上海花千坊会所

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.”

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.”

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.

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?’”

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.”