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Albatrossity2



Posts: 2780
Joined: Mar. 2007

(Permalink) Posted: Jan. 29 2010,10:41   

Quote (Utunumsint @ Jan. 29 2010,10:14)
OK, so its obvious that I'm laking in education on this subject matter, so perhaps people could suggest to me some intro level reading that I can do on my own. I have three kids and very little time, but I am certainly interested in the subject.

Preferable, not something polemical, but a good intro series of books into the subject of evolution. Especially ones that deal with the microbiological issues.

Cheers,
Ut

Carl Zimmer's Evolution: The Triumph of an Idea. Eminently readable, not polemical.

For microbiological issues, see Microcosm, also by Zimmer.

Enjoy.

--------------
Flesh of the sky, child of the sky, the mind
Has been obligated from the beginning
To create an ordered universe
As the only possible proof of its own inheritance.
                        - Pattiann Rogers

   
RDK



Posts: 229
Joined: Aug. 2009

(Permalink) Posted: Jan. 29 2010,11:09   

Quote (afarensis @ Jan. 28 2010,18:35)
 
Quote (Richardthughes @ Jan. 28 2010,17:49)
YOU GUYS ARE TEH MEANIES

HAHAHAHA this is Richard!

I found our boy FL:

http://redwing.hutman.net/~mreed/warriorshtm/ferouscranus.htm

Byers would fit nicely here too.

--------------
If you are not:
Leviathan
please Logout under Meta in the sidebar.

‘‘I was like ‘Oh my God! It’s Jesus on a banana!’’  - Lisa Swinton, Jesus-eating pagan

  
fnxtr



Posts: 3504
Joined: June 2006

(Permalink) Posted: Jan. 29 2010,11:42   

Quote (Albatrossity2 @ Jan. 29 2010,08:41)
Quote (Utunumsint @ Jan. 29 2010,10:14)
OK, so its obvious that I'm laking in education on this subject matter, so perhaps people could suggest to me some intro level reading that I can do on my own. I have three kids and very little time, but I am certainly interested in the subject.

Preferable, not something polemical, but a good intro series of books into the subject of evolution. Especially ones that deal with the microbiological issues.

Cheers,
Ut

Carl Zimmer's Evolution: The Triumph of an Idea. Eminently readable, not polemical.

For microbiological issues, see Microcosm, also by Zimmer.

Enjoy.

I also recommend Microcosm, well-written and very engaging. Not pedantic but still a wealth of information.

--------------
"[A] book said there were 5 trillion witnesses. Who am I supposed to believe, 5 trillion witnesses or you? That shit's, like, ironclad. " -- stevestory

"Wow, you must be retarded. I said that CO2 does not trap heat. If it did then it would not cool down at night."  Joe G

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Jan. 29 2010,12:10   

OK. Thanks all.

How about some good books against ID, without too much rankor?

Cheers,
Ut

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Jan. 29 2010,12:47   

Quote (Utunumsint @ Jan. 29 2010,12:10)
OK. Thanks all.

How about some good books against ID, without too much rankor?

Cheers,
Ut

If you've not already, check out the Dover trial transcripts.

http://www.talkorigins.org/faqs/dover/day11pm.html
Quote

Q Under that same definition astrology is a scientific theory under your definition, correct?

A [Behe] Under my definition, a scientific theory is a proposed explanation which focuses or points to physical, observable data and logical inferences. There are many things throughout the history of science which we now think to be incorrect which nonetheless would fit that -- which would fit that definition. Yes, astrology is in fact one, and so is the ether theory of the propagation of light, and many other -- many other theories as well.

Q The ether theory of light has been discarded, correct?

A That is correct.

Q But you are clear, under your definition, the definition that sweeps in intelligent design, astrology is also a scientific theory, correct?

A Yes, that's correct. And let me explain under my definition of the word "theory," it is -- a sense of the word "theory" does not include the theory being true, it means a proposition based on physical evidence to explain some facts by logical inferences. There have been many theories throughout the history of science which looked good at the time which further progress has shown to be incorrect. Nonetheless, we can't go back and say that because they were incorrect they were not theories. So many many things that we now realized to be incorrect, incorrect theories, are nonetheless theories.

If ID could make a case, it would have made it there. It was not made.

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Albatrossity2



Posts: 2780
Joined: Mar. 2007

(Permalink) Posted: Jan. 29 2010,12:48   

Quote (Utunumsint @ Jan. 29 2010,12:10)
OK. Thanks all.

How about some good books against ID, without too much rankor?

Cheers,
Ut

If you read those other books, and gain a good understanding of how science (and particularly evolution) works, you won't need a book to show you how ID fails.

You will easily figure it out for yourself.

--------------
Flesh of the sky, child of the sky, the mind
Has been obligated from the beginning
To create an ordered universe
As the only possible proof of its own inheritance.
                        - Pattiann Rogers

   
Robin



Posts: 1431
Joined: Sep. 2009

(Permalink) Posted: Jan. 29 2010,15:52   

Quote (Utunumsint @ Jan. 29 2010,09:26)

[/quote]
Quote (oldmanintheskydidntdoit @ Jan. 29 2010,09:17)
[/quote]
Quote (Utunumsint @ Jan. 29 2010,09:06)
It took a negavite mutation, like sickle cell anemia to provide some measure of defence.

What could a "positive" mutation have done then? What is a negative mutation and how do you determine if a given mutation is negative or positive? Can a negative mutation be a positive mutation really, depending on the environment?

Overall, if more people survive infection by malaria because of this "negative" mutation in what way is it negative (ignoring obviously the human suffering aspect of SSA)?

Survival rates increase. Deaths from malaria decrease. You call that "negative"?

Ut-Well it seems to be a trade off between one bad situation for another bad situation. SSA just kills you much more slowly. It also make  you much weaker. Do you see this as a net benefit?

Cheers,
Ut

I got to get back to my day job.... :) I'll check back in tonight....


Hmmm...perhaps an analogy will provide a different framework to evaluate the concept of 'positive' vs 'negative' mutation.

There are a very large number of folk in the US with End-stage Renal Disease (ESRD). The specific statistics for ESRD are not pertinent to this analogy, but I'll be happy to provide them if you wish. At any rate, lots - in the 300,000-400,000 person range - in the US with ESRD. ESRD used to be an automatic cause of death; No functioning kidneys = not long to live. Dialysis, a mechanical process that takes the blood out and takes out many of the impurities (but not all) was developed and people no longer died immediately* from ESRD. However, they were extremely tired due to the chemical effects of the dialysate used to filter the blood and over time doctors discovered that dialysis lead to heart failure in many, if not most, patients due to stress. Now, it was still used - those with ESRD didn't die immediately, so it was better than nothing.

Even the transplantation we have today has fairly severe drawbacks. The drugs one takes for immuno-suppression, which is required to prevent the body from rejecting the foreign organ, happen to be nephrotoxic - that means 'kidney damaging' to the layman.

The point is, while certainly the best solution from our perspective to issues that result in death would be one that has no downsides, that isn't always feasible or the first thing discovered. When faced with the alternative of issue with death vs ehhh solution with not so hot side-effects, most times the latter is preferencial since it buys some time to do a few more things. And what you need to keep in mind is that evolution *does not have the foresight* that humans do. It doesn't 'know' about the concept of death or even illness or inconvenience. The only thing propelling it along is survival. So, if someone lives longer with SSA than with malaria, those folks - and here's the crux of evolution - [/i]have a better chance[/i] of producing offspring who will survive than those who do not have SSA in a malaria area.

So is SSA a 'negative' mutation? Not by my standards.

--------------
we IDists rule in design for the flagellum and cilium largely because they do look designed.  Bilbo

The only reason you reject Thor is because, like a cushion, you bear the imprint of the biggest arse that sat on you. Louis

  
Wesley R. Elsberry



Posts: 4991
Joined: May 2002

(Permalink) Posted: Jan. 29 2010,17:37   

Quote (Utunumsint @ Jan. 29 2010,12:10)
OK. Thanks all.

How about some good books against ID, without too much rankor?

Cheers,
Ut

There is a link at the bottom of each page here called Useful Links. There are a number of books linked to their Amazon pages. You owe it to yourself to read "Why Intelligent Design Fails", but many of the books deserve your attention.

--------------
"You can't teach an old dogma new tricks." - Dorothy Parker

    
Timothy McDougald



Posts: 1036
Joined: Dec. 2006

(Permalink) Posted: Jan. 29 2010,19:45   

Quote (Zachriel @ Jan. 28 2010,20:24)
Quote (afarensis @ Jan. 28 2010,18:45)
Zhang's work on digestive Rnases in ruminants and colobines - such as this article - seems relevant here. Although I have never heard it mentioned.

Zhang provides a good summary of a few basic principles.

Quote
These results suggest that (1) an evolutionary problem can have multiple solutions, (2) the same amino acid substitution may have opposite functional effects in homologous proteins, (3) the stochastic processes of mutation and drift play an important role even at functionally important sites, and (4) protein sequences may diverge even when their functions converge.

Well, yes. But I was thinking of the nine mutations that occured in the pancreatic Rnase. Several of which allowed it to work in a low PH environment and several more of which helped it extract nitrogen from the plant digesting bacteria of course the ability of the Rnase to process double stranded RNA was reduced but overall the trade off was beneficial. Incidentally, Zhang calculated the number of different paths that could be taken to achieve these results - I'm not sure if it was in this paper or one of his others on the same subject. Turns out there are over forty ways to get from the initial pancreatic Rnase to the digestive one. One can see something kind of similar in some of the pesticide resistance stuff in flies. Some of the initial mutations, although they provide some resistance to pesticides, lower fitness. But then other mutations happen, mutations that moderate the detrimental effects and enhance the beneficial. So Behe's contention that that evolution runs up against an edge after one or two mutations is pure BS.

--------------
Church burning ebola boy

FTK: I Didn't answer your questions because it beats the hell out of me.

PaV: I suppose for me to be pried away from what I do to focus long and hard on that particular problem would take, quite honestly, hundreds of thousands of dollars to begin to pique my interest.

   
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,08:29   

Quote (Albatrossity2 @ Jan. 29 2010,10:41)
Quote (Utunumsint @ Jan. 29 2010,10:14)
OK, so its obvious that I'm laking in education on this subject matter, so perhaps people could suggest to me some intro level reading that I can do on my own. I have three kids and very little time, but I am certainly interested in the subject.

Preferable, not something polemical, but a good intro series of books into the subject of evolution. Especially ones that deal with the microbiological issues.

Cheers,
Ut

Carl Zimmer's Evolution: The Triumph of an Idea. Eminently readable, not polemical.

For microbiological issues, see Microcosm, also by Zimmer.

Enjoy.

I bought an audio version of Sean Carroll's The Making of the Fittest. I'll be listening to it as soon as I'm done absorbing Behe's Edge of Evolution. Carroll claims to vapourize creationist arguments, and specifically IDers.

Do you know if the Zimmer books are available in audio? I couldn't find them on Audible.

Cheers,
Ut

  
Albatrossity2



Posts: 2780
Joined: Mar. 2007

(Permalink) Posted: Feb. 01 2010,08:33   

Quote (Utunumsint @ Feb. 01 2010,08:29)
Do you know if the Zimmer books are available in audio? I couldn't find them on Audible.

Don't have a clue. I don't learn well by listening to audio (or lectures, or phone conversation), so I don't pay attention to audio book matters. I learn best by reading, so I read books.

--------------
Flesh of the sky, child of the sky, the mind
Has been obligated from the beginning
To create an ordered universe
As the only possible proof of its own inheritance.
                        - Pattiann Rogers

   
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,08:35   

Quote (Robin @ Jan. 29 2010,15:52)
Quote (Utunumsint @ Jan. 29 2010,09:26)
[/quote]
Quote (oldmanintheskydidntdoit @ Jan. 29 2010,09:17)
[/quote]
 
Quote (Utunumsint @ Jan. 29 2010,09:06)
It took a negavite mutation, like sickle cell anemia to provide some measure of defence.

What could a "positive" mutation have done then? What is a negative mutation and how do you determine if a given mutation is negative or positive? Can a negative mutation be a positive mutation really, depending on the environment?

Overall, if more people survive infection by malaria because of this "negative" mutation in what way is it negative (ignoring obviously the human suffering aspect of SSA)?

Survival rates increase. Deaths from malaria decrease. You call that "negative"?

Ut-Well it seems to be a trade off between one bad situation for another bad situation. SSA just kills you much more slowly. It also make  you much weaker. Do you see this as a net benefit?

Cheers,
Ut

I got to get back to my day job.... :) I'll check back in tonight....


Hmmm...perhaps an analogy will provide a different framework to evaluate the concept of 'positive' vs 'negative' mutation.

There are a very large number of folk in the US with End-stage Renal Disease (ESRD). The specific statistics for ESRD are not pertinent to this analogy, but I'll be happy to provide them if you wish. At any rate, lots - in the 300,000-400,000 person range - in the US with ESRD. ESRD used to be an automatic cause of death; No functioning kidneys = not long to live. Dialysis, a mechanical process that takes the blood out and takes out many of the impurities (but not all) was developed and people no longer died immediately* from ESRD. However, they were extremely tired due to the chemical effects of the dialysate used to filter the blood and over time doctors discovered that dialysis lead to heart failure in many, if not most, patients due to stress. Now, it was still used - those with ESRD didn't die immediately, so it was better than nothing.

Even the transplantation we have today has fairly severe drawbacks. The drugs one takes for immuno-suppression, which is required to prevent the body from rejecting the foreign organ, happen to be nephrotoxic - that means 'kidney damaging' to the layman.

The point is, while certainly the best solution from our perspective to issues that result in death would be one that has no downsides, that isn't always feasible or the first thing discovered. When faced with the alternative of issue with death vs ehhh solution with not so hot side-effects, most times the latter is preferencial since it buys some time to do a few more things. And what you need to keep in mind is that evolution *does not have the foresight* that humans do. It doesn't 'know' about the concept of death or even illness or inconvenience. The only thing propelling it along is survival. So, if someone lives longer with SSA than with malaria, those folks - and here's the crux of evolution - [/i]have a better chance[/i] of producing offspring who will survive than those who do not have SSA in a malaria area.

So is SSA a 'negative' mutation? Not by my standards.

I think I misrepresented Behe's arguments. In the book, he describes how sickle cell anemia is a clear example of evolution in action. It did work and still works in providing malaria resistance. He also describes the benefits and limitations of the various types of sickle cell anaemias, such as Haemoglobin C, sickle cell, Harlem C, as well asl other blook disorders, such as Thallesemias, and a few others that I forget for the moment.

The bottom line is that they are evolutionary success stories, according to Behe. But from a functional perspective, they also weaken those with this desease. And they do not occur in the immune system.

But from what I can tell, no one in evolutionary circles would see that as an argument against evolution. Neither does Behe. But perhaps he sees it as an argument against evolution's ability to create complex micro machines?

Cheers,
Ut

Cheers,
Ut

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,08:39   

Quote (afarensis @ Jan. 29 2010,19:45)
Quote (Zachriel @ Jan. 28 2010,20:24)
Quote (afarensis @ Jan. 28 2010,18:45)
Zhang's work on digestive Rnases in ruminants and colobines - such as this article - seems relevant here. Although I have never heard it mentioned.

Zhang provides a good summary of a few basic principles.

 
Quote
These results suggest that (1) an evolutionary problem can have multiple solutions, (2) the same amino acid substitution may have opposite functional effects in homologous proteins, (3) the stochastic processes of mutation and drift play an important role even at functionally important sites, and (4) protein sequences may diverge even when their functions converge.

Well, yes. But I was thinking of the nine mutations that occured in the pancreatic Rnase. Several of which allowed it to work in a low PH environment and several more of which helped it extract nitrogen from the plant digesting bacteria of course the ability of the Rnase to process double stranded RNA was reduced but overall the trade off was beneficial. Incidentally, Zhang calculated the number of different paths that could be taken to achieve these results - I'm not sure if it was in this paper or one of his others on the same subject. Turns out there are over forty ways to get from the initial pancreatic Rnase to the digestive one. One can see something kind of similar in some of the pesticide resistance stuff in flies. Some of the initial mutations, although they provide some resistance to pesticides, lower fitness. But then other mutations happen, mutations that moderate the detrimental effects and enhance the beneficial. So Behe's contention that that evolution runs up against an edge after one or two mutations is pure BS.

Interesting. Thanks for this. Do you have a link to the study?

Another issue that has been gnawing at me as I read Behe's book is that he makes a one to one comparison between the evolution rate of Malaria in developing Chloroquine resistance, to that of human beings developing similar complex mutations over time.

My issue with this is that it seems to be overlooking the fact that each human beings are made up of trillions of microorganisms that alre also replicating within each person. Isn't it oversimplistic to make a one to one comparison between a microorganism's rate of evolution and that of a human being, made of of trillions of microorganisms?

Cheers,
Ut

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Feb. 01 2010,09:18   

Quote (Utunumsint @ Feb. 01 2010,08:35)
But from a functional perspective, they also weaken those with this desease.

Is being "weakened" better or worse then "dead"?

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,09:24   

Quote (oldmanintheskydidntdoit @ Feb. 01 2010,09:18)
Quote (Utunumsint @ Feb. 01 2010,08:35)
But from a functional perspective, they also weaken those with this desease.

Is being "weakened" better or worse then "dead"?

Definitly better, from an evolutionary perspective. And Aferensis provided that study that showed that even though there may be an initial weakening, evolution can also just as easily provide mittigating mutations to strengthen the organism.

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Feb. 01 2010,09:53   

Quote (Utunumsint @ Feb. 01 2010,09:24)
   
Quote (oldmanintheskydidntdoit @ Feb. 01 2010,09:18)
   
Quote (Utunumsint @ Feb. 01 2010,08:35)
But from a functional perspective, they also weaken those with this desease.

Is being "weakened" better or worse then "dead"?

Definitly better, from an evolutionary perspective. And Aferensis provided that study that showed that even though there may be an initial weakening, evolution can also just as easily provide mittigating mutations to strengthen the organism.

Evolution stops working when things die before they can replicate! So there might be an "initial weakening" but compared to the rest of the group (who died) there really was no weakening at all.

Would you say that the loss of eyesight in blind cave fish was a "weakening"? Or could it only be seen as such if those blind fish were moved to a place where there was light and other fish could see? Sure, then perhaps the blind fish are worse off, but move the sighted fish to the black cave and who's "weakened" then?

However IANAB! So take what I say with a pinch of salt eh?

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,09:59   

Quote (oldmanintheskydidntdoit @ Feb. 01 2010,09:53)
Quote (Utunumsint @ Feb. 01 2010,09:24)
   
Quote (oldmanintheskydidntdoit @ Feb. 01 2010,09:18)
     
Quote (Utunumsint @ Feb. 01 2010,08:35)
But from a functional perspective, they also weaken those with this desease.

Is being "weakened" better or worse then "dead"?

Definitly better, from an evolutionary perspective. And Aferensis provided that study that showed that even though there may be an initial weakening, evolution can also just as easily provide mittigating mutations to strengthen the organism.

Evolution stops working when things die before they can replicate! So there might be an "initial weakening" but compared to the rest of the group (who died) there really was no weakening at all.

Would you say that the loss of eyesight in blind cave fish was a "weakening"? Or could it only be seen as such if those blind fish were moved to a place where there was light and other fish could see? Sure, then perhaps the blind fish are worse off, but move the sighted fish to the black cave and who's "weakened" then?

However IANAB! So take what I say with a pinch of salt eh?

Well you seem to have read a great deal more than I have, so thanks.

Sean Carroll made the same kind of distinction when talking about the Notothenioidei fish that can survive in salt water that is as cold as -2 celcius (Behe also talks about these as clear examples of evolution). If global warming predictions were to happen, these fish would quickly die out because they can no longer survive in warmer temperatures. So their adaptation is beneficial, only so long as it provides them with a significan advantage in their environment.

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Feb. 01 2010,10:10   

Quote
So their adaptation is beneficial, only so long as it provides them with a significan advantage in their environment.

And that's true of every adaption. It's all environmentally dependent.

One of the common arguments used (by IDiots) is the "parent environment study".

1) A organism has been shown to have a mutation that benefits it (e.g. developing the ability to digest citrate).

2) The objection is made "but that ability comes from damaging part of the organism, it's been made "worse" by the mutation".

3) To prove that the IDiot says "put the mutated organism in the same envrioment as it's parent. If it cannot out compete it's parent it's "damaged". The form it was given at creation, in the garden of eden, has become degenerated and it's inability to out-compete it's parent proves that as it's parent is logically closer to perfection then the mutated descendant".

I hope you can see the fallacy here. And this argument, honestly, is used many times.

The "parent" cannot digest citrate so who's worse off? It depends on the environment.

I can't swim well, but all life came from the sea. If I take a fish and put it on land and it dies does that prove anything? If I got for a swim and drown, what does that prove? That the "parent" of me got damaged and so I lost my gills?

etc etc.

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,11:21   

Quote (oldmanintheskydidntdoit @ Feb. 01 2010,10:10)
Quote
So their adaptation is beneficial, only so long as it provides them with a significan advantage in their environment.

And that's true of every adaption. It's all environmentally dependent.

One of the common arguments used (by IDiots) is the "parent environment study".

1) A organism has been shown to have a mutation that benefits it (e.g. developing the ability to digest citrate).

2) The objection is made "but that ability comes from damaging part of the organism, it's been made "worse" by the mutation".

3) To prove that the IDiot says "put the mutated organism in the same envrioment as it's parent. If it cannot out compete it's parent it's "damaged". The form it was given at creation, in the garden of eden, has become degenerated and it's inability to out-compete it's parent proves that as it's parent is logically closer to perfection then the mutated descendant".

I hope you can see the fallacy here. And this argument, honestly, is used many times.

The "parent" cannot digest citrate so who's worse off? It depends on the environment.

I can't swim well, but all life came from the sea. If I take a fish and put it on land and it dies does that prove anything? If I got for a swim and drown, what does that prove? That the "parent" of me got damaged and so I lost my gills?

etc etc.

Agreed. This strategy doesn't seem to make sense.

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,11:23   

Quote (Utunumsint @ Feb. 01 2010,08:39)
Quote (afarensis @ Jan. 29 2010,19:45)
Quote (Zachriel @ Jan. 28 2010,20:24)
 
Quote (afarensis @ Jan. 28 2010,18:45)
Zhang's work on digestive Rnases in ruminants and colobines - such as this article - seems relevant here. Although I have never heard it mentioned.

Zhang provides a good summary of a few basic principles.

 
Quote
These results suggest that (1) an evolutionary problem can have multiple solutions, (2) the same amino acid substitution may have opposite functional effects in homologous proteins, (3) the stochastic processes of mutation and drift play an important role even at functionally important sites, and (4) protein sequences may diverge even when their functions converge.

Well, yes. But I was thinking of the nine mutations that occured in the pancreatic Rnase. Several of which allowed it to work in a low PH environment and several more of which helped it extract nitrogen from the plant digesting bacteria of course the ability of the Rnase to process double stranded RNA was reduced but overall the trade off was beneficial. Incidentally, Zhang calculated the number of different paths that could be taken to achieve these results - I'm not sure if it was in this paper or one of his others on the same subject. Turns out there are over forty ways to get from the initial pancreatic Rnase to the digestive one. One can see something kind of similar in some of the pesticide resistance stuff in flies. Some of the initial mutations, although they provide some resistance to pesticides, lower fitness. But then other mutations happen, mutations that moderate the detrimental effects and enhance the beneficial. So Behe's contention that that evolution runs up against an edge after one or two mutations is pure BS.

Interesting. Thanks for this. Do you have a link to the study?

Another issue that has been gnawing at me as I read Behe's book is that he makes a one to one comparison between the evolution rate of Malaria in developing Chloroquine resistance, to that of human beings developing similar complex mutations over time.

My issue with this is that it seems to be overlooking the fact that each human beings are made up of trillions of microorganisms that alre also replicating within each person. Isn't it oversimplistic to make a one to one comparison between a microorganism's rate of evolution and that of a human being, made of of trillions of microorganisms?

Cheers,
Ut

It seems, then, that this is the core of his argument, and the one part of his book that I need to have clarified before I can really put it down.

Quote
Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 1020. I then wrote that ‘‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’’ (Behe 2007) (because that is the extrapolated time that it would take to produce 1020 humans).

  
fnxtr



Posts: 3504
Joined: June 2006

(Permalink) Posted: Feb. 01 2010,11:40   

[quote=Utunumsint,Feb. 01 2010,09:23]
Quote (Utunumsint @ Feb. 01 2010,08:39)

 
Quote
Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 1020. I then wrote that ‘‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’’ (Behe 2007) (because that is the extrapolated time that it would take to produce 1020 humans).

This is the kind of mathematical shenanigans that Behe and his crowd are famous for.

The quoted estimate would only be true if every human ever born comes with just 1 "mutation", wouldn't it?

And since every child is a mix of genomes from mother and father, even before factoring in imperfect replication during fertilization and embryonic development, you can count on slightly higher genetic variety than that.

--------------
"[A] book said there were 5 trillion witnesses. Who am I supposed to believe, 5 trillion witnesses or you? That shit's, like, ironclad. " -- stevestory

"Wow, you must be retarded. I said that CO2 does not trap heat. If it did then it would not cool down at night."  Joe G

  
Albatrossity2



Posts: 2780
Joined: Mar. 2007

(Permalink) Posted: Feb. 01 2010,11:48   

Quote (Utunumsint @ Feb. 01 2010,11:23)
It seems, then, that this is the core of his argument, and the one part of his book that I need to have clarified before I can really put it down.

Easy enough.

From Nick Matzke's http://www.sciencedirect.com/science....16b73ddreview of EoE

Quote


   [Behe] attempts to use the evolution of chloroquine resistance (CQR) in Plasmodium falciparum to establish that the origin of multiprotein complexes requires ID. First, Behe admits that CQR evolves naturally but contends that it requires a highly improbable simultaneous double mutation, occurring in only one in 1020 parasites. Second, he asserts that protein-protein binding sites require several simultaneous point mutations and that their occurrence is, therefore, even less probable than that of the alleged double mutation required for CQR. His last step is to square 1020 to produce 1040, the number of organisms required to evolve two binding sites linking three proteins. Given that fewer organisms than this have existed during the history of the Earth, any complex of three or more proteins is beyond the reach of mutations not guided by ID.

   The argument collapses at every step. Behe obtains the crucial 1020 number from an offhand estimate in the literature that considered only the few CQR alleles that have been detected because they have taken over regional populations. What is needed, however, is an estimate of how often any weak-but-selectable CQR originates. A study conducted in an area where CQR is actively evolving [5] showed that high-level CQR is more complex than just two substitutions but that it is preceded by CQR alleles having fewer substitutions; moreover, Behe’s two mutations do not always co-occur. As a result, CQR is both more complex and vastly more probable than Behe thinks. This sinks his one in 1020 estimate for CQR, in addition to his notion that protein-protein binding sites are more complex and, therefore, less probable than CQR. Behe’s decision to square the probability for two binding sites depends on the assumption that two binding sites would have to evolve at once; however, the assumption is false for the same reasons that his ‘irreducible complexity’ argument failed in the first place [1-3]. The squaring assumption is further contradicted by any experiment that accidentally evolves two proteins binding to different sites on a target protein instead of just one [6].

   […]

   1 A. Bottaro et al., Immunology in the spotlight at the Dover ‘Intelligent Design’ trial, Nat. Immunol. 7 (2006), pp. 433–435.

   2 M.J. Pallen and N.J. Matzke, From The Origin of Species to the origin of bacterial flagella, Nat. Rev. Microbiol. 4 (2006), pp. 784–790.

   3 E.C. Scott and N.J. Matzke, Biological design in science classrooms, Proc. Natl. Acad. Sci. U. S. A. 104 (suppl. 1) (2007), pp. 8669–8676.

   4 L.J. Briggs et al., More than one way to build a flagellum: comparative genomics of parasitic protozoa, Curr. Biol. 14 (2004), pp. R611–R612.

   5 P. Mittra et al., Progressive increase in point mutations associated with chloroquine resistance in Plasmodium falciparum isolates from India, J. Infect. Dis. 193 (2006), pp. 1304–1312.

   6 V.A. Petrenko et al., Alpha-helically constrained phage display library, Protein Eng. 15 (2002), pp. 943–950.



--------------
Flesh of the sky, child of the sky, the mind
Has been obligated from the beginning
To create an ordered universe
As the only possible proof of its own inheritance.
                        - Pattiann Rogers

   
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Feb. 01 2010,11:48   

Quote (Utunumsint @ Feb. 01 2010,11:23)
It seems, then, that this is the core of his argument, and the one part of his book that I need to have clarified before I can really put it down.

http://findarticles.com/p....ntagged
 
Quote
Finally, Behe notes that for one prespecified pair of mutations in one gene in humans with the first one neutral, we obtain a "prohibitively long waiting time" of 216 million years. However, there are at least 20,000 genes in the human genome and for each gene tens if not hundreds of pairs of mutations that can occur in each one. Our results show that the waiting time for one pair of mutations is well approximated by an exponential distribution. If there are k nonoverlapping possibilities for double mutations, then by an elementary result in probability, the waiting time for the first occurrence is theminimum of k independent exponentials and hence has an exponential distribution with a mean that is divided by k. From this we see that, in the case in which the first mutant is neutral or mildy deleterious, double mutations can easily have caused a large number of changes in the human genome since our divergence from chimpanzees. Of course, if the first mutant already confers an advantage, then such changes are easier.


--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Feb. 01 2010,12:01   

Utunumsint,
What you'll find, I believe, the more you look into Behe et al is that they are not interested in progressing their "science". If they were they would be publishing their work where other scientists could comment on it, tear it apart, reproduce it and improve it. I.E. the peer reviewed literature.

But you don't need to engage with your critics when you publish a book. You just need to sound "sciency" enough that people read your book and think "my viewpoint is supported by science. I might not understand all the details but Behe has done that for me already".

The back and forth I linked to is the exception rather then the rule.

Just ask yourself. Why is he publishing books instead of papers? Why are comments disabled on his blogs? Why does he never join in the comment wars at UncommonDescent, where he is name checked daily?

Why? I doubt he believes more then a fraction of what he writes. He's already said that he 100% believes in common descent.
Quote
Michael Behe
Not all intelligent-design advocates are like Nelson. Michael Behe (1996, 176 1) claims to accept the common descent of all life:

   "I believe the evidence strongly supports common descent."

He repeated this statement in a later publication (Behe 2001, 697 2):

   ". . . since I dispute the mechanism of natural selection, not common descent."


http://home.planet.nl/~gkorthof/korthof84.htm

It's all about the $$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$. If it was not, where is the science? They've had 20 years+ to show some "intelligent design" science, some positive evidence. But no, it's all "XYZ is too improbable" when we don't even know a fraction of all we could know about life.

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,12:02   

Quote
Behe attempts to use the evolution of chloroquine resistance (CQR) in Plasmodium falciparum to establish that the origin of multiprotein complexes requires ID. First, Behe admits that CQR evolves naturally but contends that it requires a highly improbable simultaneous double mutation, occurring in only one in 1020 parasites. Second, he asserts that protein-protein binding sites require several simultaneous point mutations and that their occurrence is, therefore, even less probable than that of the alleged double mutation required for CQR. His last step is to square 1020 to produce 1040, the number of organisms required to evolve two binding sites linking three proteins. Given that fewer organisms than this have existed during the history of the Earth, any complex of three or more proteins is beyond the reach of mutations not guided by ID.

  The argument collapses at every step. Behe obtains the crucial 1020 number from an offhand estimate in the literature that considered only the few CQR alleles that have been detected because they have taken over regional populations. What is needed, however, is an estimate of how often any weak-but-selectable CQR originates. A study conducted in an area where CQR is actively evolving [5] showed that high-level CQR is more complex than just two substitutions but that it is preceded by CQR alleles having fewer substitutions;


So basically, there is a step by step path to the two mutations Behe talks about with regard to Malaria, slowly increasing the CQR. But only the full blown version of CQR really takes off. So Behe's mathematical model does not take into account weaker mutation, and therefore his application of the model to our own evolution is flawed from the start.... Is this correct?

Quote
moreover, Behe’s two mutations do not always co-occur. As a result, CQR is both more complex and vastly more probable than Behe thinks. This sinks his one in 1020 estimate for CQR, in addition to his notion that protein-protein binding sites are more complex and, therefore, less probable than CQR. Behe’s decision to square the probability for two binding sites depends on the assumption that two binding sites would have to evolve at once; however, the assumption is false for the same reasons that his ‘irreducible complexity’ argument failed in the first place [1-3]. The squaring assumption is further contradicted by any experiment that accidentally evolves two proteins binding to different sites on a target protein instead of just one [6].


I think it might be time for me to put the book down and read something else.... Has he responded to this review anywhere?

Thanks for the info. :)

Cheers,
Ut

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,12:10   

Quote (oldmanintheskydidntdoit @ Feb. 01 2010,11:48)
Quote (Utunumsint @ Feb. 01 2010,11:23)
It seems, then, that this is the core of his argument, and the one part of his book that I need to have clarified before I can really put it down.

http://findarticles.com/p....ntagged
 
Quote
Finally, Behe notes that for one prespecified pair of mutations in one gene in humans with the first one neutral, we obtain a "prohibitively long waiting time" of 216 million years. However, there are at least 20,000 genes in the human genome and for each gene tens if not hundreds of pairs of mutations that can occur in each one. Our results show that the waiting time for one pair of mutations is well approximated by an exponential distribution. If there are k nonoverlapping possibilities for double mutations, then by an elementary result in probability, the waiting time for the first occurrence is theminimum of k independent exponentials and hence has an exponential distribution with a mean that is divided by k. From this we see that, in the case in which the first mutant is neutral or mildy deleterious, double mutations can easily have caused a large number of changes in the human genome since our divergence from chimpanzees. Of course, if the first mutant already confers an advantage, then such changes are easier.

He has responded to this one, and does not agree with some of their assumptions in make their own calculations. Whether he is right or not, I don't know. But the other article posted by Albatrossity2 seems to nix his argument at the very root....

Cheers,
Ut

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,12:16   

Quote (oldmanintheskydidntdoit @ Feb. 01 2010,12:01)
Utunumsint,
What you'll find, I believe, the more you look into Behe et al is that they are not interested in progressing their "science". If they were they would be publishing their work where other scientists could comment on it, tear it apart, reproduce it and improve it. I.E. the peer reviewed literature.

But you don't need to engage with your critics when you publish a book. You just need to sound "sciency" enough that people read your book and think "my viewpoint is supported by science. I might not understand all the details but Behe has done that for me already".

The back and forth I linked to is the exception rather then the rule.

Just ask yourself. Why is he publishing books instead of papers? Why are comments disabled on his blogs? Why does he never join in the comment wars at UncommonDescent, where he is name checked daily?

Why? I doubt he believes more then a fraction of what he writes. He's already said that he 100% believes in common descent.
 
Quote
Michael Behe
Not all intelligent-design advocates are like Nelson. Michael Behe (1996, 176 1) claims to accept the common descent of all life:

   "I believe the evidence strongly supports common descent."

He repeated this statement in a later publication (Behe 2001, 697 2):

   ". . . since I dispute the mechanism of natural selection, not common descent."


http://home.planet.nl/~gkorthof/korthof84.htm

It's all about the $$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$. If it was not, where is the science? They've had 20 years+ to show some "intelligent design" science, some positive evidence. But no, it's all "XYZ is too improbable" when we don't even know a fraction of all we could know about life.

I don't know if I can be that cynical about their motivations, but perhaps it is their religious views that are clouding their judgement. I know that Behe was initially motivated by Denton's book. Still...

I know that IDers often claim that they are not even allowed to publish their findings in peer reviewed articles, and that they are systematically denied the chance.

But at the same time, their support from the religious right seems to have come at a price. Creationists want to highjack their (seemingly) legitimate academic studies to their own purposes, and often try to coopt their arguments for their own literalistic understanding of the Bible.

As a religious person myself, its kind of embarassing....

Cheers,
Ut

  
Utunumsint



Posts: 103
Joined: Jan. 2010

(Permalink) Posted: Feb. 01 2010,12:33   

Quote (Utunumsint @ Feb. 01 2010,12:02)
Quote
Behe attempts to use the evolution of chloroquine resistance (CQR) in Plasmodium falciparum to establish that the origin of multiprotein complexes requires ID. First, Behe admits that CQR evolves naturally but contends that it requires a highly improbable simultaneous double mutation, occurring in only one in 1020 parasites. Second, he asserts that protein-protein binding sites require several simultaneous point mutations and that their occurrence is, therefore, even less probable than that of the alleged double mutation required for CQR. His last step is to square 1020 to produce 1040, the number of organisms required to evolve two binding sites linking three proteins. Given that fewer organisms than this have existed during the history of the Earth, any complex of three or more proteins is beyond the reach of mutations not guided by ID.

  The argument collapses at every step. Behe obtains the crucial 1020 number from an offhand estimate in the literature that considered only the few CQR alleles that have been detected because they have taken over regional populations. What is needed, however, is an estimate of how often any weak-but-selectable CQR originates. A study conducted in an area where CQR is actively evolving [5] showed that high-level CQR is more complex than just two substitutions but that it is preceded by CQR alleles having fewer substitutions;


So basically, there is a step by step path to the two mutations Behe talks about with regard to Malaria, slowly increasing the CQR. But only the full blown version of CQR really takes off. So Behe's mathematical model does not take into account weaker mutation, and therefore his application of the model to our own evolution is flawed from the start.... Is this correct?

Quote
moreover, Behe’s two mutations do not always co-occur. As a result, CQR is both more complex and vastly more probable than Behe thinks. This sinks his one in 1020 estimate for CQR, in addition to his notion that protein-protein binding sites are more complex and, therefore, less probable than CQR. Behe’s decision to square the probability for two binding sites depends on the assumption that two binding sites would have to evolve at once; however, the assumption is false for the same reasons that his ‘irreducible complexity’ argument failed in the first place [1-3]. The squaring assumption is further contradicted by any experiment that accidentally evolves two proteins binding to different sites on a target protein instead of just one [6].


I think it might be time for me to put the book down and read something else.... Has he responded to this review anywhere?

Thanks for the info. :)

Cheers,
Ut

Well I'm speechless....

http://pandasthumb.org/archives/2007/11/behe-replies-to.html

Cheers,
Ut

  
oldmanintheskydidntdoit



Posts: 4999
Joined: July 2006

(Permalink) Posted: Feb. 01 2010,12:45   

Quote (Utunumsint @ Feb. 01 2010,12:16)
I know that IDers often claim that they are not even allowed to publish their findings in peer reviewed articles, and that they are systematically denied the chance.

Yet Dembski can publish "ID supporting" papers without a problem, and when IDers are asked for the rejection letters for the papers they've tried to publish they simply can't provide them.

I know this for a fact as I have personally asked several times at UD for such rejection letters.

Link
   
Quote

Would such papers, if submitted, have rejection letters detailing the reasons for rejection? Have ID advocates already attempted to do what you say (publish in Nature or Science?) and if not, how do you know for certain they would be rejected out of hand? A positive attitude in this regard may pay dividends, whereas you can be certain if no ID advocate attempts to publish a paper in Nature or Science none will ever be published in Nature or Science

As they say for the Lottery, “you’ve got to be in it, to win it”.


As before, this claim that "IDers are not even allowed to publish their findings in peer reviewed articles" is simply an unsupported claim until some actual evidence is provided. It's really a convenient excuse as to why no such papers have been published (*see footnote).

And the same people who make that claim also, somehow, manage to point to this list
http://www.discovery.org/a/2640
   
Quote
In any case, the scientists who advocate the theory of intelligent design have published their work in a variety of appropriate technical venues, including peer-reviewed scientific journals, peer-reviewed scientific books (some in mainstream university presses), trade presses, peer-edited scientific anthologies, peer-edited scientific conference proceedings and peer-reviewed philosophy of science journals and books.

We provide below an annotated bibliography of technical publications of various kinds that support, develop or apply the theory of intelligent design.

So, when it's convenient they cry "censorship" but depending on the audience they can flip over to "but there are so peer reviewed papers that support ID.

Which is it?

Show me a single rejection letter from a reputable journal  that says "We're not publishing this because it supports ID"

If IDers can't publish, what of this?
William A. Dembski and Robert J. Marks II, “Bernoulli’s Principle of Insufficient Reason and Conservation of Information in Computer Search,” Proceedings of the 2009 IEEE International Conference on Systems, Man, and Cybernetics. San Antonio, TX, USA – October 2009, pp. 2647-2652.

*EDIT* I say no ID supporting paper exists, and if you look at Dembski's paper you'll find that despite him claiming that it supports ID I doubt you'll be able to determine how it does. I know what his claim entails at it's core but can you spot it? Nonetheless, the phrase "intelligent design" or the word "designer" does not appear once in the paper. And it's not even about biology in any case.

--------------
I also mentioned that He'd have to give me a thorough explanation as to *why* I must "eat human babies".
FTK

if there are even critical flaws in Gauger’s work, the evo mat narrative cannot stand
Gordon Mullings

  
Quack



Posts: 1961
Joined: May 2007

(Permalink) Posted: Feb. 01 2010,15:12   

Quote (oldmanintheskydidntdoit @ Feb. 01 2010,12:01)
Utunumsint,
What you'll find, I believe, the more you look into Behe et al is that they are not interested in progressing their "science". If they were they would be publishing their work where other scientists could comment on it, tear it apart, reproduce it and improve it. I.E. the peer reviewed literature.

But you don't need to engage with your critics when you publish a book. You just need to sound "sciency" enough that people read your book and think "my viewpoint is supported by science. I might not understand all the details but Behe has done that for me already".

The back and forth I linked to is the exception rather then the rule.

Just ask yourself. Why is he publishing books instead of papers? Why are comments disabled on his blogs? Why does he never join in the comment wars at UncommonDescent, where he is name checked daily?

Why? I doubt he believes more then a fraction of what he writes. He's already said that he 100% believes in common descent.
     
Quote
Michael Behe
Not all intelligent-design advocates are like Nelson. Michael Behe (1996, 176 1) claims to accept the common descent of all life:

   "I believe the evidence strongly supports common descent."

He repeated this statement in a later publication (Behe 2001, 697 2):

   ". . . since I dispute the mechanism of natural selection, not common descent."


http://home.planet.nl/~gkorthof/korthof84.htm

It's all about the $$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$$. If it was not, where is the science? They've had 20 years+ to show some "intelligent design" science, some positive evidence. But no, it's all "XYZ is too improbable" when we don't even know a fraction of all we could know about life.

IMHO it can't be stressed too often; not only WRT to life but WRT knowledge by and large about most aspects of 'reality'. Reading ID/creationist arguments it seems they are 100 years behind the times. While in reality, we realize we know much less than we once may have thought we did. And yet, that doesn't invalidate all that we after all do know. Am I on the right track?

--------------
Rocks have no biology.
              Robert Byers.

  
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