March 12, 2010
Category: Politics • Psychology • Social science
This article is reposted from the old Wordpress incarnation of Not Exactly Rocket Science.
For all the millions that are poured into electoral campaigns, a voter's choice can be influenced by the subtlest of signals. Israeli scientists have found that even subliminal exposure to national flags can shift a person's political views and even who they vote for. They managed to affect the attitudes of volunteers to the Israeli-Palestine conflict by showing them the Israeli flag for just 16 thousandths of a second, barely long enough for the image to consciously register.
These results are stunning - even for people right in the middle of the one of the modern age's most deep-rooted conflicts, the subconscious sight of a flag drew their sympathies towards the political centre.
In some ways, it's not surprising. The last decades of experimental psychology have shown us that the our conscious view of the world is a construct created by our brain. We simply cannot consciously process the barrage of information constantly arriving through our senses and to save us from a mental breakdown, our brain does a lot of subconscious computing. The upshot of this is that our decisions can be strongly influenced by sights, sounds and other stimuli that we're completely unaware of. Have a look at this video of mind-manipulator Derren Brown for a classic example of this.
Our political views are no different. In an ideal world, we would base them on a rational consideration of the relevant facts and our own beliefs, but in the real one, subliminal symbols pull on the puppet-strings too. National flags should be capable of this; to many people, they carry a weighty importance out of all proportion to their nature as rectangular sheets of cloth
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Posted by Ed Yong at 8:30 AM • 2 Comments • 0 TrackBacks
March 11, 2010
Category: Animal behaviour • Animals • Butterflies and moths • Genetics • Genomics • Insects • Invertebrates • Medicine & health • Mimicry • Sex and reproduction
Not Exactly Pocket Science is a set of shorter write-ups on new stories with links to more detailed takes by the world's best journalists and bloggers. It is meant to complement the usual fare of detailed pieces that are typical for this blog.
Geneticist sequences own genome, finds genetic cause of his disease
If you've got an inherited disease and you want to find the genetic faults responsible, it certainly helps if you're a prominent geneticist. James Lupski (right) from the Baylor College of Medicine suffers from an incurable condition called Charcot-Marie-Tooth (CMT) disease, which affects nerve cells and leads to muscle loss and weakness.
Lupski scoured his entire genome for the foundations of his disease. He found 3.4 million placed where his genome differed from the reference sequence by a single DNA letter (SNPs) and around 9,000 of these could actually affect the structure of a protein. Lupski narrowed down this list of candidates to two SNPs that both affect the SH3TC2 gene, which has been previously linked to CMT. One of the mutations came from his father and the other from his mother. Their unison in a single genome was the cause of not just Lipson's disease but that of four of his siblings too.
It's a great example of how powerful new sequencing technologies can pinpoint genetic variations that underlie diseases, which might otherwise have gone unnoticed. The entire project cost $50,000 - not exactly cheap, but far more so than the sequencing efforts of old. The time when such approaches will be affordable and commonplace is coming soon. But in this case, Lupski's job was easier because SH3TC2 had already been linked to CMT. A second paper tells a more difficult story.
Jared Roach and David Gallas sequenced the genomes of two children who have two inherited disorders - Miller syndrome and primary ciliary dyskinesia - and their two unaffected parents. We don't know the genetic causes of Miller syndrome and while the four family genomes narrow down the search to four possible culprits, they don't close the case.
For great takes on these stories and their wider significance, I strongly recommend you to read Daniel Macarthur's post on Genetic Future, Mark Henderson's piece in the Times and Nick Wade's take in the NYT (even if he does flub a well-known concept). Meanwhile, Ivan Oranksy has an interesting insight into the political manoeuvres that go into publicising two papers from separate journals. And check out this previous story I wrote about how genome sequencing was used to reverse the wrong diagnosis of a genetic disorder.
Reference: http://dx.doi.org/10.1056/NEJMoa0908094 and http://dx.doi/org/10.1126/science.1186802
Male moths freeze females by mimicking bats
Flying through the night sky, a moth hears the sound of danger - the ultrasonic squeak of a hunting bat. She freezes to make herself harder to spot, as she always does when she hears these telltale calls. But the source of the squeak is not a bat at all - it's a male moth. He is a trickster. By mimicking the sound of a bat, he fooled the female into keeping still, making her easier to mate with.
The evolutionary arms race between bats and moths has raged for millennia. Many moths have evolved to listen out for the sounds of hunting bats and some jam those calls with their own ultrasonic clicks, produced by organs called tymbals. In the armyworm moth, only the males have these organs and they never click when bats are near. Their tymbals are used for deceptive seductions, rather than defence.
Ryo Nakano found that the male's clicks are identical to those of bats. When the males sung to females, Nakano found that virtually all of them mated successfully. If he muffled them by removing the tymbals, they only got lucky 50% of the time. And if he helped out the muted males by playing either tymbal sounds or bat calls through speakers, their success shot back up to 100%. Nakano says that this is a great example of an animal evolving a signal to exploit the sensory biases of a receiver.
More on bats vs. moths from me
Reference: Biology Letters http://dx.doi.org/10.1098/rsbl.2010.0058
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Posted by Ed Yong at 2:53 PM • 1 Comments • 0 TrackBacks
March 10, 2010
Category: Animals • Birds • Genetics • Sex and reproduction
The animal on the right is no ordinary chicken. Its right half looks like a hen but its left half (with a larger wattle, bigger breast, whiter colour and leg spur) is that of a cockerel. The bird is a 'gynandromorph', a rare sexual chimera. Thanks to three of these oddities, Debiao Zhao and Derek McBride from the University of Edinburgh have discovered a truly amazing secret about these most familiar of birds - every single cell in a chicken's body is either male or female. Each one has its own sexual identity. It seems that becoming male or female is a very different process for birds than it is for mammals.
In mammals, it's a question of testicles, ovaries and the hormones they produce. Embryos live in sexual limbo until the sex organs (gonads) start to develop. This all depends on a sexual dictator called SRY, a gene found on the Y chromosome. If it's present, the indifferent gonads go down a male route; if not, they take a female one. The sex organs then secrete a flush of hormones that trigger changes in the rest of the body. The sex chromosomes are only relevant in the cells of the gonads.
But the gynandomorphs show that something very different happens in birds. Birds have Z and W chromosomes; males are ZZ and females are ZW. Zhao and McBride used glow-in-the-dark molecules that stick to the two chromosomes to show that the gynandromorphs do indeed have a mix of ZZ and ZW cells. However, they aren't split neatly down the middle. Their entire bodies are suffused with a mix of both types, although the male half has more ZZ cells and the female half has more ZW ones.
Even though the three chickens were both male and female, one of them only had a testicle on one side, the second only had an ovary on one side, and the third had a strange hybrid organ that was part testis and part ovary. These malformed organs pumped the same soup of hormones throughout the birds' bodies but, clearly, each side responded differently.
Zhao and McBride started to suspect that each cell has its very own sexual identity, and that this individuality exists from the chicken's first days of embryonic life. They proved that by transplanting cells from embryonic sex organs from one animal to another. All the transplants produced a glowing green protein so Zhao and McBride could track their whereabouts, and those of their daughters.
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Posted by Ed Yong at 1:40 PM • 17 Comments • 0 TrackBacks
Category: Journalism
If anyone's in London or thereabouts on the 31st of March, come and see me and a few other science journalists discuss the state of science in the media at City University. The discussion follows a recent government report, entitled Science in the Media: Securing the Future. The report declared that science coverage (in the UK, at least) was in "rude health", while is somewhat different to the picture that others have painted.
I'll be discussing the report as well as, presumably, other matters about science journalism along with a panel of veteran UK journalists. I assume that I have been recruited as the voice of youthful dissent and indeed, those of you who were at my panel at ScienceOnline may remember me reading out a passage from this same report to the sound of laughter from the crowd.
Personally, I think the report has a lot of good things to say, but it's missing any substantial discussion about the new ecosystem of online science journalism and the changing nature of those who can legitimately call themselves science journalists. But enough for now - come along and join the discussion. It should be a good one.
The official description is below and you need to reserve a place.
I'd also like to encourage people who attend to tweet it. Perhaps #scimedia as a hashtag.
- Date: Wednesday 31 March 2010
- Time: 6.30pm
- Location: City University London, Northampton Square, London EC1V 0HB
A recent government report on science in the media declared that it was in "rude health", while other commentators think that it is ailing and in crisis.
Join the debate with a panel of leading science journalists including:
Posted by Ed Yong at 8:30 AM • 0 Comments • 0 TrackBacks
March 9, 2010
Category: Ancient DNA • Animals • Birds • Genetics • Palaeontology
Even extinction and the passing of millennia are no barriers to clever geneticists. In the past few years, scientists have managed to sequence the complete genome of a prehistoric human and produced "first drafts" of the mammoth and Neanderthal genomes. More controversially, some groups have even recovered DNA from dinosaurs. Now, a variety of extinct birds join the ancient DNA club including the largest that ever lived - Aepyornis, the elephant bird.
In a first for palaeontology, Charlotte Oskam from Murdoch University, Perth, extracted DNA from 18 fossil eggshells, either directly excavated or taken from museum collections. Some came from long-deceased members of living species including the emu, an owl and a duck. Others belonged to extinct species including Madagascar's 3-metre tall elephant bird and the giants moas of New Zealand. A few of these specimens are just a few centuries old, but the oldest came from an emu that lived 19,000 years ago.
It turns out that bird eggshells are an excellent source of ancient DNA. They're made of a protein matrix that is loaded with DNA and surrounded by crystals of calcium carbonate. The structure shelters the DNA and acts as a barrier to oxygen and water, two of the major contributors to DNA damage. Eggshells also stop microbes from growing and it seems that ancient ones still do the same. Oskam found that the fossil shells had around 125 times less bacterial DNA than bones of the same species did.
This is important - bacteria are a major problem for attempts to extract ancient DNA and they force scientists to search for uncontaminated sources, like frozen hair. Eggshells, it seems, provide similarly bacteria-free samples. Still, Oskam's team took every precaution to prevent contamination. They used clean rooms and many control samples. Many of their sequences, like those of Aepyornis, were checked by two independent laboratories.
The Aepyornis sequences are particularly encouraging because many scientists have previously tried to extract DNA from the bones of this giant and failed. Eggshells seem like a more promising source and it certainly helps that the eggs of many of these giant species were massive and thick. But Oskam did also recover DNA from a fossil duck egg, which suggests that it should be possible to sequence the genes of even small extinct birds, like the dodo.
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Posted by Ed Yong at 7:00 PM • 11 Comments • 0 TrackBacks
Category: Animal behaviour • Animals • Eye evolution • Fish • Lizards • Predators and prey • Reptiles
Cold-proof tongue allows early chameleon to catch early insect
Chameleons are some of the most versatile of lizards. They live in baking deserts and freezing mountaintops and part of their success hinges on a weapon that works just as well in the warmth as in the cold - its tongue. Relying on stored elastic power for its ballistic strike, the chameleon's tongue is largely cold-proof. At temperatures that would flummox most reptile muscles, the tongue carries on snatching insects with great efficiency.
Chameleon tongues can reach twice the length of their body in less than a tenth of a second, latching onto prey with a sticky, grasping tip. Rather than pushing it forward with muscle power, like a spear-thrower, the chameleon behaves more like an archer. It ratchets the tongue backwards by slowly contracting its muscles, as if it was drawing an arrow on a bow. It fires by relaxing its muscles, and the whole sticky snare shoots forward on its own momentum. Once the prey is caught, long muscles pull the tongue back into the mouth.
Christopher Anderson and Stephen Deban from the University of South Florida filmed veiled chameleons with a high-speed camera as they shot their tongues at dangling crickets. Their performance certainly improved as the temperature increased from 15 to 35C, but not by much. Even at low temperatures, the tongue shot out with impressive acceleration, speed and power that fell by just 10-20% across a ten degree gradient. When it retracted under muscular control, the effects of the chill were more obvious and a similar gradient led to a 40-60% fall in performance.
By freeing their killer strike from the constraints of temperature, chameleons have been able to exploit chilly windows of opportunity denied to other lizards. They can hunt during the early morning hours when insects are very active and they can expand across a wide range of habitats. They also have to waste less energy on the simple business of keeping warm. After all, why bother with central heating when you can catch food at body temperatures of 3.5C, as some chameleons can?
Reference: PNAS http://dx.doi.org/10.1073/pnas.0910778107If this link isn't working, read why here
Image by Christopher V Anderson
More from Jennifer Viegas at Discovery News and from NERS on the mayfly-like chameleon that lives mostly as an egg
Zebrafish babies shut off their eyes at night
Many animals find it harder to see in the darkness of night, but the larvae of zebrafish must find it particularly difficult. Every night, they essentially shut down their eyes, losing the ability to see. Fairda Emran found that the retinas of the baby fish responded normally to light during the day, but they were almost totally impassive after 90 minutes of darkness. The fish themselves totally failed to follow a moving target.
The babies' body clocks drove this cycle of blindness. It kicked in every night and even if the fish were kept in darkness for several days, they always anticipated the arrival of daylight by restoring their sight. Only a flash of light at night managed to break this tidy cycle, restoring the zebrafishes' vision at a time when they would normally be blind.
At five days of age, baby zebrafish have just used up all the yolk from their eggs and are starting to find their own food. For them, energy is a precious commodity and eyes are energy-guzzling appliances, even when they're set to standby at night. It makes sense to just shut them off instead.
Reference: PNAS http://dx.doi.org/10.1073/pnas.0914718107 If this link isn't working, read why here
More from NERS on how animal eyes cope with darkness, including animals that use DNA as lenses, squid that have bacterial flashlights and the bizarre double-eyes of the spookfish,
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Posted by Ed Yong at 8:30 AM • 2 Comments • 0 TrackBacks
March 8, 2010
Category: Altruism • Cooperation • Game theory • Psychology • Social science
Ever wonder if acts of kindness or malice really do ripple outwards? If you give up a seat on a train to a stranger, do they go onto "pay it forward" to others? Likewise, if you steal someone's seat, does the bad mood you engender topple over to other people like a set of malicious dominoes? We'd all probably assume that the answers to both questions were yes, but James Fowler and Nicholas Christakis think they have found experimental evidence for the contagious nature of cooperation and cheating.
The duo analysed data from an earlier psychological experiment by Ernst Fehr and Simon Gachter, where groups of four volunteers had to decide how much money to put in a public pot. For every unit they chipped in, each member would get 0.4 back. So any donations represent a loss to the donor, but a gain to the group as a whole. The best way for the group to benefit would be for everyone to put in all their money, but each individual player could do even better by putting in nothing and feeding off their peers' generosity.
This "public goods game" went on for six rounds. At the end of each one, the players were told what their other comrades did, although everyone's identities were kept secret. The groups were shuffled between rounds so that players never played with each other more than once.
Fowler and Christakis found that the volunteers' later moves were influenced by the behaviour of their fellow players. Each act of generosity by an individual influenced the other three players to also give more money themselves, and each of them influenced the people they played with later. One act became three, which became nine. Likewise, players who experienced stingy strategies were more likely to be stingy themselves.
Even though the groups swapped every time, the contagious nature of generous or miserly actions carried on for at least three degrees of separation. You can see an example of one such cascade in the diagram below. Eleni contributes some money to the public pot and her fellow player, Lucas, benefits (one degree). In the next round, Lucas himself offers money for the good of the group, which benefits Erika (two degrees), who gives more when paired with Jay in her next game (three degrees). Meanwhile, the effects of Eleni's initial charity continue to spread throughout the players as Lucas and Erika persist in their cooperation in later rounds.
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Posted by Ed Yong at 3:00 PM • 7 Comments • 0 TrackBacks
March 7, 2010
Category: Animal behaviour • Animals • Medicine & health • Sex and reproduction
Sex might be fun but it's not without risks. As your partner exposes themselves to you, they also expose you to whatever bacteria, viruses or parasites they might be carrying. But some animals have a way around that. Ekaterina Litvinova has found that when male mice get a whiff of female odours, their immune systems prepare their airways for attack, increasing their resistance to flu viruses.
Litvinova worked with a group of mice that were exposed to bedding that had previously been soiled by females in the sexually receptive parts of their cycle. She compared them to a second more monastic group that were isolated from female contact.
Male mice use smells to track down females who are ready to mate. They'll follow markings of faeces and urine and when they actually find the female, they'll continue sniffing her nose and genitals. Each of these nasal encounters could be a source of infection. She then pitted both groups against a flu virus. Influenza doesn't affect wild populations of house mice, so the virus in this case is acting as more of an indicator of the animals' defences, rather than a representative of a real threat.
Both groups of mice lost a bit of weight, but at certain doses of virus, those that had been exposed to female aromas kept more of their grams on. They also fared better in the long run - just 20% of them died, compared to 46% of those that had only smelled male odours.
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Posted by Ed Yong at 12:00 PM • 2 Comments • 0 TrackBacks
March 5, 2010
Category: Animals • Bacteria • Dinosaurs • Material science • Medicine & health • Not Exactly Pocket Science • Obesity • Palaeontology
The Not Exactly Pocket Science experiment continues after the vast majority of people who commented liked the pilot post. I'm really enjoying this, for quite unexpected reasons. It's forcing me to flex writing muscles that usually don't get much of a workout. Writing short pieces means being far more economical with language and detail than usual. It means packing in as much information as possible while still keeping things readable. And it means blitz-reading papers and writing quickly without losing any accuracy.
One quick note before the good stuff: last time, a few people suggested that I put each NEPS item in a separate post, but the majority preferred multiple items per post. For now, I'm keeping it that way because otherwise, the longer pieces would be diluted by the smaller ones. We'll see how that works for the foreseeable future.
Rising DAMPs - when enslaved bacteria turn our bodies against themselves
Our immune systems provide excellent defence against marauding hordes of bacteria, viruses and parasites, using sentinel proteins to detect the telltale molecules of intruders. But these defences can be our downfall if they recognise our own bodies as enemies.
All of our cells contain small energy-supplying structures called mitochondria. They're descendents of ancient bacteria that were engulfed and domesticated by our ancestor cells. They've come a long way but they still retain enough of a bacterial flavour to confuse our immune system, should they break free of their cellular homes. An injury, for example, can set them free. If cells shatter, fragments of mitochondria are released into the bloodstream including their own DNA and amino acids that are typical of bacteria. Qin Zhang showed that trauma patients have far higher levels of such molecules in their blood than unharmed people. Our white blood cells have sentinel proteins that latch onto these molecules and their presence (incorrectly) says that a bacterial invasion is underway.
This discovery solves a medical mystery. People who suffer from severe injuries sometimes undergo a dramatic and potentially fatal reaction called "systemic inflammatory response syndrome" or SIRS, where inflammation courses through the whole body and organs start shutting down. This looks a lot like sepsis, an equally dramatic response to an infection. However, crushing injuries and burns can cause SIRS without any accompanying infections. Now we know why - SIRS is caused by the freed fragments of former bacteria setting off a false alarm in the body. The technical term for these enemies within is "damage-associated molecular patterns" or DAMPs.
More from Heidi Ledford at Nature News
Reference: Nature DOI:10.1038/nature08780
Different gut bacteria lead to mice to overeat
On Wednesday, I wrote about the hidden legions residing up your bum - bacteria and other microbes, living in their millions and outnumbering your cells by ten to one. These communities wield a big influence over our health, depending on who their members are. Matam Vijay-Kumar found that different species colonise the guts of mice with weakened immune systems, and this shifted membership is linked to metabolic syndrome, a group of obesity-related symptoms that increase the risk of heart disease and type 2 diabetes.
Vijay-Kumar's mice lacked the vital immune gene TLR5, which defends the gut against infections. Their bowels had 116 species of bacteria that were either far more or less common than usual. They also overate, became fat, developed high blood pressure and became resistant to insulin - classic signs of metabolic syndrome. When Vijay-Kumar transplanted the gut menagerie from the mutant mice to normal ones, whose own bacteria had been massacred with antibiotics, the recipients also developed signs of metabolic syndrome. It was clear evidence that the bacteria were causing the symptoms and not the other way round.
Vijay-Kumar thinks that without the influence of TLR5, the mice don't know what to make of their unusual gut residents. They react by releasing chemicals that trigger a mild but persistent inflammation. These same signals encourage the mice to eat more, and they make local cells resistant to the effects of insulin. Other aspects of the metabolic syndrome soon follow. The details still need to be confirmed but for now, studies like this show us how foolish it is to regard obesity as a simple matter of failing willpower. It might all come down to overeating and inactivity, but there are many subtle reasons why an individual might eat too much. The microscopic community within our guts are one of them.
Read an amazing take on this from Carl Zimmer at the Loom and a previous post from me
Reference: Science DOI:10.1126/science.1179721
The stretchy iron-clad beards of mussels
For humans, beards are for catching food, looking like a druid, and getting tenure. But other animals have beards with far more practical purposes - mussels literally have beards of iron that they use as anchors. The beard, or byssus, is a collection of 50-100 sticky threads. Each is no thicker than a human hair but they're so good at fastening the mussels to wave-swept rocks that scientists are using them as the inspiration for glue. So they should. The byssus is a marvel of bioengineering - hard enough to hold the mussel in place, but also stretchy enough so that they can extend without breaking.
The mussel secretes each thread with its foot, first laying down a protein-based core and then covering it in a thick protective layer that's much harder. When Matthew Harrington looked at the strands under a microscope, he saw that the outer layer is a composite structure of tiny granules amid a looser matrix. The granules consist of iron and a protein called mfp-1, heavily linked to one other - this makes the byssus hard. The matrix is a looser collection of the same material, where mfp-is 1 heavily coiled but easy to straighten - this lets the byssus stretch. The granules have a bit of give to them but at higher strains, they hold firm while the matrix continues extending. If cracks start to form, the granules stop them from spreading.
It's unclear how the mussel creates such a complicated pattern, but Harrington suggests that it could be deceptively simple - changing a single amino acid in the mfp-1 protein allows it to cross-link more heavily with iron. That's the difference between the tighter granular bundles, and the looser ones they sit among.
More from Eric Bland at Discovery News and stories of bioengineering from me, including triple-armoured snails, shatter-proof teeth and sharp squid beaks.
Reference: Science DOI:10.1126/science.1181044
Cause of dinosaur extinction revealed confirmed
Sixty-five million years ago, the vast majority of dinosaurs were wiped out. Now, a new paper reveals the true cause of their demise - legions of zombies armed with chaingu... wait... oh. Right. An asteroid. You knew that.
More from Mark Henderson at the Times
Reference: Science DOI:10.1126/science.1177265
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Posted by Ed Yong at 9:35 AM • 5 Comments • 0 TrackBacks
