To help self-driving cars drive safely, scientists are looking to an unlikely place: the sea.
A new type of camera inspired by the eyes of mantis shrimps could help autonomous vehicles better gauge their surroundings, researchers report October 11 in Optica. The camera — which detects polarized light, or light waves vibrating on a single plane — has roughly half a million sensors that each capture a wide range of light and dark spots within a single frame, somewhat similar to how mantis shrimps see the world. The researchers wanted to “mimic the animals’ ability to detect a wide range of light intensities,” says coauthor Viktor Gruev, a bioengineer at the University of Illinois at Urbana-Champaign. The crustaceans’ visual system allows them to see both light and dark areas while moving in and out of dark crevices in shallow waters, he says.
The newly devised camera can take in a wider range of light intensities, measured in decibels, than other digital or polarization cameras. Previously, the best polarization cameras operated with a dynamic range of about 60 decibels; the new one works within a 140 decibel range, resulting in a clearer mapping of objects in the same frame.
Depending on the maker, autonomous vehicles currently use a mixture of methods to map the world around them, including lidar (light detection and ranging equipment), cameras and GPS. But the cameras currently guiding autonomous vehicles aren’t good at handling sharp lighting transitions and have trouble detecting features in foggy weather (SN: 12/24/16, p. 34). Because the new cameras are small and use many of the same parts as common digital cameras, Gruev says they could cost as little as $10.
From 2007 to 2016, the U.S. Food and Drug Administration flagged nearly 800 over-the-counter dietary supplements as tainted with potentially harmful pharmaceutical drugs, a study shows. Fewer than half of those products were recalled by their makers, scientists found.
Researchers analyzed the FDA’s public database of tainted supplements, identifying both the type of contaminating ingredients they contained and how the products were marketed. Most of these supplements, which are allowed to contain only dietary ingredients, included drugs such as steroids, the active ingredient in Viagra and a weight loss drug banned from the U.S. market eight years ago. The products had been marketed primarily for sexual enhancement, weight loss or muscle building, scientists report online October 12 in JAMA Network Open.
More than half of American adults have reported taking dietary supplements, such as vitamins, minerals and other specialty products. More than 85,000 supplements are estimated to be available in the United States, and the FDA says it cannot test all of them. No No’s These pharmaceutical ingredients are not permitted in dietary supplements, but were found to be contaminating supplements.
Sildenafil What it is: A medication that dilates blood vessels in the penis, and is the active ingredient in Viagra Health issue: Can lower blood pressure to levels that are unsafe for people taking medications for diabetes, high blood pressure or high cholesterol Supplement type: Sexual enhancement Sibutramine What it is: An appetite suppressant removed from the U.S. market in 2010 Health issue: Increased risk of heart attack or stroke Supplement type: Weight loss Phenolphthalein What it is: A laxative removed from the U.S. market in 1999 Health issue: Potential carcinogen Supplement type: Weight loss Anabolic steroids What they are: Chemicals related to the male sex hormone testosterone Health issue: Associated with liver injury, kidney damage, heart attack and stroke Supplement type: Muscle building Aromatase inhibitors What they are: A class of drugs that lower estrogen levels, and are used to treat breast cancer Health issue: Associated with decreased bone growth, infertility, liver dysfunction Supplement type: Muscle building These supplements aren’t subject to the same regulations, testing and approval process that are required for pharmaceutical drugs. But if the FDA identifies tainted supplements after they’re on the market, the agency can issue public warnings or suggest the company voluntarily remove the product.
Whether that approach is effective raises questions, though, says general internist Pieter Cohen of Cambridge Health Alliance in Cambridge, Mass., who was not involved in the new work. Voluntary recalls don’t necessarily mean a product is completely removed from shelves or that consumers become aware and stop using a product, Cohen’s research has found.
And only 360 of the 776 supplements flagged as tainted from 2007 to 2016 were recalled, the study found. “What really jumped out at me,” Cohen says, is that “when the FDA detects drugs in supplements, more than half the time the product isn’t even recalled.”
Supplement use does carry health risks. A 2015 study estimated that 23,000 emergency room visits each year are due to health problems related to dietary supplements. Of those, about 2,100 patients are hospitalized annually, commonly for symptoms related to heart trouble. In 2013, 20 percent of drug-induced liver injury cases recorded in the Drug-Induced Liver Injury Network registry were caused by dietary supplements. That’s up from 7 percent in 2004. Liver damage can be fatal or require a liver transplant. A 2013 report by the U.S. Centers for Disease Control and Prevention on 29 cases of liver injury found that 24 of those patients reported using a dietary supplement for weight loss.
“The law allows companies to advertise supplements as if they’re good for your health, even if there’s no evidence in humans that that’s the case,” Cohen says. He began studying dietary supplements after noting that his patients developed health problems, including panic attacks, chest pain and kidney failure, related to weight-loss supplements. One patient was suspended from his job when his urine tested positive for amphetamine; a chemical derivative of the drug was found in the weight-loss pills that he was taking.
Cohen’s recommendation? Avoid supplements “that promise you anything.”
The Neil Armstrong biopic, opening October 12, follows about eight years of the life of the first man on the moon, and spends about eight minutes depicting the lunar surface. Instead of the triumphant ticker tape parades that characterize many movies about the space race, First Man focuses on the terror, grief and heartache that led to that one small step.
“It’s a very different movie and storyline than people expect,” says James Hansen, author of the 2005 biography of Armstrong that shares the film’s name and a consultant on the film. The story opens shortly before Armstrong’s 2-year-old daughter, Karen, died of a brain tumor in January 1962. That loss hangs over the rest of the film, setting the movie’s surprisingly somber emotional tone. The cinematography is darker than most space movies. Colors are muted. Music is ominous or absent — a lot of scenes include only ambient sound, like a pen scratching on paper, a glass breaking or a phone clicking into the receiver. Karen’s death also seems to motivate the rest of Armstrong’s journey. Getting a fresh start may have been part of the reason why the grieving Armstrong (portrayed by Ryan Gosling) applied to the NASA Gemini astronaut program, although he never explicitly says so. And without giving too much away, a private moment Armstrong takes at the edge of Little West crater on the moon recalls his enduring bond with his daughter.
Hansen’s book also makes the case that Karen’s death motivated Armstrong’s astronaut career. Armstrong’s oldest son, Rick, who was 12 when his father landed on the moon, agrees that it’s plausible. “But it’s not something that he ever really definitively talked about,” Rick Armstrong says.
Armstrong’s reticence about Karen — and almost everything else — is true to life. That’s not all the film got right. Gosling captured Armstrong’s gravitas as well as his humor, and Claire Foy as his wife, Janet Armstrong, “is just amazing,” Rick Armstrong says.
Beyond the performances, the filmmakers, including director Damien Chazelle and screenwriter Josh Singer, went to great lengths to make the technical aspects of spaceflight historically accurate. The Gemini and Apollo cockpits Gosling sits in are replicas of the real spacecraft, and he flipped switches and hit buttons that would have controlled real flight. Much of the dialog during space scenes was taken verbatim from NASA’s control room logs, Hansen says.
The result is a visceral sense of how frightening and risky those early flights were. The spacecraft rattled and creaked like they were about to fall apart. The scene of Armstrong’s flight on the 1966 Gemini 8 mission, which ended early when the spacecraft started spinning out of control and almost killed its passengers, is terrifying. The 1967 fire inside the Apollo 1 spacecraft, which killed astronauts Ed White, Gus Grissom and Roger Chaffee, is gruesome.
“We wanted to treat that one with extreme care and love and get it exactly right,” Hansen says. “What we have in that scene, none of it’s made up.”
Even when the filmmakers took poetic license, they did it in a historical way. A vomit-inducing gyroscope that Gosling rides in during Gemini astronaut training was, in real life, used for the earlier Mercury astronauts, but not for Gemini, for instance. Since the Mercury astronauts never experienced the kind of dizzying rotation that the gyroscope mimicked, NASA dismantled it before the next group of astronauts arrived.
“They probably shouldn’t have dismantled it,” Hansen says — it did simulate what ended up happening in the Gemini 8 accident. So the filmmakers used the gyroscope experience as foreshadowing.
Meanwhile, present-day astronauts are not immune to harrowing brushes with death: a Russian Soyuz capsule carrying two astronauts malfunctioned October 11, and the astronauts had to evacuate in an alarming “ballistic descent.” NASA is currently talking about when and how to send astronauts back to the moon from American soil. The first commercial crew astronauts, who will test spacecraft built by Boeing and SpaceX, were announced in August.
First Man is a timely and sobering reminder of the risks involved in taking these giant leaps.
Animated characters can learn from online tutorials, too.
A new computer program teaches virtual avatars new skills, such as dances, acrobatic stunts and martial art moves, from YouTube videos. This kind of system, described in the November ACM Transactions on Graphics, could render more physically coordinated characters for movies and video games, or serve as a virtual training ground for robots.
“I was really impressed” by the program, says Daniel Holden, a machine-learning researcher at Ubisoft La Forge in Montreal not involved in the work. Rendering accurate, natural-looking movements based on everyday video clips “has always been a goal for researchers in this field.” Animated characters typically have learned full-body motions by studying motion capture data, collected by a camera that tracks special markers attached to actors’ bodies. But this technique requires special equipment and often works only indoors.
The new program leverages a type of computer code known as an artificial neural network, which roughly mimics how the human brain processes information. Trained on about 100,000 images of people in various poses, the program first estimates an actor’s pose in each frame of a video clip. Then, it teaches a virtual avatar to re-create the actor’s motion using reinforcement learning, giving the character a virtual “reward” when it matches the video actor’s pose in a frame.
Computer scientist Jason Peng and colleagues at the University of California, Berkeley, fed YouTube videos into the system to teach characters to do somersaults, backflips, vaulting and other stunts. Even characters such as animated Atlas robots with bodies drastically different from those of their human video teachers mastered these motions (SN: 12/13/14, p. 16). Characters could also perform under conditions not seen in the training video, like cartwheeling while being pelted with blocks or moving across terrain riddled with holes. The work, also reported October 8 at arXiv.org, is a step “toward making motion capture easier, cheaper and more accessible,” Holden says. Videos could be used to render virtual versions of outdoor activities, since motion capture is difficult to do outdoors, or to create lifelike avatars of large animals that would be difficult to stick with motion capture markers.
This kind of program may also someday be used to teach robots new skills, Peng says. An animated version of a robot could master skills in a virtual environment before that learned computer code powered a machine in the physical world.
These animated characters still struggle with nimble dance steps, such as the “Gangnam Style” jig, and learn from short clips featuring only a single person. David Jacobs, a computer scientist at the University of Maryland in College Park not involved in the work, looks forward to future virtual avatars that can reenact longer, more complex actions, such as pairs of people dancing or soccer teams playing a game.
“That’s probably a much harder problem, because [each] person’s not as clearly visible, but it would be really cool,” Jacobs says. “This is only the beginning.”
SAN DIEGO — Mice yanked out of their community and held in solitary isolation show signs of brain damage.
After a month of being alone, the mice had smaller nerve cells in certain parts of the brain. Other brain changes followed, scientists reported at a news briefing November 4 at the annual meeting of the Society for Neuroscience.
It’s not known whether similar damage happens in the brains of isolated humans. If so, the results have implications for the health of people who spend much of their time alone, including the estimated tens of thousands of inmates in solitary confinement in the United States and elderly people in institutionalized care facilities.
The new results, along with other recent brain studies, clearly show that for social species, isolation is damaging, says neurobiologist Huda Akil of the University of Michigan in Ann Arbor. “There is no question that this is changing the basic architecture of the brain,” Akil says. Neurobiologist Richard Smeyne of Thomas Jefferson University in Philadelphia and his colleagues raised communities of multiple generations of mice in large enclosures packed with toys, mazes and things to climb. When some of the animals reached adulthood, they were taken out and put individually into “a typical shoebox cage,” Smeyne said.
This abrupt switch from a complex society to isolation induced changes in the brain, Smeyne and his colleagues later found. The overall size of nerve cells, or neurons, shrunk by about 20 percent after a month of isolation. That shrinkage held roughly steady over three months as mice remained in isolation. To the researchers’ surprise, after a month of isolation, the mice’s neurons had a higher density of spines — structures for making neural connections — on message-receiving dendrites. An increase in spines is a change that usually signals something positive. “It’s almost as though the brain is trying to save itself,” Smeyne said.
But by three months, the density of dendritic spines had decreased back to baseline levels, perhaps a sign that the brain couldn’t save itself when faced with continued isolation. “It’s tried to recover, it can’t, and we start to see these problems,” Smeyne said.
The researchers uncovered other worrisome signals, too, including reductions in a protein called BDNF, which spurs neural growth. Levels of the stress hormone cortisol changed, too. Compared with mice housed in groups, isolated mice also had more broken DNA in their neurons.
The researchers studied neurons in the sensory cortex, a brain area involved in taking in information, and the motor cortex, which helps control movement. It’s not known whether similar effects happen in other brain areas, Smeyne says.
It’s also not known how the neural changes relate to mice’s behavior. In people, long-term isolation can lead to depression, anxiety and psychosis. Brainpower is affected, too. Isolated people develop problems reasoning, remembering and navigating.
Smeyne is conducting longer-term studies aimed at figuring out the effects of neuron shrinkage on thinking skills and behavior. He and his colleagues also plan to return isolated mice to their groups to see if the brain changes can be reversed. Those types of studies get at an important issue, Akil says. “The question is, ‘When is it too far gone?’”
The cause of a rare polio-like disease continues to elude public health officials even as the number of U.S. cases grows.
Confirmed cases of acute flaccid myelitis cases have risen to 90 in 27 states, out of a possible 252 under investigation, the U.S. Centers for Disease Control and Prevention announced November 13. That’s up from 62 confirmed cases out of 127 suspected just a month ago (SN Online: 10/16/18). There were a record 149 cases in 2016. “I understand parents want answers,” Nancy Messonnier, director of the CDC’s National Center for Immunization and Respiratory Diseases in Atlanta, said at a news conference. The agency continues to investigate the disease, which causes weakness in one or more limbs and primarily affects children. But “right now the science doesn’t give us an answer,” she said.
A deep dive into 80 of the confirmed cases offered some details about the course of AFM. In most, fever or respiratory symptoms like coughing and congestion, or both, preceded limb weakness by three to 10 days. Most cases involved weakness in an upper limb, researchers report online November 13 in the Morbidity and Mortality Weekly Report.
Only two samples of cerebrospinal fluid — the clear fluid that bathes the brain and spinal cord — tested positive for a pathogen, each for a different enterovirus. Since 2014, when the first big outbreak of AFM occurred, most AFM spinal fluid samples haven’t produced a culprit, Messonnier said. The body may clear the pathogen or it hides in tissues, she said, or the body’s own immune response to a pathogen may lead to spinal cord damage.
“This time of year, many children have fever and respiratory symptoms [and] most of them do not go on to develop AFM,” Messonnier said. “We’re trying to figure out what the triggers are that would cause someone to develop AFM later.”
A proton’s mass is more than just the sum of its parts. And now scientists know just what accounts for the subatomic particle’s heft.
Protons are made up of even smaller particles called quarks, so you might expect that simply adding up the quarks’ masses should give you the proton’s mass. However, that sum is much too small to explain the proton’s bulk. And new, detailed calculations show that only 9 percent of the proton’s heft comes from the mass of constituent quarks. The rest of the proton’s mass comes from complicated effects occurring inside the particle, researchers report in the Nov. 23 Physical Review Letters.
Quarks get their masses from a process connected to the Higgs boson, an elementary particle first detected in 2012 (SN: 7/28/12, p. 5). But “the quark masses are tiny,” says study coauthor and theoretical physicist Keh-Fei Liu of the University of Kentucky in Lexington. So, for protons, the Higgs explanation falls short.
Instead, most of the proton’s 938 million electron volts of mass is due to complexities of quantum chromodynamics, or QCD, the theory which accounts for the churning of particles within the proton. Making calculations with QCD is extremely difficult, so to study the proton’s properties theoretically, scientists rely on a technique called lattice QCD, in which space and time are broken up into a grid, upon which the quarks reside. Using this technique, physicists had previously calculated the proton’s mass (SN: 12/20/08, p. 13). But scientists hadn’t divvied up where that mass comes from until now, says theoretical physicist André Walker-Loud of Lawrence Berkeley National Laboratory in California. “It’s exciting because it’s a sign that … we’ve really hit this new era” in which lattice QCD can be used to better understand nuclear physics.
In addition to the 9 percent of the proton’s mass that comes from quarks’ heft, 32 percent comes from the energy of the quarks zipping around inside the proton, Liu and colleagues found. (That’s because energy and mass are two sides of the same coin, thanks to Einstein’s famous equation, E=mc2.) Other occupants of the proton, massless particles called gluons that help hold quarks together, contribute another 36 percent via their energy.
The remaining 23 percent arises due to quantum effects that occur when quarks and gluons interact in complicated ways within the proton. Those interactions cause QCD to flout a principle called scale invariance. In scale invariant theories, stretching or shrinking space and time makes no difference to the theories’ results. Massive particles provide the theory with a scale, so when QCD defies scale invariance, protons also gain mass.
The results of the study aren’t surprising, says theoretical physicist Andreas Kronfeld of Fermilab in Batavia, Ill. Scientists have long suspected that the proton’s mass was made up in this way. But, he says, “this kind of calculation replaces a belief with scientific knowledge.”
Locust: The Opera finds a novel way to doom a soprano: species extinction.
The libretto, written by entomologist Jeff Lockwood of the University of Wyoming in Laramie, features a scientist, a rancher and a dead insect. The scientist tenor agonizes over why the Rocky Mountain locust went extinct at the dawn of the 20th century. He comes up with hypotheses, three of which unravel to music and frustration.
The project hatched in 2014. “Jeff got in his head, ‘Oh, opera is a good way to tell science stories,’ which takes a creative mind to think that,” says Anne Guzzo, who composed the music. Guzzo teaches music theory and composition at the University of Wyoming. locust brought famine and ruin to farms across the western United States. “This was a devastating pest that caused enormous human suffering,” Lockwood says. Epic swarms would suddenly descend on and eat vast swaths of cropland. “On the other hand, it was an iconic species that defined and shaped the continent.” Lockwood had written about the locust’s mysterious and sudden extinction in the 2004 book Locust , but the topic “begged in my mind for the grandeur of opera.” He spent several years mulling how to create a one-hour opera for three singers about the swarming grasshopper species. Then the ghost of Hamlet’s father, in the opera “Amleto,” based on Shakespeare’s play, inspired a breakthrough. Lockwood imagined a spectral soprano locust, who haunted a scientist until he figured out what killed her kind.
To make one locust soprano represent trillions, Guzzo challenged her music theory class to find ways of evoking the sound of a swarm. They tried snapping fingers, rattling cardstock and crinkling cellophane. But “the simplest answer was the most elegant,” Guzzo says — tasking the audience with shivering sheets of tissue paper in sequence, so that a great wave of rustling swept through the auditorium.
For the libretto, Lockwood took an unusually data-driven approach. After surveying opera lengths and word counts, he paced his work at 25 to 30 words per minute, policing himself sternly. If a scene was long by two words, he’d find two to cut. He wrote the dialogue not in verse, but as conversation, some of it a bit professorial. Guzzo asked for a few line changes. “I just couldn’t get ‘manic expressions of fecundity’ to fit where I wanted it to,” she says. Eventually, the scientist solves the mystery, but takes no joy in telling the beautiful locust ghost that humans had unwittingly doomed her kind by destroying vital locust habitat. For tragedy, Lockwood says, “there has to be a loss tinged with a kind of remorse.”
The opera, performed twice in Jackson, Wyo., will next be staged in March in Agadir, Morocco.
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.