Mooching roommates are an ancient problem. Certain species of beetles evolved to live with and leech off social insects such as ants and termites as long ago as the mid-Cretaceous, two new beetle fossils suggest. The finds date the behavior, called social parasitism, to almost 50 million years earlier than previously thought.

Ants and termites are eusocial — they live in communal groups, sharing labor and collectively raising their young. The freeloading beetles turn that social nature to their advantage. They snack on their hosts’ larvae and use their tunnels for protection, while giving nothing in return.

Previous fossils have suggested that this social parasitism has been going on for about 52 million years. But the new finds push that date way back. The specimens, preserved in 99-million-year-old Burmese amber, would have evolved relatively shortly after eusociality is thought to have popped up.

One beetle, Mesosymbion compactus, was reported in Nature Communications in December 2016. A different group of researchers described the other, Cretotrichopsenius burmiticus, in Current Biology on April 13. Both species have shielded heads and teardrop-shaped bodies, similar to modern termite-mound trespassers. Those adaptations aren’t just for looks. Like a roommate who’s found his leftovers filched one too many times, termites frequently turn against their pilfering housemates.

A hard look at experimental setups may start to explain dueling predictions on whether ocean acidification will boost, or choke, vital marine nitrogen fixers. So far, the new look trends toward choking.

As people release more and more carbon dioxide into the air, the ocean takes up the gas and edges closer toward acidity. In these shifting waters, marine microbes called Trichodesmium could falter in adding nitrogen, a critical input for marine food webs, says Dalin Shi of Xiamen University in China. And the problem could be exacerbated in acidifying seas where iron is scarce — for instance, in wide swaths of tropical and subtropical waters such as the southern Atlantic and Pacific oceans, Shi and colleagues report April 27 in Science.
The question of how Trichodesmium cyanobacteria are reacting to the changing ocean makes a big difference in predicting how other marine life, from whales to mere specks of floating plankton, will react, too. Nitrogen, essential to life for such basic processes as building DNA and proteins, makes up much of Earth’s atmosphere. Yet most living things can’t do any chemistry with the atmospheric form, two nitrogen atoms fiercely triple-bonded to each other. Trichodesmium microbes, however, can crack those bonds and transform nitrogen into more usable forms. These cyanobacteria may account for up to half of the nitrogen fixed in the ocean.

Lab research in the past 10 years generally suggested that increasing CO2 encouraged the photosynthetic Trichodesmium to grow more abundantly and supply more usable nitrogen. The rates varied, however. But when Shi and colleagues tried their version of the experiment, they found a decrease in nitrogen fixation, not an increase. “I was very excited, and I was really puzzled,” says Shi, who published the results in 2012.

After a string of detailed lab work, from culturing lab microbes to sampling wild cyanobacteria, he and colleagues propose an explanation for the contradictions. For one thing, much of the previous lab work used a recipe for artificial seawater that permitted contamination by toxic metals and forms of nitrogen, the researchers concluded. These unwanted additions introduced unexplained variety to the results.

Also, Shi and collaborators demonstrated that rising CO2 alone can stimulate the microbes’ growth but that the watery slide toward ocean acidity can depress the microbes’ ability to fix nitrogen. And if the cyanobacteria are growing in water short on iron, an essential nutrient for them, the slowdown in nitrogen fixation can overwhelm any positive growth effects from extra CO2.

The paper could be a big help in resolving the contradictions among experiments, says oceanographer Douglas Capone of the University of Southern California in Los Angeles.

Orly Levitan, an author of what may have been the first study of acidification boosting nitrogen fixation, says she would consider changing her seawater recipe based on the new paper if she were to revisit this work. Yet Levitan, who studies plankton at Rutgers University in New Brunswick, N.J., cautions against extrapolating too far. A look at wild Trichodesmium suggests that the cyanobacteria may have unexpected ways of compensating in iron-starved waters, enhancing the capture of minerals from dust settling out of the air, for instance. It’s too early, she says, to close discussion on what will happen in the complexities of the real ocean.

Oxygen on comets might not date all the way back to the birth of the solar system.

Instead, interactions between water, particles streaming from the sun and grains of sand or rust on the comet’s surface could generate the gas. Those interactions could explain the surprising abundance of O2 detected in the fuzzy envelope of gas around comet 67P/Churyumov-Gerasimenko in 2015 (SN: 11/28/15, p. 6), researchers report May 8 in Nature Communications. Such reactions might also reveal how oxygen forms in other regions of space.
“Molecular oxygen is very hard to find out there in the universe,” says Caltech chemical engineer Konstantinos Giapis. When the Rosetta spacecraft detected oxygen around comet 67P, astronomers argued it must be primordial, trapped in water ice as the comet formed roughly 4.6 billion years ago. Intrigued by the result, Giapis and Caltech colleague Yunxi Yao wanted to see if an alternative way to create O2 existed. Drawing on their work with fast-moving charged particles and materials such as silicon, they performed experiments that showed that charged water particles could slam into rust or sand grains and generate O2.

Something similar could happen on comet 67P, they suggest. As the sun evaporates water from the comet’s surface, ultraviolet light could strip an electron from the water, giving it a positive charge. Then, fast-moving particles in the solar wind could shoot the ionized water back toward the comet’s surface, where it could collide with rust or sand particles. Atoms of oxygen from the water could pair with atoms of oxygen from the rust or sand, creating O2.

The idea is plausible, says Paul Goldsmith, an astrophysicist at NASA’s Jet Propulsion Laboratory in Pasadena, Calif. He helped discover O2 in the Orion nebula and says the reaction might happen in places where young stars are forming and in other regions of space.

Rosetta mission scientist Kathrin Altwegg of the University of Bern in Switzerland calls the result interesting, but is skeptical it can explain comet 67P’s oxygen abundance. As the comet gets closer to the sun, a protective bubble develops around 67P, data from the mission showed; that bubble would prevent solar wind particles or other ionized particles from reaching the comet’s surface, Altwegg says. Also, the ratio of oxygen to un-ionized water also stays constant over time. It should be more variable if this chemical reaction were generating oxygen on the comet, she says.

Goldsmith, however, suggests researchers keep an open mind and design missions with instruments to test whether this newly detected reaction does, in fact, generate oxygen in space.

For black adults, moving out of a racially segregated neighborhood is linked to a drop in blood pressure, according to a new study. The finding adds to growing evidence of an association between a lack of resources in many predominately black neighborhoods and adverse health conditions among their residents, such as diabetes and obesity.

Systolic blood pressure — the pressure in blood vessels when the heart beats — of black adults who left their highly segregated communities decreased just over 1 millimeter of mercury on average, researchers report online May 15 in JAMA Internal Medicine. This decline, though small, could reduce the overall incidence of heart failure and coronary heart disease.
“It’s the social conditions, not the segregation itself, that’s driving the relationship between segregation and blood pressure,” says Thomas LaVeist, a medical sociologist at George Washington University in Washington, D.C., who was not involved with the study. “Maybe hypertension is not so much a matter of being genetically predisposed.” That’s important, LaVeist adds, because it means that racial health disparity “can be fixed. It’s not necessarily contained in our DNA; it’s contained in the social DNA.”

Racial segregation can impact a neighborhood’s school quality, employment opportunities or even whether there is a full-service grocery store nearby. Social policies that improve residents’ access to education, employment and fresh foods can “have spillover effects in health,” says Kiarri Kershaw, an epidemiologist at Northwestern University Feinberg School of Medicine in Chicago.

Kershaw and colleagues examined data from a study of how cardiovascular disease progresses in healthy adults, aged 18 to 30, who were recruited from four locations: Chicago, Minneapolis, Oakland, Calif., and Birmingham, Ala. The researchers specifically looked at blood pressure readings for 2,280 black participants, recorded at six points over 25 years, and noted their addresses at the time of each reading. A neighborhood’s designation of high, medium or low racial segregation was based on the percentage of black residents in the neighborhood compared with the larger metropolitan area or county, Kershaw says.

At the start of the study in the mid-1980s, 1,861 participants were living in highly segregated neighborhoods. A temporary move to a less segregated neighborhood, the researchers found, was associated with a 1 millimeter of mercury drop in blood pressure on average.

If the change of address was permanent — as it was for 243 participants — the impact was greater. On average, blood pressure dropped close to 6 millimeters of mercury for those who moved to low-segregation neighborhoods, and nearly 4 millimeters for a move to a medium-segregation neighborhood.
A 2015 study in the Journal of the American Heart Association estimates that a decrease in systolic blood pressure of 1 millimeter of mercury could result in several thousand fewer cases of heart failure, stroke and coronary heart disease annually in the U.S. population of black adults aged 45 to 64, Kershaw says.

Along with other research on racial segregation and health, the findings suggest that policies that improve housing conditions, educational resources and employment opportunities “will have implications for the health of individuals,” LaVeist says. “Social policy is health policy.”

Smarty-pants have 40 new reasons to thank their parents for their powerful brains. By sifting through the genetics of nearly 80,000 people, researchers have uncovered 40 genes that may make certain people smarter. That brings the total number of suspected “intelligence genes” to 52.

Combined, these genetic attributes explain only a very small amount of overall smarts, or lack thereof, researchers write online May 22 in Nature Genetics. But studying these genes, many of which play roles in brain cell development, may ultimately help scientists understand how intelligence is built into brains.
Historically, intelligence research has been mired in controversy, says neuroscientist Richard Haier of the University of California, Irvine. Scientists disagreed on whether intelligence could actually be measured and if so, whether genes had anything at all to do with the trait, as opposed to education and other life experiences. But now “we are so many light-years beyond that, as you can see from studies like this,” says Haier. “This is very exciting and very positive news.”

The results were possible only because of the gigantic number of people studied, says study coauthor Danielle Posthuma, a geneticist at VU University Amsterdam. She and colleagues combined data from 13 earlier studies on intelligence, some published and some unpublished. Posthuma and her team looked for links between intelligence scores, measured in different ways in the studies, and variations held in the genetic instruction books of 78,308 children and adults. Called a genome-wide association study or GWAS, the method looks for signs that certain quirks in people’s genomes are related to a trait.

This technique pointed out particular versions of 22 genes, half of which were not previously known to have a role in intellectual ability. A different technique identified 30 more intelligence genes, only one of which had been previously found. Many of the 40 genes newly linked to intelligence are thought to help with brain cell development. The SHANK3 gene, for instance, helps nerve cells connect to partners.

Together, the genetic variants identified in the GWAS account for only about 5 percent of individual differences in intelligence, the authors estimate. That means that the results, if confirmed, would explain only a very small part of why some people are more intelligent than others. The gene versions identified in the paper are “accounting for so little of the variance that they’re not telling us much of anything,” says differential developmental psychologist Wendy Johnson of the University of Edinburgh.

Still, knowing more about the genetics of intelligence might ultimately point out ways to enhance the trait, an upgrade that would help people at both the high and low ends of the curve, Haier says. “If we understand what goes wrong in the brain, we might be able to intervene,” he says. “Wouldn’t it be nice if we were all just a little bit smarter?”

Posthuma, however, sees many roadblocks. Beyond ethical and technical concerns, basic brain biology is incredibly intricate. Single genes have many jobs. So changing one gene might have many unanticipated effects. Before scientists could change genes to increase intelligence, they’d need to know everything about the entire process, Posthuma says. Tweaking genetics to boost intelligence “would be very tricky.”

Lots of newborn decorations come in black and white, so that young babies can better see the shapes. But just because it’s easier for babies to see bold blacks and whites doesn’t mean they can’t see color.

Very few studies of color vision in newborns exist, says Anna Franklin, a color researcher at the University of Sussex in England. “But those that have been conducted suggest that newborns can see some color, even if their color vision is limited,” she says. Newborns may not be great at distinguishing maroon from scarlet, but they can certainly see a vivid red.

But as babies get a little older, they get remarkably adept at discerning the world’s palette, new research shows. Babies ages 4 months to 6 months old are able to sort colors into five categories, researchers report in the May 23 Proceedings of the National Academy of Sciences.

These preverbal color capabilities offer insight into something scientists have long wondered: Without words for individual colors, how do babies divvy up the hues across the color wheel, telling when blue turns to green, for instance?

Along with Franklin and colleagues, psychologist Alice Skelton, also of the University of Sussex, bravely approached this question. The team coaxed 179 4- to 6-month-old babies to calmly and repeatedly look at two squares, each 1 of 14 various colors.

After showing babies two squares of the same color over and over, the researchers made one of the squares a new color. Gazing at the new hue longer was a sign that the baby recognized the color as new. In this meticulous way, the researchers worked their way around the entire color wheel for each baby.

The experiment required stamina, from both Skelton and the young participants. “Sometimes you can have whole weeks where the babies just don’t want to do it,” she says. Despite that, she found the process enjoyable: “Babies are nice people.”
Babies, like adults, bin hues into red, yellow, green, blue and purple, Skelton and her colleagues found. “Given the commonalities and patterns you see in the way that languages divide up the color spectrum, we did expect that we would see some evidence of these same patterns in the way babies divide up the spectrum,” Skelton says. “What was surprising, for me at least, was how nicely it fell out.”

That discernment comes even though the babies probably don’t know the words for the colors. This suggests that babies are most likely born with these categories preprogrammed in their brains. The babies in the study came from just one culture. But “we anticipate that infants from different cultures would categorize color similarly,” Franklin says.

The results offer an interesting window into what’s happening in a baby’s brain as she learns about her world. And the results also come with a gentle suggestion: Don’t restrict your newborn’s art to black and white. She may already harbor a fondness for blue.

Acting like miniature trees that soak up sunlight and release oxygen, photosynthetic bacteria injected into the heart may lighten the damage from heart attacks, a new study in rats suggests.

When researchers injected the bacteria into rats’ hearts, the microbes restored oxygen to heart tissue after blood supply was cut off as in a heart attack, researchers at Stanford University report June 14 in Science Advances.

“It’s really out of the box,” says Himadri Pakrasi, a systems biologist at Washington University in St. Louis who was not involved in the research. “It reads like science fiction to me, but it’s fantastic if it works.”
The organism, called Synechococcus elongatus, has been used recently to produce biofuels, but this may be the first time the cyanobacteria have ever been used in a medical setting, he says.

Other researchers also reacted enthusiastically to the study. “It’s outrageous, but outrageous in a good way,” says Susan Golden, who studies cyanobacteria at the University of California, San Diego. Cardiovascular scientist Matthias Nahrendorf of Massachusetts General Hospital in Boston says, “I enjoy the idea. It’s really fresh.”

Bringing oxygen to starved tissues is what Stanford cardiovascular surgeon Joseph Woo had in mind when he and colleagues dreamed up the plan to put light-harvesting bacteria into the heart. In a heart attack, clogged arteries or blood clots cut off blood flow to the organ. Without oxygen supplied by the blood, heart cells die.

Woo wanted a way for the heart to make its own oxygen or access another supply until doctors could open blocked vessels and restore blood flow. Plants make oxygen from carbon dioxide and sunlight, so Woo wondered, “Why not bring the tree to your heart?”

He and colleagues started by grinding up kale and spinach to harvest chloroplasts, the organelles within plant cells that carry out photosynthesis. But the chloroplasts didn’t survive outside the cells. That’s when the researchers learned about S. elongatus, a photosynthetic organism that Golden and other researchers have long used to study circadian rhythms.
After finding that cyanobacteria could provide oxygen to heart cells in a lab dish, the next step was to see how the cyanobacteria would fare in an animal. The researchers stopped blood flow to part of rats’ hearts and after 15 minutes injected either cyanobacteria or a saline solution. Oxygen in tissue with bacteria increased to about three times the levels measured right after the heart attack, similar to what saline-treated rats experienced.
That was in the dark: When researchers exposed the heart to light, rats that got the bacteria had 25 times higher oxygen levels than they did after the heart attack. Four weeks after the treatment, these rats had less heart damage than untreated rodents, indicating long-term benefits. In fact, the hearts of photosynthesis-treated rats were beating strongly: Blood flow out of the heart was 30 percent higher in rats treated with cyanobacteria and light than those treated with the bacteria in the dark. That extra blood flow could make the difference between life and death for some patients, Woo says. The results indicate that the bacteria need light to supply heart cells with enough oxygen to stave off damage. That presents a difficulty if the cyanobacteria are ever to be used in people: Getting light into the heart is a major hurdle.

“It will be next to impossible to open the chest to light,” says Nahrendorf. “A day on the beach won’t do the trick.” Woo says the researchers are working with engineers at Stanford to make devices that can shine light through bones and skin to reach the heart and other deep tissues.

Injecting bacteria into the heart is also a risky proposition. “What you’re doing is infecting a tissue, and that’s rarely a good thing,” says Nahrendorf. But the cyanobacteria were cleared from the rats’ bodies within 24 hours and didn’t provoke the immune system to attack the heart, the researchers found. Some other cyanobacteria produce toxins, says Golden. “But this organism is benign,” she says.

Cyanobacteria might also supply oxygen to tissues in other diseases, such as brain injuries, strokes or nonhealing wounds in people with diabetes, says Arnar Geirsson, a cardiovascular scientist at Yale University. Photosynthetic bacteria might also help preserve organs for transplant.

“I’m quite impressed,” Geirsson says. “It’s a really unique way to deliver oxygen.”

Julius Caesar could have stayed home on March 15, 44 B.C. But mocking the soothsayer who had predicted his death, the emperor rode in his litter to Rome’s Forum. There he met the iron daggers of 60 senators.

As he lay in a pool of blood, he may have gasped a final incrimination to his protégé Brutus: You too, my son? Or maybe not. But he certainly would have breathed a dying breath, a final exhalation of some 25 sextillion gas molecules. And it’s entirely possible that you just breathed in one of them.
In fact, calculating the probability of a particle of Caesar’s dying breath appearing in any given liter of air (the volume of a deep breath) has become a classic exercise for chemistry and physics students. If you make a few assumptions about the mixing of gases and the lifetimes of molecules in the atmosphere, it turns out that, on average, one molecule of “Caesar air” — or any other historic liter of air, for that matter — appears in each breath you take.

Author Sam Kean begins his book Caesar’s Last Breath with this exercise, noting that “we can’t escape the air of those around us.” It’s all recycled, and every day we breathe in a bit of our, and Earth’s, history. “The story of Earth,” he writes, “is the story of its gases.”

Kean, author of a best seller about the periodic table, The Disappearing Spoon, then tells that story. As he did in his fascinating portraits of the elements, Kean profiles individual gases such as nitrogen and oxygen primarily through the scientists and entrepreneurs who discovered or sought to harness them. These are quirky men (and they are mostly men) — every bit as obsessed, greedy and brilliant as one could hope for in a page-turner.

Along with lesser-known backstories of textbook heroes such as James Watt, Antoine-Laurent Lavoisier and Albert Einstein (who was surprisingly obsessed with building a better refrigerator), Kean clearly delights in weaving in the unexpected. In the discussion of helium, we learn about Joseph-Michel Montgolfier, the papermaker who was inspired to build the first hot-air balloon as he watched his wife’s pantaloons billowing suggestively above a fire. And in a chapter on the radioactive elements carried in nuclear fallout, there’s Pig 311, a sow that survived a nuclear test blast only to be used as propaganda for the weapons’ supposed safety.

Along the way, Kean threads in the history of Earth’s atmosphere in a surprisingly compelling narrative of geologic history. He steps aside from Lavoisier’s work on life-giving oxygen, for example, to describe the Great Oxygenation Event, which infused the atmosphere a couple billion years ago with a gas that, at the time, was toxic to most living things. The explanations of science here and throughout the book are written clearly and at a level that should be understandable with a high school education. And while they’re straightforward, the explanations have enough depth to be satisfying; by the end of the book, you realize you’ve learned quite a bit.
Even those who rarely read science will enjoy the drama — death, for instance, plays a big role in these stories. Over and over, we learn, men have taken gases’ powers too lightly, or wielded their own power too cruelly, and paid the price. Fritz Haber, for instance, could have died a hero for finding a way to make fertilizer from the nitrogen in air. Instead, he died broke and loathed for his World War I work on gas warfare.

Then there was Harry Truman — not that Truman, but the one who refused to leave his home when scientists warned of an impending volcanic eruption. Truman contended that officials were “lying like horses trot” right up until Mount St. Helens blew searing gases that erased him from the mountainside.

The links between these stories can seem at first as ephemeral as the gases, but together they tell the story of the birth of the atmosphere and humans’ history in it. In the end, like Caesar’s breath, it all comes full circle.

A common pin dropped on a table from a height of one-eighth of an inch generates about 10 ergs of energy, obviously a minuscule amount. That 10 ergs raises temperature, and even that tiny amount is “much too much” to be allowed in the experiment during which Dr. Arthur Spohr of the Naval Research Laboratory reached the lowest temperature yet achieved — within less than a millionth of a degree of absolute zero. — Science News, July 8, 1967.

Update
Today, scientists can make clouds of atoms at temperatures as low as 50 trillionths of a degree above absolute zero (SN: 5/16/15, p. 4). Late this year or early next year, NASA will launch its Cold Atom Laboratory to the International Space Station so scientists can study ultra­cold atoms reaching 100 trillionths of a degree or less. In orbit, gravity doesn’t drag atoms down, so the clouds can stay intact for scientists’ observations for up to 10 seconds — longer than is possible on Earth.

Boosting the activity of certain brain cells can help a mouse climb the social ladder.

Nerve cells in a region called the dorsomedial prefrontal cortex appear to control whether male mice are dominant or submissive to other males, researchers report in the July 14 Science. The finding adds to previous evidence that this brain region is involved in social interactions in mammals.

Like men flexing muscles or flaunting sports cars to win status, male mice compete to establish a social pecking order. When every mouse knows his place, there can be less social conflict in the long run, says James Curley, a neurobiologist at the University of Texas at Austin who wasn’t part of the study.
In dominance tests, researchers pitted mice head-to-head in a plastic tube too narrow for the animals to pass each other. With no way forward, the lower-ranking mouse eventually retreats, pushed out of the tube by the more dominant mouse.

Researchers recorded the activity of individual nerve cells, or neurons, in mice’s brains while they engaged in the tube test. A group of neurons in the dorsomedial prefrontal cortex fired faster when mice were pushing forward to claim space in the tube, and fired more slowly as the mice retreated, says study coauthor Hailan Hu, a neuroscientist at Zhejiang University in Hangzhou, China.

Hu’s team then manipulated the activity of those neurons and once again measured the mice’s performance in the tube. Mice with these neurons inactivated via druglike small molecules didn’t try as hard on the tube task and were more likely to lose the competition, the researchers found. Mice with those neurons amped up with light, on the other hand, won against opponents who had previously beaten them. If those mice won enough times in one day, they’d even keep their newly elevated status for two or three days.
Other studies have also suggested a role for the prefrontal cortex in controlling social dynamics in several species, including humans, Curley says. The new study adds detail by allowing the researchers to track how neural firing influences behavior immediately and then follow the effect over time.

However, the tube experiment measures dominance dynamics in pairs of mice, Curley points out, rather than in larger groups. “Whether the same mechanism underlies social dominance under all contexts is yet to be discovered,” he says.

Other factors, such as an animal’s size, can also influence its ability to win a fight. But Hu says that persistence is key, and that this group of neurons appears to affect that quality. “In risk tests, what’s important is how much effort you want to put into the competition,” she says. “Some mice quit easily.”

Mouse studies like this one don’t translate directly to humans. But they allow scientists to study the neurobiology of dominance behaviors in levels of detail that aren’t possible in human subjects.

The study tested only male mice. In the future, Hu wants to find out whether a similar brain mechanism holds for female mice, too.