Category: Not Exactly Pocket Science

Pocket Science – a psychopath's reward, and the mystery of the shark-bitten fossil poo

By Ed Yong | March 15, 2010 8:30 am

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.

The rewarding side of being a psychopath

Nucleus_accumbens_psychopat.jpgWhat goes on in the brains of psychopaths? They can seem outwardly normal and even charming, but tthese people typically show a lack of empathy, immoral behaviour and an impulsive streak. Joshua Buckholtz found that the last of these traits – impulsivity – may stem from a hyperactive reward system in the brain and unusually high levels of the signalling chemical dopamine.

When given small doses of amphetamines, people who come out as more impulsive on tests of psychopathy also released more dopamine in a part of their brain called the nucleus accumbens. This region plays many roles in feelings of reward, pleasure and addiction. This link between it and the impulsive side of psychopathy remained even after adjusting for other personality traits. Even the prospect of winning money, as opposed to a physical drug, triggered a hyperactive response from the nucleus accumbens.

When a psychopath imagines a future reward, the explosion of dopamine in their brain provides them with incredible motivation to get that reward. This extra motivation could underlie the increased drug use and the impulsive streaks that accompany the condition. It could even explain some of the antisocial behaviour – dopamine’s most familiar as a chemical linked to feelings of reward and pleasure but studies in mice suggest that its presence in the nucleus accumbens is vital for aggression.

Previous research in this area has focused on the emotionally cold side of psychopathy, which may stem from problems in other parts of the brain like the amygdala, involved in emotions, and the ventromedial prefrontal cortex (vmPFC), involved in fear and risk. The impulsive side of the disorder has typically been overlooked but it predicts many of the problems associated with psychopathy, including drug abuse and violent criminal behaviour.

Reference: Nature Neuroscience http://dx.doi.org/10.1038/nn.2510

Image by Gregory R.Samanez-Larkin and Joshua W. Buckholtz

Why did the shark bite the poo?

Coprolite.jpgThe specimen on the right is a most unusual one. It’s a coprolite, a piece of fossilised dung. That’s not unique in itself; such specimens are often found and they tell us a lot about what extinct animals ate. But this one has a line of grooves running down its middle. They were made by a shark.

Stephen Godfrey and Joshua Smith found two such specimens in Maryland’s Chesapeake Bay. The identity of the coprolites’ maker is a mystery, but its chemical composition suggests that they were excreted by a meat-eating vertebrate. The identity of the biter is clearer. The duo poured liquid rubber into the grooves to make a model cast of the teeth that made them. These model teeth made it clear that the biter was a shark and the duo even managed to narrow its identity down to one of two species -a tiger shark, or Physogaleus, a close extinct relative.

Why would a shark bite a piece of dung? Tiger sharks are notorious for their ability to eat just about anything, but obviously, neither piece of dung was actually swallowed. No known shark eats poo for a living. The shark may have had an exploratory bite and didn’t like what they tasted. But Godfrey and Smith’s favourite explanation is that the bites were the result of collateral damage – the shark attacked an animal and during its assault, it happened to bite through the bowels. These specimens are the enduring remains of a battle between two predators, as suggested by this wonderful drawing in the paper by T Schierer of the Calvert Marine Museum.

Shark-vs-crocodile.jpg

Reference: Godfrey, S., & Smith, J. (2010). Shark-bitten vertebrate coprolites from the Miocene of Maryland Naturwissenschaften DOI: 10.1007/s00114-010-0659-x

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Pocket Science – when enslaved bacteria go bad, gut microbes and fat mice, and stretchy beards of iron

By Ed Yong | March 5, 2010 9:35 am

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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Not Exactly Pocket Science – panic aboard the Titanic, the rise of polar bears and emasculated frogs

By Ed Yong | March 2, 2010 9:30 am

I’m trying something new. Right from the start, I’ve always tried to write fairly long and detailed write-ups of new papers but this means that on any given week, there are always more stories than time and my desktop gets littered with PDFs awaiting interpretation.

So, I’m going to start doing shorter write-ups of papers that don’t make the cut, linking to more detailed treatments on other quality news sources. This is something that I hope science journalists will do more of. It stems from a Twitter conversation where I asked if I should (a) write up short versions of these stories, (b) ignore them, or (c) link to other pieces. People chose a combo of A and C. And if we’re being honest, I was really pleased with “Not Exactly Pocket Science” and the name needed a feature to go with it!

These shorter pieces will still be written from primary papers rather than press releases or existing news stories. Give me feedback. Do these add to the NERS experience, or do short articles go against what you expect of this blog? And also let me know if you find better pieces on the same stories, or you don’t like the ones I’ve linked to. Let’s turn NEPS into a way of highlighting good journalism elsewhere on the web too.

Panic on a sinking ship – Titanic vs Lusitania

Titanic.jpgIn 1912, the Titanic famously sank after colliding with an iceberg. Three years later, the Lusitania also met the ocean floor thanks to torpedoes from a German U-boat. Both ships had similar proportions of crew and demographics of passengers. Neither had enough lifeboats and as a result, only about a third of the passengers on either vessel survived. Over a thousand people died in each tragedy. But Bruno Frey thinks that differences in the type of people who died tell us something about human behaviour under crisis situations. The key factor, he thinks, is time.

The Titanic sank in a leisurely 2 hours and 40 minutes, with plenty of time for social norms to influence who made it onto the lifeboats. The Lusitania went under in just 18 minutes, creating a situation where it was literally every man for himself. In both cases, the captains told crew to save “women and children first”. But their orders were only deferred to on the Titanic, where women and children were indeed more likely to survive than other passengers. On the Lusitania, people aged 16-35 (their supposed physical prime) were around 10% more likely to survive than other age groups. Likewise, first-class passengers had higher odds of survival aboard the Titanic, when class issues had enough time to manifest themselves but they actually fared worse than the third-class passengers on the Lusitania.  

I usually enjoy attempts to view history through a scientific lens, but in this case, it’s difficult to see how much you could really tell from two data points though. Grey’s data are certainly consistent with the hypothesis that selfish behaviour is more likely to emerge in crises that unfold more quickly. But so many other factors could have influenced the outcomes – the structure of the ship, the fact that the Lusitania sank during war-time, the fact that they probably knew about the events aboard the Titanic, different perceptions of the odds of rescue, and so on. Indeed, Grey mentions all of these and says that, “There can be no absolute proof of the hypothesis that only time led to such behavioural differences. Ideally, more observations (comparable shipwrecks) are needed to better isolate the potential relevance of time.”

More from Mark Henderson at the Times and Jeff Wise at the Extreme Fear blog

Reference: Frey, B., Savage, D., & Torgler, B. (2010). Interaction of natural survival instincts and internalized social norms exploring the Titanic and Lusitania disasters Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0911303107

Jawbone reveals the rise of the polar bear

Polar-bear.jpgA lots of news coverage is devoted to discussing the fate of polar bears, but it’s their origins that are now getting some attention. A new fossil jaw from Svalbard gave Charlotte Lindqvist the opportunity to trace the history of climate change’s flagship species. Polar bears live and die on sea ice, their remains either sink without a trace or are scavenged, so every new fossil is an exciting find. The new jawbone is approximately 130,000 to 110,000 years old but Lindqvist managed to extract enough DNA from it to sequence the genome of its mitochondria – small power plants within every animal cell, each containing their own genome.

She also sequenced extra mitochondrial genomes from two living polar bears and four brown bears from different areas. A family tree built from these sequences revealed that the jawbone’s owner was remarkably similar to the last common ancestor of brown and polar bears, sitting just at the point where the two lineages diverged. By analysing the carbon isotopes of the fossil’s canines, Lindqvist deduced that this ancient bear ate sea-going mammals just like its modern cousins do.

Together, this single bone paints the portrait of an evolutionary success story. Within 10,000-30,000 years of their split from brown bears, the polar bears had adapted magnificently to their frosty kingdom and risen to the rank of top predator. Within the next 100,000 years, they had spread across the entire polar realm. As Lindqvist says, they’re “an excellent example of “evolutionary opportunism”. Whether they’ll be swift enough to cope with the current changes to their habitat is another matter.

More from Brandon Keim at Wired

Reference: Lindqvist, C., Schuster, S., Sun, Y., Talbot, S., Qi, J., Ratan, A., Tomsho, L., Kasson, L., Zeyl, E., Aars, J., Miller, W., Ingolfsson, O., Bachmann, L., & Wiig, O. (2010). Complete mitochondrial genome of a Pleistocene jawbone unveils the origin of polar bear Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0914266107

Common pesticide turns Kermits into Kermitas

Kermit.jpgTheir testicle shrinks, their testosterone depletes, their sperm count falls, and they stop trying to have sex. Becoming emasculated and impotent isn’t a pretty fate for a male frog, but thanks to a pesticide called atrazine, it could be a common one. Atrazine is an “endocrine disruptor”, a substance that mimics the effects of sex hormones in the body. Tyrone Hayes has found that it can chemically castrate male African clawed frogs.

Around 10% of the animals actually became fully functional females despite being genetically male. They could even mate with other males to produce viable eggs (albeit ones that only hatched into genetic males). In others, the changes were less drastic but they were still feminised enough to seriously affect their odds of mating successfully. This isn’t the first time that atrazine has been linked to feminised frogs and according to previous studies, it affects other groups of animals, from salmon to crocodiles, in the same way. In these species, atrazine switches on the manufacture of aromatase, an enzyme that, in turn, stimulates the production of oestrogen. This flood of hormone may also be behind the feminised Kermits.

Frogs and other amphibians are particularly vulnerable to chemicals like atrazine because of their absorbent skins. Indeed, Hayes emasculated his frogs with just 2 parts per billion of atrazine, a dose that animals would frequently encounter in contaminated areas, and well within levels occasionally found in rainfall. Because of the environmental risks, atrazine was banned in the EU in 2004, but the US still sprays 80 million pounds of this persistent chemical every year. Obviously, this study didn’t assess the impact that the chemical could have on frog populations but there’s every reason to suspect it as a “contributor to global amphibian declines“.

More from Janet Raloff at Science News

More on amphibian conservation:

Reference: Lindqvist, C., Schuster, S., Sun, Y., Talbot, S., Qi, J., Ratan, A., Tomsho, L., Kasson, L., Zeyl, E., Aars, J., Miller, W., Ingolfsson, O., Bachmann, L., & Wiig, O. (2010). Complete mitochondrial genome of a Pleistocene jawbone unveils the origin of polar bear Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0914266107

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Not Exactly Rocket Science

Dive into the awe-inspiring, beautiful and quirky world of science news with award-winning writer Ed Yong. No previous experience required.
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