Thousands of onlookers gathered on Sunday to watch and film the planned implosion of the Texas Stadium in Dallas. The 65,000-seat-stadium was home to the Dallas Cowboys for 38 years and was witness to some thrilling football moments–but all good things must come to an end. The stadium was demolished because the team moved to the new billion-dollar, state-of-the-art Cowboys Stadium last season.

An 11-year-old named Casey Rogers, the winner of a local essay-writing contest, pushed the button that triggered the implosion, and thus set off 1.5 tons of explosives that brought down the stadium in a systematic manner. In the end, just three pillars stood leaning, leading Herbert Gears, mayor of the Dallas suburb of Irving where the stadium was located, to joke to AFP: “Now we’ve got Stonehenge.”

Not only were curious onlookers on hand to observe the implosion, but so were a group of seismologists. In a project nicknamed “Demolicious,” a team led by Jay Pulliam of Baylor University in Waco, Texas used seismometers around the stadium to try and get a clearer picture of the region’s geological features.

Nature News reports:

Pulliam and his team hope that seismic waves from the planned explosion can help to image Earth’s crust in the region, an area of interest to seismologists because it is where the Ouachita deformation was created when a supercontinent of Africa and South America crashed into North America about 300 million years ago. The team also hopes to improve understanding of why small earthquakes occurred in the region in 2008–09 after waste water was pumped deep underground in the process of extracting natural gas from shale.

Earlier last month, Pulliam and his team set up their instruments–a seismometer, an accelerometer, and a clock linked to a GPS–near the stadium. The instruments were set up to record the exact timing of the implosion and the rate at which the seismic waves traveled through the ground. However, Pulliam wasn’t quite sure what to expect from the implosion’s seismic waves. Speaking to Nature News before the big event, he called the process a “terrific experiment.”

Meanwhile, here’s a video of the implosion:

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Image: Dallas Morning Observer

People with Williams syndrome are some of the friendliest people you’ll ever meet. They are incredibly sociable, almost unnervingly so, and they approach strangers with the openness that most people reserve for close friends.

Their sociable streak is the result of a genetic disorder caused by the loss of around 26 genes. This missing chunk of chromosome leaves people with a distinctive elfin face, a risk of heart problems, and a characteristic lack of social fear. They don’t experience the same worries or concerns that most of us face when meeting new people. And now, Andreia Santos from the University of Heidelberg has suggested that they have an even more unique trait – they seem to lack racial bias.

Typically, children start overtly gravitating towards their own ethnic groups from the tender age of three. Groups of people from all over the globe and all sorts of cultures show these biases. Even autistic children, who can have severe difficulties with social relationships, show signs of racial stereotypes. But Santos says that the Williams syndrome kids are the first group of humans devoid of such racial bias, although, as we’ll see, not everyone agrees.

Santos compared the behaviour of 20 white children with Williams syndrome, aged 7 to 16, and 20 typical white children of similar backgrounds and mental ages. To do so, she used a test called the Preschool Racial Attitude Measure (PRAM-II), which is designed to tease out traces of gender or racial biases in young children.

PRAM-II consists of a picture book where every page includes a pair of people of different genders or skin types. The researcher tells a selection of stories to accompany the images and the children have to point to the person whom they think the story is about. As they hear positive or negative adjectives, they reveal any underlying racial bias if they point to light-skinned or dark-skinned people, or men or women, more frequently.

The typical children showed a strong tendency to view light-skinned people well and dark-skinned people poorly. Out of their responses, 83% were consistent with a pro-white bias. In contrast, the children with Williams syndrome only showed such responses 64% of the time, which wasn’t significantly different from chance.

Santos suggests that children with Williams syndrome don’t develop the same biases that their peers do, because they don’t experience social fear. Andreas Meyer-Lindenberg, who led the study, says, “There are hyper-social, very empathetic, very friendly, and do not get danger signals.” And because they’ll freely interact with anyone, they are less likely to cultivate a preference for people of their own ethnic groups. Alternatively, it could be that because they don’t fall prey to stereotypes, they’re more likely to socialise with everyone.

Santos is quick to rule out alternative explanations for this result. Some of the children with Williams syndrome were more intelligent or mentally advanced than the others, but they behaved in the same way. Nor could it be that they suffered from a general inability to assess people’s features, for both groups of children showed a bias towards their own gender.

But not everyone is convinced. Aliya Saperstein from the University of Oregon praised the study’s “clever research design” and said that it shows the Williams Syndrome children are clearly less biased than normal ones. That is interesting in itself, but Saperstein is sceptical that they lack racial bias entirely. In the PRAM-II test, Santos claims that children without any biases should make pro-white responses half of the time, but she showed that the Williams syndrome children did so 64% of the time. This wasn’t significantly different from a chance result but the estimate was based on a very small sample size. Given larger numbers, those extra fourteen percentage points might indicate an important difference.

Robert Livingston from Northwestern University agrees. He says, “I think that it’s problematic to make strong conclusions on the basis of null findings, particularly with a sample as small as 20 WS children.”

It’s also worth noting that the PRAM-II test doesn’t give children the option of a truly unbiased response. They can’t say that the story could fit either image equally – they can only give fewer pro-white answers. As Saperstein says, “The results don’t demonstrate or prove an absence of bias. And like all similar tests, the study may tap partly into one’s knowledge of social stereotypes not just one’s personal biases.”

Livingston also notes that when we’re talking about racial bias, there is a difference between stereotypes, which are based on our beliefs, and prejudices, which are based on our feelings and evaluations of other people. The Williams Syndrome children may not show prejudice, but Livingston says, “Very few if any people who do not show stereotypes.”

Regardless of whether the Williams Syndrome children lack racial bias altogether, it’s clear that they aren’t affected by it to the same extent as normal children. Santos’s results also suggest that racial and gender biases have different origins. The former is borne at least partly out of social fear while the latter has different roots.

The link between social fear and racial stereotypes fits with the results of previous brain-scanning studies. In people with Williams syndrome, the amygdala, a part of the brain involved in processing emotional memories, is far less reactive to threatening social situations. The connections between the amygdala and the fusiform face area, which is specialised for recognising faces, are also unusually weak.

The same areas might play a role in understanding information about people’s race: the fusiform face area tends to be more active when we look at people from the same ethnic group; and one study found that the amygdala is more active when both white and black people look at black faces. This will, of course, need to be tested in more experiments.

Reference: Current Biology; citation unavailable at time of writing

More on race:

• Even on mute, TV can perpetuate racial bias
• Social status shapes racial identity
• People overestimate their reactions to racism
• They don’t all look the same – could better facial discrimination lead to less racial discrimination?
• Simple writing exercise helps break vicious cycle that holds back black students

Astronomers have discovered the closest new star to us that’s been spotted in 63 years. Though “star” might be a stretch, depending upon whom you ask.

The new find, UGPS 0722-05, is less than 10 light years from here. But sky-watchers missed it for so long because it’s a brown dwarf, a member of the murky class of celestial objects that linger between gas giant planets and low-mass stars. Brown dwarfs have so little mass that they never get hot enough to sustain the nuclear fusion reactions that power stars like the sun. Still, they do shine, because they glow from the heat of their formation, then cool and fade [New Scientist]. This dwarf’s temperature is somewhere between 266 and 446 degrees Fahrenheit, making it the coldest scientists have even seen. With its minimal activity, the brown dwarf gives off just 0.000026 percent the amount of light that our sun does.

Like dwarf planets, which cast aside the 9-planet solar system of our childhoods and riled Pluto-philes everywhere, brown dwarfs don’t lend themselves to simple scientific definitions. The International Astronomical Union sets the planet–brown dwarf boundary at 13 times the mass of Jupiter. But that mass limit is an imperfect definition—what of brown dwarf–size bodies that orbit stars, behaving themselves like supersized planets [Scientific American]? The nomenclature could get even messier when the details of this new find are confirmed. Study leader Philip Lucas and his colleagues suggest that the newly discovered brown dwarf is so cool that it might be the first member of a new class of ultralow temperature dwarfs. Although one fingerprint of such a new class, absorption of infrared light by ammonia, appears to be missing, only “time will tell” if the discovery merits a new classification, the researchers note [Science News].

Lucas’ team’s paper is currently being submitted to the journal Nature, where the peer-review process should help to verify how close the team was with its parallax measurement of the brown dwarf’s distance. If they’re correct, UGPS 0722-05 will not only beat out the previous record-holders for proximity to Earth—a binary set of brown dwarfs in the Epsilon Indi system, about 11.8 light-years away—it would also suggest that perhaps more of these shadowy celestial objects linger even closer to us.

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Image: NASA/JPL-Caltech/R. Hurt (SSC/Caltech)

The bottom of the sea is a strange and marvelous frontier, as we were reminded last week by the discovery of the first known animals to live without oxygen. Today a team of British researchers say their undersea robotic explorers have found something new down in the depths of the Caribbean Sea: the deepest hydrothermal vents ever seen.

The black smokers, named for how they spew out an iron sulfide compound that’s black, sit 3.1 miles deep in the Cayman Trough in the Caribbean [FoxNews]. They beat out the previous record holders, which were located 2.6 miles below the surface in the middle of the Atlantic Ocean. As the National Oceanography Centre team sailed across the sea in its research vessel, the James Cook, the scientists deployed their robot explorers down to the inhospitable depths. One, called Autosub6000, mapped the seafloor while another, HyBIS, carried high-resolution cameras to capture these images.

Marine biologist Dr Jon Copley said: “Seeing the world’s deepest black-smoker vents looming out of the darkness was awe-inspiring.” He added: “Super-heated water was gushing out of their two-storey-high mineral spires, more than three miles beneath the waves” [BBC News]. The heat record held by the vents in the mid-Atlantic is a scorching 867 degrees Fahrenheit, but Copley and the other researchers say they don’t know yet whether this one is hotter. Geologist Bramley Murton reports mats of microbes covering the vents, but the team is conferring with other scientists before they announce exactly what they found. Whatever lives down there, it’s certainly got grit. The pressure at the bottom of the trough, which is 500 times normal atmospheric pressure, would be the equivalent to the weight of a large family car pushing down on every square inch of the creatures that live there, the researchers say [FoxNews].

You can keep up with the voyage of the James Cook on the team’s Web site. They’ll be cruising the Cayman Trough until the 20th of this month.

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Once again: If you haven't yet, I encourage you to download or stream my fourth (and so far, I think, best) Point of Inquiry program--with Eli Kintisch on the subject of geoengineering. All this week on the blog, I'm going to be discussing issues raised on the show--so having heard it will be kind of an essential baseline. I'm always trying to become a better interviewer, so with this next post, I want to zoom in on an area where I failed to press my interview subject as I probably should have. And that is the relationship between religious beliefs and opposition to geoengineering. At around minute 9:15, I asked Eli about religious opposition to geoengineering--basically, about the folks who say that we shouldn't "play God." He gave a very detailed answer, essentially signaling that, hey, yeah, this is a lot like genetically modified foods--some people think the impulse to interfere with "nature," to remake it in the way that only "God" is supposed to do, is wrong. I have no doubt this impulse is out there. But I don't find it to be at all a rational argument, or a sound basis for public policy. When it comes to the genetics of ...

In January through April of 2002, the Larsen B ice shelf collapsed in the Antarctic.

This was a huge sheet of ice, about 3250 square kilometers (1250 square miles) in area, roughly equal to a square 57 km (34 miles) on a side. There had been a series of warm summers that weakened the shelf, and then the very warm summer of 2002 spelled doom for it.

The Landsat 7 satellite took many images of the collapse, but the Earth Observatory Image of the Day just released two dramatic shots of its impact:

The top image was taken on April 6, 2002 — about two months after the shelf collapsed — and the bottom one on February 20, 2003. What you’re seeing is the Crane glacier which flowed out into the ice shelf. See how the end of the glacier has retreated so far back into the bay? The Larsen B ice shelf helped stabilize the glacier, but with the shelf gone, the glacier was free to break off as well. The end result is the glacier edge effectively retreating up the channel. You can see icebergs floating in the bay, some hundreds of meters across.

It’s hard not to wonder about climate change when looking at this. As we reality-based folks are fond of saying, weather (short-term, local environment) is not climate (long-term, larger environment). On the other hand, how many episodes of weather over how large a region does it take to add up to climate?

One of the great things about evolutionary theory is that it is a formal abstraction of specific concrete aspects of reality and dynamics. It allows us to squeeze inferential juice from incomplete prior knowledge of the state of nature. In other words, you can make predictions and models instead of having to observe every last detail of the natural world. But abstractions, models and formalisms often leave out extraneous details. Sometimes those details turn out not to be so extraneous. Charles Darwin’s original theory of evolution had no coherent or plausible mechanism of inheritance. R. A. Fisher and others imported the empirical reality of Mendelism into the logic of evolutionary theory, to produce the framework of 20th century population genetics. Though accepting the genetic inheritance process of Mendelism this is original synthesis was not informed by molecular biology, because it pre-dated molecular biology. After James Watson and Francis Crick uncovered the biophysical basis for Mendelism molecular evolution came to the fore, and neutral theory emerged as a response to the particular patterns of genetic variation which new molecular techniques were uncovering. And yet through this much of R. A. Fisher’s image of an abstract genetic variant floating against a statistical soup of background noise variation persisted, sometimes dismissed as “bean bag genetics”.

We’ve come a long way from the first initial wave of discussions which were prompted by the molecular genetic revolution. We have epigenetics, evo-devo and variation in gene regulation. None of these processes “overthrow” evolutionary biology, though in some ways they may revolutionize aspects of it. Science is over the long haul after all an eternal revolution, as the boundaries of comprehension keep getting pushed outward. A few days ago I pointed to Sean Carroll’s recent work, which emphasizes that one must think beyond the sequence level, and focus on particular features such as cis-regulartory elements. Here we’ve been tunneling down to the level of the gene, but what about the traits, the phenotypes, which are affected by genetic variation?

It is well known that the sparest abstraction of genotypic-phenotypic relationship can be illustrated like so:

genetic variation ? phenetic variation

But each element of this relation has to be examined greater detail. What type of genetic variation? Sequence level variation? Epigenetic variation? The second component is perhaps the most fraught, with the arrow waving away the myriad details and interactions which no doubt lurk between genotype and phenotype. And finally you have the phenotype itself. Are they all created alike in quality so that we can ascribe to them dichotomous values and quantities?

A new paper in PNAS examines the particulars of morphological phenotypes and physiological phenotypes, and their genetic control, as well as rates of evolution. Contrasting genetic paths to morphological and physiological evolution:

The relative importance of protein function change and gene expression change in phenotypic evolution is a contentious, yet central topic in evolutionary biology. Analyzing 5,199 mouse genes with recorded mutant phenotypes, we find that genes exclusively affecting morphological traits when mutated (dubbed “morphogenes”) are grossly enriched with transcriptional regulators, whereas those exclusively affecting physiological traits (dubbed “physiogenes”) are enriched with channels, transporters, receptors, and enzymes. Compared to physiogenes, morphogenes are more likely to be essential and pleiotropic and less likely to be tissue specific. Morphogenes evolve faster in expression profile, but slower in protein sequence and gene gain/loss than physiogenes. Thus, morphological and physiological changes have a differential molecular basis; separating them helps discern the genetic mechanisms of phenotypic evolution.

Morphology here refers to gross anatomical features. The sort of traits and characteristics which a paleontologist or anatomist might take interest in. Physiology is more about function, and the physical structures which enable that function. It is naturally closer to the scale of molecular biology as physiology melts into biochemistry. Of course at the other end physiology also merges with anatomy as physiology occurs within features of interest to the anatomist. By way of generalization perhaps physiology may be considered more granular, while morphology more gross, in the context of this paper.

They used the mouse because it’s a species which has long served as a model organism, and there are a host of well known and characterized mutations for both physiology and morphology. Utilization of mice in these fields in the context of evolutionary research dates back to the early 20th century. So systems biologists have a lot of research that’s already been done to work with. They found 5199 mouse genes with known phenotypes in the Mouse Genome Informatics database. 821 affected only morphological traits and 912 affected only physiological traits.

Figure 1 shows the breakdown by Gene Ontology:

Going by what little I know about these topics the second to the fourth panels aren’t surprising. Morphological traits are built from molecular structures, while the transporter activity classes are a more cellular scale, and so would seem to be below the threshold of salience for morphological traits. The first panel is not something I’d expected, but it makes sense after the fact. Figure 2 clarifies. The right panels have proportions, the left counts.

The primary point is this: morphogenes seem to affect more traits than physiogenes, and, their affect is less tissue specific when it comes to a particular trait. When this pattern is highlighted the enrichment toward transcriptional regulation makes more sense to me it is transcriptional regulation might allows for more trait by trait level control of variation. If there is a relationship of many traits to one gene that would probably impose a constraint on the sequence level to a greater extent than if the gene was implicated in variation on one trait. The gap in pleiotropy is closed somewhat when you constrain to essential genes, those whose mutation results in decrease of fitness to zero (through death or lack of ability to reproduce). Pleiotropy presumably is constraining the genetic landscape toward particular fitness peaks. Tissue specificity seems understandable when you consider the localization of many physiological processes, and their biochemical complexities (I’m thinking of the vagaries of gene expression in the liver here).

But they looked at more than how the traits and genes distribute now, they tried to sniff out if there were differences in the rate of evolution of morphogenes and physiogenes contingent upon the class of genetic variants. Remember that you have sequent level changes on exons which can alter proteins. You have cis-acting elements as critical cogs in gene regulation. And you have more gross genomic features such as gene duplication or deletion.

Figure 3 shows the differences between mice and humans on particular genes in relation to sequence level substitutions as well as gene expression profiles. Specifically in the case of the former you want to know the rate of nonsynonymous substitution, those substitutions at base pairs which change the amino acid translated, standardized by the overall mutation rate. So panel C is the one to focus on. Note that physiogenes seem to have evolved more since the last divergence between human and mice lineages than morphogenes. Why might this be? An immediate thought that comes to mind is that tissue-specific expressing physiological processes are liable to be modulated more often than gross morphology, which might be controlled by genes with a lot of pleiotropic effects and so constrained. Even when you control to tissue-specificity the pattern remains, as evident in panel D. The pattern seems somewhat inverted in relation to rate of evolution when it comes to gene expression profiles, as you can see in the last three panels. Evolution happens, but by somewhat different genetic means in these cases. The authors finger pleiotropy in particular as the problem for sequence level evolution in morphogenes, as changes in proteins are much more likely to be problematic if those proteins are upstream from many more traits.

In a way these results show that evolution has to be a versatile designer. When it comes to physiogenes the illustrator is in charge, creating new traits from the most basic genetic raw material, changes in a base pair here and a base pair there. But for morphogenes evolution has to use the tools and tricks of photoshopping, making recourse to extant elements and rearranging or tweaking things here and there so as not to upset the complex applecart while modulating on the margins.

What about cis-acting regulatory elements? In the paper they allude to the argument of Sean Carroll that cis-acting regulatory elements are critical for the evolution of morphological traits. That would imply that morphogenes should be enriched vis-a-vis physiogenes for changes on these elements. They didn’t find that in figure 4. On the contrary.

But I don’t think they perceive their result as a rock-solid refutation of Carroll because it was somewhat indirect. I’ll quote from the paper:

…Because experimentally confirmed mammalian cis elements are few, are likely to have been confirmed in only one species, and are potentially biased toward certain classes of genes,we tested the above hypothesis by using cis-elements that were predicted exclusively by motif sequence conservation among a set of vertebrate genome sequences and recorded in the cisRED database (20). In cisRED, 8,440 predicted mouse cis-elements and 7,688 predicted human cis-elements were found to be in the proximity of 586 mouse morphogenes and their human orthologs, respectively. Similarly, 7,082 mouse cis-elements and 7,215 human cis-elements were predicted for 621 physiogenes….

I’m inclined to accept this result and its generalizability, but there’s a layer of analysis and modeling in this case which doesn’t exist in the others. Additionally, Carroll’s thesis is about the whole animal kingdom and a mouse-human comparison may be atypical.

Finally they wanted to look at gene duplication. They found:

Together with the D_fam result, our analyses show that, whereas physiogene families expand/contract faster than morphogene families, the rate of expansion/contraction is relatively constant across lineages for a given family.

I wonder if the duplication here might have something to do with modulating dosages of various substrates in biochemical processes. This may have more direct relevance to physiological processes.

It is important to note as they did that the category “morphogene” and “physiogene” is somewhat artificial, as is the distinction between morphology and physiology. Nature is fundamentally one, and we break it apart as particular joints for ease of our own abstractions and categorizations. Additionally all genes presumably have some effect on morphology and physiology, and though this exploration looks under the hood a bit more than some of the older abstractions it too is a simplification. The key is that the argument here seems to be that these breaking apart of categories and processes gives us useful marginal return in comprehension of evolutionary dynamics. A trait is not always just a trait. Different classes of phenotypes may have different evolutionary genetic implications by their very nature. Some of this is common sense, those traits which are less functionally significant will exhibit more genic variation. But distinctions in terms of form and function themselves are at a further level of detail. And, I presume that generalizations that we make from mouse-human comparisons as here have some limitations across the tree of life.

Citation: Liao BY, Weng MP, & Zhang J (2010). Contrasting genetic paths to morphological and physiological evolution. Proceedings of the National Academy of Sciences of the United States of America PMID: 20368429