Archives for category: 2012

In the 1930s, the Austrian biologist Karl von Frisch, of waggle-dancing honey bee fame, performed some little-known experiments on dancing minnows. The fish weren’t dancing for fun.

Von Frisch showed that when a minnow’s skin cells are damaged, as happens during a predator attack, the fish releases a chemical into the water that triggers nearby fish to flee. Von Frisch called the chemical “Schreckstoff,” German for “scary stuff,” and yesterday, scientists described its chemical makeup.

The research team first separated the skin mucous of zebrafish into its different chemical components and then tested how each affects the behavior of a group of fish in a tank. One of the chemicals, a sugar called chondroitin sulfate, caused a dramatic fear response.

Read more (and watch the video!) at…

Smithsonian’s Surprising Science, February 2012.

 

The new study, certainly not the last word on DNA, was published last week in The EMBO Journal. The music is Chopin’s Minute Waltz, the subject of another post.

First published on…

The Last Word on Nothing, February 2012.

For the past 10 years or so, there’s been a surge of interest among archaeologists in the people who discovered the New World. Most of the buzz revolves around when, exactly, those nomads crossed the Bering land bridge into Alaska, with a focus on the distinctive stone tools they used. Nobody talks much about the artistic leanings of the first Americans, simply because examples of their cave paintings, jewelry or other symbolic creations are few and far between.

But in July 2009, after seven years of excavation work, researchers found a humble stick figure engraved in bedrock in Lapa do Santo, in central Brazil. In their report, published yesterday in PLoS ONE, the scientists call it the “oldest, indisputable testimony of rock art in the Americas.”

Read more at…

Smithsonian’s Surprising Science, February 2012.

When human urban habitat runs into the terrain of other species, the results can be traumatic for many of the parties involved.

Take coastal southern California, which has seen a big population boom in the past couple of decades. As people built skyscrapers and condos and highways to accommodate their growing numbers, they inadvertently split up the natural habitats of lizards and birdsbobcats and coyotes, and loads of other species. Isolated to much smaller patches of habitat (not to mention surrounded by metal, concrete and plastic), the animals wind up with a much smaller gene pool, making them more susceptible to disease, climate change and natural disaster.

Since the 1960s, a solution often trumpeted by conservationists is to build a “wildlife corridor”: a green pathway that connects one patch of habitat to another, allowing species to move across wider areas despite human developments. These corridors exist or are being built all over the world, from jaguar habitat in the Americas to hardwood forests in Bhutan to tropical rainforests in Australia.

But two active corridor builders are now questioning whether the approach is a good one.

Read more at…

Smithsonian’s Surprising Science, February 2012.

Nature, for all of its free-wheeling weeds and lightning strikes, is also full of biological regularity: the rows of an alligator’s teeth, the stripes on a zebrafish, the spacing of a chicken’s feathers. How do these patterns arise?

Sixty years ago, with nothing but numbers, logic and some basic biological know-how, mathematician Alan Turing (best known for his pioneering work on artificial intelligence) came up with an explanation. He proposed that two chemicals—an “activator” and an “inhibitor”—work together, something like a pencil and eraser. The activator’s expression would do something—say, make a stripe—and the inhibitor would shut off the activator. This repeats, and voilà, stripe after stripe after stripe.

On Sunday, researchers reported the first experimental evidence that Turing’s theory is correct, by studying the eight evenly spaced ridges that form on the roof of a mouse’s mouth. (People, by the way, have four such ridges on each side, which help us feel and taste food.)

Read more at…

Smithsonian’s Surprising Science, February 2012.

The development of white matter tracts, the nerve bundles that join one brain region to another, is different in babies who go on to develop autism compared with those who do not, according to a new study.

Researchers scanned the brains of infant siblings of children with autism — who have an increased risk of developing the disorder themselves — several times during their first two years of life. The so-called ‘baby sibs’ who go on to receive a diagnosis of autism at 24 months of age have distinct brain patterns at 6 months and abnormal neural development from 6 to 24 months, according to the study. The results were published 17 February in the American Journal of Psychiatry.

“The story is that autism is an unfolding process, not something that happens in the third trimester and then is done,” says lead investigator Joseph Piven, professor of psychiatry at the University of North Carolina-Chapel Hill. “We see the brain changing over time in a dynamic way.”

Read more at…

SFARI, February 2012.

Just over a year ago, I wrote about a handful of research groups creating robots that can engage children who have autism using speech, facial expressions or body movements. These ‘social’ bots ranged from a miniature dinosaur and a dancing yellow snowman to several sophisticated, full-size humanoids.

The eclectic collection now includes a boy that can sense when it’s touched, a floating female head that expresses a wide range of emotions and a low-cost fuzzy penguin that can track a child’s eye movements. Descriptions of all three appear in the latest conference proceedings of the IEEE Engineering in Medicine and Biology Society.

Read more at…

SFARI, February 2012.

By screening the genomes of hundreds of people with autism and analyzing the effect of newly identified mutations in cultured neurons, researchers have clarified the disorder’s complex link to a gene called SHANK2.

Functional mutations in SHANK2 crop up about twice as often in individuals with autism as in typical controls, according to a study published 9 February in PLoS Genetics.

The SHANK2 protein buttresses the synapse, or junction between neurons. The new findings add to already robust evidence from genetic studies and animal models that synaptic proteins — notably SHANK3, neurexins and neuroligins — are important in autism, the researchers say.

But a more surprising finding helps to explain why not everyone who has a SHANK2 mutation has autism. The three individuals with autism known to carry SHANK2 deletions also carry rare deletions or duplications — so-called copy number variations, or CNVs — in an autism-linked segment of chromosome 15. This supports the idea that autism arises not from a single genetic glitch, but from multiple hits to the genome.

“I think many people are still thinking about the genome like the old black-and-white movies from the 1950s: The good guy was in white, the bad guy was in black, and everybody knew what was going on,” says lead investigator Thomas Bourgeron, professor of genetics at the University of Paris Diderot.

But studies like this show that a ‘bad’ genetic glitch isn’t necessarily the only bad guy.

“When we find a single mutation in a patient with autism, we can’t say that we’re done,” Bourgeron says. “We still have to work on the whole genome of these patients to understand exactly what’s going on.”

Read more at…

SFARI, February 2012.

Some 40 years ago, researchers at the University of Missouri were searching for an alternative to the condom — a cheap, trustworthy and reversible form of male birth control.

For their first study, published in 1975, they strapped anesthetized rats, face-down, to a plexiglass platform with a cut-out cup full of water for their dangling scrota. The scientists then exposed the animals’ testicles to a variety of things.

Heat, for example, can kill sperm (which is thought to explain why the testes hang outside of the body). So some of the animals got a 140-degree Fahrenheit water bath for 15 minutes. Others received a dose of infrared radiation, or short blasts of microwaves or ultrasound. After treatment, the animals had constant access to females until they impregnated them.

Rats given the hot water bath didn’t conceive for 35 days. Infrared radiation doubled that sterile window, to 75 days. Sometimes microwave treatment worked, sometimes it didn’t. The best protocol, by far, was ultrasound, which the researchers transmitted through the water cup. One 5-minute exposure to these high-frequency sound waves led to seven months of sterility. Histology studies of the tissue confirmed that the animals showed a big loss of developing sperm at two months post-ultrasound, but were back to normal by 10 months.

Read more at…

The Last Word on Nothing, February 2012.