NASA’s Juno spacecraft will stay in its current 53-day orbit around Jupiter instead of closing into a 14-day orbit as originally planned, the Juno team announced February 17.

An issue with two helium check valves, which are tied to the spacecraft’s main engine, had scientists concerned. The valves took several minutes to open when the team pressurized the spacecraft’s propulsion system in October. During previous main engine firings, the valves took only a few seconds to open.

Another main engine burn to put the spacecraft into a shorter orbit poses a risk to completing the science goals of the mission, mission scientists say.

Juno has been circling Jupiter since July 4. Staying in the longer orbit will not change the date of the next flyby, nor will it affect voting for which Jovian features to be imaged with JunoCam. It will allow the team to probe Jupiter’s magnetic field in more depth than originally planned. And it may also help to maintain the health of the spacecraft because Juno will spend less time exposed to the planet’s radiation belts, the team noted.

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.

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 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.

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.

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

Update
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.

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.

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.

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.

Pancreatic cancer is hard to detect early, when the disease is most amenable to treatment. But a new study describes a blood test that may aid the diagnosis of pancreatic cancer and someday make earlier screening feasible, the authors say.

The test detects a combination of five tumor proteins that appear to be a reliable signature of the disease, the researchers report in the May 24 Science Translational Medicine. In patients undergoing pancreatic or abdominal surgery, the test was 84 percent accurate at picking out those who had pancreatic cancer.
“What’s exciting about the study is that it further favors the belief that one biomarker by itself may not be able to successfully identify a disease,” says Raghu Kalluri, a cancer biologist at the University of Texas MD Anderson Cancer Center in Houston who was not involved in the study. By putting the five protein biomarkers together, he says, “the power of the analysis might be more beneficial in differentiating healthy individuals and ones with pancreatic cancer.”

The National Cancer Institute estimates that in 2017 there will be more than 53,000 new cases of pancreatic cancer in the United States and just over 43,000 deaths from the cancer. Individuals with the most common form of pancreatic cancer, called pancreatic ductal adenocarcinoma, have a five-year survival rate of less than 10 percent. The cancer is usually caught late because the symptoms, including weight loss and abdominal pain, often don’t arise until the cancer has spread. And current imaging technology can’t detect the cancer at the start, says study coauthor Cesar Castro, a translational oncologist at Massachusetts General Hospital in Boston.

“The unmet need here is finding some other form of detection before a cancer grows large enough for the CT scan to detect it,” Castro says.

In their hunt for better detection methods, the researchers turned to tumor-derived extracellular vesicles, small sacs shed by tumor cells that circulate in the bloodstream. The sacs “are almost like mini-mes” of the parent tumor, Castro says, because they contain proteins and genetic material that often match the tumor.

The researchers selected five promising protein biomarkers from tumor-derived extracellular vesicles. Using a gold-coated silicon chip covered with antibodies and sporting nanopores, the team tested how well the biomarkers signaled the presence of pancreatic cancer in plasma samples from patients. When light shining through the pores encountered the extracellular vesicles, bound to the chip because of the interaction between the protein biomarkers and the antibodies, the light’s wavelength changed — signaling the presence of a tumor.
In plasma samples taken from 43 patients before scheduled surgery for a medical issue in the pancreas or abdomen, the panel of five biomarkers distinguished pancreatic ductal adenocarcinoma from pancreatitis — an inflammation of the pancreas — and from benign cysts as well as from control patients’ samples. A pathology report after the surgeries confirmed the results.

Using their sensing device, the researchers report that the combined five biomarkers correctly identified whether a patient had pancreatic ductal adenocarcinoma or not in 84 percent of cases. The highest accuracy for any one of these biomarkers used by itself was just 70 percent.

The next step is to test patients at high risk for pancreatic cancer, and eventually those who are healthy, to see if these biomarkers are effective at early screening. “What we need to do now is pivot towards precancerous lesions,” Castro says. “Can they pick up any precancerous changes?”

“I’m excited about anything that can happen for these patients who are in desperate need for biomarkers and treatment,” Kalluri says. But he cautions that studies reporting the effectiveness of biomarkers as cancer screening tools often use different technologies for their assessments, making it hard for academic laboratories to reproduce the results. “There’s a tremendous lack of organized effort in the biomarker field,” he says, and if there is no way to come to a consensus on which biomarkers are most promising, “it’s very difficult for a patient to realize any benefit.”