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Intelligent Design - theory, examples, implications


Lolic

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Did Saul Spiegleman create life?

 

Going off the top of my head. Didn't he do an experiment where a replicating molecule, instead of increasing in complexity, grew shorter and shorter? Something like that? Once his molecule got to the minimum size it was stuck there, wasn't it? If so, no, he did not create life. In the OOL sense, life is a self-sustaining, self-replicating system capable of evolution. His final product was stuck.

 

Lolic: Impossibility of life happening by chance, and more.

 

Yes and no. It's no impossible for life to happen by chance: there's no law of physics or chemistry that strictly forbids nucleotides from forming and then linking up into a sequence capable of self-replication. What it might be is astronomically improbable.

 

It is true that science still does not have a complete series of plausible prebiotic events that could lead from simple inorganic compounds to life. As a skeptic, I suspend judgment on the hypotheses for the origin of life until enough evidence can be presented for or against them.

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Lolic has posted a VERY good point by mentioning the extreme improbability that hemoglobin evolved. You guys are on the hook to prove it, because you claim evolution is true. Don't give us pap answers - give us some 'solid' evidence,

not your presumptous and pompous theorizations.

 

Did you not read the quotes from Behe I posted where he says the case for design of hemoglobin is weak and far from convincing? That given myoglobin as a starting point, he can envision evolution 'tweaking' it (so to speak) to create hemoglobin?

 

****************************

EDIT: After reading farther down the posts I see that you did see me mention this, but you reject Behe's statements. Guess you are more of a Creationist than and IDist.

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There is no discussion of the complexity...

 

What complexity exactly? Off the top of my head, Nillson started with an ocellus and had it evolve into a simple camera-type eye. His model would then already subsume the basic complexity: photoreceptors, neurons hooked up to the photoreceptors and then joining to form an optic nerve, which would run back to a ganglion.

 

Lolic: ... the information to integrate the various parts...

 

Weren't the various parts already integrated at the beginning? If so, it was already there.

 

Lolic: ... the number of mutations required to acquire all these parts ...

 

From what I've read previously, his model did give an estimate of the number of mutations it would have taken.

 

Lolic: ... the thousands of mutations that would be negative that would harm the evolving family of critters.

 

That is included in any model of evolution. The negative mutations decrease the fitness of the possessors and they don't get propagated into future generations at the same frequency as those that confer an advantage upon their possessors.

 

There is an important idea related to natural selection's handling of mutations that I'm not sure you are familiar with: have you heard of functional constraint?

 

 

Lolic: If it were true, then we should have millions of intermediary fossils from other "hard" body structures forming in this manner. Where's the beef?

 

I can think of a few that might meet your criteria: the general increase in skull sizes of human ancestors as well as the skeletal adaptations needed for upright bipedal mobility, the evolution of the middle ear ossicles we have from reptilian jaw bones, and the evolution of the horse hoof.

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In artificial intelligence, we've been building neural networks for years to do image processing: it learns using evolutionary techniques via random mutation! And it works amazingly well and can even be faster than than the human brain. Its primary weakness to date has been the need to coordinate the pattern recognition with a large enough database to disambiguate complex forground and background images in visual image recognition. Its also being used quite effectively though by the NSA and CIA to monitor voice traffic for suspicious words and phrases.

Why don't you go into this in more detail and explain what portions of the project use intelligence and what parts don't. I worked in a research lab some years ago where the Air Force was working in this area...it was not without programmers, funding, project plans, etc. it was a project being run by intelligent people. No free lunch. No naturalistic miracles. Good hard work with thinking involved.

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Since we've gotten back to discussing the eye...

 

In “Darwin’s Black Box”, Michael Behe discusses how Darwin tried to explain the evolution of our camera-type eye from a simple eyespot, apparently not finding anything in Darwin’s explanation that needed to be countered. On pages 18-21 Behe explains the details of the complex visual system at the biochemical level, where he does doubt evolution’s ability to create the starting point of Darwin’s scenario. Those not familiar with biochemistry might wrongly believe that the molecules and mechanisms used in vision are unique to that system…another unspannable gap that science can’t explain. This is not so. There are analogous molecules/mechanisms that evolution could have co-opted for use in vision.

 

One such example is rhodopsin kinase activity.

 

“Third, while all of this is going on, metarhodopsin II is chemically modified by an enzyme called rhodopsin kinase.” (Darwin’s Black Box, Michael Behe, Free Press, 1996, p21)

 

First, modification of biochemistry by the action of many different types of phosphorylating enzymes (called kinases) is quite common. So the general mechanism is nothing new or out of the ordinary.

 

Second, the only thing left is the specific action of rhodopsin kinase, and like several other molecules/mechanisms in vision, it too is not a “complexity island”: BARK is its “close neighbor”.

 

“The mechanism by which rod-cell activity is controlled by rhodopsin kinase is similar to adaptation (or desensitization) of the [beta]-adrenergic receptor to high levels of hormone (see Figure 20-47). Indeed, rhodopsin kinase is very similar to [beta]-adrenergic receptor kinase (BARK), the enzyme that phosphorylates and inactivates only the ligand-occupied [beta]-andrenergic receptor, and each kinase can phosphorylate the other’s substrate. Moreover, a homolog of arrestin binds to BARK-phosphorylated [beta]-andrenergic receptors, blocking their activation of G5 proteins.” (Molecular Cell Biology: Fourth Edition, Harvey Lodish, Arnold Berk, S. Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell, W. H. Freeman & Co., 2000, p957)

 

Another protein Behe mentions in the complexity of vision is arrestin. Again, it is not a “complexity island”: it has a homolog that binds to “BARK” molecules (which themselves are quite similar to rhodopsin kinase molecules).

 

"At high ambient light (such as noontime outdoors), the level of opsin phosphorylation is such that the protein arrestin binds to opsin. Arrestin binds to the same site of opsin as does transducin, totally blocking activation of transducin and causing a shutdown of all rod-cell activity. … [A] homolog of arrestin binds to BARK-phosphorylated [beta]-andrenergic receptors, blocking their activation of G5 proteins.” (Molecular Cell Biology: Fourth Edition, Harvey Lodish, Arnold Berk, S. Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell, W. H. Freeman & Co., 2000, p957)

 

Another of the biochemical players in vision Behe repeatedly references in cGMP. Cyclic GMP (cGMP) can adopt either of two stable forms: “normal” GMP (guanosine monophosphate, a nucleic acid nucleotide) and cyclic GMP. The normal form of GMP is converted into the cyclic from by an enzyme, called guanylate cyclase. Another enzyme, cGMP phosphodiesterase, serves to convert cGMP back into GMP.

 

“GTP-transducin-metarhodopsin II now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to metarhodopsin II and its entourage, the phosphodiesterase acquires the chemical ability to “cut” a molecule of cGMP (a chemical relative of GDP and GTP).” (Darwin’s Black Box, Michael Behe, Free Press, 1996, p 20)

 

But there is not just a single type of cGMP phosphodiesterase, nor is either cGMP or cGMP phosphodiesterase used only in photoreceptors. Again, more key molecules of vision that are not a “complexity islands".

 

“We have been interested in studying the regulation of the cGMP-binding, cGMP-specific phosphodiesterase (PDE5) in intestinal cells. PDE5 is the target for the drug sildenafil citrate, or Viagra, used in the treatment of male impotence.

 

PDE5 is expressed in human colonic cells and in intestinal tissue and we have shown that its activity is regulated by intracellular cGMP levels in these cells…” (http://www.mrdg.iisc.ernet.in/bundle/pde.htm)

 

“The expression and regulation of the cGMP-binding, cGMP-specific phosphodiesterase, PDE5, was studied in intestinal cells. … Our results therefore represent the first study on the expression and regulation of PDE5 in intestinal tissue, and indicate that mechanisms to control its activity may have important consequences in intestinal physiology.” (The cGMP-binding, cGMP-specific phosphodiesterase (PDE5): intestinal cell expression, regulation and role in fluid secretion, Sopory S, Kaur T, Visweswariah SS., Cell Signal. 2004 Jun;16(6):681-92)

 

Two more "players" rendered "unspecial".

 

As Behe explains (even if not explicitly), rod cells have cGMP-gated channel proteins. That is, the cyclic form of GMP binds directly to a protein that is part of the ion channel to cause a change in its functioning.

 

First, although rod cells use cGMP-gated ion channels, some other cells use cAMP-gated ion channels, which are nearly identical (it appears the main 'structural' difference is just that one binds cAMP while the other binds cGMP – that is, the single nucleotide-binding site differs).

 

Second, the two types of nucleotide-gated ion channels are very similar in structure to a very common ion channel called a voltage-regulated K+ channel. Both the voltage-gated K+ channel and the two types of nucleotide-gated channels :

 

(1) exist as tetramers (i.e., they consist of four separate polypeptides that join together to form a single functional protein)

 

(2) each of the monomeric polypeptides in the tetramers consists of six membrane-spanning alpha helices.

 

(3) each of the channels are formed by the non-helical pore segments between helices 5 and 6.

 

(source is: Figure 21-27 of Molecular Cell Biology: Fourth Edition, Harvey Lodish, Arnold Berk, S. Lawrence Zipursky, Paul Matsudaira, David Baltimore, and James Darnell, W. H. Freemand & Co., 2000, p934)

 

Another player in vision rendered "unspecial".

 

So far that makes cGMP, cGMP phosphodiesterase, cGMP-gated ion channels, retinal, seven-spanning transmembran proteins (rhodopsin and bacteriorhodopsin), and rhodopsin kinase activity all "non-special" players in vision. That should be enough to make the point: co-option cannot be simply ruled out.

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Interesting to read but hardly proof. If it were true, then we should have millions of intermediary fossils from other "hard" body structures forming in this manner.

 

If you were to go out and study the kinds of eyes that exist in nature today, you will find just about every single step on the evolutionary ladder: from simple light detectors to advanced optically shaped recepticels like the human eye.

 

One thing this proves, "theory savers" will go to no end to keep an intelligent foot out of their evolutionary sandbox. They almost act as though they have something to lose

 

I see you have no intention to stop your mindless ridicule. It does work, however, if your goal is to appear like a fool.

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Why don't you go into this in more detail and explain what portions of the project use intelligence and what parts don't. I worked in a research lab some years ago where the Air Force was working in this area...it was not without programmers, funding, project plans, etc.
Actually the hard work is in getting the networks trained, which only takes time. In practical applications, its more important to get things to work quickly rather than to prove that they'd work if left alone to build the whole system itself, so virtually all of those programmers and thought are being used to short circuit the process to get results. In addition, neurons in the brain work *completely* differently than the vonNeumann machines that have become popular: the work by having billions of processors which can modify their connections over time, and they use analog rather than digital inputs. Virtually all of the "intelligent" work that goes into this is simply getting today's hardware and software to work like neurons. Once you have them, they are amazingly simple in operation:

  1. Inspect inputs
  2. Compute against current formula
  3. Produce outputs
  4. Inspect feedback
  5. If negative feedback, randomly modify the formula, possibly skipping previously attempted modifications
  6. Go to 1

This is over simplified, but here are two useful links:

[*]This is a good explanation of the simplest type of neural network known as a "perceptron" (there are lots more complicated ones now as referenced at the end of the page): http://www.cs.stir.ac.uk/~lss/NNIntro/InvSlides.html

[*]This site actually provides an open source java development kit for building neural networks if you're interested in working with them: http://www.generation5.org/content/2000/nnintro.asp

The thing about these networks is that they start out with no initial knowledge of their inputs, the formulas don't appear to have anything to do with the problem being solved (in fact there's some evidence that the more random the initial formulas, the better the final results, although they may take many more learning iterations to develop consistent and reliable results), and the performance over time exceeds that of any pre-programmed algorithm! The basic structures are based on neurons that are *less* complex than we see in the simplest creatures with neurons. It does not require any real significant programming or even thinking to make them work. And of course the neurons in the biological world have had billions of years of feedback loops to adjust their formulas, yet we get results after a few thousand iterations. These systems are great examples of self organization, and even if you want to argue that "intelligence" was required for the initial setup, the operation of the resulting system *far* exceeds the information "programmed in". And again as I said earlier, most neural networks are programming stuff in to save time, so they can't really be used as an argument that they are all completely dependent on initial programming.

 

A side note on the Air Force's problems: The algorithms for guiding anti-missle systems and detecting decoys that are failing so famously right now is not having problems due to the neural net-based algorithms, its in dealing with the problems of physics of how fast the targets are moving, how far away they have to be in order to adjust trajectories in time, and the inability of CCDs/radar and other detection mechanisms to resolve useful inputs at such great distances, often through obscuring physical media (air, clouds, sun glare, etc.). The algorithms themselves appear to work great under when the inputs are decent...

 

Cheers,

Buffy

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More on cooption and the eye.

 

The transparent proteins that make the lens of the eye clear are called crystallins. But contrary to the long held belief that crystallins were unique to the eye, scientists back in the 1990s found that the proteins are used by most other cells in our bodies, but there are used for different purposes.

 

”The lens is a remarkable transparent structure filled with proteins called crystallins, which have been an object of study for more than a century. Found in great quantities in the lens and perfectly arranged to focus light, crystallins were long thought to be highly specialized lens proteins that evolved solely to allow animals to see.

 

But as researchers studying these proteins are discovering, the evolution of the lens may have been a lot simpler than was imagined and may begin to lessons in how such complex structures arise in general.

 

Many crystallins, scientists are finding, are actually the same proteins as the common housekeeping enzymes that govern the cell’s basic chemical metabolism. One crystalline, for example, is also known from its humbler role as lactase dehydrogenase, an ordinary metabolic enzyme. Researches say these proteins evolved first for their humdrum housekeeping tasks and only later were adapted to the entirely different and specialized task of building the lens.” (The Wizard of Eyes: Evolution Creates Novelty by Varying the Same Old Tricks, Carol Kaesuk Yoon, November 2004, from the book: The Science Times Book of Fossils and Evolution, p175)

 

and ...

 

"5.5 Orthologous proteins that have gained additional functions

 

Gene sharing

 

A special situation arises when a gene product is used to serve an additional function without losing its original function. This phenomenon, termed gene sharing, was discovered in the case of lens crystallins, which are used in the eye lens to maintain transparency (Tomarev & Piatigorsky 1996). Many types of crystallins were found to be identical with catalytically active enzymes, such as [alpha]-enolase ([one type of] crystallin), glyceraldehyde-3-phosphate dehydrogenase ([pi]-crystallin), lactate dehydrogenase ([epsilon]-crystallin), aldehyde dehydrogenase ([another type of] crystallin), argininosuccinate lyase ([another type of] crystallin), and NADPH: quininone oxidoreducatase ([another type of] crystallin)." (Protein Evolution, Laszlo Patthy, Blackwell Science, 2000, p84)

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to appear like a fool.

Ouch. Now that just wasn't nice. I don't believe I said anything that is not in the literature. The "facts" are not so clearly agreed upon as some may think or suggest.

 

I'm going through "Icons of Evolution" again. Dr Wells does a great job of bringing out many points and showing informantion on both sides. But there area real controvercies. As a science writer you should love that stuff. I bet if you read it you would find a story there, because some of the stuff people are posting here and taking for granted is shown to be incorrect by research in the last decade or so. He even does a good job of discussing the "facts" of evolution and helping to explain how things get misconstrued.

 

You can call me a fool, but based on the information Dr Wells presents, and shown otherplaces, I will wear that badge with honor. Now if you read it and point out his shortcomings with evidence, I'll change my tune. :hyper:

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Here's a good short summary paragraph from "Icons of Evolution" page 54.

 

"So the branching-tree pattern of evolution is inconsistent wth the major features of the fossil and molecular evidence. The Cambrian explosin demonstrates that the hightest categories of animals appeared first, thus turning Darwin's tree of life upside down. The molecular evidence, far from saving it, uproots it entirely. Yet the tree of life still dominates the iconography of evolution, because Darwinists have decalared it to be a fact."

 

Dr Wells includes a nice discussion of using DNA to try to make a tree of life, (work being preformed by pro-evolutionists) and the work has gone against Darwin's theory. Interesting reading.

 

The "tree of life" isn't a fact. It's a theory that does not appear to be true based upon the current evidence.

 

Later he makes an interesting quote from a Chinese paleontologist who's area is Cambrian fossils, "In China we can criticize Darwin, but not the government; in America, you can criticize the government, but not Darwin."

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You can call me a fool, but based on the information Dr Wells presents, and shown otherplaces, I will wear that badge with honor.

 

First of all, I did not call you a fool. Please read my post again.

 

I am not commenting upon what you read and what you think. I am talking about your persistent ridicule of others' posts here.

 

I don't care what you think about ID or how much you feel opressed by evolution, Lolic. I care about how you are presenting yourself and it is not looking pretty.

 

I have decided to keep out of this discussion because it is completely fruitless due to endless circular logic, dodging of questions (like your last post where you ignored TeleMad's post about the eye and simply asked for something else). When someone points out a fallacy in your line of argument you simply skip to another line and ignore the criticism. It is probably a clever way to not have to answer to anything but it is also what makes you appear foolish. I do not for a second believe that you are, though, so take it as advice from someone who has lived with these forums for 3 years.

 

I hope to get my "faith/atheism" book soon - it was delayed from Amazon but I got a "shipped" notice today so it whould be here in a week or so.

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What complexity exactly?

 

have you heard of functional constraint?

 

I can think of a few that might meet your criteria: the general increase in skull sizes of human ancestors as well as the skeletal adaptations needed for upright bipedal mobility, the evolution of the middle ear ossicles we have from reptilian jaw bones, and the evolution of the horse hoof.

My understandng from reading and viewing is that a mutation may change the DNA to create a new protein, but there is still a need within the cell for instructions for assemblying the new protein into something more, doing it in the correct order, transporting it to the structure, and that there would also be instructions for tissues, organs, body plans. I will try to find this reference but believe it came from Dr Stephen Meyer. This is a main reason I am so doubtful about the beneficail affect of mutations, because they are only a part of the story as I understand it, and the rest of the story needs to be integreated with the new protein which I don't see happening without intelligence being invovled. Fishteacher tried to answer this once but he assumed I ment something I didn't. (I may still not have made it clear)

 

I will plead no memory to "functional constraint" but sounds like a linear programming term.

 

Can you provide any links to these transitional items? (I never should have responded to that eye post, I wanted to stick with the flagellum for awhile, darn)

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Here's a good short summary paragraph from "Icons of Evolution" page 54.

 

First of all, Darwin is not evolution and evolution is not Darwin. If someone refutes some things Darwin wrote that doesn't refute evolution. Darwin made many errors because he wrote his book back in the 1800s. Behe says that at that time scientists viewed the cell as little more than a miniature lump of simple, gelatinous protoplasm. Darwin didn't know about genes, chromosomes, lateral gene transfer, etc., heck, he didn't even know how inheritance worked. So of course we would expect him to not have gotten everything right: how could he? How could anyone back then?

 

Second, even if some textbooks continue to print a tree of life based on Darwin's views, and that is no longer valid, that still doesn't disprove evolution.

 

Let me turn this type of argument around. There is no God and I can prove it. The modern Bibles in the USA continue to mistranslate "the sea of reeds" as "the Red Sea". In the original texts, it was the see of reeds that Moses parted, but the Bibles in the US have continued to print the error, long after it was known to be an error. So, since they continue to print something that's wrong, then everything related to the Bible and religion must also be wrong. Right? Therefore, there is no God.

 

Surely you see how the logic is messed up now.

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I will plead no memory to "functional constraint" but sounds like a linear programming term.

 

As you have said, mutations that would disrupt a structure occur much more frequently than mutations that would improve a structure. But if the disruptive change occurs in some structure that needs to continue to function for the organism to be fit, then those changes will be eliminated. If the structure is not needed for fitness, then there is no functional constraint and the mutation is not selected against.

 

We can see this in eyes. Eyes are very important to both prey and predators: if you have defective eyes, you die, either because you can't escape with the rest of your group, or because you can't catch things to eat. So eyes are under functional constraint: deleterious mutations to eyes are eliminated by natural selection. (At the same time, neutral mutations can accumulate and natural selection will also tend to preserve any advantageous mutations that happen to arise)

 

But what about organisms that once needed their eyes but have moved to a new habitat where they don't? For example, some cave-dwelling fish still have very partial eyes form, even though the eyes can't form images, nor can they detect light (there is no light in the caves). These fish used to have eyes, which is plain to see, but because the functional constraint on eyes for these fish was removed when they permanently moved into lightless conditions within caves, mutations that were disruptive to eyes were able to accumulate: natural selection did not eliminate those mutations, unlike it would have if the fish remained in their original habitat. Over a relatively short period of time, the fish lost their eyes.

 

The point is that we can see that natural selection does in fact continually work to eliminate disruptive mutations if the structure is under functional constraint. If it didn't, all animals would be blind like the cave-dwelling fish.

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My understandng from reading and viewing is that a mutation may change the DNA to create a new protein, but there is still a need within the cell for instructions for assemblying the new protein into something more, doing it in the correct order, transporting it to the structure, and that there would also be instructions for tissues, organs, body plans.

 

Sticking with just a protein with a new function, a change in the nucleotide sequence of DNA can produce the instructions for a new protein. One way this can occur is by exon shuffling. An exon is the part of a gene that gets translated (introns are the other part: intervening sequences that get spliced out). Some exons serve a particular function because of the particular shape that their protein will fold up into spontaneously. Many proteins are largely composed of various exons stitched together. And, many proteins share exons with other proteins. So it is possible that an exon can transpose to a region flanking an existing gene and add a new functional portion to the protein that gets produced.

 

However the gene for a protein with a new function arises, the machinery to construct that new protein - transcription from DNA to mRNA, translation of the mRNA into a protein by means of a ribosome - is already in place and functioning in the cell. If it weren't the cell would die.

 

Many protein structures self-assemble. Viruses are like this: their indivual parts - both proteins and nucleic acids - are produced separately and then they come together and self-assemble into viruses. I don't know what fraction of structures made of protein self-assemble, just that it does occur.

 

Cells also already have "taxis" that carry proteins to different targets. The delivery system wouldn't need to be created or modified, the new protein would just have to have an appropriate carbohydrate tag on it so the system routed it somewhere.

 

Tissue and higher levels are basically just particular types of cells that come together to perform a particular function. It is the cells (and their secretions) that make a tissue, the tissue is not some separate, different kind of biological thing. If you have the right cells, you have the right tissue.

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