There’s a long way to go in understanding the brain

Scientists pour a lot of brainpower into understanding how their experimental equipment works.

You don’t want to be fooled into thinking you’ve made a great discovery because of some quirk in the apparatus you didn’t know about. Just the other day, a new paper published online suggested that the instruments used to detect gravitational waves exhibited such a quirk, tricking scientists into claiming the detection of waves that maybe weren’t really there.

It appears that gravity wave fans can relax, though. A response to the challenge pretty much establishes that the new criticism doesn’t undermine the wave discoveries. Of course, you never know — supposedly well-established results sometimes do fade away. Often that’s because scientists have neglected to understand the most important part of the entire experimental apparatus — their own brains.

It’s the brain, after all, that devises experiments and interprets their results. How the brain perceives, how it makes decisions and judgments, and how those judgments can go awry are at least as important to science as knowing the intricacies of nonbiotic experimental machinery. And as any brain scientist will tell you, there’s still a long way to go before understanding the brain will get crossed off science’s to-do list. But there has been progress. A recent special issue of the journal Neuron offers a convenient set of “perspective” papers exploring the current state of understanding of the brain’s inner workings. Those papers show that a lot is known. But at the same time they emphasize that there’s a lot we don’t know.

Glancing at the table of contents reveals the first lesson about understanding the brain: It’s a complex problem that needs to be approached from multiple perspectives.

On one level, there’s the dynamics of electrical currents that constitute the main signaling method of the brain’s nerve cells. Then on a higher level there’s the need to figure out the rules by which nerve cells make connections (synapses) and create the neural circuitry for processing sensory input, learning and behaving. Another challenge is understanding how nerve cell networks represent memories and how you recall what you’ve learned. And it’s essential to understand how neurobiological processing conducted by molecules and cells and electrical signaling gets translated into behaviors, from simple bodily movements to complex social interactions.

Nerve cells in the brain, or neurons, are known to communicate among themselves by transmitting electrical signals, aided by chemical signaling at the synapses connecting the neurons. But there are gaps in understanding how that process takes the brain from perceptions to thoughts to actions. Each of Neuron’s perspective papers both describes what’s already known about how the brain works and offers speculations where scientists lack full knowledge about how the brain does it jobs.

Much of the effort to explain the brain involves mapping the electrical signaling throughout the entire network of nerve cell connections. Per Roland of the University of Copenhagen, for instance, discusses how those signals vary in space and time. He emphasizes the important balance between signaling that incites neurons to send signals and the messaging that inhibits signaling, keeping some neurons quiet.
Sophie Denève and colleagues of the Ecole Normale Supérieure in Paris also emphasize the balance between excitation and inhibition in neural circuitry. That balance is important, they say, for understanding how the whole brain can learn to do things based on changes in the connections between individual neurons. Somehow the rules governing synaptic connections between cells enable such “local” activity to modify the “global” neural circuitry that carries out the brain’s many functions. Excitation-inhibition balance, plus feedback from the global network influencing synapse strength, “can ensure that global functions can be learned with local learning rules,” Denève and colleagues write.

Almost all these approaches to figuring out the brain involve how it manipulates information. In a sense, the ultimate key question is how the brain conducts the mysterious process by which it absorbs information in the form of lights and colors, sounds, smells and tactile inputs and transforms them into physical actions — ideally behaviors that are appropriate responses to the inputs. Just (OK, not “just,” but sort of) as in a computer, the brain transforms input into output; information about the external world is manipulated to produce information about how to react to it.

But because sensory input has its limits, and some of it is ambiguous, the informational variables of the external world cannot be gauged with certainty, Xaq Pitkow and Dora Angelaki of Baylor College of Medicine and Rice University in Houston point out in their perspective. So the brain’s behavioral choices must be based on some method of computing probabilities to infer the likely state of the world — and then choosing the wisest (probably) actions in response.

“It is widely accepted that the brain somehow approximates probabilistic inference,” Pitkow and Angelaki write. But nobody really knows how the brain does it. Pitkow and Angelaki propose that multiple populations of the brain’s neurons perform various computations to make appropriate behavioral decisions.

Patterns of electrical signaling by these neurons must represent the original sensory stimuli — that is, the patterns in the stimuli are encoded in the patterns of electrical signaling among the neurons. Those neural signaling patterns, in Pitkow and Angelaki’s description, are then recoded into another set of patterns; that process sorts out the important variables in the environment from those that don’t matter. Those patterns are then decoded in the process of generating behavioral actions.

In sum, the brain appears to implement algorithms for collecting and assessing information about the environment and encoding that information in messages that tell the body what to do. Somehow those algorithms allow the brain to conduct statistical computations that combine beliefs about the environment with the expected outcome of different behaviors.

Pitkow and Angelaki present sophisticated speculation about the possible ways the brain could accomplish this task. It’s clearly an unimaginably complicated process, and figuring out how the brain does it will require more sophisticated experiments than neuroscientists have so far imagined. Much research on brain function in animals, for instance, offers the animal a choice of two options, given various external conditions. But tasks of that nature are vastly simpler than the jobs that evolution optimized brains for.

“The real benefit of complex inferences like weighing uncertainty may not be apparent unless the uncertainty has complex structure,” Pitkow and Angelaki argue. “Overly simple tasks” are “ill-suited to expose the inferential computations that make the brain special.”

And so truly understanding the brain, it seems, will require better experiments — using apparatus that is more fully understood than the brain now is — of sufficient complexity to be worthy of probing the brain’s abilities.

These record-breaking tube worms can survive for centuries

Some deep-sea tube worms get long in the tooth … er, tube. Living several decades longer than its shallow-water relatives, Escarpia laminata has the longest known life span for a tube worm, aging beyond 300 years, researchers report in the August Science of Nature.

E. laminata lives 1,000 to 3,300 meters deep in the Gulf of Mexico, near seafloor vents that seep energy-rich compounds that feed bacteria that feed the tube worms. In 2006, biologists marked 356 E. laminata in their natural habitat and measured how much the creatures had grown a year later. To estimate the ages of tube worms of different sizes, the researchers plugged E. laminata’s average yearly growth rate — along with estimates of birthrates and death rates, based on observations of another 1,046 tube worms — into a simulation. The species’s typical life span is 100 to 200 years, the researchers calculate, but some larger tube worms may be more than 300 years old.

With few large predators, deep-sea tube worms have got it good, says study coauthor Alanna Durkin, a biologist at Temple University in Philadelphia. “Once they find a seat at the buffet, they’re pretty set for hundreds of years.” The researchers’ methodology appears robust, says ocean scientist David Reynolds of Cardiff University in Wales, who was not involved in the work. Although variable environmental conditions could affect growth rate over time, he says.

Giant larvaceans could be ferrying ocean plastic to the seafloor

Everybody poops, but the poop of bloblike filter feeders called giant larvaceans could be laced with microplastics.

Every day, these gelatinous creatures (Bathochordaeus stygius) build giant disposable mucus mansions to round up zooplankton into their stomachs — sometimes sifting through around 80 liters of seawater per hour. Kakani Katija and her colleagues at the Monterey Bay Aquarium Research Institute now suggest that tiny plastic particles also make their way in — and out — of giant larvaceans’ guts.

Microplastics pervade the ocean. Their combined mass could reach 250 million metric tons by 2025. Scientists don’t know a lot about where microplastics stick around in open water ecosystems.

To see if plastics could end up on the larvacean menu, Katija and colleagues tried feeding the animals brightly colored microplastics. An underwater robot equipped with camera gear helped the researchers monitor plastic intake from above. Some animals did end up scarfing down the particles, and some of those particles ended up in the organism’s waste, which showers down on the seafloor, Katija and colleagues report August 16 in Science Advances.

“Plastics are sometimes seen as a sea surface issue, and more and more we’re seeing that’s not necessarily true,” Katija says.

Just how much plastic ends up passing through giant larvaceans in the wild remains unclear. But the researchers suspect that the creatures’ poop, as well as their mucus houses, could transfer microplastics from the water’s surface to the depths of the sea (along with nutrients such as carbon that cycle through the environment). And that pollution transfer may impact the ecosystems at either end.

CRISPR/Cas9 can reverse multiple diseases in mice

A new twist on gene editing makes the CRISPR/Cas9 molecular scissors act as a highlighter for the genetic instruction book. Such highlighting helps turn on specific genes.

Using the new tool, researchers treated mouse versions of type 1 diabetes, kidney injury and Duchenne muscular dystrophy, the team reports December 7 in Cell. The new method may make some types of gene therapy easier and could be a boon for researchers hoping to control gene activity in animals, scientists say.
CRISPR/Cas9 is a two-part molecular scissors. A short, guide RNA leads the DNA-cutting enzyme Cas9 to specific places in the genetic instructions that scientists want to slice. Snipping DNA is the first step to making or fixing mutations. But researchers quickly realized the editing system could be even more versatile.

In the roughly five years since CRISPR/Cas9 was first wielded, researchers have modified the tool to make a variety of changes to DNA (SN: 9/3/16, p. 22). Many of those modifications involve breaking the Cas9 scissors so they cannot cut DNA anymore. Strapping other molecules to this “dead Cas9” allows scientists to alter genes or change the genes’ activities.

Gene-activating CRISPR/Cas9, known as CRISPRa, could be used to turn on dormant genes for treating a variety of diseases. For instance, doctors might be able to turn on alternate copies of genes to compensate for missing proteins or to reinvigorate genes that grow sluggish with age. So far, researchers have mostly turned on genes with CRISPRa in cells growing in lab dishes, says Charles Gersbach, a biomedical engineer at Duke University not involved in the new study.

Being able to precisely turn on genes within an animal and influence the animal’s health is a “great advance,” Gersbach says. It has been difficult to do before because CRISPR activators are too big to fit inside viruses needed to deliver the tools to body cells.
In the new study, Juan Carlos Izpisua Belmonte of the Salk Institute for Biological Studies in La Jolla, Calif., and colleagues shrank the tool. This time, the researchers “killed” and modified the guide RNA instead of the DNA-cutting enzyme. The team used short guide RNAs, just 14 or 15 units long, instead of the usual 20 to 22.
The short leash can still lead Cas9 to specific spots in DNA, but once there, the enzyme — although still capable of cutting — doesn’t snip the DNA. Another piece of RNA tacked onto the “dead” guide attracts proteins that help turn genes on. The pieces of the dead guide activators are small enough to fit in gene therapy viruses.

In one experiment, the team wanted to restore the ability of mice with a version of type 1 diabetes to make insulin, a hormone that controls blood sugar. In type 1 diabetes, the immune system destroys the pancreas, the organ that normally makes insulin. Since pancreatic cells are gone, the researchers needed a new type of cell to take over the pancreas’s job.

So Belmonte’s group infected diabetic mice with viruses carrying the dead guide activators. The researchers used the dead guide RNAs to turn on the Pdx gene in the mice’s livers, which caused the liver cells to produce insulin, reversing the mice’s diabetes. Essentially the liver cell was transformed into one that does an important job of the pancreas.

“Labs have been trying to do that for decades,” says Kirk Wangensteen, a physician scientist at the University of Pennsylvania Perelman School of Medicine. Such experiments will help scientists understand what factors determine a cell’s identity.

But to do the gene therapy in humans, scientists would need to tackle another problem. In the diabetes experiment, they could use mice already engineered to make their own Cas9. But people don’t naturally make Cas9, and the entire dead guide activator and Cas9 system won’t fit in a single virus. So Belmonte’s team wanted to know if two viruses could be used at once to deliver all the pieces to target cells.

The Salk researchers tested their system in mice with a muscle-wasting disease that mimics Duchenne muscular dystrophy. Duchenne muscular dystrophy is caused by mutations in a huge gene called dystrophin. There’s no way to cram the dystrophin gene into a virus to do traditional replacement gene therapy, but researchers have found that turning on other genes can compensate and bulk up muscles. So in the dual-virus experiment, the scientists turned on a muscle-building gene called follistatin.

This time, the dead guide activator for turning on the follistatin gene was packaged in one virus and Cas9 in another virus. Both viruses were used to infect muscle cells in the hind legs of mice that had muscular dystrophy. Treated mice had more muscle mass in their hind legs than untreated mice did.

Much higher levels of gene activity were triggered in these experiments than scientists have achieved before, says Michael Hemann, a cancer biologist at MIT. High levels of activity are probably needed to produce enough protein to correct diseases.

Hemann and others say the new activator system will be useful for research, but some challenges remain before the therapy can be used in people. Researchers always have a challenge getting the therapy to the right place in the body, he says. The technology’s safety and efficacy must also be demonstrated.

Worries grow that climate change will quietly steal nutrients from major food crops

2017 was a good year for worrying about nutrient losses that might come with a changing climate.

The idea that surging carbon dioxide levels could stealthily render some major crops less nutritious has long been percolating in plant research circles. “It’s literally a 25-year story, but it has come to a head in the last year or so,” says Lewis Ziska, a plant physiologist with the U.S. Agricultural Research Service in Beltsville, Md.

Concerns are growing that wheat, rice and some other staple crops could, pound for pound, deliver less of some minerals and protein in decades to come than those crops do today. In 2017, three reports highlighted what changes in those crops could mean for global health. Also this year, an ambitious analysis made an almost-global assessment of sources of selenium, a trace element crucial for health, and warned of regions where climate change might cut the element’s availability (SN: 4/1/17, p. 14).
Crop responses to rising CO2 might affect nutrition and health for billions of people, Ziska says, but the idea has been difficult to convey to nonspecialists. One complication is that though plants certainly need CO2 to grow, providing more of it doesn’t mean that all aspects of plant biology change in sync. In hoping for a farming bonus, Ziska warns, people often overlook the disproportionate zest of weeds. An outdoor experiment wafting extra CO2 through a forest has already shown, for example, that poison ivy grew faster than the trees.

In the 2017 Annual Review of Public Health, Samuel Myers of Harvard University and colleagues wrote that global shortfalls in human nutrition are already “staggering.” More than a billion people aren’t getting enough zinc now, raising risks of premature birth, stunted childhood growth and weak immune systems. To estimate future shortfalls, Myers and colleagues turned to nutrient data they published in 2014 in Nature.

That report compared staple crops grown in various outdoor setups on three continents at either ambient or enhanced atmospheric CO2 concentrations. Fancy research piping boosted ambient levels of 363 to 386 parts per million to 546 and 584 ppm. (A moderate scenario puts late-century levels at 580 to 720 ppm.)
Decreases in zinc concentrations, including in rice and wheat, could plunge an additional 150 million to 200 million people into zinc deficiency, the researchers calculate. Likewise, predicted declines in iron content in some grains and legumes look worrisome for countries with anemia rates already higher than 20 percent, such as India and Algeria, Myers and colleagues reported in August in GeoHealth. Such high-anemia nations have a lot of people especially at risk, including 1.4 billion young children and women of childbearing age.

An expanded set of experiments suggested that protein content in rice and wheat could sink by roughly 8 percent, Myers and colleagues wrote in the August Environmental Health Perspectives. Thus, rising CO2 could add some 148 million people worldwide to the roughly 1.4 billion expected to be short of protein by 2050.

Also this year, grazing cattle joined the list of animals facing a protein downturn in their food. (Ziska and colleagues raised the issue for bees in 2016.) For cattle, 22 years and more than 36,000 fecal measurements suggest that plants on U.S. grazing lands have grown poorer in protein, ecologist Joseph Craine of Jonah Ventures, in Boulder, Colo., and colleagues reported April 10 in Environmental Research Letters. For every kilogram of plants that cattle ate in 2015, there were 10.6 grams less protein than there had been 22 years before. The yearly loss is equivalent to the protein available in $1.9 billion worth of soy meal — and rising CO2 is a possible culprit.

Plant reactions will be varied and complex, Ziska points out. An Artemisia plant’s anti-malarial compound, artemisinin, can get more concentrated as CO2 increases, possibly good news for plant-based medicine. But the mix of urushiols, oils that put the itch in poison ivy, can become more allergy-provoking when exposed to extra CO2, a test suggested. Ziska is now looking into how much caffeine will turbocharge future coffee beans.

Whatever the changes, concern is growing, says mathematical biologist Irakli Loladze of Bryan College of Health Sciences in Lincoln, Neb. He, Ziska and nine coauthors included nutritional erosion in the 2016 U.S. scientific assessment of the impacts of climate change on human health. To raise the public profile of the issue, though, Myers says, “We have a ways to go.”

Our first interstellar visitor may be a camouflaged comet

An itinerant interstellar asteroid may actually be a comet in disguise.

Known as ‘Oumuamua, the object was detected in October and is the first visitor from another star spotted touring our solar system (SN: 11/ 25/17, p. 14). Early observations suggested the vagabond was rocky. But after additional analysis, a team of researchers suggests December 18 in Nature Astronomy that the object might have an icy core.

In general, comets are icy and asteroids are rocky. Ice gives comets their characteristic tails: As a comet passes near the sun, the heat warms the ice, causing it to sublimate, releasing gas and dust. Because no tail appeared despite ‘Oumuamua’s passage by the sun, the mysterious visitor was dubbed an asteroid — a surprising conclusion since the vast majority of objects ejected from star systems are expected to be icy.
“Everybody’s been assuming that this is just a lump of rock,” says astronomer Alan Fitzsimmons of Queen’s University Belfast in Northern Ireland. “This may not be the case.” So ‘Oumuamua might not be as odd as originally thought.

Fitzsimmons and colleagues used the Very Large Telescope in Chile and the William Herschel Telescope in La Palma, Spain to capture the object’s spectrum — its light sliced up according to wavelength. “It’s an impressive piece of work,” says astronomer Olivier Hainaut of the European Southern Observatory in Garching, Germany, who was not involved with the research. “It was a very faint object and to observe such a faint moving target is horribly difficult.”

The object’s spectrum revealed a reddish hue with no signs of ice. But ‘Oumuamua could have an exterior crust — about half a meter thick or thicker — which hid the ice and insulated it from the sun’s heat, the researchers calculated. “You could have a lot of ice in this thing and really not know it,” says astronomer Jessica Sunshine of the University of Maryland in College Park, who was not involved with the research. Such a crust could have formed as energetic particles known as cosmic rays bombarded the object over its lifetime, creating an ice-free surface rich in organic compounds. ‘Oumuamua’s spectrum is similar to those of other objects in the solar system suspected of concealing such icy interiors.
Studies of ‘Oumuamua continue — with some researchers looking for evidence of even more surprising hypotheses. Using the Green Bank Telescope in West Virginia, scientists with the Breakthrough Listen project are searching for signatures of artificial origin — that is, aliens — on the off chance that the object might be an interstellar spacecraft. Sorry, X-Files fans: So far no such signals have been detected.

These 2017 discoveries could be big news, if they turn out to be true

Some reports from 2017 hint at potentially big discoveries — if the research holds up to additional scientific scrutiny.

Under pressure
Putting the squeeze on hydrogen gas turned it into a long-elusive metal that may superconduct, Harvard University physicists claimed (SN: 2/18/17, p. 14). A diamond vise, supercold temperatures and intense pressure made the element reflective — a key property of metals. But other researchers in the field don’t buy it; one experiment with a slew of caveats isn’t enough to confirm the claim, those scientists say.
Woman warrior?
The skeleton of a 10th century Viking woman buried in full warrior regalia has scientists sparring over women’s roles in Viking society (SN: 10/14/17, p. 6). Researchers who confirmed the skeleton’s sex through DNA analysis contend that the woman was a high-ranking Viking warrior, the first Viking woman warrior known. But other archaeologists argue that the bones — with no obvious signs of injury or strenuous physical activity — are too pristine to have seen battle.
A far-flung star’s extra wink, spotted in data from the Kepler space telescope and further probed by the Hubble Space Telescope, may be the first evidence for an exomoon — a moon orbiting a planet orbiting a distant star. If it exists, the Neptune-sized candidate moon (dubbed Kepler 1625b i) is roughly 4,000 light-years away and orbits a planet a tad larger than Jupiter (SN: 8/19/17, p. 15).

Rooting out hominid origins
The first members of the human evolutionary family may have originated in Europe, not Africa. New analyses of a fossilized jaw (shown) and teeth from Graecopithecus, a chimpanzee-sized primate that lived in southeastern Europe roughly 7 million years ago, suggest that it may be the earliest known hominid (SN: 6/24/17, p. 9). But more complete fossils are needed to determine whether Graecopithecus was truly a hominid.

Light pollution can prolong the risk of sparrows passing along West Nile virus

SAN FRANCISCO — Even moderate light pollution can roughly double the time a house sparrow remains a risk for passing along the worrisome West Nile virus.

House sparrows, about as widespread across the United States as artificial lighting itself, make a useful test species for a first-of-its-kind study of how night illumination might contribute to disease spread, said Meredith Kernbach, an eco-immunologist at the University of South Florida in Tampa. Passer domesticus brought into the lab and kept dimly illuminated at night were slower in fighting off West Nile infections than lab sparrows allowed full darkness, Kernbach reported January 7 at the annual meeting of the Society for Integrative and Comparative Biology.
Sparrows kept under a dim night light typically had enough virus in their bloodstreams for at least four days to turn biting mosquitoes into disease spreaders, she said. Sparrows housed in darkness had high virus concentrations for only about two days. Doubling the time a bird can pass along a big dose of virus could in theory increase the likelihood that a disease will spread.

The broader question of whether light pollution affects human health has been a concern for shift workers. Researchers have also looked at possible changes in reproduction and other behavior in wildlife (SN: 12/26/15, p. 29).

Kernbach’s project opens new territory by testing the effects of light on physiological factors that control how diseases that can infect humans might hopscotch among animals, says Jenny Ouyang, of the University of Nevada, Reno. As light pollution studies go, “I don’t know of anything like this,” says Ouyang, an integrative physiologist who also has studied light pollution and birds.

The tests intensify Ouyang’s curiosity about whether light might affect the spread of malaria among humans. There have been hints and speculation in the scientific literature, she says, that vector mosquitoes might be drawn to light sources in some circumstances, which could mean that excess illumination might compound urban disease risks.
Kernbach based much of her lab test on real-world conditions. The viral dose she gave the birds was strong enough to kill about 40 percent of them, and it was well within what a mosquito might pick up vampirizing birds or mammals. She used white incandescent lighting, basically the last century’s universal light bulb, which is still common despite inroads by LED lighting.

The white incandescence in the experiment has plenty of warmer tones, but does include some of blue wavelengths from common cool white LEDs, or light-emitting diodes. The sparrows on average experienced about 8 lux of this white incandescence during their seven-hour nights. (A heavily overcast day, by comparison, ranks at about 100 lux.)

Other studies in birds are showing that artificial night lighting can affect concentrations of the hormone corticosterone, which helps orchestrate reactions of the immune system. But Kernbach said she found no signs in her experiment that corticosterone controlled the results she saw in house sparrows.

What lights do to the birds is only part of the story, points out Davide Dominoni, an eco-physiologist at the Netherlands Institute of Ecology in Wageningen. Researchers will also need to look for effects on the virus itself. And on the mosquitoes.

Trio of dead stars upholds a key part of Einstein’s theory of gravity

OXON HILL, Md. — Observations of a trio of dead stars have confirmed that a foundation of Einstein’s gravitational theory holds even for ultradense objects with strong gravitational fields.

The complex orbital dance of the three former stars conforms to a rule known as the strong equivalence principle, researchers reported January 10 at a meeting of the American Astronomical Society. That agreement limits theories that predict Einstein’s theory, general relativity, should fail at some level.
According to general relativity, an object’s composition has no impact on how gravity pulls on it: Earth’s gravity accelerates a sphere of iron at the same rate as a sphere of lead. That’s what’s known as the weak equivalence principle. A slew of experiments have confirmed that principle — beginning with Galileo’s purported test of dropping balls from the Leaning Tower of Pisa (SN: 1/20/18, p. 9).

But the strong equivalence principle is more stringent and difficult to test than the weak version. According to the strong equivalence principle, not only do different materials fall at the same rate, but so does the energy bound up in gravitational fields. That means that an incredibly dense, massive object with a correspondingly strong gravitational field, should fall with the same acceleration as other objects.

“We’re asking, ‘How does gravity fall?’” says astronomer Anne Archibald of the University of Amsterdam, who presented the preliminary result at the meeting. “That sounds weird, but Einstein says energy and mass are the same.” That means that the energy bound up in a gravitational field can fall just as mass can. If the strong equivalence principle were violated, an object with an intense gravitational field would fall with a different acceleration than one with a weaker field.

To test this theory, scientists measured the timing of signals from a pulsar — a spinning, ultradense collapsed star that emits beams of electromagnetic radiation that sweep past Earth at regular intervals. The pulsar in question, PSR J0337+1715, isn’t just any pulsar: It has two companions (SN: 2/22/14, p.8). The pulsar orbits with a type of burnt-out star called a white dwarf. That pair is accompanied by another white dwarf, farther away.
If the strong equivalence principle holds, the paired-up pulsar and white dwarf should both fall at the same rate in the gravitational field of the second white dwarf. But if the pulsar, with its intense gravitational field, fell faster toward the outermost white dwarf than its nearby companion, the pulsar’s orbit would be pulled toward the outermost white dwarf, tracing a path in the shape of a rotating ellipse.

Scientists can use the timing of a pulsar’s signals to deduce its orbit. As a pulsar moves away from Earth, for example, its pulses fall a little bit behind its regular beat. So if J0337+1715’s orbit were rotating, signals received on Earth would undergo regular changes in their timing as a result. Archibald and colleagues saw no such variation. That means the pulsar and the white dwarf must have had matching accelerations, to within 0.16 thousandths of a percent.

Many physicists expect the strong equivalence principle to be violated on some level. General relativity doesn’t mesh well with quantum mechanics, the theory that reigns on very small scales. Adjustments to general relativity that attempt to combine these theories tend to result in a violation of the strong equivalence principle, says physicist Clifford Will of the University of Florida in Gainesville, who was not involved with the research.

The strong equivalence principle might still fail at levels too tiny for this test to catch. So the door remains open for adjustments to general relativity. But the new measurement constrains many such theories better than any previous test. The result is “really tremendous,” says Will. It’s “a great improvement in this class of theories … which is why this triple system is so beautiful.”

Spaceships could use blinking dead stars to chart their way

OXON HILL, Md. — Future spacecraft could navigate by the light of dead stars.

Using only the timing of radiation bursts from pulsating stellar corpses, an experiment on the International Space Station was able to pinpoint its location in space in a first-ever demonstration. The technique operates like a stellar version of GPS, researchers with the Station Explorer for X-ray Timing and Navigation Technology experiment, SEXTANT, reported at a news conference January 11 during a meeting of the American Astronomical Society.
Known as pulsars, the dead stars emit beams of radiation that sweep past Earth at regular intervals, like the rotating beams from a lighthouse. Those radiation blips could allow a spaceship to find its location in space (SN: 12/18/10, p. 11). It’s similar to how GPS uses the timing of satellite signals to determine the position of your cell phone – and it would mean spacecraft would no longer have to rely on radio telescope communications to find their coordinates. That system becomes less accurate the further a spaceship gets from Earth.

SEXTANT used an array of 52 X-ray telescopes to measure the signals from five pulsars. By analyzing those signals, the researchers were able to locate SEXTANT’s position to within 10 kilometers as it orbited Earth on the space station, astronomer Keith Gendreau of NASA’s Goddard Space Flight Center in Greenbelt, Md., reported.

On Earth, knowing your location within 10 kilometers isn’t that impressive — GPS can do much better. But “if you’re going out to Pluto, there is no GPS navigation system,” Gendreau said. Far from Earth, pulsar navigation could improve upon the position estimates made using radio telescopes.