This issue marks the second year that Science News has reached out to science notables and asked: Which up-and-coming scientist is making a splash? Whose work impresses you? Tell us about early- to mid-career scientists who have the potential to change their fields and the direction of science more generally.
This year, we expanded the pool of people we asked. We reached out to Nobel laureates again and added recently elected members of the National Academy of Sciences. That allowed us to consider shining lights from a much broader array of fields, from oceanography and astronomy to cognitive psychology. Another difference this year: We spent time face-to-face with many of those selected, to get a better sense of them both as scientists and as people. The result is the SN 10, a collection of stories not only about science, but also about making a life in science. They are stories of people succeeding because they have found what they love, be it working in the lab on new ways to probe molecular structures or staring up to the stars in search of glimmers of the early universe. In my interviews with chemist Phil Baran, I was struck by his drive to do things in new ways, whether devising chemical reactions or developing ideas about how to fund research. (If you can, he says, go private.) Laura Sanders, who met with neuroscientist Jeremy Freeman, was intrigued by his way of seeing a problem (siloed data that can’t be easily shared or analyzed) and figuring out solutions, even if those solutions were outside his area of expertise.
Of course, there are many ways to identify noteworthy scientists — and there’s plenty more fodder out there for future years. Our approach was to seek standouts, asking who deserved recognition for the skill of their methods, the insights of their thinking, the impacts of their research. Not all of the SN 10’s work has made headlines, but they all share something more important: They are participants in building the science of the future.
Notably, many of them do basic research. I think that’s because it’s the type of work that other scientists notice, even if it’s not always on the radar of the general public. But that’s where fundamental advances are often made, as scientists explore the unknown.
That edge of what’s known is where Science News likes to explore, too. Such as the bet-ending, head-scratching results from the Large Hadron Collider, which have failed to reveal the particles that the equations of supersymmetry predict. As Emily Conover reports in “Supersymmetry’s absence at LHC puzzles physicists,” that means that either the theory must be more complicated than originally thought, or not true, letting down those who looked to supersymmetry to help explain a few enduring mysteries, from the nature of dark matter to the mass of the Higgs boson.
Other mysteries may be closer to a solution, as Sanders reports in “New Alzheimer’s drug shows promise in small trial.” A new potential treatment for Alzheimer’s disease reduced amyloid-beta plaques in patients. It also showed hints of improving cognition. That’s standout news, a result built on decades of basic research by many, many bright young scientists.
In smart homes of the future, computers may identify inhabitants and cater to their needs using a tool already at hand: Wi-Fi. Human bodies partially block the radio waves that carry the wireless signal between router and computer. Differences in shape, size and even gait among household members yield different patterns in the received Wi-Fi signals. A computer can analyze the signals to distinguish dad from mom, according to a report posted online August 11 at arXiv.org.
Scientists built an algorithm that was nearly 95 percent accurate when attempting to discern two adults walking between a wireless router and a computer. For six people, accuracy fell to about 89 percent. Scientists tested the setup on men and women of various sizes, but it should work with children as well, says study coauthor Bin Guo of Northwestern Polytechnical University in Xi’an, China.
In a home rigged with Wi-Fi and a receiver, the system could eventually identify family members and tailor heating and lighting to their preferences — maybe even cue up a favorite playlist.
Nature’s rarest type of atomic nucleus is not giving up its secrets easily.
Scientists looking for the decay of an unusual form of the element tantalum, known as tantalum-180m, have come up empty-handed. Tantalum-180m’s hesitance to decay indicates that it has a half-life of at least 45 million billion years, Bjoern Lehnert and colleagues report online September 13 at arXiv.org. “The half-life is longer than a million times the age of the universe,” says Lehnert, a nuclear physicist at Carleton University in Ottawa. (Scientists estimate the universe’s age at 13.8 billion years.) Making up less than two ten-thousandths of a percent of the mass of the Earth’s crust, the metal tantalum is uncommon. And tantalum-180m is even harder to find. Only 0.01 percent of tantalum is found in this state, making it the rarest known long-lived nuclide, or variety of atom.
Tantalum-180m is a bit of an oddball. It is what’s known as an isomer — its nucleus exists in an “excited,” or high-energy, configuration. Normally, an excited nucleus would quickly drop to a lower energy state, emitting a photon — a particle of light — in the process. But tantalum-180m is “metastable” (hence the “m” in its name), meaning that it gets stuck in its high-energy state. Tantalum-180m is thought to decay by emitting or capturing an electron, morphing into another element — either tungsten or hafnium — in the process. But this decay has never been observed. Other unusual nuclides, such as those that decay by emitting two electrons simultaneously, can have even longer half-lives than tantalum-180m. But tantalum-180m is unique — it is the longest-lived isomer found in nature. “It’s a very interesting nucleus,” says nuclear physicist Eric Norman of the University of California, Berkeley, who was not involved with the study. Scientists don’t have a good understanding of such unusual decays, and a measurement of the half-life would help scientists pin down the details of the process and the nucleus’ structure. Lehnert and colleagues observed a sample of tantalum with a detector designed to catch photons emitted in the decay process. After running the experiment for 176 days, and adding in data from previous incarnations of the experiment, the team saw no evidence of decay. The half-life couldn’t be shorter than 45 million billion years, the scientists determined, or they would have seen some hint of the process. “They did a state-of-the-art measurement,” says Norman. “It’s a very difficult thing to see.”
The presence of tantalum-180m in nature is itself a bit of a mystery, too. The element-forging processes that occur in stars and supernovas seem to bypass the nuclide. “People don’t really understand how it is created at all,” says Lehnert.
Tantalum-180m is interesting as a potential energy source, says Norman, although “it’s kind of a crazy idea.” If scientists could find a way to tap the energy stored in the excited nucleus by causing it to decay, it might be useful for applications like nuclear lasers, he says.
Two trillion galaxies. That’s the latest estimate for the number of galaxies that live — or have lived — in the observable universe, researchers report online October 10 at arXiv.org. This updated headcount is roughly 10 times greater than previous estimates and suggests that there are a lot more galaxies out there for future telescopes to explore.
Hordes of relatively tiny galaxies, weighing as little as 1 million suns, are responsible for most of this tweak to the cosmic census. Astronomers haven’t directly seen these galaxies yet. Christopher Conselice, an astrophysicist at the University of Nottingham in England, and colleagues combined data from many ground- and space-based telescopes to look at how the number of galaxies in a typical volume of the universe has changed over much of cosmic history. They then calculated how many galaxies have come and gone in the universe.
The galactic population has dwindled over time, as most of those 2 trillion galaxies collided and merged to build larger galaxies such as the Milky Way, the researchers suggest. That’s in line with prevailing ideas about how massive galaxies have been assembled. Seeing many of these remote runts, however, is beyond the ability of even the next generation of telescopes. “We will have to wait at least several decades before even the majority of galaxies have basic imaging,” the researchers write.
Crucial immune system proteins that make it harder for viruses to replicate might also help the attackers avoid detection, three new studies suggest. When faced with certain viruses, the proteins can set off a cascade of cell-to-cell messages that destroy antibody-producing immune cells. With those virus-fighting cells depleted, it’s easier for the invader to persist inside the host’s body.
The finding begins to explain a longstanding conundrum: how certain chronic viral infections can dodge the immune system’s antibody response, says David Brooks, an immunologist at the University of Toronto not involved in the research. The new studies, all published October 21 in Science Immunology, pin the blame on the same set of proteins: type 1 interferons. Normally, type 1 interferons protect the body from viral siege. They snap into action when a virus infects cells, helping to activate other parts of the immune system. And they make cells less hospitable to viruses so that the foreign invaders can’t replicate as easily.
But in three separate studies, scientists tracked mice’s immune response when infected with lymphocytic choriomeningitis virus, or LCMV. In each case, type 1 interferon proteins masterminded the loss of B cells, which produce antibodies specific to the virus that is being fought. Normally, those antibodies latch on to the target virus, flagging it for destruction by other immune cells called T cells. With fewer B cells, the virus can evade capture for longer.
The proteins’ response “is driving the immune system to do something bad to itself,” says Dorian McGavern, an immunologist at the National Institute of Neurological Disorders and Stroke in Bethesda, Md., who led one of the studies.
The interferon proteins didn’t directly destroy the B cells; they worked through middlemen instead. These intermediaries differed depending on factors including the site of infection and how much of the virus the mice received. T cells were one intermediary. McGavern and his colleagues filmed T cells actively destroying their B cell compatriots under the direction of the interferon proteins. When the scientists deleted those T cells, the B cells didn’t die off even though the interferons were still hanging around. Another study found that the interferons were sending messages not just through T cells, but via a cadre of other immune cells, too. Those messages told B cells to morph into cells that rapidly produce antibodies for the virus. But those cells die off within a few days instead of mounting a longer-term defense.
That strategy could be helpful for a short-term infection, but less successful against a chronic one, says Daniel Pinschewer, a virologist at the University of Basel in Switzerland who led that study. Throwing the entire defense arsenal at the virus all at once leaves the immune system shorthanded later on.
But interferon activity could prolong even short-term viral infections, a third study showed. There, scientists injected lower doses of LCMV into mice’s footpads and used high-powered microscopes to watch the infection play out in the lymph nodes. In this case, the interferon stifled B cells by working through inflammatory monocytes, white blood cells that rush to infection sites.
“The net effect is beneficial for the virus,” says Matteo Iannacone, an immunologist at San Raffaele Scientific Institute in Milan who led the third study. Sticking around even a few days longer gives the virus more time to spread to new hosts.
Since all three studies looked at the same virus, it’s not yet clear whether the mechanism extends to other viral infections. That’s a target for future research, Iannacone says. But Brooks thinks it’s likely that other viruses that dampen antibody response (like HIV and hepatitis C) could also be exploiting type 1 interferons.
Joining a gang doesn’t necessarily make a protein a killer, a new study suggests. This clumping gets dangerous only under certain circumstances.
A normally innocuous protein can be engineered to clump into fibers similar to those formed by proteins involved in Alzheimer’s, Parkinson’s and brain-wasting prion diseases such as Creutzfeldt-Jakob disease, researchers report in the Nov. 11 Science. Cells that rely on the protein’s normal function for survival die when the proteins glom together. But cells that don’t need the protein are unharmed by the gang activity, the researchers discovered. The finding may shed light on why clumping proteins that lead to degenerative brain diseases kill some cells, but leave others untouched. Clumpy proteins known as prions or amyloids have been implicated in many nerve-cell-killing diseases (SN: 8/16/08, p. 20). Such proteins are twisted forms of normal proteins that can make other normal copies of the protein go rogue, too. The contorted proteins band together, killing brain cells and forming large clusters or plaques.
Scientists don’t fully understand why these mobs resort to violence or how they kill cells. Part of the difficulty in reconstructing the cells’ murder is that researchers aren’t sure what jobs, if any, many of the proteins normally perform (SN: 2/13/10, p. 17).
A team led by biophysicists Frederic Rousseau and Joost Schymkowitz of Catholic University Leuven in Belgium came up with a new way to dissect the problem. They started with a protein for which they already knew the function and engineered it to clump. That protein, vascular endothelial growth factor receptor 2, or VEGFR2, is involved in blood vessel growth. Rousseau and colleagues clipped off a portion of the protein that causes it to cluster with other proteins, creating an artificial amyloid.
Masses of the protein fragment, nicknamed vascin, could aggregate with and block the normal activity of VEGFR2, the researchers found. When the researchers added vascin to human umbilical vein cells grown in a lab dish, the cells died because VEGFR2 could no longer transmit hormone signals the cells need to survive. But human embryonic kidney cells and human bone cancer cells remained healthy. Those results suggest that some forms of clumpy proteins may not be generically toxic to cells, says biophysicist Priyanka Narayan of the Whitehead Institute for Biomedical Research in Cambridge, Mass. Instead, rogue clumpy proteins may target specific proteins and kill only cells that rely on those proteins for survival.
Those findings may also indicate that prion and amyloid proteins, such as Alzheimer’s nerve-killing amyloid-beta, normally play important roles in some brain cells. Those cells would be the ones vulnerable to attack from the clumpy proteins. The newly engineered ready-to-rumble protein may open new ways to inactivate specific proteins in order to fight cancer and other diseases, says Salvador Ventura, a biophysicist at the Autonomous University of Barcelona. For instance, synthetic amyloids of overactive cancer proteins could gang up and shut down the problem protein, killing the tumor.
Artificial amyloids might also be used to screen potential drugs for anticlumping activity that could be used to combat brain-degenerating diseases, Rousseau suggests.
The stories of dinosaurs’ lives may be written in fossilized pigments, but scientists are still wrangling over how to read them.
In September, paleontologists deduced a dinosaur’s habitat from remnants of melanosomes, pigment structures in the skin. Psittacosaurus, a speckled dinosaur about the size of a golden retriever, had a camouflaging pattern that may have helped it hide in forests, Jakob Vinther and colleagues say. The dinosaur “was very much on the bottom of the food chain,” says Vinther, of the University of Bristol in England. “It needed to be inconspicuous.” Identifying ancient pigments can open up a wide new world of dinosaur biology and answer all sorts of lifestyle questions, says zoologist Hannah Rowland of the University of Cambridge. “You might be able to take a fossil … and infer a dinosaur’s life history just from its pigment patterns,” she says. “That’s the most exciting thing.”
Not so fast, says paleontologist Mary Schweitzer of North Carolina State University in Raleigh. Evidence for ancient pigments can be ambiguous. In some cases, microscopic structures that appear to be melanosomes may actually be microbes, she says. “Both hypotheses remain viable until one is shot down with data.” Until then, she says, inferring dinosaur lifestyles from alleged ancient pigments is impossible.
Vinther’s work, published in the Sept. 26 Current Biology, is the latest in a long-simmering debate in the field of paleo color, the study of fossil pigments and what they can reveal about ancient animals. Disputes over his team’s findings and what’s needed to clearly identify fossilized melanosomes point to current pitfalls of the field.
But the promise is clear: Paleo color could paint a vivid picture of a dinosaur’s life, offering clues about behavior, habitat and evolution.
“This is a crucial new piece in the puzzle of how the past looked,” Vinther says. Color me dino Psittacosaurus (model shown) was a parrot-beaked herbivore about the size of a large dog. Researchers found signs of pigmentation (black specks) on its tail region, back leg and elsewhere that hint at its habitat.
Tap the image below to see signs of pigmentation from Psittacosaurus fossils. A field emerges Scientists have been puzzling over animals of the past for centuries, but eight years ago, paleontology got a wake-up call. That’s when Vinther and colleagues proposed that microscopic structures in a roughly 125-million-year-old fossil feather were actually a type of melanosome (SN: 8/2/08, p. 10). These pigment pouches rest inside pigment cells and, in this particular fossil feather, might have delivered a blackish hue, like a blackbird’s.
Scientists had noticed similar structures inside fossilized skin and feathers since the early 1980s. But people assumed that these structures were remnants of bacteria — perhaps decomposers that feasted on the dead animals, says paleontologist Martin Sander of the University of Bonn in Germany.
The new, colorful interpretation sparked a flurry of research, and scientists have since spotted what appear to be melanosomes in all kinds of fossilized animals. Paleontology, in fact, is now awash in colors and patterns. Pigment pods may have painted reddish-brown speckles on the face of a Late Jurassic theropod, brushed chestnut stripes on a long-tailed dino from China and made the plumage of a four-winged dinosaur called Microraptor iridescent. That shimmery dinosaur “probably had a weak, glossy iridescence all over its body,” says evolutionary biologist Matthew Shawkey of Ghent University in Belgium. His team deduced Microraptor’s color from the shape of its melanosomes. Modern melanosomes generally carry a mixture of two melanin pigments: dark brown-black eumelanin and red-yellow pheomelanin. Scientists have linked color in mammals and birds to melanosome shape — a meatball shape for reddish brown hues, for example, and a sausage shape for darker colors.
In iridescent feathers, melanosomes tend to be even thinner, Shawkey says. Microraptor’s melanosomes looked like skinny sausages — similar to those seen in the feathers of modern crows and ravens, says Shawkey, who reported the findings with Vinther and colleagues in Science in 2012 (SN Online: 3/9/12).
Three years later, Vinther laid out the case for inferring color — and ancient histories — from fossilized pigments in a review in Bioessays. Not only can the distinctive shapes of melanosomes offer clues, he noted, but chemical tests can help detect the presence of melanin itself. Finding this pigment in fossils, he argued, puts the old bacteria hypothesis to rest.
Schweitzer and colleagues disagreed with Vinther’s take in a review published in Bioessays later in 2015. Researchers need to be cautious when deducing the hues of extinct animals, the scientists wrote. Any melanosome look-alikes in fossilized feathers or skin could actually be microbes. After all, microbes are everywhere. “These animals died in an environment that was not sterile and free from microbes,” Schweitzer says. “Think about it. If you take a piece of chicken and throw it out in your backyard, how long does it take for microbes to overgrow that chicken?”
The tiny organisms are hardy, too. Both microbes and the sticky biofilms they form are preserved in the fossil record. And, Schweitzer says, microbes and melanosomes overlap completely in shape and size, which makes the two tough to tell apart. What’s more, some microbes actually make melanin themselves; detecting the pigment in a fossil is not a rock-solid sign that the ancient animal was black, brown or freckled.
It’s not that Schweitzer or Bioessays coauthor Johan Lindgren, a geologist at Lund University in Sweden, doubt that melanosomes can leave traces in the fossil record. The issue, Lindgren says, is that not all round structures you find are melanosomes.
Chemical tests could help distinguish the two. Bacteria, for example, leave behind traces that can be identified with pyrolysis gas chromatography-mass spectrometry. But that requires samples to be vaporized. “It can mean destroying much of what you are trying to study,” says geochemist Roy Wogelius of the University of Manchester in England. “So it’s not always possible.”
Vinther’s new work isn’t likely to settle the debate. In fact, people were arguing both sides in October at a meeting of the Society of Vertebrate Paleontology in Salt Lake City.
Arindam Roy, a Bristol colleague of Vinther’s, reported size differences between fossilized melanosomes and bacteria growing on decaying chicken feathers in the lab. Alison Moyer, an N.C. State colleague of Schweitzer’s, said that looks weren’t enough. Finding keratin, a protein that typically surrounds melanosomes, could serve as evidence for pigments in fossils.
From color to camouflage The fossil described in Vinther’s new paper is “spectacular,” Schweitzer says. “It’s got skin all over the place. I can’t think of too many dinosaur specimens that are preserved like this.”
The dinosaur lies on its back, flattened in a slab of volcanic rock. Skin covers a completely intact skeleton, and dozens of long bristles poke from the tail. Psittacosaurus, an herbivore that lived some 120 million years ago, walked on two legs and would have reached about half a meter in height. “It would have been a supercute animal,” Vinther says. “It’s got this wide face and looks a little bit like E.T.”
Black material speckles the dinosaur’s body, tail and face. Vinther believes the material is the ancient remains of pigment. His team examined samples chipped from the fossil and saw what he considers the telltale orbs of melanosomes — mostly impressions in the rock but also some microbodies, the 3-D structures themselves.
Based on the dinosaur’s pigment patterns, it would have had a dark back that faded to a lighter belly. That type of coloring, called countershading, shows up in animals from penguins to fish and may act as a form of camouflage. It lightens parts of the body typically in shadow, and darkens parts typically exposed to light. “If you want to hide, it makes sense to try and obliterate those shadows,” Rowland says.
Their prediction for diffuse light matched the model painted like Psittacosaurus. “It’s like what we see in forest-living animals,” Vinther says. “This thing was camouflaged.” Lingering doubts Going from fossil to forest may be more of a leap than a step, other scientists suggest.
Psittacosaurus’ skin very well may contain ancient pigments, Wogelius says. “I don’t think it’s a crazy idea.” But, he adds, of Vinther’s group: “I don’t think they’ve proved what they claim.”
Vinther’s team, for exampl e, used just four tiny fossil samples to extrapolate the coloring of the whole dinosaur. “I think it’s a bit of an overreach,” Wogelius says.
Schweitzer also notes that the specimen was varnished, presumably to protect the bones and soft tissues. It happened before Vinther and colleagues got their hands on the dinosaur and makes it impossible to perform the chemical tests that would bolster the claim for pigments. “Varnish is horribly destructive to fossils,” she says. “It totally ruins the specimen for other types of analysis.”
Vinther argues that his team has chemically analyzed other fossils and found evidence of melanin — not bacteria. The microbodies in those fossils look just like the ones in Psittacosaurus, he says.
Vinther’s team also saw evidence of just one kind of microbody, and it had a distinct round shape. If the structures were actually bacteria, he says, you’d expect to see a whole range of shapes and sizes. “Some of them would be shaped like corkscrews, some would have flagella, some would be humongous, some would be tiny.”
That’s the tricky part with bacteria, counters Lindgren. “In some cases you can have a huge consortium, but in other cases you can have one single type.” Vinther’s interpretation has its supporters. “I was skeptical at first,” Sander says, “but now there’s been such an array of these little bodies that it’s pretty clear that at least some of them are not bacteria.” Despite some continuing controversy, Sander says many paleontologists now accept that microstructures in fossils may be melanosomes.
Additional research, though, “would help the entire community,” he says, “so that there are no longer any lingering doubts.”
Along with chemical tests, Schweitzer suggests, researchers could try transmission electron microscopy, a technique that blasts an electron beam through a thinly sliced sample. With TEM, melanosomes appear as black blobs. Bacteria tend to look different — in some cases, more like fried eggs.
Shawkey, for one, is looking to chemistry. In a paper published online November 14 in Palaeontology, his team used a technique called Raman spectroscopy to help build a case for feather color in a bird that died some 120 million years ago. In the feathers, the researchers spotted the skinny sausages of iridescent melanosomes and chemical signs of the pigment eumelanin. Shawkey thinks the chemical evidence could help “head off any criticism that we might encounter.”
Working through the field’s snags, paleontologists might come together to fill in the hues and tints, and potentially the habits and habitats, of ancient animals that until recently had been known primarily by their bones.
A pair of simultaneous nuclear explosions, one more than 1.6 miles underground and the other 1,000 feet above it, have been proposed as a way to extract huge quantities of natural gas from subterranean rock. Each blast would be … about 2.5 times the size of the bomb used at Hiroshima. By breaking up tight gas-bearing rock formations, a flow of presently inaccessible gas may be made available.… A single-blast experiment, called Project Gasbuggy, is already planned. — Science News, December 17, 1966 Update On December 10, 1967, Project Gasbuggy went ahead, with a 29-kiloton nuclear explosion deep underground in northwestern New Mexico. The blast released natural gas, but the gas was radioactive. The area is still regularly monitored for radioactive contamination. Today, natural gas trapped below Earth’s surface is often extracted via fracking, which breaks up rock using pressurized fluid (SN: 9/8/12, p. 20). Though less extreme, potential links to drinking water contamination and earthquakes have stoked fears about the technique.
It was barely more than half a century ago that the Nobel Prize–winning virologist Sir Frank Macfarlane Burnet mused about the demise of contagions. “To write about infectious disease,” he wrote in 1962, “is almost to write of something that has passed into history.”
If only. In the past several decades, over 300 infectious pathogens have either newly emerged or emerged in new places, causing a steady drumbeat of outbreaks and global pandemic scares.
Over the course of 2016, their exploits reached a crescendo. Just as the unprecedented outbreak of Ebola in West Africa was collapsing in early 2016, the World Health Organization declared Zika virus, newly erupted in the Americas, an international public health emergency. What would balloon into the largest outbreak of yellow fever in Angola in 30 years had just begun. A few months later, scientists reported the just-discovered “superbug” mcr-1 gene in microbes collected from humans and pigs in the United States (SN Online: 5/27/16). The gene allows bacteria to resist the last-ditch antibiotic colistin, bringing us one step closer to a looming era of untreatable infections that would transform the practice of medicine. Its arrival presaged yet another unprecedented event: the convening of the United Nations General Assembly to consider the global problem of antibiotic-resistant bugs. It was only the fourth time over its 70-plus-year history that the assembly had been compelled to consider a health challenge. It’s “huge,” says University of Toronto epidemiologist David Fisman. But even as UN delegates arrived for their meeting in New York City in September, another dreaded infection was making headlines again. The international community’s decades-long effort to end the transmission of polio had unraveled. In 2015, the WHO had declared Nigeria, one of the three last countries in the world that suffered the infection, free of wild polio. By August 2016, it was back. Millions would have to be vaccinated to keep the infection from establishing a foothold. Three fundamental, interrelated factors fuel the microbial comeback, experts say. Across the globe, people are abandoning the countryside for life in the city, leading to rapid, unplanned urban expansions. In crowded conditions with limited access to health care and poor sanitation, pathogens like Ebola, Zika and influenza enjoy lush opportunities to spread. With more infections mingling, there are also more opportunities for pathogens to share their virulence genes.
At the same time, global demand for meat has quadrupled over the last five decades by some estimates, driving the spread of industrial livestock farming techniques that can allow benign microbes to become more virulent. The use of colistin in livestock agriculture in China, for example, has been associated with the emergence of mcr-1, which was first discovered during routine surveillance of food animals there. Genetic analyses suggest that siting factory farms full of chickens and pigs in proximity to wild waterfowl has played a role in the emergence of highly virulent strains of avian influenza. Crosses of Asian and North American strains of avian influenza caused the biggest outbreak of animal disease in U.S. history in 2014–2015. Containing that virus required the slaughter of nearly 50 million domesticated birds and cost over $950 million. Worryingly, some strains of avian influenza, such as H5N1, can infect humans. The thickening blanket of carbon dioxide in the atmosphere resulting from booming populations of people and livestock provides yet another opportunity for pathogens to exploit. Scientists around the world have documented the movement of disease-carrying creatures including mosquitoes and ticks into new regions in association with newly amenable climatic conditions. Climate scientists predict range changes for bats and other animals as well. As the organisms spread into new ranges, they carry pathogens such as Ebola, Zika and Borrelia burgdorferi(a bacterium responsible for Lyme disease) along with them. Since we can rarely develop drugs and vaccines fast enough to stanch the most dangerous waves of disease, early detection will be key moving forward. Researchers have developed a welter of models and pilot programs showing how environmental cues such as temperature and precipitation fluctuations and the insights of wildlife and livestock experts can help pinpoint pathogens with pandemic potential before they cause outbreaks in people. Chlorophyll signatures, a proxy for the plankton concentrations that are associated with cholera bacteria, can be detected from satellite data, potentially providing advance notice of cholera outbreaks.
Even social media chatter can be helpful. Innovative financing methods, such as the World Bank’s recently launched Pandemic Emergency Financing Facility — a kind of global pandemic insurance policy funded by donor countries, the reinsurance market and the World Bank — could help ensure that resources to isolate and contain new pathogens are readily available, wherever they take hold. Right now, emerging disease expert Peter Daszak points out, “we wait for epidemics to emerge and then spend billions on developing vaccines and drugs.” The nonprofit organization that Daszak directs, EcoHealth Alliance, is one of a handful that instead aim to detect new pathogens at their source and proactively minimize the risk of their spread.
Burnet died in 1985, two years after the discovery of HIV, one of the first of the latest wave of new pathogens. His vision of a contagion-free society was that of a climber atop a foothill surrounded by peaks, mistakenly thinking he’d reached the summit. The challenge of surviving in a world of pathogens is far from over. In many ways, it’s only just begun.
SAN FRANCISCO — One climate doomsday scenario can be downgraded, new research suggests.
Decades of atmospheric measurements from a site in northern Alaska show that rapidly rising temperatures there have not significantly increased methane emissions from the neighboring permafrost-covered landscape, researchers reported December 15 at the American Geophysical Union’s fall meeting.
Some scientists feared that Arctic warming would unleash large amounts of methane, a potent greenhouse gas, into the atmosphere, worsening global warming. “The ticking time bomb of methane has clearly not manifested itself yet,” said study coauthor Colm Sweeney, an atmospheric scientist at the University of Colorado Boulder. Emissions of carbon dioxide — a less potent greenhouse gas — did increase over that period, the researchers found. The CO2 rise “is still bad, it’s just not as bad” as a rise in methane, said Franz Meyer, a remote sensing scientist at the University of Alaska Fairbanks who was not involved in the research. The measurements were taken at just one site, though, so Meyer cautions against applying the results to the entire Arctic just yet. “This location might not be representative,” he said.
Across the Arctic, the top three meters of permafrost contain 2.5 times as much carbon as the CO2 released into the atmosphere by human activities since the start of the Industrial Revolution. As the Arctic rapidly warms, these thick layers of frozen soil will thaw and some of the carbon will be converted by hungry microbes into methane and CO2, studies that artificially warmed permafrost have suggested. That carbon will have a bigger impact on Earth’s climate as methane than it will as CO2. Over a 100-year period, a ton of methane will cause about 25 times as much warming as a ton of CO2.
A research station in Alaska’s northernmost city, Barrow, has been monitoring methane concentrations in the Arctic air since 1986 and CO2 since 1973. An air intake on a tower about 16.5 meters off the ground constantly sniffs the air, taking measurements. Barrow has warmed more than twice as fast as the rest of the Arctic over the last 29 years. This rapid warming “makes this region of the Arctic a great little incubation test to see what happens when we have everything heating up much faster,” Sweeney said.
Over the course of a year, methane concentrations in winds wafting from the nearby tundra rise and fall with temperatures, the Barrow data show. Since 1986, though, seasonal methane emissions have remained largely stable overall. But concentrations of CO2 in air coming from over the tundra, compared with over the nearby Arctic Ocean, have increased by about 0.02 parts per million per year since 1973, the researchers reported.
The lack of an increase in methane concentrations could be caused by the thawing permafrost allowing water to escape and drying the Arctic soil, Sweeney proposed. This drying would limit the productivity of methane-producing microbes, potentially counteracting the effects of warming. Tracking Arctic wetness will be crucial for predicting future methane emissions in the region, said Susan Natali, an Arctic scientist at the Woods Hole Research Center in Falmouth, Mass. Studies have shown increased methane emissions from growing Arctic lakes, she points out. “We’re going to get both carbon dioxide and methane,” she said. “It depends on whether areas are getting wetter or drier.”
