That past-its-prime bag of spinach buried in the back of your fridge should probably hit the compost heap instead of your dinner plate. The watery gunk that accumulates at the bottom of bagged salad mix is the perfect breeding ground for Salmonella bacteria that could make people sick, researchers report November 18 in Applied and Environmental Microbiology.

The culprit? The juice that oozes out of cut or damaged leaves. After five days in the fridge, small amounts of plant juice sped up Salmonella growth. The bacteria grew avidly on the bag and stuck persistently to the salad leaves, so much so that washing didn’t remove the microbes.

Salmonella’s success inside bagged salads means it’s important for producers to avoid bacterial contamination from the get-go — and for consumers to eat those greens before they get soggy. Popeye would approve.

Clearing tropical forests may raise the risk of people being exposed to a gruesome disease called Buruli ulcer, a new study suggests.

Mycobacterium ulcerans, the bacteria that cause Buruli skin lesions and bone deformities, can thrive in a wide range of wild creatures, especially tiny insects grazing on freshwater algae, says Aaron Morris, now at Imperial College London. Surveying more than 3,600 invertebrates and fish from both pristine forests and cleared land in French Guiana, Morris and colleagues found the bacteria flourishing in altered landscapes. As species are lost from once-complex food webs, there’s an intermediate zone where bacteria-friendly species thrive, Morris and colleagues propose online December 7 in Science Advances.
When people push into tropical forests to build farms, roads and towns, the food web of the forest grows simpler, Morris says. Aquatic predators that once kept smaller predators and grazers in check have dwindled, the analysis suggests. This shift in the food web allows some grazers that bacteria multiply abundantly in to thrive in the environment. Thus people might face more risk of picking up the disease. (The exact routes of transmission aren’t clear, according to the U.S. Centers for Disease Control and Prevention.)

Yet the relationship between forest loss and bacterial boom times isn’t a straight line, the researchers found. As people change the landscape even more drastically toward urbanization, the niches for the bacteria-carriers appears to start shrinking again. This may mean that some of the bacteria’s favorite hosts are dwindling away, too.

Other work has examined the way that landscape change affects people’s risks of catching infectious diseases, says Kate Jones of University College London, who has studied Lassa fever in Africa. Yet she cautions that recent research suggests that the interplay of infectious disease and disturbance depends strongly on the location. Some evidence has linked degraded ecosystems to rising numbers of small rodents that spread, for instance, Lyme disease. But in cases with diseases spread by monkeys and apes, their habitat needs mean they tend to be among the first animals to disappear as people take over land, taking particular disease risks with them.

Just how the rise in bacteria for Buruli ulcer translates into numbers of human cases will take more study. The new study focused on the animals and landscape and did not look at human prevalence of the disease. Worldwide, some 5,000 to 6,000 new cases of Buruli ulcer are reported each year from a total of 15 countries, says the CDC. The disease is also found in at least 18 more countries not included in the statistics. Buruli ulcer can occur in temperate as well as tropical regions but is especially a risk for children and young teens in sub-Saharan Africa.

In a hotel ballroom in Seoul, South Korea, early in 2016, a centuries-old strategy game offered a glimpse into the fantastic future of computing.

The computer program AlphaGo bested a world champion player at the Chinese board game Go, four games to one (SN Online: 3/15/16). The victory shocked Go players and computer gurus alike. “It happened much faster than people expected,” says Stuart Russell, a computer scientist at the University of California, Berkeley. “A year before the match, people were saying that it would take another 10 years for us to reach this point.”
The match was a powerful demonstration of the potential of computers that can learn from experience. Elements of artificial intelligence are already a reality, from medical diagnostics to self-driving cars (SN Online: 6/23/16), and computer programs can even find the fastest routes through the London Underground. “We don’t know what the limits are,” Russell says. “I’d say there’s at least a decade of work just finding out the things we can do with this technology.”

AlphaGo’s design mimics the way human brains tackle problems and allows the program to fine-tune itself based on new experiences. The system was trained using 30 million positions from 160,000 games of Go played by human experts. AlphaGo’s creators at Google DeepMind honed the software even further by having it play games against slightly altered versions of itself, a sort of digital “survival of the fittest.”

These learning experiences allowed AlphaGo to more efficiently sweat over its next move. Programs aimed at simpler games play out every single hypothetical game that could result from each available choice in a branching pattern — a brute-force approach to computing. But this technique becomes impractical for more complex games such as chess, so many chess-playing programs sample only a smaller subset of possible outcomes. That was true of Deep Blue, the computer that beat chess master Garry Kasparov in 1997.

But Go offers players many more choices than chess does. A full-sized Go board includes 361 playing spaces (compared with chess’ 64), often has various “battles” taking place across the board simultaneously and can last for more moves.

AlphaGo overcomes Go’s sheer complexity by drawing on its own developing knowledge to choose which moves to evaluate. This intelligent selection led to the program’s surprising triumph, says computer scientist Jonathan Schaeffer of the University of Alberta in Canada. “A lot of people have put enormous effort into making small, incremental progress,” says Schaeffer, who led the development of the first computer program to achieve perfect play of checkers. “Then the AlphaGo team came along and, incremental progress be damned, made this giant leap forward.”

Real-world problems have complexities far exceeding those of chess or Go, but the winning strategies demonstrated in 2016 could be game changers.

Drug use continued to threaten the health and safety of the American public in 2016, while a hidden menace in drinking water remained a major worry for the people of Flint, Mich.

Teen vaping
Vaping has surpassed cigarette smoking among U.S. high school students, according to a report released in 2016 from the National Youth Tobacco Survey. Estimates suggest that some 2.39 million U.S. high school kids vaped in 2015, compared with an estimated 1.37 million who smoked cigarettes (SN: 5/28/16, p. 4). The popularity of e-cigarettes has increased recently despite a lack of evidence showing that they are safer than conventional tobacco products, according to the U.S. Food and Drug Administration, which in May extended its regulatory authority to e-cigarettes. Studies reported in 2016 show a host of potential health risks, including effects on the brain, immune system and fertility (SN: 3/5/16, p. 16).
Opioid epidemic
Against a backdrop of rising prescription opioid addiction, deaths related to opioid use have become an issue of national importance. A surge in fentanyl-spiked drugs emerged as a primary concern in 2016 (SN: 9/3/16, p. 14). U.S. deaths from synthetic opioids rose from 3,105 in 2013 to 5,544 in 2014, a change that could not be explained by fentanyl prescription rates, according to a report released in August by the Centers for Disease Control and Prevention. Drug enforcement seizures involving fentanyl more than doubled from 2014 to 2015.

Fallout in Flint
After lead in the drinking water in Flint, Mich., launched a public health crisis (SN: 3/19/16, p. 8), a federal state of emergency remained in effect into August. The most recent tests conducted by the U.S. Environmental Protection Agency show that levels of lead, which is toxic to the brain, are below those considered dangerous and that filtered tap water is safe to drink. Many residents are still relying on bottled water, however. There’s also growing concern that lead contamination and testing is not being taken seriously elsewhere in the United States.

The moon is made of moons, new simulations suggest. Instead of a single colossal collision forming Earth’s cosmic companion, researchers propose that a series of medium to large impacts created mini moons that eventually coalesced to form one giant moon.

This mini-moon amalgamation explains why the moon has an Earthlike chemical makeup, the researchers propose January 9 in Nature Geoscience.

“I think this is a real contender in with the other moon-forming scenarios,” says Robin Canup, a planetary scientist at the Southwest Research Institute in Boulder, Colo., who was not involved in the new work. “This out-of-the-box idea isn’t any less probable — and it might be more probable — than the other existing scenarios.”
A collision between Earth and a Mars-sized object called Theia around 4.5 billion years ago is the current leading candidate for how the moon formed. This impact would have been a glancing blow rather than a dead-on collision, with most of the resulting building materials for the moon coming from Theia. But the moon and Earth are compositional dead ringers for one another, casting doubts on a mostly extraterrestrial origin of lunar material and thus the single impact explanation.
Planetary scientist Raluca Rufu of the Weizmann Institute of Science in Rehovot, Israel, and colleagues dusted off a decades-old, largely disregarded hypothesis that the moon instead formed from multiple impacts. In this scenario, the early Earth was hit by a series of objects a hundredth to a tenth of Earth’s mass. Each impact could have created a disk of debris around Earth that assembled into a moonlet, the researchers’ simulations show. Over tens of millions of years, about 20 moonlets could have ultimately combined to form the moon.
Multiple impacts help explain why Earth and the moon are chemically similar. For example, each impact may have hit Earth at a different angle, excavating more earthly material into space than a singular impact would.

The single impact hypothesis has about a 1 to 2 percent chance of yielding the right lunar mix based on the makeup of potential impactors in the solar system. In the researchers’ simulations, the multiple impact scenario is correct tens of percent of the time. Further investigation of the interiors and composition of the Earth and moon, the researchers say, should reveal whether this explanation is correct.

The last time Earth’s thermostat was cranked as high as it is today, sea levels were high enough to completely drown New Orleans (had it existed at the time), new research suggests.

Ocean surface temperatures around 125,000 years ago were comparable to those today, researchers report in the Jan. 20 Science. Previous estimates suggested that this period, the height of the last warm phase in the ongoing ice age, was as much as 2 degrees Celsius warmer.
Climate scientists often use the last interglacial period as a reference point for predicting how rising temperatures will affect sea levels. The new results, the researchers write, will help scientists better predict how Earth’s oceans and climate will respond to modern warming. Warming 125,000 years ago raised sea levels 6 to 9 meters above present-day levels.

The global scale of that warming has been difficult to estimate. Chemical clues inside dozens of seafloor sediment samples collected from around the world provide only regional snapshots of the ancient climate. Combining 104 of these dispersed data points, climate scientist Jeremy Hoffman of Oregon State University in Corvallis and colleagues pieced together a global climate picture.

Average global sea surface temperatures around 125,000 years ago were indistinguishable from the 1995 to 2014 average, the researchers estimate.

The playground ditty “first the worst, second the best” isn’t always true when it comes to dengue fever. Some patients who contract the virus a second time can experience more severe symptoms. A rogue type of antibody may be to blame, researchers report in the Jan. 27 Science. Instead of protecting their host, the antibodies are commandeered by the dengue virus to help it spread, increasing the severity of the disease.

Four closely related viruses cause dengue, a mosquito-transmitted disease marked by fever, muscle pain and other flulike symptoms. When a previously infected person contracts a second type of dengue, leftover antibodies can react with the new virus.
Fewer than 15 percent of people with a second infection develop severe dengue disease. Those who do may produce a different type of antibody, says Taia Wang, an infectious diseases researcher with the Stanford University School of Medicine.

Wang and colleagues found that dengue patients with a dangerously low blood platelet count — a sign of severe dengue disease — had an abundance of these variant antibodies.

Tests in mice supported the connection. “We found that when we transferred the antibodies from patients with severe disease into mice, they triggered platelet loss,” Wang says.

Wang says it’s not known why some people have this alternate antibody. She and her team want to determine that, along with how these antibodies are regulated by the immune system. With further research, they may be able to screen people to identify those more susceptible to severe dengue disease, Wang says.

Anna Durbin, a dengue vaccine researcher at the Johns Hopkins Bloomberg School of Public Health, doesn’t see a strong connection between this type of antibody and the severity of dengue disease. But she says that the research was interesting in how it connected dengue to low platelet count, a condition known as thrombocytopenia.

“There’s a lot of different theories out there about the role of dengue antibodies and thrombocytopenia, and whether or not the virus itself can enter platelets,” Durbin says. “I think this paper may provide more insight into what is the pathogenic mechanism of thrombocytopenia and dengue, and raises some good avenues for further research.”

Fearful, flighty chickens raised for eating can hurt themselves while trying to avoid human handlers. But there may be a simple way to hatch calmer chicks: Shine light on the eggs for at least 12 hours a day.

Researchers at the University of California, Davis bathed eggs daily in light for different time periods during their three-week incubation. When the chickens reached 3 to 6 weeks old, the scientists tested the birds’ fear responses. In one test, 120 chickens were randomly selected from the 1,006-bird sample and placed one by one in a box with a human “predator” sitting visibly nearby. The chickens incubated in light the longest — 12 hours — made an average of 179 distress calls in three minutes, compared with 211 from birds incubated in complete darkness, animal scientists Gregory Archer and Joy Mench report in January in Applied Animal Behaviour Science.

Chickens exposed to lots of light as eggs “would sit in the closest part of the box to me and just chill out,” Archer says. The others spent their time trying to get away. How light has its effect is unclear. On commercial chicken farms, eggs typically sit in warm, dark incubation rooms. The researchers are now testing light’s effects in large, commercial incubators. Using light exposure to raise less-fearful chickens could reduce broken bones during handling at processing plants, Archer says. It might also decrease harmful anxious behaviors, such as feather pecking of nearby chickens.

Babies are born germy, and that’s a good thing. Our microbiomes — the microbes that live on and in us — are gaining cred as tiny but powerful keepers of our health.

As microbes gain scientific stature, some scientists are trying to answer questions about how and when those germs first show up on babies. Birth itself may be an important microbe-delivery event, some researchers suspect. A trip through the birth canal can coat a baby with bacteria from his mother. A C-section, some evidence suggests, might introduce different bacteria, at least right after birth.

That difference forms the basis of the practice of vaginal seeding, which involves wiping vaginal fluids onto a baby born by C-section to introduce microbes the baby would have encountered in a vaginal birth.

Even while some parents are asking for the procedure, there’s dissent in the ranks of research about its benefits. Scientists don’t agree yet on how — or even whether — type of birth affects the microbiome. “It’s murky,” says obstetrician and maternal-fetal medicine specialist Kjersti Aagaard of the Baylor College of Medicine in Houston. Existing studies don’t clearly distinguish the effects of the C-section itself from those of certain diseases or conditions that can make a C-section more likely, such as maternal diabetes or obesity, she says. Other issues, like whether a baby received antibiotics or is breastfed, also muddy the waters. “You are left saying, ‘Wait a minute. Is it the surgery or not the surgery? What’s going on here?’” Aagaard says.

In a search for clarity, Aagaard and her colleagues surveyed the microbiomes of 81 pregnant women. Later on, the researchers added a second group of 82 women, whose microbiomes were assessed at the birth of their children.

Just after birth, babies who had been delivered by C-section had different mouth, nose and skin microbiomes than babies born vaginally. One possible explanation is that these babies are handled differently just after birth, Aagaard says. The microbiomes of the babies’ meconium, or stool, appeared to be similar, regardless of how the babies were born.

But between four and six weeks later, these C-section/vaginal birth differences on the mouth, nose and skin were largely gone, Aagaard says. The microbes living in and on the babies born by C-section and those born vaginally were nearly indistinguishable, the researchers reported online January 23 in Nature Medicine.
Depending on where they lived, the populations of microbes had already taken on distinct identities by about a month after birth, the researchers found. Communities of nose-dwelling microbes were easy to distinguish from those living in the gut, for instance. These regional differences are signs of surprising microbial maturity, Aagaard says. “Postnatal microbiomes start looking like adults a little sooner than we may have appreciated,” she says.

The results raise an interesting question: If the type of birth isn’t one of the main shapers of microbiomes, then how and when do microbes get into babies? It’s possible that microbes from mothers slip into fetuses during pregnancy — a plausible idea, given some earlier results. Genetically tagged bacteria fed to pregnant mice showed up in their fetuses’ guts a day before the predicted due date, a result that suggests the bacteria traveled from mother to fetus. And Aagaard and colleagues have found evidence of microbes in the placenta of human mothers. They are now studying whether microbes, or perhaps pieces of them, move through the placenta from mother to baby. If that turns out to be the case, then babies meet their microbes, for better or worse, well before their birthday.

Humans and Neandertals are still in an evolutionary contest, a new study suggests.

Geneticist Joshua Akey of the University of Washington in Seattle and colleagues examined gene activity of more than 700 genes in which at least one person carried a human and a Neandertal version of the gene. Human versions of some genes are more active than Neandertal versions, especially in the brain and testes, the researchers report February 23 in Cell. In other tissues, some Neandertal versions of genes were more active than their human counterparts.
In the brain, human versions were favored over Neandertal variants in the cerebellum and basal ganglia. That finding may help explain why Neandertals had proportionally smaller cerebellums than humans do. Neandertal versions of genes in the testes, including some needed for sperm function, were also less active than human varieties. That finding is consistent with earlier studies that suggested male human-Neandertal hybrids may have been infertile, Akey says.

But Neandertal genes don’t always lose. In particular, the Neandertal version of an immunity gene called TLR1 is more active than the human version, the researchers discovered.

Lopsided gene activity may help explain why carrying Neandertal versions of some genes has been linked to human diseases, such as lupus and depression (SN: 3/5/16, p. 18). Usually, both copies contribute equally to a gene’s total activity. Less robust activity of a version inherited from Neandertals might cause total activity to dip to unhealthy levels, for instance.