A summertime cold snap can, quite literally, take the bloom off the rose. Not so for Scotch heather — and now scientists know why.

Thick cell walls and narrow plumbing in the alpine shrub’s stems stop deadly ice crystals from spreading to its fragile flowers during sudden summer freezes, researchers report September 15 in PLOS ONE. That lets the flowers survive and the plant make seeds even if temperatures dip below freezing.

Once ice crystals start to form inside of a plant, they can spread very quickly, says Gilbert Neuner, a botanist at the University of Innsbruck in Austria who led the study. Those sharp crystals can destroy plant cells — and flowers are particularly sensitive. So plants living in cold climes have developed strategies to confine ice damage to less harmful spots.
Neuner and his team used infrared imaging to measure heat given off by Scotch heather (Calluna vulgaris) plants as they freeze. That technique revealed where and when ice was forming. And looking at thin slices of the plant under a microscope let the scientists pick apart the structure of the plant’s ice barrier.
Cells at the base of the flower stalks had thicker walls and were packed more closely together than elsewhere in the plant, the team found. In the same area, the pipelines that carry water up the plant — called xylem — were narrower and had fewer points where ice could potentially sneak through. Those modifications let the plants “supercool” their flowers. That is, even when the flowers chilled to below zero degrees Celsius, they contained liquid water instead of ice. Ice didn’t form in the Scotch heather flowers until far below normal freezing temperatures, ‒22° C, and ice that formed elsewhere in the plant didn’t spread to the flowers.
Other species sometimes put up temporary ice blockades, for instance to protect overwintering buds. But that usually cuts off the flow of water through the xylem — fine if a plant is dormant over the winter, but flowers facing a sudden summer freeze need a continuous supply of water. Scotch heather gets around this problem by threading its xylem right through the icy barrier.

Membranes let water pass between the xylem cells, and these membranes might ultimately control the spread of ice crystals in C. vulgaris, Neuner suspects. Tiny pores in the membranes are too small to let ice crystals through the barrier. And when water molecules are found inside such small holes, the molecules are bound so tightly to the structures around them that they behave more like a gel instead of crystalizing into ice. The team hopes to test the idea in future studies.
Other flowering alpine plants could use a similar strategy. “I don’t think that this is unique to this plant,” says Sanna Sevanto, a tree physiologist at Los Alamos National Laboratory in New Mexico who wasn’t involved in the study. “It’s just that nobody has looked at it.”

Concussions, particularly those among children playing sports, are on parents’ minds. The fervor over NFL players’ brains and those of other elite athletes has trickled all the way down to mini-kicker soccer teams and peewee football leagues. And parents are right to be worried. Concussions seem to be on the rise. From 1990 to 2014, the rate of concussions in youth soccer players jumped by over 1,000 percent, a recent study estimated.

This increase might be driven in part by more inclusive definitions of concussion, a common form of traumatic brain injury that can come with headaches, confusion and memory trouble. More awareness might also drive numbers up; because parents, coaches and referees are more alert to the possibility of a concussion, more kids might be getting the diagnosis. But games may have become more competitive, too, leading to more body clashes that jolt the brain.

When a kid gets concussed, the instinct of many parents, myself included, is to cocoon their child, limiting social interaction, activity and even sleep, a recent poll conducted by researchers at UCLA suggests. The survey asked about 500 parents about how they would handle a child who had symptoms a week after a concussion. Eighty-four percent of the respondents said they would restrict their child’s physical activity for the week after the injury, 62 percent said they would take away their child’s electronics and 77 percent said they’d even wake their child up during the night. But those measures “can certainly be unhelpful,” says pediatric neurologist Christopher Giza of UCLA. “There’s some evidence it may be harmful.”

Giza points out that each child is unique, and the recovery process ought to be tailored by his or her medical team to best help the individual. But in general, excessive rest and isolation might work against kids. Last year, scientists found that children and teenagers who strictly rested for five days reported more symptoms than those who rested for one to two days. What’s more, recovery took longer for the kids who got the five-day break.

Complete isolation and rest may cause children to grow anxious and despondent, Giza says. With their normal routines interrupted, they may focus more on their symptoms. Social interactions, even those that come via a screen, may help kids feel better sooner. Gentle exercise, such as walks and swimming, is also a good thing. And despite what parents may have heard, children with concussions need sleep to recover. “Waking the kid up every few hours only worsens symptoms,” Giza says. It’s not surprising that a week of poor sleep can dial up fatigue, irritability and slow thinking.

There is one very important limit that should still be respected for kids recovering from concussions: No more head knocks. Concussions in quick succession can be extra pernicious for the brain. That means kids shouldn’t return to any sport that puts them at risk for a second concussion until they are fully recovered. In a concussion’s aftermath, reflexes are blunted, balance may be off and thinking may be slow, Giza says. Those deficits put children at more risk for getting hit.

Some sports leagues have begun changing their rules to make the game safer. This season, 5- to 10-year-olds playing in a Pop Warner football game, for instance, will no longer have kickoffs, a game-starting play responsible for an inordinate amount of concussions. Game tweaks like that, along with more vigilant coaches and parents, will help protect these little brains.

You don’t need a degree in science to monitor backyard owls or measure trees. And anyone with a computer can help scientists track seal populations in Antarctica. Citizen science projects like these — which depend on crowdsourced data — are booming. And when faced with a planet scarred by industrialization and climate change, these efforts might be exactly what we need, environmental journalist Mary Ellen Hannibal argues in Citizen Scientist.
What we call “citizen science” was once just “science.” After all, many early conservationists and natural historians — people like John Muir — weren’t academics. As species disappear faster and faster, scientists can’t work alone. They need the eyes and ears of passionate people who are watching as flowers bloom earlier each year and butterflies become sparser.

Hannibal dips her toes into some of the citizen science projects happening within driving distance of her home in San Francisco. She chronicles efforts to count, track and save a variety of species, including sea otters and redwood trees.

Along the way, Hannibal discovers heroes both modern and historical: For instance, Rebecca Moore, who leads Google Earth Outreach, originally developed the mapping tool in the early 2000s to help stop logging in the Santa Cruz Mountains. And Alice Eastwood, botany curator at the California Academy of Sciences in the early 1900s, helped build the museum’s plant collection. Lacking a college degree, she collected specimens for nearly 60 years — and even saved part of the collection from the 1906 San Francisco earthquake.

While Hannibal is contemplating extinction and habitat destruction, her father is dying from cancer. Her field expeditions become a lens through which she processes her dad’s death. The parallels make Citizen Scientist part memoir, part science tale and part history book. Hannibal has a conversational writing style that moves quickly from topic to topic, punctuated with humorous and thoughtful asides.

Although centered in California, the book has a global message: Humans have much in common with the species we’re trying to save. Grizzlies and wolves, for instance, “leave their natal home, light out for a huge territory, find a mate, and establish a new base of operations,” Hannibal writes. The human heroes in our storybooks aren’t so different.

A genetic study of HIV viruses from the 1970s may finally clear the name of a man long identified as the source of the AIDS epidemic in the United States. HIV came to New York City between 1969 and 1973, long before the man known as Patient Zero became infected, researchers report October 26 in Nature.

Using techniques developed to decipher badly degraded ancient DNA from fossils, researchers reconstructed the genetic instruction books of eight HIV viruses from blood samples collected in 1978 and 1979 in New York City and San Francisco. The viral DNA was so genetically diverse that the viruses must have been circulating in the cities for years, picking up variations, says evolutionary biologist Michael Worobey of the University of Arizona in Tucson.
Worobey and colleagues calculate that the virus probably first jumped to the United States in 1970 or 1971. So HIV spread for about a decade before AIDS was recognized in 1981 and found to be caused by a retrovirus in 1983.
Examining the relationships between the New York City and San Francisco viruses with HIV strains from elsewhere let researchers trace the virus’s path. The eight American samples all came from the same branch of the HIV family tree as ones from the Caribbean. That suggests that HIV spread from Africa to the Caribbean before making its way to the United States. New York HIV samples were more diverse than those from California, indicating that New York City was probably the hub of early HIV spread and the virus arrived in San Francisco later.
Worobey and colleagues also examined HIV DNA from Patient Zero. Also known as Case 57, he was part a 1984 study of gay men with AIDS in Los Angeles who had either a rare cancer called Kaposi’s sarcoma or Pneumocystis carinii pneumonia, both complications of the disease. Researchers from the Centers for Disease Control and Prevention found that many of the men had had sexual contact with each other, helping to establish that HIV is sexually transmitted.
Later, in the book And the Band Played On, author Randy Shilts identified Patient Zero as an Air Canada flight attendant named Gaëtan Dugas. It was widely interpreted that Dugas was the first case of HIV in the United States, even though the CDC never claimed — and has repeatedly refuted — that, says epidemiologist James Curran, a coauthor of the 1984 study who is now at Emory University in Atlanta. Part of the confusion may have been that Patient Zero was supposed to be identified as Patient O (for “outside of California”).

Dugas became a flight attendant in 1974 and began traveling to the United States shortly after, says Richard McKay, coauthor of the new study and a medical historian at the University of Cambridge. Dugas estimated that he had about 250 male sexual partners each year between 1979 and 1981. Shilts and others contended that Dugas was intentionally spreading the virus to others, though he was diagnosed with Kaposi’s sarcoma in 1980 before anyone knew what AIDS was or that it was caused by a virus.

Now, the genetic analysis confirms that Dugas was not carrying the earliest version of the virus. “This individual was simply one of thousands infected before HIV/AIDS was recognized,” McKay says.

The new study is a cautionary tale against trying to pin the spread of an infectious disease on any one person, says Robert Remien, a behavioral scientist at Columbia University Medical Center. “There’s no blame or cause to be laid on any of those people in those early years.”

Editor’s note: This story was updated November 10, 2016, to fix the alignment of the timeline with the phylogenetic tree and to update the number of sequential diagnoses in the Patient Zero cluster of AIDS cases.

Many preschoolers take a surprisingly long and bumpy mental path to the realization that people can have mistaken beliefs — say, thinking that a ball is in a basket when it has secretly been moved to a toy box. Traditional learning curves, in which kids gradually move from knowing nothing to complete understanding, don’t apply to this landmark social achievement and probably to many other types of learning, a new study concludes.

Kids ranging in age from 3 to 5 often go back and forth between passing and failing false-belief tests for several months to more than one year, say psychologist Sara Baker of the University of Cambridge and her colleagues. A small minority of youngsters jump quickly from always failing to always passing these tests, the scientists report October 20 in Cognitive Psychology.
“If these results are replicated, it will surprise a lot of researchers that there is such a low level of sudden insight into false beliefs,” says psychologist Malinda Carpenter, currently at the Max Planck Institute for Evolutionary Anthropology in Leipzig. Early childhood researchers generally assume that preschoolers either pass or fail false-belief tests, with a brief transition between the two, explains Carpenter, who did not participate in the new study. Grasping that others sometimes have mistaken beliefs is a key step in social thinking.

False-belief understanding may start out as something that can be indicated nonverbally but not described. Human 2-year-olds and even chimpanzees tend to look toward spots where a person would expect to find a hidden item that only the children or apes have seen moved elsewhere (SN Online: 10/6/16).

Numerous investigations suggest that neurologically healthy kids between ages 3 and 5 consciously appreciate when others have formed mistaken beliefs. But those studies report average scores on false-belief tests for groups of preschoolers. That leaves unexamined how individual kids progress — or not — as mind readers.

Baker’s team generated individual scoring profiles for 52 children repeatedly assessed for false-belief understanding between ages 3 and 5. Trials occurred over roughly one to two years. Two types of false-belief tasks were alternately presented about every two to six weeks, either at a preschool, in a lab or at a child’s home.

In one task, an experimenter used pictures to help describe a situation in which someone moves an object from one location to another once a friend leaves — say, taking a ball from a basket and putting it in a toy box. Children were asked where the friend would later look for the object.
In a second task, children observed a container’s unexpected contents, such as a sock in a crayon box or a toy cow in an egg carton. Kids reported what they originally thought was inside the container and what another person would think is inside it.

Nine children, including some of the youngest ones, passed their first three trials. All except one of the nine continued to pass trials at a high rate. The remaining 43 children failed at least one of the first three trials. A statistical analysis calculated the likelihood that a series of scores for a particular child reflected gains, losses or no change in false-belief understanding.

Five of the 43 children achieved rapid insights into false beliefs, consistently passing trials immediately after a string of failed trials. Another 22 youngsters showed different patterns of improvement, such as going from a 12 percent likelihood of passing trials to a 50 percent chance by the study’s end. None of them moved gradually and steadily from failing to passing false belief tests. Smooth learning curves are statistical illusions created by averaging group scores, the researchers suspect.

Four kids started out failing false-belief tests and showed no signs of improvement over time. Another 10 children sometimes passed and sometimes failed throughout the study. Statistical profiles were inconclusive for two children.

Related findings, although based on group statistics, nonetheless suggest that grade-schoolers shift among various problem-solving strategies when learning mathematical concepts (SN: 3/17/01, p. 172). Baker’s statistical method could enhance the study of how individual children develop math skills and other forms of reasoning, says psychologist Rose Scott of the University of California, Merced.

SAN DIEGO — A nerve-zapping headset caused people to shed fat in a small preliminary study.

Six people who had received the stimulation lost on average about 8 percent of the fat on their trunks in four months, scientists reported November 12 at the annual meeting of the Society for Neuroscience.

The headset stimulated the vestibular nerve, which runs just behind the ears. That nerve sends signals to the hypothalamus, a brain structure thought to control the body’s fat storage. By stimulating the nerve with an electrical current, the technique shifts the body away from storing fat toward burning it, scientists propose.
Six overweight and obese people received the treatment, consisting of up to four one-hour-long sessions of stimulation a week. Because it activates the vestibular system, the stimulation evoked the sensation of gently rocking on a boat or floating in a pool, said study coauthor Jason McKeown of the University of California, San Diego.

After four months, body scans measured the trunk body fat for the six people receiving the treatment and three people who received sham stimulation. All six in the treatment group lost some trunk fat, despite not having changed their activity or diet. In contrast, those in the sham group gained some fat. Researchers suspect that metabolic changes are behind the difference. “The results were a lot better than we thought they’d be,” McKeown said.

Earlier studies had found that vestibular nerve stimulation causes mice to drop fat and pack on muscle, resulting in what McKeown called Schwarzenegger mice. Though small, the current study suggests that the approach has promise in people. McKeown and colleagues have started a company based on the technology and plan to test it further, he said.

SAN ANTONIO — Early Christian monks’ vows of silence may have attracted not only the devout but also a fair number of hearing-impaired men with a sacred calling.

A team led by bioarchaeologist Margaret Judd of the University of Pittsburgh found that a substantial minority of Byzantine-era monks buried in a communal crypt at Jordan’s Mount Nebo monastery display skeletal signs of hearing impairments. Judd presented these results November 19 at the annual meeting of the American Schools of Oriental Research.
Judd has directed excavations at Mount Nebo since 2007. Her new results focus on a two-chambered crypt containing skeletons of at least 57 men presumed to have been monks. Oil lamps found in the crypt date to the 700s.

About 16 percent of these men displayed damage to middle ear bones caused by infections known as otitis media. This condition frequently occurs in childhood and can lead to lasting hearing problems even if the infection clears up quickly (SN Online: 3/10/10). Monks showing signs of otitis media probably suffered mild to moderate hearing loss.

Damage to one middle ear bone, the stapes, in two other individuals likely caused severe hearing loss in one ear each. In another case, a fracture above the left eye could have damaged middle ear bones, Judd proposed. Finally, one skull’s thickened bone may have resulted from Paget’s disease, a viral infection in adulthood that can impair hearing.

Hearing loss would have had little effect on monks’ daily lives, since they communicated with hand signals, nods and other gestures, Judd said. Even if some developed hearing ailments after joining the monastery, those conditions must have largely gone undetected by affected monks and their peers who rarely or never spoke, she suggested.

Brilliant births and destructive deaths of stars might take a runt of a galaxy and stretch it to become a ghostly behemoth, new computer simulations show. This process could explain the origin of recently discovered dark galaxies, which can be as wide as the Milky Way but host roughly 1 percent as many stars.

Since 2015, astronomers have found hundreds of these shadowy systems lurking in and around several clusters of galaxies (SN: 12/10/16, p. 18). How these dark galaxies form is a puzzle. But prolific star formation and blast waves from exploding stars could be responsible, researchers suggest in a paper to appear in Monthly Notices of the Royal Astronomical Society Letters.
“The mystery is: Are these galaxies like the Milky Way, or are they dwarf galaxies?” says study coauthor Arianna Di Cintio, an astrophysicist at the University of Copenhagen in Denmark. “Our mechanism could be a nice formation scenario for these galaxies and prove that they are dwarfs.”

Di Cintio and colleagues ran computer simulations of galaxy evolution and found that some runts can be inflated by stellar energy. Radiation from young massive stars heats up interstellar gas, preventing it from forming more stars. And a flurry of supernova explosions can toss that gas out of the galaxy. The gravity of the galaxy drops, and so does its ability to hold on to stars and dark matter, an enigmatic substance thought to help hold galaxies together. “Dark matter particles fly outward and start the expansion,” says Di Cintio. “This happens to the stellar population as well.”

Those galaxies that remain as runts in the simulations go through this process just once, whereas giant dark galaxies regurgitate their gas multiple times. And that provides a way to test this idea, says Di Cintio. First astronomers need to find dark entities far away from galaxy clusters where the environment can also take its toll. Then researchers can estimate the ages of stars in the galaxy to see if there have been multiple bursts of star formation. If this hypothesis is correct, dark galaxies might also be loaded up with lots of hydrogen gas that allows them to sustain several rounds of gas purging.

“It is very interesting to see that, in some cases, [supernovas] can be efficient enough to expand dwarf galaxies,” says Nicola Amorisco, also at the University of Copenhagen. He helped put forth an idea that dark galaxies start as runts that get stretched because of rapid rotation. Recent observations also show that some dark systems have masses that are similar to dwarf galaxies (though one is as hefty as the Milky Way). “It is even possible that a combination of — or the interplay between — a few different mechanisms could be responsible,” says Amorisco. “It will be very exciting to understand whether that is the case.”

At first glance, the stories taking the top two spots in Science News’ review of 2016 have little in common. Scientists began searching decades ago for gravitational waves. Discussions of these subtle signals from dramatic and distant phenomena appear dozens of times in the SN archive starting as early as the 1950s. Their long-awaited discovery, our No. 1 story of the year, touched off celebration of a new era in astronomy.

Less expected, and far from subtle, was the sudden rise in Brazil of microcephaly cases, linked this year to Zika virus infections — our No. 2 story. Little was known about Zika before the outbreak, which delivered devastation and fear across the Americas. In fact, only a single previous mention of Zika exists in the SN archive, in a book review from the 1990s.
But the stories have at least one thing in common: Both highlight the power of scientific discoveries to trigger our deepest human emotions. Pure elation as well as overwhelming dread can accompany research advances.

2016 brought many more sentiments, too. There was enthusiasm for the discovery of the exoplanet Proxima b, concern for the prospects of three-parent babies and feelings of potential but also impending peril in the openings of Arctic passageways.

The editors and writers at Science News also recognize that some of the best and most moving stories are those that are still unfolding. So, in addition to the discoveries of 2016, we review milestones, setbacks and other tales of unsteady progress. Sonia Shah writes about a new wave of infectious diseases; Tom Siegfried explores convergent failures in the field of particle physics; and Laurel Hamers covers key challenges for self-driving cars. Then, Science News writers share what science news they’re most excited about in the year to come. — Elizabeth Quill

Four proteins that can transform adult cells into embryonic-like ones can also turn back the aging clock, a new study in mice suggests.

Partial reprogramming of cells within prematurely aging mice’s bodies extended the rodents’ average life span from 18 weeks to 24 weeks, researchers report December 15 in Cell. Normal mice saw benefits, too: Muscles and pancreas cells healed better in middle-aged mice that got rejuvenation treatments than in mice that did not. The experiment could be evidence that epigenetic marks — chemical tags on DNA and proteins that change with age, experience, disease and environmental exposures — are a driving factor of aging. Some marks accumulate with age while others are lost.
“It’s an inspiring paper,” says Jan van Deursen, a biologist at the Mayo Clinic in Rochester, Minn., who studies diseases of aging. He gives the paper an “A” for sparking imagination, but lower marks for practical applications to human aging because it would involve gene therapy and could be risky. “It’s all cool, but I don’t see that it could ever be applied in medicine,” he says. “We could be terribly wrong. Hopefully we are.”

Researchers reset the mice’s aging clock by genetically engineering the animals to make four proteins when the rodents were treated with the antibiotic doxycycline. Those four proteins — Oct4, Sox2, Klf4 and c-Myc — are known as “Yamanaka factors” after Shinya Yamanaka. The Nobel Prize‒winning scientist demonstrated in 2006 that the proteins could turn an adult cell into an embryonic-like cell known as an induced pluripotent stem cell, or iPS cell (SN: 11/3/12, p. 13; SN: 7/14/07, p. 29).
The factors help strip away epigenetic marks that enable cells to know whether they are heart, brain, muscle or kidney cells, for example. As a result, stripped cells revert to the ultraflexible pluripotent state and are capable of becoming nearly any type of cell. Other researchers have used the Yamanaka factors to reprogram cells within living mice before, but those attempts resulted in the growth of tumors. (Cancer cells resemble stem cells in that they don’t have a specific identity and are “undifferentiated.”)
Those tumors indicated to Alejandro Ocampo and colleagues that the proteins were rewriting epigenetic programming to take cells back to an undifferentiated state. But “you don’t need to go all the way back to pluripotency” to erase the marks associated with aging, says Ocampo, a stem cell biologist at the Salk Institute for Biological Studies in La Jolla, Calif. A milder reprogramming treatment might reverse aging without stripping away cells’ identity, leading to cancer, Ocampo and colleagues thought.

The researchers put genetically engineered mice with a premature aging disease called progeria on a regimen in which the animals were treated with doxycycline two days per week to turn on the Yamanaka factors. Mice that made the reprogramming proteins lived six weeks longer on average than mice that didn’t get the treatment. The mice didn’t get cancer, but still died prematurely (lab mice usually live two to three years on average). “We are far away from perfection,” Ocampo says.

Normally aging mice also got benefits from the treatment. When the animals were 1 year old (roughly middle-aged), the researchers treated them with doxycycline two days per week for three weeks. Treated mice were better able to repair muscles and replace insulin-producing cells in the pancreas than untreated mice. Not all organs fared as well, Ocampo says, citing preliminary evidence. Ongoing experiments will determine whether the epigenetic reprogramming can make the mice live any longer or healthier.
People probably won’t be genetically engineered the way mice are. But chemicals and small molecules might also be able to wipe away epigenetic residue that builds up with aging and restore marks that were lost over time, returning to a pattern seen in youth, Ocampo suggests.

Researchers still don’t know whether all cells are rejuvenated by the treatment. Yamanaka factors may breathe new life into aging stem cells, allowing them to replenish damaged tissues. Or the factors may wake up senescent cells — cells that have shut down normal functions and cease to divide, but may send signals to neighboring cells that cause them to age (SN: 3/5/16, p. 8). Reviving senescent cells could be dangerous, says van Deursen; the body shuts cells down to prevent them from becoming cancerous.

Plenty of evidence indicates that resetting epigenetic programming can extend life, says Ocampo. He points to a recent report that Dolly the Sheep’s cloned sisters are aging normally (SN: 8/20/16, p. 6) as a hopeful sign that reprogramming probably isn’t dangerous, and might one day safely prevent many of the diseases associated with aging in people, if not lengthening life spans.