ScienceBlogs Select

Dark Energy: Where did the Light go? (Part 3) [Starts With A Bang]

Ethan Siegel none@example.com — Wed, 11 Nov 2009 21:25:25 -0500

Though the Sun is gone, I have a light. -Kurt Cobain

Last time we visited dark energy, we discussed its initial discovery. This came about from the fact that supernovae observed with a certain redshift (i.e., moving away from us) appear to be systematically fainter than we were able to explain.

But we weren't satisfied with simply saying that there must be dark energy. We asked a lot of critical questions about why these supernovae might appear so faint.

First off, we asked the question, "Could these supernovae from far away be different than the type Ia supernovae we have today?"

Unfortunately, the answer is a resounding no. So long as atoms work exactly the same way, they require the same pressure to collapse at all points, times, and places in the Universe. The process of forming a Type Ia Supernova -- having a white dwarf accrete mass until the core collapses and it explodes -- should be independent of location and time.

Well, if the supernovae are constant, could the environments that they form in be different than the environments today? Of course they could. So, is there any way to make them appear fainter without them actually being fainter, and without having to resort to dark energy? Sure, you might say, block some of that light! All you need is some dust, like so.

What a simple idea, right? Problem solved?

Not so fast. Dust, in real life, is made up of real particles (atoms, molecules, grains, etc.), with real sizes. This means they affect light differently at different wavelengths. Not just red, green, and blue, but X-rays, ultraviolet, infrared, and more. We don't see this light dimmed more in one spectral band than any other; it's dimmed equally at all wavelengths!

So, real dust is out. But what if we invented some new type of dust that absorbed light the same at all wavelengths? We can give it a name: grey dust. We have no idea what would cause it, but it's a lot more believable that there's some new kind of dust out there than there is a whole new type of energy pervading the Universe.

Well, if this grey dust were there, then the light from distant supernovae would simply continue to appear dimmer and dimmer the farther away they were. Whereas, if the Universe had dark energy, the supernovae should start to appear relatively brighter beyond a certain distance. Take a look at the graph below to compare some different theories with the data.

As you can see, grey dust (the top line) is as inconsistent as a Universe with only normal matter (bottom line) when compared to the data.

So you can't simply blame it on a trick of the light. In fact, if we look at the most modern supernova data, it clearly favors dark energy significantly over even a flat, low-density Universe.

Other "light-blocking" schemes, such as photon-axion oscillations, suffer from the same problem; they don't give the right turn-over as shown above. If we've got the right laws of gravity, there's pretty much no way around dark energy.

But we don't like relying on only one source of data. Supernovae are nice, but what happens when we look at all the other evidence? Does that tell us there must be dark energy too, or could it be that the supernova data just cannot be trusted? Seems like a job for part 4, and so I'll see you then!

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Guess the Dow, Win Chow! [The Quantum Pontiff]

Dave Bacon none@example.com — Wed, 11 Nov 2009 20:05:01 -0500

Last month a local restaurant group, Chow foods---among whose restaurants is one of our favorite Sunday breakfast spots, The Five Spot---ran a contest/charity event: "Chow Dow." The game: guess the value of the Dow Jones Industrial Average at the close of the market on October 29th, 2009. The closest bet under the closing value which did not go over the value would be the winner. The prize was the value of Dow in gift certificates to the Chow restaurants: i.e. approximately $10K in food (or as we would say in Ruddock House at Caltech: "Eerf Doof!" We said that because it fit nicely with another favorite expression, "Eerf Lohocla!", this later phrase originating in certain now obscure rules enforced by administrative teetotalers.) I love games like this, and I especially love games where the rules are set up in an odd way. Indeed what I found amusing about this game was that, as a quick check of the rules on the Chow website showed, you could enter your guesses at anytime up until October 28th. Relevant also: maximum of 21 bets per person with a suggested donation of $1 per guess. So what would your strategy be optimizing your probability of winning, assuming that you are going to enter 21 times?

Below the fold: my strategy, the amazing power of the X-22 computer, and....chaos!

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Two Articles on Predictions & Hype in Science [Framing Science]

Matthew C. Nisbet none@example.com — Wed, 11 Nov 2009 19:28:34 -0500

Earlier this year, in an article at Nature Biotechnology, I joined with several colleagues in warning that the biggest risk to public trust in science is not the usual culprits of religious fundamentalism or "politicization" but rather the increasing tendency towards the stretching of scientific claims and predictions by scientists, university press offices, scientific journals, industry, and journalists. As I detail with Dietram Scheufele in a separate article at the America Journal of Botany,(PDF) each time a scientific prediction or claim goes beyond the available evidence and proves to be false, it serves as a vivid negative heuristic for the public.

This past week, two important articles describing the perils of prediction in the life sciences and climate sciences appeared at The Scientist magazine and Nature Reports Climate Change respectively. In a cover article for the The Scientist, Stuart Blackman identifies several factors driving the tendency towards hype. As Blackman notes, scientists are under increasing pressure to publish at ever more competitive flagship journals, meaning that the conclusions of a paper have to be that much more provocative. Granting agencies are also putting stronger emphasis on the public impacts portion of funding proposals, again creating an incentive to sometimes promise too much. A third and major factor is the increasing privatization of university-based science with strong incentives and rewards for commercialization, a route that usually involves a heavy dose of promotion. In his article, Blackman draws on the insights of some of the top social scientists studying these trends including Brian Wynne, Christine Hauskeller, and Daniel Sarewitz. A useful sidebar summarizes advice on how researchers can avoid hype in communicating with the public, policymakers, and/or the media.

In a commentary at Nature Reports Climate Change, Mike Hulme, Roger Pielke, Jr and Suraje Dessai warn against promising that climate science can "supply on-demand climate predictions to governments, businesses and individuals," estimating impacts on certain regions and sectors.

"Scientists and decision-makers alike should treat climate models not as truth machines to be relied upon for making adaptation decisions, but instead as one of a range of tools to explore future possibilities," they write. And as they aptly observe, it's not just a matter of technical certainty. Even in cases where forecasts might be accurate in a formal statistical sense, effectively communicating the complexity of these findings to the public and decision-makers will prove a difficult task. Here's the key take away from their commentary:

For scientists, the lesson here is clear. Caution is warranted when promising decision-makers a clarified view of the future. Guaranteeing precision and accuracy over and above what science can credibly deliver risks contributing to flawed decisions. We are not suggesting that scientists abandon efforts to model the behaviour of the climate system. Far from it. Models as exploratory tools can help identify physically implausible outcomes and illuminate the boundaries where uncertain knowledge meets fundamental ignorance. But using models in this way will require a significant rethink on the role of predictive climate science in decision-making. In some cases the prudent course of action will be to let policymakers know the very real limitations of predictive science. For decision-makers, the lesson is to plan for a range of possible alternatives. Instead of seeking certainty, decision-makers need to ask questions of scientists such as 'What physically could not happen?' or 'What is the worst that could happen?'

The authors' warning is important to the U.S. context. Perhaps the most effective way to convey the significance of climate change is to communicate to Americans how it is impacting the region or area in which they live. Yet as effective as this strategy might be, these communication efforts need to proceed cautiously, otherwise they risk opening the door to counter-claims that scientists and government agencies are going beyond available scientific evidence.

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23andMe gets scooped on hair curl genes [Genetic Future]

Daniel MacArthur none@example.com — Wed, 11 Nov 2009 19:15:00 -0500

Medland et al. (2009). Common Variants in the Trichohyalin Gene Are Associated with Straight Hair in Europeans. The American Journal of Human Genetics DOI: 10.1016/j.ajhg.2009.10.009

A couple of weeks ago I reported on a presentation by 23andMe's Nick Eriksson at the American Society of Human Genetics meeting in Honolulu, in which Eriksson presented data on a series of genome-wide association studies performed by the company using genetic and trait data from its customers.

Along with genetic analysis of a variety of other traits (such as asparagus anosmia and photic sneeze) Eriksson presented data on two novel regions significantly associated with hair curl, one close to the TCHH gene and a second near WNT10A (see the abstract for details). I noted at the time that 23andMe appears to be doing a pretty good job of running genome-wide association studies, although of course the real test of this is independent replication.

Well, now we have replication (of a sort) for at least two of 23andMe's novel findings - but unfortunately for the 23andMe crew the "replication" study has beaten them into print.

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Levels of selection & the full Price Equation [Gene Expression]

Razib Khan none@example.com — Wed, 11 Nov 2009 16:34:31 -0500

In the post below on the Price Equation I stayed true to George Price's original notation in his 1970 paper where he introduced his formalism. But here is a more conventional form, the "Full Price Equation," which introduces a second element on the right-side.

Δz = Cov(w, z) / w

One can specifically reformulate this verbally for a biological context:

Change in trait = Change due to selection on individuals + Change due to individual transmission

The first element on the right-side is explicable as selection upon a heritable trait. w is the conventional letter used for "fitness," so w is population mean fitness, and serves to normalize the relation. "z" is the trait. The term "individual" can mean any set of entities. The straightforward plain interpretation may be that "individual" means a bounded physical entity, so that the covariance is measuring selection across individuals within a population conditional upon a correlation between trait value and fitness.

What then is the second element? The "E" represents expectation, just as "Cov" represents covariance. Purely abstract statistical concepts which can be drafted to various ends. In the frame I presented above, it is transmission bias from the individual to their offspring. In a deterministic system without stochasticity this is often just 0, so it is omitted from original Price Equation, but, it can be understood genetically as meiotric drive, mutation, random drift or biases introduced through Mendelian segregation. In other words, the covariance is measuring the change across the whole population due to processes which apply on the level of the population, while the expectation is simply tracking parent-offspring dynamics independent of that covariance.

But "individuals" need not be conceived of as physical individuals. One could imagine individuals being cells within a multicellular organism. The application of this in terms of the spread of cancers is obvious. Or, one could move "up a level," and conceive of the individuals as a collection of individuals, groups. Then, the second element, the expectation, could be transmission bias within the groups. So the verbal form of the equation would be:

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Google's New Language: Go [Good Math, Bad Math]

Mark C. Chu-Carroll none@example.com — Wed, 11 Nov 2009 16:08:33 -0500

I've been being peppered with questions about Go, the new programming language just released as open-source by Google. Yes, I know about it. And yes, I've used it. And yes, I've got some strong opinions about it.

Go is an interesting language. I think that there are many fantastic things about it. I also think that there are some really dreadful things about it.

A warning before I go on: this post is definitely a bit of a rush job. I wanted to get something out before my mailbox explodes :-). I'll probably try to do a couple of more polished posts about Go later. But this should give you a first taste.

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Revisiting FOXP2 and the origins of language [Not Exactly Rocket Science]

Ed Yong none@example.com — Wed, 11 Nov 2009 13:00:40 -0500

Today, a new paper published in Nature adds another chapter to the story of FOXP2, a gene with important roles in speech and language. The FOXP2 story is a fascinating tale that I covered in New Scientist last year. It's one of the pieces I'm proudest of so I'm reprinting it here with kind permission from Roger Highfield, and with edits incorporating new discoveries since the time of writing.

The FOXP2 Story (2009 edition)

Imagine an orchestra full of eager musicians which, thanks to an incompetent conductor, produces nothing more than an unrelieved cacophony. You're starting to appreciate the problem faced by a British family known as KE. About half of its members have severe difficulties with language. They have trouble with grammar, writing and comprehension, but above all they find it hard to coordinate the complex sequences of face and mouth movements necessary for fluid speech.

Thanks to a single genetic mutation, the conductor cannot conduct, and the result is linguistic chaos. In 2001, geneticists looking for the root of the problem tracked it down to a mutation in a gene they named FOXP2. Normally, FOXP2 coordinates the expression of other genes, but in affected members of the KE family, it was broken.

It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 "the language gene" or the "grammar gene". Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited - the discovery sparked a frenzy of research aiming to uncover the gene's role.

Several years on, and it is clear that talk of a "language gene" was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. "When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language," recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours. "It gives us a really important lesson," says Fisher. "Speech and language didn't just pop up out of nowhere. They're built on very highly conserved and evolutionarily ancient pathways."

Two amino acids, two hundred thousand years

The first team to compare FOXP2 in different species was led by Wolfgang Enard from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. In 2001, they looked at the protein that FOXP2 codes for, called FOXP2, and found that our version differs from those of chimpanzees, gorillas and rhesus macaques by two amino acids out of a total of 715, and from that of mice by three. This means that the human version of FOXP2 evolved recently and rapidly: only one amino acid changed in the 130 million years since the mouse lineage split from that of primates, but we have picked up two further differences since we diverged from chimps, and this seems to have happened only with the evolution of our own species at most 200,000 years ago.

The similarity between the human protein FOXP2 and that of other mammals puts it among the top 5 per cent of the most conserved of all our proteins. What's more, different human populations show virtually no variation in their FOXP2 gene sequences. Last year, Enard's colleague Svante Pääbo made the discovery that Neanderthals also had an identical gene, prompting questions over their linguistic abilities (see "Neanderthal echoes below).

"People sometimes think that the mutated FOXP2 in the KE family is a throwback to the chimpanzee version, but that's not the case," says Fisher. The KEs have the characteristically human form of the gene. Their mutation affects a part of the FOXP2 protein that interacts with DNA, which explains why it has trouble orchestrating the activity of other genes.

There must have been some evolutionary advantage associated with the human form of FOXP2, otherwise the two mutations would not have spread so quickly and comprehensively through the population. What this advantage was, and how it may have related to the rise of language, is more difficult to say. Nevertheless, clues are starting to emerge as we get a better picture of what FOXP2 does - not just in humans but in other animals too.

During development, the gene is expressed in the lungs, oesophagus and heart, but what interests language researchers is its role in the brain. Here there is remarkable similarity across species: from humans to finches to crocodiles, FOXP2 is active in the same regions. With no shortage of animal models to work with, several teams have chosen songbirds due to the similarities between their songs and human language: both build complex sequences from basic components such as syllables and riffs, and both forms of vocalisation are learned through imitation and practice during critical windows of development.

Babbling birds

All bird species have very similar versions of FOXP2. In the zebra finch, its protein is 98 per cent identical to ours, differing by just eight amino acids. It is particularly active in a part of the basal ganglia dubbed "area X", which is involved in song learning. Constance Scharff at the Max Planck Institute for Molecular Genetics in Berlin, Germany, reported that finches' levels of FOXP2 expression in area X are highest during early life, which is when most of their song learning takes place. In canaries, which learn songs throughout their lives, levels of the protein shoot up annually and peak during the late summer months, which happens to be when they remodel their songs.

So what would happen to a bird's songs if levels of the FOXP2 protein in its area X were to plummet during a crucial learning window? Scharff found out by injecting young finches with a tailored piece of RNA that inhibited the expression of the FOXP2 gene. The birds had difficulties in developing new tunes and their songs became garbled: they contained the same component "syllables" as the tunes of their tutors, but with syllables rearranged, left out, repeated incorrectly or sung at the wrong pitch.

The cacophony produced by these finches bears uncanny similarities to the distorted speech of the afflicted KE family members, making it tempting to pigeonhole FOXP2 as a vocal learning gene - influencing the ability to learn new communication sounds by imitating others. But that is no more accurate than calling it a "language gene". For a start, songbird FOXP2 has no characteristic differences to the gene in non-songbirds. What's more, among other species that show vocal learning, such as whales, dolphins and elephants, there are no characteristic patterns of mutation in their FOXP2 that they all share.

Instead, consensus is emerging that FOXP2 probably plays a more fundamental role in the brain. Its presence in the basal ganglia and cerebellums of different animals provides a clue as to what that role might be. Both regions help to produce precise sequences of muscle movements. Not only that, they are also able to integrate information coming in from the senses with motor commands sent from other parts of the brain. Such basic sensory-motor coordination would be vital for both birdsong and human speech. So could this be the key to understanding FOXP2?

Moving mice

New work by Fisher and his colleagues supports this idea. In 2008, his team engineered mice to carry the same FOXP2 mutation that affects the KE family, rendering the protein useless. Mice with two copies of the dysfunctional FOXP2 had shortened lives, characterised by motor disorders, growth problems and small cerebellums. Mice with one normal copy of FOXP2 and one faulty copy (as is the case in the affected members of the KE family) seemed outwardly healthy and capable of vocalisation, but had subtle defects.

For example, they found it difficult to acquire new motor skills such as learning to run faster on a tilted running wheel. An examination of their brains revealed the problem. The synapses connecting neurons within the cerebellum, and those in a part of the basal ganglia called the striatum in particular, were severely flawed. The signals that crossed these synapses failed to develop the long-term changes that are crucial for memory and learning. The opposite happened when the team engineered mice to produce a version of FOXP2 with the two characteristically human mutations. Their basal ganglia had neurons with longer outgrowths (dendrites) that were better able to strengthen or weaken the connections between them.

A battery of over 300 physical and mental tests showed that the altered mice were generally healthy. While they couldn't speak like their cartoon equals, their central nervous system developed in different ways, and they showed changes in parts of the brain where FOXP2 is usually expressed (switched on) in humans.

Their squeaks were also subtly transformed. When mouse babies are moved away from their nest, they make ultrasonic distress calls that are too high for us to hear, but that their mothers pick up loudly and clearly. The altered Foxp2 gene subtly changed the structure of these alarm calls. We won't know what this means until we get a better understanding of the similarities between mouse calls and human speech.

For now, the two groups of engineered mice tentatively support the idea that human-specific changes to FOXP2 affect aspects of speech, and strongly support the idea that they affect aspects of learning. "This shows, for the first time, that the [human-specific] amino-acid changes do indeed have functional effects, and that they are particularly relevant to the brain," explains Fisher. "FOXP2 may have some deeply conserved role in neural circuits involved in learning and producing complex patterns of movement." He suspects that mutant versions of FOXP2 disrupt these circuits and cause different problems in different species.

Pääbo agrees. "Language defects may be where problems with motor coordination show up most clearly in humans, since articulation is the most complex set of movements we make in our daily life," he says. These circuits could underpin the origins of human speech, creating a biological platform for the evolution of both vocal learning in animals and spoken language in humans.

Holy diversity, Batman

The link between FOXP2 and sensory-motor coordination is bolstered further by research in bats. Sequencing the gene in 13 species of bats, Shuyi Zhang and colleagues from the East China Normal University in Shanghai discovered that it shows incredible diversity. Why would bats have such variable forms of FOXP2 when it is normally so unwavering in other species?

Zhang suspects that the answer lies in echolocation. He notes that the different versions seem to correspond with different systems of sonar navigation used by the various bat species. Although other mammals that use echolocation, such as whales and dolphins, do not have special versions of FOXP2, he points out that since they emit their sonar through their foreheads, these navigation systems have fewer moving parts. Furthermore, they need far less sensory-motor coordination than flying bats, which vocalise their ultrasonic pulses and adjust their flight every few milliseconds, based on their interpretation of the echoes they receive.

These bats suggest that FOXP2 is no more specific to basic communication than it is to language, and findings from other species tell a similar tale. Nevertheless, the discovery that this is an ancient gene that has assumed a variety of roles does nothing to diminish the importance of its latest incarnation in humans.

Since its discovery, no other gene has been convincingly implicated in overt language disorders. FOXP2 remains our only solid lead into the genetics of language. "It's a molecular window into those kinds of pathways - but just one of a whole range of different genes that might be involved," says Fisher. "It's a starting point for us, but it's not the whole story." He has already used FOXP2 to hunt down other key players in language.

The executive's minions

FOXP2 is a transcription factor, which activates some genes while suppressing others. Identifying its targets, particularly in the human brain, is the next obvious step. Working with Daniel Geschwind at the University of California, Los Angeles, Fisher has been trying to do just that, and their preliminary results indicate just what a massive job lies ahead. On their first foray alone, the team looked at about 5000 different genes and found that FOXP2 potentially regulates hundreds of these.

Some of these target genes control brain development in embryos and its continuing function in adults. Some affect the structural pattern of the developing brain and the growth of neurons. Others are involved in chemical signalling and the long-term changes in neural connections that enable to learning and adaptive behaviour. Some of the targets are of particular interest, including 47 genes that are expressed differently in human and chimpanzee brains, and a slightly overlapping set of 14 targets that have evolved particularly rapidly in humans.

Most intriguingly, Fisher says, "we have evidence that some FOXP2 targets are also implicated in language impairment." Last year, Sonja Vernes in his group showed that FOXP2 switches off CNTNAP2, a gene involved in not one but two language disorders - specific language impairment (SLI) and autism. Both affect children, and both involve difficulties in picking up spoken language skills. The protein encoded by CNTNAP2 is deployed by nerve cells in the developing brain. It affects the connections between these cells and is particularly abundant in neural circuits that are involved in language.

Verne's discovery is a sign that the true promise of FOXP2's discovery is being fulfilled - the gene itself has been overly hyped, but its true worth lies in opening a door for more research into genes involved in language. It was the valuable clue that threw the case wide open. CNTNAP2 may be the first language disorder culprit revealed through FOXP2 and it's unlikely to be the last.

Most recently, Dan Geschwind compared the network of genes that are targeted by FOXP2 in both chimps and humans. He found that the two human-specific amino acids within this executive protein have radically altered the set of genetic minions that it controls.

The genes that are directed by human FOXP2 are a varied cast of players that influence the development of the head and face, parts of the brain involved in motor skills, the growth of cartilage and connective tissues, and the development of the nervous system. All those roles fit with the idea that our version of FOXP2 has been a lynchpin in evolving the neural circuits and physical structures that are important for speech and language.

The FOXP2 story is far from complete, and every new discovery raises fresh questions just as it answers old ones. Already, this gene has already taught us important lessons about evolution and our place in the natural world. It shows that our much vaunted linguistic skills are more the result of genetic redeployment than out-and-out innovation. It seems that a quest to understand how we stand apart from other animals is instead leading to a deeper appreciation of what unites us.

Box - Neanderthal echoes

The unique human version of the FOXP2 gives us a surprising link with one extinct species. Last year, Svante Pääbo's group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from the bones of two Neanderthals, one of the first instances of geneticists exploring ancient skeletons for specific genes. They found that Neanderthal FOXP2 carries the same two mutations as those carried by us - mutations accrued since our lineage split from chimps between 6 and 5 million years ago.

Pääbo admits that he "struggled" to interpret the finding: the Neanderthal DNA suggests that the modern human's version of FOXP2 arose much earlier than previously thought. Comparisons of gene sequences of modern humans with other living species had put the origins of human FOXP2 between 200,000 and 100,000 years ago, which matches archaeological estimates for the emergence of spoken language. However, Neanderthals split with humans around 400,000 years ago, so the discovery that they share our version of FOXP2 pushes the date of its emergence back at least that far.
"We believe there were two things that happened in the evolution of human FOXP2," says Pääbo. "The two amino acid changes - which happened before the Neanderthal-human split - and some other change which we don't know about that caused the selective sweep more recently." In other words, the characteristic mutations that we see in human FOXP2 may indeed be more ancient than expected, but the mutated gene only became widespread and uniform later in human history. While many have interpreted Pääbo's findings as evidence that Neanderthals could talk, he is more cautious. "There's no reason to assume that they weren't capable of spoken language, but there must be many other genes involved in speech that we yet don't know about in Neanderthals."

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AMA Advocates Change in Marijuana Classification [The Scientific Activist]

Nick Anthis none@example.com — Wed, 11 Nov 2009 12:37:28 -0500

Yesterday, the influential AMA (American Medical Association) announced that it would cease its opposition to the concept of medical marijuana and instead advocate for a change in federal classification of the drug. From the LA Times:

The American Medical Assn. on Tuesday urged the federal government to reconsider its classification of marijuana as a dangerous drug with no accepted medical use, a significant shift that puts the prestigious group behind calls for more research.

The nation's largest physicians organization, with about 250,000 member doctors, the AMA has maintained since 1997 that marijuana should remain a Schedule I controlled substance, the most restrictive category, which also includes heroin and LSD.

In changing its policy, the group said its goal was to clear the way to conduct clinical research, develop cannabis-based medicines and devise alternative ways to deliver the drug.

"Despite more than 30 years of clinical research, only a small number of randomized, controlled trials have been conducted on smoked cannabis," said Dr. Edward Langston, an AMA board member, noting that the limited number of studies was "insufficient to satisfy the current standards for a prescription drug product."

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Great Observatories View of the Milky Way Centre [Dynamics of Cats]

Wed, 11 Nov 2009 12:09:04 -0500

Awesome combined image from Hubble, Spitzer and Chandra, showing deep view of the centre of the Milky Way, in celebration of the International Year of Astronomy.

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The amazing disappearing asymmetric magnetic reversals [Highly Allochthonous]

Chris Rowan none@example.com — Wed, 11 Nov 2009 12:00:00 -0500

Interpreting the record of the Earth's magnetic field preserved in rocks - palaeomagnetism - is a complicated business, but at the heart of it is one very simple assumption: except when it is reversing, if you average over a few thousand years or so, the geomagnetic field resembles a dipole aligned with the Earth's geographic poles.

This relatively uncomplicated shape means that there is a very simple relationship between latitude and the magnetic inclination (the angle magnetic field lines make with the horizontal); it is zero at the equator, and gradually increases to 90 degrees at the poles. If you measure the direction of the fossil field direction carried by rocks at a particular site, a simple formula converts the inclination of this ancient magnetisation into the palaeolatitude of that particular chunk of crust at the time the rocks formed. Because the field is symmetric, a reversal changes the polarity, but not the shape, of the field; for example, an inclination value of 50 and -50 degrees both always correspond to a latitude of 30 degrees.

But what if our simple assumption is wrong, and the Earth's magnetic field has not always been a dipole? There are more complicated quadropole and octopole components in the present geomagnetic field, but they are fairly minor and, except during a magnetic reversal, seem to average out to zero over a few thousand years. But what if at some point in the geological past these components were not only a more significant part of the geomagnetic field, but also did not average to zero over geological time? This would produce an asymmetric long-term field geometry, as in the figure below, where 15% of the earth's magnetic field energy is in the quadropole component. For a point at mid-to low northern latitudes, rocks forming in a normal polarity field would have a shallow magnetic inclination, whilst rocks forming in a reversed polarity field would have a much steeper inclination. The warped field geometry means that there is no longer a one-to-one relationship between inclination and latitude, which makes working out the plate motions recorded by all of those ancient magnetic directions much more difficult.

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Swine Flu Strikes a Colleague: Afarensis Hospitalized [Living the Scientific Life (Scientist, Interrupted)]

"GrrlScientist" none@example.com — Wed, 11 Nov 2009 11:05:10 -0500

My friend and former ScienceBlogs colleague, Afarensis, is in the hospital with pneumonia, a complication of a probable case of "swine" flu; H1N1 Influenza. His youngest daughter posted a message to his blog yesterday, so let's all head over there to leave our best wishes for his speedy and uneventful recovery! I know from experience that it's all of you, your kind words and your funny comments, who can really make a difference!

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The doctorate is the new bachelor's? [DrugMonkey]

DrugMonkey none@example.com — Wed, 11 Nov 2009 10:29:38 -0500

Commenter qaz raised an issue the I think I last took up following an observation of Larry Moran. That was also in the context of discussing so-called over-production of PhDs. The new comment from qaz frames the issue as follows:

I AM advocating graduate PhD-level science training for the rest of the population - imagine if our politicians actually understood science (or even critical thinking) for example. A lot of professions would be improved by having scientific training. (But they don't need it, you say. I say, why can't they have it? Why can't spending five years doing some good science not be a part of someone's path in life, even if they don't go on to do NIH-R01-Research?)

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