爱上海龙凤

Frog brains get busy long before they’re fully formed. Just a day after fertilization, embryonic brains begin sending signals to far-off places in the body, helping oversee the layout of complex patterns of muscles and nerve fibers. And when the brain is missing, bodily chaos ensues, researchers report online September 25 in Nature Communications.

The results, from brainless embryos and tadpoles, broaden scientists’ understanding of the types of signals involved in making sure bodies develop correctly, says developmental biologist Catherine McCusker of the University of Massachusetts Boston. Scientists are familiar with short-range signals among nearby cells that help pattern bodies. But because these newly described missives travel all the way from the brain to the far reaches of the body, they are “the first example of really long-range signals,” she says.
Celia Herrera-Rincon of Tufts University in Medford, Mass., and colleagues came up with a simple approach to tease out the brain’s influence on the growing body. Just one day after fertilization, the scientists lopped off the still-forming brains of African clawed frog embryos. These embryos survive to become tadpoles even without brains, a quirk of biology that allowed the researchers to see whether the brain is required for the body’s development.
The answer was a definite — and surprising — yes, Herrera-Rincon says. Long before the brain is mature, it’s already organizing and guiding organ behavior, she says. Brainless tadpoles had bungled patterns of muscles. Normally, muscle fibers form a stacked chevron pattern. But in tadpoles lacking a brain, this pattern didn’t form correctly. “The borders between segments are all wonky,” says study coauthor Michael Levin, also of Tufts University. “They can’t keep a straight line.”
Nerve fibers that crisscross tadpoles’ bodies also grew in an abnormal pattern. Levin and colleagues noticed extra nerve fibers snaking across the brainless tadpoles in a chaotic pattern, “a nerve network that shouldn’t be there,” he says.

Muscle and nerve abnormalities are the most obvious differences. But brainless tadpoles probably have more subtle defects in other parts of their bodies, such as the heart. The search for those defects is the subject of ongoing experiments, Levin says.
In addition to keeping patterns on point, the young frog brain may protect its body from chemical assaults. A molecule that binds to certain proteins on cells in the body had no effect on normal embryos. But when given to brainless embryos, the same molecule caused their spinal cords and tails to grow crooked. These results suggest that early in development, brains keep embryos safe from agents that would otherwise cause harm.

“The brain is instructing cells that are really a long way away from it,” Levin says. While the precise identities of these long-range signals aren’t known, the researchers have some ideas. When brainless embryos were dosed with a drug that targets cells that typically respond to the chemical messenger acetylcholine, the muscle pattern improved. Similarly, the addition of a protein called HCN2 that can tweak the activity of cells also seemed to improve muscle development. More work is needed before scientists know whether these interventions are actually mimicking messaging from the early brain, and if so, how.

Frog development isn’t the same as mammalian development, but frog development “is pretty applicable to human biology,” McCusker says. In fundamental ways, humans and frogs are built from the same molecular toolbox, she says. So the results hint that a growing human brain might also interact similarly with a growing human body.

The weird glowing blob of gas known as Hanny’s Voorwerp was a 10-year-old mystery. Now, Lia Sartori of ETH Zurich and colleagues have come to a two-pronged solution.

Hanny van Arkel, then a teacher in the Netherlands, discovered the strange bluish-green voorwerp, Dutch for “object,” in 2008 as she was categorizing pictures of galaxies as part of the Galaxy Zoo citizen science project.

Further observations showed that the voorwerp was a glowing cloud of gas that stretched some 100,000 light-years from the core of a massive nearby galaxy called IC 2497. The glow came from radiation emitted by an actively feeding black hole in the galaxy.
To excite the voorwerp’s glow, the black hole and its surrounding accretion disk, the active galactic nucleus, or AGN, should have had the brightness of about 2.5 trillion suns; its radio emission, however, suggested the AGN emitted the equivalent of a relatively paltry 25,000 suns. Either the AGN was obscured by dust, or the black hole slowed its eating around 100,000 years ago, causing its brightness to plunge.

Sartori and colleagues made the first direct measurement of the AGN’s intrinsic brightness using NASA’s NuSTAR telescope, which observed IC 2497 in high-energy X-rays that cut through the dust.

They found that the AGN is obscured by dust and it is dimmer than expected; the feeding has slowed way down. The team reported on arXiv.org on November 20 that IC 2497’s heart is as bright as 50 billion to 100 billion suns, meaning it dropped in brightness by a factor of 50 in the past 100,000 years — a less dramatic drop than previously thought.
“Both hypotheses that we thought before are true,” Sartori says.

Sartori plans to analyze NuSTAR observations of other voorwerpjes to see if their galaxies’ black holes are also in the process of shutting down — or even booting up.

“If you look at these clouds, you get information on how the black hole was in the past,” she says. “So we have a way to study how the activity of supermassive black holes varies on superhuman time scales.”

Editor’s note: This story was updated December 5, 2017, to clarify that the brightness measured by the researchers came from the accretion disk around an actively eating black hole, not the black hole itself.

Out of the hundreds of species of carnivorous plants found across the planet, none attract quite as much fascination as the Venus flytrap. The plants are native to just a small section of North Carolina and South Carolina, but these tiny plants can now be found around the world. They’re a favorite among gardeners, who grow them in homes and greenhouses.

Scientists, too, have long been intrigued by the plants and have extensively studied the famous trap. But far less is known about the flower that blooms on a stalk 15 to 35 centimeters above — including what pollinates that flower.
“The rest of the plant is so incredibly cool that most folks don’t get past looking at the active trap leaves,” says Clyde Sorenson, an entomologist at North Carolina State University in Raleigh. Plus, notes Sorenson’s NCSU colleague Elsa Youngsteadt, an insect ecologist, because flytraps are native to just a small part of North and South Carolina, field studies can be difficult. And most people who raise flytraps cut off the flowers so the plant can put more energy into making traps.

Sorenson and Youngsteadt realized that the mystery of flytrap pollination was sitting almost literally in their backyard. So they and their colleagues set out to solve it. They collected flytrap flower visitors and prey from three sites in Pender County, North Carolina, on four days in May and June 2016, being careful not to damage the plants.

“This is one of the prettiest places where you could work,” Youngsteadt says. Venus flytraps are habitat specialists, found only in certain spots of longleaf pine savannas in the Carolinas. “They need plenty of sunlight but like their feet to be wet,” says Sorenson. In May and June, the spots of savanna where the flytraps grow are “just delightful,” he says. And other carnivorous plants can be found there, too, including pitcher plants and sundews.
The researchers brought their finds back to the lab for identification. They also cataloged what kind of pollen was on flower visitors, and how much.
Nearly 100 species of arthropods visited the flowers, the team reports February 5 in American Naturalist. “The diversity of visitors on those flowers was surprising,” says Youngsteadt. However, only three species — a sweat bee and two beetles — appeared to be the most important, as they were either the most frequent visitors or carriers of the most pollen.
The study also found little overlap between pollinators and prey. Only 13 species were found both in a trap and on a flower, and of the nine potential pollinators in that group, none were found in high numbers.

For a carnivorous plant, “you don’t want to eat your pollinators,” Sorenson says. Flytraps appear to be doing a good job at that.

There are three ways that a plant can keep those groups separate, the researchers note. Flowers and traps could exist at different times of the year. However, that’s not the case with Venus flytraps. The plants produce the two structures at separate times, but traps stick around and are active during plant flowering.

Another possibility is the spatial separation of the two structures. Pollinators tend to be fliers while prey were more often crawling arthropods, such as spiders and ants. This matches up with the high flowers and low traps. But the researchers would like to do some experiments that manipulate the heights of the structures to see just how much that separation matters, Youngsteadt says.

The third option is that different scents or colors produced by flowers and traps might lure in different species to each structure. That’s another area for future study, Youngsteadt says. While attraction to scent and color are well documented for traps, little is now known about those factors for the flowers.

Venus flytraps are considered vulnerable to extinction, threatened by humans, Sorenson notes. The plant’s habitat is being destroyed as the population of the Carolinas grows. What is left of the habitat is being degraded as fires are suppressed (fires help clear vegetation and keep sunlight shining on the flytraps). And people steal flytraps from the wild by the thousands.

While research into their pollinators won’t help with any of those threats, it could aid in future conservation efforts. “Anything we can do to better understand how this plant reproduces will be of use down the road,” Sorenson says.

But what really excites the scientists is that they discovered something new so close to home. “One of the most thrilling parts of all this,” Sorenson says, “is that this plant has been known to science for [so long], everyone knows it, but there’s still a whole lot of things to discover.”

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.

First Man is not a movie about the moon landing.

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.

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.”

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.