Saturn’s ‘Death Star’ moon may not conceal ocean after all

An ocean of liquid water probably doesn’t lurk beneath the icy surface of Mimas, Saturn’s smallest major moon, new calculations suggest. In 2014, scientists had proposed the ocean to help explain an odd wobble in the moon’s orbit (SN: 11/15/14, p. 16).

Other ocean-harboring moons, such as Jupiter’s Europa and Saturn’s Enceladus, are crisscrossed by fractures opened by strong tides that cause their oceans to bulge outward. Mimas, though freckled with craters, lacks any such cracks.

Planetary scientist Alyssa Rhoden of Arizona State University in Tempe and colleagues calculated whether Mimas’ icy shell could withstand the stress of a subsurface ocean pushing outward. Taking into account the moon’s elongated orbit, the team estimates that a subsurface ocean would produce tidal stresses larger than those on crack-riddled Europa. Mimas therefore probably doesn’t have an ocean, the researchers conclude February 24 in the Journal of Geophysical Research: Planets.

Warming soils may belch much more carbon

As the planet warms, carbon stashed in Earth’s soils could escape into the atmosphere far faster than previously thought. In the worst-case scenario for climate change, carbon dioxide emissions from soil-dwelling microbes could increase by 34 to 37 percent by 2100, researchers report online March 9 in Science. Previous studies predicted a more modest 9 to 12 percent rise if no efforts are taken to curb climate change. Those extra emissions could further intensify global warming.

Much of that extra CO2 will originate from soils at depths overlooked by previous measurements, says study coauthor Margaret Torn, a biogeochemist at Lawrence Berkeley National Laboratory in California. “We ignore the deep at our peril,” she says.
Soils cover about two-thirds of Earth’s ice-free land area and store nearly 3 trillion metric tons of organic carbon — more than three times the amount of carbon in the atmosphere. Dead organisms such as plants contribute to this carbon stockpile, and carbon-munching microbes belch some of that carbon into the atmosphere as CO2. Rising temperatures will spur the microbes to speed up their plant consumption, scientists warn, releasing more CO2 into the air. And the data back up that fear.

Scientists have mimicked future warming by heating the top 5 to 20 centimeters of experimental soil plots and measuring the resulting CO2 emissions. Those studies missed deeper soils, though, known to contain more than half of all soil carbon. Warming such deep soils is technically challenging and scientists had generally assumed that any emission increases from so far down were insignificant, says study coauthor Caitlin Hicks Pries, an ecosystem ecologist at Lawrence Berkeley.

Using heating coils and rods embedded in the soil, Hicks Pries, Torn and colleagues warmed a plot of soil for over two years in the forested foothills of California’s Sierra Nevada. The warmth extended to a meter below ground, the full depth of the soil in the area. That heating replicated the roughly 4 degrees Celsius of warming expected by the end of the century in a worst-case scenario. Annual carbon emissions from the soil jumped from 1,100 grams per square meter to 1,450 grams per square meter. Around 40 percent of this emissions increase originated below a depth of 15 centimeters, with 10 percent originating below 30 centimeters.

Assuming other soils behave similarly, by 2100, the increase in the CO2 emission rate from just the soils deeper than 30 centimeters could equal modern-day CO2 emission rates from oil burning, the researchers estimate.

While only 13.5 percent of Earth’s soils resemble the woodland soils examined in the study, Torn says that the experiment shows that scientists need to consider deep soils when calculating future climate change. Studies already in the works will test if the results hold true for other soil types.

The new experiment is exciting and well executed, says Katherine Todd-Brown, a biogeochemist at the Pacific Northwest National Laboratory in Richland, Wash. The net impact soils will have on future climate change, however, remains unclear, she says. The amount of carbon from the atmosphere entering soils could also increase as higher CO2 concentrations and warmer environments promote plant growth. That increased carbon drawdown could offset the climate impacts of the increased emissions, though the magnitude of that effect is still debated (SN Online: 9/22/16). “You really have to take both the inputs and outputs into account,” Todd-Brown says.

Genetic switch offers clue to why grasses are survival masters

Grasses have top-notch border control to conserve water in their leaves. Now, scientists have identified the genetic switch that makes them such masters at taking in carbon dioxide without losing water. The find might eventually help scientists create more drought-resistant crop plants, the researchers report in the March 17 Science.

Adjustable pores called stomata on the undersides of leaves help plants take in CO2 while minimizing water loss. Like pupils responding to sunlight, plants open and close their stomata in response to changing light, humidity and temperature. Grass stomata can open wider and respond more quickly than those in other plants, which helps grasses photosynthesize more efficiently.
This ability might help explain why grasses grow successfully in so many places on Earth, says Brent Helliker, a plant ecologist at the University of Pennsylvania who wasn’t part of the new study. For instance, grasses are particularly well equipped to deal with the rapidly changing weather and strong winds that can hit plains and prairies.

In most plant stomata, two kidney bean–shaped cells, one on each side of the pore, swell or deflate like balloons to control the size of the opening. But in grass, each of these cells is shaped like a dumbbell instead. And each dumbbell is linked to two other cells called subsidiary cells.
Scientists have long suspected that grasses’ subsidiary cells might give the dumbbells, known as guard cells, an assist by making it easier for them to open and close. But that’s been hard to test in a controlled way.
When a stoma opens, “it’s elbowing its way into the neighbor cells,” says study coauthor Dominique Bergmann, a biologist at Stanford University. “If the neighbors don’t want to move, you’re stuck.” But subsidiary cells have some squish. As guard cells inflate, their neighboring subsidiary cells deflate.
Bergmann and her colleagues mutated a gene called MUTE in purple false brome (Brachypodium distachyon) so that the grass didn’t make the MUTE protein. Without MUTE, plants didn’t make subsidiary cells. And without the helping hand, the plants were less efficient than usual at opening and closing their stomata.

Grasses aren’t the only plants that have the MUTE gene, Bergmann says. But in other plants, the gene provides instructions to help make guard cells, not subsidiary cells. At some point in grasses’ evolution, the MUTE gene took on a function that differs from the rest of the plant kingdom.

Although the new work confirms that subsidiary cells and guard cells work together to make grass stomata more responsive, more research is still needed to understand exactly how subsidiary cells lend a hand. “It would be really nice to show that there’s actually an exchange of ions between the two cell types,” says Michael Blatt, a plant physiologist at the University of Glasgow in Scotland. Sharing ions could incentivize water to flow from one cell type to the other, controlling which one is more inflated.

More responsive stomata may have helped grasses survive during periods when Earth’s climate was warm and dry. “Grasses got lucky,” says study coauthor Michael Raissig, also at Stanford. As Earth’s climate continues to change, Raissig says, these genetic innovations might be exploited to help other plants make it through, too.

Dengue fever spreads in a neighborly way

Dengue is a bit of a homebody. By mapping the spread of the virus across Bangkok, scientists found that infections were most likely to occur within a few minutes’ walk of the home of the first person infected.

Pinpointing where dengue is likely to be transmitted can better focus efforts to stop the spread of the disease, the researchers report in the March 24 Science.

“We often think of transmission and infection as occurring in this ubiquitous, pervasive and amorphous way,” says study coauthor Derek Cummings. But there is a pattern to how dengue spreads. This study, he adds, shows that scientists are “starting to have the tools and methods to really track how infectious diseases move across a population.”
Dengue is a viral disease transmitted by Aedes aegypti mosquitoes and can cause fever and muscle pain so excruciating that it’s also known as “breakbone fever.” In some cases, it can be deadly, resulting in more than 20,000 deaths per year.
Cummings and colleagues looked at both the genetics and locations of about 18,000 cases of dengue from 1994 to 2010 in Thailand, most from the capital Bangkok. If two cases of dengue evolved from the same parent strain of the virus within a season, or about six months, researchers considered the pair to belong to the same transmission chain, which connects dengue infections that spread from one person to the next. About 160 chains occur in Bangkok in a season.

The researchers found that 60 percent of dengue cases within a 200-meter radius in Bangkok were closely related. These infections with a particular dengue strain belonged to the same transmission chain, says Cummings, an epidemiologist at the University of Florida in Gainesville. In contrast, only three percent of cases separated by a greater distance, between one to five kilometers, were from the same transmission chain.
The new study’s combination of genetic and location information provides more details on the ecology of dengue than previous research, says Caroline Buckee, an infectious disease epidemiologist at the Harvard School of Public Health. “It would be great to see this kind of approach become a standard for studies of dengue transmission and epidemiology.”

When the researchers mapped the locations of cases within the same transmission chain, they found that the home of the person originally infected by a mosquito bite, the first link in the chain, is a good indicator of where new cases of dengue will occur.

Thailand’s Ministry of Public Health responds to dengue infections by spraying to kill mosquitoes. “Now, we have some quantitative details to start targeting control technologies,” Cummings says, to better focus spraying in high-priority areas.

The data may also be helpful for a vaccine. Though there is a dengue vaccine licensed for use in Thailand, Cummings says, researchers don’t know yet whether the vaccine will need to be updated with more strains of the virus over time, like the flu shot. Understanding the diversity of dengue strains and how they spread across Bangkok in a season may help researchers address this vaccine concern, he adds.

“Once we can understand these detailed patterns of how things spread, then we might be able to refine how we respond to the pathogen,” Cummings says.

SpaceX launches and lands its first reused rocket

In a spaceflight first, the aerospace company SpaceX has successfully launched and landed a previously used rocket.

The Falcon 9 rocket blasted off March 30 from NASA’s Kennedy Space Flight Center in Florida at 6:27 p.m. EDT carrying a commercial telecommunications satellite. After separating from the rest of the rocket and its payload, the refurbished first stage of the rocket touched back down smoothly on a platform in the Atlantic Ocean. The stage is the same one SpaceX used in its first successful landing on an ocean barge in April 2016.

Although the aerospace company has recovered eight Falcon 9 rockets after previous launches, this homecoming marks the first time it has reflown one of those used boosters. In September, a Falcon 9 rocket and its payload exploded on the launchpad at Cape Canaveral during a routine test.

In the past, the spent first stages of rockets have been lost to the ocean. Capturing and reusing rockets may lead to cheaper spaceflights, the company says.

50 years ago, contraception options focused on women

The pill is a sledgehammer approach to contraception…. A second-generation of [drugs] is being designed to do the job without upsetting a woman’s normal cycle of ovulation and menstruation…. A contraceptive administered to the man can be given only for a short time without actually affecting the development of sperm … and, therefore, is not being considered for actual clinical use. —Science News, April 15, 1967

Contraceptives have come a long way since 1967. Women can choose low-dose pills, hormonal rings, implants and intrauterine devices — effective methods that can be less disruptive to normal menstrual cycles. Men have far fewer options, but that may eventually change. A long-acting gel injected into 16 adult male rhesus monkeys’ reproductive tracts completely prevented pregnancy in their partners over one to two breeding periods. The gel works like a vasectomy but is less invasive and can be reversed more easily, researchers report February 7 in Basic and Clinical Andrology.

Vaccinating pregnant women protects newborns from whooping cough

When I was pregnant, my pronoun shifted automatically. My “I” turned into “we,” as in, “What are we going to eat for dinner?” and, “Should we sit in that hot tub?” I thought about that shift to the majestic plural as we got our Tdap shot in our third trimester.

The Tdap vaccine protects against tetanus, diphtheria and pertussis, or whooping cough. Doctors recommend that women receive a dose with each pregnancy because the diseases can be particularly dangerous for young babies. But good, hard evidence for the benefits of vaccinating women while pregnant instead of shortly after giving birth has been lacking. A new study of nearly 150,000 newborns fills that gap for whooping cough.

Researchers at the Kaiser Permanente Vaccine Study Center in Oakland, Calif., studied the medical records of mothers who gave birth to babies between 2010 and 2015. Overall, about 46 percent of the mothers received a Tdap vaccine at least 8 days before giving birth.

Seventeen of the 150,000 babies got whooping cough by the time they were 2 months old. Of these 17 babies, only one had been born to a mother who had received the Tdap vaccine during her pregnancy. And this baby, the researchers note, had a mild case of whooping cough and wasn’t admitted to the hospital.

The maternal protection against whooping cough stuck around beyond 2 months, the researchers found. Though babies got their own vaccines in their first year of life, those babies who got their mothers’ antibodies during pregnancy were less likely to get whooping cough before their first birthdays than babies whose mothers had not been vaccinated while pregnant.

Babies whose mothers were vaccinated after giving birth didn’t get similar protection. The researchers found no evidence that postpartum Tdap vaccinations for mothers prevented whooping cough in babies. “Our results demonstrate the substantial benefit of vaccinating during pregnancy rather than waiting until after birth,” pediatrician and vaccine researcher Nicola Klein and colleagues wrote online April 3 in Pediatrics.

Since 2013, doctors have recommended that women get Tdap shots during every pregnancy between weeks 27 and 36 of pregnancy, a window that’s thought to be prime for antibody sharing. Babies usually get their first vaccine against whooping cough at 2 months of age. The new study shows how antibodies received in utero from mom can shepherd babies through this vulnerable unvaccinated period.

These days, whooping cough is making a comeback. That reemergence comes in part from a switch in the 1990s to a vaccine that comes with fewer side effects but is less effective. Changes in the bacterial culprit itself and lower vaccination rates also contribute to whooping cough’s reemergence. One of the best things mothers-to-be can do to keep their newborns healthy, the study shows, is to themselves deliver those antibodies to their babies by getting vaccinated during pregnancy.

Autism, ADHD risk not linked to prenatal exposure to antidepressants

Taking antidepressants during pregnancy does not increase the risk of autism or attention-deficit/hyperactivity disorder, two new large studies suggest. Genetic or environmental influences, rather than prenatal exposure to the drugs, may have a greater influence on whether a child will develop these disorders. The studies are published online April 18 in JAMA.

Clinically, the message is “quite reassuring for practitioners and for mothers needing to make a decision about antidepressant use during pregnancy,” says psychiatrist Simone Vigod, a coauthor of one of the studies. Past research has questioned the safety of expectant moms taking antidepressants (SN: 6/5/10, p. 22).
“A mother’s mood disturbances during pregnancy are a big public health issue — they impact the health of mothers and their children,” says Tim Oberlander, a developmental pediatrician at the University of British Columbia in Vancouver. About one in 10 women develop a major depressive episode during pregnancy. “All treatment options should be explored. Nontreatment is never an option,” says Oberlander, who coauthored a commentary, also published in JAMA.

Untreated depression during pregnancy creates risks for the child, including poor fetal growth, preterm birth and developmental problems. Some women may benefit from psychotherapy alone. A more serious illness may require antidepressants. “Many of us have started to look at longer term child outcomes related to antidepressant exposure because mothers want to know about that in the decision-making process,” says Vigod, of Women’s College Hospital in Toronto.

Previous studies indicated that the use of antidepressants came with its own developmental risks: autism spectrum disorder, ADHD, premature birth and poor fetal growth. “The key question is whether those risks are due to the actual medication,” says psychologist Brian D’Onofrio of Indiana University Bloomington. “Could the negative outcomes be due to the depression itself, or stress or genetic factors?” D’Onofrio and his group authored the other study.

To attempt to isolate the impact of antidepressants on exposed children, both studies relied on big sample sizes and sophisticated statistical techniques. D’Onofrio’s team looked at more than 1.5 million Swedish children born from 1996 to 2012 to nearly 950,000 mothers. More than 22,000, or 1.4 percent, of these kids had mothers who reported using antidepressants, mostly selective serotonin reuptake inhibitors, in the first trimester.
The researchers compared siblings in families where the mother used antidepressants in one pregnancy but not the other. “This helps account for all of the factors that make siblings similar — their shared genetics and environment,” D’Onofrio says.
In the sibling matchup, the children had essentially the same risk for autism, ADHD and poor fetal growth whether they were exposed to antidepressants in the womb or not. There remained a small increased risk of preterm birth among exposed siblings compared to their unexposed siblings.

In the whole sample, looking at antidepressant use only without accounting for other possible influences, “children have roughly twice the risk of having autism if the mother takes antidepressant medication during the first trimester,” says D’Onofrio. “But that association goes completely away when you compare siblings.” Although it’s not clear exactly what’s responsible for the increased risk — depression, stress, genetic factors, poor prenatal care — “our results suggest that it is actually not due to the medication itself,” he says.

Vigod and colleagues looked at mothers who qualified for public drug coverage in Ontario, Canada, from 2002 to 2010. The women gave birth to 35,906 children; in 2,837 of those pregnancies, nearly 8 percent, the women took antidepressants, also primarily selective serotonin reuptake inhibitors. The team compared exposed children to their unexposed siblings, too, and found no association between autism risk and antidepressant use.

“The use of sibling matches in both studies is a very innovative way to account for genetics and a shared environment,” says Oberlander. “We can’t ignore the fact that there are shared genetic mechanisms that might relate autism and depression. The genetic reason that brought the mom to use the drug may say more about the risk of autism in the child.”

Ötzi the Iceman froze to death

NEW ORLEANS — Ever since Ötzi’s mummified body was found in the Italian Alps in 1991, researchers have been trying to pin down how the 5,300-year-old Tyrolean Iceman died. It now looks like this Copper Age hunter-gatherer simply froze to death, perhaps after suffering minor blood loss from an arrow wound to his left shoulder, anthropologist Frank Rühli of the University of Zurich reported April 20 at the annual meeting of the American Association of Physical Anthropologists.

“Freezing to death is quite likely the main cause of death in this classic cold case,” Rühli said. Ötzi succumbed to exposure within anywhere from a few minutes to a few hours, he estimated.

New analyses of the Iceman’s body, based on X-rays and CT scans, argue against the idea that Ötzi died from a stone arrowhead shot into his shoulder (SN: 9/6/14, p. 6). Surprisingly shallow penetration of that weapon into Ötzi’s shoulder ruptured a blood vessel but caused no major tissue damage, Rühli said. Internal bleeding totaled only about 100 milliliters, or a half cup, he and his colleagues concluded. That’s enough of a poke to cause plenty of discomfort but not death, Rühli said.

Several depressions and fractures on the Iceman’s skull also couldn’t have proven fatal, he added. Some researchers regard those injuries as signs that Ötzi was clubbed to death. Rühli’s team found that those skull injuries are more consistent with the ancient man having accidentally fallen and hit his head while walking over rough ground. The Iceman was found with fur headgear that probably helped to protect his noggin when he took a headlong tumble, Rühli suggested.

How a mushroom gets its glow

The enzyme that turns on the light for a glow-in-the-dark mushroom seems “promiscuous.” But in a good way.

Researchers have worked out new details of how two Neonothopanus fungi shine softly green at night. The team had earlier figured out that the basic starting material for bioluminescence in these fungi is a compound called hispidin, found in some other fungi as well as plants such as horsetails. Those plants don’t spontaneously give off light, but in the two Neonothopanus mushroom species, an enzyme rejiggers a form of hispidin into a compound that glows.

The enzyme that turns a fungus into a natural night-light isn’t that fussy as enzymes go, says Cassius V. Stevani of the University of São Paulo in Brazil. He and colleagues can tweak the compound that the enzyme normally reacts with and still get a glow, the researchers report April 26 in Science Advances.

This easygoing chemistry has allowed the team to develop blue to orange glows instead of just the natural yellowish-green. These bonus colors might mark the beginnings of a new labeling tool for molecular biologists, the researchers say.