Editor’s note: This story will be periodically updated as new images are released.
NASA’s InSight lander touched down on Mars on November 26 for a study of the Red Planet’s insides.
“Touchdown confirmed, InSight is on the surface of Mars!” said Christine Szalai, a spacecraft engineer at NASA’s Jet Propulsion Laboratory in Pasadena, Calif., in a live broadcast from mission control. The lander sent its first picture — which mostly showed the inside of the dust cover on its camera lens — shortly after landing. The landing of InSight, short for Interior Exploration using Seismic Investigations, Geodesy and Heat Transport, brings the total number of successful NASA Mars landings to eight. InSight touched down at about 2:55 p.m. Eastern time in a wide, flat plain called Elysium Planitia, near Mars’ equator. News of the landing was relayed by a pair of tiny satellites called MarCO that travelled to Mars with InSight as an in-house communications team (SN Online: 11/18/18).
Over the next Martian year (about two Earth years), InSight will use a seismometer to listen for “Marsquakes” and other seismic waves rippling through the planet (SN: 5/26/18, p. 13). The lander will also drill five meters into Mars’ surface to measure the planet’s internal heat flow, a sign of how geologically active Mars is today. Update, November 27, 2018: InSight has opened its solar panels and is charging its batteries. In the next few days, the Mars lander will stretch out its robotic arm and take photos of the ground so the InSight team can decide where to place its scientific instruments. The first image from the Instrument Deployment Camera, taken shortly after landing November 26 and beamed back at 8:30 p.m. Eastern Standard Time, shows the spacecraft’s body, the folded-up robotic arm and the wide flat expanse of Elysium Planitia.
The U.S.S. Leviathan set sail from Hoboken, N.J., on September 29, 1918, carrying roughly 10,000 troops and 2,000 crewmen. The ship, bound for the battlefields in France, had been at sea less than 24 hours when the first passengers fell ill. By the end of the day, 700 people had developed signs of the flu.
The medical staff tried to separate the sick from the healthy, but that soon proved impossible. The poorly ventilated bunkrooms filled with the stench of illness. The floor grew slippery with blood from many nosebleeds, and the wails of the sick and dying echoed below deck. Bodies piled up and began decomposing, until finally the crew was forced to heave them into the sea. It was the stuff of nightmares. This is just one of the grisly scenes in Pandemic 1918 by historian Catharine Arnold. The book details how the movement of troops during World War I helped drive the spread of a deadly strain of influenza around the globe — from the American Midwest to Cape Town, South Africa, to New Zealand and beyond.
Scientists have yet to conclusively determine where that flu originated; Arnold suggests it was on a massive military base in Étaples, France. But all agree that the pandemic that became known as the Spanish flu didn’t begin in Spain. And the disease, which ultimately killed more than 50 million people, wasn’t caused by any ordinary influenza strain. Grim eyewitness accounts chronicle the gory details of how this virus differed. Victims often bled from the nose or mouth, writhed in pain and grew delirious with fever. Their faces turned dusky blue as their lungs filled with pus. Healthy men and women in their prime were dying, sometimes within days of falling ill. And there was a smell associated with the sick, “like very musty straw,” recalled one survivor. Arnold’s graphic depictions of the carnage make for some gripping scenes, but the book is perhaps too ambitious. She zigzags between so many people and places that only the most careful reader will be able to keep track of who fell ill where.
Another book tied to the 100th anniversary of the Spanish flu, Influenza, by long-time emergency room doctor Jeremy Brown, covers some of the same ground. Both Arnold and Brown, for instance, chronicle the hunt for the 1918 virus in bodies buried in Arctic permafrost and efforts to reconstruct the virus’s genetic code. But while Arnold’s book is rooted primarily in the past, Brown spends more time on recent research. He provides an in-depth look at what scientists now know about the 1918 strain, an H1N1 virus that originated in birds and spent time in an unknown mammalian host before infecting humans. In 2005, researchers managed to re-create the virus and test it in mice. The experiment provided insight into how the virus might have wrought so much damage in the lungs, but it also renewed a debate over the ethics of reconstructing deadly viruses. These kinds of experiments can help scientists better understand the inner workings of pathogens, but might also help people build biological weapons.
Brown also provides a fascinating look at the factors that make the more common seasonal flu so challenging to predict and prevent. Because data collection relies on the generosity of health care workers and because doctors rarely test for influenza, researchers can’t get a full picture of the scope of the disease. And because the virus mutates easily, scientists struggle to accurately predict what next year’s outbreak might look like. The strains circulating when pharmaceutical companies begin making vaccines might not be the strains that are circulating when the vaccines reach clinics and pharmacies. That’s why the flu shot’s efficacy varies from about 10 to 60 percent each year (SN: 10/28/17, p. 18).
Both books provide fresh perspectives on the 1918 pandemic and the influenza virus that caused it. Readers interested in a deep dive into the harrowing details and eyewitness accounts from that dark time should pick up Arnold’s book. For those who want more science with a frank discussion of the challenges influenza still poses, Brown delivers a clear and captivating overview. Together the books offer an unsettling picture of the damage influenza inflicted on the world 100 years ago and the misery that this virus might yet bring again.
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.”
Off the Pacific coast of Costa Rica sits a deep-sea chimera of an ecosystem. Jacó Scar is a methane seep, where the gas escapes from sediment into the seawater, but the seep isn’t cold like the others found before it. Instead, geochemical activity gives the Scar lukewarm water that enables organisms from both traditionally colder seeps and scalding hot hydrothermal vents to call it home.
One resident of the Scar is a newly identified species of small, purplish fish called an eelpout, described for the first time on January 19 in Zootaxa. This fish is the first vertebrate species found at the Scar and could help scientists understand how the unique ecosystem developed. Jacó Scar was discovered during exploration of a known field of methane seeps off the Costa Rican coast and named for the nearby town of Jacó. It is “a really diverse place” with many different organisms living in various microhabitats, says Lisa Levin, a marine ecologist at Scripps Institution of Oceanography in La Jolla, Calif.
Levin was on one of the first expeditions to the Scar but wasn’t involved in the new study. She recalls the team finding and collecting one of the fish during this early excursion, but the researchers didn’t recognize it as a new species.
Several more specimens were snagged during later submersible dives. Charlotte Seid, an invertebrate biologist at Scripps who is working on a checklist of organisms found at the Costa Rican seeps, brought the fishy finds to ichthyologist Ben Frable, also of Scripps, for formal identification.
Frable says he knew the fish was an eelpout. They look exactly as one would expect based on their name: like frowning eels, though they aren’t true eels. But he was having trouble determining what type. Eelpouts are a diverse family of fish comprised of nearly 300 species that can be found all over the world at various ocean depths.
Because the physical differences between species can be subtle, they are “kind of a tricky group” to identify, Frable says. “I just was not really getting anywhere.” So the team turned to eelpout expert Peter Rask Møller of the Natural History Museum of Denmark in Copenhagen, sending him X-rays, pictures and eventually one of the fish specimens.
Møller narrowed the enigmatic eelpout to the genus Pyrolycus, meaning “fire wolf.” Turns out, the tool, called a dichotomous key, that Frable had been using to identify the specimens was outdated, made before Pyrolycus was described in 2002. “I did not know that genus existed,” Frable says.
Because the other two known Pyrolycus species live far away in the western Pacific and have different physical features, the team dubbed the mystery fish P. jaco — a new species.
The first eelpouts most likely evolved in cold waters, Frable says, but many have since made their home in the scalding waters of hydrothermal vents. Of the 24 known fish species that live only at hydrothermal vents, “13 of them are eelpouts,” Frable says. The new finding raises questions about how the known Pyrolycus species came to live so far apart. It may have to do with the fact that methane seeps are more common than previously thought on the ocean floor, and if some are lukewarm like Jacó Scar, the new species could have used them as refuges while moving east.
And by comparing P. jaco to its vent-living relatives, researchers may be able to figure out how it adapted to live in the tepid waters of the Scar — which may provide clues to how other species living there did too.
The eelpout is part of a medley of other species that form Jacó Scar’s composite ecosystem, along with, for example, clams typically found at cold seeps and bacteria found at hydrothermal vents. Jacó Scar is a “mixing bowl” of species found in other parts of the world, Seid says. Figuring out how this eclectic bunch interacts “is part of the fun.”
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).
Editor’s note: On April 10, the Event Horizon Telescope collaboration released a picture of the supermassive black hole at the center of galaxy M87. Read the full story here.
We’re about to see the first close-up of a black hole.
The Event Horizon Telescope, a network of eight radio observatories spanning the globe, has set its sights on a pair of behemoths: Sagittarius A*, the supermassive black hole at the Milky Way’s center, and an even more massive black hole 53.5 million light-years away in galaxy M87 (SN Online: 4/5/17). In April 2017, the observatories teamed up to observe the black holes’ event horizons, the boundary beyond which gravity is so extreme that even light can’t escape (SN: 5/31/14, p. 16). After almost two years of rendering the data, scientists are gearing up to release the first images in April.
Here’s what scientists hope those images can tell us.
What does a black hole really look like? Black holes live up to their names: The great gravitational beasts emit no light in any part of the electromagnetic spectrum, so they themselves don’t look like much.
But astronomers know the objects are there because of a black hole’s entourage. As a black hole’s gravity pulls in gas and dust, matter settles into an orbiting disk, with atoms jostling one another at extreme speeds. All that activity heats the matter white-hot, so it emits X-rays and other high-energy radiation. The most voraciously feeding black holes in the universe have disks that outshine all the stars in their galaxies (SN Online: 3/16/18). The EHT’s image of the Milky Way’s Sagittarius A, also called SgrA, is expected to capture the black hole’s shadow on its accompanying disk of bright material. Computer simulations and the laws of gravitational physics give astronomers a pretty good idea of what to expect. Because of the intense gravity near a black hole, the disk’s light will be warped around the event horizon in a ring, so even the material behind the black hole will be visible. And the image will probably look asymmetrical: Gravity will bend light from the inner part of the disk toward Earth more strongly than the outer part, making one side appear brighter in a lopsided ring.
Does general relativity hold up close to a black hole? The exact shape of the ring may help break one of the most frustrating stalemates in theoretical physics.
The twin pillars of physics are Einstein’s theory of general relativity, which governs massive and gravitationally rich things like black holes, and quantum mechanics, which governs the weird world of subatomic particles. Each works precisely in its own domain. But they can’t work together.
“General relativity as it is and quantum mechanics as it is are incompatible with each other,” says physicist Lia Medeiros of the University of Arizona in Tucson. “Rock, hard place. Something has to give.” If general relativity buckles at a black hole’s boundary, it may point the way forward for theorists.
Since black holes are the most extreme gravitational environments in the universe, they’re the best environment to crash test theories of gravity. It’s like throwing theories at a wall and seeing whether — or how — they break. If general relativity does hold up, scientists expect that the black hole will have a particular shadow and thus ring shape; if Einstein’s theory of gravity breaks down, a different shadow.
Medeiros and her colleagues ran computer simulations of 12,000 different black hole shadows that could differ from Einstein’s predictions. “If it’s anything different, [alternative theories of gravity] just got a Christmas present,” says Medeiros, who presented the simulation results in January in Seattle at the American Astronomical Society meeting. Even slight deviations from general relativity could create different enough shadows for EHT to probe, allowing astronomers to quantify how different what they see is from what they expect. Do stellar corpses called pulsars surround the Milky Way’s black hole? Another way to test general relativity around black holes is to watch how stars careen around them. As light flees the extreme gravity in a black hole’s vicinity, its waves get stretched out, making the light appear redder. This process, called gravitational redshift, is predicted by general relativity and was observed near SgrA* last year (SN: 8/18/18, p. 12). So far, so good for Einstein.
An even better way to do the same test would be with a pulsar, a rapidly spinning stellar corpse that sweeps the sky with a beam of radiation in a regular cadence that makes it appear to pulse (SN: 3/17/18, p. 4). Gravitational redshift would mess up the pulsars’ metronomic pacing, potentially giving a far more precise test of general relativity.
“The dream for most people who are trying to do SgrA* science, in general, is to try to find a pulsar or pulsars orbiting” the black hole, says astronomer Scott Ransom of the National Radio Astronomy Observatory in Charlottesville, Va. “There are a lot of quite interesting and quite deep tests of [general relativity] that pulsars can provide, that EHT [alone] won’t.”
Despite careful searches, no pulsars have been found near enough to SgrA* yet, partly because gas and dust in the galactic center scatters their beams and makes them difficult to spot. But EHT is taking the best look yet at that center in radio wavelengths, so Ransom and colleagues hope it might be able to spot some.
“It’s a fishing expedition, and the chances of catching a whopper are really small,” Ransom says. “But if we do, it’s totally worth it.” How do some black holes make jets? Some black holes are ravenous gluttons, pulling in massive amounts of gas and dust, while others are picky eaters. No one knows why. SgrA* seems to be one of the fussy ones, with a surprisingly dim accretion disk despite its 4 million solar mass heft. EHT’s other target, the black hole in galaxy M87, is a voracious eater, weighing in at between about 3.5 billion and 7.22 billion solar masses. And it doesn’t just amass a bright accretion disk. It also launches a bright, fast jet of charged subatomic particles that stretches for about 5,000 light-years.
“It’s a little bit counterintuitive to think a black hole spills out something,” says astrophysicist Thomas Krichbaum of the Max Planck Institute for Radio Astronomy in Bonn, Germany. “Usually people think it only swallows something.”
Many other black holes produce jets that are longer and wider than entire galaxies and can extend billions of light-years from the black hole. “The natural question arises: What is so powerful to launch these jets to such large distances?” Krichbaum says. “Now with the EHT, we can for the first time trace what is happening.”
EHT’s measurements of M87’s black hole will help estimate the strength of its magnetic field, which astronomers think is related to the jet-launching mechanism. And measurements of the jet’s properties when it’s close to the black hole will help determine where the jet originates — in the innermost part of the accretion disk, farther out in the disk or from the black hole itself. Those observations might also reveal whether the jet is launched by something about the black hole itself or by the fast-flowing material in the accretion disk.
Since jets can carry material out of the galactic center and into the regions between galaxies, they can influence how galaxies grow and evolve, and even where stars and planets form (SN: 7/21/18, p. 16).
“It is important to understanding the evolution of galaxies, from the early formation of black holes to the formation of stars and later to the formation of life,” Krichbaum says. “This is a big, big story. We are just contributing with our studies of black hole jets a little bit to the bigger puzzle.”
Editor’s note: This story was updated April 1, 2019, to correct the mass of M87’s black hole; the entire galaxy’s mass is 2.4 trillion solar masses, but the black hole itself weighs in at several billion solar masses. In addition, the black hole simulation is an example of one that uphold’s Einstein’s theory of general relativity, not one that deviates from it.
