Modern rattlesnakes have pared down their weaponry stockpile from their ancestor’s massive arsenal. Today’s rattlers have irreversibly lost entire toxin-producing genes over the course of evolution, narrowing the range of toxins in their venom, scientists report September 15 in Current Biology.

“After going through all the work of evolving powerful toxins, over time, some snakes have dispensed with them,” says study coauthor Sean B. Carroll, an investigator with the Howard Hughes Medical Institute who is at the University of Wisconsin–Madison. These modern rattlesnakes produce smaller sets of toxins that might be more specialized to their prey.
Carroll, an evolutionary biologist, and his colleagues focused on a family of enzymes called phospholipase A2, or PLA2. Genes in the PLA2 family are one of the main sources of toxic proteins in the deadly cocktail of rattlesnake venom. This set of genes can be shuffled around, added to and deleted from to yield different collections of toxins.

Data from the genome — the complete catalog of an organism’s genetic material — can reveal how those genetic gymnastics have played out over time. Carroll’s team looked at the relevant genome regions in three modern rattlesnake species (western diamondback, eastern diamondback and Mojave) and also measured molecules that help turn genetic instructions into proteins. That showed not just how the genes were arranged, but which genes the snakes were actually using. Then, the scientists blended that data with genetic information about other closely related rattlesnakes to construct a potential evolutionary story for the loss of PLA2 genes in one group of snakes.

The most recent common ancestor of this group probably had a large suite of PLA2 genes 22 million years ago, the scientists found. That collection of genes, which probably came about through many gene duplications, coded for toxins affecting the brain, blood and muscles of the snake’s prey. But 4 million to 7 million years ago, some rattlesnake species independently dropped different combinations of those genes to get smaller and more specialized sets of venom toxins. For instance, three closely related rattlesnake species in the group lost the genes that made their venom neurotoxic.

“The surprise is [the genes’] wholesale loss at two levels: complete disappearance from the venom and complete disappearance from the genome,” Carroll says. In other words, some of the genes are still lurking in the genome but aren’t turned on. The proteins those genes produce don’t show up in the venom in modern snakes. But other genes have left the genome entirely — a more dramatic strategy than simple changes in gene regulation.

Environmental shifts might have encouraged this offloading of evolutionary baggage, Carroll says. If a certain snake species’ main food source stopped responding to a neurotoxin, the snake would waste energy producing a protein that didn’t do anything helpful.
Plus, a rattlesnake doesn’t just invest in producing venom. It also needs to produce antibodies and other proteins to protect itself from its own poison, says Todd Castoe, an evolutionary biologist at the University of Texas at Arlington who wasn’t involved in the study. As a snake’s weapon becomes more complex, its shield does too — and that protection can use up resources.

Researchers also found that venom genes might not be consistent even within a single species of rattlesnake, perhaps because snakes in different areas specialize in different prey. One western diamondback rattlesnake that Carroll’s team sampled had unexpected extra genes that the other western diamondbacks didn’t have. His lab is currently looking into these within-species differences in venom composition to see how dynamic the PLA2 genome region still is today.

As for the ancestral rattlesnake, it’s impossible to say exactly how powerful the now-extinct reptile’s venom was, Carroll says. But the wider variety of enzymes this rattlesnake could hypothetically produce would have given it more flexibility to adapt its poison to environmental curveballs — an ability that Castoe describes as “the pinnacle of nastiness.”

PASADENA, Calif. — The Schiaparelli Mars lander, scheduled to touch down on the Red Planet on October 19 at 10:48 a.m. EDT, went silent a few minutes before touchdown, leaving mission scientists hanging on whether the lander safely made it to the surface. Meanwhile, its counterpart, the Trace Gas Orbiter, appears to have successfully entered orbit around Mars.

“We can say the mission is not nominal, but it’s too early to speculate about what happened,” ESA planetary scientist Olivier Witasse said at an October 19 news briefing. “We’re hoping for the best of course.”

The Schiaparelli lander is part of the European Space Agency’s ExoMars mission to, in part, test technology needed for a future European Mars rover. The lander was only expected to survive on the surface for a few Martian days.

A radio signal was received from the Giant Meterwave Radio Telescope in India as the lander descended, indicating the probe survived initial entry into the atmosphere. Subsequent hiccups in the radio signal suggested that the parachute deployed on schedule. The Mars Express orbiter also detected a signal from the lander. But both signals cut out a few minutes before the scheduled landing.

The next chance to learn more will be in the next few hours when the Mars Reconnaissance Orbiter transmits telemetry that it recorded from the lander. The Trace Gas Orbiter also recorded data from the lander, which will be transmitted soon. The European Space Agency will provide an update October 20 at 4 a.m. EDT.

The battle against Zika may have some new firepower. A single dose of a human antibody called ZIKV-117 can shield mouse fetuses from the virus’s damaging effects, researchers report online November 7 in Nature.

In humans, Zika virus infection during pregnancy has been linked to a suite of birth defects including a condition known as microcephaly, which leaves babies with shrunken heads and brains (SN: 4/2/16, p. 26). It’s not yet clear whether a new treatment based on the antibody would work in humans (or even in monkeys). But if it does, ZIKV-117 could potentially offer pregnant women a way to defend themselves — and their babies — from a virus that tore through Brazil and has now encroached upon the United States.

SAN FRANCISCO — Zika causes fetal brain cells neighboring an infected cell to commit suicide, David Doobin of Columbia University Medical Center reported December 6 at the annual meeting of the American Society for Cell Biology. In work with mice and rats, Doobin and colleagues found hints that the cell death might be the body’s attempt to limit the virus’ spread.

The scientists applied techniques they had used to investigate a genetic cause of microcephaly to narrow when in pregnancy the virus is most likely to cause the brain to shrink. Timing of the virus’s effect varied by strain. For one from Puerto Rico, brain cell die-off happened in mice only in the first two trimesters. But a strain from Honduras could kill developing brain cells later in pregnancy.

Discoveries in a richly appointed 2,600-year-old burial chamber point to surprisingly close ties between Central Europe’s earliest cities and Mediterranean societies. Dated to 583 B.C., this grave also helps pin down when people inhabited what may have been the first city north of the Alps.

An array of fine jewelry, luxury goods and even a rare piece of horse armor found in the grave indicates that “there were craftsmen working in the early Celtic centers north of the Alps who learned their crafts south of the Alps,” says archaeologist Dirk Krausse of the Archaeological State Office of Baden-Württemberg, Germany.
Previous research has established that speakers of Celtic languages inhabited parts of Europe as early as 3,300 years ago. Celtic iron makers appeared in Central Europe by around 2,700 years ago — marking the beginning of that region’s Iron Age — and founded what’s now called the Hallstatt culture.

The grave and a smaller adjoining burial lie in a German cemetery situated across the Danube River from an early Iron Age hill fort called the Heuneburg. Along with yielding insights into long-distance trade and the timing of Europe’s first Iron Age cities, these graves provide the earliest evidence of Hallstatt people elaborately interring women and even children, Krausse and colleagues report in the February Antiquity.

“The main burial represents one of the oldest examples of an exceptionally rich female grave and serves as further testimony of the important social role of certain women in Hallstatt communities,” says archaeologist Manuel Fernández-Götz of the University of Edinburgh, who did not participate in the new study.
While surveying earthen mounds covering graves at the German site in 2005, Krausse’s team noticed a gold-plated bronze brooch fragment lying on the ground. An excavation revealed that the brooch came from the grave of a 2- to 4-year-old child whose skeleton was surrounded by gold and gold-plated jewelry.
It turned out that the child’s grave was an addition to a larger burial chamber. Because farming activity threatened the site, cranes were used in 2010 to hoist out the chamber and surrounding soil in a block weighing 80 metric tons. Researchers excavated the tomb at Krausse’s facility.

Planks of oak and silver fir formed the chamber. Comparisons of growth rings in the planks with previously dated tree rings in the region indicate that the tomb was built in 583 B.C. Previous excavations over the past decade had suggested that the Heuneburg and several other early Iron Age settlements in Germany and France were the first cities north of the Alps, but the grave provides the most precise date yet. Prior to this find, settlements dating to between 2,200 and 2,000 years ago have traditionally been considered the first Central European cities.

Inside the chamber, the team discovered a 30- to 40-year-old woman’s headless skeleton. Her lower jaw and skull were found at two other spots in the grave. Objects placed on and around the skeleton included gold, bronze, amber and jet jewelry and brooches. Decorative styles of some items showed Mediterranean influences. Researchers also found two pairs of boar tusks mounted on large pendants. Each pair of tusks curves around two bronze strips and bronze bells hanging from a smaller pendant.

Another woman’s skeleton and pieces of bronze jewelry rested in a corner of the chamber. It’s unclear whether both bodies were buried at the same time.

A decorated bronze sheet found near the second skeleton’s feet was a piece of armor, called a chamfron, that covered a horse’s forehead, the researchers say. Traces of plant netting and fur preserved on the inside surface of the sheet come from padding, they suspect. CT scans revealed remains of an iron horse bit at one end of the sheet, where it fit in the mouth.

This is the first chamfron found at a Hallstatt site. It resembles horse armor from around the same time found in several Mediterranean cultures, Krausse says.

“The tide is finally shifting” toward accepting links between early European Iron Age cities and societies south of the Alps, says anthropologist Bettina Arnold of the University of Wisconsin–Milwaukee. She suspects that, as at some other Iron Age graves, the elite woman’s burial chamber was looted or material was removed for ritual reasons shortly after interment. Such burials typically included a wagon and metal vessels, but these are missing in the woman’s spacious grave. “This grave is a puzzle, and Hallstatt culture is still enigmatic,” Arnold says.

Amid a flurry of cabinet appointments and immigration policies, the Trump administration has announced one thing it will not do: pursue policies that protect transgender children in public schools.

The Feb. 22 announcement rescinds Obama administration guidelines that, among other protections, allow transgender kids to use bathrooms and participate in sports that correspond with their genders, and to be called by their preferred names and pronouns.

In a Feb. 23 news briefing, White House press secretary Sean Spicer said that this is a states’ rights issue. “States should enact laws that reflect the values, principles, and will of the people in their particular state,” he said. “That’s it, plain and simple.”

But this “plain and simple” move could be quite dangerous, even deadly, science suggests. Transgender children, who are born one biological sex but identify as the other, already face enormous challenges as they move through a society that often doesn’t understand or accept them. Consider this: Nearly half (46.5 percent) of young transgender adults have attempted suicide at some point in their lives, a recent survey of over 2,000 people found. Nearly half. For comparison, the attempted suicide rate among the general U.S. population is estimated to be about 4.6 percent.

What’s more, a 2015 study in the Journal of Adolescent Health found that transgender youth are two to three times as likely as their peers to suffer from depression and anxiety disorders, or to attempt suicide or harm themselves. These troublesome stats, based on a sample of 180 transgender children and young adults in Boston ages 12 to 29, applied equally to those who underwent male-to-female transitions and those who underwent female-to-male transitions.

The science is clear: Many transgender kids already have to overcome big challenges. To have the federal government proclaim that it won’t stop states from denying equal protection to transgender children makes a difficult situation even worse.

The American Academy of Pediatrics agrees. On February 23, AAP president Fernando Stein issued a statement condemning the new guidelines. “Policies excluding transgender youth from facilities consistent with their gender identity have detrimental effects on their physical and mental health, safety and well-being,” he wrote. “No child deserves to feel this way, especially within the walls of their own school.”

As that statement points out, policies that run counter to a child’s gender identity can cause harm in several ways. One obvious way comes from the physical effects of not having access to bathrooms. In a study of 93 transgender adults, 68 percent reported having been verbally harassed while trying to use a public bathroom, and 18 percent said they had been turned away from a bathroom. To avoid these confrontations, transgender people often resort to not drinking water or simply holding in their urine, measures that can cause dehydration or urinary tract infections, that same survey found.
Those are the experiences of transgender adults who were aware of the health effects of not using the bathroom. Now think about how a young transgender child in school might navigate that situation. A school bathroom can be a scary place for any first grader, let alone one who risks ridicule or worse for walking into the boys’ or girls’ room.

Beyond the physical harms of not having access to a bathroom, restrictive policies also carry heavy psychological harms. Rules that fail to recognize these children’s genders create stigma, and these policies may have harmful consequences on mental health.

The story of same-sex marriage legalization, an issue that’s been around for decades, holds lessons in how policy can influence mental health. Before the U.S. Supreme Court’s 2015 decision to uphold the right of people of the same sex to marry, states had piecemeal policies, creating a natural experiment of sorts. In states that had recently legalized same-sex marriage, fewer teenagers attempted suicide, scientists reported February 20 in JAMA Pediatrics. In the states’ study, the drop was particularly steep for gay, lesbian and bisexual teens, health and social policy researcher Julia Raifman of Johns Hopkins Bloomberg School of Public Health and colleagues found. Although that study can’t determine the cause of the drop, Raifman suspects that the same-sex laws helped reduce negative stigma, and as a result, improved mental health. Mental health benefits have been documented in gay, lesbian and bisexual adults who are in legally recognized relationships. Marriage bans, on the other hand, had a negative effect.

Raifman says that the announcement from the Trump administration “suggests that transgender youth are different, negatively stereotypes transgender youth, gives transgender youth lesser rights, and allows for states or municipalities to use their power to enforce lesser rights.”

Gender is not a choice. Transgender children are quite clear on their gender identity, often from an early age. It’s easy to lose sight of the fact that behind these dreary statistics is someone’s daughter or son, a vulnerable child that the science clearly shows is at a greater risk of suffering simply because of how he or she was born.

Even in the wilderness, humans are making a ruckus.

In 63 percent of America’s protected places — including parks, monuments and designated wilderness areas — sounds made by human activity are doubling the volume of background noise. And in 21 percent of protected places, this racket can make things 10 times noisier.

Enough clatter from cars, planes and suburban sprawl is seeping into wild places to diminish animals’ ability to hear mating calls and approaching predators, a team of researchers based in Colorado reports in the May 5 Science. Human noise doesn’t always have to be loud to override natural sounds, though. Some places are so quiet to begin with that even the smallest amount of human noise can dominate, the researchers found.

“The world is changing, and protected areas are getting louder — the last strongholds of diversity,” says Jesse Barber, an ecologist at Boise State University in Idaho. Studies like this one that show the impact of human-related noise across the entire country instead of in a single park are important, he says, because “this is the scale at which conservation occurs.”
Researchers measured the reach of human noise by tapping into a National Park Service dataset containing long-term audio recordings from 492 sites across the United States. At each site, the scientists linked the sound volume in decibels (averaged over weeks of recording and adjusted to prioritize the frequencies that human ears are most sensitive to) to the presence or absence of dozens of possible features. Such factors include whether the terrain was mountainous or flat, if there was a river nearby, and how close the site was to a highway or a farm.

Machine learning algorithms then predicted the volume in areas without audio monitors, based on the features of that place — and figured out how much of the noise in any given location came from human sources compared with natural ones.
The answer: quite a lot, even in the wilderness. In 12 percent of designated wilderness areas, for instance, human-made noises increase the median sound level 3 decibels above the predicted natural levels of noise. That means the area over which a bird’s squawk would register in human ears would be cut in half in those places.

The more stringent the protections on the land, the lower the noise pollution, says study coauthor Rachel Buxton, an ecologist at Colorado State University in Fort Collins. For example, some categories of land protection allow mining and timber harvesting in limited amounts, which can boost noise levels. Areas labeled as wilderness ban such activity almost entirely, though do permit livestock grazing. Overall, protected areas were 35 percent less noisy than nearby spots that weren’t protected in any way.

Land managed by the federal government also tended to be less impacted by human noise than land under local control. That might come as a surprise to anyone who’s faced a traffic jam trying to find a parking spot in Yosemite or Shenandoah national parks on a summer weekend. But unlike other U.S. land management agencies, the National Park Service “considers natural sounds to be a natural resource,” Buxton says.
Many national parks have instituted restrictions on airplanes flying overhead, for instance, and implemented public transit to decrease park traffic. So while the area around the visitor center might feel like an amusement park, chirping birds and gurgling streams can dominate the soundscape deeper in the park. This study suggests those noise control efforts might be making a difference.

Still, even a little extra noise can take a toll on the surrounding ecosystem. A humming highway can drown out birds’ mating calls or prevent predators from hearing rustling prey (SN: 2/21/15, p. 22). And species don’t need ears to be affected — the effects of excess noise “can really trickle through a community,” Buxton says. Plants often depend on birds to spread their seeds, or on bees to get pollinated. If noise changes those animals’ behavior, then the plants can face consequences, too.

“Noise is not strictly an urban phenomenon,” says Clint Francis, an ecologist at California Polytechnic State University in San Luis Obispo. There’s hope for wild areas, though. “Solutions to noise are often readily available,” he says. Quieter car engines and different types of road surfaces can all help reduce traffic noise, for example.

Quieter wild places can benefit humans, too. “When you’re in a park and you’re appreciating some sight, like the Grand Canyon, you also experience the sound of the river going by, the sound of the birds in the trees,” Buxton says. “It totally enhances your experience.”

Immune cells can turn certain invaders on themselves, forcing them to prematurely self-destruct, researchers have discovered.

In mice, when white blood cells in the lungs engulf spores of a common airborne fungus, these immune cells release an enzyme that sends the fungal cells into programmed cell death. That prevents the spores from setting up shop in the lungs and sparking a potentially deadly lung infection, the researchers report in the Sept. 8 Science.

Found naturally in soil and decaying organic matter, the fungus, Aspergillus fumigatus, releases airborne spores that are found in small doses in the air people breathe every day. The finding may help explain why most people can regularly inhale the spores and not get sick. In people with weakened immune systems, though, this natural defense system doesn’t work. This research could eventually lead to better treatments for these patients.
Programmed cell death is a natural part of a cell’s life cycle — a way for organisms to break down old cells and make way for new ones. “Research in the last couple of decades has shown that microbes can exploit [cell death] pathways to cause disease,” says study coauthor Tobias Hohl, an infectious disease researcher at Memorial Sloan Kettering Cancer Center in New York City. But this study shows that the tables can be turned. “Not only can microbes exploit this in hosts, but host cells can exploit these pathways to instruct certain microbes to kill themselves.”

“The idea that the host triggers the mechanism of [programmed cell death] as a way of defending against infection is very cool,” says Borna Mehrad, a pulmonologist at the University of Florida College of Medicine in Gainesville who wasn’t part of the study.

Hohl and colleagues identified a gene in A. fumigatus that puts the brakes on programmed cell death. The gene, AfBIR1, shares an ancestor with the human gene survivin, which also regulates cell death.

When the researchers amped up the activity of AfBIR1 in a strain of the fungus, half the mice infected with the spores died during the eight-day study period. (Mice infected with unmodified spores were fine.) Cues that would normally send fungal cells to their death didn’t register, so the fungus was able to grow in the mice’s lungs.

In another experiment, the scientists gave mice a drug called S12, which took away AfBIR1’s brake effect. As a result, the mice were able to fight off the infection. “Those two findings suggested to us that this fungal [cell death] pathway really is critical,” Hohl says.
Hohl did this research with a special variety of A. fumigatus that changes color when its suicide instructions kick in. That advance allowed the researchers to make observations that weren’t possible before, Mehrad says.

For instance, Hohl and his colleagues noticed that fungal cells being engulfed by neutrophils, a type of white blood cell, appeared to be undergoing programmed cell death. That suggested that neutrophil activity might set off fungal programmed cell death.

Neutrophils release an enzyme called NADPH oxidase, and mice deficient in the enzyme weren’t as good at fending off the fungus, Hohl found. That makes sense with clinical data in humans too. People with a genetic mutation that causes a deficiency in NADPH oxidase are particularly at risk for developing an Aspergillus infection, Hohl says. People who have fewer neutrophils, due to chemotherapy or HIV infection, for instance, also make less of the enzyme and are less able to resist a fungal infection.

Survival rates vary, but the U.S. Centers for Disease Control and Prevention estimates that 41 percent of organ transplant recipients who contract aspergillosis die within a year. Seventy-five percent of stem cell transplant recipients with the infection die in that same time frame. Someday, a version of S12 that’s modified to work in humans might be able to boost these patients’ defenses against A. fumigatus infections, Hohl suggests.

In the future, he wants to see whether the same mechanisms extend to other fungal species too.

Finding a great glue is a sticky task — especially if you want it to attach to something as slick as the inside of the human body. Even the strongest human-made adhesives don’t work well on wet surfaces like tissues and organs. For surgeons closing internal incisions, that’s more than an annoyance. The right glue could hold wounds together as effectively as stitches and staples with less damage to the surrounding soft tissue, enabling safer surgical procedures.

A solution might be found under wet leaves on a forest floor, recent research suggests. Jianyu Li of McGill University in Montreal and colleagues have created a surgical glue that mimics the chemical recipe of goopy slime that slugs exude when they’re startled. The adhesive stuck to a pig heart even when the surface was coated in blood, the team reported in the July 28 Science. Using the glue to plug a hole in the pig heart worked so well that the heart still held in liquid after being inflated and deflated tens of thousands of times. Li, who did the research while at Harvard University, and colleagues also tested the glue in live rats with liver lacerations. It stopped the rats’ bleeding, and the animals didn’t appear to suffer any bad reaction from the adhesive.
The glue has “excellent, excellent properties,” says Andrew Smith, a biologist at Ithaca College in New York.
And slugs aren’t the only biological inspiration for new adhesives. Clues to better glues have long been hiding out in damp, soggy and downright wet places. For slugs, mussels, marine worms and a cadre of other critters, secreting sticky substances that attach strongly to soaked surfaces is just a fact of life. That’s why scientists are studying the structures of those substances to design new and better surgical adhesives.

“There’s really a big need to develop new ways of sealing tissues, of affixing devices to tissues — in particular, for minimally invasive procedures,” says Jeff Karp, a biomedical engineer at Brigham and Women’s Hospital in Boston. While existing medical-grade superglue is great at sealing up fingertip cuts, it is too toxic to use inside the body. Other alternatives just aren’t sticky enough to fully replace stitches. With a better glue, surgeons could also make snips that are too tiny to be stitched or stapled closed. Smaller incisions speed healing time and decrease risk of complications, Karp says.

Smith says he isn’t surprised that slug slime could lead to a big advance. For several years, he’s been trying to understand how the slug Arion subfuscus builds its ooze. For his research, Smith prods slugs gently with the tip of a metal spatula to startle them, and scoops up the slime as it’s released. “If you get it on your hands, it’ll set within seconds into an extremely sticky material,” he says.
The goo, Smith and others have found, overcomes a major challenge that adhesive designers face. It seems obvious that glue should be sticky. Yet the molecules in glue need to adhere not just to the things you’re trying to stick together, but also to each other. And that stickiness can’t come at the expense of flexibility, especially for medical applications. Soft, squishy organs are going to jiggle; skin is going to stretch. Without some bendiness, the glue might attach securely to each of the surfaces being stuck together, but the glob of glue itself might snap or shear under stress.

Slug defense slime solves that problem with two interwoven networks of molecules, tangled together like strings of holiday lights. One network is rigid, with chemical bonds that break easily, Smith says. The other is deformable, stretching substantially without breaking. This combo makes the goo simultaneously tough, flexible and sticky.

Li’s slug-inspired adhesive takes a similar approach. One layer of the material is a polymer, a type of material made from long molecules built from many repeated subunits, like a string of beads. Positively charged appendages dangling off the polymers are drawn to wet tissue surfaces by the same forces underlying static electricity. This first layer weaves into another layer, a water-based gel. The gel layer acts like a shock absorber in a car, Li says. It soaks up energy that might otherwise dislodge or snap the adhesive.

Despite being 90 percent water, the material is both sticky and tough, Li says. The fact that it’s mostly water makes it more likely to be nontoxic to humans.
Though Li’s adhesive has been tested only in human cell cultures and in lab animals, another bio-inspired glue has made its way into human trials. It’s based on work published by Karp and colleagues in 2014 in Science Translational Medicine. Karp’s team developed a viscous liquid that solidifies into a tough but stretchy glue when illuminated by light, and demonstrated that the liquid can seal holes in hearts.

“Nothing we create is really that similar to anything you see in nature, but some of the ideas gave us critical insights,” Karp says. The researchers realized, for example, that a lot of natural glues that work in water have hydrophobic elements that help clear away the water for a better stick. The research sparked Karp and colleagues to found a company, Gecko Biomedical, which Karp now advises. On September 11, the company announced the completion of a small clinical trial of its adhesive: The sealant immediately stopped blood flow after an artery-clearing operation in about 85 percent of 22 participants. Because of that success, Gecko Biomedical now has approval to market the glue in Europe.

Bio-inspired adhesives can do more than patch up incisions, though. Russell Stewart, a bioengineer at the University of Utah in Salt Lake City, is tapping into marine-dwelling sandcastle worms for a different glue goal: He wants to create a better embolic agent — a way to deliberately block blood flow to certain tissues. Embolic agents can cut blood flow to a tumor, say, or stem internal bleeding. Often, these materials are liquids that reach their target through a catheter and then solidify into a sticky mass to block tiny vessels. But such glues can be difficult to control — they need to harden at just the right time and current options often rely on harsh materials that require special equipment and can cause pain for patients.

Inspired by the sandcastle worm (Phragmatopoma californica), Stewart has designed a new — and he thinks better — embolic agent. A sandcastle worm uses fingerlike appendages coming out of its face to arrange grains of sand into expansive tubular reefs. It squirts small dabs of a liquid adhesive out of these appendages to make the grains stick together. That glue’s structure is quite different from slug slime, Stewart has found. It’s a solution of oppositely charged proteins strongly attracted to each other. The proteins make up a dense liquid that doesn’t mix with water. A worm packages each ingredient in the glue separately, so the proteins combine only once secreted. After mixing, the glue solidifies in about 30 seconds.

Stewart’s mimic also starts out as a liquid that transforms into a hard foamlike material within a few seconds of hitting blood, his team reported in 2016 in Advanced Healthcare Materials. That means the material can be injected as a liquid and doesn’t harden until it’s in the right place. Early tests have been promising: The foam completely blocked the arteries of rabbits’ kidneys without moving into tissue where it didn’t belong.

The range of biological adhesives is impressive, says Jonathan Wilker, a chemist at Purdue University in West LaFayette, Ind. “They’re so wildly different,” both in terms of chemical makeup and functional properties. That diversity provides a wide palette for scientists seeking glues for specialized applications. And Wilker’s own work adds mussels to the list.

Mussels secrete a strong adhesive that helps them stick tenaciously to rocks and ship hulls. Their secret is a molecule called DOPA, Wilker says. DOPA, or 3,4-dihydroxyphenylalanine, sticks well to other DOPA molecules and to other substances. That gives it the same balance of toughness and stickiness that’s also found in slug slime. Certain amino acids found in mussel proteins might also aid the underwater adhesion. For example, an amino acid called lysine that hangs off of mussel adhesion proteins appears to help clear water molecules out of the way, leaving a drier surface for proteins glomming on.
Wilker’s copycat adhesive is made up of long chains of polystyrene molecules (essentially, Styrofoam) with units of DOPA mixed in. Those long chains of tricked-out polystyrene molecules tangle together and cross-link to create a strong adhesive. He’s made different varieties of the mimic, tailored for different applications. After being immersed in water, one version held on tighter underwater than the glue made by mussels themselves, Wilker’s team reported in February in Applied Materials Interfaces. Another version is biodegradable.

If he can make the glues nontoxic to cells, they could possibly be used inside the body. In one recent study, Wilker created an artificial adhesive protein that mimics the natural protein elastin. The artificial version excelled in both dry and damp test environments, his team reported in April in Biomaterials.

Bringing animal-inspired adhesives into the human body won’t necessarily be a simple task, though. It requires tackling some problems that other animals don’t need to solve, Karp says. A slug, for instance, produces its slime as it needs it. It doesn’t stockpile gallons of glue in its tiny body, or instantly churn out a year’s supply. A successful real-world glue, however, will need to be easy to produce in large quantities and safe to store for months at a time, Karp points out. Those are problems humans will have to solve on their own. That’s the next challenge.

Some bridges could really put a swing in your step.

Crowds walking on a bridge can cause it to sway — sometimes dangerously. Using improved simulations to represent how people walk, scientists have now devised a better way to calculate under what conditions this swaying may arise, researchers report November 10 online in Science Advances.

When a bridge — typically a suspension bridge — is loaded with strolling pedestrians, their gaits can sync, causing the structure to shimmy from side to side. The new study “allows us to better predict the crowd size at which significant wobbling can appear abruptly,” says mathematician Igor Belykh of Georgia State University in Atlanta.
Engineers might eventually use the researchers’ results to avoid debacles like the one that befell the Millennium Bridge in London. This suspension bridge temporarily shut down just days after it opened in 2000 due to the large wobble that occurred when many people tromped across it at once (SN: 11/24/07, p. 331), necessitating costly repairs to fix the problem.

Pedestrians crossing a bridge can cause slight sideways motion of the bridge as they push with their feet. This swaying may lead to the crowd unintentionally falling into lockstep because it’s easier to go with the flow of the swinging bridge than fight it. That synchronization, in turn, creates larger and larger oscillations.
“It’s a dangerous phenomenon that could cause a bridge to collapse if it went unchecked,” says applied mathematician Daniel Abrams of Northwestern University in Evanston, Ill., who was not involved with the research.

Previous mathematical models of the phenomenon “didn’t realistically capture how people exerted force on the bridge,” Abrams says, “but this new model is pretty realistic.” Whereas earlier simulations focused on the timing of footfalls or the amount of force produced with each step, the new work takes both into account.

Tests of the Millennium Bridge showed that the lurching occurred only after a critical number of people — around 165 — entered the bridge. Likewise, in their simulations, Belykh and his colleagues find that oscillations begin abruptly above a certain threshold number of walkers, depending on the properties of the bridge.

The research challenges some previous assumptions. For instance, in the new simulations, the onset of the wobbling began just before the walkers joined in lockstep. This suggests that the synchrony of the crowd might not be a root cause but instead acts as a feedback effect that amplifies preexisting small-scale wobbles. That insight could be relevant for wobbles that occur in certain bridges without pedestrians syncing, Belykh says. Future work will further investigate how the swaying starts.