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