New York Times, May 2013
Link

With the unofficial start of summer on Monday, many people will get up close and personal with the element that carries 17 protons.

I speak, of course, of chlorine.

Over the next few months, chlorine will ensure that countless swimming pools don’t turn into microbe-choked petri dishes. That’s only one of many uses we’ve found for the element. We sprinkle it on our food as table salt — a k a sodium chloride. We pump water through pipes made of polyvinyl chloride. Perchlorate, a combination of chlorine and oxygen atoms, fuels rockets and ignites fireworks.

But in other incarnations, chlorine is a bane of our existence. In World War I, the German army unleashed clouds of chlorine gas and killed or injured thousands of enemy -soldiers. The Hudson River is burdened with cancer-causing dioxins, chlorine-bearing compounds dumped from factories along its banks.

Still, chlorine’s threats today are nothing compared with its menace on the early Earth.

Read more

The Atlantic, May 2013
Link

When Jeannie Peeper was born in 1958, there was only one thing amiss: her big toes were short and crooked. Doctors fitted her with toe braces and sent her home. Two months later, a bulbous swelling appeared on the back of Peeper’s head. Her parents didn’t know why: she hadn’t hit her head on the side of her crib; she didn’t have an infected scratch. After a few days, the swelling vanished as quickly as it had arrived.

When Peeper’s mother noticed that the baby couldn’t open her mouth as wide as her sisters and brothers, she took her to the first of various doctors, seeking an explanation for her seemingly random assortment of symptoms. Peeper was 4 when the Mayo Clinic confirmed a diagnosis: she had a disorder known as fibrodysplasia ossificans progressiva (FOP).

The name meant nothing to Peeper’s parents—unsurprising, given that it is one of the rarest diseases in the world. One in 2 million people have it.

Peeper’s diagnosis meant that, over her lifetime, she would essentially develop a second skeleton. Within a few years, she would begin to grow new bones that would stretch across her body, some fusing to her original skeleton. Bone by bone, the disease would lock her into stillness. The Mayo doctors didn’t tell Peeper’s parents that. All they did say was that Peeper would not live long.

“Basically, my parents were told there was nothing that could be done,” Peeper told me in October. “They should just take me home and enjoy their time with me, because I would probably not live to be a teenager.” We were in Oviedo, Florida, in an office with a long, narrow sign that read The International Fibrodysplasia Ossificans Progressiva Association. Peeper founded the association 25 years ago, and remains its president. She was dressed in a narrow-waisted black skirt and a black-and-white striped blouse. A large ring in the shape of a black flower encircled one of her fingers. Her hair was peach-colored.

Read the entire article at The Atlantic

New York Times, May 2013
Link

Imagine a wolf catching a Frisbee a dozen times in a row, or leading police officers to a stash of cocaine, or just sleeping peacefully next to you on your couch. It’s a stretch, to say the least. Dogs may have evolved from wolves, but the minds of the two canines are profoundly different.

Dog brains, as I wrote last month in The New York Times, have become exquisitely tuned to our own. Scientists are now zeroing in on some of the genes that were crucial to the rewiring of dog brains.

Their results are fascinating, and not only because they can help us understand how dogs turned into man’s best friend. They may also teach us something about the evolution of our own brains: Some of the genes that evolved in dogs are the same ones that evolved in us.

To trace the change in dog brains, scientists have first had to work out how dog breeds are related to one another, and how they’re all related to wolves. Ya-Ping Zhang, a geneticist at the Chinese Academy of Sciences, has led an international network of scientists who have compared pieces of DNA from different canines. They’ve come to the conclusion that wolves started their transformation into dogs in East Asia.

Read more

New York Times, April 2013
Link

From North Carolina to Connecticut, billions of creatures with eyes the color of blood and bodies the color of coal are crawling out of the earth. Periodical cicadas are emerging en masse, clambering into trees and singing a shivering chorus that can be heard for miles.

What makes this emergence truly remarkable, however, is how long it’s been in the making. This month’s army of periodical cicadas was born in 1996. Their mothers laid their eggs in the branches of trees, where they developed for a few weeks before hatching and heading for the ground. “They just jumped out and rained down out of the trees,” said Chris Simon, a cicada biologist at the University of Connecticut.

Those Clinton-era larvae then squirmed into the dirt and spent the next 17 years sucking fluid from tree roots. Now, at last, they are ready to produce the next generation. The adult males are snapping rigid plates on their abdomens to produce their courtship song. The females are clicking their wings to signal approval. They will mate and then die shortly afterward. Their time in the sun is short, but their 17-year life span makes them the longest-lived insects known.

Read more

Outside Magazine, April 2013
Link

I’m tailing a Ford pickup truck along the eastern bank of the Connecticut River. When we reach a sign for Lord Creek Farm, the pickup turns off the road and I follow up a dusty driveway. We park in the shadow of an enormous red horse barn, next to paddocks full of jump gates, where riding lessons are under way.

I get out of my car and climb into the passenger side of the pickup. It’s driven by Scott Williams, a wildlife biologist from the Connecticut Agricultural Experiment Station in New Haven. Williams, 38, has the poise and scale of a bear standing upright. He wears a faded peach T-shirt that reads, DO I LOOK LIKE A @&#@& PEOPLE PERSON? Next to him is Megan Floyd, 24, and riding in the bed in back is Michael Short, 51, both research technicians.

Williams drives us across the farm, past freshly groomed meadows, and into the forest. The morning is magnificent, the sunlight slipping through gaps in the canopy. But we’re not here to admire the scenery. We’re here on a hunt, and our quarry is the black-legged tick. If you want to find black-legged ticks, you could not ask for a more spectacularly infested piece of land than Lord Creek Farm.

“You get absolutely astronomical abundance here—maybe 1,000 ticks an acre,” Williams declares. He sounds both appalled and delighted.

Lord Creek Farm holds another attraction for Williams: it is located in the town of Lyme. As in Lyme disease, caused by bacteria known as Borrelia burgdorferi. As in the town where Lyme disease was first discovered in the late 1970s, before it was recognized across the United States, from New York to California. Today, a quarter of a century after its discovery, Lyme, Connecticut, is still a great place to study Lyme disease. Seventy percent of the ticks on Lord Creek Farm are infected with Borrelia. I’m hoping one of them doesn’t find me today.

Williams, Floyd, and Short climb out of the truck and grab blue plastic crates from the back. I follow Williams into the woods, walking over jewelweed, wine raspberries, and Japanese barberry, which stabs our legs with hypodermic thorns.

Read more

New York Times, April 2013
Link

In 1995, Brian Hare began to wonder what his dog Oreo was thinking.

At the time, he was a sophomore at Emory University, where he was studying animal psychology with Michael Tomasello. Dr. Tomasello was comparing the social intelligence of humans and other animals.

Humans, it was known at the time, are exquisitely sensitive to signals from other humans. We use that information to solve problems that we might struggle to figure out on our own.

Read more

National Geographic, April 2013
Link

On July 30, 2003, a team of Spanish and French scientists reversed time. They brought an animal back from extinction, if only to watch it become extinct again. The animal they revived was a kind of wild goat known as a bucardo, or Pyrenean ibex. The bucardo (Capra pyrenaica pyrenaica) was a large, handsome creature, reaching up to 220 pounds and sporting long, gently curved horns. For thousands of years it lived high in the Pyrenees, the mountain range that divides France from Spain, where it clambered along cliffs, nibbling on leaves and stems and enduring harsh winters.

Then came the guns. Hunters drove down the bucardo population over several centuries. In 1989 Spanish scientists did a survey and concluded that there were only a dozen or so individuals left. Ten years later a single bucardo remained: a female nicknamed Celia. A team from the Ordesa and Monte Perdido National Park, led by wildlife veterinarian Alberto Fernández-Arias, caught the animal in a trap, clipped a radio collar around her neck, and released her back into the wild. Nine months later the radio collar let out a long, steady beep: the signal that Celia had died. They found her crushed beneath a fallen tree. With her death, the bucardo became officially extinct.

Read more

Discover, March 2013
Link

David Reich, a geneticist at the Harvard Medical School, has redrawn our species’ family tree. And today, in his office overlooking Avenue Louis Pasteur in Boston, he picks up a blue marker, walks up to a blank white wall, and shows the result to me. He starts with a pair of lines—one for humans and one for Neanderthals—that split off from a common ancestor no more than 700,000 years ago. The human branch divides into lineages of Africans, Asians, and Europeans, and then into twigs for smaller groups like the people of New Guinea or the residents of the remote Andaman Islands in the Indian Ocean. Reich also creates a branch off the Neanderthal line for the Denisovans, a paleolithic lineage geneticists discovered only a few years ago.

All well and good. This is the sort of picture you’d expect if we and our humanlike relatives diverged neatly through evolution. It looks a lot like the tree of life that Darwin included in The Origin of Species. But then Reich violates his tree.

Read more

Discover, February 2013
Link

After spending a few days in bed with the flu, you may have felt a bit stupid. It is a common sensation, that your sickness is slowing down your brain. At first blush, though, it doesn’t make much sense. For one thing, flu viruses infect the lining of the airways, not the neurons in our brains. For another, the brain is walled off from the rest of the body by a series of microscopic defenses collectively known as the blood-brain barrier. It blocks most viruses and bacteria while allowing essential molecules like glucose to slip through. What ails the body, in other words, shouldn’t interfere with our thinking.

But over the past decade, Jonathan Kipnis, a neuroimmunologist in the University of Virginia School of Medicine’s department of neuroscience, has discovered a possible link, a modern twist on the age-old notion of the body-mind connection. His research suggests that the immune system engages the brain in an intricate dialogue that can influence our thought processes, coaxing our brains to work at their best.

Read more

New York Times, February 2013
Link

In 1855, Charles Darwin took up a new hobby. He started raising pigeons.

In the garden of his country estate, Darwin built a dovecote. He filled it with birds he bought in London from pigeon breeders. He favored the fanciest breeds — pouters, carriers, barbs, fantails, short-faced tumblers and many more.

“The diversity of the breeds is something astonishing,” he wrote a few years later in “On the Origin of Species” — a work greatly informed by his experiments with the birds.

Read more

New York Times, January 2013
Link

In November, a team of biologists journeyed to Maria Island, three miles off the Australian island state of Tasmania, taking with them 15 plastic cylinders. They loaded the cylinders into S.U.V.’s, drove them to an abandoned farm and scattered them in the fields.

Before long 15 Tasmanian devils emerged from the containers, becoming the first ever to inhabit the island.

“All indications are that they’re doing very well,” Phil Wise, a government wildlife biologist who leads the project, said of the devils — fierce-looking, doglike marsupials that have become an endangered species on the much larger island for which they are named.

Read more

Yale Environment 360, January 2013
Link

It rises from the chimneys of mansions and from simple hut stoves. It rises from forest fires and the tail pipes of diesel-fueled trucks rolling down the highway, and from brick kilns and ocean liners and gas flares. Every day, from every occupied continent, a curtain of soot rises into the sky.

What soot does once it reaches the atmosphere has long been a hard question to answer. It’s not that scientists don’t know anything about the physics and chemistry of atmospheric soot. Just the opposite: it does so many things that it’s hard to know what they add up to.

To get a clear sense of soot — which is known to scientists as black carbon — an international team of 31 atmospheric scientists has worked for the past four years to analyze all the data they could. This week, they published a 232-page report in the Journal of Geophysical Research. “It’s an important assessment of where we stand now,” says Veerabhadran Ramanathan of the Scripps Institution for Oceanography, an expert on atmospheric chemistry who was not involved in the study.

Read more

Wired, February 2013
Link

On September 19, 2011, Evan Snitkin sat staring at a computer monitor, its screen cluttered with Perl script and row after row of 0s sprinkled with the occasional 1. To Snitkin, a bioinformatician at the National Institutes of Health, it read like a medical thriller. In this raw genetic-sequencing data, he could see the hidden history of a deadly outbreak that was raging just a few hundred yards from where he sat.

Snitkin was, in a sense, a medical historian: a genetic epidemiologist who traced the paths of disease outbreaks. But now, for the first time in history, he was trying to use his genetic toolkit to reroute an outbreak while it was in progress—and before it turned disastrous. A few weeks earlier, a handful of patients at the NIH Clinical Center, a 243-bed research hospital on the NIH campus in Bethesda, Maryland, had been hit by a vicious strain of bacteria known as KPC. Shorthand for carbapenem-resistant Klebsiella pneumoniae, KPC can hitch a ride on healthy people, setting up residence on their skin. From them it can spread to people with weak defenses—like hospital patients—and bloom into an overwhelming infection that spreads via the bloodstream into the whole body, swiftly shutting down one organ after another. In the past decade, KPC has evolved the ability to withstand every known antibiotic. As a result, roughly half of people who develop an active infection of KPC will die.

Read the entire article at Wired