Peppered moths and copycat butterflies owe their wing color-changing abilities to a single gene, two independent studies suggest.
A genetic tweak in a portion of the cortex gene that doesn’t make protein painted the speckled gray wings of peppered moths black, researchers report online June 1 in Nature. Genetic variants in DNA interspersed with and surrounding the cortex gene also help some tasty species of Heliconius butterflies mimic unpalatable species and avoid getting eaten by predators, a second team of scientists reports, also June 1 in Nature. In the often-told evolutionary tale, the color shift in moths began as factories in Britain started to darken the skies with coal smoke during the Industrial Revolution in the 1800s. Victorian naturalists took note as a newly discovered, all-black carbonaria form of peppered moths (Biston betularia) blended into soot-covered backgrounds; the light-colored typica moths, which lacked the mutation, were easily picked off by birds. By 1970, nearly 99 percent of peppered moths were black in some localities. As air pollution decreased in the late 20th century, black moths became more visible to birds. As a result, carbonaria moths are now rare.
“This begins to unravel exactly what the original mutation was that produced the black … moths that were favored by natural selection” during much of the last century, says evolutionary biologist Paul Brakefield of the University of Cambridge in England. “It adds a new and exciting element to the story.”
Wing pattern changes in butterflies and peppered moths are textbook examples of natural selection, but the molecular details behind the adaptation have eluded scientists for decades. In 2011, researchers tracked the traits to a region of a chromosome all the species have in common (SN: 5/7/11, p. 11; SN: 9/24/11, p. 16). Which of the many genes in that region might be responsible remained a mystery. In peppered moths, the region of interest stretches over about 400,000 DNA bases and contains 13 genes and two microRNAs. “There aren’t really any genes that scream out to you, ‘I’m involved in wing patterning,’” says evolutionary geneticist Ilik Saccheri at the University of Liverpool in England. Saccheri and colleagues compared that region in one black moth and three typical moths. The researchers found 87 places where the black moth differed from the light-colored moths. Most of the differences were changes in single DNA bases — the information-carrying chemicals in DNA. Such genetic variants are known as SNPs for single nucleotide polymorphisms. One difference was the insertion of a 21,925-base-long stretch of DNA into the region. This big chunk of DNA contained multiple copies of a transposable element, or jumping gene. Transposable elements are viruslike pieces of DNA that copy and insert themselves into a host’s DNA.
By examining the DNA of hundreds more typica moths and ruling out mutations one by one, the team ended up with one candidate: the large transposable element that had landed in the cortex gene. But the jumping gene didn’t land in the DNA that encodes the protein. Instead it landed in an intron — a stretch of DNA that gets chopped out after the gene is copied into RNA and before a protein is made.
The jumping gene first landed in the cortex intron in about 1819, the researchers calculated from historical measurements of how common the trait was throughout history. That timing gave the mutation about 20 to 30 moth generations to spread through the population before people first reported sightings of the black moths in 1848. Saccheri and colleagues found the transposable element in 105 of 110 wild-caught carbonaria moths and none of the 283 typica moths tested. The remaining five moths are black because of another, unknown, genetic variation.
Similarly, Nicola Nadeau, an evolutionary geneticist at the University of Sheffield in England, and colleagues combed through more than 1 million DNA bases in each of five species of Heliconius butterflies. The researchers were looking for genetic variants associated with the presence or absence of yellow bands on the wings.
Nadeau’s team found 108 SNPs in all H. erato favorinus butterflies that have a yellow band on their hind wings. Most of those SNPs were in introns of the cortex gene or outside of the gene. Butterflies that lack the yellow band don’t have those SNPs.
Other DNA changes were found to draw yellow bars on the wings of different species of Heliconius butterflies, suggesting that evolution acted multiple times on the cortex gene with similar results.
The finding that the same gene influences wing patterns in butterflies and moths supports an idea that some genes are hot spots of natural selection, says Robert Reed, an evolutionary biologist at Cornell University.
None of the genetic differences in the butterflies or peppered moths change the cortex gene itself. That leaves open the possibility that the transposable element and SNPs aren’t doing anything to cortex, but may be regulating a different gene. But the evidence that cortex really is the gene upon which natural selection has acted is strong, says Reed. “I’d be surprised if they were wrong.”
Still, it’s not obvious how cortex changes wing patterns, says Saccheri. “We’re both equally puzzled about how it is doing what it appears to be doing.” The teams have evidence that cortex helps determine when certain wing scales grow. In butterflies and moths, the timing of wing scale development affects the color of the wings, says Reed. “You see colors popping up almost like a paint-by-numbers.”
Yellow, white and red scales develop first. Black scales come later. Cortex is known to be involved in cell growth. So varying levels of the protein may speed up development of wing scales, causing them to become colored, or slow their growth, allowing them to turn black, the researchers speculate.
A sloppy light system may be just what a squid needs to hide from predators. Bioluminescent cells in some glass squid work in a surprisingly inefficient way — leaking a lot of light rather than fully channeling it, a new study suggests.
Glass squid have largely transparent bodies, helpful for inconspicuous swimming in deep open water. Marine predators often scan the waters above them for the telltale silhouettes of prey blocking sunlight, but there’s little to betray a glass squid — except for a few notable features such as the shadow-making eyes on its head. Underneath those eyes, squid in the genus Galiteuthis grow silvery patches of cells that act as undersurface bioluminescence, a camouflage technique that has evolved in various marine creatures, making their shadows less conspicuous to hunters below.
Biophysicist Alison Sweeney of the University of Pennsylvania in Philadelphia had hypothesized that the cells, called photophores, act like microscopic cables that channel the bioluminescent glow of the squid down or out in a specific direction. The skinny, cablelike cells are surrounded by thin, protein-dense layers that create a silver tube that reminds Sweeney of Saran Wrap. But in the first detailed look at these structures, Sweeney and Pennsylvania colleague Amanda Holt found that the channels performed poorly, letting most of the light leak away sideways. That efficiency, it turns out, could be useful, Sweeney and Holt report June 8 in the Journal of the Royal Society Interface. “We always expect that the most ‘perfect’ or efficient mechanism will be the pinnacle of evolution, but this study shows that there are many ways to solve challenges imposed by the environment,” says marine biologist Steven Haddock of Monterey Bay Aquarium Research Institute in California.
Inefficiency might sound like an improbable scenario for success. But, says visual ecologist Justin Marshall of the University of Queensland in Brisbane, Australia, “I believe it.”
Other researchers had discussed the idea that certain sea creatures show a great deal of subtlety in disguising their silhouettes, but Sweeney knew of no other study trying to figure out how supposed cables work. It turns out that the squid structures were “really bad at being fiber-optic cables,” Sweeney says. The cells are about 50 micrometers long, longish for a cell but short for a cable. And the cells couldn’t guide light even over that short distance without losing much of it. Looking at the cross sections of the photophores under a microscope showed big, uneven gaps in the layers. When she first recognized this, she expected to write “a boring paper that’s, ‘Gee, squid cells kind of sort of guide light, but not really.’”
Then came the “of course” moment for Sweeney and her puzzling measurements. “The lesson that keeps coming back to us,” she says, “is that these things are meaningless until you consider the habitat.” After calculating the light environment where wild squid swim, the researchers realized that the overall effect of the leaking tubes created a plausible approximation for the twilightlike haze in which the squid live. A glowing blur might actually make the eyes less conspicuous to predator approaching from a variety of angles.
Irregularities in the sheathing and shapes of the leaky cables might even make the living cables more remarkable, Sweeney speculates. Dividing them into five rough types, the researchers investigated the kinds of light effects each produced and matched those effects with ocean conditions at two locations off Hawaii. If squid can pick which cable doodads to use and when, the animals could improve the match between their under-eye shine and conditions in the ocean.
Other squid with opaque skin flicker, darken and quick-change their tiny color-making structures, she points out. So, the suggestion that eye-glow structures might change, too, “is not crazy,” Sweeney says.
Spoiler alert: Scientists can gauge a film’s emotional tenor from the gasps of its audience. Sure, the audible sounds are a cue, but so are the chemicals exhaled with each sigh and scream. These gases could point the way to a subtle form of human communication.
“There’s an invisible concerto going on,” says Jonathan Williams, an atmospheric chemist at the Max Planck Institute for Chemistry in Mainz, Germany. “You hear the music and see the pictures, but you don’t realize there are chemical signals in the air.” Williams started out measuring the air in a soccer stadium to see if human breath had a noticeable impact on the concentration of greenhouse gases in the atmosphere. The answer was no, at least on a small scale. But he noticed that levels of carbon dioxide and other gases fluctuated wildly whenever the crowd cheered. That got him wondering: Maybe humans’ emissions are influenced by emotions. So he went to the movies.
Williams and colleagues measured air samples collected over six weeks in two movie theaters in Germany. Overall, 9,500 moviegoers watched 16 films — a mix of comedy, romance, action and horror that included The Hunger Games: Catching Fire, Walking With Dinosaurs and Carrie. The researchers classified scenes from the movies using such labels as “suspense,” “laughter” and “crying.” Then they looked for associations between movie scenes and hundreds of compounds in the air.
Certain scenes, primarily those that had people laughing or on the edge of their seats, had distinct chemical fingerprints, the researchers write May 10 in Scientific Reports. During screenings of The Hunger Games: Catching Fire, CO2 and isoprene emissions consistently peaked at two suspenseful moments. Williams and colleagues attribute the spikes in CO2 to increased pulse and breathing rate. The spikes in isoprene — a chemical associated with muscle action — were probably due to tense movie moments.
The researchers had to account for chemicals wafting into the air that may not have been a reaction to onscreen action. People emit chemicals from their perfume, shampoo and even the snacks they munch such as popcorn or beer. During screenings of The Secret Life of Walter Mitty, for instance, the researchers noticed a spike in ethanol corresponding with a scene in which Mitty orders a beer. Williams speculates that the scene reminded movie-goers to take a swig of their own alcoholic beverages.
Scientists need more data to make robust connections between human emotion and chemical emissions. But Williams sees potential practical applications. Marketers, for example, could quickly measure the air during consumer testing to see how people feel about products. He envisions future studies involving heart rate, body temperature and other physiological measurements.
“We have scratched the surface and it’s made a funny smell,” he says. “It’s something to investigate.”
SAN DIEGO — While astrophysicists celebrate the second detection of ripples in spacetime (SN Online: 6/15/16), they are also looking ahead to figuring out what led to these cosmic quakes. Black holes colliding in remote galaxies sent the gravitational waves our way. But how these duos ended up in an ill-fated embrace in the first place is unknown.
With only two clear detections from the Advanced Laser Interferometer Gravitational-Wave Observatory, and a third marginal candidate, there isn’t enough information to figure out for sure how these binary black holes formed. But there are two leading ideas.
One is that two heavyweight stars, each more than roughly 20 times as massive as the sun, are born, live and detonate together. Their deaths would leave behind a pair of black holes snuggled up to one another. They would eventually spiral together in a spectacular collision (SN: 3/19/16, p. 5).
Another idea is that the black holes find each other in the hustle and bustle of a dense star cluster. Within these crowded clusters, stars and black holes gravitationally shove each other around. “My graduate student calls it a black hole mosh pit,” Frederic Rasio, an astrophysicist at Northwestern University in Evanston, Ill., said June 15 during a news briefing at a meeting of the American Astronomical Society.
Rasio and colleagues developed computer simulations that investigate how denizens of these clusters interact with one another. Black holes settle into the center of the cluster, where some get caught in another’s gravitational embrace. Continued run-ins with other wandering black holes fling these pairings from the cluster, leaving the couple to soar across the galaxy and eventually merge into a single black hole.
There’s no way to tell if the two black hole pairs found by LIGO formed as stellar siblings or cluster cousins. But tests could be done as more are found.
Measuring the spins of the black holes could distinguish between formation scenarios, says Rasio. Black holes from previously paired stars will be spinning the same way; those that hooked up in a star cluster are more likely to be spinning in random directions. While LIGO researchers report that one of the black holes in the latest detection was twirling, they can’t tell which one it was or which way its spin axis was pointing. Another test requires finding collisions over a range of distances from Earth. Because it takes time for gravitational waves to reach us, more distant impacts happened earlier in cosmic history. If astronomers notice an uptick in collisions happening around the same time that star formation peaked in the early universe, then pairings of massive stars are the more likely culprit, says Vicky Kalogera, an astrophysicist also at Northwestern.
“This has great potential to tell us how binary black holes formed,” she says. “But we need a larger sample.”
With improved detectors, researchers could eventually listen in on the entire observable universe — and all of cosmic history back to the first wave of star formation. “Big black holes come from big stars,” says Jonah Kanner, a Caltech astrophysicist. And the first stars are thought to have been hundreds of times more massive than our sun. If LIGO had 10 times its current sensitivity, he says, “we could learn about the first generation of stars. That’s exciting astrophysics.”
Such a leap would require a much more ambitious facility, such as a souped-up LIGO with 40-kilometer-long arms, says Kanner (today’s LIGO is one-tenth that size). “That’s the kind of concept where I can daydream,” he says. It’s just a pipedream for now, but over the coming years, new observatories will come online and bring with them incremental improvements in how far researchers can probe.
LIGO itself is undergoing an upgrade, and will be switched back on this fall. The VIRGO detector in Italy should return to service in early 2017 after five-plus years of refurbishment. In Japan, the KAGRA facility is under construction with plans to begin operation in 2018. And the Indian government recently gave the go-ahead to build a third LIGO facility.
“This is just the beginning of gravitational wave astronomy,” said VIRGO spokesperson Fulvio Ricci, a physicist at the Sapienza University of Rome. “We did it, then we did it again, and we will do it again in the future.”
Lightning seen as cause of puzzling chondrules — Lightning flashes in the huge cloud of primeval dust and gas from which the planets in the solar system condensed may have caused formation of the puzzling objects known as chondrules … the tiny, rounded granules about the size of poppy seeds found in stony meteorites…. Dry lightning flashes could have been the source of the fast heating that, followed by quick cooling, [explains] the glassy structure of chondrules. — Science News, July 16, 1966
Update Chondrules are among the oldest pieces of planetary building blocks, formed roughly 4.6 billion years ago during the solar system’s first few million years. How they formed is still up for debate. But the lightning hypothesis has mostly fallen out of favor. One leading idea is that chondrules emerged in the wake of shock waves that rippled through the planet nursery. Those shock waves may have been triggered by collisions of embryonic planets, gas waves spiraling around the sun or strong solar flares.
By age 25, Patrick Schnur had cycled through a series of treatment programs, trying different medications to kick his heroin habit. But the drugs posed problems too: Vivitrol injections were painful and created intense heroin cravings as the drug wore off. Suboxone left him drowsy, depressed and unable to study or go running like he wanted to. Determined to resume the life he had before his addiction, Schnur decided to hunker down and get clean on his own.
In December 2015, he had been sober for two years and had just finished his first semester of college, with a 4.0 grade point average. Yet, just before the holidays, he gave in to the cravings. Settling into his dorm room he stuck a needle in his vein. It was his last shot. Scientists are searching for a different kind of shot to prevent such tragedies: a vaccine to counter addiction to heroin and other opioids, such as the prescription painkiller fentanyl and similar knockoff drugs. In some ways, the vaccines work like traditional vaccines for infectious diseases such as measles, priming the immune system to attack foreign molecules. But instead of targeting viruses, the vaccines zero in on addictive chemicals, training the immune system to usher the drugs out of the body before they can reach the brain.
Such a vaccine may have helped Schnur, a onetime computer whiz who grew up in the Midwest, far removed from the hard edges of the drug world. His overdose death reflects a growing heroin epidemic and alarming trend. In the 1960s, heroin was seen as a hard-core street drug abused mostly in inner cities. Now heroin is a problem in many suburban and rural towns across America, where it is used primarily by young, white adults — male and female, according to research published by psychiatrist Theodore Cicero of Washington University in St. Louis and colleagues in 2014 in JAMA Psychiatry. His team’s surveys of nearly 2,800 patients in substance abuse treatment programs suggest a shift in the demographics of heroin users in recent years. In the 1960s, more than 80 percent of users took heroin as their first opioid. From 2000 to 2010, 75 percent of heroin users came to the drug because it was easier to get and less expensive than the prescription opioids they had been taking.
In recent decades, overdoses of both illicit and prescription drugs have surged. In 2014, overdose deaths surpassed deaths from motor vehicle accidents, the U.S. Centers for Disease Control and Prevention reported in January. In that year, 28,647 people died of opioid-related overdoses, primarily from prescription pain relievers and heroin.
“The opioid epidemic is devastating and the number of people dying demands an urgent intervention,” says Nora Volkow, director of the U.S. National Institute on Drug Abuse.
A family of drugs The term opioid refers to a host of painkillers derived from the opium poppy as well as synthetic versions of its active compounds. Heroin is processed from morphine, which is extracted from the plant. Prescription medications such as Vicodin, Percocet, OxyContin and fentanyl are made from synthetic morphine, altered to produce different effects.
Currently, three medications, sold under various brand names, are available to help people with heroin or opioid addiction get clean and stay drug-free: methadone, buprenorphine and naltrexone. The treatments work, Volkow says, but not perfectly. Some addicted patients, such as Schnur, experience unwanted side effects from the daily or monthly treatments and stop using them. Others lack access to treatments due to high costs and strict federal limits on dispensing the drugs.
“Unfortunately, only a small percentage — about 25 percent — of people who could benefit from treatment actually get these medications,” Volkow says. Round two for vaccines Vaccines could offer an alternative to patients who have kicked their habit and want to stay clean, scientists say. The vaccines aim to make an addict immune to a drug’s effects, decreasing the motivation to seek more of the drug. That’s important, Volkow says, because over time the treatment may allow recovery of the overactive circuitry in the brain that pushes drug users to keep using.
The idea of antidrug vaccines isn’t new. Scientists began working on formulations in the 1970s, but those efforts were eclipsed by the availability of methadone. Methadone, a synthetic opioid, relieves withdrawal symptoms and cravings for heroin or prescription painkillers by acting on the same brain targets as the drugs, but in a slow, controlled manner, so patients can function normally without feeling high. But the treatment is a method for harm reduction, not a cure for addiction, and must be taken daily to be effective.
In the late 1990s, scientists resumed antidrug vaccine efforts, focusing on vaccines for everything from cocaine to nicotine to heroin (SN: 2/10/07, p. 90). Vaccines for nicotine and cocaine were tested in people, but worked for only a small percentage.
Now, to help combat the growing opioid addiction crisis, two vaccines for heroin users are advancing toward human trials and other antiopioid vaccines are in the pipeline, including one for fentanyl, now a popular street drug.
Among the antiheroin vaccines being tested, one — developed at the Scripps Research Institute in La Jolla, Calif. — spurs the immune system to attack heroin and helps eliminate it from the body so effectively that it can neutralize even lethal levels of the drug in animals. A second antiheroin vaccine, developed at the Walter Reed Army Institute of Research in Silver Spring, Md., goes after two closely linked problems: It keeps heroin from reaching the brain while preventing HIV infection.
Addiction’s grip Once a person is addicted, the fight to stay clean never ends, Volkow says. That’s because heroin and other addictive substances alter the brain’s pleasure circuits, producing changes that persist long after users stop taking the drug. Volkow, who has studied these effects for more than two decades, says addiction is a brain disease because of the structural and functional changes that occur. Drugs of abuse produce their high by interacting with cells located in brain areas that govern reward, including the nucleus accumbens, a key region in the pleasure circuit. Though each type of drug works in a slightly different way, all addictive drugs increase the amount of the chemical dopamine in this area. Dopamine is a neurotransmitter, carrying signals between nerve cells, or neurons.
Opioids boost dopamine levels by stimulating molecules called mu receptors that sit on the surface of certain neurons. Normally, these receptors are activated by hormones and brain chemicals made in the body, such as endorphins, to reinforce pleasurable behavior such as eating, having sex or listening to music. A single dose of heroin, however, releases many times the amount of dopamine produced by a favorite food or song.
Dopamine fuels the high that people feel from taking an addictive drug, but other molecules help to get people hooked. Glutamate, a neurotransmitter that increases the chatter among cells in areas that govern learning and boost motivation, helps engrave the experience of a drug’s high into the brain. Memories of the high become so enduring that years later they can be reawakened. This long-lasting pull is why more than 60 percent of people with addiction experience relapse within the first year after they are discharged from treatment.
Taken over time, drugs of abuse can change signaling in a number of the brain’s circuits. Last year in Cell, Volkow and NIDA biochemist Marisela Morales outlined two common features of the addicted brain: a decreased sensitivity in the brain’s reward centers and disruption of circuits involved in self-control.
With repeated drug use, the number of dopamine receptors declines as the brain attempts to calm down, Volkow says. With fewer receptors available to take up dopamine molecules, it takes more stimulation to produce feelings of pleasure. Addicts soon find that they are no longer motivated by everyday activities that had been enjoyable or exciting, and they need higher doses of the drug to get the euphoric feelings once provided by smaller doses.
“The brain rapidly learns that the only thing that’s going to stimulate these pleasure circuits is the drug,” Volkow says. “That’s one of the components that drives drug-seeking behavior.” Eventually, the drug no longer produces a high. Instead, it becomes a necessity to stave off feelings of anxiety and despair.
Addiction also impairs dopamine functioning in the prefrontal cortex, an area of the brain that includes regions involved in analysis, decision making and self-control. “Taking drugs interferes with one’s capacity to make good decisions” and follow through, Volkow says. “An addict might say ‘I don’t want to take that drug.’ But they don’t have the capacity to easily change their behavior.”
Protect the brain Vaccines, potentially, offer a “transformative” way to treat addiction, Volkow says, because the treatments can train the immune system to attack drug molecules before they reach the brain. Vaccines typically contain an agent that resembles a disease-causing virus, teaching the immune system to respond quickly when it encounters the invader. In designing vaccines, scientists try to provoke at least one of the human body’s primary immune responders: T cells, which attack infected cells, or B cells, which release antibodies that recognize hostile molecules and attach to them, targeting them for destruction.
Easier said than done. For starters, drug molecules are tiny, much smaller than a bacterium or virus, and are not easily detected by the immune system. In addition, the body’s immune system is set up to fight invaders that arrive in small groups. When an influenza virus makes its way into a body, the initial levels of virus in the blood are very low, Volkow says. But when people inject heroin, for example, many millions of drug molecules and their breakdown products quickly rush into the bloodstream. In recent years, researchers have found new ways to help call the immune system’s attention to such surges of “invading” drugs.
While developing one heroin vaccine, chemist Kim Janda of Scripps and colleagues noticed that antibodies to heroin molecules alone didn’t stop animals from getting high. That’s because once heroin gets into the body — whether it’s injected, snorted or smoked — it is broken down into its active components, 6-acetylmorphine, or 6-AM, and morphine. “Those two metabolites are the real drugs in heroin,” Janda says.
Typically, vaccines lead to production of antibodies that target a single invader. To get the immune system to notice both heroin and its metabolites, Janda joined forces with neurobiologist George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, to design a multitarget vaccine. The vaccine “cocktail,” as Janda calls it, has three components: a large protein that carries the druglike molecules into the body; a molecule called a hapten, chemically designed to induce an immune response to heroin and its metabolites 6-AM and morphine; and finally, alum, an agent commonly added to vaccines to stimulate release of cytokines, proteins that help rally the immune cells to fight invaders.
Over the last six years, Janda’s group has tinkered with the hapten to help the antibodies get a tight grip on heroin, 6-AM and morphine. The hapten, along with the protein carrier, draws attention from the immune system’s T cells, which learn to recognize the drug molecules as invaders. Later, if heroin or its metabolites are detected in the blood, the T cells will “remember” the invaders and remove them. In rats, the three-pronged vaccine generated high numbers of antibodies against the drug and its metabolites, blocking heroin’s action on the brain. Once vaccinated, the formerly addicted rats were unable to get high, even when injected with extremely high doses of the drug, Janda’s group reported in 2013 in the Proceedings of the National Academy of Sciences. The result was decreased drug-seeking behavior in the vaccinated rats. By contrast, control rats, and those vaccinated only against morphine, continued to seek higher doses of the drug.
The vaccine showed similar effectiveness in nonhuman primates, Janda reported in May at the American Psychiatric Association’s annual meeting in Atlanta. In addition, the vaccine is specific to heroin metabolites, not other opiates. A vaccine that’s too broad could potentially make patients immune to the effects of all prescription opioids, leaving them vulnerable if they become injured and need pain relief.
Janda’s team recently tested another antiopioid vaccine in animals, one that arms the body against fentanyl. When given to mice, the vaccine trained the animals’ immune systems to generate antibodies that bind to fentanyl and prevent it from traveling to the brain from the bloodstream. The results, published March 7 in Angewandte Chemie, showed that in mice, the antibodies neutralized high levels of the drug — more than 30 times a normal dose — for months after a series of three shots. By blocking the effects of the drug and its high, the vaccine could potentially curb drug-seeking behavior.
Another group is going after heroin and its strong tie to high HIV infection rates worldwide. Scientists at the Walter Reed Army Institute of Research are developing a dual-purpose vaccine, called H2, to treat heroin addiction while preventing HIV infection.
Biochemist Gary Matyas and his group at Walter Reed first designed a vaccine to stimulate antibodies against heroin. Similar to Janda’s antiheroin vaccine, haptens are bound to a protein carrier, spurring the immune system to create high levels of antibody to bind heroin and its metabolites in the blood and prevent it from crossing the blood-brain barrier. Users will then experience no euphoria or addictive reactions.
The researchers plan to combine the heroin vaccine with an HIV vaccine, a combination that’s much trickier to develop. Scientists have long been frustrated by the ability of the AIDS virus to mutate and evade the immune system. The virus constantly changes the makeup of the proteins on its surface so that antibodies have difficulty recognizing and attacking it. But researchers have found that targeting a region called V2 on the surface of the virus decreased the risk of HIV infection.
The vaccine, tested in volunteers in Thailand by the country’s Ministry of Public Health and Walter Reed scientists, protected about a third of participants against HIV infection, according to a 2009 report.
There’s no timeline for moving the H2 vaccine into human trials, Matyas says. His hope is that the vaccine will concurrently address the entwined epidemics. “If you can reduce heroin use, you can reduce the spread of HIV,” he says. “That’s why we’re focusing on both heroin and HIV in one vaccine.”
Extra help While vaccines can’t be the only treatment for the opioid epidemic, they could offer users who want to abstain an additional and much needed option to deal with addiction. It’s not unusual for people to relapse, or to require more than one type of treatment, before finding a course of recovery that suits them, Volkow says. Treating addiction like a disease that needs to be managed, such as diabetes or high blood pressure, with a multiplicity of treatment options would help addicts find a treatment that works well for them over the long haul, she says.
“Addiction is an extremely serious disease, with a high mortality rate and devastating consequences,” Volkow says. “We need to treat it very aggressively, and we need to have a variety of interventions so if one doesn’t work we have something else to offer the patient.”
Because relapse is common in addiction, Janda says he thinks that the antidrug vaccines’ value will come in helping people who want to abstain, but might falter in a weak moment. “Even if they try to do the drug, they’re not going to get the reward effects of the drug,” he says. “That means that they won’t spiral out of control and have to start all over again.”
Kathy Schnur, Patrick’s mother, remembers how, years into her son’s treatment, when the conversation turned to heroin — its euphoric high and mysterious spell — her son would confess to a desire to taste the drug “one more time.” A heroin vaccine would have taken a relapse off the table, she says. He would no longer have needed to make a daily decision to stay clean.
“If he knew he couldn’t get what he expected from the drug, it would remain a nonevent,” Schnur says. “Or, if he slipped up and tried it just one more time, the vaccine would prevent an overdose.”
Mars’ misshapen moons, Phobos and Deimos, might be all that’s left of a larger family that arose in the wake of a giant impact with the Red Planet billions of years ago, researchers report online July 4 in Nature Geoscience.
The origin of the two moons has never been clear; they could be captured asteroids or homegrown satellites. But their orbits are hard to explain if they were snagged during a flyby, and previous calculations have had trouble reproducing locally sourced satellites. The new study finds that a ring of rocks blown off of the planet by a collision with an asteroid could have been a breeding ground for a set of larger satellites relatively close to the planet. Those moons, long since reclaimed by Mars, could have herded remaining debris in the sparsely populated outer part of the ring to form Phobos and Deimos. Pascal Rosenblatt, a planetary scientist at the Royal Observatory of Belgium in Brussels, and colleagues ran computer simulations to show how the helper moons formed, did their duty and then fell to Mars, leaving behind a pair of moons similar to Phobos and Deimos.
The rain of moons is not over. While Deimos is in a stable orbit, Phobos is developing stress fractures as it slowly inches toward the Red Planet (SN: 12/12/15, p. 11).
Capuchins in northeast Brazil have wielded stones to crack open cashew nuts for 600 to 700 years, researchers report July 11 in Current Biology. Unearthed “hammers” and “anvils” are the earliest evidence of monkey tool use to date.
Today, Brazilian bearded capuchin monkeys (Sapajus libidinosus) still open cashews by placing them on the flat surfaces of anvil rocks and pounding the nuts with large stones. Unlike pebbles and other rocks, the tool stones are distinctively heavy, blemished with wear marks, greased with cashew residue and clustered under cashew trees, Michael Haslam of the University of Oxford and colleagues found. The team mapped where the monkeys left these modern tools scattered under cashew trees. When the researchers dug beneath dense, ancient cashew groves, they found 69 more stone tools — clustered in similar arrangements to modern tools, of similar heft and with the same distinctive wear marks — buried in three sequentially deeper layers of sediment. Radiocarbon dating of charcoal shows that the deepest tools rest in a layer of excavated soil dating back as early as 1266, suggesting that capuchins have been using stone tools to crack nuts for hundreds of years. The new findings are “incredibly important,” says archaeologist Huw Barton of the University of Leicester in England. They “will help us reassess the earliest evidence of tool use by our own ancestors.”
Capuchins are the only monkeys in South America that frequently use tools. It’s a habit they evolved independently from other inventive primates, such as humans and chimps. (The three species last shared a common ancestor some 35 million years ago.) Understanding why capuchins picked up the skill could point to situations that inspired the rise of tool use across species, says primatologist and study coauthor Tiago Falótico of the University of Sao Paulo.
Elisabetta Visalberghi, a primatologist at the Institute of Cognitive Sciences and Technologies in Rome, agrees that it’s likely that the monkeys “used tools in the past as they do now.” But she doubts that wear-and-tear scratches — which Haslam’s team used to identify buried stones as tools — were indeed produced by cracking cashews. The nuts are relatively soft; so are the stones, she says. While Haslam’s team compared markings on modern and ancient tools, they didn’t test if new marks appear on modern stones after they are used by capuchins. Visalberghi says those experiments are “fundamental to evaluate the relevance of the results.” SUBSCRIBE While this is not the first archaeological evidence of monkey tool use, it is the oldest by far. Haslam, Falótico and colleagues reported the first evidence last month in the Journal of Human Evolution: 10- to 50-year-old buried tools used by long-tailed macaques in Thailand. Before that, chimpanzees were the only primates other than humans with an ancient track record of tool use, dating back thousands of years (SN: 02/17/07, p. 99).
Compared with that of chimps, the record of capuchin tools is relatively young. But 600 to 700 years isn’t a final estimate, the researchers say. Even older monkey tools could rest in deeper soil under the cashew trees.
Turtle shells didn’t get their start as natural armor, it seems. The reptiles’ ancestors might have evolved partial shells to help them burrow instead, new research suggests. Only later did the hard body covering become useful for protection.
The findings might also help explain how turtles’ ancestors survived a mass extinction 250 million years ago that wiped out most plants and animals on earth, scientists report online July 14 in Current Biology.
Most shelled animals, like armadillos, get their shells by adding bony scales all over their bodies. Turtles, though, form shells by gradually broadening their ribs until the bones fuse together. Fossils from ancient reptiles with partial shells made from thickened ribs suggest that turtles’ ancestors began to suit up in the same way. It’s an unusual mechanism, says Tyler Lyson, a paleontologist at the Denver Museum of Nature and Science who led the study. Thicker ribs don’t offer much in the way of protection until they’re fully fused, as they are in modern turtles. And the modification makes critical functions like moving and breathing much harder — a steep price for an animal to pay. So Lyson suspected there was some advantage other than protection to the partial shells.
He and his colleagues examined fossils from prototurtles, focusing on an ancient South African reptile called Eunotosaurus africanus.
Eunotosaurus shared many characteristics with animals that dig and burrow, the researchers found. The reptile had huge claws and large triceps in addition to thickened ribs. “We could tell that this animal was very powerful,” says Lyson. Broad ribs “provide a really, really strong and stable base from which to operate this powerful digging mechanism,” he adds. Like a backhoe, Eunotosaurus could brace itself to burrow into the dirt.
Thanks to a lucky recent find of a fossil preserving the bones around the eyes, the team was even able to tell that the prototurtles’ eyes were well adapted to low light. That’s another characteristic of animals that spend time underground.
Swimming and digging use similar motions, Lyson says, so you would expect to find similar skeletal adaptations in water-dwelling animals. But large claws good for moving dirt suggest a life on land.
Fossils from other prototurtle species also have wider ribs and big claws. So the researchers think these traits may have been important for early turtle evolution in general, not just for Eunotosaurus.
Not everyone is entirely convinced. “It’s a very plausible idea, although many other animals burrow but don’t have these specializations,” says Hans Sues, a paleontologist at the Smithsonian Institution’s National Museum of Natural History. Sues says that it will be important to find and study other turtle ancestors well-adapted to digging to bolster the explanation.
Lyson thinks the prototurtles’ burrowing tendencies might have helped them survive the end-Permian mass extinction around 250 million years ago (SN: 9/19/15, p. 10).
“Lots of animals at this time period burrowed underground to avoid the very, very arid environment that was present in South Africa,” Lyson says. “The burrow provides more climate control.”
There are plenty of reasons to tell kids not to bite their nails or suck their thumbs. Raw fingernail areas pick up infection, and thumbs can eventually move teeth into the wrong place. Not to mention these habits slop spit everywhere. But these bad habits might actually good for something: Kids who sucked their thumbs or chewed their nails had lower rates of allergic reactions in lab tests, a new study finds.
The results come from a group of more than 1,000 children in New Zealand. When the kids were ages 5, 7, 9 and 11, their parents were asked if the kids sucked their thumbs or bit their nails. At age 13, the kids came into a clinic for an allergen skin prick test. That’s a procedure in which small drops of common allergens such as pet dander, wool, dust mites and fungus are put into a scratch on the skin to see if they elicit a reaction.
Kids whose parents said “certainly” to the question of thumb-sucking or nail-biting were less likely to react to allergens in the skin prick test, respiratory doctor Robert Hancox of the University of Otago in New Zealand and colleagues report July 11 in Pediatrics. And this benefit seemed to last. The childhood thumb-suckers and nail-biters still had fewer allergic reactions at age 32.
The results fit with other examples of the benefits of germs. Babies whose parents cleaned dirty pacifiersby popping them into their own mouths were more protected against allergies. And urban babies exposed to roaches, mice and cats had fewer allergies, too. These scenarios all get more germs in and on kids’ bodies. And that may be a good thing. An idea called the hygiene hypothesis holds that exposure to germs early in life can train the immune system to behave itself, preventing overreactions that may lead to allergies and asthma.
It might be the case that germy mouths bring benefits, but only when kids are young. Hancox and his colleagues don’t know when the kids in their study first started sucking thumbs or biting nails, but having spent time around little babies, I’m guessing it was pretty early.
So does this result mean that parents shouldn’t discourage — or even encourage — these habits? Hancox demurs. “We don’t have enough evidence to suggest that parents change what they do,” he says. Still, the results may offer some psychological soothing, he says. “Perhaps if children have habits that are difficult to break, there is some consolation for parents that there might be a reduced risk of developing allergy.”
