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An Unlikely Driver of Evolution: Arsenic
New York Times, March 12, 2015

Around 11,000 years ago, humans first set foot in the driest place on Earth.

The Atacama Desert straddles the Andes Mountains, reaching into parts of Chile, Peru, Bolivia and Argentina. Little rain falls on the desert — some spots haven’t received a single drop in recorded history.

But the people who arrived at the Atacama managed to turn it into a home. Some Atacameños, as they are known today, fished the Pacific. Others hunted game and herded livestock in the highlands. They mummified their dead, decorating them with ceremonial wigs before leaving them in the mountains.

Those mummies reveal a hidden threat in the Atacama. When scientists analyzed the hair in 7,000-year-old mummy wigs, they discovered high levels of arsenic. Through their lives, the Atacameños were gradually poisoned.

Arsenic can poison people today through exposure to pesticides and pollution. But arsenic is also naturally present in the water and soil in some parts of the world. The Atacama Desert, sitting on top of arsenic-rich volcanic rock, is one of them. The concentration of arsenic in Atacama drinking water can be 20 times higher than the level considered safe for human consumption.

Protection without a Vaccine
New York Times, March 9, 2015

Last month, a team of scientists announced what could prove to be an enormous step forward in the fight against H.I.V.

Scientists at Scripps Research Institute said they had developed an artificial antibody that, once in the blood, grabbed hold of the virus and inactivated it. The molecule can eliminate H.I.V. from infected monkeys and protect them from future infections.

But this treatment is not a vaccine, not in any ordinary sense. By delivering synthetic genes into the muscles of the monkeys, the scientists are essentially re-engineering the animals to resist disease. Researchers are testing this novel approach not just against H.I.V., but also Ebola, malaria, influenza and hepatitis.

“The sky’s the limit,” said Michael Farzan, an immunologist at Scripps and lead author of the new study.

Is Most of Our DNA Garbage?
New York Times, March 8, 2015

T. Ryan Gregory’s lab at the University of Guelph in Ontario is a sort of genomic menagerie, stocked with creatures, living and dead, waiting to have their DNA laid bare. Scorpions lurk in their terrariums. Tarantulas doze under bowls. Flash-frozen spiders and crustaceans — collected by Gregory, an evolutionary biologist, and his students on expeditions to the Arctic — lie piled in beige metal tanks of liquid nitrogen. A bank of standing freezers holds samples of mollusks, moths and beetles. The cabinets are crammed with slides splashed with the fuchsia-stained genomes of fruit bats, Siamese fighting fish and ostriches.

Gregory’s investigations into all these genomes has taught him a big lesson about life: At its most fundamental level, it’s a mess. His favorite way to demonstrate this is through what he calls the “onion test,” which involves comparing the size of an onion’s genome to that of a human. To run the test, Gregory’s graduate student Nick Jeffery brought a young onion plant to the lab from the university greenhouse. He handed me a single-edged safety razor, and then the two of us chopped up onion stems in petri dishes. An emerald ooze, weirdly luminous, filled my dish. I was so distracted by the color that I slashed my ring finger with the razor blade, but that saved me the trouble of poking myself with a syringe — I was to supply the human genome. Jeffery raised a vial, and I wiped my bleeding finger across its rim. We poured the onion juice into the vial as well and watched as the green and red combined to produce a fluid with both the tint and viscosity of maple syrup.

Two Strains of H.I.V. Cut Vastly Different Paths
New York Times, March 2, 2015

Thirty-four years ago, doctors in Los Angeles discovered that some of their patients were succumbing to a normally harmless fungus. It soon became clear that they belonged to a growing number of people whose immune systems were hobbled by a virus, eventually known as human immunodeficiency virus, or H.I.V.

To date, an estimated 78 million people have become infected, 39 million of whom have died.

As the true scale of the virus’s devastation began to emerge, a number of scientists set out to investigate its origins. Piece by piece, year after year, the scientists reconstructed its history. Their research slowly revealed that the virus did not make a single leap from animals, but several.

On Monday, a team of researchers filled in the final gaps in the history. It’s now clear, they say, that the virus originated in humans on 13 separate occasions, evolving in humans from ancestral viruses that infected monkeys, chimpanzees and gorillas.

“We’ve got an amazing amount of the story nailed down, more than any reasonable person could have expected in the 1980s,” said Michael Worobey, a professor of ecology and evolutionary biology at the University of Arizona, who was not involved in the new study.

The first clue to the evolution of H.I.V. emerged in 1985, when scientists discovered a virus in macaque monkeys that was closely related to H.I.V. As it turned out, forty African primate species harbored H.I.V.-like viruses, called simian immunodeficiency viruses, or S.I.V. It became clear that H.I.V. had evolved from an S.I.V. ancestor.

But looking for H.I.V.’s precise origins proved a difficult task.

In Short-Lived Fish, Secrets to Aging
New York Times, February 27, 2015

The turquoise killifish lives in a fleeting world: the ponds that appear only during the rainy season in East Africa.

As a new pond forms, turquoise killifish eggs buried in the mud spring from suspended animation. The eggs hatch, and in just 40 days the fish grow to full size, about 2.5 inches. They feed, mate and lay eggs. By the time the ponds dry up, the fish are all dead.

Even when hobbyists pamper them in aquariums, turquoise killifish survive only a few months, making them among the shortest-lived vertebrates on Earth. So the turquoise killifish may not seem the best animal to study to discover the secrets of a long life.

But researchers are finding that this tiny fish ages much as we do, only at a much faster pace. “It’s a compressed life span,” said Itamar Harel, a postdoctoral researcher at Stanford University. Dr. Harel and his colleagues recently developed a set of tools to probe the biology of the turquoise killifish.

Old people may seem a more logical focus for scientists looking to discover the mechanics of aging, but progress would be glacial.

“Who has 70 years to study somebody else’s aging process?” asked Sarah J. Mitchell, a postdoctoral researcher at the National Institute on Aging.

A New Theory on How Neanderthal DNA Spread in Asia
New York Times, February 19, 2015

In 2010, scientists made a startling discovery about our past: About 50,000 years ago, Neanderthals interbred with the ancestors of living Europeans and Asians.

Now two teams of researchers have come to another intriguing conclusion: Neanderthals interbred with the ancestors of Asians at a second point in history, giving them an extra infusion of Neanderthal DNA.

The findings are further evidence that our genomes contain secrets about our evolution that we might have missed by looking at fossils alone. “We’re learning new, big-picture things from the genetic data, rather than just filling in details,” said Kirk E. Lohmueller, a geneticist at the University of California, Los Angeles, and co-author of one of the new studies.

The oldest fossils of Neanderthals date back about 200,000 years, while the most recent are an estimated 40,000 years old. Researchers have found Neanderthal bones at sites across Europe and western Asia, from Spain to Siberia.

Some of those bones still retain fragments of Neanderthal DNA. Scientists have pieced those DNA fragments together, reconstructing the entire Neanderthal genome. It turns out that Neanderthals had a number of distinct genetic mutations that living humans lack. Based on these differences, scientists estimate that the Neanderthals’ ancestors diverged from ours 600,000 years ago.

Studying Oversize Brain Cells for Links to Exceptional Memory
New York Times, February 12, 2015

In 2010, a graduate student named Tamar Gefen got to know a remarkable group of older people.

They had volunteered for a study of memory at the Feinberg School of Medicine at Northwestern University. Although they were all over age 80, Ms. Gefen and her colleagues found that they scored as well on memory tests as people in their 50s. Some complained that they remembered too much.

She and her colleagues referred to them as SuperAgers. Many were also friends. “A couple tried to set me up with their grandsons,” Ms. Gefen said.

She was impressed by their resilience and humor: “It takes wisdom to a whole new level.”

Recently, Ms. Gefen’s research has taken a sharp turn. At the outset of the study, the volunteers agreed to donate their brains for medical research. Some of them have died, and it has been Ms. Gefen’s job to look for anatomical clues to their extraordinary minds.

“I had this enormous privilege I can’t even begin to describe,” she said. “I knew them and tested them in life and in death. At the end, I was the one looking at them through a microscope.”

Breakthrough DNA Editor Borne of Bacteria
Quanta Magazine, February 6, 2015

On a November evening last year, Jennifer Doudna put on a stylish black evening gown and headed to Hangar One, a building at NASA’s Ames Research Center that was constructed in 1932 to house dirigibles. Under the looming arches of the hangar, Doudna mingled with celebrities like Benedict Cumberbatch, Cameron Diaz and Jon Hamm before receiving the 2015 Breakthrough Prize in life sciences, an award sponsored by Mark Zuckerberg and other tech billionaires. Doudna, a biochemist at the University of California, Berkeley, and her collaborator, Emmanuelle Charpentier of the Helmholtz Centre for Infection Research in Germany, each received $3 million for their invention of a potentially revolutionary tool for editing DNA known as CRISPR.

Doudna was not a gray-haired emerita being celebrated for work she did back when dirigibles ruled the sky. It was only in 2012 that Doudna, Charpentier and their colleagues offered the first demonstration of CRISPR’s potential. They crafted molecules that could enter a microbe and precisely snip its DNA at a location of the researchers’ choosing. In January 2013, the scientists went one step further: They cut out a particular piece of DNA in human cells and replaced it with another one.

In the same month, separate teams of scientists at Harvard University and the Broad Institute reported similar success with the gene-editing tool. A scientific stampede commenced, and in just the past two years, researchers have performed hundreds of experiments on CRISPR. Their results hint that the technique may fundamentally change both medicine and agriculture.

In Bedbugs, Scientists See a Model of Evolution
New York Times, February 5, 2015

In the closing sentence of “The Origin of Species,” Charles Darwin marvels at the process of evolution, observing how “from so simple a beginning endless forms most beautiful and most wonderful have been, and are being, evolved.”

Few people would describe bedbugs as most beautiful or most wonderful. Yet this blood-feeding pest may represent an exceptional chance to observe the emergence of Darwin’s “endless forms”: New research indicates that some bedbugs are well on their way to becoming a new species.

“For something that is so hated by so many people, it might just be a perfect model organism for evolutionary questions,” said Warren Booth, a biologist at the University of Tulsa and a co-author of the new study, published in Molecular Ecology.

Scientists have been very slow to appreciate the biology of bedbugs despite the fact that the insects have infiltrated human shelters for thousands of years. That’s because the insects practically vanished at the dawn of modern biology in the 1940s, thanks to the widespread use of DDT.

Bedbugs have returned with a vengeance in recent years, partly because they have evolved resistance to pesticides, and scientists are struggling to learn more about these pests. It’s a much bigger challenge than examining, say, monarch butterflies.

In the Way Cancer Cells Work Together, a Possible Tool for Their Demise
New York Times, January 29, 2015

A tumor, as strange as it may sound, is a little society. The cancer cells that make it up cooperate with one another, and together they thrive.

Scientists are only starting to decipher the rules of these communities. But if they can understand how these cells work together, then they may be able to stop the tumor. “You can drive it to collapse,” said Marco Archetti, a biologist at the University of East Anglia and at the Icahn School of Medicine at Mount Sinai.

Cancer starts when healthy cells mutate and lose the safeguards that normally keep their growth in check. The cells start to multiply quickly, and their descendants gain new mutations, some of which make the cells even better at multiplying.

As tumors rapidly develop, they outgrow their blood supply, and stores of nutrients and growth-stimulating chemicals, known as growth factors, run low. As it turns out, cancer cells survive this harsh new environment by helping one another.

New mutations can cause cancer cells to start making their own growth factors, and they don’t keep these essential chemicals to themselves. Growth factors seep throughout the tumor, affecting all the cells. “It’s one of the hallmarks of cancer,” Dr. Archetti said.

Even Elusive Animals Leave DNA, and Clues, Behind
New York Times, January 22, 2015

You wouldn’t think hellbenders would be hard to find: The huge salamanders, the biggest amphibians in North America, can grow up to 30 inches long. Yet hellbenders make themselves scarce, living on the bottoms of mountain streams, lurking under massive rocks.

As a result, locating hellbenders takes a crew of scientists. First, some of them must wedge a long pole under a rock to hoist it up, and then their colleagues must plunge into the chilly water to catch their quarry.

A couple of years ago, Stephen Spear, a conservation scientist at the Orianne Society in Athens, Ga., heard about a possible alternative. Instead of finding rare animals, some experts were gathering animal DNA from their habitats. That way, they didn’t have to track down a species to be sure it was there.

Dr. Spear decided to try. He traveled to rivers in the Southeast where he and his colleagues had found hellbenders, and scooped water into jugs.

Raising Alarm, Study Finds Oceans on Brink of Wave of Extinctions
New York Times, January 15, 2015

A team of scientists, in a groundbreaking analysis of data from hundreds of sources, has concluded that humans are on the verge of committing unprecedented damage to the oceans and the animals living in them.

“We may be sitting on a precipice of a major extinction event,” said Douglas J. McCauley, an ecologist at the University of California, Santa Barbara, and a co-author of the new research, which was published on Thursday in the journal Science.

But there is still time to avert catastrophe, Dr. McCauley and his colleagues also found. Compared with the continents, the oceans are mostly intact, still wild enough to bounce back to ecological health.

“We’re lucky in many ways,” said Malin L. Pinsky, a marine biologist at Rutgers University and a co-author of the new report. “The impacts are accelerating, but they’re not so bad we can’t reverse them.”

Unraveling the Key to a Cold Virus’s Effectiveness
New York Times, January 8, 2015

If there is a champion among contagions, it may well be the lowly rhinovirus, responsible for many of the coughs and sniffles that trouble us this time of year. Rhinoviruses are spectacularly effective at infecting humans. Americans suffer one billion colds a year, and rhinoviruses are the leading cause of these infections.

Scientists have never been sure why they are so effective, but now a team at Yale University may have found a clue. The scientists argue that rhinoviruses have found a blind spot in the human immune system: They take advantage of the cold air in our noses.

In the 1960s, researchers first noticed that if they incubated rhinoviruses a few degrees below body temperature, the viruses multiplied much faster. It was an intriguing finding, since rhinoviruses often infect the lining of the nostrils, which are cooled by incoming air.

In subsequent years, scientists searched for an explanation. “People have taken the virus apart and studied its parts,” said Akiko Iwasaki, an immunobiologist at Yale. “But none of this really added up to explain why the virus replicated faster at a lower temperature.”

Can Hermaphrodites Teach Us What It Means To Be Male?
This View of Life, January 4, 2015

The vinegar worm (officially known as Caenorhabditis elegans) is about as simple as an animal can be. When this soil-dwelling nematode reaches its adult size, it measures a millimeter from its blind head to its tapered tail. It contains only a thousand cells in its entire body. Your body, by contrast, is made of 36 trillion cells. Yet the vinegar worm divides up its few cells into the various parts you can find in other animals like us, from muscles to a nervous system to a gut to sex organs.

In the early 1960s, a scientist named Sydney Brenner fell in love with the vinegar worm’s simplicity. He had decided to embark on a major study of humans and other animals. He wanted to know how our complex bodies develop from a single cell. He was also curious as to how neurons wired into nervous systems that could perceive the outside world and produce quick responses to keep animals alive. Scientists had studied these two questions for decades, but they still knew next to nothing about the molecules involved. When Brenner became acquainted with the vinegar worm in the scientific literature, he realized it could help scientists find some answers.

Its simplicity was what made it so enticing. Under a microscope, scientists could make out every single cell in the worm’s transparent body. It would breed contentedly in a lab, requiring nothing but bacteria to feed on. Scientists could search for mutant worms that behaved in strange ways, and study them to gain clues to how their mutations to certain genes steered them awry.

A Weakness in Bacteria’s Fortress
Scientific American, January 2015

At the University of Zurich, Rolf Kümmerli investigates new drugs to stop deadly infections. He spends his days in a laboratory stocked with petri dishes and flasks of bacteria—exactly the place where you would expect him to do that sort of work. But Kümmerli took an odd path to get to that lab. As a graduate student, he spent years hiking through the Swiss Alps to study the social life of ants. Only after he earned a Ph.D. in evolutionary biology did he turn his attention to microbes.

The path from ants to antibiotics is not as roundabout as it may seem. For decades scientists have studied how cooperative behavior evolves in animal societies such as ant colonies, in which sterile female workers raise the eggs of their queen. A new branch of science—sometimes called “sociomicrobiology”—is revealing that some of the same principles that govern ants can explain the emergence of bacterial societies. Like ants, microbes live in complex communities, where they communicate with one another to cooperate for the greater good. This insight of social evolution suggests a new strategy for stopping infections: instead of attacking individual bacteria, as traditional antibiotics do, scientists are exploring the notion of attacking entire bacterial societies.

New strategies are exactly what is needed now. Bacteria have evolved widespread resistance to antibiotics, leaving doctors in a crisis. For example, the Centers for Disease Control and Prevention estimates that 23,000 people die in the U.S. every year of antibiotic-resistant infections. Strains of tuberculosis and other pathogens are emerging that are resistant to nearly every drug. “It already is a substantial problem,” says Anthony S. Fauci, director of the National Institute of Allergy and Infectious Disease. “And there's every reason to believe it's going to get even worse.”

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