WASHINGTON — There’s a long-standing joke that NASA is always 20 years from putting astronauts on Mars. Mission details shared at a recent summit shows that the space agency is right on schedule. A to-do list from 2015 looks remarkably similar to one compiled in 1990. One difference: NASA is now building a rocket and test-driving technologies needed to get a crew to Mars. But the specifics for the longest road trip in history — and what astronauts will do once they arrive — remain an open question.
“Are we going to just send them there to explore and do things that we could do robotically though slower, or can we raise the bar?” asked planetary scientist Jim Bell during the Humans to Mars summit. “We need to make sure that what these folks are being asked to do is worthy of the risk to their lives,” said Bell, of Arizona State University in Tempe. The three-day symposium, which ended May 19, was organized by Explore Mars Inc., a nonprofit dedicated to putting astronauts on Mars by the 2030s.
While the summit didn’t break new scientific ground, it did bring together planetary scientists , space enthusiasts and representatives from both NASA and the aerospace industry to talk about the challenges facing a crewed mission to Mars and rough ideas for how to get there.
Part of the appeal in sending humans is the pace of discovery. Drilling just one hole with the Curiosity rover, which has been exploring Gale Crater on Mars since August 2012 (SN: 5/2/2015, p. 24), currently takes about a week. “It’s a laborious, frustrating, wonderful — frustrating — multiday process,” said Bell.
Humans also can react to novel situations, make quick decisions and see things in a way robotic eyes cannot. “A robot explorer is nowhere near as good as what a human geologist can do,” says Ramses Ramirez, a planetary scientist at Cornell University. “There’s just a lot more freedom.”
Researchers saw the human advantage firsthand in 1997 when they sent a rover called Nomad on a 45-day trek across the Atacama Desert in Chile. Nomad was controlled by operators in the United States to simulate operating a robot on another planet. Humans at the rover site provided a reality check on the data Nomad sent back. “There was a qualitative difference,” says Edwin Kite, a planetary scientist at the University of Chicago. And it wasn’t just that the geologists could do things faster. “The robots were driving past evidence of life that humans were finding very obvious.” To get astronauts ready to explore Mars, the Apollo program is a good template, said Jim Head, a geologist at Brown University who helped train the Apollo astronauts. “Our strategy was called t-cubed: train them, trust them and turn them loose.” While each of the moon expeditions had a plan, the astronauts were trusted to use their judgment. Apollo 15 astronaut David Scott, for example, came across a chunk of deep lunar crust that researchers hoped to find although it wasn’t at a planned stop. “He spotted it three meters away,” said Head. “He saw it shining and recognized it immediately. That’s exploration.”
Despite a lack of clear goals for a jaunt to Mars, NASA is forging ahead. The Orion crew capsule has already been to space once; a 2014 launch atop a Delta IV Heavy rocket sent an uncrewed Orion 5,800 kilometers into space before it splashed down in the Pacific Ocean (SN Online: 12/5/2014). And construction of the Space Launch System, a rocket intended to hurl humans at the moon and Mars, is under way. The first test flight, scheduled for October 2018, will send Orion on a multiday uncrewed trip around the moon. NASA hopes to put astronauts onboard for a lunar orbit in 2021.
Meanwhile, the crew aboard the International Space Station is testing technologies that will keep humans healthy and happy during an interplanetary cruise. Astronaut Scott Kelly recently completed a nearly yearlong visit to the station intended to reveal the effects of long-duration space travel on the human body (SN Online: 2/29/2016). And on April 10, a prototype inflatable habitat — the Bigelow Expandable Activity Module — arrived at the station and was attached to a docking port six days later. The station crew will inflate the module for the first time on May 26. No one will live in it, but over the next two years, astronauts will collect data on how well the habitat handles radiation, temperature extremes and run-ins with space debris. Beyond that, the plans get fuzzy. The general idea is to construct an outpost in orbit around the moon as a testing and staging ground starting in the late 2020s. The first crew to Mars might land on the planet — or might not. One idea is to set up camp in Mars orbit; from there, astronauts could operate robots on the surface without long communication delays. Another idea has humans touching down on one of Mars’ two moons, Phobos or Deimos. When crews do land on the Martian surface, NASA envisions establishing a base from which astronauts could plan expeditions.
With so few details, it’s difficult for the space agency to identify specific technologies to invest in. “There have been lots of studies — we get a lot of grief that it’s nothing but studies,” said Bret Drake, an engineer at the Aerospace Corp. in El Segundo, Calif. “But out of the studies, there are a lot of common things that come to the top no matter what path you take.”
Any mission to Mars has to support astronauts for roughly 500 to 1,000 days. The mission has to deal with round-trip communication delays of up to 42 minutes. It will need the ability to land roughly 40-ton payloads on the surface of Mars (current robotic missions drop about a ton). Living off the land is also key, making use of local water and minerals. And astronauts need the ability to not just survive, but drive around and explore. “We want to land in a safe place, which is going to be geologically boring, but we want to go to exciting locations,” said Drake.
The technical and logistical challenges might be the easiest part. “We do know enough to pull this off,” Ramirez says. “The biggest problem is political will.” Congress has yet to sign off on funding this adventure (nor has NASA presented a budget — expected to be in the hundreds of billions of dollars), and future administrations could decide to kill it.
Multiple summit speakers stressed the importance of using technology that is proven or under development — no exotic engines or rotating artificial gravity habitats for now. And a series of small missions —baby steps to the moon and an asteroid before committing to Mars — could show progress that might help keep momentum (and public interest) alive.
“We thought going to the moon was impossible, but we got there,” says Ramirez. “If we dedicate ourselves as a nation to do something crazy, we’ll do it. I have no doubt.”
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.
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).
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.”
A puzzling mismatch is plaguing two methods for measuring how fast the universe is expanding. When the discrepancy arose a few years ago, scientists suspected it would fade away, a symptom of measurement errors. But the latest, more precise measurements of the expansion rate — a number known as the Hubble constant — have only deepened the mystery.
“There’s nothing obvious in the measurements or analyses that have been done that can easily explain this away, which is why I think we are paying attention,” says theoretical physicist Marc Kamionkowski of Johns Hopkins University. If the mismatch persists, it could reveal the existence of stealthy new subatomic particles or illuminate details of the mysterious dark energy that pushes the universe to expand faster and faster.
Measurements based on observations of supernovas, massive stellar explosions, indicate that distantly separated galaxies are spreading apart at 73 kilometers per second for each megaparsec (about 3.3 million light-years) of distance between them. Scientists used data from NASA’s Hubble Space Telescope to make their estimate, presented in a paper to be published in the Astrophysical Journal and available online at arXiv.org. The analysis pegs the Hubble constant to within experimental errors of just 2.4 percent — more precise than previous estimates using the supernova method.
But another set of measurements, made by the European Space Agency’s Planck satellite, puts the figure about 9 percent lower than the supernova measurements, at 67 km/s per megaparsec with an experimental error of less than 1 percent. That puts the two measurements in conflict. Planck’s result, reported in a paper published online May 10 at arXiv.org, is based on measurements of the cosmic microwave background radiation, ancient light that originated just 380,000 years after the Big Bang.
And now, another team has weighed in with a measurement of the Hubble constant. The Baryon Oscillation Spectroscopic Survey also reported that the universe is expanding at 67 km/s per mega-parsec, with an error of 1.5 percent, in a paper posted online at arXiv.org on July 11. This puts BOSS in conflict with the supernova measurements as well. To make the measurement, BOSS scientists studied patterns in the clustering of 1.2 million galaxies. That clustering is the result of pressure waves in the early universe; analyzing the spacing of those imprints on the sky provides a measure of the universe’s expansion.
Although the conflict isn’t new (SN: 4/5/14, p. 18), the evidence that something is amiss has strengthened as scientists continue to refine their measurements. The latest results are now precise enough that the discrepancy is unlikely to be a fluke. “It’s gone from looking like maybe just bad luck, to — no, this can’t be bad luck,” says the leader of the supernova measurement team, Adam Riess of Johns Hopkins. But the cause is still unknown, Riess says. “It’s kind of a mystery at this point.” Since its birth from a cosmic speck in the Big Bang, the universe has been continually expanding. And that expansion is now accelerating, as galaxy clusters zip away from one another at an ever-increasing rate. The discovery of this acceleration in the 1990s led scientists to conclude that dark energy pervades the universe, pushing it to expand faster and faster.
As the universe expands, supernovas’ light is stretched, shifting its frequency. For objects of known distance, that frequency shift can be used to infer the Hubble constant. But measuring distances in the universe is complicated, requiring the construction of a “distance ladder,” which combines several methods that build on one another.
To create their distance ladder, Riess and colleagues combined geometrical distance measurements with “standard candles” — objects of known brightness. Since a candle that’s farther away is dimmer, if you know its absolute brightness, you can calculate its distance. For standard candles, the team used Cepheid variable stars, which pulsate at a rate that is correlated with their brightness, and type 1a supernovas, whose brightness properties are well-understood.
Scientists on the Planck team, on the other hand, analyzed the cosmic microwave background, using variations in its temperature and polarization to calculate how fast the universe was expanding shortly after the Big Bang. The scientists used that information to predict its current rate of expansion.
As for what might be causing the persistent discrepancy between the two methods, there are no easy answers, Kamionkowski says. “In terms of exotic physics explanations, we’ve been scratching our heads.”
A new type of particle could explain the mismatch. One possibility is an undiscovered variety of neutrino, which would affect the expansion rate in the early universe, says theoretical astrophysicist David Spergel of Princeton University. “But it’s hard to fit that to the other data we have.” Instead, Spergel favors another explanation: some currently unknown feature of dark energy. “We know so little about dark energy, that would be my guess on where the solution most likely is,” he says.
If dark energy is changing with time, pushing the universe to expand faster than predicted, that could explain the discrepancy. “We could be on our way to discovering something nontrivial about the dark energy — that it is an evolving energy field as opposed to just constant,” says cosmologist Kevork Abazajian of the University of California, Irvine.
A more likely explanation, some experts say, is that a subtle aspect of one of the measurements is not fully understood. “At this point, I wouldn’t say that you would point at either one and say that there are really obvious things wrong,” says astronomer Wendy Freedman of the University of Chicago. But, she says, if the Cepheid calibration doesn’t work as well as expected, that could slightly shift the measurement of the Hubble constant.
“In order to ascertain if there’s a problem, you need to do a completely independent test,” says Freedman. Her team is working on a measurement of the Hubble constant without Cepheids, instead using two other types of stars: RR Lyrae variable stars and red giant branch stars.
Another possibility, says Spergel, is that “there’s something missing in the Planck results.” Planck scientists measure the size of temperature fluctuations between points on the sky. Points separated by larger distances on the sky give a value of the Hubble constant in better agreement with the supernova results. And measurements from a previous cosmic microwave background experiment, WMAP, are also closer to the supernova measurements.
But, says George Efstathiou, an astrophysicist at the University of Cambridge and a Planck collaboration member, “I would say that the Planck results are rock solid.” If simple explanations in both analyses are excluded, astronomers may be forced to conclude that something important is missing in scientists’ understanding of the universe.
Compared with past disagreements over values of the Hubble constant, the new discrepancy is relatively minor. “Historically, people argued vehemently about whether the Hubble constant was 50 or 100, with the two camps not conceding an inch,” says theoretical physicist Katherine Freese of the University of Michigan in Ann Arbor. The current difference between the two measurements is “tiny by the standards of the old days.”
Cosmological measurements have only recently become precise enough for a few-percent discrepancy to be an issue. “That it’s so difficult to explain is actually an indication of how far we’ve come in cosmology,” Kamionkowski says. “Twenty-five years ago you would wave your hands and make something up.”
Cancer goes way, way back. A deadly form of this disease and a noncancerous but still serious tumor afflicted members of the human evolutionary family nearly 2 million years ago, two new investigations of fossils suggest.
If those conclusions hold up, cancers are not just products of modern societies, as some researchers have proposed. “Our studies show that cancers and tumors occurred in our ancient relatives millions of years before modern industrial societies existed,” says medical anthropologist Edward Odes of the University of the Witwatersrand in Johannesburg, a coauthor of both new studies. Today, however, pesticides, longer life spans and other features of the industrialized world may increase rates of cancers and tumors. A 1.6-million- to 1.8-million-year-old hominid, either from the Homo genus or a dead-end line called Paranthropus, suffered from a potentially fatal bone cancer, Odes and colleagues say in one of two papers published in the July/August South African Journal of Science. Advanced X-ray techniques enabled identification of a fast-growing bone cancer on a hominid toe fossil previously unearthed at South Africa’s Swartkrans Cave site, the researchers report. This malignant cancer consisted of a mass of bone growth on both the toe’s surface and inside the bone.
Until now, the oldest proposed cancer in hominids consisted of an unusual growth on an African Homo erectus jaw fragment dating to roughly 1.5 million years ago. Critics, though, regard that growth as the result of a fractured jaw, not cancer.
A second new study, led by biological anthropologist Patrick Randolph-Quinney, now at the University of Central Lancashire in England, identifies the oldest known benign tumor in a hominid in a bone from an Australopithecus sediba child. This tumor penetrated deep into a spinal bone, close to an opening for the spinal cord. Nearly 2-million-year-old partial skeletons of the child and an adult of the same species were found in an underground cave at South Africa’s Malapa site ( SN: 8/10/13, p. 26 ). Although not life-threatening, this tumor would have interfered with walking, running and climbing, the researchers say. People today, especially children, rarely develop such tumors in spinal bones.
“This is the first evidence of such a disease in a young individual in the fossil record,” Randolph-Quinney says.
X-ray technology allowed scientists to create and analyze 3-D copies of the inside and outside of the toe and spine fossils.
But studies of fossil bones alone, even with sophisticated imaging technology, provide “a very small window” for detecting cancers and tumors, cautions paleoanthropologist Janet Monge of the University of Pennsylvania Museum of Archaeology and Anthropology in Philadelphia. Microscopic analysis of soft-tissue cells, which are typically absent on fossils, confirms cancer diagnoses in people today, she says.
Without additional evidence of bone changes in and around the proposed cancer and tumor, Monge won’t draw any conclusions about what caused those growths.
Monge led a team that found a tumor on a 120,000- to 130,000-year-old Neandertal rib bone from Eastern Europe. Whether the tumor was cancerous or caused serious health problems can’t be determined, the scientists concluded in 2013 in PLOS ONE.
For the first time, scientists can see where molecular tags known as epigenetic marks are altered in the brain.
These chemical tags — which flag DNA or its protein associates, known as histones — don’t change the genes but can change gene activity. Abnormal epigenetic marks have been associated with brain disorders such as Alzheimer’s disease, schizophrenia, depression and addiction.
Researchers at Massachusetts General Hospital in Boston devised a tracer molecule that latches on to a protein that removes one type of epigenetic mark known as histone acetylation.
The scientists then used PET scans to detect where a radioactive version of the tracer appeared in the brains of eight healthy young adult men and women, the researchers report in the Aug. 10 Science Translational Medicine. Further studies could show that the marks change as people grow older or develop a disease. The team studied only healthy young volunteers so can’t yet say whether epigenetic marking changes with age or disease.
A star that made headlines for its bizarre behavior has got one more mystery for astronomers to ponder.
Tabby’s star, also known as KIC 8462852, has been inexplicably flickering and fading. The Kepler Space Telescope caught two dramatic drops in light — by up to 22 percent — spaced nearly two years apart. Photographs from other telescopes dating back to 1890 show that the star also faded by roughly 20 percent over much of the last century. Possible explanations for the behavior range from mundane comet swarms to fantastical alien engineering projects (SN Online: 2/2/16). A new analysis of data from Kepler, NASA’s premier planet hunter, shows that Tabby’s star steadily darkened throughout the telescope’s primary four-year mission. That’s in addition to the abrupt flickers already seen during the same time period. Over the first 1,100 days, the star dimmed by nearly 1 percent. Then the light dropped another 2.5 percent over the following six months before leveling off during the mission’s final 200 days.
Astronomers Benjamin Montet of Caltech and Josh Simon of the Observatories of the Carnegie Institution of Washington in Pasadena, Calif., report the findings online August 4 at arXiv.org.
The new data support a previous claim that the star faded between 1890 and 1989, a claim that some researchers questioned. “It’s just getting stranger,” says Jason Wright, an astronomer at Penn State University. “This is a third way in which the star is weird. Not only is it getting dimmer, it’s doing so at different rates.” The slow fading hadn’t been noticed before because data from Kepler are processed to remove long-term trends that might confuse planet-finding algorithms. To find the dimming, Montet and Simon analyzed images from the telescope that are typically used only to calibrate data. “Their analysis is very thorough,” says Tabetha Boyajian, an astronomer at Yale University who in 2015 reported the two precipitous drops in light (and for whom the star is nicknamed). “I see no flaws in that at all.”
While the analysis is an important clue, it doesn’t yet explain the star’s erratic behavior. “It doesn’t push us in any direction because it’s nothing that we’ve ever encountered before,” says Boyajian. “I’ve said ‘I don’t know’ so many times at this point.”
An object (or objects) moving in front of the star and blocking some of the light is still the favored explanation — though no one has figured out what that object is. The drop in light roughly 1,100 days into Kepler’s mission is reminiscent of a planet crossing in front of a star, Montet says. But given how slowly the light dropped, such a planet (or dim star) would have to live on an orbit more than 60 light-years across. The odds of catching a body on such a wide, slow orbit as it passed in front of the star are so low, says Montet, that you would need 10,000 Kepler missions to see just one. “We figure that’s pretty unlikely.”
An interstellar cloud wandering between Earth and KIC 8462852 is also unlikely, Wright says. “If the interstellar medium had these sorts of clumps and knots, it should be a ubiquitous phenomenon. We would have known about this for decades.” While some quasars and pulsars appear to flicker because of intervening material, the variations are minute and nothing like the 20 percent dips seen in Tabby’s star.
A clump of gas and dust orbiting the star — possibly produced by a collision between comets — is a more likely candidate, although that doesn’t explain the century-long dimming. “Nothing explains all the effects we see,” says Montet.
Given the star’s unpredictable nature, astronomers need constant vigilance to solve this mystery. The American Association of Variable Star Observers is working with amateur astronomers to gather continuous data from backyard telescopes around the globe. Boyajian and colleagues are preparing to monitor KIC 8462852 with the Las Cumbres Observatory Global Telescope Network, a worldwide web of telescopes that can keep an incessant eye on the star. “At this point, that’s the only thing that’s going to help us figure out what it is,” she says.
