prove me wrong on evolution

[Endless]

Firstly he was not asked any question. Second of all he was not asked to explain things simply. Thirdly he was trying to explain the basics - which he explained incorrectly. Not that he wasn't specific enough - he was wrong.
Is it any wonder you don't understand what i'm talking about - barr Opethian by the looks of it.

Any uncyclopedia readers here?

It would make you wonder....:bonk:

 

[JerryL]

Firstly he was not asked any question. Second of all he was not asked to explain things simply. Thirdly he was trying to explain the basics - which he explained incorrectly. Not that he wasn't specific enough - he was wrong.

Like you were with your statement that people with down's syndrome were not fertile? Or with the statement you were attempting to infer that added chormosomes result in sterility because of some mythic barrier to "novel new" genes?

What about your failure to address any mechanism to prevent "novel new" genes, nor any ability to even give a definition for "kind", while asserting that "kind-change" can't happen? Where's your refutation of my point that both new and novel have happened and you are creating an ever moving "line in the sand"?

You've not supported your argument. You've not responded to my clear and detailed refutations. In your appeal to your own authority, you've not addressed the fact that the scientific world embraces evolution almost universally. Your assertions about ignorance are pretty contrary to that fact and you've not offered even a little bit of explanaion.

You've picked on spelling to avoid answering the issue, you've picked on word choice (notice that even with my comment corrected by me, you've not discussed the topic at all).

The short list of logical fallacies:
Appeal to authoriy: Your assertion that you are right because you've read a book.
Reversal of proof: Your failure to meet the burden of proof your assertions carry.
Ad Hominim: Your focus on soemone else's spelling or education rather than the substance of their post.
Straw-Man: Your creation of your own criteria (such as "novel new") and then hacking at your own argument.

The list goes on. Support your claim that there is a real meachinsm of grouping animals with an actuall barrier to group-change. Define the barrier and illustrare it.

 

[Endless]

Support your claim that there is a real meachinsm of grouping animals with an actuall barrier to group-change. Define the barrier and illustrare it.

I would if i could even get that far. To be honest there is little point in discussing these things with people who don't understand the basics - because unless you have a good grasp of them then you won't understand what i am talking about and you have demonstrated time and time again that you don't.

Firstly i don't understand the first part in the quote. Remember that i was talking about microevolution and macroevolution and going to illustrate the difference that i perceive between them...

What about your failure to address any mechanism to prevent "novel new" genes, nor any ability to even give a definition for "kind", while asserting that "kind-change" can't happen? Where's your refutation of my point that both new and novel have happened and you are creating an ever moving "line in the sand"?

There is not a mechanism as such to prevent it. What i was saying is that we don't observe genes coming into existance as a result of mutation which code for new structures - like the sting example we talked about ages ago. Nor do we observe existing genes mutating into genes that code for a protein with a completely different yet still useful function in the cell's biochemical environment. I've already spoken about the definition of a kind in the other topic. Your examples of 'new and novel' genes are not examples of what i just described above.
DS like i said many many times before is simply a duplication of the existing genetic material - the same information copied. It doesn't matter what effect that has - we still aren't getting new information that codes for new structures which is a mechanism that is needed for the first simple organism to evolve to all organisms that we see today.

You've not supported your argument. You've not responded to my clear and detailed refutations. In your appeal to your own authority, you've not addressed the fact that the scientific world embraces evolution almost universally. Your assertions about ignorance are pretty contrary to that fact and you've not offered even a little bit of explanaion.

Umm, yes i did. But you didn't understand the refutations. You mentioned sickle cell anaemia as an example of a mutation to a gene which produces new information that codes for new structures - yet you jump to assume that this somehow is an example of mutation that can get you from the first simple organism to all others.
It isn't - mutation has damaged the gene - it cannot perform it's function properly, it still needs the undamaged 'copy of the gene' for the organism to survive. So it's at a slight disadvantage - but this disadvantage is kept when malaria is present, because it's harder for infection to occur. But simply showing an example of damage to a gene and how a damaged gene won't be removed by natural selection is not an example of mutation that leads to simply organism to all others. Keep having mutations which damage the genes and you are in big difficulty - the simple organism will not evolve.

You've picked on spelling to avoid answering the issue, you've picked on word choice (notice that even with my comment corrected by me, you've not discussed the topic at all).

What like correcting your spelling of 'midochondria' to 'mitochondria' - listen if i thought you would understand a discussiong about mitochondria we would have had one already.

Appeal to authoriy: Your assertion that you are right because you've read a book.
Reversal of proof: Your failure to meet the burden of proof your assertions carry.
Ad Hominim: Your focus on soemone else's spelling or education rather than the substance of their post.
Straw-Man: Your creation of your own criteria (such as "novel new") and then hacking at your own argument.

Not because i've read a book - but because i've been educated in it, in evolutionary theory - the same education that the 99% of biologists you keep talking about have been educated in. Well obviously education differs from place to place, but it is essentially the same.
The second point - it is only you that thinks i haven't met my burden of proof - you have not understood what i was talking about or what i was trying to show you.
Third - focusing on that - pointing it out rather (more than once).
Fourth - Had you understood what it takes for the first simple organism to evolve to all others you would have understood what i meant when i wrote and tried to explain that to you.

Like you were with your statement that people with down's syndrome were not fertile? Or with the statement you were attempting to infer that added chormosomes result in sterility because of some mythic barrier to "novel new" genes?

The first section i was wrong about and i admitted it - i was half right because the males are sterile - bar the very rare cases. The second part of the quote i haven't a clue what you are talking about.

 

[JerryL]

I would if i could even get that far. To be honest there is little point in discussing these things with people who don't understand the basics - because unless you have a good grasp of them then you won't understand what i am talking about and you have demonstrated time and time again that you don't.

You have a positive claim. Support your claim.

Firstly i don't understand the first part in the quote. Remember that i was talking about microevolution and macroevolution and going to illustrate the difference that i perceive between them...

The only definition you've given is the appearance of a "novel new", which you've asserted there is a barrier preventing.

What is the barrier preventing it. How can you establish your claim that this barrier exists?

There is not a mechanism as such to prevent it. What i was saying is that we don't observe genes coming into existance as a result of mutation which code for new structures - like the sting example we talked about ages ago. Nor do we observe existing genes mutating into genes that code for a protein with a completely different yet still useful function in the cell's biochemical environment.

Sickle-cell gene. Different protien, resists malaria.

DS like i said many many times before is simply a duplication of the existing genetic material - the same information copied. It doesn't matter what effect that has - we still aren't getting new information that codes for new structures which is a mechanism that is needed for the first simple organism to evolve to all organisms that we see today.

So "new information" = "different combination of base pairs"? Ok. Sickle-cell.

It isn't - mutation has damaged the gene - it cannot perform it's function properly

No, non sickle-cell has a damaged gen which cannot protect from malaria properly.

See how you are just making up a "which one's right"? You could assert that feathers are a defective gene which prevent the function of scale formation, or that a 4 chambered heart is a defective 2 chambered heart.

Words like "defective", as you use them, are extremely biased. The sickle-cell and non-sickl-cell versions of the gene contain different information and do different things. Whether one is advantageous cannot be determined at the genetic level.

Where is the mechanism preventing one gene from mutating into another? If there is none, where is your suppor that it cannot happen?

So it's at a slight disadvantage - but this disadvantage is kept when malaria is present, because it's harder for infection to occur. But simply showing an example of damage to a gene and how a damaged gene won't be removed by natural selection is not an example of mutation that leads to simply organism to all others.

GATTACTTA
TTCGTCHAC

Which of the above segments is "damaged" and which one is not? Assume they both make protiens (as do both variations of the red-cell gene). You want to talk genetic level? OK, there's two genes.

What like correcting your spelling of 'midochondria' to 'mitochondria' - listen if i thought you would understand a discussiong about mitochondria we would have had one already.

Pompus boasting. You are simply asserting it because you are unable to have a discussion supporting your position as you have no support for your position.

There's a saying in martial arts: The proof is on the mat. If you prefer (since you've mentioned GIGO), the real proof of a programmer's skill is in how the program runs.

You've writtten at length about yourself and others, I'm witing for you to disccuss the topic.

Not because i've read a book - but because i've been educated in it, in evolutionary theory - the same education that the 99% of biologists you keep talking about have been educated in. Well obviously education differs from place to place, but it is essentially the same.

Still waiting for you to explain that 99% in light of your "I'm right because I'm educated" logical fallacy.

The second point - it is only you that thinks i haven't met my burden of proof - you have not understood what i was talking about or what i was trying to show you.

Rhetoric. Prove that it is impossible for [insert gene here] to mutate to [insert gene here]. Prove that it's impossible for junk DNA to mutate into a functioning gene. Prove that it's impossible for a copied gene (say the one in DS) to mutate after copy or to function after it mutates.

The mechanisms have been shown true. Mutation happens. In assigning a limitation to a known event, you create a positive claim. Prove it.

Fourth - Had you understood what it takes for the first simple organism to evolve to all others you would have understood what i meant when i wrote and tried to explain that to you.

You have a positive claim. Support it. What mechanism prevents the appearance of a "novel new" gene through mutation.

The first section i was wrong about and i admitted it - i was half right because the males are sterile - bar the very rare cases. The second part of the quote i haven't a clue what you are talking about.

Your standard not mine.

 

[Endless]

No, non sickle-cell has a damaged gen which cannot protect from malaria properly.

See how you are just making up a "which one's right"? You could assert that feathers are a defective gene which prevent the function of scale formation, or that a 4 chambered heart is a defective 2 chambered heart.

Words like "defective", as you use them, are extremely biased. The sickle-cell and non-sickl-cell versions of the gene contain different information and do different things. Whether one is advantageous cannot be determined at the genetic level.

It only partially protects against malaria and only in the first few years of childhood - children with sickle cell trait are more likely to survive the first malaria infections than those without the trait. After this clinical immunity sets in and you don't really need the sickle cell trait. See here However by selecting for this trait the population will eventually run into serious difficulties with the high incidence of sickle cell anaemia in their offspring - more heterozygotes = greater chance of reproduction resulting in sickle cell anaemia = death when they get malaria.
The reasons behind the mutation causing increased malaria resistance are still being researched as far as i know - possible that the reactive oxygen species being produced as a result of the mutation in RBCs interfere with the infection, or perhaps the sickling of infected RBCs which then get them removed by the immune system.
Anyway, the gene has been damaged, because the beta globin function is impaired. No one will argue this - homozygosity proves this. So the only thing this is an example of is how mutation causing damage can be selected for by natural selection.
However this protein isn't forming any new function - it isn't doing a job it didn't do before. Therefore how is this an example of how evolution of the first simple organism to all other organisms happened? Lets damage the genes in the first simple organism - no new information has been produced to increase complexity - the protein is not doing a new job that it didn't do before. It is still performing the same function but not as well. But not as well, is better because of the benefits of protecting from evolution. But it's still doing the same function of transporting oxygen.

So "new information" = "different combination of base pairs"? Ok. Sickle-cell.

No, the whole protein has to be doing something. Different combinations of content yes, but not of information. Information will lead to a function - so new information leads to a new function. By new function i'm talking about a completely different function to what it had before - only in this way can the first simple organism evolve in complexity and evolve new structures and biochemical pathways as it must have done.

The mechanisms have been shown true. Mutation happens. In assigning a limitation to a known event, you create a positive claim. Prove it.

I don't have to - it has never been observed to happen, even with all the testing and mutations performed on bacteria which replicate quickly. No new (as defined above) genes have arisen. You've got to ask yourself why. Why dont we see this happening, why can we not reproduce it either. Therefore the burden of proof is to show that the mechanism can surmount the odds and actually happen. I don't think you realise quite how complex it all is.

 

[JerryL]

It only partially protects against malaria and only in the first few years of childhood - children with sickle cell trait are more likely to survive the first malaria infections than those without the trait. After this clinical immunity sets in and you don't really need the sickle cell trait.

"trait"? "need"? doesn't sound like your talking about genetics to me (recall, it's you that tried to set evrything at the genetic level). To me it sounds like yuo are discussing traits and envyronment.

The reasons behind the mutation causing increased malaria resistance are still being researched as far as i know - possible that the reactive oxygen species being produced as a result of the mutation in RBCs interfere with the infection, or perhaps the sickling of infected RBCs which then get them removed by the immune system.

I'd be a great deal more interested in that fact if you could show any relevence to your claim that new information is impossible to get trhough mutation.

Anyway, the gene has been damaged, because the beta globin function is impaired. No one will argue this - homozygosity proves this. So the only thing this is an example of is how mutation causing damage can be selected for by natural selection.

Again with the biased language. "impaired" sounds a lot like "inhibited" but negative.

You were discussing a genetic level.... the appearance of "new information" and "functioning genes" and the like.

The sickle-cell information doesn't exist in a non-sickle-cell gene. It functions differently and it functions. As a bonus it confers different traits at a macroscopic level.

However this protein isn't forming any new function - it isn't doing a job it didn't do before

You mean that the old version conferred malaria resistance? Support that?

Did the old chromosome 34 (not that any such one exists in non DS patients) also change the X-inactivation? Is that a function that it was doing before it existed?

Your making statements that are blatently false.

no new information has been produced to increase complexity

And you make another, different, claim "mutations cannot increase complexity". Since you've asserted that this is all genetic, "complexity" must occur in the potential energy of the molecule (thermodynamics) in which case we are discussing length. DNA most ceratinly can get longer though mutation and such mutation certainly has been observed.

Or you could be discussing the number of protiens made. Again, DS DNA makes more than non DS DNA. Again your claim is demostrably false.

Here's a question for you: How complex is human DNA? How many base-pairs? How many protiens? How many genes?

Here's another: Which is more complex GATA or TCGT?

No, the whole protein has to be doing something.

What does that even mean? If it does something no other protien does than it's not an old protien to have something different to do.

But OK. An example of a protien appearing in a human which does something no other protien is doing is Downs Syndrome, where the protiens on Chromosome 34 do things no others do (give Downs Syndrome)

By new function i'm talking about a completely different function to what it had before - only in this way can the first simple organism evolve in complexity and evolve new structures and biochemical pathways as it must have done.

Propping up your own theory and then hacking it down? Straw Man Logical Fallacy.

I don't have to - it has never been observed to happen, even with all the testing and mutations performed on bacteria which replicate quickly. No new (as defined above) genes have arisen

We can discuss "didn't" later. You've said "can't". Why "can't" it? Where is your support for your positive claim?

You've got to ask yourself why.

You need to ask yourself why 99% of biologists disagree with your assessment. I've certainly asked that question.

But Ok. Why?

Why dont we see this happening, why can we not reproduce it either. Therefore the burden of proof is to show that the mechanism can surmount the odds and actually happen.

Odds? I thought you said it couldn't happen? Are you now conceding that "macroevolution" is possible, just "unlikely"? I don't think you have the educational background to make such a statistical claim (what do you knwo of pre and post prediction odds in complex systems. Do you understand the difference between random and chaotic? What is your statistical background?).

 

[Opethian]

From talkorigins.com:

It is hard to understand how anyone could make this claim, since anything mutations can do, mutations can undo. Some mutations add information to a genome; some subtract it. Creationists get by with this claim only by leaving the term "information" undefined, impossibly vague, or constantly shifting. By any reasonable definition, increases in information have been observed to evolve. We have observed the evolution of

• increased genetic variety in a population (Lenski 1995; Lenski et al. 1991)
• increased genetic material (Alves et al. 2001; Brown et al. 1998; Hughes and Friedman 2003; Lynch and Conery 2000; Ohta 2003)
• novel genetic material (Knox et al. 1996; Park et al. 1996)
• novel genetically-regulated abilities (Prijambada et al. 1995)

If these do not qualify as information, then nothing about information is relevant to evolution in the first place.

A mechanism that is likely to be particularly common for adding information is gene duplication, in which a long stretch of DNA is copied, followed by point mutations that change one or both of the copies. Genetic sequencing has revealed several instances in which this is likely the origin of some proteins. For example:

Two enzymes in the histidine biosynthesis pathway that are barrel-shaped, structural and sequence evidence suggests, were formed via gene duplication and fusion of two half-barrel ancestors (Lang et al. 2000).

• RNASE1, a gene for a pancreatic enzyme, was duplicated, and in langur monkeys one of the copies mutated into RNASE1B, which works better in the more acidic small intestine of the langur. (Zhang et al. 2002)
• Yeast was put in a medium with very little sugar. After 450 generations, hexose transport genes had duplicated several times, and some of the duplicated versions had mutated further. (Brown et al. 1998)

The biological literature is full of additional examples. A PubMed search (at http://www.ncbi.nlm.nih.gov/entrez/query.fcgi) on "gene duplication" gives more than 3000 references.

According to Shannon-Weaver information theory, random noise maximizes information. This is not just playing word games. The random variation that mutations add to populations is the variation on which selection acts. Mutation alone will not cause adaptive evolution, but by eliminating nonadaptive variation, natural selection communicates information about the environment to the organism so that the organism becomes better adapted to it. Natural selection is the process by which information about the environment is transferred to an organism's genome and thus to the organism (Adami et al. 2000).

The process of mutation and selection is observed to increase information and complexity in simulations (Adami et al. 2000; Schneider 2000).

 

[Fade]

Good find Opethian. I'd frubal you if I didn't have to spread them around some more.

 

[Endless]

"trait"? "need"? doesn't sound like your talking about genetics to me (recall, it's you that tried to set evrything at the genetic level). To me it sounds like yuo are discussing traits and envyronment.

To be honest i'll probably not be having this conversation with you again - if you had done a bit of reading you would have realised that when a person is heterozygous with the Sickle cell mutation (they have one unmutated and one mutated) then the name given is 'Sickle cell trait' - google it if you want.

The function of any protein is at the biochemical level - the function of the protein is not now to infer malaria resistance, the protein function is the same - it transports oxygen. It's not performing any other function. The changing in structure under lower oxygen conditions is what now makes it harder for malaria to infect the red blood cells. But the protein is still doing the same function of transporting oxygen. Under low oxygen conditions it does not have a different function - but the mutation allows structural change, which results in 'sickled cells'.

But OK. An example of a protien appearing in a human which does something no other protien is doing is Downs Syndrome, where the protiens on Chromosome 34 do things no others do (give Downs Syndrome)

How could duplicates of proteins not perform the same function - they are clones. You are talking absolute rubbish because you do not understand how the 'inactivation' occurs. I'm not about to waste my time explaining it either.

By new function i'm talking about a completely different function to what it had before - only in this way can the first simple organism evolve in complexity and evolve new structures and biochemical pathways as it must have done.

Propping up your own theory and then hacking it down? Straw Man Logical Fallacy.

Again, a load of rubbish. You obviously don't grasp that organisms have genes coding for proteins which perform different kinds of functions - therefore in order to have evolved from the first simple organism we have to have proteins coming into being with functions completely different - how else could we possibly have got them.

Here's another: Which is more complex GATA or TCGT?

That is a prime example of your ignorance of the subject we are talking about. I'm not talking about complexity from a thermodynamic viewpoint - i'm talking at the biochemical level. Things had to have become more complex as the simple organism evolved to all we have today - therefore the mutations had to give rise to increasing complexity (genes) - which coded for different proteins with new biochemical functions that fitted in with the existing biochemical pathways in the organism.

Odds? I thought you said it couldn't happen? Are you now conceding that "macroevolution" is possible, just "unlikely"? I don't think you have the educational background to make such a statistical claim (what do you knwo of pre and post prediction odds in complex systems. Do you understand the difference between random and chaotic? What is your statistical background?).

Again ignorance - you can get odds which represent a statistical impossiblity - ie, it will never happen. Like you dropping bowling balls on top of each other and doing this trying to get 7 balanced. You could get odds for that - but they would represent a statistical impossiblity - ie. it is not going to happen.

You need to ask yourself why 99% of biologists disagree with your assessment. I've certainly asked that question.

Disagree with my assertion? - i don't think you even understand what i am asserting...
I'm through with repeating myself Jerry - read the basics mate even Opethian knows you don't have a grasp of them, and he's not biased as you would see me. Nor am i being patronising - just advising.

 

[Endless]

Opethian,

It is hard to understand how anyone could make this claim, since anything mutations can do, mutations can undo. Some mutations add information to a genome; some subtract it. Creationists get by with this claim only by leaving the term "information" undefined, impossibly vague, or constantly shifting. By any reasonable definition, increases in information have been observed to evolve. We have observed the evolution of

Yep, anything mutations can do they can undo if the circumstances allow them. Again, at this point notice that they do not put a precise definition on 'information'. Some mutations add information to a genome - but they don't define what they mean by information. If they mean addition etc of nucleotides - certainly. But then is sections of DNA which have no function classed as information? Personally i would say it doesn't.
Does disrupting a gene count as a mutation which causes information? It's just removed a gene - ie. Just removed a pile of information. But it has now left a different combination of existing information, which some people may class as 'new information' - but all that's happened is information has been removed, not what i would call addition of new information.
What about gene duplication - no creationist would deny that this happens. So is this an example of a mutation causing new information? Well, certainly it's a duplication of existing information - so how can the information be new? To me it's obvious this isn't new information.
So what is new information. If i described a situation where mutations in a duplicated gene built up until the protein had a new function which was different to the original - now that would be new information. Better still, the original still exists, now we've also got a protein that does something different to the original - maybe it's an enzyme which breaks down a new substrate. That is new information.
Then the new information has to be in the right context for natural selection to select it - but that's another part of the story.

Lets have a look at each of those papers mentioned and if any qualify:

1.increased genetic variety in a population (Lenski 1995; Lenski et al. 1991)

Cannot find these papers in PubMed (have references in original talk article). So cannot comment on this. You able to read them Opethian?

2.increased genetic material (Alves et al. 2001; Brown et al. 1998; Hughes and Friedman 2003; Lynch and Conery 2000; Ohta 2003)

Don't have to look at this - i am well aware of duplication and accept that it occurs. I also don't think this is new information as i am sure you don't.

3. novel genetic material (Knox et al. 1996; Park et al. 1996)

I have looked at these papers' abstracts. Knox 1996 looks at two genes he thinks may have evolved an ancestoral protein. Conclusion is that they may have. This paper is extrapolating backwards what they think may have happened.
Park 1996 - seems more interesting. They've taken two homologues, which they think might have evolved from a common ancestor. They've mutated the active site of one and induced the antibiotic resistance that the other had. I don't have access to the full paper - i'd be very interested in seeing how many mutations occurred in the active site and whether they were able to keep original enzyme activity through each of the stages of mutation. If not then this would not happen in nature as once the mutation knocks out enzyme activity the enzyme the mutation would be removed by natural selection. Maybe you have access to the paper Opethian?

4.novel genetically-regulated abilities (Prijambada et al. 1995)
This to me is perhaps the most interesting. The ability to metabolise xenobiotic compounds such as a by product of nylon manufacture. There are other papers that i could point you to should you be interested in this, but no doubt you should be able to find them yourself.
This paper shows how quickly the bacteria gains the ability to digest these compounds - we are talking 9 days here. This was not and could not have been caused by mutation. It was caused by some other process acting on the existing genetic variation. Yomo et al has a few papers - statement he made from his research was:

These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes.

It's an interesting read, so there is something else acting that allows this remarkable adaptation of the P.aeruginosa. I've talked to a few evolutionists and they had commented on maybe writing to the talk origins site to get that section removed from it. But as yet, it hasn't been.

So again we have never observed mutation giving rise to this new information...

 

[Fade]

Okay so what qualifies as "new" information in your ever so humble book?

 

[Endless]

I already gave an example in my previous post.

 

[Fade]

so why is what is presented not new info?

 

[Endless]

for the reasons i mentioned in my previous post.

 

[Opethian]

The function of any protein is at the biochemical level - the function of the protein is not now to infer malaria resistance, the protein function is the same - it transports oxygen. It's not performing any other function. The changing in structure under lower oxygen conditions is what now makes it harder for malaria to infect the red blood cells. But the protein is still doing the same function of transporting oxygen. Under low oxygen conditions it does not have a different function - but the mutation allows structural change, which results in 'sickled cells'.

This is exactly the way evolution happens. Small changes in structure of the protein pile up over time and slight changes that at first do not alter the function of the protein, may after time when more alterations have occured result in a protein with a new function.
We have to take DNA for what it is: blind information. Mutations are blind too. It is the process of natural selection that results in the structured information of DNA in organisms on the earth today. The beauty is, that if this earth was not there, the information would be useless, and it is exactly the earth that shaped the information because of the fact that the information had to survive on the earth to be able to reproduce and exist.
Over the billions of years of time the information has had to mutate and change by chance, certain alterations gave the information benefits to reproduce and stay 'alive'. This is how the information evolved. This still goes on today, though it is hard to show impressive modern changes, since the process is dependant on large quantities of time. But even then, evidence from the past is more than enough to even show the most stubborn-headed that evolution is a fact.
Endless, with your knowledge on Biochemistry, I simply cannot understand that you deny evolution. You accept that mutations occur do you? You accept that these mutations change DNA, which results in the translation of new proteins? You accept that a very small percentage of the time, this results in a new protein (1 altered amino acid can give rise to to the destruction or creation of certain bridges that held together the protein's secundairy structure, completely altering its form and thus its capability to interact with different molecules) that is not harmful for the organism and maybe even beneficial? Do you accept that, in this case, the new DNA will be reproduced in offspring of the mutated organism, and over time, this will result in a large population of the new mutant? Do you accept that, when this occurs multiple times in the same organism (given the huge amount of time), it can give rise to large changes in the proteome? And everybody knows that this can have some drastic changes on the phenotype of the organism, which most would accept as 'macroevolution'.
And this is just one little part of the way DNA can be changed. Bacteria can exchange large chunks of DNA between each other (fages) to give each other a benefit. Sometimes plants have their DNA duplicated giving rise to stronger polyploid plants (you probably eat corn from time to time or wheat?). And what if a certain gene is accidentily duplicated and the 2 initially identical genes undergo different mutations? The possibilities are endless! If you have all this knowledge of Biochemistry, and still deny evolution, you have either A) not read enough Biology, B) been completely brainwashed by creationists, C) are the most stubborn man in the universe.

Edit: Be glad that I couldn't find my book of Biochemistry from last year, or this post would've been 10 times longer full of evolutionary links within the biochemistry of the human body. But you may expect that soon if I can find time and the book.
If you are interested: http://www.amazon.com/gp/product/0716730510/qid=1141677107/sr=2-2/ref=pd_bbs_b_2_2/103-3834306-0790227?s=books&v=glance&n=283155

 

[Opethian]

Cannot find these papers in PubMed (have references in original talk article). So cannot comment on this. You able to read them Opethian?

Nope

I have looked at these papers' abstracts. Knox 1996 looks at two genes he thinks may have evolved an ancestoral protein. Conclusion is that they may have. This paper is extrapolating backwards what they think may have happened.
Park 1996 - seems more interesting. They've taken two homologues, which they think might have evolved from a common ancestor. They've mutated the active site of one and induced the antibiotic resistance that the other had. I don't have access to the full paper - i'd be very interested in seeing how many mutations occurred in the active site and whether they were able to keep original enzyme activity through each of the stages of mutation. If not then this would not happen in nature as once the mutation knocks out enzyme activity the enzyme the mutation would be removed by natural selection. Maybe you have access to the paper Opethian?

Given the fact that 'macro'evolution is such a slow process, extrapolating backwards is about all we can do to achieve something that satisfies the creationist crowd. I don't have access to the full paper either.
I just quickly read it and copy pasted it here which is something I usually don't do but I didn't have time to write something myself.
But one fact remains: You say we have never observed mutation giving rise to new information. Yet, the very essence of mutations is giving rise to new information. The changing of one base pair into another is the birth of new information. I think you just expect way too much from this new information because you don't realise the earth is 4,6 billion years old and life had more than 3 billion years to evolve. Small changes are what makes the difference.

 

[Endless]

Would you care to explain why science has never observed mutation giving rise to new information in the context that i defined information before? Because it takes a long time? - we can control the environment, increase the mutation rates, use bacteria which replicate quickly etc. Why don't we see it happening?

 

[Opethian]

In this context, we have given rise to new information on many occasions. Genetically engineered bacteria and plants have been made numerous times. I really don't know why you don't see it happening.

 

[Fade]

Endless has a magic goal post instead of a valid definition of 'new' information. As soon as the ball looks like it's about to go in the back of the net they miraculously move and Endless pretends he's made a brilliant diving save.

 

[Opethian]

The funny thing is that I've seen threads like these on other forums as well, with exactly the same pointless discussion about information. What's even funnier is that these claims come from creationist websites.