The planet Mercury is about to throw some shade at Earth.

For about seven hours on Monday, May 9, the innermost planet will trek across the face of the sun and cast a shadow on our planet. During its journey, a rare event known as a transit, Mercury will appear as a tiny black speck on the sun. The transit will begin at 7:12 a.m. Eastern Daylight Time and end at 2:42 p.m. It will be visible from most countries, though folks in Japan, Australia, New Zealand, and islands in the West Pacific are out of luck.

Transits of Mercury happen on average about eight times a century and only in May or November. The last one was in 2006; the next one won’t be until 2019.

Don’t stare at the sun to try and see it. Seriously. Don’t do that. Staring at the sun is dangerous. Plus, Mercury is tiny. A solar-filtered telescope with at least 50x magnification is the best and safest way to enjoy the show. Many astronomy clubs and organizations will have viewing events. And there will be many ways to see it online such as NASA TV, the Virtual Telescope Project and the Slooh Observatory.

Packing on a few pounds may not be such a bad thing.

As a group, overweight people are living the longest nowadays, suggests an almost four-decade study in Denmark published May 10 in JAMA. And obese people seem to be at no higher risk of dying than those of normal weight. The new analysis fuels ongoing debate about what’s a healthy body mass index — especially in light of rising obesity rates (SN: 5/14/16, p. 5), improved heart health treatments and other factors influencing health and longevity.
“This is a very carefully done study,” says Rexford Ahima, a physician who studies endocrine disorders at the University of Pennsylvania School of Medicine. The findings strengthen the notion that “BMI as a number alone may not be sufficient to predict health and risk of death. It has to be taken within context.” Ahima was not involved in the research but has analyzed previous studies urging a rethink of how BMI influences mortality.

Researchers screen for obesity by calculating BMI — a popular but fairly crude measurement of body fat reached by dividing a person’s weight in kilograms by the square of height in meters. People with BMIs between 18.5 and 24.9 are considered normal. A BMI between 25 and 29.9 is “overweight”; 30 and above is “obese.”

Many studies suggest that obese individuals face a higher risk of heart disease, stroke and other ills. But some analyses have found that heavier folks may not in fact be in such dire straits. In one study of type 2 diabetes patients, those with normal weight when diagnosed were more likely to die than those who were overweight or obese (SN: 9/8/12, p. 13). And a 2013 meta-analysis of 97 studies found that being overweight was associated with lower risk of death than having a normal BMI — a surprising finding that echoed a 2005 study by the same researchers.

In this new analysis, clinical biochemist Børge Nordestgaard of Copenhagen University Hospital and his team studied more than 100,000 adults. The three groups of white Danes, recruited about 15 years apart, reflected the general population in Copenhagen.

From 1976 to 2013, BMI associated with lowest risk of death increased from 23.7 to 27. That falls squarely in the overweight category. What’s more, obese individuals had the same mortality risk as people in the normal range, the analysis found. That trend held even when researchers took into account potentially confounding factors including age, sex, smoking and a history of cardiovascular disease or cancer.
While some might misinterpret the study to mean “you can eat as much as you like,” this is not what the findings suggest, Nordestgaard says. Rather, the results indicate that people who are moderately overweight might not need to worry as much as they had in the past. That might be because better treatments are now available for high blood pressure, high cholesterol and other risk factors for heart disease, Nordestgaard speculates. “So maybe you can be overweight if you have [these conditions] treated.” But the study was not designed to address whether improved heart health care actually caused “healthy” BMI values to creep up over time.

It’s also unclear whether the results apply to other ethnic groups. A substantial fraction of Asians, for instance, develop type 2 diabetes and heart disease despite having BMIs lower than the existing cutoff point for being overweight.

The findings underscore the idea that a person’s BMI does not tell the whole story. While this measure is good for comparing populations, it is not as useful for evaluating individuals and their risk for disease and death, Ahima says. Interpreting an individual’s BMI depends on many other factors, including “whether you are man or woman, how much muscle you have, how physically fit you are and what diseases you have.”

COLD SPRING HARBOR, N.Y. — Garbled signals from cellular antennas may have grounded the Galápagos cormorant.

Galápagos cormorants (Phalacrocorax harrisi) are the only cormorant species with wings too small to lift the birds’ large bodies off the ground. Broken primary cilia —antennas that cells need to receive key developmental messages — left the cormorants with stunted wings, UCLA evolutionary biologist Alejandro Burga suggested May 12 at the Biology of Genomes meeting.

Burga and colleagues compared DNA of flightless Galápagos cormorants with that of their close relatives, including double-crested cormorants (Phalacrocorax auritus), which have large wings and can fly. The researchers found more than 23,000 differences in more than 12,000 genes. Those changes have occurred within the last 2 million years, a short time by evolutionary standards.
Many of those genes probably have nothing to do with wing size. So Burga and colleagues narrowed down which genes might have had the biggest effect on cormorant evolution using a computer program that predicts whether a change in a gene will affect its function. Genes that have mutations that damage function may have big evolutionary consequences. Of the genes predicted to have altered function, the researchers selected the 3.3 percent that have changed most drastically in Galápagos cormorants.

To determine what these genes do, Burga examined whether any of the human versions of these genes cause problems when they are mutated in people. Eight of the banged-up genes were associated with limb defects caused by faulty primary cilia, hairlike structures that grow from cells. The cilia receive signals important for the development and proper functioning of cells (SN: 11/3/12, p.16). In people, genetic mutations that damage primary cilia lead to a wide variety of diseases, including developmental defects.

Normal versions of those eight genes are necessary for primary cilia to pick up signals sent by an important protein called hedgehog. Those genes are so crucial for normal development that evolution has not allowed them to change much in 300 million years. Three other genes that are mutated in the flightless cormorants affect other aspects of the primary cilia. In people, mutant versions of all 11 cilia genes can cause small limbs, extra fingers and short ribs, Burga said.

It wasn’t clear whether the cilia defects were the primary cause of the birds’ flightlessness. So Burga further narrowed his focus to 10 of the altered Galápagos cormorant genes predicted by the computer program to give the biggest functional and evolutionary disadvantages. Those genes would be the most important wing shrinkers, Burga and his colleagues reasoned.

One of those top 10 candidates is a gene called CUX1. The protein it produces helps turn on other genes. Vertebrates from primitive coelacanths to people have nearly identical versions of the gene. But in flightless cormorants, four amino acids have been lost from the protein, suggesting that it can no longer do its job or does it poorly. In chickens, a defective form of CUX1 can shrink wings. That finding indicates the Galápagos cormorant’s altered form of CUX1 might also make wings smaller because it fails to turn on limb growth genes.
Many researchers would have left the story at that point, says Ludovic Orlando, an evolutionary biologist at the University of Copenhagen. “But they didn’t simply stop there,” Orlando says. “They made an effort to validate their findings. It’s unusual.”

Burga and colleagues wondered whether CUX1 and the primary cilia changes were related. The researchers injected cells used to mimic skeletal development in lab dishes with the normal vertebrate version of CUX1. Activity levels of two cilia genes rose by about 50 percent. That is evidence that CUX1 normally helps to regulate activity of primary cilia genes.

But the Galápagos cormorant version of CUX1 barely budged activity of the cilia genes. It also was not as good at stimulating growth and development of bone cells as the normal version, the researchers found. Those findings strengthen the case that CUX1 and primary cilia together were involved in shrinking the flightless fowl’s wings.

It’s still a mystery why Galápagos cormorants have normal size legs, Burga said.

Houseflies stretch their legs to land. Bumblebees hover, then slowly descend. Now, insect-sized flying robots have a way to stick the landing, too.

A tiny aerial bot about the size of a bee (nicknamed RoboBee) uses static electricity to cling to the underside of a leaf and perch on other materials, study coauthor Robert Wood of Harvard University and colleagues report in the May 20 Science.

RoboBee, a bot with shiny, flapping wings and four pinlike legs, is the first of its size that can fly, perch on a surface and then take off again. This energy-saving feat could one day extend mission time in search and rescue operations, the researchers say.
For robots, tackling the problem of flight has been easier than figuring out how to land. “Engineers have been trying to build perching mechanisms for flying robots nearly as long as we have been creating flying robots,” Wood says.
Researchers have had success with bigger, bird-sized bots (SN: 2/7/15, p. 18), but their landing mechanisms are tricky to scale down. For the microbot, Wood and colleagues wanted something simple: lightweight and without moving parts.

The team created an “electroadhesive” patch with electrodes that can be charged, letting the patch stick to different surfaces, like a balloon sticking to the wall after being rubbed on someone’s hair.

Switch the electrodes on and the patch, a circular disc on top of the robot, helps RoboBee hang out on overhanging pieces of glass or plywood, for example. Switch the electrodes off and the bot detaches, free to fly again. The sticky contraption lets RoboBee rest between flights: The bot used about a thousandth as much energy perching than hovering, the researchers found.

The cooling effect of pollution may have been exaggerated.

Fossil fuel burning spews sulfuric acid into the air, where it can form airborne particles that seed clouds and cool Earth’s climate. But that’s not the only way these airborne particles can form, three new studies suggest. Tree vapors can turn into cooling airborne particles, too.

The discovery means these particles were more abundant before the Industrial Revolution than previously thought. Climate scientists have therefore overestimated cooling caused by air pollution, says atmospheric chemist Urs Baltensperger, who coauthored the three studies.
Simulating unpolluted air in a cloud chamber, Baltensperger and colleagues created microscopic particles from vapors released by trees. In the real world, cosmic rays whizzing into the atmosphere foster the development of these particles, the researchers propose in the May 26 Nature. Once formed, the particles can grow large enough to form the heart of cloud droplets, the researchers show in a second paper in Nature. After sniffing the air over the Swiss Alps, some of the same researchers report in the May 27 Science the discovery of the particles in the wild.

“These particles don’t just form in the laboratory, but also by Mother Nature,” says Baltensperger, of the Paul Scherrer Institute in Villigen, Switzerland.

Airborne particles, called aerosols, are microscopic bundles of molecules. Some aerosols start fully formed, such as dust and salts from sea spray, while others assemble from molecules in the atmosphere.

Since the 1970s, scientists have suspected that sulfuric acid is a mandatory ingredient for aerosols assembled in the air. Sulfuric acid molecules react with other molecules to form clusters that, if they grow large enough, can become stable. Human activities such as coal burning have boosted sulfuric acid concentrations in the atmosphere, subsequently boosting the abundance of aerosols that seed clouds and reflect sunlight like miniature disco balls. That aerosol boost partially offsets warming from greenhouse gases.

A cloud chamber at the CERN laboratory near Geneva allowed Baltensperger and his collaborators to simulate the atmosphere when sulfuric acid was scarce. The researchers added alpha-pinene, the organic vapor that gives pine trees their characteristic smell, to pristine air and watched for growing aerosols. Previous, though inconclusive, work suggested that the pine vapors might form aerosols.
Alpha-pinene molecules reacted with ozone in the air and formed molecules that reacted and bundled together to form aerosols, the researchers observed. The researchers added an extra layer of realism by using one of CERN’s particle beams to mimic ions from the cosmic rays bombarding Earth’s atmosphere. The “rays” led to the formation of as many as 100 times the number of aerosols. The added ions help stabilize the growing aerosols, the researchers propose.

Further testing showed that the newborn aerosols can rapidly grow from around 2 nanometers wide — roughly the diameter of a DNA helix — to 80 nanometers across, large enough to seed cloud droplets.

At a research station high in the Swiss Alps, researchers observed aerosol formation during atmospheric conditions with low sulfuric acid concentrations and abundant molecules akin to alpha-pinene. The researchers couldn’t confirm the rapid growth seen in the lab, though.

Quantifying the overall climate influence of fossil fuel burning in light of the new discovery will be tricky, says Renyi Zhang, an atmospheric chemist at Texas A&M University in College Station. “Atmospheric processes are complex,” he says. “They had a pure setup, but in reality the atmosphere is loaded with chemicals. It’s hard to draw direct conclusions at this point.”

Painkillers in the opium family may actually make pain last longer. Morphine treatment after a nerve injury doubled the duration of pain in rats, scientists report the week of May 30 in the Proceedings of the National Academy of Sciences.

The results raise the troubling prospect that in addition to having unpleasant side effects and addictive potential, opioids such as OxyContin and Vicodin could actually extend some types of pain. If a similar effect is found in people, “it suggests that the treatment is actually contributing to the problem,” says study coauthor Peter Grace, a neuroscientist at the University of Colorado Boulder.
Scientists have known that opioid-based drugs can cause heightened sensitivity to pain for some people, a condition called opioid-induced hyperalgesia. The new study shows that the effects linger weeks after use of the drugs is stopped. Male rats underwent surgery in which their sciatic nerves, which run down the hind legs, were squeezed with a stitch — a constriction that causes pain afterward. Ten days after surgery, rats received a five-day course of either morphine or saline.

Rats that didn’t receive morphine took about four weeks to start recovering, showing less sensitivity to a poke. Rats that got morphine took about eight weeks to show improvements — double the time. “That’s far bigger than we had anticipated,” Grace says. “We were definitely surprised by that.”

These experiments were done with male rats, but unpublished data indicate that morphine extends pain even longer in female rats, Grace says, results that fit with what’s known about differences in how males and females experience pain.

Longer-lasting pain in the rats came courtesy of an inflammatory response in the spinal cord. The immune system sees morphine as a threat, the researchers suspect, and responds by revving up inflammation through specialized cells called microglia. Experiments that shut down this process in microglia shortened the duration of the pain.

Many questions remain. Scientists don’t yet know if a similar immune reaction happens in people. Nor is it known whether all opioid-based painkillers would behave like morphine.
Understanding the details of how the process works has important implications for doctors, many of whom may be unaware of opioids’ complex relationship with pain, says internal medicine physician Jonathan Chen of Stanford University School of Medicine. Clarity on how opioids influence pain could change doctors’ prescribing habits and encourage the search for better pain treatments, he says.

Grace points out that the experiments were done in genetically similar rats, and that people may have more varied responses to opioids. That variability might mean that not everyone would be at risk for such long-lasting pain, he says. “But clearly these data suggest that there may be a subset of people who might be in trouble.”

Radiation from the 23 nuclear tests conducted near Bikini Atoll in the 1940s and ’50s has lingered far longer than previously predicted.

Radioactive material such as cesium-137 currently produces, on average, 184 millirems of radiation per year on Bikini Atoll. And some parts of the island hit 639 millirems per year, researchers report online the week of June 6 in the Proceedings of the National Academy of Sciences. Those measurements, made last year, surpass the 100 millirems per year safety standard set by the United States and the Republic of the Marshall Islands, which controls the island.

Scientists had predicted that, by now, radiation levels would have dropped to 16 to 24 millirems per year. But those estimates came from extrapolating from measurements made in the 1970s. The mismatch probably stems from incorrect assumptions about how rapidly radioactive material washes off the island, proposes study coauthor Emlyn Hughes, a physicist at Columbia University.

Whether the higher radiation levels pose a serious health risk to caretakers who live on the island for part of the year depends on how long they stay on the island and whether the local fruit they eat is safe, Hughes says.

A new technique turns climate-warming carbon emissions to stone. In a test program in Iceland, more than 95 percent of the carbon dioxide injected into basaltic lava rocks mineralized into solid rock within two years. This surprisingly fast transformation quarantined the CO2 from the atmosphere and could ultimately help offset society’s greenhouse gas emissions, scientists report in the June 10 Science.

“It’s working, it’s feasible and it’s fast enough to be a permanent solution for storing CO2 emissions,” says study coauthor Juerg Matter, a geochemist at the University of Southampton in England.
Many existing carbon storage schemes pump CO2 underground, though the approach has been prone to leaks. Targeting basalt, the cooled remains of volcanic outpourings, may offer an advantage over other types of rock. As much as 25 percent of basalt is made up of elements that react with CO2 to form solid carbonate minerals such as limestone, a process that occurs naturally during rock weathering. Since it was thought that this mineralization process takes hundreds to thousands of years in most rock, it seemed far too slow to be useful in combating near-term climate change.
In Iceland, Matter and colleagues blended groundwater with 230 tons of CO2 emissions from a geothermal power plant to create a kind of seltzer water. The researchers then injected the mixture 400 to 800 meters belowground into basaltic rock. After about two years, the team collected samples of the deep rock — and discovered that almost all of the CO2 had mineralized.

At $17 per ton, mineralizing carbon emissions is roughly twice as expensive as existing storage methods, though doesn’t require long-term monitoring to prevent leaks, Matter says. Additionally, the approach only requires water and basalt, he says, and “we have enough basalt globally to take care of all anthropogenic CO2 emissions, theoretically.”

Another research group’s work backs up the new findings. Peter McGrail, a geochemist at the Pacific Northwest National Laboratory in Richland, Wash., and colleagues conducted similar tests using pure CO2 without water. The as-yet-unpublished findings revealed rapid mineralization similar to that reported by Matter and colleagues, McGrail says.

If you want to lock new information into your brain, try working up a sweat four hours after first encountering it.

This precisely timed trick, described June 16 in Current Biology, comes courtesy of 72 people who learned the location of 90 objects on a computer screen. Some of these people then watched relaxing nature videos, while others worked up a sweat on stationary bikes, alternating between hard and easy pedaling for 35 minutes. This workout came either soon after the cram session or four hours later.

Compared with both the couch potatoes and the immediate exercisers, the people who worked out four hours after their learning session better remembered the objects’ locations two days later. The delayed exercisers also had more consistent activity in the brain’s hippocampus, an area important for memory, when they remembered correctly. That consistency indicates that the memories were stronger, Eelco van Dongen of the Donders Institute in the Netherlands and colleagues propose.

The researchers don’t yet know how exercise works its memory magic, but they have a guess. Molecules sparked by aerobic exercise, including the neural messenger dopamine and the protein BDNF, may help solidify memories by reorganizing brain cell connections.

Australia has seen zero mass shootings in the 20 years since it enacted strict gun control laws and a mandatory gun buyback program, researchers report June 22 in JAMA.

Key to this success is probably the reduction in people’s exposure to semiautomatic weapons, Johns Hopkins University health policy researcher Daniel Webster writes in an accompanying editorial.

“Here’s a society that recognized a public safety threat, found it unacceptable, and took measures to address the problem,” Webster says.
In April 1996, a man with two semiautomatic rifles shot and killed 35 people in Tasmania and wounded at least 18 others. Two months after the shooting, known as the Port Arthur massacre, Australia began implementing a comprehensive set of gun regulations, called the National Firearms Agreement.

The NFA is famous for banning semiautomatic long guns (including the ones used by the Port Arthur shooter), but, as Webster points out, it also made buying other guns a lot harder too. People have to document a “genuine need,” pass a safety test, wait a minimum of 28 days, have no restraining orders for violence and demonstrate good moral character, among other restrictions, Webster writes.

“In Australia, they look at someone’s full record and ask, ‘Is this a good idea to let this person have a firearm?’” Webster says. In the United States, “we do pretty much the opposite. The burden is on the government to show that you are too dangerous to have a firearm.”

Australia also initiated a mandatory gun buyback program in 1996, leading to the purchase and destruction of more than 650,000 semiautomatic and pump-action rifles and shotguns.

Simon Chapman of the University of Sydney and colleagues tallied up mass shootings before and after the NFA and analyzed 35 years of mortality data from the Australian Bureau of Statistics.
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From 1979 to 1996, Australia had 13 fatal mass shootings involving five or more victims (not including the shooter), Chapman and colleagues report. From 1997 to May 2016, the country has had none. (Three shootings, however, have killed three or four victims.) Chapman’s team also found that the rate of gun deaths dropped rapidly after 1996 but can’t confirm that this reduction is due to the gun laws.