Nobel Laureate: Earl W. Sutherland, Jr.

 

The Nobel Prize in Physiology or Medicine 1971.

"for his discoveries concerning the mechanisms of the action of hormones"

Earl W. Sutherland, Jr. (1915-1974) received the Nobel Prize in Physiology or Medicine for his work on the mechanism of action of hormones, particularly epinephrine. Sutherland was very much influenced by Carl Cori [Nobel Laureates: Carl Ferdinand Cori and Gerty Theresa Cori] who worked on the pathways of glycogen breakdown and glucose synthesis in mammalian liver cells. Sutherland is responsible for discovering how the hormone epinephrine regulates glycogen synthesis [Regulating Glycogen Metabolism]. Along the way, Sutherland discovered the second messenger cyclic AMP (cAMP), which was Monday's Molecule #39.

The presentation speech was delivered by Peter Reichard of the Karolinska Medico-Chirurgical Institute. Note the opening line that refers to Monod's famous quote"What is true of E. coli is also true of the elephant." It was 1971 and Chance and Necessity had just come out. For years scientists had thought that the action of hormones demonstrated that so-called "higher" organisms used higher-level processes to regulate metabolism. Hormones needed whole tissues and organs to show an effect. What Sutherland proved was that hormones work at the cellular and molecular level just like the molecules that regulated activity in bacteria.

Your Majesty, Your Royal Highnesses, Ladies and Gentlemen,

What applies to bacteria also applies to elephants. This free quotation after the French Nobel prize winner, Jacques Monod, illustrates with some exaggeration one important principle of biology: that of the identity of the fundamental life processes.

Yet one need not be a Nobel prize winner to know the difference between bacteria and an elephant. The latter is not only much larger. The decisive difference lies in the fact that bacteria are unicellular organisms and that all the functions of life are contained in a single cell. In higher organisms on the other hand, there occurs a division of labor between different types of highly specialized cells. Nevertheless, the elephant must function as an integrated unity. The cells in the different organs must be coordinated in such a way that they rapidly adapt to the changing requirements of the environment.

The hormones form part of such a coordinating system. Among other things, the difference between a bacterium and an elephant lies in the fact that the latter - as well as all of us here - for the sustainment of his life is completely dependent of the proper function of hormones, while bacteria can do without them.

What then is the function of hormones? Ever since the first hormone was discovered about 70 years ago this has been a central theme of research for many scientists. This question is also of considerable medical importance. Many diseases are hormone diseases, amongst them diabetes. In spite of this the mechanism of hormone action remained a complete mystery until recently. The answer did not come until Earl Sutherland started his investigations on the function of the hormone epinephrine.

This hormone is produced in the adrenal glands and is transported to different organs of the body by the blood. It is formed in increased amounts during stress and adapts the individual to new situations. One of its important functions lies in the liberation of glucose inside the cells for the production of energy. Epinephrine serves as a chemical signal, as a messenger, which is sent out from the adrenals to activate different organs essential for the defense of the individual.

Sutherland investigated the effect of epinephrine on the formation of glucose in liver and muscle cells. He discovered a new chemical substance which serves as an intermediate during the function of the hormone. This substance is called cyclic AMP. It transmits the signal from epinephrine to the machinery of the cell, and Sutherland therefore called it a "second messenger". Furthermore, Sutherland made the important discovery that cyclic AMP is formed in the cell membrane. This means that epinephrine never enters the cell. We may visualize the hormone as a messenger which arrives at the door of the house and there rings the bell. The messenger is not allowed to enter the house. Instead the message is given to a servant, cyclic AMP, which then carries it to the interior of the house.

Sutherland suggested already around 1960 that cyclic AMP participates as a second messenger in many hormone mediated reactions, and that its effect thus is not limited to the action of epinephrine. First this generalization was not willingly accepted by the scientific community, since it was difficult to visualize how a single chemical substance could give rise to all the diverse effects mediated by various hormones. By now Sutherland and many other scientists have provided convincing evidence, however, that many hormones exert their effects by giving rise to the formation of cyclic AMP in the cell membrane. Sutherland had discovered a new biological principle, a general mechanism for the action of many hormones.

How can one then explain the specificity of different hormones? A good part of the explanation lies in the fact that different cells in their membranes possess specific receptors for various hormones. The different messengers thus must find their way to the right door in order to deliver their messages.

Cyclic AMP was discovered in connection with investigations concerning the function of hormones. It came therefore as a big surprise when Sutherland in 1965 reported that cyclic AMP also occurred in bacteria which apparently had no use for hormones. It was soon found that cyclic AMP was produced by other unicellular organisms, too. In all these cases cyclic AMP was shown to have important regulatory functions which aid the cells in their adaptation to the environment. Maybe we can look upon cyclic AMP as the first primitive hormone, regulating the behaviour of unicellular organisms. We then may look upon the true hormones of higher organisms as components of an overriding principle which was added during the course of evolution. Thus the difference between uni- and multicellular organisms does not, after all, appear to be so great, and with respect to cyclic AMP we can turn around Monod's dictum and say that what applies to elephants also applies to bacteria.

Dr. Sutherland,

Hormones were known in biology and medicine for a long time. The mechanism for hormone action remained a mystery, however, until you discovered cyclic AMP and its function as a second messenger. In recent years it has become apparent that cyclic AMP also serves as an important regulatory signal in microorganisms, and that its action thus is not limited to the function of hormones. When you discovered cyclic AMP you discovered one of the fundamental principles involved in the regulation of essentially all life processes. For this you have been awarded this year's Nobel prize in physiology or medicine. On behalf of the Karolinska Institute I wish to convey to you our warmest congratulations, and I now ask you to receive the prize from the hands of his Majesty the King.

Google Sky

 
If you haven't updated your copy of Google Earth then you should do so right now. A new feature called "Sky" has been added [Celestial add-on points Google Earth at the stars.

The image on the right shows us what the sky will look like tomorrow night when Mercury, Saturn, and Venus are close together in Leo. Saturn is going to be very close to Regulus. Unfortunately, the program won't tell me if I can see this from where I live. I don't know if this feature is missing or if I just can't find it.

You can click on the galaxy icons to get more information and you can click on each star to find out it's name, distance, spectral type etc.

Pretty cool. I wonder if Phil Plait of Bad Astronomy will comment? I'd like to know what he thinks of the program.

Identity of the Product of Mendel's Green Cotyledon Gene

 
This posting has been replaced by Identity of the Product of Mendel's Green Cotyledon Gene (Update).


Another of Mendel's seven genes has been identified. This one is described in his 1865 paper Experiments in Plant Hybridization [MendelWeb] as character number 2.

2. To the difference in the color of the seed albumen (endosperm). The albumen of the ripe seeds is either pale yellow, bright yellow and orange colored, or it possesses a more or less intense green tint. This difference of color is easily seen in the seeds as their coats are transparent.

Mendel's reference to the color of albumin, or endosperm, is inaccurate. He was actually observing the color of the cotyledons—the "seed leaves" that surround the embryo in the pea seed. These tiny leaves are covered by a seed coat that is partially transparent.

In wild-type peas the seeds turn yellow as they mature (i) but certain mutants exhibit a "stay-green" phenotype where the peas retain their green color (I). The figure shows seeds from a plant with the II genotype (top) and the ii genotype (bottom). The seed coat has been removed from the lower pair of each group of four peas.

In a paper just published in the Proceedings of the National Academy of Sciences (USA) a group in Japan has identified the "stay green" gene that Mendel worked with (Sato et al., 2007). It turns out that the gene, called SGR (stay-green), encodes an enzyme that is localized to chloroplasts and plays a role in the degradation of chlorophyll during senescence and maturation of seeds. When the enzyme is defective chlorophyll isn't broken down and the tissue stays green.

This brings to three the number of Mendel's genes that have a known function. The wrinkled pea phenotype is caused by a defect in the gene for starch branching enzyme (Bhattacharya et al., 1990) [Biochemist Gregor Mendel Studied Starch Synthesis]. The tall/short phenotypes are caused by defects in the gene for gibberellin 3β-hydroxylase (Martin et al., 1997). Gibberellins are plant growth hormones.

---

[Photo Credit: The photograph of mutant and wild-type pea seeds is taken from Figure 1 of Sato et al. (2007)]

Bhattacharyya, M. K., Smith, A. M., Ellis, T. H., Hedley, C., and Martin, C. (1990) The wrinkled-seed character of a pea described by Mendel is caused by a transposon-like insertion in a gene encoding starch-branching enzyme. Cell 60:115-122.

Martin D.N., Proebsting W.M., Hedden P. (1997) Mendel's dwarfing gene: cDNAs from the Le alleles and function of the expressed proteins. Proc. Natl. Acad. Sci. (USA) 94:8907–8911.

Sato Y., Morita R., Nishimura M., Yamaguchi H., and Kusaba M. (2007) Mendel’s green cotyledon gene encodes a positive regulator of the chlorophyll-degrading pathway. Proc. Natl. Acad. Sci. (USA) (early publication, [August 20, 2007]).

Monday's Molecule #39

 
Today's molecule is complex but it has a very simple common name. The common name is not sufficient—you must supply the formal IUPAC name to win the prize. There's a direct connection between this Monday's Molecule and Wednesday's Nobel Laureate.

The reward (free lunch) goes to the person who correctly identifies the molecule and the Nobel Laureate(s). Previous free lunch winners are ineligible for one month from the time they first collected the prize. There's only one (Marc) ineligible candidate for this Wednesday's reward since many recent winners haven't collected their prize. The prize is a free lunch at the Faculty Club.

In preparation for the beginning of classes in three weeks I'm going to start requesting email responses. Send your guess to Sandwalk (sandwalk(at)bioinfo.med.utoronto.ca) and I'll pick the first email message that correctly identifies the molecule and the Nobel Laureate. All responses will be posted tomorrow along with the time that their message was received on my server. This way I may select multiple winners if several people get it right.

Comments will be blocked for 24 hours. Comments are now open.

Like a Broken Record ...

 
Matt Nisbet is at it again. His particular spin frame on the rationalism vs. superstition debate is that the rationalists are making too much noise. According to Nisbet, we atheists are hurting the "cause" (what cause?) by speaking out loudly against superstition in the form of religion. Apparently it would be better to tone down the rhetoric in order to avoid offending those who believe in superstition. This is the strategy that has been followed by Americans for the last 100 years or so. No matter how stupid the religious extremists are, whether from the pulpit or on talk radio, we mustn't say that they are stupid because that would hurt their feelings. Or rather, it would hurt the feelings of the moderate believers who tolerate and support the religious extremists.

Of course Matt doesn't recognize that this is just his personal opinion. Oh no, that wouldn't be right, would it? If you are going to attack Dawkins, Hitchins, and Harris then you'd better frame it make it sound like an attack based on solid scientific reasoning. Here's what Matt Nisbet says in his latest posting [Why the New Atheist Noise Machine Fails].

Everything we know from social science research on attitude formation and beliefs predicts that the communication strategy of the New Atheist noise machine will only further alienate moderately religious Americans, the very same publics who might otherwise agree with secularists on many social issues.

Everything we know from history predicts that social change is often stimulated and led by vocal "extremists" who dare to speak out even if it offends those who prefer the status quo. This was true of the women's movement, the civil rights movement, and the gay rights movement. In those cases it was the moderate male chauvinists, the moderate racists, and the moderate homophobes who were initially offended. They didn't like being told that their long-held beliefs were wrong. In all those cases I suspect there were Matt Nisbets who tried to silence the outspoken leaders because they were offending the average moderate citizen.

If social science "research" says that the cause of outspoken individuals always fails then that says a lot more about the so-called "research" of social scientists than it does about reality.

The Dawkins/Hitchens PR campaign provides emotional sustenance and talking points for many atheists, but when it comes to selling the public on either non-belief or science, the campaign is likely to boomerang in disastrous ways.

The experiment is under way. Up until 2005, atheism was pretty much hidden under a bushel and religious superstition was rarely confronted in public. The result is that America is the most religious country in the industrialized world and evolution isn't taught in schools. Let's see if there's any change in the status quo over the next decade as the Dawkins/Hitchens framing PR campaign continues. According the Nisbet, the country will become even more religious because of the backlash. I'm betting that religion will become less important to Americans when they realize that there are other options.

There are times when I wonder which side Nisbet is on. It sounds to me like he's perfectly happy with the way things have been for the past several decades.

Don't Mess with Canadians

 
I recently returned from spending a week in a foreign country. I did not behave like the Canadian in this video although there were times ...



[Hat Tip: Canadian Cynic]

The Cause of Variation in a Population

John Dennehy of The Evilutionary Biologist has posted a wonderful article on This Week's Citation Classic. The classics are two back-to-back papers on genetic variation in fruit flies (Hubby and Lewontin (1966), Lewontin and Hubby (1966)). That's Lewontin on the left.

Please get on over to The Evilutionary Biologist and read what John has to say. These were very important and groundbreaking papers when they came out and everyone needs to know why.

Here's some background.

In the olden days there were two competing theories to explain variation (heterozygosity) in a population. The classical theory said that mutations are constantly being removed from the population by positive natural selection or purifying selection. Variation is a transient phenomenon that would disappear entirely if it weren’t for new mutations that arise at a significant rate.

The balance theory maintains that variation in a population is often due to balancing selection. The best known example of balancing selection is the allele for sickle cell disease. In the heterozygous state it confers resistance to malaria but in the homozygous state it is often lethal. Both the sickle cell allele and the wild type allele are maintained in the human population by balancing selection.

Hubby and Lewontin (1966) discovered that there was a huge amount of genetic variation in fruit flies. Their data suggested that 50% of all loci had multiple alleles. This is difficult to reconcile with the balance theory and it was also a big surprise to those who supported the classic theory. It seemed unlikely that at any given point in the evolutionary history of a species that so many genes could be undergoing selection. Further work confirmed that other species contained a huge amount of variation.

The solution to this surprising observation was the recognition that most of the alleles were neutral. The variation is explained by fact that fixation by random genetic drift is much slower than fixation by natural selection. Thus, while the variation is transient in the sense that it is a snapshot of an ongoing process, the process is not selection but drift.

The results of Hubby and Lewontin (1966) led directly to Neutral Theory.

The neutral theory also asserts that most intraspecific variability at the molecular level (including DNA and protein polymorphisms) is selectively neutral, and is maintained in the species by the balance between mutational input and random extinction. In other words, the neutral theory regards protein and DNA polymorphisms as a transient phase of molecular evolution and rejects the notion that the majority of such polymorphisms are adaptive and actively maintained in the species by some form of balancing selection.
                M. Kimura

This explanation is also known as the Neoclassical Theory. Balancing selection is now thought to play only a minor and insignificant role in the cause of variation in a population.

... the neoclassical theory is not refuted by occasional observations of overdominance for fitness, because the theory does not deny that cases exist but only that they are common and explain a significant proportion of natural variation. So it is no use trotting out that tired old Bucephalus, sickle-cell anemia, as a proof that single-locus heterosis can exist. Anyone who has taught genetics for a number of years is tired of sickle-cell anemia and embarrassed by the fact that it is the only authenticated case of overdominace available. “If balancing selection is so common," the neoclassicists say, "why do you always end up talking about sickle-cell anemia?"
                R. Lewontin

---

[Photo credit: The photograph of Richard Lewontin is from (Photographs of Participants in the Molecular Evolution Workshop)]

Where's the Evidence for Intelligent Design Creationism?

 
Denyse O'Leary has friend named David Warren. Warren writes articles for newspapers and he and Denyse are friends because they both worship at the church of anti-Darwinism. Over on Post-Darwinist Denyse brags about the latest article written by her friend [ Another Toronto journalist takes swat at Darwinists (or Darwinoids)]. Note the title of the blog article. It's more of the same old, same old, "Darwinist" baiting. Turns out that 99.9% of the IDiot movement is about attacking evolution (their version) and 0.1% is about presenting evidence for intelligent design. (And even that tiny amount of evidence has been refuted or shown to be irrelevant.)

So what about David Warren? Is he any different—don't hold your breath. Here's the article that he wrote for some Canadian newspapers [Panspermianism]. The main point of the article is supposed to be that panspermia is ruled out because scientists have shown that DNA won't survive in outer space (*yawn*). But the real purpose of the article is to whine about the evil atheist materialists and how they are suppressing the IDiots.

Much of the “star chamber” atmosphere, that has accompanied the public invigilation of microbiologists such as Michael J. Behe, and other very qualified scientists working on questions of design in organisms and natural systems, can only be explained in this way. The establishment wants such research to be stopped, because it challenges the received religious order, of atheist materialism. Any attempt, or suspected attempt, to acknowledge God in scientific proceedings, must be exposed and punished to the limit of the law; or by other ruthless means where the law does not suffice.

There's more, but you get the idea. The IDiot movement is scientifically bankrupt. They have no scientific evidence to back them up so the only thing they can do is lash out at their opponents. When is the last time you've seen an article from an IDiot that explains any evidence for the existence of an Intelligent Designer? That's right, hardly ever. Is there a reason why they don't support their case with real data? Yep, you bet there is. And that's exactly why they have to stoop to attacking "Darwinism" at every chance they get. They don't have any other option. Pathetic, isn't it?

[Image credit: The photograph is from one of my students, Zarna. That's her in the picture. She took it last December in India (Oh My God)]

Should Cloning Humans Be Legal?

 
In the July 21 issue of New Scientist, Hugh McLachlan thinks that we should legalize cloning of humans [Let's legalise cloning].

But why are we so against the idea of cloned human babies? As a bioethicist specialising in reproductive issues, I believe it has more to do with an irrational fear of cloning than any logical reason. All the arguments in favour of a ban describe risks that we accept quite easily and naturally in other areas of reproduction.

One argument against human cloning is the idea that it is morally wrong or undesirable to create replicas of people. But although a clone has the same gene set as the adult from which it was cloned, environmental factors will ensure that the resulting individual is not an identical copy, either psychologically or physically. What's more, we accept genetically identical people in the form of twins. If anything, clones would be less alike than twins because they would be different ages and be brought up in different contexts. Objecting to cloning on these grounds makes no sense.

I agree with McLachlan. Aside from the safety issue, there doesn't seem to be any good reason to forbid the cloning of humans.

This is a topic that's frequently discussed in "ethics" classes. I've never really understood what "ethics" actually means—but I'm working on it. The cloning of humans isn't an ethical issue for me personally because there isn't a conflict between two versions of what I think I ought to do. However, maybe it's an ethical issue for society as a whole because there are some people who think that it is unethical to clone people. Is that right? What's unethical about it?

Do we define "ethical" issues in terms of conflict between different groups? If so, is there a way of distinguishing between issues where the two sides are almost equally represented and those where one side has an overwhelming majority? For example, is the cloning of humans still an ethical issue in a society where 99% of the population is opposed? Does it cease to be an ethical issue if 99% are persuaded to accept human cloning?

Amazing Grace

 
Last night we saw a screening of the film Amazing Grace in a small cozy theater. At the end of the movie there was a fascinating talk by one of the producers Ken Wales. We learned a lot about how the film was made.

The film follows the efforts of William Wilberforce to abolish slavery in the British Empire at the end of the eighteenth century. Wilberforce and his close friend William Pitt the Younger, who became Prime Minister in 1783, finally succeeded in eliminating slavery by 1807.

There's mention of the fact that Wilberforce was a Christian and some of his allies were preachers but this isn't an important theme. The movie makes it clear that Pitt, who was a prime mover in social change, did not share Wilberforce's beliefs. During the discussion afterward it was clear that the religious motivation was important to some people.

The title of the movie comes from the song Amazing Grace whose words were composed by John Newton, an ex-slave trader who converted to Christianity. Newton, who has a significant part in the movie, influenced Wilberforce and served as his mentor.

One interesting scene depicts a debate in the House of Commons in 1778. The newly elected Wilberforce is advocating the withdrawal of British forces from America, thus abandoning the attempt to put down the rebellion. Wilberforce is attacked and challenged to distinguish between appeasement and surrender. "It's merely a question of timing," he says.

This scene, and many others, reveal that Great Britain was a functioning democracy at the time of the American Revolution. It contrasts markedly with the general impression of Americans who tend to think that this sort of representative democracy was invented by them in 1776.

William Wilberforce's third son was Samuel Wilberforce ("Soapy Sam") who became the Bishop of Oxford and debated evolution with Thomas Huxley in 1860.

Tangled Bank #86

 

The 86th issue of the Tangled Bank has been posted on Fish Feet [Tangled Bank #86].

Peter Lawrence on What's Wrong with Science

 
Peter Lawrence is a Professor at the University of Cambridge in Cambridge, UK. He has worked on various aspects of fruit fly development for almost 40 years. Readers may know him as one of the authors of Wolpert's Principles of Development or as the author of The Making of a Fly.

Peter is a very smart guy. He thinks a lot about the "big picture" and not just the minutiae of day-to-day work in a competitive environment. That's why his article in this month's issue of Current Biology is worth reading. Lawrence writes about what's wrong with modern science [The Mismeasure of Science].

For most scientists, there won't be any revelations in the article but it's put together well and covers all the bases. The main point is that today's scientists have to worry far too much about "productivity" in order to get funded. The system is geared towards artificial measurements of research success that may, or may not, reward creativity and innovation.

Modern science, particularly biomedicine, is being damaged by attempts to measure the quantity and quality of research. Scientists are ranked according to these measures, a ranking that impacts on funding of grants, competition for posts and promotion. The measures seemed, at first rather harmless, but, like cuckoos in a nest, they have grown into monsters that threaten science itself. Already, they have produced an “audit society” [2] in which scientists aim, and indeed are forced, to put meeting the measures above trying to understand nature and disease.

The journals are evaluated according to impact factors, and scientists and departments assessed according to the impact factors of the journals they publish in. Consequently, over the last twenty years a scientist's primary aim has been downgraded from doing science to producing papers and contriving to get them into the “best” journals they can [3]. Now there is a new trend: the idea is to rank scientists by the numbers of citations their papers receive. Consequently, I predict that citation-fishing and citation-bartering will become major pursuits.

You need to read the full article to get all the details.

So, what can we do about it? It's an old complaint, one that's been openly discussed even since I first met Peter Lawrence back in the mid-1970's. If a bunch of (relatively) smart scientists can't figure out how to fix the problem then maybe it's unfixable.

Here's where I think Lawrence drops the ball. He proposes the same tired old "remedies" that we've never adopted in the past in spite of the fact that we all pay lip service to their benefits. He wants us all to pay attention to "quality" and "originality" over quantity. He wants us to be more careful about putting authors names on a paper. He wants a code of ethics for scientists. He wants to reform the peer review process in the leading journals. None of this is going to happen as long as money is tight and the granting agencies have to come up with defensible policies for turning down 75% of grant applications.

The short term solution is to put more money into the grant system and to stop hiring more scientists. The long term solution is to look for better ways of funding. I like the idea of giving large block grants to departments and letting the researchers divide it up as they see fit. This would have worked well in any department I've been in but I hear horror stories about other departments.

---

[Photo Credit: The photograph of Peter Lawrence is from his website at the University of Cambridge (Peter A. Lawrence]

Lawrence, P.A. (2007) The mismeasurement of science. Current Biology 17:R583-R585.

Half-Truths in Sicko?

 
Jim Giles reviewed Michael Moore's Sicko in the July 14th issue of New Scientist [Review: Sicko, directed by Michael Moore]. Like many reviews, this one conceded that Moore has a point about the shape of health care in the USA but was reluctant to admit that other countries are doing better. One paragraph mentioned "half-truths."

For the most part, Moore makes his case by absenting himself from the screen and allowing those who have been let down by the system to do the talking. Then he travels to the UK and France and finds that what conservatives in the US damn as "socialised medicine" actually works well. He does the same in Cuba, ferrying ill Americans to the island where they receive excellent healthcare at almost no cost. The result is a moving, funny and shocking film. It is a powerful call for change, despite its half-truths.

In last week's issue of New Scientist, a letter writer challenged Giles to produce his "half-truths," pointing out that the Sicko website documents every claim in the movie.

Here's how Jim Giles responded ...

The most obvious half-truths were the slanted depictions of the healthcare systems in the UK, France, and Cuba. The British NHS can be great, but waiting lists are often long and access to certain drugs can depend on where a patient lives. France's system is indeed highly rated, but Moore did not mention the very high taxes there. Cuba's public health is far above what would be expected for a country with limited resources and suffering the consequences of the US trade embargo, but it also restricts access to certain drugs and technologies.

Some of these sound very much like half-truths to me. Yes, waiting lists for non-lifethreatening procedures are often longer in countries with socialized medicine. That is, they are longer than the wait for similar procedures in a fully private system where people can afford to pay for it. On the other hand, the waiting time in the UK is a lot shorter than it is for Americans who can't afford decent health insurance, isn't it?

Access to certain drugs is restricted in all socialized medicine systems. For example, the system won't pay for drugs that don't work and haven't been approved. This is bad news for quacks who generally do much better under a private system. Socialized medicine often won't pay for expensive drugs if a cheaper alternative is available. Is this what Giles meant?

It's true that taxes are higher in countries that provide universal access to medical treatments. This isn't a half-truth in Sicko. As I recall, it's one of the main points. The US system is more expensive in spite of the fact that it's run by the private sector.

Gene Genie #13

 




Gene Genie #13 has been posted on The Genetic Geneologist [Gene Genie #13: Into the Future].

The Hominid Bush

 
Brian Switek of Laelaps has posted a wonderful essay on Homo sapiens: The Evolution of What We Think About Who We Are. Read it.

In a just world, the IDiots like Jonathan Wells would read what Brian, and others, have to say and stop spreading lies about what scientists think.

[Photo Credit: The photograph of Hamlet is from The Young Shakespeare Workshop]