爱上海龙凤

Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons.

Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old.

Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find.

With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain.Martha Carlin married the love of her life in 1995. She and John Carlin had dated briefly in college in Kentucky, then lost touch until a chance meeting years later at a Dallas pub. They wed soon after and had two children. John worked as an entrepreneur and stay-at-home dad. In his free time, he ran marathons.

Almost eight years into their marriage, the pinky finger on John’s right hand began to quiver. So did his tongue. Most disturbing for Martha was how he looked at her. For as long as she’d known him, he’d had a joy in his eyes. But then, she says, he had a stony stare, “like he was looking through me.” In November 2002, a doctor diagnosed John with Parkinson’s disease. He was 44 years old.

Carlin made it her mission to understand how her seemingly fit husband had developed such a debilitating disease. “The minute we got home from the neurologist, I was on the internet looking for answers,” she recalls. She began consuming all of the medical literature she could find.

With her training in accounting and corporate consulting, Carlin was used to thinking about how the many parts of large companies came together as a whole. That kind of wide-angle perspective made her skeptical that Parkinson’s, which affects half a million people in the United States, was just a malfunction in the brain.
“I had an initial hunch that food and food quality was part of the issue,” she says. If something in the environment triggered Parkinson’s, as some theories suggest, it made sense to her that the disease would involve the digestive system. Every time we eat and drink, our insides encounter the outside world.

John’s disease progressed slowly and Carlin kept up her research. In 2015, she found a paper titled, “Gut microbiota are related to Parkinson’s disease and clinical phenotype.” The study, by neurologist Filip Scheperjans of the University of Helsinki, asked two simple questions: Are the microorganisms that populate the guts of Parkinson’s patients different than those of healthy people? And if so, does that difference correlate with the stooped posture and difficulty walking that people with the disorder experience? Scheperjans’ answer to both questions was yes.

Carlin had picked up on a thread from one of the newest areas of Parkinson’s research: the relationship between Parkinson’s and the gut. Other than a small fraction of cases that are inherited, the cause of Parkinson’s disease is unknown. What is known is that something kills certain nerve cells, or neurons, in the brain. Abnormally misfolded and clumped proteins are the prime suspect. Some theories suggest a possible role for head trauma or exposure to heavy metals, pesticides or air pollution.
People with Parkinson’s often have digestive issues, such as constipation, long before the disease appears. Since the early 2000s, scientists have been gathering evidence that the malformed proteins in the brains of Parkinson’s patients might actually first appear in the gut or nose (people with Parkinson’s also commonly lose their sense of smell).
From there, the theory goes, these proteins work their way into the nervous system. Scientists don’t know exactly where in the gut the misfolded proteins come from, or why they form, but some early evidence points to the body’s internal microbial ecosystem. In the latest salvo, scientists from Sweden reported in October that people who had their appendix removed had a lower risk of Parkinson’s years later (SN: 11/24/18, p. 7). The job of the appendix, which is attached to the colon, is a bit of a mystery. But the organ may play an important role in intestinal health.

If the gut connection theory proves true — still a big if — it could open up new avenues to one day treat or at least slow the disease.

“It really changes the concept of what we consider Parkinson’s,” Scheperjans says. Maybe Parkinson’s isn’t a brain disease that affects the gut. Perhaps, for many people, it’s a gut disease that affects the brain.

Gut feeling
London physician James Parkinson wrote “An essay on the shaking palsy” in 1817, describing six patients with unexplained tremors. Some also had digestive problems. (“Action of the bowels had been very much retarded,” he reported of one man.) He treated two people with calomel — a toxic, mercury-based laxative of the time — and noted that their tremors subsided.

But the digestive idiosyncrasies of the disease that later bore Parkinson’s name largely faded into the background for the next two centuries, until neuroanatomists Heiko Braak and Kelly Del Tredici, now at the University of Ulm in Germany, proposed that Parkinson’s disease might arise from the intestine. Writing in Neurobiology of Aging in 2003, they and their colleagues based their theory on autopsies of Parkinson’s patients.
The researchers were looking for Lewy bodies, which contain clumps of a protein called alpha-synuclein. The presence of Lewy bodies in the brain is a hallmark of Parkinson’s, though their exact role in the disease is still under investigation.

Lewy bodies form when alpha-synuclein, which is produced by neurons and other cells, starts curdling into unusual strands. The body encapsulates the abnormal alpha-synuclein and other proteins into the round Lewy body bundles. In the brain, Lewy bodies collect in the cells of the substantia nigra, a structure that helps orchestrate movement. By the time symptoms appear, much of the substantia nigra is already damaged.

Substantia nigra cells produce the chemical dopamine, which is important for movement. Levodopa, the main drug prescribed for Parkinson’s, is a synthetic replacement for dopamine. The drug has been around for a half-century, and while it can alleviate symptoms for a while, it does not slow the destruction of brain cells.

In patient autopsies, Braak and his team tested for the presence of Lewy bodies, as well as abnormal alpha-s­ynuclein that had not yet become bundled together. Based on comparisons with people without Parkinson’s, the researchers found signs that Lewy bodies start to form in the nasal passages and intestine before they show up in the brain. Braak’s group proposed that Parkinson’s disease develops in stages, migrating from the gut and nose into the nerves to reach the brain.

Neural highway
Today, the idea that Parkinson’s might arise from the intestine, not the brain, “is one of the most exciting things in Parkinson’s disease,” says Heinz Reichmann, a neurologist at the University of Dresden in Germany. The Braak theory couldn’t explain how the Lewy bodies reach the brain, but Braak speculated that some sort of pathogen, perhaps a virus, might travel along the body’s nervous system, leaving a trail of Lewy bodies.

There is no shortage of passageways: The intestine contains so many nerves that it’s sometimes called the body’s second brain. And the vagus nerve offers a direct connection between those nerves in the gut and the brain (SN: 11/28/15, p. 18).

In mice, alpha-synuclein can indeed migrate from the intestine to the brain, using the vagus nerve like a kind of intercontinental highway, as Caltech researchers demonstrated in 2016 (SN: 12/10/16, p. 12). And Reichmann’s experiments have shown that mice that eat the pesticide rotenone develop symptoms of Parkinson’s. Other teams have shown similar reactions in mice that inhale the chemical. “What you sniff, you swallow,” he says.

To look at this idea another way, researchers have examined what happens to Parkinson’s risk when people have a weak or missing vagus nerve connection. There was a time when doctors thought that an overly eager vagus nerve had something to do with stomach ulcers. Starting around the 1970s, many patients had the nerve clipped as an experimental means of treatment, a procedure called a vagotomy. In one of the latest studies on vagotomy and Parkinson’s, researchers examined more than 9,000 patients with vagotomies, using data from a nationwide patient registry in Sweden. Among people who had the nerve cut down low, just above the stomach, the risk of Parkinson’s began dropping five years after surgery, eventually reaching a difference of about 50 percent compared with people who hadn’t had a vagotomy, the researchers reported in 2017 in Neurology.
The studies are suggestive, but by no means definitive. And the vagus nerve may not be the only possible link the gut and brain share. The body’s immune system might also connect the two, as one study published in January in Science Translational Medicine found. Study leader Inga Peter, a genetic epidemiologist at the Icahn School of Medicine at Mount Sinai in New York City, was looking for genetic contributors to Crohn’s disease, an inflammatory bowel condition that affects close to 1 million people in the United States.

She and a worldwide team studied about 2,000 people from an Ashkenazi Jewish population, which has an elevated risk of Crohn’s, and compared them with people without the disease. The research led Peter and colleagues to suspect the role of a gene called LRRK2. That gene is involved in the immune system — which mistakenly attacks the intestine in people who have Crohn’s. So it made sense for a variant of that gene to be involved in inflammatory disease. The researchers were thrown, however, when they discovered that versions of the gene also appeared to increase the risk for Parkinson’s disease.

“We refused to believe it,” Peter says. The finding, although just a correlation, suggested that whatever the gene was doing to the intestine might have something to do with Parkinson’s. So the team investigated the link further, reporting results in the August JAMA Neurology.

In their analysis of a large database of health insurance claims and prescriptions, the scientists found more evidence of inflammation’s role. People with inflammatory bowel disease were about 30 percent more likely to develop Parkinson’s than people without it. But among those who had filled prescriptions for an anti-inflammatory medication called antitumor necrosis factor, which the researchers used as a marker for reduced inflammation, Parkinson’s risk was 78 percent lower than in people who had not filled prescriptions for the drug.

Belly bacteria
Like Inga Peter, microbiologist Sarkis Mazmanian of Caltech came upon Parkinson’s disease almost by accident. He had long studied how the body’s internal bacteria interact with the immune system. At lunch one day with a colleague who was studying autism using a mouse version of the disease, Mazmanian asked if he could take a look at the animals’ intestines. Because of the high density of nerves in the intestine, he wanted to see if the brain and gut were connected in autism.

Neurons in the gut “are literally one cell layer away from the microbes,” he says. “That made me feel that at least the physical path or conduit was there.” He began to study autism, but wanted to switch to a brain disease with more obvious physical symptoms. When he learned that people with Parkinson’s disease often have a long history of digestive problems, he had his subject.

Mazmanian’s group examined mice that were genetically engineered to overproduce alpha-synuclein. He wanted to know whether the presence or absence of gut bacteria influenced symptoms that developed in the mice.

The results, reported in Cell in 2016, showed that when the mice were raised germ free — meaning their insides had no microorganisms — they showed no signs of Parkinson’s. The animals had no telltale gait or balance problems and no constipation, even though their bodies made alpha-synuclein (SN: 12/24/16 & 1/7/17, p. 10). “All the features of Parkinson’s in the animals were gone when the animals had no microbiome,” he says.

However, when gut microbes from people diagnosed with Parkinson’s were transplanted into the germ-free mice, the mice developed symptoms of the disease — symptoms that were much more severe than those in mice transplanted with microbes from healthy people.

Mazmanian suspects that something in the microbiome triggers the misfolding of alpha-synuclein. But this has not been tested in humans, and he is quick to say that this is just one possible explanation for the disease. “There’s likely no one smoking gun,” he says.

Microbial forces
If the microbiome is involved, what exactly is it doing to promote Parkinson’s? Microbiologist Matthew Chapman of the University of Michigan in Ann Arbor thinks it may have something to do with chemical signals that bacteria send to the body. Chapman studies biofilms, which occur when bacteria form resilient colonies. (Think of the slime on the inside a drain pipe.)

Part of what makes biofilms so hard to break apart is that fibers called amyloids run through them. Amyloids are tight stacks of proteins, like columns of Legos. Scientists have long suspected that amyloids are involved in degenerative diseases of the brain, including Alzheimer’s. In Parkinson’s, amyloid forms of alpha-synuclein are found in Lewy bodies.

Despite amyloids’ bad reputation, the fibers themselves aren’t always undesirable, Chapman says. Sometimes they may provide a good way of storing proteins for future use, to be snapped off brick by brick as needed. Perhaps it’s only when amyloids form in the wrong place, like the brain, that they contribute to disease. Chapman’s lab group has found that E. coli bacteria, part of the body’s normal microbial population, produce amyloid forms of some proteins when they are under stress.

When gut bacteria produce amyloids, the body’s own cells could also be affected, wrote Chapman in 2017 in PLOS Pathogens with an unlikely partner: neurologist Robert Friedland of the University of Louisville School of Medicine in Kentucky. “This is a difficult field to study because it’s on the border of several fields,” Friedland says. “I’m a neurologist who has little experience in gastro­enterology. When I talked about this to my colleagues who are gastroenterologists, they’ve never heard that bacteria make amyloid.”
Friedland and collaborators reported in 2016 in Scientific Reports that when E. coli in the intestines of rats started to produce amyloid, alpha-synuclein in the rats’ brains also congealed into the amyloid form. In their 2017 paper, Chapman and Friedland suggested that the immune system’s reaction to the amyloid in the gut might have something to do with triggering amyloid formation in the brain.

In other words, when gut bacteria get stressed and start to produce their own amyloids, those microbes may be sending cues to nearby neurons in the intestine to follow suit. “The question is, and it’s still an outstanding question, what is it that these bacteria are producing that is, at least in animals, causing alpha-synuclein to form amyloids?” Chapman says.

Head for a cure
There is, in fact, a long list of questions about the microbiome, says Scheperjans, the neurologist whose paper Martha Carlin first spotted. So far, studies of the microbiomes of human patients are largely limited to simple observations like his, and the potential for a microbiome connection has yet to reach deeply into the neurology community. But in O­ctober, for the second year in a row, Scheperjans says, the International Congress of Parkinson’s Disease and Movement Disorders held a panel discussing connections to the microbiome.

“I got interested in the gastrointestinal aspects because the patients complained so much about it,” he says. While his study found definite differences in the bacteria of people with Parkinson’s, it’s still too early to know how that might matter. But Scheperjans hopes that one day doctors may be able to test for microbiome changes that put people at higher risk for Parkinson’s, and restore a healthy microbe population through diet or some other means to delay or prevent the disease.
One way to slow the disease might be shutting down the mobility of misfolded alpha-synuclein before it has even reached the brain. In Science in 2016, neuroscientist Valina Dawson and colleagues at Johns Hopkins University School of Medicine and elsewhere described using an antibody to halt the spread of bad alpha-synuclein from cell to cell. The researchers are working now to develop a drug that could do the same thing.

The goal is to one day test for the early development of Parkinson’s and then be able to tell a patient, “Take this drug and we’re going to try to slow and prevent progression of disease,” she says.

For her part, Carlin is doing what she can to speed research into connections between the microbiome and Parkinson’s. She quit her job, sold her house and drained her retirement account to pour money into the cause. She donated to the University of Chicago to study her husband’s microbiome. And she founded a company called the BioCollective to aid in microbiome research, providing free collection kits to people with Parkinson’s. The 15,000 microbiome samples she has collected so far are available to researchers.

Carlin admits that the possibility of a gut connection to Parkinson’s can be a hard sell. “It’s a difficult concept for people to wrap their head around when you are taking a broad view,” she says. As she searches for answers, her husband, John, keeps going. “He drives, he runs biking programs in Denver for people with Parkinson’s,” she says. Anything to keep the wheels turning toward the future.One way to slow the disease might be shutting down the mobility of misfolded alpha-synuclein before it has even reached the brain. In Science in 2016, neuroscientist Valina Dawson and colleagues at Johns Hopkins University School of Medicine and elsewhere described using an antibody to halt the spread of bad alpha-synuclein from cell to cell. The researchers are working now to develop a drug that could do the same thing.

The goal is to one day test for the early development of Parkinson’s and then be able to tell a patient, “Take this drug and we’re going to try to slow and prevent progression of disease,” she says.

For her part, Carlin is doing what she can to speed research into connections between the microbiome and Parkinson’s. She quit her job, sold her house and drained her retirement account to pour money into the cause. She donated to the University of Chicago to study her husband’s microbiome. And she founded a company called the BioCollective to aid in microbiome research, providing free collection kits to people with Parkinson’s. The 15,000 microbiome samples she has collected so far are available to researchers.

Carlin admits that the possibility of a gut connection to Parkinson’s can be a hard sell. “It’s a difficult concept for people to wrap their head around when you are taking a broad view,” she says. As she searches for answers, her husband, John, keeps going. “He drives, he runs biking programs in Denver for people with Parkinson’s,” she says. Anything to keep the wheels turning toward the future.

Magnetism transforms a weird new material from soft to rigid in a split second.

This metamaterial — a synthetic structure designed to behave in ways that natural materials don’t — comprises a gridlike network of plastic tubes filled with fluid that becomes more viscous in a magnetic field, causing the tubes to firm up. The material could help make more adaptable robots or body armor, researchers report online December 7 in Science Advances.

Christopher Spadaccini, a materials engineer at Lawrence Livermore National Laboratory in California, and colleagues 3-D printed lattices composed of plastic struts 5 millimeters long and injected them with a mixture of tiny iron particles and oil. In the absence of a magnetic field, the iron microparticles remain scattered randomly throughout the oil, so the liquid is runny. But close to a magnet, these iron microparticles align into chains along the magnetic field lines, making the fluid viscous and the lattices stiffer.
A solid hunk of iron microparticle–filled material would be heavy and expensive to make. Building tubular structures that are mostly open space makes this tunable material more lightweight, says coauthor Julie Jackson, an engineer at Lawrence Livermore.
The researchers tested individual “unit cells” of the new material — hollow, die-shaped structures that can collectively form the larger lattices. Moving one unit cell from about eight centimeters to one centimeter away from a magnet increased its stiffness by about 62 percent.

In future technologies, this material could be paired with devices that use electricity to generate magnetic fields, called electromagnets. Material that becomes softer or stiffer on demand could be used to make next-generation sports pads or helmets with tunable impact absorption, Jackson says. Robots with changeable stiffness could squeeze into small spaces, but then be sturdy enough to carry or move other objects.

In the classic fairy tale, Hansel and Gretel dropped bread crumbs while walking through a treacherous forest so they wouldn’t lose their way. Rovers may one day use a similar trick to traverse other planets without losing their data.

Typically, if a rover permanently loses communication during a mission, all the information that it has gathered is lost. To avoid this, researchers suggest using a multi-rover system in which a smaller rover piggybacks on a larger “mother rover.” The smaller rover would then venture into any especially uncertain territory, such as a cave or lava tubes, deploying sensors the size of an AirPods case like bread crumbs as it goes.
The sensors could then communicate with each other via a wireless network and funnel any collected data back to the mother rover, theoretical physicist Wolfgang Fink and colleagues propose February 11 in Advances in Space Research. As proof of concept, the team built prototype sensors that communicate via Wi-Fi.

It’s not that the smaller rover would be following the “bread crumbs” back the way it came. Instead, “we use [the sensors] for the data to find its way communication-wise out of the cave to the mother rover,” says Fink, of the University of Arizona in Tucson.

The technology could also be useful here on Earth, especially after a natural disaster such as an earthquake. A rover could be sent with the deployable sensors into rubble where it’s too dangerous for people to perform search-and-rescue missions (SN: 12/3/14).

The bread crumb–like communication network could allow researchers to “cater to the essence of scientific exploration,” Fink says, by allowing rovers to overcome some of the constraints posed by tricky terrain. “To get to the real exciting science, you most of the time have to go to exotic places, hard-to-get-to places.”

Race should no longer be used to describe populations in most genetics studies, a panel of experts says.

Using race and ethnicity to describe study participants gives the mistaken impression that humans can be divided into distinct groups. Such labels have been used to stigmatize groups of people, but do not explain biological and genetic diversity, the panel convened by the U.S. National Academies of Sciences, Engineering and Medicine said in a report on March 14.
In particular, the term Caucasian should no longer be used, the committee recommends. The term, coined in the 18th century by German scientist Johann Friedrich Blumenbach to describe what he determined was the most beautiful skull in his collection, carries the false notion of white superiority, the panel says.

Worse, the moniker “has also acquired today the connotation of being an objective scientific term, and that’s what really led the committee to take objection with it,” says Ann Morning, a sociologist at New York University and a member of the committee that wrote the report. “It tends to reinforce this erroneous belief that racial categories are somehow objective and natural characterizations of human biological difference. We felt that it was a term that … should go into the dustbin of history.”

Similarly, the term “black race” shouldn’t be used because it implies that Black people are a distinct group, or race, that can be objectively defined, the panel says.

Racial definitions are problematic “because not only are they stigmatizing, they are historically wrong,” says Ambroise Wonkam, a medical geneticist at Johns Hopkins University and president of the African Society of Human Genetics. Race is often used as a proxy for genetic diversity. But “race cannot be used to capture diversity at all. Race doesn’t exist. There is only one race, the human race,” says Wonkam, who was not involved with the National Academies’ panel.

Race might be used in some studies to determine how genetic and social factors contribute to health disparities (SN: 4/5/22), but beyond that race has no real value in genetic research, Wonkam adds.

Researchers could use other identifiers, including geographical ancestry, to define groups of people in the study, Wonkam says. But those definitions need to be precise.

For instance, some researchers group Africans by language groups. But a Bantu-speaking person from Tanzania or Nigeria where malaria is endemic would have a much higher genetic risk of sickle cell disease than a Bantu-speaking person whose ancestors are from South Africa, where malaria has not existed for at least 1,000 years. (Changes in genes that make hemoglobin can protect against malaria (SN: 5/2/11), but cause life-threatening sickle cell disease.)
Genetic studies also have to account for movements of people and mixture between multiple groups, Wonkam says. And labeling must be consistent for all groups in the study, he says. Current studies sometimes compare continent-wide racial groups, such as Asian, with national groups, such as French or Finnish, and ethnic groups, such as Hispanic.

An argument for keeping race in rare cases
Removing race as a descriptor may be helpful for some groups, such as people of African descent, says Joseph Yracheta, a health disparities researcher and the executive director of the Native BioData Consortium, headquartered on the Cheyenne River Sioux reservation in South Dakota. “I understand why they want to get rid of race science for themselves, because in their case it’s been used to deny them services,” he says.

But Native Americans’ story is different, says Yracheta, who was not part of the panel. Native Americans’ unique evolutionary history have made them a valuable resource for genetics research. A small starting population and many thousands of years of isolation from humans outside the Americas have given Native Americans and Indigenous people in Polynesia and Australia some genetic features that may make it easier for researchers to find variants that contribute to health or disease, he says. “We’re the Rosetta stone for the rest of the planet.”

Native Americans “need to be protected, because not only are our numbers small, but we keep having things taken away from us since 1492. We don’t want this to be another casualty of colonialism.” Removing the label of Indigenous or Native American may erode tribal sovereignty and control over genetic data, he says.

The panel does recommend that genetic researchers should clearly state why they used a particular descriptor and should involve study populations in making decisions about which labels to use.

That community input is essential, Yracheta says. The recommendations have no legal or regulatory weight. So he worries that this lack of teeth may allow researchers to ignore the wishes of study participants without fear of penalty.

Still seeking diversity in research participants
Genetics research has suffered from a lack of diversity of participants (SN: 3/4/21). To counteract the disparities, U.S. government regulations require researchers funded by the National Institutes of Health to collect data on the race and ethnicity of study participants. But because those racial categories are too broad and don’t consider the social and environmental conditions that may affect health, the labels are not helpful in most genetic analyses, the panel concluded.

Removing racial labels won’t hamper diversity efforts, as researchers will still seek out people from different backgrounds to participate in studies, says Brendan Lee, who is president of the American Society of Human Genetics. But taking race out of the equation should encourage researchers to think more carefully about the type of data they are collecting and how it might be used to support or refute racism, says Lee, a medical geneticist at Baylor College of Medicine in Houston, who was not part of the panel.

The report offers decision-making tools for determining what descriptors are appropriate for particular types of studies. But “while it is a framework, it is not a recipe where in every study we do A, B and C,” Lee says.

Researchers probably won’t instantly adopt the new practices, Lee says. “It is a process that will take time. I don’t think it is something we can expect in one week or one evening that we’ll all change over to this, but it is a very important first step.”

Saturn’s rings are painting its innermost moons.

Data from NASA’s now-defunct Cassini spacecraft show that five odd-shaped moons embedded in Saturn’s rings are different colors, and that the hues come from the rings themselves, researchers report. That observation could help scientists figure out how the moons were born.

“The ring moons and the rings themselves are kind of one and the same,” says planetary scientist Bonnie Buratti of NASA’s Jet Propulsion Laboratory in Pasadena, Calif. “For as long as the moons have existed, they’ve been accreting particles from the rings.”
Saturn has more than 60 moons, but those nearest to the planet interact closely with its main band of rings. Between December 2016 and April 2017, Cassini passed close to five of these ring-dwelling moons: ravioli-shaped Pan and Atlas (SN Online: 3/10/17), ring-sculpting Daphnis and Pandora (SN: 9/2/17, p. 16) and potato-shaped Epimetheus. The flybys brought Cassini between two and 10 times closer to the moons than it had ever been, before the spacecraft deliberately crashed into Saturn in September 2017 (SN Online: 9/15/17).

Examining those close-ups, Buratti and her colleagues noticed that the moons’ colors vary depending on the objects’ distances from Saturn. And the moon hues are similar to the colors of the rings that the objects are closest to, the team reports online March 28 in Science.
Close-in Pan was the reddest moon, while the farthest-out Epimetheus was the bluest. The researchers think the red material comes from Saturn’s dense main rings, and mostly consists of organics and iron (SN Online: 10/4/18). The blue material is probably water ice from Saturn’s more distant E ring, which is created by plumes erupting from the larger, icy moon Enceladus.
The team thinks that the rings are continually depositing material onto the moons. “It’s an ongoing process,” Buratti says. She notes that “skirts” of material at Atlas and Pan’s equators are probably made of accreted ring debris, too.

The overall similarity between the moons and rings led the researchers to conclude that these small moons are leftover shards of a destructive event that created the rings in the first place. But it’s unknown whether that event was a collision between long-gone, larger moons, the shredding of one moon by Saturn’s gravity, or some other occurrence (SN: 1/20/18, p. 7).

Saturn, its rings and its moons are “very dynamic,” says planetary scientist Matija Ćuk of the SETI Institute in Mountain View, Calif. The idea that the rings are still shedding material onto the moons today “sounds perfectly reasonable.” He isn’t sure the moons formed at the same time as the rings, though. It’s possible “they formed from the rings since that catastrophic event,” he says.

Just a few powerful storms in Antarctica can have an outsized effect on how much snow parts of the southernmost continent get. Those ephemeral storms, preserved in ice cores, might give a skewed view of how quickly the continent’s ice sheet has grown or shrunk over time.

Relatively rare extreme precipitation events are responsible for more than 40 percent of the total annual snowfall across most of the continent — and in some places, as much as 60 percent, researchers report March 22 in Geophysical Research Letters.
Climatologist John Turner of the British Antarctic Survey in Cambridge and his colleagues used regional climate simulations to estimate daily precipitation across the continent from 1979 to 2016. Then, the team zoomed in on 10 locations — representing different climates from the dry interior desert to the often snowy coasts and the open ocean — to determine regional differences in snowfall.

While snowfall amounts vary greatly by location, extreme events packed the biggest wallop along Antarctica’s coasts, especially on the floating ice shelves, the researchers found. For instance, the Amery ice shelf in East Antarctica gets roughly half of its annual precipitation — which typically totals about half a meter of snow — in just 10 days, on average. In 1994, the ice shelf got 44 percent of its entire annual precipitation on a single day in September.

Ice cores aren’t just a window into the past; they are also used to predict the continent’s future in a warming world. So characterizing these coastal regions is crucial for understanding Antarctica’s ice sheet — and its potential future contribution to sea level rise.
Editor’s note: This story was updated April 5, 2019, to correct that the results were reported March 22 (not March 25).

We live in a sea of neutrinos. Every second, trillions of them pass through our bodies. They come from the sun, nuclear reactors, collisions of cosmic rays hitting Earth’s atmosphere, even the Big Bang. Among fundamental particles, only photons are more numerous. Yet because neutrinos barely interact with matter, they are notoriously difficult to detect.

The existence of the neutrino was first proposed in the 1930s and then verified in the 1950s (SN: 2/13/54). Decades later, much about the neutrino — named in part because it has no electric charge — remains a mystery, including how many varieties of neutrinos exist, how much mass they have, where that mass comes from and whether they have any magnetic properties.
These mysteries are at the heart of Ghost Particle by physicist Alan Chodos and science journalist James Riordon. The book is an informative, easy-to-follow introduction to the perplexing particle. Chodos and Riordon guide readers through how the neutrino was discovered, what we know — and don’t know — about it, and the ongoing and future experiments that (fingers crossed) will provide the answers.

It’s not just neutrino physicists who await those answers. Neutrinos, Riordon says, “are incredibly important both for understanding the universe and our existence in it.” Unmasking the neutrino could be key to unlocking the nature of dark matter, for instance. Or it could clear up the universe’s matter conundrum: The Big Bang should have produced equal amounts of matter and antimatter, the oppositely charged counterparts of electrons, protons and so on. When matter and antimatter come into contact, they annihilate each other. So in theory, the universe today should be empty — yet it’s not (SN: 9/22/22). It’s filled with matter and, for some reason, very little antimatter.

Science News spoke with Riordon, a frequent contributor to the magazine, about these puzzles and how neutrinos could act as a tool to observe the cosmos or even see into our own planet. The following conversation has been edited for length and clarity.

SN: In the first chapter, you list eight unanswered questions about neutrinos. Which is the most pressing to answer?

Riordon: Whether they’re their own antiparticles is probably one of the grandest. The proposal that neutrinos are their own antiparticles is an elegant solution to all sorts of problems, including the existence of this residue of matter we live in. Another one is figuring out how neutrinos fit in the standard model [of particle physics]. It’s one of the most successful theories there is, but it can’t explain the fact that neutrinos have mass.
SN: Why is now a good time to write a book about neutrinos?

Riordon: All of these questions about neutrinos are sort of coming to a head right now — the hints that neutrinos may be their own antiparticles, the issues of neutrinos not quite fitting the standard model, whether there are sterile neutrinos [a hypothetical neutrino that is a candidate for dark matter]. In the next few years, a decade or so, there will be a lot of experiments that will [help answer these questions,] and the resolution either way will be exciting.

SN: Neutrinos could also be used to help scientists observe a range of phenomena. What are some of the most interesting questions neutrinos could help with?

Riordon: There are some observations that simply have to be done with neutrinos, that there are no other technological alternatives for. There’s a problem with using light-based telescopes to look back in history. We have this really amazing James Webb Space Telescope that can see really far back in history. But at some point, when you go far enough back, the universe is basically opaque to light; you can’t see into it. Once we narrow down how to detect and how to measure the cosmic neutrino background [neutrinos that formed less than a second after the Big Bang], it will be a way to look back at the very beginning. Other than with gravitational waves, you can’t see back that far with anything else. So it’ll give us sort of a telescope back to the beginning of the universe.

The other thing is, when a supernova happens, all kinds of really cool stuff happens inside, and you can see it with neutrinos because neutrinos come out immediately in a burst. We call it the “cosmic neutrino bomb,” but you can track the supernova as it’s going along. With light, it takes a while for it to get out [of the stellar explosion]. We’re due for a [nearby] supernova. We haven’t had one since 1987. It was the last visible supernova in the sky and was a boon for research. Now that we have neutrino detectors around the world, this next one is going to be even better [for research], even more exciting.

And if we develop better instrumentation, we could use neutrinos to understand what’s going on in the center of the Earth. There’s no other way that you could probe the center of the Earth. We use seismic waves, but the resolution is really low. So we could resolve a lot of questions about what the planet is made of with neutrinos.

SN: Do you have a favorite “character” in the story of neutrinos?

Riordon: I’m certainly very fond of my grandfather Clyde Cowan [he and Frederick Reines were the first physicists to detect neutrinos]. But Reines is a riveting character. He was poetic. He was a singer. He really was this creative force. I mentioned [in the book] that they put this “SNEWS” sign on their detector for “supernova early warning system,” which sort of echoed the ballistic missile early warning systems at the time [during the Cold War]. That’s so ripe.

In the classic fairy tale, Hansel and Gretel dropped bread crumbs while walking through a treacherous forest so they wouldn’t lose their way. Rovers may one day use a similar trick to traverse other planets without losing their data.

Typically, if a rover permanently loses communication during a mission, all the information that it has gathered is lost. To avoid this, researchers suggest using a multi-rover system in which a smaller rover piggybacks on a larger “mother rover.” The smaller rover would then venture into any especially uncertain territory, such as a cave or lava tubes, deploying sensors the size of an AirPods case like bread crumbs as it goes.
The sensors could then communicate with each other via a wireless network and funnel any collected data back to the mother rover, theoretical physicist Wolfgang Fink and colleagues propose February 11 in Advances in Space Research. As proof of concept, the team built prototype sensors that communicate via Wi-Fi.

It’s not that the smaller rover would be following the “bread crumbs” back the way it came. Instead, “we use [the sensors] for the data to find its way communication-wise out of the cave to the mother rover,” says Fink, of the University of Arizona in Tucson.

The technology could also be useful here on Earth, especially after a natural disaster such as an earthquake. A rover could be sent with the deployable sensors into rubble where it’s too dangerous for people to perform search-and-rescue missions (SN: 12/3/14).

The bread crumb–like communication network could allow researchers to “cater to the essence of scientific exploration,” Fink says, by allowing rovers to overcome some of the constraints posed by tricky terrain. “To get to the real exciting science, you most of the time have to go to exotic places, hard-to-get-to places.”

For the first time, astronomers have caught a glimpse of shock waves rippling along strands of the cosmic web — the enormous tangle of galaxies, gas and dark matter that fills the observable universe.

Combining hundreds of thousands of radio telescope images revealed the faint glow cast as shock waves send charged particles flying through the magnetic fields that run along the cosmic web. Spotting these shock waves could give astronomers a better look at these large-scale magnetic fields, whose properties and origins are largely mysterious, researchers report in the Feb. 17 Science Advances.
Finally, astronomers “can confirm what so far has only been predicted by simulations — that these shock waves exist,” says astrophysicist Marcus Brüggen of the University of Hamburg in Germany, who was not involved in the new study.

At its grandest scale, our universe looks something like Swiss cheese. Galaxies aren’t distributed evenly through space but rather are clumped together in enormous clusters connected by ropy filaments of dilute gas, galaxies and dark matter and separated by not-quite-empty voids (SN: 10/3/19).

Tugged by gravity, galaxy clusters merge, filaments collide, and gas from the voids falls onto filaments and clusters. In simulations of the cosmic web, all that action consistently sets off enormous shock waves in and along filaments.

Filaments make up most of the cosmic web but are much harder to spot than galaxies (SN: 1/20/14). While scientists have observed shock waves around galaxy clusters before, shocks in filaments “have never been really seen,” says astronomer Reinout van Weeren of Leiden University in the Netherlands, who was not involved in the study. “But they should be basically all around the cosmic web.”

Shock waves around filaments would accelerate charged particles through the magnetic fields that suffuse the cosmic web (SN: 6/6/19). When that happens, the particles emit light at wavelengths that radio telescopes can detect — though the signals are very weak.
A single shock wave in a filament “would look like nothing, it’d look like noise,” says radio astronomer Tessa Vernstrom of the International Centre for Radio Astronomy Research in Crawley, Australia.

Instead of looking for individual shock waves, Vernstrom and her colleagues combined radio images of more than 600,000 pairs of galaxy clusters close enough to be connected by filaments to create a single “stacked” image. This amplified weak signals and revealed that, on average, there is a faint radio glow from the filaments between clusters.

“When you can dig below the noise and still actually get a result — to me, that’s personally exciting,” Vernstrom says.

The faint signal is highly polarized, meaning that the radio waves are mostly aligned with one another. Highly polarized light is unusual in the cosmos, but it is expected from radio light cast by shock waves, van Weeren says. “So that’s really, I think, very good evidence for the fact that the shocks are likely indeed present.”
The discovery goes beyond confirming the predictions of cosmic web simulations. The polarized radio emissions also offer a rare peek at the magnetic fields that permeate the cosmic web, if only indirectly.

“These shocks,” Brüggen says, “are really able to show that there are large-scale magnetic fields that form [something] like a sheath around these filaments.”

He, van Weeren and Vernstrom all note that it’s still an open question how cosmic magnetic fields arose in the first place. The role these fields play in shaping the cosmic web is equally mysterious.

“It’s one of the four fundamental forces of nature, right? Magnetism,” Vernstrom says. “But at least on these large scales, we don’t really know how important it is.”

An uncomfortable truth is that there is another influenza pandemic in humankind’s future. Whether it will be a relative of the lethal avian flu strain currently wreaking havoc in bird populations around the globe is anyone’s guess.

Because the virus, called H5N1, can be deadly to birds, mammals and people, researchers closely monitor reports of new cases. Worryingly, a new variant of H5N1 that emerged in 2020 has not only spread farther than ever before among birds, but has also spilled over into other animals, raising the specter of a human outbreak (SN: 12/12/22).

The variant was linked to a seal die-off in Maine last summer. In October, there was an H5N1 outbreak on a mink farm in Spain, researchers reported in January in Eurosurveillance. (It’s unclear how the mink were exposed, but the animals were fed poultry by-products.) Sea lions off the coast of Peru and wild bears, foxes and skunks, which prey upon or scavenge birds, in the United States and Europe have also tested positive for the virus.

Globally, hundreds of millions of domestic poultry have been culled or died from the new variant. It’s also likely that millions of wild birds have died, though few governmental agencies are counting, says Michelle Wille a viral ecologist at the University of Sydney who studies avian influenza. “This virus is catastrophic for bird populations.”

A handful of human cases have also been reported, though there’s no evidence that the virus is spreading among people. Of seven cases, six people recovered and one person from China died. In February, health officials in China reported an eighth case in a woman whose current condition is unknown.

What’s more, four of the reported human cases — including a U.S. case from Colorado and two workers linked to the Spanish mink farm — were in people who didn’t have any respiratory symptoms. That leaves open the possibility that those people were not truly infected. Instead, tests may have picked up viral contamination, say in the nose, that the people breathed in while handling infected birds.

The impossibility of predicting which avian influenza viruses might make the jump to people and spark an outbreak is in part related to knowledge gaps. These bird pathogens don’t typically easily infect or circulate among mammals including humans. And scientists don’t have a full grasp on how these viruses might need to change for human transmission to occur.

For now, it’s encouraging that so few people have gotten infected amid such a large outbreak among birds and other animals, says Marie Culhane, a food animal veterinarian at the University of Minnesota in St. Paul. Still, experts around the globe are diligently watching for any signs the virus may be evolving to spread more easily between people.

The good news is that flu drugs and vaccines that work against the virus already exist, Wille says. Compared with where the world was when the coronavirus behind the COVID-19 pandemic came on the scene, “we are already ahead of the game.”

How the virus would need to change to spread among people is a big unknown
This new iteration of bird flu is what’s called a highly pathogenic avian influenza, one that is particularly lethal for both domestic and wild birds. Aquatic birds such as ducks naturally carry avian flus with no or minor signs of infection. But when influenza viruses shuffle between poultry and waterfowl, variants with changes that make them lethal to birds can emerge and spread.

Avian viruses can be severe or even deadly for people. Since 2003, there have been 873 human cases of H5N1 infections reported to the World Health Organization. A little less than half of those people died. In February, an 11-year-old girl in Cambodia died after she developed severe pneumonia from an avian flu virus, the country’s first reported infection since 2014. Her father was also infected with the virus — a different variant than the one behind the widespread outbreak in birds —though he has not developed symptoms. It’s unknown how the two people were exposed.

Some of what scientists know about H5N1’s pandemic potential comes from controversial research on ferrets done more than a decade ago (SN: 6/21/13). Experiments showed that some changes to proteins that help the virus break into cells and make more copies of itself could help the virus travel through the air to infect ferrets, a common laboratory stand-in for humans in influenza research.

While researchers know these mutations are important in lab settings, it’s still unclear how crucial those changes are in the real world, says Jonathan Runstadler, a disease ecologist and virologist at Tufts University’s Cummings School of Veterinary Medicine in North Grafton, Mass.
Viruses change constantly, but not all genetic tweaks work together. A change may help one version of the virus transmit better, while also hurting another variant and making it less likely to spread.

“We’re not sure how critical or how big a difference or how much to worry about those mutations when they happen in the wild,” Runstadler says. “Or when they happen five years down the road when there are other changes in the virus’s genetic background that are impacting those [original] mutations.”

That doesn’t stop researchers from trying to pinpoint specific changes. Runstadler and his team look for viruses in nature that have jumped into new animals and work backward to figure out which mutations were crucial. And virologist Louise Moncla says her lab is trying to develop ways to scan entire genetic blueprints of viruses from past outbreaks to look for signatures of a virus that can jump between different animal species.

“There’s a ton that we don’t know about avian influenza viruses and host switching,” says Moncla, of the University of Pennsylvania.

Genetic analyses of H5N1 circulating on the mink farm in Spain, for instance, revealed a change known to help the virus infect mice and mammalian cells grown in the lab. Such a change could make it easier for the virus to spread among mammals, including people. There could have been mink-to-mink transmission on the farm, the researchers concluded, but it remains unclear how much of a role that specific mutation played in the outbreak.

It’s a numbers game for when influenza viruses with the ability to transmit among mammals might make the jump from birds, Runstadler says. “The more chances you give the virus to spill over and adapt, the higher the risk will be that one of those adaptations will be effective [at helping the virus spread among other animals] or take root and be a real problem.”

The ongoing outbreak is still a big problem for birds
Irrespective of our inability to forecast human’s future with H5N1, it’s clear that many species of birds — and some other animals that eat them — are dying now. And more species of birds are dying in this outbreak than previous ones, Culhane and Wille say.

“We have seen huge outbreaks in raptors and seabirds, which were never really affected before,” Wille says. It’s possible that genetic changes have helped the virus to spread more efficiently among birds than previous versions of H5N1, but that’s unknown. “There are a number of studies underway to try and figure it out,” Wille says.
Historically, these deadly avian flus have not been a persistent problem in the Americas, Moncla says. Sporadic outbreaks of H5N1 variants are typically limited to places such as parts of Asia, where the virus has circulated in birds since its emergence in the late 1990s, and northern Africa.

North America’s last big avian flu outbreak was in 2015, when experts detected more than 200 cases of a different bird flu virus in commercial and backyard poultry across the United States. The poultry industry culled more than 45 million birds to stop that virus’s spread, Culhane says. “But it didn’t go away from the rest of the world.”

The latest version of H5N1 arrived on North American shores from Europe in late 2021, first popping up in Canada in Newfoundland and Labrador. From there, it spread south into the United States, where so far tens of millions of domestic poultry have been culled to prevent transmission on farms where the virus has been detected. By December 2022, the virus had made it to South America. In Peru, tens of thousands of pelicans and more than 700 sea lions have died since mid-January.

It’s important to understand exactly how nonbird animals are getting exposed, Culhane says. Highly pathogenic avian influenzas infect every organ of a bird’s body. So, a fox chowing down on an infected bird is exposing its own mouth, nose and stomach to a lot of virus as it eats its meal.

For now, experts are keeping an eye on infected animals to raise the alarm early if H5N1 starts transmitting among mammals.

“I do think that the mink outbreak, and then the sea lion outbreak, is a wake-up call,” Moncla says. “We should be doing our very best to implement all the science we can to try and understand what’s happening with these viruses so that if the situation does change, we are better prepared.”