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Res, you're at it again, insulting people's religious beliefs.

And you say Christians are persecuted?

Similar to NokX's "show me a fish with legs!" bit to counter evolution, I'm sticking with "explain my appendix" as a counter to ID.

resedit wrote:

jerwin wrote:

At last, a formula for computing entropy!

Shannon entropy (Sn) values were calculated as a measure of genetic complexity. They incorporate the number of sequence variants, the frequency of each variant, and the total number of variants analyzed

   
where N = total number of sequences and pi = frequency of each sequence. Sn values can range from 0 (when 1 variant is present) to 1 (where each variant occurs once).

source

I'm using the same definition of entropy used by that link that jerwin provided where they used shanon entropy to describe genetic diversity.

OK, then. We're getting somewhere. The link says that Sn ranges from zero to one. But how much information corresponds to an Sn of zero? How much to an Sn of one? Can we assume that one extreme Sn is just random noise, and the other, evidence of the hand of god?

ShnickyShnack wrote:

You're using reason again. ID has nothing to do with reason.

Neither does Mother Russia, but I love it.

What's the real story behind ID and creationism? Where does it all come from?

Americans are woefully ignorant on the subject of science

Dr. Miller's data reveal some yawning gaps in basic knowledge. American adults in general do not understand what molecules are (other than that they are really small). Fewer than a third can identify DNA as a key to heredity. Only about 10 percent know what radiation is. One adult American in five thinks the Sun revolves around the Earth, an idea science had abandoned by the 17th century.

Rr. Miller, who was raised in Portsmouth, Ohio, when it was a dying steel town, attributes much of the nation's collective scientific ignorance to poor education, particularly in high schools. Many colleges require every student to take some science, but most Americans do not graduate from college. And science education in high school can be spotty, he said.

"Our best university graduates are world-class by any definition," he said. "But the second half of our high school population - it's an embarrassment. We have left behind a lot of people."

And those people -- they vote. They're devout. And evidently they expect things to be done their way.

resedit wrote:

That entropy link you provided has nothing to do with how the information got there, it is just using the information that is there for the purposes of studying genetic diversity - which is quite commonly done.

Such inquisitiveness!
Shall we go back to the original text?

Oh yes. Yes, we shall.

Most studies assessing the diversity of hepatitis C virus (HCV) quasispecies are conducted by amplifying selected portions of the genome by PCR, isolating individual subgenomic fragments by a cloning procedure, and then characterizing the nucleotide sequence of each clone 15, 17, 20.

Hmm. These numbers are interesting. Might they shed some light on our queries?

Let's go look at the endnotes.

15.     Manzin, A., L. Solforosi, E. Petrelli, G. Macarri, G. Tosone, M. Piazza, and M. Clementi. 1998. Evolution of hypervariable region 1 of hepatitis C virus in primary infection. J. Virol. 72:6271-6276

17.     McAllister, J., C. Casino, F. Davidson, J. Power, E. Lawlor, P. L. Yap, P. Simmonds, and D. B. Smith. 1998. Long-term evolution of the hypervariable region of hepatitis C virus in a common-source-infected cohort. J. Virol. 72:4893-4905

20.     Ni, Y. H., M. H. Chang, P. J. Chen, H. H. Lin, and H. Y. Hsu. 1997. Evolution of hepatitis C virus quasispecies in mothers and infants infected through mother-to-infant transmission. J. Hepatol. 26:967-974

In this case, reference 15 provides the goods. You can investigate the others, should you wish, though. The last, sadly, is only available in abstract form, at least to the proletariat.

Manzin et al. wrote:

Hepatitis C virus (HCV), a positive-strand RNA virus of about 9.4 kb (3, 4, 9) included in the family Flaviviridae (21), is the major causative agent of non-A, non-B acute and chronic hepatitis. After primary HCV infection, progression to viral persistence is observed in most patients (1, 28). The HCV genome in persistently infected hosts is described as a dynamic population of heterogeneous, closely related variants designated quasispecies (11, 15, 20). Recent biological and molecular data strongly suggest that HCV variability plays a crucial role in escaping the host immune surveillance and establishing the chronic carrier state (8, 11, 12, 29-31). A high degree of variability has been revealed in two discrete sequences of the putative envelope-encoding E2 region of HCV RNA, which have been designated hypervariable regions 1 and 2 (HVR-1 and HVR-2). Notably, the 27-amino-acid HVR-1, located in the N-terminal portion of the HCV envelope protein, bears major neutralizing epitopes (25, 34). More recently, the role of the humoral immune response to HCV in driving viral genetic variability has been studied in vivo by analyzing chronically infected, immunocompromised patients (14, 16, 23); the results support the general hypothesis that the immune response acts as a major selective force during HCV persistence, even though the involvement of different, nonimmunological mechanisms, as observed in other RNA viruses (5), cannot be excluded.

The error-prone nature of viral RNA polymerases provides the biochemical basis for the variability observed in most RNA viruses. However, conflicting hypotheses have been advanced to explain the mechanisms of viral evolution in infected hosts; these include mutation-driven evolution (27), neutral evolution (7), and viral fitness for a selective environment. One method for the evaluation of the selective pressure envisages the analysis of Ka and Ks values and the Ka/Ks ratio, where Ka is the frequency of nonsynonymous (antonymous) substitutions per nonsynonymous site and Ks is the frequency of synonymous substitutions per synonymous site (17, 18); the higher the Ka/Ks ratio, the stronger the selective pressure for amino acid changes.

Of course, to discover which factor is most responsible for quasispecies diversity, you'll just have to read the papers.

So, umm, we were discussing entropy, and we were discussing information.

Are the two directly proportional? Inversely Proportional? Locked in a continuously variable struggle for dominance?

dN1/dt = r1*N1 ((K1 – N1 – (a *N2))/ K1)
dN2/dt = r2*N2 (K2 – N2 - (b *N1))/ K2)

Last edited by jerwin (2005-08-30 8:57 pm)

resedit wrote:

yeast

By all means, read the yeast paper and discover that it is not a loss of function, but an increase in function (and it is not "one" gene, but several, for that matter)

Also, please read my post #209 because you've successfully ignored it in your above post.

Also, please, please read the monkey paper (linked in post #194) because there you will see a duplication with the duplicate gaining a NEW function, NOT LOSING function.

You can "suspect" all you want, but you're wrong.

resedit wrote:

jerwin wrote:

Resedit.

Please define information.

Thanks.

DNA contains very specific sequences, much like grammar in a book.

Grammar in the absence of meaning

Last edited by jerwin (2005-08-30 9:45 pm)

donQ wrote:

Podesta wrote:

I think some Christians think not accepting what they believe is persecuting them.

I was going to add something to this thread, but will probably start another one instead.  It has gotten too long, and, I think, drifted away from the core problem with so-called intelligent design:  The so-called theory has no content.

Isn' t that the problem? ID was created to sneak a religious idea into science class.

So you agree that Moses was a prophet?

http://www.nytimes.com/2005/08/30/scien … oref=login
(requires free login)

Here's a really neat article about a group of scientist doing research in to a method of evolution. It talks about some work they did in determining how exactly the bits of DNA in chromosomes flip to cause certain changes, and some of it even relates somewhat to Res's confusion about how DNA can change to create new species, which is also tied to his whole "informational entropy" thing.

excerpt of article wrote:

Then they compared the macaque map to a corresponding map of the human genome. The order of thousands of genes was the same.

"About half of the chromosomes are pretty much intact," said William Murphy, a member of the team, now at Texas A&M University.

The other chromosomes had become rearranged over the past 25 million years, but Dr. Murphy and his colleagues were able to reconstruct their evolution. Periodically, a chunk of chromosome was accidentally sliced out of the genome, flipped around and inserted backward.

In other cases, the chunk was ferried to a different part of the chromosome. All told, 23 of these transformations took place, and within these blocks of DNA, the order of the genes remained intact.

"It's fairly easy to see how you can convert the chromosomes from the macaque to the human," Dr. Murphy said.

Then they compared the macaque map to a corresponding map of the human genome. The order of thousands of genes was the same.

"About half of the chromosomes are pretty much intact," said William Murphy, a member of the team, now at Texas A&M University.

Why would you require that an intelligent designer wouldn't re-use what works?
It is what our human "intelligent" designers do all the time.

A TI-89 has a m68k processor in it.
So does the Centris 610 sitting in my shed.
So does the Plus in my closes.

That doesn't mean a TI-89 evolved from an Amiga.

resedit wrote:

Then they compared the macaque map to a corresponding map of the human genome. The order of thousands of genes was the same.

"About half of the chromosomes are pretty much intact," said William Murphy, a member of the team, now at Texas A&M University.

Why would you require that an intelligent designer wouldn't re-use what works?
It is what our human "intelligent" designers do all the time.

A TI-89 has a m68k processor in it.
So does the Centris 610 sitting in my shed.
So does the Plus in my closes.

That doesn't mean a TI-89 evolved from an Amiga.

Hahaha... Have you heard of the idea of omphalism? God/gods could have created the universe as is last week if they wanted, it doesn't mean they did, and if they did, there's no way we could really know for sure. If that's what you believe, then there is absolutely no point in even discussing the issue, for either side.

The study shows a specific way in which the genes changed to create the different species. In one, or even a dozen, human lifetimes, we will never directly observe this process because it takes millions of years, but by comparing genomes, and using what we know of how mutations happen, these scientist are able to determine the evolutionary path the species may have taken.

Also, if you read the article, you will note that the breaks in the chromosomes happen in the same place, suggesting this "weakness" was exploited by evolution/natural selection to cause the various mutations. Consistent with omphalism, God could have put that there to fool us, but why would you choose to believe that? The other theory could be that god guided the evolution, exploiting the laws of nature...

Last edited by mo' ron (2005-08-30 11:04 pm)