In 2007, Jan Souman dropped three volunteers into the Sahara desert and watched as they walked for several miles, in an attempt to walk in a straight line. Souman was interested in the widespread belief that lost travelers end up walking in circles, a belief that has never been properly tested but has nonetheless become firmly entrenched in the popular consciousness. Just think about Frodo and Sam’s hike through Mordor or the three hapless teens in the Blair Witch Project.

To see how non-fictional humans would fare, Souman tracked a group of volunteers using GPS as they walked through a thick German forest or a featureless Tunisian desert, as well as others who strolled through a large field blindfolded. The result: they did indeed go in circles but with no preference for any direction and only when they couldn’t see or when the sun or moon weren’t visible.

It seems that with some sort of reference point, we’re entirely capable of walking in a straight line, even in a featureless desert where dunes obscure the horizon or a busy forest that’s riddled with obstacles. The sun’s good enough for these purposes, even though it’s position changes as the hours pass. Without any such cues, we quickly veer off course.

The two volunteers who walked through in the forest on a sunny day managed to keep to a perfectly straight line, wandering only in the first fifteen minutes when the sun was behind a cloud. The four people who walked on much cloudier days all ambled in circles, repeatedly crossing their own path without knowing it. The desert walkers fared about as well – those who walked during the heat of the day veered slightly but kept reasonably straight. A third man walked at night; he too kept a direct course when the moon was visible but when it vanished behind clouds, a couple of sharp turns sent him back in the direction he came from.

Scientists have put forward many explanations for the circular rambles of lost walkers. Some say that most people have one leg that’s longer or stronger than the other and over time, these differences add up to a curving course. Others say that asymmetries in our very brains set up a tendency to turn in one direction. Without a guiding light or landmark, these small biases would make their presence felt.

But Souman thinks otherwise. He set a group of 15 blindfolded people loose in a large field, told them to walk straight ahead and watched them for 50 minutes. All of them walked in very random paths, including large flamboyant loops and, on occasion, surprisingly small circles of as little as 20 metres in diameter (little enough to fit within a basketball court).

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Whether it’s a goalkeeper who needs to decide which way to dive, or a motorist who needs to swerve to avoid a pedestrian, people often have to make decisions in a small amount of time, based on a complex onrush of information. But even as their muscles launch them towards one particular fate, there is still room for indecisiveness. Arbora Resulaj from the University of Cambridge has found that people often change their decisions in the split-seconds after making them because of late-arriving information. 

Neuroscientists have come up with several possible explanations for what happens in our brains when we make decisions. For example, the popular “drift-diffusion model” looks at simple choices with two possible outcomes. Take a motorist’s decision about whether to swerve right or left to avoid a crash. They have to weigh up a lot of information: the speed of their car; the position of the pedestrian; the presence of surrounding traffic; and more.

The brain must wade through all of this noisy information and extract meaningful patterns. Once these signals pass a certain threshold – a “decision bound” – the brain commits to a choice and the car swerves either left or right.  But this simplistic model can’t account for the fact that people sometimes change their minds after decisions are made. The driver, for example, could rapidly swerve the other way. These are the last-minute changes of heart that Resulaj was interest in.

Working in the lab of Michael Shadlen (whose work I have covered before), Resulaj watched three people as they carried out a simple task, where they monitored a set of dots that each moved left or right at random. They had to decide on the overall direction of the dots and indicate their choice by moving a joystick left or right towards one of two targets.

According to the drift-diffusion model, people watch the dots until they get an overall sense of their movement. Their brains accumulate evidence until it gets enough to cross one of two thresholds – one for leftward decisions and one for rightward ones. But things weren’t so simple. On a few of the tasks, the volunteers would change their minds, initially moving towards one target but then swapping for the other. In almost all cases, this sudden swap led to the more accurate answer.

The key to the experiment was that as soon as the volunteers moved at all, the dots disappeared, effectively cutting off their supply of information. So they weren’t changing their plans based on new information. Instead, Resulaj thinks that their change of heart was driven by information that was still in transit at the time when they started to move.

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Several million years ago, at a time when dinosaurs walked the earth, a flying reptile – a pterosaur – came in for a landing. As it approached, it used its powerful wings to slow itself down and hit the ground feet first. It took a short hopping step before landing a second time. On solid ground, it leant forward, put its arms down and walked away on all fours.

The landing made quite an impression on the underlying limestone mud and in the following millennia, the creature’s tracks became fossilised. Now, they have been unearthed by Jean-Michel Mazin from the University of Lyon at a site near Crayssac in southwestern France.

The area is home to at least 30 sets of pterosaur tracks, which have earned it the nickname of Pterosaur Beach.  Some of these tracks have confirmed that some pterosaurs walked on four legs while land-bound, in the manner of many modern bats. But one bizarre set stood out to Mazin – they simply didn’t fit the typical walking gait of the French pterosaurs. The most plausible explanation is that they preserved a landing, and they’re the first set of fossils that have done so.

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In a Swiss laboratory, a group of ten robots is competing for food. Prowling around a small arena, the machines are part of an innovative study looking at the evolution of communication, from engineers Sara Mitri and Dario Floreano and evolutionary biologist Laurent Keller.

They programmed robots with the task of finding a “food source” indicated by a light-coloured ring at one end of the arena, which they could “see” at close range with downward-facing sensors. The other end of the arena, labelled with a darker ring was “poisoned”. The bots get points based on how much time they spend near food or poison, which indicates how successful they are at their artificial lives.

They can also talk to one another. Each can produce a blue light that others can detect with cameras and that can give away the position of the food because of the flashing robots congregating nearby. In short, the blue light carries information, and after a few generations, the robots quickly evolved the ability to conceal that information and deceive one another.

Their evolution was made possible because each one was powered by an artificial neural network controlled by a binary “genome”. The network consisted of 11 neurons that were connected to the robot’s sensors and 3 that controlled its two tracks and its blue light. The neurons were linked via 33 connections – synpases – and the strength of these connections was each controlled by a single 8-bit gene. In total, each robot’s 264-bit genome determines how it reacts to information gleaned from its senses.

In the experiment, each round consisted of 100 groups of 10 robots, each competing for food in a separate arena. The 200 robots with the highest scores – the fittest of the population – “survived” to the next round. Their 33 genes were randomly mutated (with a 1 in 100 chance that any bit with change) and the robots were “mated” with each other to shuffle their genomes. The result was a new generation of robots, whose behaviour was inherited from the most successful representatives of the previous cohort.

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This article is reposted from the old WordPress incarnation of Not Exactly Rocket Science.

Twenty-two thousand sounds like a huge number. It’s happens to be number of eastern Pacific gray whales currently swimming off the coast of North America. It’s certainly much larger than 140, the number of whales that aboriginal people of this area are allowed to hunt. And it’s far, far bigger than zero, the population size that the whales were rapidly approaching in the mid 20^th century.

Obviously, it’s all relative. Twenty-two thousand is still much less than ninety-six thousand. That’s the size of the original gray whale population and it’s three to five times the current count. Not exactly cause for conservational complacency, then.

Previously, conservationists and whalers alike could only speculate on the number of whales that lived before their flirtation with extinction. But now, Elizabeth Alter and Stephen Palumbi from Stanford University have managed to pin down a figure by looking at the genetic diversity of living whales. And their results suggest that despite a rebound that Hollywood would envy, the grays are still a pale shadow of their former strength.

The gray whale is often touted as a poster child for successful conservation. In the 19^th century, they were hunted to near extinction by eager whalers, but they were given a new lease of life in 1949, when the International Whaling Commission granted them protection from hunting. Today, the western Pacific population remains critically endangered, but the eastern Pacific whales have bounced back. On average, recent censuses put their numbers at about 22,000. Despite once skirting the brink of extinction, the eastern Pacific gray is now the most common whale in the western seaboard.

Cries of ‘full recovery’ were sounded, bolstered by the fact that several gray whales have recently been seen suffering from starvation. The assumption was that they had reached a population plateau, filling up the ecological niche that can support their large bulk. Even the American Cetacean Society claims that the whales are ‘probably close to their original population size.’But Alter argues that these celebrations are premature.

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A very brief note to say that today, Not Exactly Rocket Science is three years old. Sniff… they grow up so fast…

They say that imitation is the sincerest form of flattery and it appears that capuchins believe it too. These very sociable monkeys gravitate towards humans that mimic their actions, spending more time in their company and even preferring to trade with them.

Annika Paukner, who studied this monkey business, thinks that imitation is a type of social glue that binds groups of monkeys together. It says, “We are alike,” and in doing so, it lays the foundation for acts of selflessness by providing a means for two individuals to form an empathic connection.

Certainly, imitation is very much a part and parcel of human life. Every day, we mimic the gestures and mannerisms of people we meet. We sit in the same way, twirl our hair, shift our accents or scratch the same spot. This “chameleon effect” is almost always unconscious and while subtle, it can have a big impact on our social success. Others like us more if our behaviour matches their own, and we in turn put more unconscious effort into imitation if we want someone to like us or if sense that we’re being ostracised.

Paukner and other biologists suggest that these unconscious acts of imitation are adaptations to a social life and she wanted to see if imitation can also strengthen relationships in other sociable primates. Capuchins certainly fit the bill. Paukner allowed monkeys to play with a rubber ball while experimenters either matched their movements with their own balls or played in a different way. The animals spent significantly more time looking at the imitating human than the other one.

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When the bacteria that cause anthrax (Bacillus anthracis) aren’t ravaging livestock or being used in acts of bioterrorism, they spend their lives as dormant spores. In these inert but hardy forms, the bacteria can weather tough environmental conditions while lying in wait for their next host. This is the standard explanation for what B.anthracis does between infections, and it’s too simple by far. It turns out that the bacterium has a far more interesting secret life involving two unusual partners – viruses and earthworms.

A dying animal can release up to a billion bacterial cells in every single millilitre of blood. This torrent of microbes provides a feast of riches for bacteriophages – viruses that infect bacteria. Raymond Schuch and Vincent Fischetti from the Rockefeller University  have found that the anthrax bacterium depends on becoming infected by phages. They began by isolating several strains of phages that specifically infect B.anthracis. The viruses hailed from a range of sources, including the soil, plant roots and worm guts. <

When these phages find bacterial targets, they inject their own DNA, which insinuates itself into the genome of the host. This process is called lysogeny and it is essential for the bacterium’s survival. The added viral DNA encodes proteins called sigma factors that change how bacterial genes are switched on. In doing so, they change the behaviour of the bacteria, giving them new abilities that boost their survival and allow them to colonise an intermediate host – the earthworm.

With their newly incorporated viral DNA, some bacteria formed spores while others were actually prevented from doing so, depending on the phage. Regardless, all the anthrax bacteria grew at almost twice the rate. The phage DNA brought out the social side of the bacteria, inducing them to cluster in groups. It also made them more likely to secreted more complex sugar molecules that form the building blocks of biofilms – the bacterial equivalent of towns and cities. Amid this matrix of sugars, the cells find shelter and protection.

Small wonder then that the infected bacteria are much better are surviving for long durations. Their advantage was so great in comparison to virus-free strains that Schuch and Fischetti suggest that phage infections may actually be necessary if anthrax bacteria are to survive in soil. Indeed, duo identified three bacterial genes that are activated by the phages and that are necessary for eking out a living in soil. When they inactivated these genes, the bacteria survived in these environments for the briefest of times.

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In a French laboratory, a team of ants is attempting a daring rescue. One of their colony-mates is trapped in a snare – a nylon thread that dastardly researchers have looped around its waist and half-buried in some sand. Thankfully, help is at hand. A crack squad of rescuers work together to dig away at the sand, expose the snare, and bite at the threads until their colleague is liberated.

Many animals help each other but actual rescue attempts, even between individuals of the same species, are rarely documented. Among back-boned animals, dolphins are famously said to help injured comrades by supporting them at the surface so that they can breathe more easily, and a lone capuchin monkey was documented to save a mother and baby from attack by a rival group.

Then, there are ants. As early as 1874, biologists noted that ants will often dig out fellows that have sunk too deeply into sand and later studies showed that they’ll also drag others out by their legs. But both limb-pulling and sand-digging are very simple actions, that could be triggered by chemical alarms released by stressed ants. You could imagine that workers have a simple programme that says “Follow the alarm smell until you find its source, then dig and pull.”

But it’s very hard to see how such simple rules could direct rescuers to uncover and bite through a nylon snare. These escapades show that ants can launch rescues that are more sophisticated and exact that anything previously reported.

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People infected with the bird flu virus – influenza A subtype H5N1 – go through the usual symptoms of fever, aching muscles and cough. The virus is so virulent that 60% of infected humans have died. But according to a study in mice, the infection could also take a more inconspicuous toll on the brain, causing the sorts of damage that could increase the risk of diseases like Parkinson’s and Alzheimer’s many years after the virus has been cleared.

The link between influenza and Parkinson’s disease is hardly old but certainly controversial. Previous studies have found no traces of flu genetic material in Parkinson’s patients, but one of the strongest pieces of evidence for a link comes from analysing an outbreak of von Economo disease  following the 1918 flu pandemic.

To date, 433 people have been infected with H5N1, and a few cases have shown problems with their nervous system, running the gamut from inflammation of the brain to coma. For the survivors, it’s too early to say if their brief time with the virus could lead to neurological problems later on in life. Instead, Haeman Jang from St Jude’s Children’s Research Hospital turned to mice for answers.

He clearly showed that the H5N1 virus can infect mouse neurons within a few days, where it causes certain proteins to gather in the sorts of clumps that are so strongly associated with neurodegenerative disease. It kills off important cells, triggers symptoms reminiscent of Parkinson’s like tremors, and even stimulates an over-the-top immune response that lasted for months after the original infection was cleared.

Jang thinks that this long-lasting immune response may be how the virus leads to a higher risk of chronic diseases long after it has left its host. It’s a hit-and-run strategy, where the initial infection paves the way for something else to come along later on in life and make a “second hit”. According to this model, the flu virus doesn’t directly cause Parkinson’s or related diseases, but it primes the neurons for other things that do. This could also explain why scientists have been unable to detect influenza RNA in Parkinson’s patients.

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