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The U.S. Environmental Protection Agency has a methane problem — and that could misinform the country’s carbon-cutting plans. Recent studies suggest that the agency’s reports fail to capture the full scope of U.S. methane emissions, including “super emitters” that contribute a disproportionate share of methane release. Those EPA reports influence the country’s actions to combat climate change and the regulation of methane-producing industries such as agriculture and natural gas production.

With EPA’s next annual methane report due to be published by April 15, early signs suggest that the agency is taking steps to fix the methane mismatch. A preliminary draft of the report revises the agency’s methane calculations for 2013 — the most recent year reported — upward by about 27 percent for the natural gas and petroleum sectors, a difference of about 2 million metric tons.
Yet it’s unclear how that and other revisions will factor into final methane emission totals in the upcoming report. The draft estimates that U.S. methane emissions from all sources in 2014 were about 28 million metric tons, up slightly from the revised estimate for 2013 and well above the original 2013 estimate of 25.453 million metric tons. But the totals in the draft don’t include updates to emission estimates from the oil and gas industry.
“EPA is reviewing the substantial body of new studies that have become available in the past year on the natural gas and petroleum sector,” says EPA spokesperson Enesta Jones. The agency is also gathering feedback from scientists and industry experts to further improve their reporting.

Methane, which makes up the bulk of natural gas, originates from natural sources, such as wetlands, as well as from human activities such as landfills, cattle ranches (SN: 11/28/15, p. 22) and the oil and gas industry. Globally, human activities release about 60 percent of the 600 million metric tons of methane emitted into the atmosphere each year. Once in the air, methane prevents some of Earth’s heat from escaping into space, causing a warming effect. Methane emissions currently account for about a quarter of human-caused global warming.

The EPA’s underestimation of U.S. methane emissions comes down to accounting. EPA samples emissions from known methane sources, such as cows or natural gas pipelines, and works out an average. That average is then multiplied by the nation’s number of cows, lengths of pipe and other methane sources. Results from this method disagree with satellite and land-based observations that measure changes in the total amount of methane in the air. A 2013 report in the Proceedings of the National Academy of Sciences found that U.S. methane emissions based on atmospheric measurements are about 50 percent larger than EPA estimates (SN Online: 11/25/13).
EPA’s reports don’t just misjudge the scale of emissions, they also miss the long-term trend, recent work suggests. EPA reported that U.S. methane emissions remained largely unchanged from 2002 to 2014. But researchers report online March 2 in Geophysical Research Letters that emissions of the greenhouse gas rose more than 30 percent over that period. The United States could be responsible for as much as 30 to 60 percent of the global increase in methane emissions over the last decade, the study’s authors conclude. “We’re definitely not a small piece of that pie,” says Harvard University atmospheric scientist Alex Turner, who coauthored the study.
Correctly tracking methane is important, Turner says, because over a 100-year period, the warming impact of methane is more than 25 times that of the same amount of CO2. Methane levels have also risen faster: Since the start of the industrial revolution, methane concentrations have more than doubled while CO2 has risen more than 40 percent.

While methane is more potent than CO2, there is about 200 times less methane in the atmosphere than CO2. Furthermore, methane stays in the atmosphere for only around 12 years before being absorbed by soil or breaking apart in chemical reactions. “If we reduce methane emissions, the climate responds very quickly and global warming would slow down almost immediately,” says Cornell University earth systems scientist Robert Howarth. “CO2, on the other hand, has an influence that will go hundreds to even thousands of years into the future.”

Turner and colleagues tracked methane across the continental United States using land stations that measure methane in the air and satellite observations that record dips in the infrared radiation frequencies absorbed and reemitted by methane. The researchers compared these methane measurements with those taken over Bermuda and the North Pacific Ocean — places upwind of the United States and far from major methane sources.

From 2002 through 2014, methane concentrations over the continental United States grew faster than those over the oceans, the researchers found. The difference was most pronounced over the central United States, where methane concentrations rose nearly twice as fast as in the rest of the country. Natural gas drilling and production boomed in in the central United States during the period studied, though the researchers could not precisely trace the source of the additional methane.

Turner and colleagues say they’re now working with EPA to reconcile the methane estimates. EPA will provide small-scale estimates of methane emissions down to a 10-kilometer-wide grid. By combining that grid with space and land observations, scientists should be able to isolate where methane mismatches are the most pronounced.

While Turner’s research can’t pinpoint the exact origins of the additional methane, other studies point to the oil and gas industry. The numbers that the EPA uses to tabulate methane emissions assume that equipment is functioning as intended, says Stanford University sustainability engineer Adam Brandt. Malfunctioning equipment can spew huge amounts of methane. That became abundantly – and visibly – clear last October when the largest U.S. methane leak in history began in an underground storage facility near Los Angeles. The leak released 97,100 metric tons of methane, equivalent to the annual greenhouse gas emissions of 572,000 cars, before being permanently sealed in February, researchers estimated in the March 18 Science.

Super methane emitters are a big problem elsewhere, too, albeit typically much smaller than the California leak, researchers report in the June 2016 Environmental Pollution. Surveying emissions from 100 natural gas leaks around Boston, the researchers found that 7 percent of leaks contributed half of the total methane released. In 2014, a different research team reported in Environmental Science & Technology that 19 percent of pneumatic controllers used at natural gas production sites accounted for 95 percent of all controller emissions.

Monitoring and quick repairs can stamp out rogue methane sources quickly, Brandt says. “This is a problem that’s easier to fix than it is to understand,” he says.

Most people do not marvel much at sand. We may enjoy how it feels under our bare feet, or get annoyed when someone tracks it into the house. But few of us see those quartz grains the way geologist Walter Alvarez does — as the product of 4.5 billion years of improbable cosmic and geologic events that defined the course of human history.

Sandy beaches exist because silicon — a relatively rare element in the solar system — happened to become concentrated on Earth during the solar system’s early days, Alvarez, of the University of California, Berkeley, writes in A Most Improbable Journey. While powerful solar particles swept lighter, gaseous elements toward the outer planets, more massive, mineral-forming elements such as silicon, magnesium and iron were left behind for Earth. Later on, in the molten crucibles between Earth’s colliding tectonic plates, these elements formed the raw materials for pivotal human inventions, including stone tools, glass and computer chips.
The 4.5 billion years of history that led to a computer chip is just one of many stories of scientific happenstance that Alvarez presents. Best known for proposing that an asteroid impact killed off the dinosaurs, Alvarez argues that rare, unpredictable cosmic, geologic and biological events — what he calls “contingencies” — are key to understanding the human condition.

Fans of Bill Bryson’s A Short History of Nearly Everything will appreciate Alvarez’s enthusiastic, clearly written tour of contingencies that have shaped our world, starting with the origins of life on Earth. No matter how distant the event, Alvarez quickly zeroes in on its eventual impact on people: For instance, the formation of oceanic crust helped expose rich deposits of copper ore on Cyprus, later an epicenter of the Bronze Age. A catastrophic Ice Age flood formed the English Channel in which the Spanish Armada would later sink. And ancient rivers in North America smoothed the terrain of the westward trail for American pioneers in covered wagons.

Not all of Alvarez’s arguments are convincing — his claim in the final chapter that every individual is a “contingency” in his or her own right, given how many other people could have been born instead, feels more flattering than important. Still, it’s hard to argue with his observation that impulsive human actions can transform the planet just as much as earthquakes, asteroids and other difficult-to-predict, occasionally world-changing phenomena.

Critics of this macro view, described in academia as “Big History,” say that the approach sacrifices important nuance and detail. At roughly 200 pages of text, however, A Most Improbable Journey does not claim to be a comprehensive account of history or a replacement for more detailed, focused examinations of the past. Instead, it makes a compelling case for Big History as a fun, perspective-stretching exercise — a way to dust off familiar topics and make them sparkle.

WASHINGTON — It has been used by an assassin wielding a poisoned umbrella and sent in a suspicious letter to a president.

Ricin, the potent toxin and bioterrorism agent, has no antidote and can cause death within days. But a cocktail of antibodies could one day offer victims at least a slim window for treatment.

A new study presented February 7 at the American Society for Microbiology’s Biothreats meeting reveals a ricin antidote that, in mice, works even days after exposure to the toxin. Another presented study offers a potential explanation for how such an antidote might work.
Doctors need some way to deal with ricin poisoning, said Patrick Cherubin, a cell biologist at the University of Central Florida in Orlando. Immunologist Nicholas Mantis agreed: “There is no specific treatment or therapy whatsoever.”

Though ricin has an innocuous origin (it’s found in castor beans), the poison is anything but harmless. It’s dangerous and relatively easy to spread — rated by the U.S. Centers for Disease Control and Prevention as a category B bioterrorism agent, just behind the highest-risk category A agents such as anthrax, plague and Ebola.

Ricin poisoning is rare but has featured in some high-profile cases. In 1978, Bulgarian writer Georgi Markov was hit in the thigh with a ricin-poisoned pellet shot from an umbrella gun. A few days later, he was dead. In 2013, a letter addressed to President Barack Obama tested positive for granules of the deadly toxin. A Texas woman had ordered castor bean seeds and lye online, for a do-it-yourself approach to making ricin. No one was injured.

Symptoms of ricin poisoning depend on how the toxin enters the body, and how much gets in. Inhaling ricin can make breathing so difficult the skin turns blue. Ingesting ricin can cause diarrhea, vomiting and seizures. Death can come as soon as 36 hours after exposure.

Ricin is known as an RIP — a scary-sounding acronym that stands for ribosome-inactivating protein, said Mantis, of the New York State Department of Health in Albany. In the cell, ribosomes serve as tiny protein factories. After ricin exposure, “the whole machinery comes to a screeching halt,” Mantis said. For cells, shutting down protein factories for too long is a death sentence.
Scientists have developed two vaccines for ricin, though neither is available yet for use in humans. A vaccine may be “good for soldiers going into the field,” said biochemist Ohad Mazor of the Israel Institute for Biological Research in Ness Ziona. But unvaccinated people are out of luck.
Mazor and colleagues developed a new treatment that could potentially help. The treatment is a mixture of three proteins called neutralizing antibodies; they grab onto ricin and don’t easily let go. With antibodies hanging onto its back, ricin has trouble slipping into cells and wreaking its usual havoc.
Even 48 hours after inhaling ricin, roughly 73 percent of mice, 22 out of 30, treated with the antibodies survived, the team reported at the meeting and in a paper published in the March 1 Toxicon. Untreated mice died within a week.

Previous antibody treatments for ricin work well only if mice are treated within hours after exposure, Mazor said. For poisoned humans, that may not be long enough to diagnose the problem. Mazor doesn’t know how his antibodies might work in people, but he’d like to follow up his mouse work with studies in monkeys or pigs.

Scientists haven’t figured out exactly how antibodies help animals recover, but another study presented at the meeting offers a clue. Cherubin and colleagues added ricin to monkey cells in a dish, and then tracked how much protein was manufactured by the cells.

At high enough levels, ricin exposure shuttered the factories as expected. But when researchers stopped exposing cells to the toxin, protein synthesis started up again and cells recovered. “You need ongoing toxin delivery to eventually kill the cell,” Cherubin said. It’s possible that antibody treatments could cut off ricin delivery to cells, letting them bounce back from poisoning, said study coauthor Ken Teter, also a cell biologist at the University of Central Florida.

A strain of wild Hawaiian worms has helped unmask long-studied genes as just plain selfish. The scammers beat the usual odds of inheritance and spread extra fast by making mother worms poison some of their offspring.

Biologists have for decades discussed how two genes in the familiar lab nematode Caenorhabditis elegans might help embryos build their organs. Working with a little-studied wild strain, however, caused a rethink of the genes’ supposedly beneficial role “that flipped it on its head,” says UCLA geneticist Leonid Kruglyak.
Instead of doing some body sculpting, the gene sup-35 doses the eggs with a toxin that will kill them after fertilization, two postdocs in the Kruglyak lab discovered. The toxin gene doesn’t poison itself out of the gene pool because it’s linked to a partner, pha-1, that lets embryos manufacture an antidote. Embryos die unless they inherit a copy of the antidote gene in either egg or sperm, and so the poison-antidote duo can spread unusually fast through populations.

Making a mom on occasion poison some of her offspring doesn’t benefit her but certainly helps the genes. Thus the long-known sup-35 and pha-1 form what’s called a selfish genetic element, Kruglyak’s team proposes May 11 in Science.

That analysis is “very clearly accurate,” says evolutionary geneticist Jack Werren of the University of Rochester in New York. The idea that a gene could behave selfishly, promoting its own spread regardless of its host’s interests, was once controversial (SN: 3/19/16, p. 12). But as molecular biology techniques have improved, researchers have found more and more examples. Many of the most dramatic forms of selfishness, the murderous cheats, come from bacteria, so Werren welcomes the C. elegans scam as a rare case discovered in animals.
Kruglyak’s lab has described an earlier example in C. elegans: a gene that doses sperm with a toxin that kills embryos unless an antidote gene rescues them. Finding a second selfish element in the nematode, he says, suggests that these may not be as rare in animals as people have thought.
The big community of researchers regularly studying C. elegans had missed discovering the selfish role for a simple reason: The main lab strain of nematodes carries the selfish element, explains study coauthor Eyal Ben-David. Whenever the standard strain mates or self-fertilizes (the species has both males and hermaphrodites), all the offspring inherit sup-35 and pha-1. Researchers see no weird die-offs.

In the Kruglyak lab, however, Ben-David and fellow postdoc Alejandro Burga were doing a project that required crossing the usual lab nematodes with the DL238 strain from Hawaii. In its natural state, this strain has somehow escaped invasion by the selfish sup-35/pha-1 pair.

A series of oddities in interbreeding the disparate strains pushed the researchers to reconsider the two genes. For instance, much higher percentages of offspring died in mixed-parent crosses than the routine few percent in same-strain pairings. And when Ben-David and Burga looked at the genes in the Hawaiian strain isolated from the wild, sup-35 and pha-1 just weren’t there.

That was a shock. Earlier experiments in the lab strain had shown that disabling pha-1 caused death in offspring — which it certainly does. The feeding tube of the dying embryos was not forming properly, so researchers at first speculated that the gene controlled tube development. Later work suggested a more nuanced role for it, Ben-David says, but the overall hypothesis remained that the genes helped regulate embryo development. The Hawaiian strain changed that thinking: “How is this wild isolate alive and happy without a gene that’s supposed to be essential for development?” Kruglyak wanted to know.

A better way of interpreting the old experiments, he and his colleagues suggest, is that the embryos died because pha-1 wasn’t providing the antidote to the sup-35 toxin. “No one had previously considered the possibility,” says David S. Fay of the University of Wyoming in Laramie, who has done much of the work exploring the role of these genes. “All the data, including a lot of our previous published and unpublished findings, seem to fit the [selfish gene] model perfectly,” he says. And perhaps the highest praise: “I wish we had somehow come up with the solution ourselves.”

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.

As far as last meals go, squid isn’t a bad choice. Cephalopod remains appear to dominate the stomach contents of a newly analyzed ichthyosaur fossil from nearly 200 million years ago.

The ancient marine reptiles once roamed Jurassic seas and commonly pop up in England’s fossil-rich coast near Lyme Regis. But a lot of ichthyosaur museum specimens lack records of where they came from, making their age difficult to place.

Dean Lomax of the University of Manchester and his colleagues reexamined one such fossil. Based on its skull, they identified the creature as a newborn Ichthyosaurus communis. Microfossils of shrimp and amoeba species around the ichthyosaur put the specimen at 199 million to 196 million years old, the researchers estimate.

Tiny hook structures stand out in the newborn’s ribs — most likely the remnants of prehistoric black squid arms. Another baby ichthyosaur fossil that lived more recently had a stomach full of fish scales. So the new find suggests a shift in the menu for young ichthyosaurs at some point in their evolutionary history, the researchers write October 3 in Historical Biology.

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.”

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?’”