that vit c gene wrecking occurred after the prosimian divergence, leaving them unnaffected. A remarkable coincidence, don’t you think?"
You are free to believe that common descent and genetic drift are the best naturalistic explanations. However, if mutations are non-random these conclusion cannot be drawn. [/QUOTE]
[/b]
I do still maintain that common descent & drift are the best explanations of non vit c synthesis. Whether the mutations are random, partly random, or COMPLETELY NON-RANDOM, matters not one iota to phylogenetic inference. A non-lethal/non-genetic death mutation is heritable either way. If it's heritable, then phylogeny can be inferred.
[QUOTE]Originally posted by peter borger:
[B]
2/ That you are able to attribute the existence of hot spots to design, when the cause of hot spots is UNKNOWN. God-Of-The-Gaps."
I (and others) have already explained that IF [my bold] the information is already present in the genome it makes it hard not to believe in design. Maybe you know a naturalistic explanation. I am very curious to hear about it. [/QUOTE]
[/b]
How can you tell if something is designed when you don’t understand the mechanism?
Also, there’s a VERY BIG IF in that sentence.
I find it odd that a designer would go to the trouble of creating vit c synthesis in an organism, then deliberately put a function wrecker in as standard. It’s like designing an aircraft so that the wings fall off. Is this evidence against design? It’s as good as evidence for design, so why not? J
quote:
Originally posted by peter borger:

3/ That non-random means directed, or pre-programmed in the sense of design, with regard to spontaneous mutations. If you think it does, rather than not-an-equal-chance-of-mutation-at-each-site, then you need to back this up. Remember, you have already told me you aren’t conflating the statistical & colloquial definitions of random/non-random."
At present the only well presented gene in subspieces of an organism is the 1G5 gene of D. mel. I invite you to study the sequences of the 13 subspecies extensively and have a careful look at the site of the mutations, and the type of substitutions. (Please do, since I am becoming a bit tired of repeating myself.)
And, what exactly did I tell you about conflating the statistical and colloquial definitions of random/non-random?

I think you’ll find it was me that warned YOU about statistical & colloquial definitions of random, not the other way around.
I’m sorry you’re getting tired of repeating yourself, because you’re going to have to get used to it if you continue to avoid pertinent questions.
For the THIRD time, & this time I’ll really labour the point.
quote:
Originally posted by peter borger:

That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab.

Let me put it another way, you can take an extant sequence, mutate it a thousand times, then examine where the sequences mutate most in order to demonstrate where the hot spots are.
THIS IS DIFFERENT TO INFERRING HOT SPOTS ON ANCESTRAL SEQUENCES, FROM ALLEGED NEUTRAL EXTANT LOCI!!!!!!!!
The best you can see from an ancestral sequence is that a loci mutated a maximum of three times, that is, from A to G, A to T, A to C, certainly not from within your paradigm. There is no way you can quantify a hotspot that has a thousand-fold higher probability of mutation than a statistically random probability. You may look at loci that appear to be random to you, but have mutated thousands of times more than adjacent loci, but because it started as A, & finished as A, you will never know.
This is probably best illustrated in the form of a question;
Q/ There is a single homologous locus in a gene in eight different related organisms. The locus is alleged to be neutral. Is there, or has there ever been a hotspot at this locus?
1/The nucleotides are A,G,T,C,A,G,T, & C.
2/The nucleotides are A,A,A,A,A,A,A, & A.
3/The nucleotides are A,A,A,A,A,A,A, & T.
No, I can't tell either.
Mark
------------------
Occam's razor is not for shaving with.
[This message has been edited by mark24, 08-09-2002]
[This message has been edited by mark24, 08-10-2002]

This message is a reply to:
 Message 34 by peter borger, posted 08-08-2002 10:33 PM peter borger has not replied

Replies to this message:
 Message 39 by wj, posted 08-10-2002 11:11 AM mark24 has replied

  
wj
Inactive Member


Message 39 of 50 (15140)
08-10-2002 11:11 AM
Reply to: Message 38 by mark24
08-09-2002 1:55 PM


Let me get some clarification on Peter Borger's frequent self-aggrandizing declarations in various threads about the demise of NDT. Does his whole argument boil down to
unequal frequency of mutations at all loci = non-random mutation = directed mutation by mechanism unknown = genomes designed to mutate in (enhancing) response to external evnironmental factors = evidence for intelligent design by designer unknown (don't say god) = demise of NDT ?

This message is a reply to:
 Message 38 by mark24, posted 08-09-2002 1:55 PM mark24 has replied

Replies to this message:
 Message 40 by mark24, posted 08-10-2002 11:30 AM wj has not replied
 Message 47 by peter borger, posted 08-14-2002 3:55 AM wj has not replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 40 of 50 (15144)
08-10-2002 11:30 AM
Reply to: Message 39 by wj
08-10-2002 11:11 AM


wj,
Yup, that about sums it up
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 39 by wj, posted 08-10-2002 11:11 AM wj has not replied

  
William E. Harris
Inactive Member


Message 41 of 50 (15150)
08-10-2002 12:19 PM
Reply to: Message 36 by monkenstick
08-09-2002 7:48 AM


Only snp mutations evolve by natural selection (which is also part of ID to be influenced by enviornmental factors). Additional new gene complexes come from ID. The chance of new gene complexes to be produced by natural selection is essentially zero.
William

This message is a reply to:
 Message 36 by monkenstick, posted 08-09-2002 7:48 AM monkenstick has not replied

Replies to this message:
 Message 42 by wj, posted 08-10-2002 12:44 PM William E. Harris has replied

  
wj
Inactive Member


Message 42 of 50 (15153)
08-10-2002 12:44 PM
Reply to: Message 41 by William E. Harris
08-10-2002 12:19 PM


quote:
Originally posted by William E. Harris:
Only snp mutations evolve by natural selection (which is also part of ID to be influenced by enviornmental factors). Additional new gene complexes come from ID. The chance of new gene complexes to be produced by natural selection is essentially zero.
William

What sort of delusion is this? What precludes multiple nucleotide insertions and deletions, gene duplication, chromosomal inversions and polyploidy from being sources of variation which can be might be acted on by natural selection? Where is the evidence for ID except in the personal incredulity of its believers? The problem for IDers is that they have no idea where to draw the line between natural processes of natural processes of mutation, natural selection, genetic drift and evolution and ID because they only invoke ID at the point where they can't believe the naturalistic explanation. But because this is a personal view and varies with such factors as knowledge of the topic, each IDer draws the line at a different point. Nothing like having a personal opinion masquerading as science!

This message is a reply to:
 Message 41 by William E. Harris, posted 08-10-2002 12:19 PM William E. Harris has replied

Replies to this message:
 Message 43 by William E. Harris, posted 08-10-2002 10:26 PM wj has not replied

  
William E. Harris
Inactive Member


Message 43 of 50 (15170)
08-10-2002 10:26 PM
Reply to: Message 42 by wj
08-10-2002 12:44 PM


wj
I realize I was a little SNPy not to include nucleotide insertions and deletions, gene duplication, chromosomal inversions, genetic drift and polyploidy. But what sort of delusion is it for you to believe that they can create new gene clusters necessary for evolution beyond speciation. Show me some evidence! Is your logic, phylogenetic evolution must have happened this way? If so, you are living by the faith you deride creationists for having.
Looking at new gene production from a statistical point of view, Stu Pullen, author of "Darwin's Mistake", has concluded that statistical models to calculate the odds of a new gene evolving from a random sequence of DNA show that new gene production by natural selection does not work. He states, "These models presented on his website (http://www.theory-of-evolution.org) change the entire complexion of the evolutionary debate. These models predict that new genes cannot evolve from random sequence of DNA. Since the models are based on math, subjective opinions are no longer relevant. If the models are correct, evolution did not happen under the guidance of naturalistic laws.
Many other scientists have reached the same conclusion. The models developed here are more accurate than previous models developed by other scientists. As it turns out, these more accurate models predict that the odds associated with a gene evolving from random chance are even lower. The probability is so small that scientists like Yockey in Information Theory and Molecular Biology have commented that anyone who believes that a novel protein can arise through chance does so on faith....
There is a point where alternatives must be sought. The evolution of new genes by natural selection does not happen. Any scientist who believes that it can either has not seen the odds or simply accepts the naturalistic axiom on faith."
I am not trying to appeal to authority, I really would like to know if there are errors in his model, I would like some input on what they are.
William

This message is a reply to:
 Message 42 by wj, posted 08-10-2002 12:44 PM wj has not replied

Replies to this message:
 Message 44 by mark24, posted 08-11-2002 7:58 AM William E. Harris has not replied
 Message 45 by mark24, posted 08-11-2002 6:13 PM William E. Harris has not replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 44 of 50 (15189)
08-11-2002 7:58 AM
Reply to: Message 43 by William E. Harris
08-10-2002 10:26 PM


Hi William,
I had trouble finding the math models, could you cite the exact page please.
Cheers,
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 43 by William E. Harris, posted 08-10-2002 10:26 PM William E. Harris has not replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 45 of 50 (15216)
08-11-2002 6:13 PM
Reply to: Message 43 by William E. Harris
08-10-2002 10:26 PM


quote:
Originally posted by William E. Harris:

I realize I was a little SNPy not to include nucleotide insertions and deletions, gene duplication, chromosomal inversions, genetic drift and polyploidy.

Actually, you were right to leave genetic drift out. GD & NS are by definition mutually exclusive.
quote:
Originally posted by William E. Harris:

These models predict that new genes cannot evolve from random sequence of DNA. Since the models are based on math, subjective opinions are no longer relevant. If the models are correct, evolution did not happen under the guidance of naturalistic laws.
Many other scientists have reached the same conclusion. The models developed here are more accurate than previous models developed by other scientists.

Many other scientists? Excellent, so these models are peer reviewed, then?
Subjective opinions are no longer relevant IF the models are 100% ABSOLUTELY correct, but then how do you know? That sentence was premature.
Mark
------------------
Occam's razor is not for shaving with.
[This message has been edited by mark24, 08-11-2002]

This message is a reply to:
 Message 43 by William E. Harris, posted 08-10-2002 10:26 PM William E. Harris has not replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024