Elections are weighing heavily on our minds. In three short months, America will see the race between Barack Obama and John McCain come to a head, while we in Britain will probably have a general election within the next few years. Some people, of course, will vote based on long-held loyalties to a specific political party, but many of us are more malleable in our choices. What affects the choices of these undecided voters?

People are given to viewing ourselves as rational beings and as such, we’d like to think that our choices are fuelled by objective and careful deliberation. So we pay attention to media coverage, we read up on policies and we listen to debates and only then, having gathered as much information as we can about the various options, do we make a choice. That’s how it plays out in our heads, but according to a new study, the reality may be quite different.

Silvia Galdi at the University of Padova, Italy, has found evidence that the final verdicts of undecided decision-makers are only weakly related to their conscious preferences and more strongly influenced by unconscious views and biases they aren’t aware of. In many cases, when people claim that they are undecided, they have secretly made up our minds, unbeknownst even to themselves.

For example, a British voter sitting on the fence might unconsciously be inclined to vote for David Cameron because they view Gordon Brown as dour, or oppositely because of a prejudice against the Tory party. Likewise, and more unfortunately, an American voter might side with John McCain because of unconscious racial prejudices against black people.

By their very nature, there unconscious associations aren’t easy to find, but psychologists have a tool for doing so – implicit association tests. Volunteers are shown a series of words or images and must classify them into one of two categories by pressing assigned keys. For example, they might have to distinguish good words (happy, joy) from bad words (anger, hate) and white faces from black faces. At first, the categories are presented separately and then in various combinations. So in one trial, you might be asked to press one key for good words and black faces and the other key for bad words and white faces.

The idea is that people perform the task more quickly and more accurately if the combinations of categories matches their unconscious associations between the two categories. So if people have a hidden prejudice against black people, they would be quicker at trials where black faces and bad words were represented by the same key, than those where black faces were twinned with good words. If you want to see these tests in action, Harvard have a large range online and I’d highly recommend having a go yourself.

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Owls may be are known for their trademark hooting noises, but a new study shows that they don’t just rely on sound for communication. With some species having very large and sensitive eyes, you might expect that they would use visual signals too and that’s exactly what a pair of Spanish biologists have found. Vincenzo Penteriani and Maria del Mar Delgado studied the eagle owl, and found that it marks its territories by recycling its meals – in more ways than one.

The eagle owl is the world’s largest and is found in mountains and hilly forests throughout Europe and Asia. As breeding pairs prepare to raise a brood of chicks, various landmarks around their nest become streaked with brilliantly white marks that are noticeable from some distance away. Some of these are streaks of droppings (“faecal posts”) and others are collections of matted feathers, plucked from dead birds (“plucking sites”).

Through a series of clever observations, Penteriani and Delgado showed that these streaks are the equivalent of owl police-tape, delineating the borders of their territory and acting as clear keep-out signs to other owls.

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I like anniversaries and it’s a good month for them.
Last Wednesday marked two years since I started Not Exactly Rocket Science at its humble WordPress beginnings.
Next Monday marks six months of blogging at ScienceBlogs.
And that last article on face recognition is the 300th post I’ve written for this blog!
A massive thanks to everyone who reads this blog, links to it and comments on it; to Ginny, Erin and the rest of the team at ScienceBlogs and SEED; to my fellow Sciblings for support and encouragement; and to Mike and Dennis for their SuperReaders skillz.
Writing here is one of the most fulfilling things I get to do and I hope to stick with it for many years to come.
Ed

When you look at someone’s face, what part do you concentrate on? Common wisdom has it that the eyes are the focal point of the face and they are the features that draw attention first. But according to a new study, that may not be universally true – while Western cultures do fixate on the eyes, East Asians tend to focus on the nose.

We owe a lot of our knowledge about the way we look at images to a Russian psychologist Alfred Yarbus. He was the first scientist to carefully record the subtle eye movements that people make when they take in a view. Yarbus’s experiments showed that our gaze rapidly flicks back and forth across an image so that our centre of vision focused on the most important parts. For example, while surfing websites, our eyes tend to focus on headings, words at the top of the page and words on the left.

The same thing happens when we look at faces. Previous studies have found that viewers tend to flick their gaze between the eyes and the mouth – an inverted triangle of important features. Some psychologists have taken this to mean that humans have a single, universal and innate strategy for processing faces. But this conclusion has a big snag – it’s only really based on experiments done with Western populations.

To get a more cross-cultural perspective, Caroline Blais and colleagues at the University of Glasgow tracked the eye movements of fourteen white Western students and fourteen East Asians, eight of whom were Chinese and six of whom were Japanese. The East Asian volunteers were all students who had recently enrolled in the university and had never been to a Western country before.

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Strip away the trendy clothes, the shiny ornaments and the cosmetically enhanced body parts and consider the naked human body. Free of decorations and distractions, what makes one body more attractive than another? According to one group of scientists, symmetry is part of the answer. William Brown and colleagues at Brunel University found that both men and women fancied symmetrical bodies over asymmetrical ones.

Many animals naturally develop asymmetric body parts; just look at the massive claw of the fiddler crab or the distorted Picasso-like face of the flatfish. But most mismatches are subtler. As a symmetrical animal develops, it is buffeted by outside forces – infections, environmental hardships and the like – that can lead to small differences between its two halves.

These small differences are known as “fluctuating asymmetries” and the theory goes that fitter and healthier individuals are better at buffering themselves against the stresses that produce them. The perfectly mirrored halves of these fittest of individuals are testament to their quality as mates, reflecting both their developmental past and their functional present. For example, symmetrical legs and hips can be signs of steady development, while also bestowing their owners with greater speed and better coordination.

This idea isn’t new, but it’s still hotly contested. While there is some evidence that it applies to our faces, two previous studies found no connection between asymmetry and attractiveness in our bodies. But measuring attractiveness in humans isn’t a simple matter; we are so easily swayed by clothing, skin colour, hairstyles and facial appearances. To get round this problem, Brown worked not with real humans, but with wireframe images.

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People in most parts of the world are living longer and longer, thanks to great leaps in medicine and sanitation over the last century. But these growing life expectancies bring with them a sense of unease. The biggest worry is the possibility that medical advances are artificially prolonging life with little regard for its quality. Old age, after all, brings with it an increased risk of chronic diseases such as cancer, as well as both physical and mental decline.

This is not just a moral question, but an economic one too. The “oldest-old” are the fastest growing demographic in Western countries. If this expanding part of the population is indeed becoming more and more dependent on care from relatives or the state, the costs to society will start to skyrocket. But new research from Denmark suggests that this grim vision of the future is a fictitious one.

Kaare Christensen and colleagues from the University of Southern Denmark found that the proportion of elderly Danes who manage to remain independent holds steady at about 30-35 percent between the ages of 90 to 100. Individual people certainly risk losing their independence as they get older but the unhealthiest ones tend to pass away earlier despite improvements in medicine. This means that from society’s point of view, exceptional long-life won’t lead to exceptional levels of disability.

The scale of Christensen’s study is unprecedented. It exploited the fact that Denmark has kept a record of everyone living in it since 1968. Each person is assigned with a 10-digit identification number that links all their information across official registries. In 1998, Christensen’s team used this resource to contact every one of the 3,600 people who were born in Denmark in 1905 and were still alive.

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They say that memory declines as age marches on, but that only applies to neurons – the immune system has a very different sort of memory and it stays fresh till the end of life. To this day, people who survived the 1918 flu pandemic carry antibodies that can remember and neutralise the murderous strain.

The 1918 influenza virus was the most devastating infections of recent history and killed anywhere from 20 to 100 million people in the space of two years. Ironically, it seems that the virus killed via the immune system of those infected. It caused immune cells to unleash a torrent of signalling chemicals – cytokines – that recruited other immune cells to the fray. These too started signalling and the resulting “cytokine storm” rages out of control.

This probably explains why the 1918 flu took such a heavy and unexpected toll on the young and healthy. Their strong immune systems would have done them little good against a virus that kills by causing those same systems to overreact. Nonetheless, many children managed to fight off the infection and they are still alive to tell the tale.

Xiaocong Yu from the Vanderbilt University Medical Center and Tshidi Tsibane from the Mount Sinai School of Medicine managed to track down 32 of these lucky survivors. Today, the youngest of the group is 91 and the oldest have seen their first century come and go. During the time of the pandemic, they could all remember one of their family being sick, making it likely that they themselves had been directly exposed to the usually lethal infection. And even though 90 years had passed, every single one of these people was still immune to the virus. To this day, their blood samples can neutralise it.

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Imagine reading the paper to find that a new wonder drug has been created that could save your life, if only you could afford it. Alternatively, put yourself in the shoes of the authorities that must decide not to offer powerful new drugs on the NHS because they simply aren’t cost-effective enough. These situations are all too common-place and are often due to the extremely high costs of drug development. But a couple of years ago, scientists at Icon Genetics and Bayer Bioscience made an exciting step toward lowering these costs for some of the most promising new treatments.

The treatments in question are called ‘monoclonal antibodies’ or ‘MAbs’, synthetic versions of the natural antibodies that our immune systems use to identify and neutralise infectious agents. MAbs are specially shaped to act like molecular gloves, sticking onto a target of choice and inactivating it by blocking interactions with other molecules.

The most famous member of this group, the breast cancer drug Herceptin, is one of a handful of currently available MAbs. But they are about to be joined by many more – over 150 MAbs are in development and the market for them is likely to exceed £10 billion.

But no matter how good these new biotechnological wunderkinds are, they will be worthless unless they reach the patients they are designed to benefit. And with the cost of treatment courses exceeding tens of thousands of pounds, that is looking unlikely. Every stage of the manufacturing process from raw materials to equipment is exorbitantly expensive and drives the inflated prices of the end product. As such, only better, cheaper and more effective production methods will enable scientists to fully realise the potential of these designer molecules. A new technique called ‘magnifection’ could be just such a method.

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Hey folks, I’ve got a feature article in this week’s New Scientist, which is my second for the magazine.  The article describes the story of FOXP2, the “language gene” that’s not really a language gene.

The story started a few years ago, when a group of scientists led by Simon Fisher found that a single genetic mutation was responsible for an inherited language disorder in a British family called KE. The gene in question – FOXP2 – was quickly touted as a “gene for language” by an overenthusiastic and sensationalist media.

Since then, researchers have probed the true nature of FOXP2 using disciplines from evolutionary biology to neuroscience to genetics, and species including humans, mice, finches and bats. And amid this growing body of surprising results, it’s now clear that the “language gene” epithet is far too simplistic.

FOXP2 is hardly a unique human innovation; it’s found in a huge variety of other animals. Nor has it changed beyond all recognition in our genome; instead it is incredibly heavily conserved, with the human and chimpanzee versions bearing only two small differences. It’s role is not specific to language, nor even to communicaiton in general; it’s probably part of an ancient system involved in learning and producing complex patterns of movement.

It’s a really interesting body of work, and definitely the most difficult thing I’ve had to write so far. It was an attempt to debunk a lot of the nonsense surrounding the gene, and I’m very pleased with how it turned out. I even had the chance to interview Simon Fisher, who led the team who first identified FOXP2, and Svante Paabo, who’s done a lot of the work on mice (and Neanderthals!).

Here’s the start and end of the piece. For the middle, you need access to New Scientist. Or you could email me and I’ll send you a sneaky copy

IMAGINE an orchestra full of eager musicians which, thanks to an incompetent conductor, produces nothing more than an unrelieved cacophony. You’re starting to appreciate the problem faced by a British family known as KE. About half of its members have severe difficulties with language. They have trouble with grammar, writing and comprehension, but above all they find it hard to coordinate the complex sequences of face and mouth movements necessary for fluid speech. Thanks to a single genetic mutation, the conductor cannot conduct, and the result is linguistic chaos. In 2001, geneticists looking for the root of the problem tracked it down to a mutation in a gene they named FOXP2. Normally, FOXP2 coordinates the expression of other genes, but in affected members of the KE family, it was broken.

It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 “the language gene” or the “grammar gene”. Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited – the discovery sparked a frenzy of research aiming to uncover the gene’s role.

Several years on, and it is clear that talk of a “language gene” was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. “When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language,” recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours. “It gives us a really important lesson,” says Fisher. “Speech and language didn’t just pop up out of nowhere. They’re built on very highly conserved and evolutionarily ancient pathways.”

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The FOXP2 story has already taught us important lessons about evolution and our place in the natural world. It shows that our much vaunted linguistic skills are more the result of genetic redeployment than out-and-out innovation. It seems that a quest to understand how we stand apart from other animals is instead leading to a deeper appreciation of what unites us.

What would you do if someone asked you to help transcribe an old book onto a website? Chances are, you’d say no on the basis that you have other things to do, or simply that it just doesn’t sound very interesting. And yet, millions of people every day are helping with precisely this task, and most are completely unaware that they’re helping out.

It’s all thanks to a computer program developing by Luis von Ahn and colleagues at Carnegie Mellon University. Their goal was to slightly alter a simple task that all web users encounter and convert it from wasted time into something productive. That task – and you will all have done this before – is to look at an image of a distorted word and type what it is in a box. It often turns up when you’re trying to post on a blog or sign up for an account.

The distorted word is called a CAPTCHA and, playing fast and loose with the spirit of acronyms, it stands for “Completely Automated Public Turing test to tell Computers and Humans Apart”. Their point is to make users prove that they are human, because modern computer programs cannot discern the distorted letters as well as humans can. The CAPTCHAs are visual sentinels that protect  against automated programs that would otherwise overbuy tickets for sale at inflated prices, set up millions of fake email accounts for spamming or inundate polls, forums and blogs with comments.

They have become so commonplace that von Ahn estimates that people type in over 100 million CAPTCHAs every day. And even though the goals of improving web security is a worthwhile one, these efforts add up to hundreds of thousands of hours that are effectively wasted on a daily basis. Now, von Ahn’s team have found a way of tapping this effort and putting it to better use – to help decipher scanned words, and usher old printed books into the digital age.

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