Here be monsters

With fiery breath... Image courtesy of Joschenbacher

With fiery breath...

Image courtesy of Joschenbacher

It seemed like a curse. Ancient texts report that the winter of 821–822 CE was long and exceptionally cold, reportedly freezing solid the Danube, Elbe, Rhine, and Seine. A great food shortage struck in 822 CE. Famine continued into 823 CE when texts record drought, horrendous hailstorms and widespread plague. The winter of 823–824 CE was long and uncommonly severe. Remarkable hailstorms again hit in 824 CE and famine persisted at least into the autumn of that year. Irish, Spanish and even Chinese sources tell similar stories. Whispers of an angered monster were rampant and now a new paper is revealing the identity of that beast to be Katla.

Sleeping beneath 700 meters of ice, Katla is Iceland's most active volcano and her activity has been well recorded ever since Vikings settled alongside her in 870 CE. Yet in 821, the Vikings were still busy pillaging the coasts of France and England and there are no precise records of what Katla was up to. Thus, the curse of 821 remained a mystery until a severe spring flood on an Icelandic river in 2003 exposed a prehistoric forest that had been buried centuries ago under sediment. A team has now used a mix of radiocarbon and tree ring analysis to study a very well preserved fossil tree at the site and found evidence suggesting that there was a serious Katla eruption in 821.  You can read more in The Economist article that I wrote on this here.

Sounds like trouble

Shall I flap the alarm? Image courtesy of Fir0002/Flagstaffotos

Shall I flap the alarm?

Image courtesy of Fir0002/Flagstaffotos

In his writings on sexual selection, Darwin devoted equal space to non-vocal and vocal communication in birds. Yet, in the years that have passed since his death, the research community has given almost no attention to non-vocal communications. This, particularly when compared to the extensive attention that bird calls have received, is a great shame. Darwin called the sounds that birds made with their feathers and feet "instrumental music" and speculated that they used these sounds to send valuable signals to one another. That hypothesis is very old and has never been tested. Now, a team is revealing that one species of pigeon creates a unique warning sound with a single wing feather when fleeing danger.

The new work was all conducted through a clever mix of video and feather-removal experiments that were able to demonstrate that a highly modified primary feather on the wings of the crested pigeon produces a distinct note during each flap of the wing. Crucially, the note changes with wing beat frequency which means that pigeons fleeing danger produce a sound that is different from pigeons that are merely taking off in a relaxed manner. You can read more in The Economist article that I wrote on this here.

Antibiotic resistance on fish farms

Looks clean but what's in the food? Image courtesy of Narek75.

Looks clean but what's in the food?

Image courtesy of Narek75.

We know that antibiotic resistance genes commonly appear in bacteria living in the muck below fish farms. Until recently, the assumption was that antibiotics used to prevent disease in these farms were the key force behind the high concentrations of resistance genes in the bacteria living below them but in 2014 a study challenged that notion by revealing that farms in parts of the Baltic, where antibiotics have been banned for years or were never used, still had sediment below them that was crawling with resistant strains of bacteria. That finding along with several others left researchers scratching their heads as to how the resistance was getting there. Now a new experiment is revealing that the food being used to feed farmed fish is where most of these resistant genes are coming from.  

The researchers behind the work knew from past studies that antibiotics had often been detected in poor quality fish food but, when they looked through the literature, they could find no studies that analysed whether fish foods on the markets were actually carrying bacteria in them with resistant genes. Curious, they analysed a bunch of commonly used fish food products and, voila, there they were. The team uncovered a whopping 132 unique resistant genes in five different fish food products. And the reason these genes are there? The fish food products are being made in facilities where sanitation is poor and genetic material in chopped up fish that are being prepared to be made into fish food are not getting heated enough to be destroyed. Friggin unbelievable.  You can read more in The Economist article that I wrote on this here.

T test

Many studies show that testosterone male animals more aggressive but how the hormone affects human decision making has, surprisingly, had little attention. Keen to take a closer look, a team ran the largest human testosterone behavioural experiment ever conducted and randomly administered a single dose of either testosterone or a placebo to a sample of 243 men. They then measured the participants' performance on both the Cognitive Reflection Test, a long used exam that assesses a person's capacity to monitor their own intuitive judgments and override them when appropriate, and a mathematics test which functioned as a control.

The researchers guessed that testosterone would increase participants’ tendency to rely on their intuitive judgments, reduce inhibition of incorrect responses and thus impair their Cognitive Reflection Test performance compared to those who were given the placebo. They expected the maths test results to not be affected. This is precisely what they found. Mathematics scores from both placebo and testosterone groups were nearly identical. However, Cognitive Reflection Test scores in those dosed with testosterone were a staggering 50% those of the placebo group.  You can read more in The Economist article that I wrote on this here.

Driven by digestion

Heartless beast. Image courtesy of Steve Childs.

Heartless beast.

Image courtesy of Steve Childs.

Sea spiders are an ancient group of animals that have a number of odd traits. Perhaps the most notable is that many of them either have teeny tiny hearts or no hearts at all. This has led many researchers to question how they get their blood to move around their bodies but, to date, nobody has been sure. Now a new experiment is revealing that they manage this vital task with guts... literally. Peristalsis, the process that moves food through our intestines, appears to be the primary force that swishes oxygen-carrying blood around the bodies of sea spiders. You can read more in The Economist article that I wrote on this here.

Colour me dangerous

Captured bandit. Image courtesy of Jakob Vinther.

Captured bandit.

Image courtesy of Jakob Vinther.

The "bandit mask" is a common colour pattern found on the faces of animals living in the open plains. With nowhere to hide, these species depend upon their mask communicating the important message that they are not to be messed with. In the case of the badger and the wolverine, the message is a simple "do not judge me by my size, I will rip your arms off." In the case of the skunk and the teledu, the message is "touch me and I will nauseate or blind you with nasty juices stored in my anal glands!" Many birds, including kingfishers, osprey and falcons also have dark bands covering their eyes both to prevent prey animals from spotting their dark eyes staring at them before an attack and to reduce glare from intense sunlight. Thus, it is fascinating that a new study is revealing that the dinosaur Sinosaurpteryx had a bandit mask on its face too. 

The new research revolves around a pigment analysis that was conducted on three exceptionally well preserved fossils of Sinosaurpteryx. While the species is known as one of the many toothy, meter-long and semi-feathered kin of Tyrannosaurus rex found in the Jehol formation of China, details about how it led its life have remained unclear. The assumption was that it lived as a forest ambush predator since the Jehol was once heavily forested but the colouration patterns on Sinosaurpteryx challenge that notion. Aside from the presence of the bandit mask, which needs to be easily seen by would be predators to be effective and would not function terribly well in a dense forest, Sinosaurpteryx also shows some lovely evidence of counter-shading. Counter-shading involves an animal having a light coloured belly and a dark back that helps mask the three-dimensional shape of its body by reducing self-shadowing, decreasing conspicuousness and thus helping to avoid detection by both predators and prey alike. Like the mask, counter-shading would be of little use in a dense forest and, indeed, it is rarely seen in such environments.



Sun cream vs multiple sclerosis

That multiple sclerosis (MS) is less common near the equator than it is in upper latitudes has led teams in recent years to explore this oddity and led one group to find that ultraviolet light (UV) suppresses the disease. Keen to take a closer look at this, a researchers applied sun cream to mice with the rodent version of MS just before exposing them to UV light. They fully expected the sun cream to block the protective effect of the light but this is not what happened. Instead, the cream granted further protection against the disease.

This surprising discovery led the researchers to run a follow up experiment with many sun creams. They found that not all were equal in their ability to suppress MS but that the few that did have a beneficial effect worked even when the mice were not exposed to UV light. Fascinated, the team broke the MS suppressing sun creams into their component parts and applied them one by one to the mice. You can read more in The Economist article that I wrote on this here.

Better training bomb sniffing dogs

Are we sure that box isn't tainted? Image courtesy of US Navy.

Are we sure that box isn't tainted?

Image courtesy of US Navy.

One of the key arguments made for replacing bomb sniffing dogs with electronic noses is that the dogs are fallible and have the potential to be distracted by the presence of sausages whereas electronic noses are not. Yet defenders of the dogs argue that it is not so much that the dogs are making mistakes as they are being poorly taught by their handlers. Canines are currently judged during training and testing by how well they find intentionally hidden explosives. This method makes intuitive sense because handlers cannot see the odours themselves and certainly cannot smell them, so their intention is used as a surrogate for whether or not an odour is actually there. However, unintentional explosive odours can easily be presented and damage dog training. Now a team is revealing the invention of a vapour analysis device with real-time detection capabilities that will allow handlers to visualise the odours they are exposing to their dogs and vastly improve training.

The new technology has a detection library of nine explosives and explosive-related materials including some of the big baddies like nitroglycerin, triacetone triperoxide (used in the Brussels blasts) and cyclohexanone. It has detection limits in the parts-per-trillion to parts-per-quadrillion range and has the ability to reveal vapour plume dynamics. The team used the device as expert trainers were training and testing their dogs and the technology revealed that handlers were making mistakes during training. For example, in one test where the handlers believed they were presenting their dogs with 28 envelopes that were tainted with traces of the potent explosive RDX (trinitroperhydrotriazine) and 68 untainted controls, the researchers found that only 27 of the envelopes were actually tainted with the explosive and that six of the controls were carrying enough of the explosive residue to be detected by the dogs. This meant that on six occasions when dogs (correctly) identified the presence of the explosive on control envelopes they were treated as if they had made an error when they truly had not. You can read more in The Economist article that I wrote on this here.  

Origin of filter feeding in whales

Once sharp and pointy. Image courtesy of NOAA.

Once sharp and pointy.

Image courtesy of NOAA.

Archaeopteryx played a pivotal part in revealing one of the greatest transitions in the history of life when dinosaurs took to the skies and fluttered away. There are not many transitions that can quite rival that evolutionary moment but, if there is one, it is the journey that the terrestrial ancestors of whales made into the sea. How the largest mammals on the planet came to lead the lives that they do today is a matter that is much shrouded in mystery. More specifically, how the blue whale and its kin ended up filtering tiny organisms out of the water with fibrous baleen when they started with sharp and pointed teeth is a subject of tremendous debate. Now a new fossil find is doing for baleen whales what Archaeopteryx did for birds by providing the first glimpse of an animal that was in the midst of a remarkable transition.

To say that the origins of baleen are controversial is an understatement. One hypothesis suggests that teeth were lost during a suction-feeding stage of whale evolution and that baleen evolved thereafter. The other suggests that baleen evolved before teeth were lost. The new fossil solidly supports the second argument. The new species, named Coronodon havensteini, dates to the Oligocene epoch roughly 30 million years ago and has an astonishing mouth. While most of its teeth indicate that it captured large prey, its broad lower molars frame narrow slots that look like that had to have been used for filter-feeding. This notion is further supported by the fact that, structurally, the rest of specimen looks like an ancient relative of the filter feeding branch of the whale family. Given this, the researchers are arguing that filter-feeding was preceded by predatory feeding, and that suction-feeding (which is seen in a few whales) evolved separately within a group that was removed from modern baleen whales. You can read more in The Economist article that I wrote on this here.

Antarctic monster

That antibiotic use fuels the rise of resistance in bacterial populations is well understood. What is less well understood is where the antibiotic resistant genes come from in the first place. Some have argued that modern antibiotic resistant traits have evolved when bacterial populations come under intense selective pressure from drugs. Others have argued that antibiotic resistant traits have always been present in wild bacterial populations and that as human use of drugs has increased this has driven the distribution of these traits to dramatically rise. Now the discovery of a worryingly resistant bacterium from Antarctica is providing strong support for the argument that resistant traits have always been around.

Antibiotic contamination in Antarctica is almost nothing. Yes, it is possible that a bacterium from a more antibiotic contaminated region of the world could migrate there through the sea, the rain or human activity but this is widely viewed as unlikely. It is for this reason that the discovery of an unstoppable bacterium on the frozen continent is so surprising.  

The species that has been found belongs to the genus Pseudomonas, the group that contains the highly troublesome Pseudomonas aeruginosa that routinely causes lethal resistant infections in nursing homes and hospitals. Yet, while P. aeruginosa is found all over the developed world and has had ample exposure to antibiotics over the years, the new species, creatively named 6A1, has never been seen by science before and appears to only occur in Antarctica. 

If 6A1 was only resistant to one or two antibiotics, that would not be particularly noteworthy but this is not the case. The bug is resistant to a lot of antibiotics and extremely resistant to a number of the best drugs on the market today. I won't get into all the details here, but its resistance to the common antibiotics amoxicillin and cefoxitin was far greater than that seen in P. aeruginosa. Resistance to erythromycin was ten times greater than that seen in P. aeruginosa. Worse, against ertapenem, a state of the art last resort antibiotic, the new species proved 180 times more resistant than P. aeruginosa.

Let us all hope that 6A1 remains sequestered in Antarctica for a very very long time.

This research published online in Polar Biology and, while I could not weave it into the science section of The Economist, you can view the original peer reviewed paper here

Stand at attention

He's paying more attention this way. Image courtesy of Rama.

He's paying more attention this way.

Image courtesy of Rama.

A new study is revealing that people are able to more quickly solve problems that test their ability to pay attention while standing up than when sitting down. This flies in the face of the long held notion that standing up requires us to pay a little bit of attention to keep our balance and that this, in turn, interferes with our ability to entirely pay attention to other matters. It is also this wrongheaded logic that has guided important exams to be taken sitting down. As it turns out, if we were take such exams standing up we'd probably perform better.

Academically, this finding suggests that a great many psychological experiments that have been conducted in the past would yield different results if participants in them were take engage in such experiments while sitting down. It will be interesting to see how the psychological community responds to this. You can read more in The Economist article that I wrote on this here,

The enemy of my enemy

Strains of antibiotic resistant tuberculosis are becoming more common and it is expected that nearly half of all cases of the disease will survive exposure to traditional front line drugs by 2050. This is driving an intense search for drugs that can bypass the resistances that are commonly seen arising in tuberculosis. Now a team is revealing that they have found a compound produced by another species of bacterium that regularly infects human lungs that looks like it has tremendous potential to control tuberculosis infections.

The compound in question is produced by the species Burkholderia gladioli. While exceptionally rare in most people, B gladioli thrives in the lungs of those suffering from cystic fibrosis. The reason the team behind the new research was attracted to this species is because, once it establishes itself in the lungs, it does an astounding job of making sure that no other bacteria encroach on its turf. This suggested that the species was producing compounds that had the potential to inhibit the growth of competition and this is precisely what the team discovered when they took a closer look. You can read more in The Economist article that I wrote on this here.


Street smart birds

Perfect pest-proofing material. Image courtesy of SillyPuttyEnemies.

Perfect pest-proofing material.

Image courtesy of SillyPuttyEnemies.

Six years ago a team revealed that the nests of birds that had cigarettes woven into them were less likely to contain blood sucking parasites than the nests of birds that did not have cigarettes in them. Further testing revealed that the nicotine content in the butts played a key part in keeping the parasites away. I wrote that up in Nature at the time and pointed out that the team behind the research did not really know if city birds were doing this by accident or had actually worked out that cigarettes were a valuable tool for use when parasites came to their nests. Now that same team is revealing evidence that the birds know perfectly well what they are doing.

Precisely why birds bring cigarettes to their nests is a matter of debate. Some argue that they collect discarded butts simply because they resemble natural materials like twigs while others argue that they know the butts repel parasites. To test out this latter idea, the team monitored house finch behaviour as they added either dead or living parasites to their nests. When live parasite numbers increased, female finches collected more butts for their nests than females that had dead parasites added. You can read more in The Economist article that I wrote on this here. Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do so here.

Simulating the smell of death

Cells sometimes intentionally kill themselves off even if they are not diseased are harmed. This often occurs during normal development (like the forming of fingers in embryos from an initially fin-like appendage). When cells die in this way, bits of them circulate and tell the immune system that their death has been an intentional and somewhat peaceful affair. This is staggeringly different from when cells die during infection. Under those circumstances, their dead fragments usually trigger a powerful immune response that creates intense inflammation. While initially useful, inflammation impairs healing if it lasts for too long. This has led to a lot of research into how inflammation can be better controlled with drugs. Now a team is revealing that they have found a way to do this by releasing compounds into the body that look an awful lot like the fragments of cells that intentionally killed themselves in a peaceful manner.  You can read more in The Economist article that I wrote on this here.

Many snake venom antidotes do not work

Saw-scaled vipers are difficult to spot as they tend to be active at night, have venom that drives people to suffer catastrophic internal haemorrhages and live in places where medical care is limited. As such, it is not surprising that they kill an awful lot of people. Antivenoms are widespread and available where these snakes are found but a team of researchers studying survival data noticed that people were still often dying even if they got the antivenom in time. Concerned and confused, the researchers ran an analysis of antivenom performance against venom milked from a number of the vipers and discovered that many of the antivenoms on the market simply do not work in regions where advertising says they should.

Are we sure we have the right antidote on hand? Image courtesy of Shantanu Kuveskar

Are we sure we have the right antidote on hand?

Image courtesy of Shantanu Kuveskar

The key issue at hand here is the fact that antivenoms are produced using venom and venom varies from snake to snake, sometimes even within the same species. So, if an antivenom is produced using a species of saw-scaled viper found in both India and Pakistan but only snakes from Pakistan have their venom collected for the creation of the drug, there is chance that the antivenom will not work very well (or at all) when used to treat snake bites in India. This is precisely what appears to have happened and the harm to people in Asia and Africa looks like it is quite significant.

Some of the antivenom companies that I spoke with were remarkably receptive to these findings. One clearly stated that they are going to re-label their bottles immediately so their drugs are only delivered to places where they do actually work. Another stated that they are going to start milking vipers from more regions to build better antivenoms. However, not all is rosy. One company flatly denied that they manufacture a very poorly performing antivenom that is advertised on their own website and another argued that the findings of the researchers were flawed.  You can read more in The Economist article that I wrote on this here.

Not born with bad teeth

Cavities are one of the most problematic chronic oral diseases suffered by children and, for decades, the assumption has been that those who develop severe cavities largely have bad luck by inheriting genes that make their teeth vulnerable to the condition. Now a new study is revealing that this notion is nonsense.

The researchers behind the new work examined the role of genetics, environment, and disease on the composition of the bacteria and fungi that live in the mouth in a whopping 485 pairs of twins. They found that while there are several species of bacteria that are heritable (or prone to grow in mouths due to heritable conditions), these species play little or no part in the formation of cavities.  

These findings prove that chronic cavities have to be almost entirely the result of bad eating behaviours and not down to inherited "bad" oral microbiology. On the larger scale, we are seeing loads of cardiovascular, immunological and respiratory diseases (including several cancers) that have strong connections to the composition of the bacterial bugs living in the gut. Some recent papers show that oral microbiota are important here too and, if that is so, then diet looks very important for preventing or controlling these diseases too while genetics look largely unimportant. You can read more in The Economist article that I wrote on this here.

Return of rain mouse

In 2014, I reported a remarkable find in The Economist where researchers used a sleeping sickness drug to treat mice suffering from the rodent equivalent of autism. Administration of the drug, known as suramin, caused the autism traits to fade away over a matter of weeks. Similarly, as the drug treatment ended, the autistic traits came back. It was astonishing stuff but my editor and I were cautious in our reporting since what works in mice often does not work in men. Well, humans trials have now finished and the findings suggest that suramin has tremendous potential.

What works in mice is now working in men. Image courtesy of Aaron Logan.

What works in mice is now working in men.

Image courtesy of Aaron Logan.

Like all first trials in humans, this one was small with just ten patients. All were autistic boys. Half were given a placebo and half were given suramin. The participants went through numerous tests throughout the treatment to monitor their behaviours and tease out whether the grip that autism had on them was weakened. All five of the kids who were given the suramin showed substantial gains while the drug was given while none of the children given the placebo did.

Obviously, this is a big deal since there is currently no drug available for treating autism but what these findings suggest from a biochemical perspective is perhaps even more important. Suramin gums up purine receptors on cells and prevents neurons (cells in the brain) in particular from entering what is known as the cellular danger response. While in this defensive mode, neurons become more resistant to a wide range of diseases but stop making connections with other neurons. This is not really a problem when someone is ill for a few days or weeks but the theory with autism is that patients with the condition have neurons that permanently get stuck in the danger response and can't stop responding to purine stimulation. The fact that suramin improves language and social skills in autistic patients while simultaneously decreasing repetitive behaviours suggests that the theory of the cellular danger response being a central cause of autism is likely correct.  

This work has to be replicated before we can take it too seriously but the fact that what works in mice is working in autism sufferers is really something extraordinary. You can read more in The Economist article that I wrote on this here.

How air pollution causes heart disease

That people chronically exposed to severe air pollution develop lung diseases is entirely logical. However, what has been a conundrum is why such patients often succumb to heart disease. Some researchers have theorised that many of the tiny particles found in air pollution are capable of migrating from the lungs to the blood vessels around the heart but evidence for this has been extremely thin. Now a new study is revealing that this is absolutely true. Indeed, the findings are worse than anyone could have imagined, showing that pollutant particles are actually attracted to blood vessels suffering from the sort of inflammation that is typically caused by plaques that build up over years of unhealthy eating. You can read more in The Economist article that I wrote on this here.

Moth larvae that eat plastic

The future of recycling? Image courtesy of D. Hobern.

The future of recycling?

Image courtesy of D. Hobern.

Plastics carry a heavy environmental impact. While roughly 26% of plastic materials are recycled and 36% are burned for purposes of energy recovery, 38% end up lingering in landfills. While many attempts have been made to get various strains of fungi and bacteria to eat this junk, success has been limited due to the colossal amount of time that it takes these tiny organisms to chew plastic up. Now a new experiment is revealing that a far better way forward would be to put moth larvae to the task.

The team behind the new work thought up their experiment while they were studying the moth species Galleria mellonella which is fond of laying its eggs inside the hives of honey bees and chewing up beeswax. Since beeswax and plastic are structurally not too different, the researchers decided to put the larvae on plastic and monitor their behaviour. Remarkably, holes started to appear in 40 minutes. The authors are arguing that the discovery lays the basis for the development of biotechnological applications that could play a pivotal role in management of plastic waste and, frankly, I'm inclined to agree with them. You can read more in The Economist article that I wrote on this here.  Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do so here.

Bacterial brain benefits

We know from work done on mice raised in entirely sterile environments that an absence of healthy bacteria leads to changes in how the blood–brain barrier functions. This matters because the barrier plays a critical part in keeping out materials and pathogens that have no business hanging around in the brain. In contrast, administration of probiotics has been shown to restore both intestinal function and brain chemistry. Given these findings, researchers have speculated that concurrent treatment of probiotics while patients are taking antibiotics should ameliorate the damage caused by the antibiotics but evidence for this has been thin. Now a new study conducted in mice is revealing that this is something that is well worth further attention. 

In the new work, researchers dosed baby mice with penicillin one week before birth and then continued giving it to them until they weaned. Throughout this process, they simultaneously monitored the bacteria in their guts, their behaviour and the integrity of their blood brain barriers. Remarkably, they found that, like mice raised in completely sterile environments, the antibiotic-treated mice had lasting changes in the bacteria found in their guts, modified blood brain barrier integrity and showed behavioural changes like increased aggression and reduced sociality. More importantly, they found that the use of probiotics partially prevented these negative effects. You can read more in The Economist article that I wrote on this here.