Methicillin-resistant Staphylococcus aureus (MRSA) is very difficult to kill. This notorious “superbug” can withstand a broad and growing range of antibiotics, and is the leading cause of hospital infections in many countries. But it’s not restricted to hospitals. According to studies coming in from all over the world, MRSA has found a new route into our bodies -piggyback.

Pig farms throughout the world have become breeding grounds for strains of MRSA that can jump from swine to humans. These strains have already been isolated in the Netherlands, Denmark and Canada, and now, the latest study adds the USA to that list. The research was led by Tara Smith from the University of Iowa, who I know as a Scibling and who many of you will recognize as the author of the excellent Aetiology blog.

Smith found widespread traces of MRSA in two different production systems in the states of Iowa and Illinois. Within the nostrils of 49% of pigs and 45% of pig farmers, her team detected traces of the “superbug” (although it’s worth noting that none of the farmers had experienced any actual infections). Piglets had the highest rates of infection and in fact, every single pig under the age of 12 weeks harboured MRSA colonies.

The high levels of the bacterium in both man and pig suggest that it can spread readily between the two species. To MRSA, both four leg and two legs are good…

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It’s been a big week. With a simple words, Barack Obama became the first black President of a country whose history has been so haunted by the spectre of racial prejudice. His election and inauguration are undoubtedly proud moments but they must not breed complacency. Things may be changing outwardly, but problems remain.

For a start, it goes without saying that many people, even the most liberal and left-wing among us, still harbour unconscious prejudices against members of other races. These “implicit biases” may be hidden, but their effects are often not. For example, a study published last year showed that unconscious biases can hold greater sway over a person’s voting decisions than their conscious, rational preferences.

Their influence becomes apparent even when we simply look at people of other races. It’s a well-known fact that people generally find it more difficult  to distinguish between the faces of people from other ethnic groups than those of their own. This so-called “other-race effect” is the phenomenon behind claims that “they all look the same”. But looks are in the eye of the beholder and the other-race effect can be negated through experience with members of different races. For example, African infants who are adopted by white families develop a bias in distinguishing between faces that matches those of white children.

Sophie Lebrecht from Brown University sensed a link between poorer facial discrimination and greater racial discrimination. Her idea is simple: if someone finds it hard to tell the difference between people of a certain race, they will be more likely to characterise that entire group with broad stereotypes. When the lines between individuals blur, generalities start seeping in and implicit biases have a stronger influence. But if that’s the case, there may be a way around it – indeed, Lebrecht found that by training people to better discriminate between faces of other races, she could help to reduce their biased attitudes towards those races.

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The area collectively known as Austronesia covers half the globe. It stretches from South-East Asia and Taiwan, across New Guinea and New Zealand, to the hundreds of small islands dotted around the Pacific. Today, it is home to about 400 million people.

They are the descendants of early humans who spread throughout the Pacific in prehistoric times. These forebears are long dead but they left several unexpectedly important legacies that are evident in their modern descendants. The languages they used evolved and splintered into over 1,200 tongues spoken by modern Austronesians. The bacteria in their bodies did the same, giving rise to distinct strains in different parts of the region.

Two new studies have used these very different hitchhikers – one cultural and one biological – to piece together the routes of this ancient mass migration. And they have come to the same general conclusion.  

The Austronesian people originated in Taiwan some 5,000 years ago. After a few centuries of settlement, they started a massive pulse of migration, spreading southwards and eastwards. They moved to the Philippines, dispersed across South-East Asia, and spread as far west as Madagascar and as far east as the Micronesian islands. They reached Fiji and other islands in Western Polynesia about 3,000 years ago and there, they paused again. About 1,500 years ago, they started a second big migration pulse that took them east across the Pacific all the way to Easter Island.

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The blood that flows into our heads is obviously important for it provides nutrients and oxygen to that most energetically demanding of organs – the brain. But for neuroscientists, blood flow in the brain has a special significance; many have used it to measure brain activity using a technique called functional magnetic resonance imaging, or fMRI.

This scanning technology has become a common feature of modern neuroscience studies, where it’s used to follow firing neurons and to identify parts of the brain that are active during common mental tasks. Its use rests on the assumption that the flow of blood (“haemodynamics” to those in the know) is a decent enough stand-in for the firing of neurons – the latter creates a shortage of nutrients and oxygen that is corrected by the former.

But Yevgeniy Sirotin and Aniruddha Das from Columbia University have found that this assumption might not be entirely valid. They used a new technique to independently measure and compare nerve activity and blood flow in the brains of live monkeys. Sure enough, they found a blood flow pattern that reliably matched the activity of the animals’ neurons.

But they also spotted something that no one has seen before – a second haemodynamic signal, of equal strength to the first, that didn’t correspond to any local brain activity. This second signal was not a sign of parts of the brain that are active, but those that may need to be active in the near future. It seems that if the brain expects a task in the future, it can anticipate which of its regions will be needed and flush them with blood in preparation.

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If the sound of eating dung all your life doesn’t sound that appealing to you, you’re not alone. A beetle called Deltochilum valgum shares your distaste, which is quite surprising given that it’s a dung beetle.

There are over 5,000 species of dung beetle and almost all of them feed mainly on the droppings of other animals (and more specifically, on the rich supply of bacteria they contain). D.valgum is the black sheep of the family, the only one that has abandoned the manure-based diet of its fellows and taken to hunting live meat for a living. 

D.valgum lives in the lowland rainforests of Peru, and stalks the forest floor looking for its favoured food – millipedes.  Having evolved from dung-rolling ancestors, D.valgum lacks the killing mouthparts that grace the heads of wasps, mantises or tiger beetles. Instead, they use a sharp, shield-like plate on the top of their heads like a chisel to decapitate their prey.

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Whalefishes, bignoses and tapetails – these three groups of deep-sea fishes couldn’t look more different. The whalefishes (Cetomimidae) have whale-shaped bodies with disproportionately large mouths, tiny eyes, no scales and furrowed lateral lines – narrow organs on a fish’s flanks that allow it to sense water pressure.

The tapetails (Mirapinnidae) are very different – they also lack scales but they have no lateral lines. They have sharply angled mouths that give them a comical overbite and long tail streamers that extend to nine times the length of their bodies.

The bignoses (Megalommycteridae) are very different still – unlike the other two groups, they have scales, their mouths are small and their noses (as their name suggests) are very large.

Based on these distinct bodies, scientists have classified these fishes into three distinct families. Now, it seems they are wrong. Amazingly enough, the three groups are all just one single family – the tapetails are the larvae, the bignoses are the males and the whalefishes are the females. The entire classification scheme for these fishes needs to be reworked, as many distinct “species” are actually different sexes or life-stages of the same animal.

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People seem inordinately keen to pit nature and nurture as imagined adversaries, but this naive view glosses over the far more interesting interactions between the two. These interactions between genes and environment lie at the heart of a new study by Rose McDermott from Brown University, which elegantly fuses two of my favourite topics – genetic influences on behaviour and the psychology of punishment.

<Regular readers may remember that I've written three previous pieces on punishment. Each was based on a study that used clever psychological games to investigate how people behave when they are given a choice to cooperate with, cheat, or punish their peers.

McDermott reasoned that the way people behave in these games might be influenced by the genes they carry and especially one called monoamine oxidase A (MAOA), which has been linked to aggressive behaviour. Her international team of scientists set out to investigate the effect that different versions of MAOA would have in a real situation, where people believe that they actually have the chance to hurt other people.

MAOA encodes a protein that helps to break down a variety of signalling chemicals in the brain, including dopamine and serotonin. It has been saddled with the tag of “warrior gene” because of its consistent link with aggressive behaviour. A single fault in the gene, which leads to a useless protein, was associated with a pattern of impulsive aggression and violent criminal behaviour among the men of a particular Dutch family. Removing the gene from mice makes them similarly aggressive.

These are all-or-nothing changes, but subtler variations exist. For example, there is a high-activity version of the gene (MAOA-H), which produces lots of enzyme and a low-activity version (MAOA-L), which produces very little. The two versions are separated by changes in the gene’s “promoter region”, which controls how strongly it is activated.

A few years ago, British scientists found that children who had been abused are less likely to develop antisocial problems if they carry the MAOA-H gene than if those who bear the low-activity MAOA-L version. An Italian group has since found the same thing. It is a truly fascinating result for it tells us that the MAOA gene not only affects a person’s behaviour, but also their reactions to other people’s behaviour.

But both studies had a big flaw – they measured aggression by asking people to fill in a questionnaire. Essentially, they relied on people to accurately say how belligerent they are and we all know that many people like to talk big. McDermott wanted to look at actions not claims.

To that end, she recruited 78 male volunteers and sequenced their MAOA gene to see which version they carried (just over a quarter had the low-activity version). The volunteers played out a scenario where they believed that they could actually physically harm another person for taking money that they had earned. Their weapon of retribution? Spicy sauce.

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You swallow the pill. As it works its way through your digestive system, it slowly releases its chemical payload, which travels through your bloodstream to your brain. A biochemical chain reaction begins. Old disused nerve cells spring into action and form new connections with each other. And amazingly, lost memories start to flood back.

The idea of a pill for memory loss sounds like pure science-fiction. But scientists from the Massachussetts Institute for Technology have taken a first important step to making it a reality, at least for mice.

Andre Fischer and colleagues managed to restore lost memories of brain-damaged mice by using a group of drugs called HDAC inhibitors, or by simply putting them in interesting surroundings.

They used a special breed of mouse, engineered to duplicate the symptoms of brain diseases that afflict humans, such as Alzheimer’s. The mice go about their lives normally, but if they are given the drug doxycycline, their brains begin to atrophy. The drug switches on a gene called p25 implicated in various neurodegenerative diseases, which triggers a massive loss of nerve cells. The affected become unable to learn simple tasks and lose long-term memories of tasks they had been trained in some weeks earlier.

Fischer moved some of the brain-damaged mice from their usual Spartan cages, to more interesting accommodation. Their new cages were small adventure playgrounds, replete with climbing frames, tunnels and running wheels, together with plentiful food and water. In their new stimulating environments, the mice returned to their normal selves. Their ability to learn improved considerably, and amazingly, seemingly lost memories were resurrected.

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Bee hives, with their regularly arranged honeycombs and permanently busy workers may seem like the picture of order. But look closer, and hives are often abuzz with secret codes, eavesdropping spies and deadly alliances.

African honeybees are victimised by the parasitic small hive beetle. The beetles move through beehives eating combs, stealing honey and generally making a mess. But at worst, they are a minor pest, for the bees have a way of dealing with them.

They imprison the intruders in the bowels of the hive and carefully remove any eggs they find. In turn, the beetle sometimes fools the bees by acting like one of their own grubs, and gets a free meal instead of imprisonment. In Africa, both species have found themselves in an evolutionary stalemate.

But in 1998, American beekeepers spotted the beetle in hives of their local European-descended honeybees. These insects are gentler versions of their aggressive African relatives, and in them, the beetles found more vulnerable victims.

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Using genetic engineering, a group of scientists have developed a way of sneaking a virus past the brain’s defences. Don’t panic – this isn’t some nightmare scenario. It could be the first step to curing a huge number of brain diseases.

The brain seems incredibly well protected amid its shell of bone and cushioning fluid. But even the strongest of forts needs supply lines, and brain is no exception.

A dense network of blood vessels carries vital oxygen to its cells. These vessels are a potential vulnerable spot, providing access for bacteria and other disease-causing organisms to migrate in from other body parts.

But even these weak spots are heavily guarded. The blood vessels in the brain are lined with a tightly packed layer of cells that restrict the flow of molecules from blood to brain. These cells form a protective shield called the blood-brain barrier, or BBB.

It is a superb defence but it can do its job too well. Not only does it block out dangerous microbes, but it can also exclude large proteins and drugs designed to treat brain diseases. Usually, these large molecules need to be distributed throughout the entire brain to be effective. With the BBB in the way, they don’t stand a chance. Now, Brian Spencer and Inder Verma from the Salk Institute of Biological Studies have come up with a way to disguise helpful molecules to sneak them past the brain’s defences

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