DNA is the glamour molecule of the genetics world. Its instructions are credited with defining appearance, personality and health. And the proteins that result from DNA’s directives get credit for doing most of the work in our cells. RNA, if mentioned at all, is considered a mere messenger, a go-between — easy to ignore. Until now.

RNAs, composed of strings of genetic letters called nucleotides, are best known for ferrying instructions from the genes in our DNA to ribosomes, the machines in cells that build proteins. But in the last decade or so, researchers have realized just how much more RNAs can do — how much they control, even. In particular, scientists are finding RNAs that influence health and disease yet have nothing to do with being messengers.

The sheer number and variety of noncoding RNAs, those that don’t ferry protein-building instructions, give some clues to their importance. So far, researchers have cataloged more than 25,000 genes with instructions for noncoding RNAs in the human genome, or genetic instruction book (SN: 10/13/18, p. 5). That’s more than the estimated 21,000 or so genes that code for proteins.

Those protein-coding genes make up less than 2 percent of the DNA in the human genome. Most of the rest of the genome is copied into noncoding RNAs, and the vast majority of those haven’t been characterized yet, says Pier Paolo Pandolfi of Boston’s Beth Israel Deaconess Medical Center. “We can’t keep studying just two volumes of the book of life. We really need to study them all.”
Scientists no longer see the RNAs that aren’t envoys between DNA and ribosomes as worthless junk. “I believe there are hundreds, if not thousands, of noncoding RNAs that have a function,” says Harvard University molecular biologist Jeannie Lee. She and other scientists are beginning to learn what these formerly ignored molecules do. It turns out that they are involved in every step of gene activity, from turning genes on and off to tweaking final protein products. Those revelations were unthinkable 20 years ago.

Back in the 1990s, Lee says, scientists thought only proteins could turn genes on and off. Finding that RNAs were in charge “was a very odd concept.”

Here are five examples among the many noncoding RNAs that are now recognized as movers and shakers in the human body, for good and ill.
Sometimes anticancer drugs stop working for reasons researchers don’t entirely understand. Take the chemotherapy drug cytarabine. It’s often the first drug doctors prescribe to patients with a blood cancer called acute myeloid leukemia. But cytarabine eventually stops working for about 30 to 50 percent of AML patients, and their cancer comes back.

Researchers have looked for defects in proteins that may be the reason cytarabine and other drugs fail, but there still isn’t a complete understanding of the problem, Pandolfi says. He and colleagues now have evidence that drug resistance may stem from problems in some of the largest and most bountiful of the newly discovered classes of RNAs, known as long noncoding RNAs. Researchers have already cataloged more than 18,000 of these “lncRNAs” (pronounced “link RNAs”).
Pandolfi and colleagues investigated how some lncRNAs may work against cancer patients who are counting on chemotherapy to fight their disease. “We found hundreds of new players that can regulate response to therapy,” he says.

When the researchers boosted production of several lncRNAs in leukemia cells, the cells became resistant to cytarabine, Pandolfi and colleagues reported in April 2018 in Cell. They also found that patients with AML who had higher than normal levels of two lncRNAs experienced a cancer recurrence sooner than people who had lower levels of those lncRNAs.

Researchers are just beginning to understand how these lncRNAs influence cancer and other diseases, but Pandolfi is hopeful that someday he and other researchers will devise ways to control the bad actors and boost the helpful ones.

MicroRNAs
Sparking a tumor’s spread

MicroRNAs are barely more than 20 RNA units, or bases, long, but they play an outsized role in heart disease, arthritis and many other ailments. These pipsqueaks can also lead to nerve pain and itchiness, researchers reported last year in Science Translational Medicine and in Neuron (SN Online: 8/13/18).

Hundreds of clinical studies are testing people’s blood and tissues to determine if microRNAs can be used to help doctors better diagnose or understand conditions ranging from asthma and Alzheimer’s disease to schizophrenia and traumatic brain injury. Some researchers are beginning to develop microRNAs as drugs and seeking ways to inhibit rogue microRNAs.

So far, the little molecules’ most firmly established roles are as promoters of and protectors against cancer (SN: 8/28/10, p. 18). Pancreatic cancer, for example, is a deadly foe. Only 8.5 percent of people are still alive five years after being diagnosed with this disease, according to U.S. National Cancer Institute statistics.

Cancer biologist Brian Lewis of the University of Massachusetts Medical School in Worcester and colleagues have learned that some microRNAs spur this lethal cancer’s initial attack and help the tumor spread from the pancreas to other organs.

MicroRNAs are mirror images of portions of the messenger RNAs that shuttle protein-making instructions from DNA to the ribosomes, where proteins are built. The microRNAs pair up with their larger messenger RNA mates and slate the bigger molecules for destruction, or at least prevent their instructions from being translated into proteins. One microRNA might have hundreds of mates, or targets, through which it influences many different body functions.

Lewis studies one gang of six microRNAs, known as the miR-17~92 cluster, the first group of microRNAs found to play a role in cancer. The six normally help strike a balance between cell growth and death, but an imbalance of these little molecules can push cells toward cancer.

Tumors in pancreatic cancer patients tend to have elevated levels of the cluster. To learn what the microRNAs were doing to goad cancer into taking hold, Lewis and colleagues used a genetic trick to remove the microRNAs from the pancreas in mice that were genetically engineered to develop pancreatic tumors. Early in their lives, mice with and without the microRNA cluster had about the same number of precancerous cells.
But by the time the animals were 9 months old, a clear difference emerged. In mice with the miR-17~92 microRNAs, nearly 60 percent of the pancreas was tending toward cancer, compared with less than 20 percent in mice lacking the cluster. The finding, reported in 2017 in Oncotarget, suggests that the microRNAs aid the cancer’s start.

The researchers developed bits of RNA that block some of the cluster members from spurring on the tumor. Using human pancreatic cancer cells grown in lab dishes, Lewis and colleagues found that taking out two of the six cluster members, miR-19a and miR-19b, stopped cancer cells from forming structures called invadopodia. As their name suggests, invadopodia allow tumors to break through blood vessel walls and other barriers to spread through the body.

Transfer RNA fragments
The virus helpers

For some young children and older adults, an infection with respiratory syncytial virus, or RSV, feels like a simple cold. But each year in the United States, more than 57,000 children younger than age 5 and about 177,000 people older than 65 are hospitalized because of the virus, the U.S. Centers for Disease Control and Prevention estimates. The infection kills hundreds of babies and about 14,000 adults over 65 annually.

Slightly higher than normal levels of some microRNAs had been linked to severe RSV infections. But molecular virologist Xiaoyong Bao of the University of Texas Medical Branch in Galveston wasn’t convinced that modestly increasing amounts of a few microRNAs could really mean the difference between a child getting a slight cold and dying from the respiratory virus.

She consulted her Texas Medical Branch colleague, cancer researcher Yong Sun Lee, for advice on studying microRNAs. Lee said Bao would need to deeply examine, or sequence, RNA in cells infected with the virus. That was an expensive proposition in 2012 when Bao started the project. “But I squeezed from my [lab’s] dry bank account,” she says, to pay for the experiment. The investment paid off. Cells infected with RSV had more of one particular RNA than did uninfected cells. Surprisingly, it was a piece of a transfer RNA. Transfer RNAs, or tRNAs, are the assembly line workers of protein building. tRNAs read instructions in a messenger RNA and deliver the amino acids the ribosome needs to make a protein.
Scientists knew that working tRNAs are essential employees. Fragments, when they were found, were considered leftover bits of decommissioned tRNAs. But the fragments that Bao and colleagues discovered aren’t just worn out bits of tRNAs. Each fragment, about 30 bases long, is precisely cut from a tRNA when RSV infects cells. The fragments aid the virus’s infection in more than one way. For instance, two fragments help the virus make copies of itself in cells, Bao and colleagues reported in 2017 in the Journal of General Virology.

tRNA fragments may also boost the body’s susceptibility to a virus. Last year, Bao’s group described in Scientific Reports how exposure to some heavy metals, via air or water pollution, can produce tRNA fragments that trigger inflammation, which may make people more susceptible to respiratory infections such as RSV.

SINE RNAs
Sacrificing infected cells

Another type of RNA may help protect against infection by certain viruses, including herpesvirus. Virologist Britt Glaunsinger has long marveled at the way viruses manipulate host cells by controlling RNAs in the cell. She became intrigued by transposons, mobile stretches of DNA that can jump from one location to another in the genome. Transposons make up nearly half of all the DNA in the human genome (SN: 5/27/17, p. 22). “We tend to think of [transposons] as parasites and things our own cells are constantly trying to shut down,” says Glaunsinger, a Howard Hughes Medical Institute investigator at the University of California, Berkeley. That’s because some are relics of ancient viruses. “While they may have initially been bad, some of them may actually be useful to us,” she says.

One class of transposons, called SINEs for short interspersed nuclear elements, are peppered throughout the genome. People have more than a million of one type of SINE known as Alu elements. Mice have similar SINEs, called B2s.

When active, SINE transposons make RNA copies of themselves. These SINE RNAs don’t carry instructions for building proteins and alone don’t enable the transposons to jump around the genome. So researchers puzzled over their role. Glaunsinger and colleagues discovered that some SINE RNAs may protect against viral infections.
Normally, cells keep a tight lock on transposons, preventing them from making any RNA. But in Glaunsinger’s experiments, cells infected with herpesvirus “were producing tons of these noncoding RNAs in response to infection,” she says. “That sort of captured our interest.”

Details of the process are still being worked out, but Glaunsinger and others have discovered that SINE RNA production triggers a cascade of events that eventually kills infected human and mouse cells. Once the RNA production gets going, Glaunsinger says, “the cell is destined to die.” Inflammation appears to be an important step in the cell-killing chain reaction. It’s all for the greater good: Killing the infected cell may protect the rest of the organism from the infection’s spread.

But there’s a wrinkle: In mice, at least, one type of herpesvirus benefits from the flood of B2 RNAs in the cells it infects. The virus hijacks part of the inflammation chain reaction to boost its own production, Glaunsinger and colleagues reported in 2015 in PLOS Pathogens. “This is an example of the back-and-forth battle that’s always going on between virus and host,” she says. “Now the ball is back in the host’s court.”

piRNAs
Shielding the brain from jumping genes

Autopsies of people who died with Alzheimer’s disease show a buildup of a protein called tau in the brain. That tau accumulation is tied to loss of some guardian RNAs, according to work by Bess Frost, a neurobiologist at UT Health San Antonio.

Frost studies fruit flies genetically engineered to make a disease-causing version of human tau in their nerve cells. Flies with the disorderly tau get a progressive nerve disease that causes movement problems and kills nerves. The insects live shorter lives than normal.

Part of the reason the flies, as well as people with tau tangles, have problems is because some RNAs known to guard the genome fall down on the job, Frost and colleagues discovered. These piwi-interacting RNAs, or piRNAs (pronounced “pie RNAs”), help keep transposons from jumping around. When transposons jump, they may land in or near a gene and mess with its activity.
Usually cells prevent jumping by stopping transposons from making messenger RNA, which carries instructions to make proteins that eventually enable the transposon to hop from place to place. If a transposon gets past the cell’s defenses and produces its messenger RNA, piRNAs will step up to pair with the messenger and cause its destruction.

When disease-causing tau builds up in flies (and maybe in people), a class of transposon with a lengthy name — class I long terminal repeat retrotransposons — makes much more RNA than usual. And when flies have the disease-causing version of tau, they also have lower than normal levels of piRNAs, Frost and colleagues reported in August 2018 in Nature Neuroscience. “Both arms of control are messed up,” Frost says. Brains of people who died with Alzheimer’s disease or supranuclear palsy, another tau-related disease, also show signs that transposons were making extra RNA, suggesting that when tau goes bad, it can beat piRNA’s defenses.

In search of a work-around, Frost’s team found that genetically boosting piRNA production in flies or giving a drug that stops transposon hops reduced nerve cell death in the insects. The researchers are preparing to test the drug in mice prone to a rodent version of Alzheimer’s disease. The team is also examining human brain tissue to see if the increase in transposon RNAs actually leads to transposon jumping in Alzheimer’s patients. If transposons don’t hop more than usual, the finding may suggest that transposon RNAs themselves can cause mischief — no jumping necessary.

This story appears in the April 13, 2019 issue of Science News with the headline, “The Secret Powers of RNA: Overlooked molecules play a big role in human health.”

Multiplying 2 x 2 is easy. But multiplying two numbers with more than a billion digits each — that takes some serious computation.

The multiplication technique taught in grade school may be simple, but for really big numbers, it’s too slow to be useful. Now, two mathematicians say that they’ve found the fastest way yet to multiply extremely large figures.

The duo claim to have achieved an ultimate speed limit for multiplication, first suggested nearly 50 years ago. That feat, described online March 18 at the document archive HAL, has not yet passed the gauntlet of peer review. But if the technique holds up to scrutiny, it could prove to be the fastest possible way of multiplying whole numbers, or integers.
If you ask an average person what mathematicians do, “they say, ‘Oh, they sit in their office multiplying big numbers together,’” jokes study coauthor David Harvey of the University of New South Wales in Sydney. “For me, it’s actually true.”

When making calculations with exorbitantly large numbers, the most important measure of speed is how quickly the number of operations needed — and hence the time required to do the calculation — grows as you multiply longer and longer strings of digits.

That growth is expressed in terms of n, defined as the number of digits in the numbers being multiplied. For the new technique, the number of operations required is proportional to n times the logarithm of n, expressed as O(n log n) in mathematical lingo. That means that, if you double the number of digits, the number of operations required will increase a bit faster, more than doubling the time the calculation takes.
But, unlike simpler methods of multiplication, the time needed doesn’t quadruple, or otherwise rapidly blow up, as the number of digits creeps up, report Harvey and Joris van der Hoeven of the French national research agency CNRS and École Polytechnique in Palaiseau. That slower growth rate makes products of bigger numbers more manageable to calculate.

The previously predicted max speed for multiplication was O(n log n), meaning the new result meets that expected limit. Although it’s possible an even speedier technique might one day be found, most mathematicians think this is as fast as multiplication can get.

“I was very much astonished that it had been done,” says theoretical computer scientist Martin Fürer of Penn State. He discovered another multiplication speedup in 2007, but gave up on making further improvements. “It seemed quite hopeless to me.”

The new technique comes with a caveat: It won’t be faster than competing methods unless you’re multiplying outrageously huge numbers. But it’s unclear exactly how big those numbers have to be for the technique to win out — or if it’s even possible to multiply such big numbers in the real world.

In the new study, the researchers considered only numbers with more than roughly 10214857091104455251940635045059417341952 digits when written in binary, in which numbers are encoded with a sequence of 0s and 1s. But the scientists didn’t actually perform any of these massive multiplications, because that’s vastly more digits than the number of atoms in the universe. That means there’s no way to do calculations like that on a computer, because there aren’t enough atoms to even represent such huge numbers, much less multiply them together. Instead, the mathematicians came up with a technique that they could prove theoretically would be speedier than other methods, at least for these large quantities.

There’s still a possibility that the method could be shown to work for smaller, but still large, numbers. That could possibly lead to practical uses, Fürer says. Multiplication of these colossal numbers is useful for certain detailed calculations, such as finding new prime numbers with millions of digits (SN Online: 1/5/18) or calculating pi to extreme precision (SN Online: 12/10/02).

Even if the method is not widely useful, making headway on a problem as fundamental as multiplication is still a mighty achievement. “Multiplying numbers is something people have been working on for a while,” says mathematical physicist John Baez of the University of California, Riverside. “It’s a big deal, just because of that.”

A nebulous void in Egypt’s Great Pyramid of Giza has been unveiled thanks to strange subatomic particles called muons.

Scientists first identified the void in 2016 using muons, heavy relatives of electrons that can penetrate through solid materials. Thought to be a corridor-shaped hole, the void was located near a chevron-shaped structure visible on the pyramid’s north face. Further muon measurements revealed new details of the void’s size and shape, scientists from the ScanPyramids team report March 2 in Nature Communications.
The new muon measurements indicate that the void is a 9-meter-long corridor about 2 meters wide by 2 meters tall, close to the pyramid’s north face. ScanPyramids researchers made additional measurements with ground-penetrating radar and ultrasonic testing, they reported March 2 in NDT & E International. The detailed measurements allowed the scientists to use an endoscope to take images inside the chamber, the team announced. The images reveal a corridor with a vaulted ceiling, presumably one that was hasn’t been seen by humans since the pyramid was built more than 4,500 years ago. The corridor’s purpose is still unclear.
Muons are created when high-energy particles from space called cosmic rays crash into the Earth’s atmosphere. Muons are partially absorbed as they rain down onto structures such as the pyramids. Using detectors placed inside the pyramid, scientists from ScanPyramids zeroed in on regions where more muons made it through, indicating they’d traversed less material, which let them map out the location of the void.

Scientists also recently used muons to probe an ancient Chinese wall (SN: 1/30/23), a nuclear reactor and various volcanoes (SN: 4/22/22).

A new biological mashup just dropped.

“Pikobodies,” bioengineered immune system proteins that are part plant and part animal, could help flora better fend off diseases, researchers report in the March 3 Science. The protein hybrids exploit animals’ uniquely flexible immune systems, loaning plants the ability to fight off emerging pathogens.

Flora typically rely on physical barriers to keep disease-causing microbes at bay. If something unusual makes it inside the plants, internal sensors sound the alarm and infected cells die. But as pathogens evolve ways to dodge these defenses, plants can’t adapt in real time. Animals’ adaptive immune systems can, making a wealth of antibodies in a matter of weeks when exposed to a pathogen.、
In a proof-of-concept study, scientists genetically modified one plant’s internal sensor to sport animal antibodies. The approach harnesses the adaptive immune system’s power to make almost unlimited adjustments to target invaders and lends it to plants, says plant immunologist Xinnian Dong, a Howard Hughes Medical Institute investigator at Duke University who was not involved in the work.

Crops especially could benefit from having more adaptable immune systems, since many farms grow fields full of just one type of plant, says Dong. In nature, diversity can help protect vulnerable plants from disease-spreading pathogens and pests. A farm is more like a buffet.

Researchers have had success fine-tuning plant genes to be disease-resistant, but finding the right genes and editing them can take more than a decade, says plant pathologist Sophien Kamoun of the Sainsbury Laboratory in Norwich, England. He and colleagues wanted to know if plant protection could get an additional boost from animal-inspired solutions.

To create the pikobodies, the team fused small antibodies from llamas and alpacas with a protein called Pik-1 that’s found on the cells of Nicotiana benthamiana, a close relative of tobacco plants. Pik-1 typically detects a protein that helps a deadly blast fungus infect plants (SN: 7/10/17). For this test, the animal antibodies had been engineered to target fluorescent proteins

Plants with the pikobodies killed cells exposed to the fluorescent proteins, resulting in dead patches on leaves, the team found. Of 11 tested versions, four were not toxic to the leaves and triggered cell death only when the pikobodies attached to the specific protein that they had been designed bind.

What’s more, pikobodies can be combined to give plants more than one way to attack a foreign invader. That tactic could be useful to hit pathogens with the nimble ability to dodge some immune responses from multiple angles.

Theoretically, it’s possible to make pikobodies “against virtually any pathogen we study,” Kamoun says. But not all pikobody combos worked together in tests. “It’s a bit hit or miss,” he says. “We need some more basic knowledge to improve the bioengineering.”

Whales are known for belting out sounds in the deep. But they may also whisper.

Southern right whale moms steer their calves to shallow waters, where newborns are less likely to be picked off by an orca. There, crashing waves mask the occasional quiet calls that the pairs make. That may help the whales stick together without broadcasting their location to predators, researchers report July 11 in the Journal of Experimental Biology.

While most whale calls are meant to be long-range, “this shows us that whales have a sort of intimate communication as well,” says Mia Nielsen, a behavioral biologist at Aarhus University in Denmark. “It’s only meant for the whale right next to you.”

Nielsen and colleagues tagged nine momma whales with audio recorders and sensors to measure motion and water pressure, and also recorded ambient noise in the nearshore environment. When the whales were submerged, below the noisy waves, the scientists could pick up the hushed calls, soft enough to fade into the background noise roughly 200 meters away.
An orca, or killer whale, “would have to get quite close in the big ocean to be able to detect them,” says biologist Peter Tyack at the University of St. Andrews in Scotland. Tyack was not involved with the study, but collaborates with one of the coauthors on other projects.

The whispers were associated with times when the whales were moving, rather than when mothers were stationary and possibly suckling their calves. Using hushed tones could make it harder for the pair to reunite if separated. But the observed whales tended to stay close to one another, about one body length apart, the team found.

Eavesdropping biologists have generally focused on the loud noises animals make, Tyack says. “There may be a repertoire among the calls of lots of animals that are specifically designed only to be audible to a partner who’s close by,” he says.

Artificial intelligence has passed the last major milestone in mastering poker: six-player no-limit Texas Hold’em.

Games like poker, with hidden cards and players who bluff, present a greater challenge to AI than games where every player can see the whole board. Over the last few years, computers have become aces at increasingly complicated forms of one-on-one poker, but multiplayer games take that complexity to the next level (SN Online: 5/13/15).

Now, a card shark AI dubbed Pluribus has outplayed more than a dozen elite professionals at six-player Texas Hold’em, researchers report online July 11 in Science. Algorithms that can plot against several adversaries using such spotty information could make savvy business negotiators, political strategists or cybersecurity watchdogs.
Pluribus honed its initial strategy by playing against copies of itself, starting from scratch and gradually learning which actions helped to win. Then, the AI used that intuition for when to hold and when to fold during the first betting round of each hand against five human players.

During subsequent betting rounds, Pluribus fine-tuned its strategy by imagining how the game might play out if it took different actions. Unlike artificial intelligence trained for two-player poker, Pluribus didn’t speculate all the way to the end of the game — which would require too many computations when dealing with so many players (SN: 4/1/17, p. 12). Instead, the AI imagined several moves ahead and decided what to do based on those hypothetical futures and different strategies that players could adopt.

In 10,000 hands of Texas Hold’em, Pluribus competed against five contestants from a pool of 13 professionals, all of whom had won more than $1 million playing poker. Every 100 hands, Pluribus raked in, on average, about $480 from its human competitors.
“This is roughly the amount that elite human professionals aspire to beat weaker players by,” implying that Pluribus was a savvier player than its human opponents, says Noam Brown of Facebook AI Research in New York City. Brown, along with Tuomas Sandholm of Carnegie Mellon University in Pittsburgh, created Pluribus.

Now that AI has poker in the bag, algorithms could test their strategic reasoning in games with more complex hidden information, says computer scientist Viliam Lisý of the Czech Technical University in Prague, who was not involved in the work. In games like Kriegspiel — a chess spin-off where players can’t see each other’s pieces — the unknowns can become far more complicated than a few cards held close to opponents’ chests, Lisý says.

Video games like StarCraft, which allow many more types of moves and free players from rigid, turn-based play, could also serve as new tests of AI cleverness (SN: 5/11/19, p. 34).

No one has ever probed a particle more stringently than this.

In a new experiment, scientists measured a magnetic property of the electron more carefully than ever before, making the most precise measurement of any property of an elementary particle, ever. Known as the electron magnetic moment, it’s a measure of the strength of the magnetic field carried by the particle.

That property is predicted by the standard model of particle physics, the theory that describes particles and forces on a subatomic level. In fact, it’s the most precise prediction made by that theory.
By comparing the new ultraprecise measurement and the prediction, scientists gave the theory one of its strictest tests yet. The new measurement agrees with the standard model’s prediction to about 1 part in a trillion, or 0.1 billionths of a percent, physicists report in the February 17 Physical Review Letters.

When a theory makes a prediction at high precision, it’s like a physicist’s Bat Signal, calling out for researchers to test it. “It’s irresistible to some of us,” says physicist Gerald Gabrielse of Northwestern University in Evanston, Ill.

To measure the magnetic moment, Gabrielse and colleagues studied a single electron for months on end, trapping it in a magnetic field and observing how it responded when tweaked with microwaves. The team determined the electron magnetic moment to 0.13 parts per trillion, or 0.000000000013 percent.

A measurement that exacting is a complicated task. “It’s so challenging that nobody except the Gabrielse team dares to do it,” says physicist Holger Müller of the University of California, Berkeley.
The new result is more than twice as precise as the previous measurement, which stood for over 14 years, and which was also made by Gabrielse’s team. Now the researchers have finally outdone themselves. “When I saw the [paper] I said, ‘Wow, they did it,’” says Stefano Laporta, a theoretical physicist affiliated with University of Padua in Italy, who works on calculating the electron magnetic moment according to the standard model.

The new test of the standard model would be even more impressive if it weren’t for a conundrum in another painstaking measurement. Two recent experiments, one led by physicist Saïda Guellati-Khélifa of Kastler Brossel Laboratory in Paris and the other by Müller, disagree on the value of a number called the fine-structure constant, which characterizes the strength of electromagnetic interactions (SN: 4/12/18). That number is an input to the standard model’s prediction of the electron magnetic moment. So the disagreement limits the new test’s precision. If that discrepancy were sorted out, the test would become 10 times as precise as it is now.
The stalwart standard model has stood up to a barrage of experimental tests for decades. But scientists don’t think it’s the be-all and end-all. That’s in part because it doesn’t explain observations such as the existence of dark matter, an invisible substance that exerts gravitational influence on the cosmos. And it doesn’t say why the universe contains more matter than antimatter (SN: 9/22/22). So physicists keep looking for cases where the standard model breaks down.

One of the most tantalizing hints of a failure of the standard model is the magnetic moment not of the electron, but of the muon, a heavy relative of the electron. In 2021, a measurement of this property hinted at a possible mismatch with standard model predictions (SN: 4/7/21).

“Some people believe that this discrepancy could be the signature of new physics beyond the standard model,” says Guellati-Khélifa, who wrote a commentary on the new electron magnetic moment paper in Physics magazine. If so, any new physics affecting the muon could also affect the electron. So future measurements of the electron magnetic moment might also deviate from the prediction, finally revealing the standard model’s flaws.

Homo sapiens who reached Europe around 54,000 years ago introduced bows and arrows to that continent, a new study suggests.

Researchers examined tiny triangular stone points and other artifacts excavated at a rock-shelter in southern France called Grotte Mandrin. H. sapiens on the move probably brought archery techniques from Africa to Europe, archaeologist Laure Metz of Aix-Marseille University in France and colleagues report February 22 in Science Advances.

“Metz and colleagues demonstrate bow hunting [at Grotte Mandrin] as convincingly as possible without being caught bow-in-hand,” says archaeologist Marlize Lombard of the University of Johannesburg, who did not participate in the new study.
No bows were found at the site. Wooden items such as bows preserve poorly. The oldest intact bows, found in northern European bogs, date to around 11,000 years ago, Metz says.

Previous stone and bone point discoveries suggest that bow-and-arrow hunting originated in Africa between about 80,000 and 60,000 years ago. And previously recovered fossil teeth indicate that H. sapiens visited Grotte Mandrin as early as 56,800 years ago, well before Neandertals’ demise around 40,000 years ago and much earlier than researchers had thought that H. sapiens first reached Europe (SN: 2/9/22).

“We’ve shown that the earliest known Homo sapiens to migrate into Neandertal territories had mastered the use of the bow,” Metz says.

No evidence suggests that Neandertals already present in Europe at that time launched arrows at prey. It’s also unclear whether archery provided any substantial hunting advantages to H. sapiens relative to spears that were thrust or thrown by Neandertals.
Among 852 stone artifacts excavated in a H. sapiens sediment layer at Grotte Mandrin dated to about 54,000 years ago, 196 triangular stone points displayed high-impact damage. Another 15 stone points showed signs of both high-impact damage and alterations caused by butchery activities, such as cutting.

Comparisons of those finds were made to damage on stone replicas of the artifacts that the researchers used as arrowheads shot from bows and as the tips of spears inserted in handheld throwing devices. Additional comparative evidence came from stone and bone arrowheads used by recent and present-day hunting groups.

Impact damage along the edges of stone points from the French site indicated that these implements had been attached at the bottom to shafts.

The smallest Grotte Mandrin points, many with a maximum width of no more than 10 millimeters, could have pierced animals’ hides only when shot from bows as the business ends of arrows, the researchers say. Experiments they conducted with replicas of the ancient stone points found that stone points less than 10 millimeters wide reach effective hunting speeds only when attached to arrow shafts propelled by a bow.

Larger stone points, some of them several times the size of the smaller points, could have been arrowheads or might have tipped spears that were thrown or thrust by hand or launched from handheld spear throwers, the researchers conclude.

Lombard, the University of Johannesburg archaeologist, suspects that the first H. sapiens at the French rock-shelter hunted with bows and arrows as well as with spears, depending on where and what they were hunting. Earlier studies directed by Lombard indicated that sub-Saharan Africans similarly alternated between these two types of hunting weapons starting between about 70,000 and 58,000 years ago.

H. sapiens newcomers to Europe may have learned from Neandertals that spear hunting in large groups takes precedence on frigid landscapes, where bow strings can easily snap and long-distance pursuit of prey is not energy efficient, Lombard says.

But learning about archery from H. sapiens may not have been in the cards for Neandertals. Based on prior analyses of brain impressions on the inside surfaces of fossil skulls, Lombard suspects that Neandertals’ brains did not enable the enhanced visual and spatial abilities that H. sapiens exploited to hunt with bows and arrows.

That’s a possibility, though other controversial evidence suggests that Neandertals behaved no differently from Stone Age H. sapiens (SN: 3/26/20).If Grotte Mandrin Neandertals never hunted with bows and arrows but still survived just fine alongside H. sapiens archers for roughly 14,000 years, reasons for Neandertals’ ultimate demise remain as mysterious as ever.

Whether it’s Katy Perry poaching dancers from once-BFF Taylor Swift or Clytemnestra orchestrating the murder of her husband Agamemnon, betrayal is a dark, persistent part of the human condition. Unlike garden-variety deception, betrayal happens in established relationships, destroying trust that has developed over time. It’s usually unexpected, and it yields a unique, often irreparable, wound. In fact, betrayers have a special place in hell, literarily: In Dante’s Inferno, they occupy the ninth and final circle; mere fraudsters dwell in the eighth.

While most of us are familiar with betrayal, investigating it is really hard. (Consider all the complications of a study that asks people in trusted relationships to betray each other.) Case studies of real betrayals can provide insight after-the-fact, but without a time machine, finding studies that reveal big picture patterns about the lead-up to treachery are scarce.

“We all know betrayal exists,” says Cristian Danescu-Niculescu-Mizil, a computer scientist at Cornell University who spends a lot of time thinking about what language reveals about relationships. “But finding relevant data is really hard.”

So when Danescu-Niculescu-Mizil heard about a Diplomacy, a strategy game rife with betrayal, he figured it might serve as a good proxy for real life treachery. And he was right: Studying the patterns of communication between the players revealed that betrayal is sometimes foreseeable. But like many relationships that collapse in betrayal, teasing out what goes wrong and who is at fault isn’t so easy.
Unlike Risk and other war games, Diplomacy is all about, well, diplomacy (John F. Kennedy and Henry Kissinger reportedly were fans). Set in Europe before World War I, the nations/players have to form alliances to win. But chance is removed from the equation; players don’t roll dice or take turns. There’s only diplomacy: a negotiation phase where players converse, form alliances and gather intelligence (these days, typically online), and a movement phase where everyone’s decisions are revealed and executed all at once. Betrayal is so integral to Diplomacy that, as noted on a “This American Life” episode, stabbing an ally in the back is referred to by the shorthand “stabbing.”

Danescu-Niculescu-Mizil, colleague and fan-of-the-game Jordan Boyd-Graber, and colleagues examined 249 games of Diplomacy with a total of 145,000 messages among players. When they used a computer program to compare exchanges between players whose relationships ended in betrayal with those whose relationships lasted, the computer discerned subtle signals of impending betrayal.

One harbinger was a shift in politeness. Players who were excessively polite in general were more likely to betray, and people who were suddenly more polite were more likely to become victims of betrayal, study coauthor and Cornell graduate student Vlad Niculae reportedJuly 29 at the Annual Meeting of the Association for Computational Linguistics in Beijing. Consider this exchange from one round:

Germany: Can I suggest you move your armies east and then I will support you? Then next year you move [there] and dismantle Turkey. I will deal with England and France, you take out Italy.

Austria: Sounds like a perfect plan! Happy to follow through. And—thank you Bruder!

Austria’s next move was invading German territory. Bam! Betrayal.

An increase planning-related language by the soon-to-be victim also indicated impending betrayal, a signal that emerges a few rounds before the treachery ensues. And correspondence of soon-to-be betrayers had an uptick in positive sentiment in the lead-up to their breach.
Working from these linguistic cues, a computer program could peg future betrayal 57 percent of the time. That might not sound like much, but it was better than the accuracy of the human players, who never saw it coming. And remember that by definition, a betrayer conceals the intention to betray; the breach is unexpected (that whole trust thing). Given that inherent deceit, 57 percent isn’t so bad.

When I spoke to Danescu-Niculescu-Mizil, he said that more important than the clues themselves is the shift in the balance of behavior in the relationship. Positive or negative sentiment of one player isn’t what matters, it’s the asymmetry of the behavior of the two people in the relationship. He likens the linguistic tells to body language: While you wouldn’t use it as a sole basis for decision-making, if you know how to interpret it, it might give you an advantage.

More work is needed to explore whether these patterns exist in real life. And while the research did reveal some patterns, it can’t say anything about cause and effect or who is at fault. Perhaps, for example, the extensive planning of the eventual victims came off as super bossy and frustrating to the eventual betrayer. After all, Clytemnestra’s betrayal of Agamemnon came after he killed their daughter Iphigenia. That kind of bad blood may be unforgivable.

HONOLULU — Perhaps most supermassive black holes — dark giants in the centers of galaxies — are just shy when they’re young.

“We have this weird problem, where on the one hand the universe makes really supermassive black holes very shortly after the Big Bang,” says Kevin Schawinski, an astrophysicist at ETH Zürich in Switzerland. “But when we look at more typical galaxies, we find no evidence for growing black holes.”

The feeding zones around voracious black holes create quasars, blazing furnaces of X-rays and other light. And yet the Chandra space telescope detects no X-rays from a cache of galaxies in the constellation Fornax that researchers think should be nourishing young black holes, Schawinski reported August 6 at a meeting of the International Astronomical Union.
Over the past several years, astronomers have found a handful of very bright quasars that lit up within the first billion years of cosmic history. These quasars are probably powered by unusually hefty supermassive black holes — ones that gobbled down gas as fast as physically possible (or even faster) for hundreds of millions of years.

“If this happens all over the universe,” says Schawinski, “then if we look at more normal-mass galaxies, we should be seeing their supermassive black holes pop out in the early universe to the same degree.”

But they don’t.
Maybe the more run-of-the-mill black holes are there but they’re not actively feeding, he says. Or perhaps something is blocking the X-rays from getting out.

Or maybe — just maybe — these black holes haven’t been born yet.

“It’s a very interesting suggestion,” says Andrea Comastri, an astronomer at the Osservatorio Astronomico di Bologna in Italy, says of the not-yet-born scenario. “But I’m not convinced.”

These images capture a relatively tiny volume of space, he says, so perhaps the researchers aren’t casting a wide enough net. The distances to these galaxies are also notoriously difficult to pin down. Many could be much closer and seen during a time when black holes have formed but quieted down a bit.

If the universe can make monstrous black holes in under a billion years, then making the relatively little guys should be straightforward and they should be everywhere, Comastri says. “It should be easier to make smaller black holes because you don’t have to work that much. They are there somewhere.”

If the black holes are confirmed to be missing, “it’s going to shake up a lot of what we think about the growth of quasars,” says Tiziana Di Matteo, an astrophysicist at Carnegie Mellon University in Pittsburgh. “But I’m very skeptical of it.”

These cosmic no-shows probably don’t suck down gas as fast as the researchers assume, she says. If these black holes only nibble at the surrounding gas — as opposed to their obese cousins who gorge themselves — then X-rays would only trickle from their dinner plates and might not be detected.

Much like with humans, black hole obesity is influenced by environment. Most galaxies need some time to build up enough mass to efficiently feed their black holes, Di Matteo says. Tiny galaxies easily lose gas every time a cluster of new stars is born or whenever a dying star explodes. “It’s only in extreme environments,” she says, at the junctions of cosmic filaments that become interstellar dumping grounds, “where gas could plunge through and not care about anything else that’s going on.” Here, fledgling black holes aren’t as reliant on their galaxy’s feeble gravity to grab food; the incoming rivers of gas are like intergalactic fire hoses.

Those unusually massive black hole starter kits are probably responsible for the dazzling quasars that switch on during the first billion years after the Big Bang. Computer simulations show that in the younger, more intimate universe, when everything was squished together a lot more than today, there are the oddball places where gas funnels onto ancestral galaxies at astounding rates, providing fast-growing black holes with an all-you-can-eat buffet.

The other less showy black holes, the ones Schawinski and colleagues are hunting for, probably spend the next several billion years quietly catching up. Finding these black holes when they’re young and struggling to grow might require searching a wider area or getting more sensitive observations.

“It’s exciting,” Schawinski says. “It’s the last major category of astrophysical objects of whose origin we know nothing about.” Planets, stars and galaxies are pretty well understood, he says. “But we have no idea how supermassive black holes form.”

Schawinski’s team plans to spend the next year or two repeating their experiment over a wider volume of space, hoping to find at least one youthful black hole in a moderate-sized galaxy. “Once you go from zero to one you have something to work with,” he says. “Right now we’ve got nothing.”