Saturn serves up the closest thing to space pasta, the latest round of images from NASA’s Cassini probe, released March 9, show.

On March 7, the spacecraft snapped a series of portraits of Pan, Saturn’s small moon that orbits within a 325-kilometer gap in one of the planet’s rings. Taken at a distance of 24,572 kilometers from the moon, these are the closest images of Pan to date.

The close-ups could help refine astronomers’ understanding of the mini moon’s geology and shape. Pan has a distinctive ridge along its equator, which in the past has prompted astronomers to liken the moon’s shape to that of a flying saucer. In the new images, Pan’s ridge isn’t uniform like that of a fictional alien spacecraft. Instead, it’s uneven, creating an overall shape that more closely resembles a ravioli or wrinkly walnut.

Still, the ridge’s distinctness is “what is so spectacular and eye-opening in these images,” says imaging team leader Carolyn Porco of the Space Science Institute in Boulder, Colo. That supports the theory that the ridge is made of material from Saturn’s rings that continued to rain down on Pan’s equator after it formed.

Cassini captured the images on one of a series of ring-grazing orbits, as part of its final few months orbiting Saturn. Though it won’t get this close to Pan again, the probe is scheduled to swing past Saturn’s other “flying saucer” moon, Atlas, on April 12.

Physicists have snagged a bounty of five new particles in one go.

Members of the LHCb experiment, located at the Large Hadron Collider near Geneva, reported the prolific particle procurement in a paper posted online March 14 at arXiv.org. The five particles are each composed of three quarks — a class of particle that makes up larger particles such as protons and neutrons. Each of the new particles comprises two “strange” quarks and one “charm” quark.

The five particles are in various excited, or high-energy, states — giving each particle a different mass and a different arrangement of quarks within. Such particles are expected to exist according to the theory of the strong nuclear force, which bundles quarks together into larger particles.

The five excited particles are named after their low-energy relative, Ωc0 or omega-c-zero. Their rather uninspiring monikers are Ωc(3000)0, Ωc(3050) 0, Ωc(3066) 0, Ωc(3090) 0 and Ωc(3119) 0. Each number in parentheses indicates the mass of the particle in millions of electron volts.

Nomadic warriors and herders known as the Huns are described in historical accounts as having instigated the fifth century fall of the Roman Empire under Attila’s leadership. But the invaders weren’t always so fierce. Sometimes they shared rather than fought with the Romans, new evidence suggests.

Huns and farmers living around the Roman Empire’s eastern border, where the Danube River runs through present-day Hungary, borrowed ways of life from each other during the fifth century, say archaeologist Susanne Hakenbeck of the University of Cambridge and colleagues. Nomadic Huns on the Roman frontier raised relatively small numbers of animals and grew some crops, while border-zone farmers incorporated more meat into what had been a wheat- and vegetable-heavy diet, the scientists report March 22 in PLOS ONE.
“Our data show that the dietary strategies of the people on both sides of the Roman frontier were not fundamentally different,” Hakenbeck says.

Their findings challenge a traditional view of the Huns as marauders who roamed hundreds of kilometers from Central Asia to Europe. There’s no evidence of major social upheavals or a geographically distinctive group of newcomers at the frontier sites, so at least some Huns may have been homegrown, Hakenbeck suggests. Rapidly forming groups of Hun warriors and herders on horseback could have emerged in southeastern Europe not far from the Roman Empire’s border, perhaps supplemented by nomadic newcomers from farther east near the Black Sea, she proposes.

Still, geographic origins of the Huns are tough to pin down, says archaeologist Ursula Brosseder of the University of Bonn in Germany. The Huns developed as a political movement that picked up members from various ethnic groups as it spread, she explains. Brosseder suspects the “Hun phenomenon” formed on the grasslands of Western Eurasia, a territory that includes regions cited by Hakenbeck. The earliest evidence of Huns in that region dates to about 2,400 years ago.
The new study supports the idea that herding communities adapted flexibly to new environments, sometimes relying only on their livestock and at other times farming to varying extents, Brosseder says. Nomadic herders in Asia probably cultivated millet, a fast-growing cereal that can be used to feed people and horses, Hakenbeck says.
Her group studied skeletons of 234 people buried at five previously excavated sites on or near the Roman frontier. Each site contained evidence of contact with Huns, including bronze artifacts and adult skulls with elongated braincases created by binding the head during childhood. Reasons for this practice are poorly understood. It may have signified affiliation with the Huns or social status of some kind.

Graves at a Roman fort and a nearby cemetery lay on Roman land, about 150 kilometers from the frontier. Another two cemeteries were situated on the banks of the Danube River, directly on the Roman frontier. A final graveyard fell outside Roman territory. It was located about 150 kilometers east of the border.

Measurements of ratios of specific forms of carbon, nitrogen and oxygen in teeth and ribs enabled the scientists to identify what types of plants and how much meat or milk individuals ate during childhood, early adulthood and toward the end of their lives.

Results pointed to considerable consumption of cultivated plants, most likely millet, as well as meat or milk at all five sites. Variations on this general pattern occurred across sites and among individuals at each site, suggesting that groups and individuals rapidly adjusted how much they farmed or herded as circumstances dictated. “This mixing and matching was likely a kind of economic insurance policy in violent and unstable times,” Hakenbeck says.

Hakenbeck’s group also measured another tooth element, strontium, to determine whether individuals at four of the sites had grown up drinking water and eating food in the locales where they were buried. Between 30 and 50 percent of individuals studied at those sites weren’t locals, and the birthplaces of these people remain a mystery, Hakenbeck says.

In many cases, both newcomers and natives to the Roman frontier substantially changed their eating habits over the course of their lives, the researchers find. That fits Hakenbeck’s “mix and match” scenario, in which a fluctuating diet aided survival on the empire’s edge.

Most visitors to a large natural history museum don’t know it, but they are only scratching the surface of the museum’s holdings, even if they check out every exhibition. Most of the scientific treasures are tucked away in collection rooms filled with millions of specimens, which scientists use in their research.

The Field Museum in Chicago, home to Sue, the famous T. rex, is displaying some of its secreted goodies in its new exhibit “Specimens: Unlocking the Secrets of Life.” The museum has more than 30 million biological specimens, mummies, minerals, cultural artifacts and other objects in its collections. At any one time, only 0.5 to 1.5 percent of the holdings are on display. For the new exhibit, curators brought out about 5,600 additional items — from preserved deep-sea creatures and fossilized brains to meteorites — to show the diversity of the museum’s hidden collections, says Rusty Russell, director of collections.
“Specimens” not only provides access to these items, but it also informs the public about what natural historians do for a living. “Field Museum’s scientists do collections-based research. Without our vast collections, we could not carry out our science,” says William Simpson, head of geological collections and collections manager of fossil vertebrates. “In fact, almost none of our collecting is done for exhibit.”

Visitors wandering the exhibit will notice that all of this collecting has helped shed light on life millions of years ago, as well as stories ripped from today’s headlines.
Remember the Miracle on the Hudson in 2009? Pilot Chesley B. “Sully” Sullenberger safely landed a plane after its engines failed in a bird strike. To identify the birds, a scientist compared the remains recovered from the plane’s engines with tissues from known birds in the museum’s collection, some of which are on display in “Specimens.” The researcher determined that the birds were migratory Canada geese, not year-round Big Apple residents.
Museum collections play central roles in all kinds of identifications, especially for classifying new species. The museum has more than 20,000 holotypes — specimens that researchers have used to define species — in its collections, most of which were identified by museum scientists. The new exhibit features about 10 of these.

One example: dinosaur bones discovered in 1900 in the Colorado Rockies. In his lab, Elmer Riggs, the Field Museum’s first paleontology curator, removed rock covering the bones and realized he had unearthed a dinosaur bigger than Brontosaurus, the largest dinosaur known at the time. Riggs named the new dinosaur Brachiosaurus altithorax.

Another holotype on display is a skull and jaw of the early mammal Morganucodon oehleri, named in 1963, from the early Jurassic Period some 200 million years ago. The fossils show evidence of key evolutionary changes in early mammal history.

Several parts of “Specimens” are more hands-on. Visitors are urged to touch a giant, 160-kilogram clamshell from the Philippines, and they can peruse a drawer full of now-extinct butterflies with silvery-blue wings. Visitors also can sort seashells into different species. An interactive touch screen offers a look at ancient insects trapped in amber a la Jurassic Park.

When specimens are collected, researchers often don’t know how they’ll be used in the future. In one recent case, researchers analyzed two Arctic ivory gulls collected in 1896 to show that mercury levels in the ocean are now 45 times higher than a century ago. In another example in the exhibit, rodent and marsupial bones found in owl pellets recovered from Australian caves document wildlife before European settlement. Managers are now using the fossils as a blueprint to re-create ecosystems with species that still live in Australia.

All of these specimens show Field visitors a world they may not have known existed behind museum walls. Other large museums would do well to highlight their hidden bounty, too.

A common and usually harmless virus may trigger celiac disease. Infection with the suspected culprit, a reovirus, could cause the immune system to react to gluten as if it was a dangerous pathogen instead of a harmless food protein, an international team of researchers reports April 7 in Science.

In a study in mice, the researchers found that the reovirus, T1L, tricks the immune system into mounting an attack against innocent food molecules. The virus first blocks the immune system’s regulatory response that usually gives non-native substances, like food proteins, the OK, Terence Dermody, a virologist at the University of Pittsburgh, and colleagues found. Then the virus prompts a harmful inflammatory response.
“Viruses have been suspected as potential triggers of autoimmune or food allergy–related diseases for decades,” says Herbert Virgin, a viral immunologist at Washington University School of Medicine in St. Louis. This study provides new data on how a viral infection can change the immune system’s response to food, says Virgin, who wasn’t involved in the study.

Reoviruses aren’t deadly. Almost everyone has been infected with a reovirus, and almost no one gets sick, Dermody says. But if the first exposure to a food with gluten occurs during infection, the virus may turn the immune system against the food protein, the researchers found.

The immune system can either allow foreign substances, such as food proteins, to pass through the body peacefully, or it can go on the attack. In people with celiac disease, gluten is treated like a harmful pathogen; the immune system response damages the lining of the small intestine, causing symptoms like bloody diarrhea.

Celiac disease has been associated with two genetic features. Though 30 to 40 percent of people in the United States have one or both of these features, only 1 percent of the population has been diagnosed with the disease. This disparity suggests that some environmental factor triggers it.

Dermody and colleagues found that the T1L reovirus may be a trigger. In mice engineered to have one of those genetic features, the virus appeared to trick the immune system into seeing gluten as an enemy.
The key interaction occurs in the mesenteric lymph nodes, where gluten meets up with dendritic cells, which are like the “orchestra conductors” of the immune system, Dermody says. These cells dictate whether the immune system ignores a substance or mounts a defense against it.

But the virus engages with the dendritic cells as well, fooling the cells into thinking that gluten, like the virus, is in some way dangerous. And then the immune system attacks the gluten.

Dermody and colleagues also found that the reovirus stimulated activity of an enzyme called tissue transglutaminase. In people with celiac disease, the enzyme makes gluten more able to trigger a harmful immune system response.

Celiac patients also had higher levels of reovirus antibodies than those found in people without the disease.

Dermody doesn’t think that the T1L reovirus is the only virus that can stimulate celiac disease. Future research will analyze the potential of other viruses and also determine whether T1L is a true trigger of the disease in humans. If it is, then a reovirus vaccine could be developed for at-risk children, which could potentially block the development of celiac disease, “and that would be pretty amazing,” Dermody says.

Some Pakistani people are real knockouts, a new DNA study finds. Knockouts in this sense doesn’t refer to boxing or a stunning appearance, but to natural mutations that inactivate, or “knock out” certain genes. The study suggests that human knockouts could prove valuable evidence for understanding how genes work and for developing drugs.

Among 10,503 adults participating in a heart disease study in Pakistan, 1,843 people have at least one gene of which both copies have been knocked out, researchers report online April 12 in Nature. Researchers also drew blood from many of the participants and used medical records to study more than 200 traits, such as heart rate, blood pressure and blood levels of sugar, cholesterol, hormones or other substances. Studying how the knockout mutations affect those traits and health could point to genes that are potentially safe and effective targets for new drugs.
Combining genetic data with medical information will provide “a rich dataset for many applications,” says Robert Plenge, a human geneticist formerly with the pharmaceutical company Merck.

Scientists have traditionally learned about genes’ roles by deleting the genes from mice and then cataloging abnormalities in how those mice developed and behaved. Such animal research will always be needed, but studies of people naturally lacking certain genes “will change the nature of the scientific investigation of the genetic basis of human disease,” Plenge wrote in a commentary in the same issue of Nature.

Often, a person will inherit a broken copy of a gene from one parent and a healthy copy from the other. But 39 percent of the people in this study had parents who were closely related — often first cousins — increasing the odds of inheriting two mutant copies of a gene. Of this study’s 1,843 participants, 1,504 had both copies of a single gene knocked out. The rest had more than one gene knocked out, including one person in whom six genes were predicted to be completely nonfunctional.
In one example from the new study, geneticist Sekar Kathiresan and colleagues found four people in which both copies of the APOC3 gene had inactivating mutations. Kathiresan and colleagues had previously found that people with one mutated copy of APOC3 are protected against heart disease. Normally, the ApoC3 protein made from the gene stops dietary fat from being cleared from the body. People who had one mutant copy of the gene were able to get rid of fat more quickly than normal, reducing the amount left to clog arteries, says Kathiresan, of the Broad Institute of MIT and Harvard. Scientists reasoned that drugs that inactivate the ApoC3 protein would also reduce heart attack risk in people who have two working copies of the gene.
But there was a problem. Scientists worried that drugs that completely abolish the activity of the ApoC3 protein might be dangerous. Previous genetic studies encompassing nearly 200,000 people had never found a person with both copies of APOC3 knocked out, indicating that people might not be able to do without the gene entirely. Finding people who have almost no ApoC3 protein in their blood indicates that it is probably safe to get rid of its activity.

Further tests on 28 family members of one man who had both copies of APOC3 knocked out showed that his wife (who was his first cousin) and all nine of the couple’s children also lacked APOC3. The researchers fed fat-filled milkshakes to 13 members of the family — six who lacked APOC3 and seven who had two functional copies of the gene. Within six hours after the milkshake, levels of triglyceride— a type of fat in the blood — shot up two to three times over premilkshake levels in people with two functional copies of the gene. But in people in which the gene was knocked out, “triglyceride levels didn’t go up. It didn’t budge at all,” Kathiresan says. That finding suggests APOC3 could be a good target for drugs that reduce triglyceride levels in the blood and fend off heart disease, he says.

The Arctic Ocean is a final resting place for plastic debris dumped into the North Atlantic Ocean, new research suggests.

A 2013 circumpolar expedition discovered hundreds of tons of plastic debris, from fishing lines to plastic films, ecologist Andrés Cózar of the University of Cádiz in Spain and colleagues report April 19 in Science Advances. While many areas remain relatively unpolluted, the density of plastic trash in the Arctic waters east of Greenland and north of Europe rivals plastic pileups in waters closer to the equator, despite few nearby human populations. Even more plastic probably lurks on the seafloor, the researchers suspect.

Ocean currents carried that plastic northward from the North Atlantic Ocean, the researchers propose. Based on the kind of plastic found, the researchers say the debris probably originated from the U.S. East Coast and Europe. While the study estimates that the Arctic contains less than 3 percent of all global floating plastic, that number will only rise as currents continue carrying pollution poleward, putting Arctic ecosystems at risk.

The March for Science, Washington, D.C. — On April 22, 2017 — Earth Day — thousands of scientists, science advocates and general enthusiasts rallied on the grounds of the Washington Monument in Washington, D.C., at the first-ever March for Science. The organizers estimate that over 600 sister marches also occurred around the world.

The march may be “unprecedented,” sociologist Kelly Moore told Rachel Ehrenberg for a blog post giving a historical perspective on scientists’ activism. “This is the first time in American history where scientists have taken to the streets to collectively protest the government’s misuse and rejection of scientific expertise.”
The March for Science took place next to the Washington Monument, opposite the White House. Grounds opened at 8 a.m. and filled up quickly.
Astronaut Leland Melvin told an entertaining anecdote about getting his start in science in sixth grade when his mom gave him “an age-inappropriate, non-OSHA-approved chemistry set.” At one point, a chemical explosion blew up her living room. But, “that’s what got me hooked on science,” he said.
Pediatrician Mona Hanna-Attisha took the stage with Amariyanna “Mari” Copeny, aka “Little Miss Flint.”

DNA from 2,000-year-old stallions is helping rewrite the story of horse domestication.

Ancient domesticated horses had much more genetic diversity than their present-day descendants do, researchers report in the April 28 Science. In particular, these ancient horses had many more varieties of Y chromosomes and fewer harmful mutations than horses do now. Previous studies based on the genetics of modern horses concluded that domestication must have squeezed out much of the diversity seen in wild horses before the Ice Age. But the new findings suggest that the lack of diversity is a more recent development.
“Today, Y chromosomes of all horses are pretty much the same,” says evolutionary geneticist Ludovic Orlando of the Natural History Museum of Denmark in Copenhagen. As a result, scientists thought that ancient people started domesticating horses by breeding only a few stallions to many different mares.

“But when we look in the past — wow! — this is a whole new planet,” Orlando says.

Horses are thought to have been domesticated by about 5,500 years ago. Orlando’s group examined DNA from the bones of 15 Iron Age stallions from the ancient Scythian civilization: Two stallions were from a 2,700-year-old grave site in Russia and 13 were sacrificed in a burial ritual about 2,300 years ago in Kazakhstan. The team also looked at a 4,100-year-old Bronze Age mare from the Sintashta culture in Russia. Nearly all of the stallions had a different type of Y chromosome, Orlando says.

That finding challenges the idea that only a few stallions participated in the early stages of domestication. Loss of Y chromosome diversity among horses must have happened within the last 2,300 years, Orlando says, and maybe as recently as 200 to 300 years ago, when people started creating specific horse breeds.
Using genetic data from modern animals to figure out what went on in the past is like flipping to the end of a novel and reading only the ending; it shows how things ended up but doesn’t indicate how the story started or unfolded. Examining ancient DNA can fill in those gaps to give a better indication of how domestication took place and how ancient people interacted with animals, says Laurent Frantz, an evolutionary biologist at Queen Mary University of London.
Modern horses also carry mutations that can be harmful (SN: 1/10/15, p. 16), including ones involved in dementia and seizures. But the ancient horses didn’t have those mutations, indicating that those DNA changes happened sometime within the last 2,300 years.

“It really shows an awful lot has changed very recently, and it’s incredibly dangerous to model the deep past from modern genetics,” says zooarchaeologist Alan Outram of the University of Exeter in England. “You really need to carry out the ancient DNA studies.”

Orlando and colleagues also determined some genetic traits that were cultivated by the Scythians. Genes involved in mammary gland development and function had variants associated with greater milk production, perhaps indicating that the Scythians milked their horses. Outram and others have evidence that horse milking started at least 5,000 years ago (SN: 3/28/09, p. 15).

Also changed were genes involved in the function of neural crest cells. Those embryonic cells migrate to different parts of the body during early development and help form parts of the brain, some facial features and other tissues. One recent hypothesis is that changes in how neural crest cells work could lead to common characteristics shared by domestic animals, such as floppy ears, juvenile faces and spotted coats (SN: 8/23/14, p. 7).

Genetic results from the ancient horses provide evidence that the hypothesis might be true, says Frantz. Geneticists will have to work with experimental biologists to confirm that neural crest cells are involved in changing the appearance of domesticated animals. But, Frantz says, “this is the first step toward testing that hypothesis correctly.”

Chemical transformations in minerals deep beneath the seafloor could explain why Indonesia’s 2004 mega-earthquake was unexpectedly destructive, researchers report in the May 26 Science.

The magnitude 9.2 quake and the tsunami that it triggered killed more than 250,000 people, flattened villages, and swept homes out to sea across Southeast Asia. It was one of the deadliest tsunamis in recorded history.

“It raised a whole bunch of questions, because that wasn’t a place in the world where we thought a magnitude 9 earthquake would occur,” says study coauthor Brandon Dugan, a geophysicist at the Colorado School of Mines in Golden.

The thick but stable layer of sediment where tectonic plates meet off the coast of the Indonesian island of Sumatra should have limited the power of an earthquake, seismologists had predicted. But instead, this quake was the third-strongest on record worldwide.
Dugan spent two months aboard a boat with 30 other scientists collaborating through the International Ocean Discovery Program. The researchers drilled down 1,500 meters below the seafloor in two places off the coast of Sumatra, extracting narrow cylinders of sediment. This sediment is very slowly moving toward the fault where the 2004 earthquake occurred — a zone where one massive tectonic plate slides over another, pushing that plate downward.

Analyzing how sediment changes with depth can give scientists a snapshot of the geological processes at play near the fault zone.

In particular, deep down, the researchers identified a layer of sediment where the water had a lower salinity than the water in the sediment above or below. Since seawater seeping into the sediment would be salty, the evidence of freshwater suggests that the water must have instead been released from within minerals in the sediment.

For tens of millions of years, Dugan proposes, minerals sat on the seafloor taking in water — baking it into their crystal structure. Then, more sediment settled on top. It got toasty under such a thick blanket of sediment, heating up the minerals beneath. The temperature increase triggered a chemical transformation within the sediment, pushing water out of the mineral crystals and into tiny pores between the grains.
The sediment sampled in this study is still dehydrating. By the time any of it reaches the plate boundary, Dugan says, it’ll be buried under kilometers of more sediment and will probably be completely dehydrated.

At first, the liberated water would have softened the material, actually decreasing the risk of a big earthquake by allowing it to absorb more force, Dugan says. As the sediment got closer to the fault over millions of years, though, the water flowed away, leaving it brittle and unstable — the perfect setup for a mega-quake.

The timing of this sediment dehydration process can make or break a quake. Had the sediment near the fault been in a softened state when the quake struck in 2004, the tremor might not have been as deadly, Dugan says. But since enough time had passed for it to become brittle again, the tectonic plates were able to rapidly slip past each other for a much greater distance during the quake. That massive motion displaced the seafloor itself, setting a tsunami into motion.
“It’s really the tsunamis from these earthquakes that prove to be the deadliest and most dangerous,” says Roland Bürgmann, a seismologist at the University of California, Berkeley who wasn’t part of the study. And quakes that displace the seafloor are far more likely to trigger tsunamis.

The findings could apply to other faults with similarly thick sediment, such as the Cascadia Subduction Zone in the Pacific Northwest, suggests study coauthor Andre Hüpers, a geophysicist at the University of Bremen in Germany.

But more evidence is needed before applying such analysis to faults beyond this one, says Bürgmann. The argument for what happened along the Sumatran fault is compelling, he says. “But nonetheless, it’s only one data point. It doesn’t yet make for a pattern.”