Remarkably preserved bones of rat-sized creatures excavated in an Indian coal mine may come from close relatives of the first primatelike animals, researchers say.
A set of 25 arm, leg, ankle and foot fossils, dating to roughly 54.5 million years ago, raises India’s profile as a possible hotbed of early primate evolution, say evolutionary biologist Rachel Dunn of Des Moines University in Iowa and her colleagues. Bones from Vastan coal mine in Gujarat, India’s westernmost state, indicate that these tiny tree-dwellers resembled the first primates from as early as 65 million years ago, the scientists report in the October Journal of Human Evolution. These discoveries add to previously reported jaws, teeth and limb bones of four ancient primate species found in the same mine. “The Vastan primates probably approximate a common primate ancestor better than any fossils found previously,” says paleontologist and study coauthor Kenneth Rose of Johns Hopkins University School of Medicine. The Vastan animals were about the size of living gray mouse lemurs and dwarf lemurs, weighing roughly 150 to 300 grams (roughly half a pound), the investigators estimate. Dunn’s group has posted 3-D scans of the fossils to Morphosource.org ( SN: 3/19/16, p. 28 ) so other researchers can download and study the material. Most Vastan individuals possessed a basic climbing ability unlike the more specialized builds of members of the two ancient primate groups that gave rise to present-day primates, the researchers say. One of those groups, omomyids, consisted of relatives of tarsiers, monkeys and apes. The other group, adapoids, included relatives of lemurs, lorises and bushbabies. The Indian primates were tree-dwellers but could not leap from branch to branch like lemurs or ascend trees with the slow-but-sure grips of lorises, the new report concludes.
Vastan primates probably descended from a common ancestor of omomyids and adapoids, the researchers propose. India was a drifting landmass headed north toward a collision with mainland Asia when the Vastan primates were alive. Isolated on a huge chunk of land, the Indian primates evolved relatively slowly, retaining a great number of ancestral skeletal traits, Rose suspects.
“It’s possible that India played an important role in primate evolution,” says evolutionary anthropologist Doug Boyer of Duke University. A team led by Boyer reported in 2010 that a roughly 65-million-year-old fossil found in southern India might be a close relative of the common ancestor of primates, tree shrews and flying lemurs (which glide rather than fly and are not true lemurs).
One possibility is that primates and their close relatives evolved in isolation on the island continent of India between around 65 million and 55 million years ago, Boyer suggests. Primates then spread around the world once India joined Asia by about 50 million years ago.
That’s a controversial idea. An increasing number of scientists suspect primates originated in Asia. Chinese primate fossils dating to 56 million to 55 million years ago are slightly older than the Vastan primates (SN: 6/29/13, p. 14; SN: 1/3/04, p. 4). The Chinese finds show signs of having been omomyids.
And in at least one respect, Boyer says, some of the new Vastan fossils may be more specialized than their discoverers claim. Vastan ankle bones, for instance, look enough like those of modern lemurs to raise doubts that the Indian primates were direct descendants of primate precursors, he holds.
Dunn, however, regards the overall anatomy of the Vastan fossils as “the most direct evidence we have” that ancestors of early primates lacked lemurs’ leaping abilities, contrary to what some researchers have argued.
Where you live and what you eat can rapidly affect the types of friendly bacteria inhabiting your body. To see how the microbes that inhabit the mouth and intestines change over time, Duke University computational biologist Lawrence David zealously chronicled his microbiome for an entire year. (For more on David and this experiment, see “Lawrence David’s gut check gets personal.”)
A stream plot (below, top graph) shows the ebb and flow of phyla of bacteria in his gut over time. The thickness of each stream indicates a bacterial group’s relative abundance in daily fecal samples. David peered closer at the data in a horizon plot (above, bottom graph; colored squares at left indicate the phylum of the bacteria represented in each row). He first determined each type of bacteria’s normal abundance in his gut, then calculated how much they differed from the median abundance. Warmer colors (red, orange, yellow) indicate that bacteria in that group increased in abundance, and cooler colors (blue, green) indicate a decrease in abundance. Living abroad from day 71 to day 122 had a dramatic — but short-lived — effect on David’s microbiome.
Using records unearthed from library storage vaults, researchers recently revealed that the sugar industry paid nutrition experts from Harvard University to downplay studies linking sugar and heart disease. Although the incident happened in the 1960s, it appears to have helped redirect the scientific narrative for decades.
The documents — which include correspondence, symposium programs and annual reports — show that the Sugar Research Foundation (as it was named at the time) paid professors who wrote a two-part review in 1967 in the New England Journal of Medicine. That report was highly skeptical of the evidence linking sugar to cardiovascular problems but accepting of the role of fat. The now-deceased professors’ overall conclusion left “no doubt” that reducing the risk of heart disease was a matter of reducing saturated fat and cholesterol, according to researchers from the University of California, San Francisco, who published their report online September 12 in JAMA Internal Medicine.
“Why does it matter today? The sugar industry helped deflect the way the research was developing,” says study coauthor Cristin Kearns, a dentist at UCSF’s Institute for Health Policy Studies. The Harvard team’s scientific favoritism had a role in directing research and policy attention toward fat and cholesterol. And in fact, the first dietary guidelines published by the federal government in 1980 said there was no convincing evidence that sugar causes heart disease, stating “the major health hazard from too much sugar is tooth decay.” Following the publication of the Harvard report, fat and cholesterol went on to hijack the scientific agenda for decades, and even led to a craze of low-fat foods that often added sugar. Kearns points out that it was only in 2015 that dietary guidelines finally made a strong statement to limit sugar. Researchers writing this year in Progress in Cardiovascular Diseases note that current studies estimate that diets high in added sugars carry a three times higher risk of death from cardiovascular disease. (For its part, the Sugar Association says in a statement on its website that “the last several decades of research have concluded that sugar does not have a unique role in heart disease.”)
The level at which the food industry continues to influence nutrition research is still a much-debated topic. The Sugar Association’s statement acknowledged the secret deal occurred, but pointed out that “when the studies in question were published, funding disclosures and transparency standards were not the norm they are today.” Journals now require all authors to list conflicts of interest, especially funding from a source has a vested interest in the outcome.
That doesn’t mean that trade groups and industry associations no longer have an influence on scientists, says Andy Bellatti, cofounder and strategic director of Dietitians for Professional Integrity, which has campaigned to push the Academy of Nutrition and Dietetics to sever its ties with industry, While a modern researcher could not take corporate money, even for speaking fees, without disclosure, the influences may be more subtle, he says. “We’re not talking about making up data, but perhaps influencing how a research question is framed.”
In a commentary published with the JAMA study, Marion Nestle, a nutrition researcher at New York University, wrote that industry influence has not disappeared. She cited recent New York Times investigations of Coca-Cola–sponsored research and Associated Press stories revealing that a candy trade group sponsored research attempting to show that children who eat sweets have a healthy body weight.
Bellatti says that researchers don’t necessarily want to be cozy with industry, but sometimes turn to commercial sources because non-biased research money is lacking. “The reason the food industry is able to do this is because there is such little public funding for nutrition and disease,” Bellatti says. For that reason, the scientific community should not reject industry money wholesale, says John Sievenpiper, a physician and nutrition researcher at the University of Toronto. A study of his was once ridiculed on Nestle’s blog because the disclosures covered two full pages. He believes that any scientist who takes industry money should adhere to an even higher standard of openness, including releasing study protocols ahead of time so reviewers can make sure the research question was not changed midstream to favor a certain conclusion.
While many parallels have been made between the food and tobacco industries, Sievenpiper believes those comparisons miss the complicated nature of the human diet. Tobacco is always bad, never good. Sugar, fat, cholesterol and other components of diet are some of both, making research into their effects much more nuanced, he says. And unlike with tobacco, the solution can’t be to never eat them. He believes solutions won’t involve turning single nutrients like fat or sugar into villains, but promoting better overall patterns of eating, like the Mediterranean diet.
Kearns, who has spent the past 10 years looking into the sugar industry’s influence on science, isn’t finished yet. She says her curiosity first arose during a conference on gum disease and diabetes in 2007, when she noticed a lack of scientific discussion of sugar. She started out simply Googling industry influences. The trail eventually led her to scour library archives, until she came across dusty boxes of records from a closed sugar company in Colorado. “The first page I looked at in that archive had a confidential memo,” she says. “I knew I had something no one else had never talked about before.”
She doesn’t see the research going sour any time soon. “This was their 226th project in 1965,” she says. “There’s a lot more to the story.”
X-rays were the iPhone 7 of the 1890s. Months after X-rays were discovered in late 1895, German physicist Walter Koenig put the latest in tech gadgetry to the test by scanning 14 objects, including the mummified remains of an ancient Egyptian child. Koenig’s image of the child’s knees represented the first radiographic investigation of a mummy.
At the time, details on the mummy itself were scant. Originally collected by explorer-naturalist Eduard Rueppell in 1817, the specimen lacked any sort of decoration that might link it to a particular dynasty or time period. Koenig’s X-ray image of the mummy served less to fill in any of those blanks and more to demonstrate the technology’s potential. Since then, radiographic images have revealed hidden artifacts, elucidated embalming techniques and even pinpointed health issues and diseases in mummies. Now, biological anthropologist and Egyptologist Stephanie Zesch of the Reiss Engelhorn Museum in Mannheim, Germany, and colleagues have examined the mummy with modern imaging techniques. CT scans show that the child was a boy. His teeth suggest that he was 4 to 5 years old when he died. Radiocarbon dating places him in the Ptolemaic period, between 378 and 235 B.C., the researchers report online July 22 in the European Journal of Radiology Open. The team also diagnosed a slew of health conditions: a common chest wall deformity called pectus excavatum, or sunken chest; bone density marks called Harris lines in his leg bones that indicate physiological stress; and an enlarged liver. The team attributes the distended liver to a parasitic infection like schistosomiasis, which is common in Egypt and sometimes lethal. Without any obvious signs of trauma, however, “it’s impossible to determine cause of death,” Zesch says.
Even with the all-seeing power of today’s CT scans, the culprit behind the boy’s demise remains under wraps.
Coral reefs are bustling cities beneath tropical, sunlit waves. Thousands of colorful creatures click, dash and dart, as loud and fast-paced as citizens of any metropolis.
Built up in tissue-thin layers over millennia, corals are the high-rise apartments of underwater Gotham. Calcium carbonate skeletons represent generations of tiny invertebrate animals, covered in a living layer of colorful coral polyps. Their structures offer shelter, and for about 114 species of fish and 51 species of invertebrates, those coral skyscrapers are lunch.
Important as they are, corals are in jeopardy. Warming oceans are causing more and more corals to bleach white and become vulnerable to destruction. A prolonged spike in temperatures, just 1 to 2 degrees Celsius, is enough to kill the marine animals. Greenhouse gas emissions also acidify the water, dissolving the calcium skeletons. In some countries, fishermen use dynamite to catch fish, leaving behind coral rubble. Today, more than 60 percent of the world’s reefs are at risk of disappearing. Threats to reefs have “dramatically escalated in the last few decades,” says marine scientist Peter Harrison of Southern Cross University in Lismore, Australia. He has studied corals for three decades. “In my time as a reef researcher,” Harrison says, “I’ve seen it get worse, firsthand.”
Thirty years ago, massive coral bleachings were unheard of. Today, reefs are suffering through a third global bleaching event since 1998. With high ocean temperatures dragging on since 2014, this summer marked the longest and most widespread episode of worldwide coral bleaching on record (SN: 7/23/16, p. 5). Australia has been hit especially hard. More than 80 percent of the northern part of the Great Barrier Reef is bleached and close to half of those corals have died, according to a report in April from Australia’s National Coral Bleaching Taskforce.
As reefs take a nose dive, scientists from Hawaii to the Philippines and the Caribbean are scrambling to save corals. Approaches that were once considered radical are “now seen as necessary in some places,” says coral biologist Ruth Gates of the Hawaii Institute of Marine Biology on Oahu.
In Florida, researchers are restoring reefs with tiny coral fragments. In Hawaii, Gates is scouring the water for stress-tolerant corals and experimenting in the lab to breed the hardiest individuals. At the 13th International Coral Reef Symposium in Honolulu in June, Harrison’s team reported early promising results of its effort to flood damaged reefs in the Philippines with tiny coral larvae.
What works on one reef won’t necessarily save another. So researchers are testing an arsenal of options to rescue a diversity of underwater communities.
A different story In the early 1980s, Harrison was a graduate student at James Cook University in Townsville, Australia, working on the Great Barrier Reef. At the time, textbooks taught that most corals reproduce by brooding: Fertilization occurred inside the body and larvae were released into the water to replenish reefs year-round. But Harrison witnessed something very different. For a few nights around a full moon in springtime, corals spawned, spewing eggs and sperm into the water to be externally fertilized. The sea was covered in a pink, oily slick.
“We found the corals hadn’t read the textbooks,” Harrison says. Eggs and sperm were meeting outside of the coral bodies, and larvae were developing while drifting in the currents.
That discovery spurred a cascade of studies on coral reproduction that led to the modern understanding that many corals reproduce only once or twice a year, in coordinated mass releases of eggs and sperm. Most of the resulting larvae die or drift out to sea, Harrison says. Only a small fraction survive to adulthood. Even so, mass spawns are “how reefs replenish themselves over time,” he says.
Just after Harrison’s discovery, the Great Barrier Reef, and then reefs around the globe, experienced bleaching on a massive scale. Normally, tiny algae live inside coral polyps. The algae make sugar and other nutrients for the coral, and can give polyps their characteristic bright colors. But when temperatures spike, algae become toxic. Corals spit out their partners, bleach white and can die if temperatures don’t cool enough for the algae to return (SN Online: 10/8/15).
Corals worldwide were bleaching more often and more severely than had been recorded in the past. Scientists began to worry that reefs were in trouble. Some researchers, like Dave Vaughan, who manages the Coral Reef Restoration program at the Mote Tropical Research Laboratory in Summerland Key, Fla., took action.
In those days, Vaughan was a fish farmer, raising saltwater fish species in captivity. He began growing corals for tropical aquarium tanks. At the time, all the corals in the aquarium trade were taken from the wild, Vaughan says. He started growing coral species in captivity as an environmentally friendly alternative.
One day, Philippe Cousteau, grandson of legendary aquanaut Jacques, toured the operation. When the young Cousteau saw that Vaughan was raising corals for aquariums, “he shook his head,” Vaughan remembers, “and said ‘Dave, if you could do this for the aquarium trade, you can do this for the reef.’”
In those earliest days, most scientists were tackling small-scale reef damage caused by dropped anchors or boat groundings, Vaughan says. To repair that kind of minor damage, scientists began breaking 3- to 5-centimeter fragments from healthy corals on a neighboring reef and transplanting the chunks in damaged spots.
Cousteau’s visit convinced Vaughan that he should try restoring reefs. While doing so, 11 years ago, Vaughan made a game-changing discovery: Tinier fragments of coral, only 1 centimeter long, repair themselves 25 to 40 times as fast as scientists had ever recorded corals growing.
Today Vaughan’s team is spreading many of these microfragments over the surface of dead coral skeletons in the Florida Keys. As those bits fuse back together, they create a fast-growing “skin” over an otherwise dead reef. Condemned buildings are refurbished rather than razed.
The hope is that thousands of microfragments will carpet a small reef in two to three years, says Chris Page, a biologist at Mote Marine Laboratory working with Vaughan. That’s super fast. “There’s no way that’s happening in nature,” Page says.
Vaughan’s team is cultivating 17 species for microfragmentation in large troughs on land, with seawater running through them. He is focused on the top six slow-growing massive species that create the foundation of the reef. Some can live for centuries, mounded into boulders the size of a truck. The Florida researchers plunged their first 200 microfragments into the ocean three years ago, at two sites in a nearshore coral reef off Big Pine Key, Fla. The colonies are now six to eight times as large as they were at planting and have begun to fuse together into areas about the size of a 5-gallon bucket lid. Since then, Vaughan and Page have planted close to 10,000 microfragments in the wild. “People were looking for some glimmer of light,” Vaughan says. “And restoration is turning out to be that in a big way.”
Seeds of reefs Fragmentation and the newer microfragmentation are both time- and labor-intensive, and therefore very expensive. And, Harrison says, they rely on cloning.
When one coral is broken into fragments, to be fattened up and then planted around a reef, each chunk is genetically identical. All those pieces have the same DNA blueprint to fight infection and to deal with stress. Unlike natural reefs, where individuals are genetically distinct and have different vulnerabilities, cloned corals share the same weaknesses.
“People have spent years growing coral gardens only to have them wiped out by the next bleaching event,” Harrison says. With more diversity, he adds, some of those corals might have survived. In a warmer world where bleaching and disease will probably become more common, “genetic diversity equals resilience.”
To address the diversity issue, Vaughan and Page are raising 20 to 30 genetic variants of each coral species, to be planted around the reef. They are also collecting eggs and sperm from wild colonies of four coral species to grow on Summerland Key.
Harrison has been thinking about genetic diversity ever since the early 1980s, when he saw corals spewing sperm and eggs into the ocean. Few of the resulting larvae would survive. Many would drift away and most would die. All while Harrison saw reefs in decline.
What if, he wondered, scientists could take millions of those diverse coral larvae and help them settle onto reefs to replenish ailing ecosystems?
Other researchers asked themselves the same question. In the late 1990s and from 2007 to 2009, two teams, in Australia and Palau, released coral larvae onto healthy reef areas in mesh tents pitched over the seabed. In both studies, thousands of larvae settled under the tents, many more than scientists would have seen naturally.
But those early results may have been misleading. Most of the early settlers in Palau died within 30 weeks. Flooding the reef with larvae didn’t make a lasting difference in coral numbers. Maybe, the researchers speculated, settlers were too crowded, which meant swamping reefs with larvae made no sense.
Harrison wasn’t ready to give up. Even though most of the new settlers had died, those studies were done on healthy reefs, he says. In battered areas, where some baby corals might naturally drift in, but not enough for the reef to self-heal, a flush of larvae could be a shot in the arm.
The idea was to find a badly damaged reef, where the worst problems, such as blast fishing, had stopped. Harrison would bring a few of the reef’s mature, sexually active corals to the lab, persuade them to release sperm and eggs in aquarium tanks, and then take more than a million of their larvae back out to the reef. The plan was to saturate the environment with settling babies, as adult corals would have done in healthier days.
In 2013, Harrison’s team, led by graduate student Dexter dela Cruz, began a small pilot experiment in the Philippines at a reef called Magsaysay, where nearly two decades of fishing with explosives had taken a toll. Blast fishing is “like hitting the reef with a sledgehammer,” Harrison says. Magsaysay’s large foundational corals were blown to bits. A once-vibrant city was now a wasteland. By 2013, the blast fishing had stopped, but Magsaysay wasn’t recovering on its own. So Harrison’s team brought in larvae from a species of fast-growing, purple-tipped coral, called Acropora tenuis, collected from a nearby healthier reef. The scientists released more than a million larvae into floorless mesh tents pitched under-water over the reef. After five days, Harrison’s team removed the mesh enclosures.
Over the next six months, most of the tiny coral settlers died. But, by the nine-month mark, the remaining populations had stabilized. Scientists expected more of the juvenile corals to die, but “incredibly and extraordinarily,” Harrison says, none have. At 3 years old, the juvenile corals have reached sexual maturity and are now the size of dinner plates. In June, dela Cruz presented the findings in Honolulu.
For slower-growing corals, Harrison’s approach will take extra patience. But for fast-growers like A. tenuis, reseeding larvae could be a quick and affordable way to help severely damaged reefs bounce back.
Winning corals Getting more larvae onto damaged reefs is the first step, Harrison says. But some individuals are stronger and more stress-tolerant than others. As they grow up, these “winners” distinguish themselves by surviving.
Across the Pacific from Magsaysay, biologist Gates is studying winners. Rows of indoor and outdoor aquariums gurgle in her lab on Coconut Island, off Oahu’s windward shore. Those tanks are full of Montipora capitata, a local and fast-growing coral collected from the patchy reefs surrounding the island.
In 2014 and 2015, unusually warm water hit Hawaii. Under stress, many corals rejected their symbiotic algae, then blanched from a healthy brown to white; some died.
Gates’ team patrolled the reefs around the island during and after the bleaching, in search of hardy M. capitata individuals that stayed brown, even in hot water. The scientists are also interested in M. capitata that bleached, but then recovered. Gates equates the work to professional sports scouting, “out at high schools, looking for the best athletes.” When she finds top performers, Gates brings them to her lab to run them through their paces, exposing each pro-performer to different temperatures and pH levels in seawater tanks. Some conditions re-create today’s oceans, while others mimic future warm and more acidic seas.
Today, Gates is breeding the strongest corals (her first batch of babies was born in June). She hopes that top performers will have “extremely talented kids” that inherit their parents’ strengths. It’s too soon to tell how the new corals will do once they’re planted out on the reef.
“We’re trying to give corals a leg up,” she says. Reefs healthy enough to survive without human intervention are the ultimate aim. In the next five years, the researchers plan to branch out from M. capitata to look for super corals of all five species found in the bay surrounding Coconut Island.
It would be ideal to find those super corals before the next big bleaching event. But for that, the researchers need another sign of resilience. That sign, Gates says, could be hidden in the way corals glow.
Some coral animals, and their symbiotic algae, are loaded with fluorescent proteins that absorb incoming light, then spit it back out by glowing. It’s unclear what fluorescent proteins do for corals; they may be a kind of sun block, protecting corals from the intense light in shallow seas, or a form of camouflage or part of the immune system.
Stress affects corals’ glowing proteins and changes their fluorescence patterns. In the Pacific and Indian Ocean species Acropora yongei, for instance, researchers reported in 2013 in Scientific Reports that the concentration of green fluorescent protein fell with temperature stress before bleaching and the coral glowed less intensely. In an earlier study, prolonged high temperatures changed the ratio of green to orange fluorescence in the endangered Caribbean coral Orbicella faveolata.
Gates expects that under stress, super corals will keep their healthy fluorescence patterns much longer than corals that are bleaching. One next step, Gates says, is to stress out tiny pieces of coral and watch what happens under a very powerful laser scanning confocal microscope. She’ll expose nubbins of coral to acidifying water or increasing temperatures in a petri dish. The microscope will pick up the fluorescence of the nubbins and may indicate which corals will stay healthy the longest. Once scientists can identify the hardiest corals, they can combine selective breeding with other rehab techniques. Approaches like microfragmentation could help super colonies mature super fast. Then, Gates says, “we would have a strategy to get the reef producing its own offspring quite quickly.”
No two approaches to saving reefs are the same, which is probably a good thing. Coral fragmentation, reseeding and selective breeding each have their pros and cons.
“The assumption that one size will fit all is completely flawed,” Gates says. What might work on the Florida coast wouldn’t necessarily work in the Pacific. Like far-flung cities, each reef has different needs and priorities. Their communities of coral vary as do the threats they face. Some problems, like warming oceans, are global in scope. Others, like pollution from roads and agricultural runoff, overfishing and dynamite fishing, are often more localized. Rehabilitation approaches will vary, depending on the type and severity of damage, and how the mosaic of coral species might respond.
Across the globe, “will the things that we do be different?” Gates asks. “Absolutely.”
Rather than competing, Gates, Vaughan and Harrison are working toward a common goal: to find the right mix of approaches to support the reefs so they no longer need human help.
Editor’s note: Science has retracted the study described in this article. The May 3, 2019, issue of the journal notes that a panel of outside experts convened by Kyoto University in Japan concluded in March 2019 that the paper contained falsified data, manipulated images and instances of plagiarism, and that these were the responsibility of lead author Aiming Lin, a geophysicist at Kyoto University. In agreement with the investigation’s recommendation, the authors withdrew the report.
A titanic volcano stopped a mega-sized earthquake in its tracks.
In April, pent-up stress along the Futagawa-Hinagu Fault Zone in Japan began to unleash a magnitude 7.1 earthquake. The rupture traveled about 30 kilometers along the fault until it reached Mount Aso, one of Earth’s largest active volcanoes. That’s where the quake met its demise, geophysicist Aiming Lin of Kyoto University in Japan and colleagues report online October 20 in Science. The quake moved across the volcano’s caldronlike crater and abruptly stopped, the researchers found.
Geophysical evidence suggests that a region of rising magma lurks beneath the volcano. This magma chamber created upward pressure plus horizontal stresses that acted as an impassable roadblock for the seismic slip powering the quake, the researchers propose. This rare meetup, the researchers warn, may have undermined the structural integrity surrounding the magma chamber, increasing the likelihood of an eruption at Aso.
The eyes may reveal whether the brain’s internal stopwatch runs fast or slow. Pupil size predicted whether a monkey would over- or underestimate a second, scientists report in the Nov. 2 Journal of Neuroscience.
Scientists knew that pupils get bigger when a person is paying attention. They also knew that paying attention can influence how people perceive the passage of time. Using monkeys, the new study links pupil size and timing directly. “What they’ve done here is connect those dots,” says neuroscientist Thalia Wheatley of Dartmouth College. More generally, the study shows how the eyes are windows into how the brain operates. “There’s so much information coming out of the eyes,” Wheatley says. Neuroscientist Masaki Tanaka of Hokkaido University School of Medicine in Japan and colleagues trained three Japanese macaques to look at a spot on a computer screen after precisely one second had elapsed. The study measured the monkeys’ subjective timing abilities: The monkeys had to rely on themselves to count the milliseconds. Just before each trial, the researchers measured pupil diameters.
When the monkeys underestimated a second by looking too soon, their pupil sizes were slightly larger than in trials in which the monkeys overestimated a second, the researchers found. That means that when pupils were large, the monkeys felt time zoom by. But when pupils were small, time felt slower.
The differences in pupil size were subtle, but Tanaka and colleagues think these changes are meaningful. Pupil size, the results suggest, offers a readout of the brain as it keeps track of passing milliseconds.
This pupil readout may reflect a specific type of signaling in the brain. As a chemical messenger called noradrenaline puts the brain into a heightened state of alertness, pupils get bigger, previous research has shown. That link is why this study makes sense, Wheatley says. Attention is known to make time fly, a distortion that would lead a monkey to think a second has elapsed sooner than it has. The opposite is also true. When the brain is a little more sluggish or not paying attention, time ticks by slower and seconds stretch out.
By finding that the eyes hold clues to how the brain perceives time, Tanaka says that the study may motivate further research into how brain cells actually make this split-second calculation (SN: 7/25/15, p. 20).
Growing planets carve rings and spiral arms out of the gas and dust surrounding their young stars, researchers report in three papers to be published in Astronomy & Astrophysics. And dark streaks radiating away from the star in one of the planet nurseries appear to be shadows cast onto the disk by the clumps of planet-building material close to the star. This isn’t the first time that astronomers have spied rings around young stars, but the new images provide a peek at what goes into building diverse planetary systems.
The three stars — HD 97048, HD 135344B and RX J1615.3-3255 — are all youthful locals in our galaxy. They sit between 460 and 600 light-years away; the oldest is roughly a mere 8 million years old. All the stars have been studied before. But now three teams of researchers have used a new instrument at the Very Large Telescope in Chile to see extra-sharp details in the planet construction zone around each star.
The new instrument, named SPHERE, was designed to record images, spectra and polarimetry (the orientations of light waves) of young exoplanet families. Flexible mirrors within the instrument adapt to atmospheric turbulence above the telescope, and a tiny disk blocks light from the star, allowing faint details around the star to come into view.
Seabird poop helps the Arctic keep its cool, new research suggests.
The droppings release ammonia into the atmosphere, where it reacts with other chemicals in the air to form small airborne particles. Those particles form the heart of cloud droplets that reflect sunlight back into space, researchers propose November 15 in Nature Communications.
Even though the poop’s presence provides only modest cooling, understanding the effect could help scientists better predict how the region will fare under future climate change, says study coauthor Greg Wentworth. “The humor is not lost on me,” says Wentworth, an atmospheric chemist at Alberta Environment and Parks in Canada. “It’s a crucial connection, albeit somewhat comical.” Arctic air temperatures are rising about twice as fast as temperatures in lower latitudes (SN: 12/26/15, p. 8), a shift that could threaten ecosystems and alter global weather patterns. Scientists still don’t fully understand Arctic climate, though.
Earlier this year, Wentworth and colleagues reported finding surprisingly abundant ammonia in Arctic air. They linked the chemical to the guano of the tens of millions of seabirds that flock to the frigid north each summer. Bacteria in the Arctic dine on the feces and release about 40,000 metric tons of ammonia annually. (The smell, Wentworth says, is awful.)
Once in the atmosphere, that ammonia reacts with sulfuric acid and water to form small particles that increase the number of cloud droplets, the researchers now propose. A cloud made up of a lot of smaller droplets will have more surface area and reflect more sunlight than a cloud made up of fewer but larger droplets.
This effect causes on average about 0.5 watts of summertime cooling per square meter in the Arctic, with more than a watt of cooling per square meter in some areas, the researchers estimate using a simulation of the Arctic’s atmospheric chemistry. For comparison, the natural greenhouse effect causes about 150 watts of warming per square meter worldwide. On top of that, carbon dioxide from human activities currently contributes about 1.6 watts per square meter of warming on average.
“Birds are in the equation now” when it comes to cloud formation, says Ken Carslaw, an atmospheric scientist at the University of Leeds in England. Understanding how climate change and human activities in the Arctic impact seabirds could be important to forecasting future temperature changes in the region, he says.
Bacteria may be a meat-eating plant’s best friends thanks to their power to reduce the surface tension of water.
The carnivorous pitcher plant Darlingtonia californica releases water into the tall vases of its leaves, creating deathtraps where insect prey drown. Water in a pitcher leaf starts clear. But after about a week, thanks to bacteria, it turns “murky brown to a dark red and smells horrible,” says David Armitage of the University of Notre Dame in Indiana. Now, he’s found that those bacteria can help plants keep insects trapped. Microbial residents reduce the surface tension of water enough for ants and other small insects to slip immediately into the pool instead of perching lightly on the surface, he reports November 23 in Biology Letters.
Armitage seeded tubes of clean water with fluid from the trap pools of pitcher plants and added dead crickets to feed the microbes. After sitting for a month, the mess had about the same surface tension properties as natural pitcher plant pools. Then, he created a series of increasingly dilute samples of pool soup and dropped harvester ants into each one. He found that the ants sank immediately in all but the bacteria-free water sample.
Bacterial populations in a pitcher leaf are akin to those in a mammal gut or bovine rumen, Armitage’s preliminary analysis finds. The microbes can help digest the prey as well as catch it, he says.