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Or maybe I know better than you do, because I've actually had to come to terms with this issue personally and watched a number of relatives (both old and young) face these questions.

Here is a medical perspective on such questions.

Thanks! I've dug out the direct link:

http://www.pnas.org/cgi/content/abstract/060238210 3v1

Here's the first paper:

http://www.pubmedcentral.gov/articlerender.fcgi?ar tid=164507

and a nice website from the research group with lots of background:

http://www1.wfubmc.edu/pathresearch/srmouse/part1. htm

Why don't we just do what we do with the Uranium in coal?!

According to this paper (which just happens to be the first sort-of-remotely-useful source I've seen in Google, rather than an exhaustive study):

Coal Samples: Coal from Stockheim, Franken, Federal Republic of Germany, having a uranium content of 554 microgramme/gramme of coal was used.

According to a US DoE report on coal production and consumption states that on 2005 prelimary data shows total coal consumption to be around 1.1 billion short tons.

If we assume that the uranium content of 554 microgrammes/gramme is rather typical then:

1.1 billion short tons is about 997,700,000 tonnes of coal, which is 997,700,000,000,000 grammes.
Multiply that by 554 microgrammes/gramme to get 552,725,800,000,000,000 microgrammes of uranium...

Which is (drum roll) 552,725.8 TONNES (about 609,400 short tons) of URANIUM!

And what happens to it all? Well, some of it is in the airborne smokey stuff, and some of it remains as part of the coal ash. And what happens to the millions and millions of tonnes of coal ash? I wonder.

Are you sure that 50,000 tons of nuclear waste is really that much of a problem in comparison?

The base sequences of these genes were examined and a common characteristic was found: a long stretch of sequence without chain-terminating base triplets, defined as a nonstop frame (NSF), is being maintained on the antisense strand. Moreover, a certain coding frame is open for both the sense and the antisense sequences, while the other frames have many stop codons. The probability of the presence of these NSFs on the antisense strand of a gene is very small (0.0001-0.0018). In addition, another gene for nylon oligomer degradation was found to have a NSF on its antisense strand, and this gene is phylogenically independent of the nylB genes. Therefore, the presence of these NSFs is very rare and improbable. Even if the common ancestral gene of the nylB family was originally endowed with a NSF on its antisense strand, the probability of this original NSF persisting in one of its descendants of today is only 0.007. Unless an unknown force was maintaining the NSF, it would have quickly disappeared by random emergences of chain terminators. Therefore, the presence of such rare NSFs on all three antisense strands of the nylB gene family suggests that there is some special mechanism for protecting these NSFs from mutations that generate the stop codons. Such a mechanism may enable NSFs to evolve into new functional genes and hence seems to be a basic mechanism for the birth of new enzymes.

"What do you think antibiotic resistance is?"

A genetic adaptive response.

"They're variant amino acid sequences for antibiotic targets that produce slightly different proteins."

Contingency loci. This is not random change.

"Or community plasmids or viral sequences that don't have any advantage normally, but the bacterial community keeps around because those that don't are periodically wiped out."

Another adaptive response.

"But if you think about it as a random genetic mutation in the structure of a blood protein that, in its heterozygous state, confers great resistance to a lethal disease"

I do think about it that way. Note that your only example thus far of an actual random mutation has been degenerative. And yes, people who die from this don't reproduce much afterwards.

"How about cystic fibrosis? If "sick things don't reproduce well", cystic fibrosis should have been history long before modern medicine got around to diagnosing it."

????

So you are saying that natural selection doesn't work?

"Try looking up "ribosomal RNA sequencing" sometime, since you say you're big on scientific papers."

rRNA sequencing conflicts with the morphological data in many cases.

"How could life arise from non-life? The Wiki entry on "origin of life" has a good summary of the theories on how that could happen. As well as the experimental proof behind them."

Yes, there's many theories. But the "proof"s simply aren't there. Try checking out:

Chance and Necessity Do Not Explain the Origin of Life

Origin of life on earth and Shannon's theory of communication.

You also have the problem that before DNA-editting enzymes, the error rate would be too high to support life, but the enzymes are encoded by DNA.

Also there's the little problem that, before enzymes, the reaction rate would be way too slow to do anything of interest before being totally destroyed.

You also seem to be misunderstanding the idea of Intelligent Design (and even creationism). First of all, ID is compatible with (but does not require) common descent. Neither creationism nor intelligent design require a designer to be continually tinkering throughout natural history. The point is that the processes in the cell are ultimately _telic_ processes. They are informational processes, guided by the information that was originally coded. The Darwinian idea is that information can generate itself. Demski has handily refuted such idea using basic math (any search space involving more than 500 bits to achieve the next fitness level is basically impossible).

The quintessential ID hypothesis is probably Davison's Prescribed Evolutionary Hypothesis (previously called the Semi-Meiotic Theory) which says that phylogeny follows a semi-directed path just like ontogeny does.

The quintessential Creationary hypothesis is probably Todd Wood's Altruistic Genetic Element hypothesis.

Also, if you're interested, two good examinations of neo-Darwinism are:

A Biochemical Mechanism for Nonrandom Mutations and Evolution

and

"It would if the genes were exactly identical. "

Why is that? Design patterns do not use the same code every time. If they did, they would just be library routines, not design patterns.

"If you like I can show you some sequence alignments, for example between human and fly Eya/PAX6 (= Eyes absent) and other species in between that show quite astonishingly how these species are related."

You can find the same kind of homologies in 6-aminohexanoate-cyclic-dimer hydrolase in Flavobacterium and Psedomonas, despite the fact that we have _observed_ their appearance as separate occurrences. In fact, I believe in the case of Pseudomonas, the gene appeared de novo after 9 days.

So, if you can have a gene that appears _separately_ in two different lineages, with that gene appearing within days and exhibitting high homology, what does that do to the rest of the molecular arguments from homology?

"Aren't you actually grossly violating that by attempting to bring forth an untruth because you're too lazy to check the evidence?"

I have checked the evidence.

"Evolution and natural selection is the cause of most, if not all, variation in the biological world."

This is simply false. Natural selection has not been able to explain hardly anything. It is simply invoked. Read some biological papers. Whenever something new is found, it is simply listed as "having evolved" without any discussion about how the evolution could even have taken place.

_Most_ of the variation that takes place is the result of Mendellian inheritance, which, by the way, was discovered by a creationist (who used it to argue _against_ transformism).

The environment induces a large part of variance. Scott Gilbert has written about many of these, include variance resulting from an animal sensing predatory animals in the environment, and specifically changing their morphology to account for it. The process of genetic assimilation will make these changes the default morphology even in absence of the predator after a certain number of generations.

Likewise, microbes can change their genome in response to the environment. They can use transposons to activate latent genes, they can induce a highly regulated mutagenesis which produces almost entirely beneficial mutations.

Natural selection explains almost nothing. All natural selection means is that dead things don't reproduce, and sick things don't reproduce well. This is a conservative, not a creative process. And random mutation has too big of a search space to do anything productive. Perhaps you should take a 21st century view of evolution rather than the 1950's version of it you are looking at now.

Please tell me what the evidence is that (a) everything shares a common ancestor, and that (b) random mutation + natural selection is sufficient for creating the diversity that exists today from that common ancestor. If you want to be really adventurous, you can also show how (c) life could have proceeded from non-life.

Also, while we're at it, you could try showing how choice can arise through material mechanisms. If choice can't arise through material mechanisms, then either (a) choice as a real entity doesn't exist, or (b) a material view of origins is insufficient.

But I would agree with the statement in the article that one or two pills would be fairly harmless as far as side effects go. This is a drug that thousands of people have stayed on for decades.

Someone brought up the issue of attacking a treated victim's testimony in court. I wouldn't be surprised if this new data means lawyers will start attacking the testimony of all witnesses on beta blockers for whatever reason. And I would bet probably 25% of Congress (I'm guessing based on age and sex) is on a beta blocker.

Here.

The authors are far more cautious in their interpretation than some of the /. readers...but then this is not that much of a surprise. PDF (a few MBs) http://www.pubmedcentral.gov/picrender.fcgi?artid= 1253627&blobtype=pdf

Here is a link to the scientific article in the Proceedings of the National Academy of Sciences which may be more informative. Abstract: Anxiety involves complex, incompletely understood interactions of genomic, environmental, and experience-derived factors, and is currently being measured by psychological criteria. Here, we report previously nonperceived interrelationships between expression variations and nucleotide polymorphisms of the chromosome 7q21-22 acetylcholinesterase-paraoxonase 1 (ACHE-PON1) locus with the trait- and state-anxiety measures of 461 healthy subjects from the Health, Risk Factors, Exercise Training, and Genetics Family Study. The AChE protein controls the termination of the stress-enhanced acetylcholine signaling, whereas the PON protein displays peroxidase-like activity, thus protecting blood proteins from oxidative stress damages. Serum AChE and PON enzyme activities were both found to be affected by demographic parameters, and showed inverse, reciprocal associations with anxiety measures. Moreover, the transient scores of state anxiety and the susceptibility score of trait anxiety both appeared to be linked to enzyme activities. This finding supported the notion of corresponding gene expression relationships. Parallel polymorphisms in the ACHE and PON1 genes displayed apparent associations with both trait- and state-anxiety scores. Our findings indicate that a significant source of anxiety feelings involves inherited and acquired parameters of acetylcholine regulation that can be readily quantified, which can help explaining part of the human variance for state and trait anxiety.

This article by Yasuko Onuma et al Univeristy of Tokyo shows how grossly different physical traits come about by small changes to sequence within key genes.

Pretty much what Onuma's team did was take the gene sequence that encodes a gene that bosses other genes around from a fly and stuck it in a frog. Now the frog has a compound eye with multiple lenses.

Of course, over evolutionary time you wouldn't need Onuma to do this, random mutagenesis could do it just fine. If there was an advantage to having compound eyes for frogs, then that frog would be populous and be easily found, along side their normal eyed ancestors (for a while at least).

The evidence of such missing link animals wouldn't show up on the fossil record - if you had a frog which could - at the change of a few base pairs in its DNA - form a compound eye, but the backup gene was working so they just had regular eyes, it's gross morphology would look like a regular frog when you dug it up.

For life to live and have kids, it has to work. You can have animals that have "half a circulatory system" (like flies which lack lungs but instead have an "open" circulatory system where blood mixes with air) but generally these look like fully fledged morphologyies because they work so well.

Exciting evolutionary events tend to happen at the molecular scale, and don't manifest until everything is ready.

Watch your children.

Um, NIH already has a well developed infrastructure for this: PubMed Central. The problem is that not many journals are contributing full text to it right now. NIH does provide the abstracts only for just about every medical journal article in existence, as well as lots of other stuff through Entrez .

I would like to point out that not only traditional publishers are challenged, but even the peer review process is under consideration, as there is no great evidence on its usefulness (BMJ 1999;318:44-45).However, it's still difficult to find something to substitute it...

Furthermore, Brown's attempts are not so new. PubMedCentral has been created for putting scientific papers (of traditional publishers) on the web for free, but it also includes a number of autonomous publications, which are free for readers; unfortunately, they are not free for authors, as administrative expenses (which exist for web-based journals too) are covered by a submission fee. Anyway, every research project includes publication costs, so this is a way for using them.

Enzo

In the medical field there is at least one great attempt of freeing the access to scientific literature: PubMedCentral, from the US government, aimed at hosting papers from traditional scientific journals. However, not so many publishers accepted such proposal. One important publisher offering free access to its journals is instead BMJ (as you can see from the above citation), available on the Web with a full range of services, including fast responses. The latter are a good way for transforming a paper on the web to a catalyst of discussion, as people may answer through the web avoiding the long times needed for a paper response.

"Informative", I hope...