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 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.

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.

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.”

Scientists have unwrapped long-sought details of embalming practices that ancient Egyptians used to preserve dead bodies.

Clues came from analyses of chemical residue inside vessels from the only known Egyptian embalming workshop and nearby burial chambers. Mummification specialists who worked there concocted specific mixtures to embalm the head, wash the body, treat the liver and stomach, and prepare bandages that swathed the body, researchers report February 1 in Nature.

“Ancient Egyptian embalmers had extensive chemical knowledge and knew what substances to put on the skin to preserve it, even without knowing about bacteria and other microorganisms,” Philipp Stockhammer, an archaeologist at Ludwig Maximilians University of Munich, said at a January 31 news conference.
The findings come courtesy of chemical residue inside 31 vessels found in an Egyptian embalming workshop and four vessels discovered in an adjacent pair of burial chambers. Writing on workshop vessels named embalming substances, provided embalming instructions (such as “to put on his head”) or both. All the artifacts — dating from Egypt’s 26th dynasty which rose to power between 664 B.C. and 525 B.C. — were excavated at a cemetery site called Saqqara in 2016. Archaeologist and study coauthor Ramadan Hussein, who died in 2022, led that project.

Newfound mummy embalming mixtures
Five of the vessels had the label antiu. The substance was thought to have been a fragrant resin called myrrh. The antiu at Saqqara, however, consisted of oil or tar from cedar and juniper or cypress trees mixed with animal fats. Writing on these jars indicates that antiu could have been used alone or combined with another substance called sefet.

Three vessels from the embalming workshop bore the label sefet, which researchers have usually described as an unidentified oil. At Saqqara, sefet was a scented, fat-based ointment with added ingredients from plants. Two sefet pots contained animal fats mixed with oil or tar from juniper or cypress trees. A third container held animal fats and elemi, a fragrant resin from tropical trees.

Clarification of the ingredients in antiu and sefet at Saqqara “takes mummification studies further than before,” says Egyptologist Bob Brier of Long Island University in Brookville, N.Y., who was not part of the research.

Egyptians may have started mummifying their dead as early as 6,330 years ago (SN: 8/18/14). Mummification procedures and rituals focused on keeping the body fresh so the deceased could enter what was believed to be an eternal afterlife.
Embalming and mummification procedures likely changed over time, says team member Maxime Rageot, a biomolecular archaeologist also at Ludwig Maximilians University. Embalmers’ mixtures at Saqqara may not correspond, say, to those used around 700 years earlier for King Tutankhamun (SN: 11/2/22).

Mummy embalming instructions
Outside surfaces of other vessels from the Saqqara embalming workshop and burial chambers sported labels and, in some cases, instructions for treatment of the head, preparation of linen mummy bandages, washing the body and treating the liver and stomach. Inscriptions on one jar referred to an administrator who performed embalming procedures, mainly on the head.

Chemical residue inside these pots consisted of mixtures specific to each embalming procedure. Ingredients included oils or tars of cedar and juniper or cypress trees, pistachio resin, castor oil, animal fats, heated beeswax, bitumen (a dense, oily substance), elemi and a resin called dammar.

Most of those substances have been identified in earlier studies of chemical residues from Egyptian mummies and embalming vessels in individual tombs, says Egyptologist Margaret Serpico of University College London. But elemi and dammar resins have not previously been linked to ancient Egyptian embalming practices and are “highly unexpected,” notes Serpico, who did not participate in the new study.

Elemi was an ingredient in the workshop mixtures used to treat the head, the liver and bandages wrapped around the body. Chemical signs of dammar appeared in a vessel from one of the burial chambers that included remnants of a range of substances, indicating that the container had been used to blend several different mixtures, the researchers say.

Specific properties of elemi and dammar that aided in preserving dead bodies have yet to be investigated, Stockhammer said.

A far-flung trade network for mummy embalming ingredients
Elemi resin reached Egypt from tropical parts of Africa or Southeast Asia, while dammar originated in Southeast Asia or Indonesia, Rageot says. Other embalming substances detected at Saqqara came from Southwest Asia and parts of southern Europe and northern Africa bordering the Mediterranean Sea. These findings provide the first evidence that ancient Egyptian embalmers depended on substances transported across vast trade networks.

Egyptian embalmers at Saqqara took advantage of a trade network that already connected Egypt to sites in Southeast Asia, Stockhammer said. Other Mediterranean and Asian societies also engaged in long-distance trade during ancient Egypt’s heyday (SN: 1/9/23).

It’s no surprise that ancient Egyptians imported embalming ingredients from distant lands, Brier says. “They were great traders, had limited [local] wood products and really wanted these substances to achieve immortality.”

No backside, no problem for some young sea spiders.

The creatures can regenerate nearly complete parts of their bottom halves — including muscles, reproductive organs and the anus — or make do without them, researchers report January 23 in Proceedings of the National Academy of Sciences.

The ability to regrow body parts isn’t super common, but some species manage to pull it off. Some sea slug heads can craft an entirely new body (SN: 3/8/21). Sea spiders and some other arthropods — a group of invertebrates with an exoskeleton — can regrow parts of their legs. But researchers thought new legs were the extent of any arthropod’s powers, perhaps because tough exteriors somehow stop them from regenerating other body parts.
A mishap first clued evolutionary biologist Georg Brenneis in that sea spiders (Pycnogonum litorale) might be able handle more complex repairs too. He accidentally injured one young specimen that he was working on in the lab with forceps. “It wasn’t dead, it was moving, so I just kept it,” says Brenneis, of the University of Vienna. Several months later, the sea spider had an extra leg instead of a scar, he and evolutionary biologist Gerhard Scholtz of Humbolt University of Berlin reported in 2016 in The Science of Nature.

In the new study, most of the 19 young spiders recovered and regrew missing muscles and other parts of their lower halves after amputation, though the regeneration wasn’t always perfect. Some juveniles sported six or seven legs instead of eight.

None of four adults regenerated. That may be because adults no longer shed their skin as they grow, suggesting that regeneration and molting are somehow linked, Brenneis says. Two young sea spiders also didn’t regenerate at all. The animals survived with only four legs and without an anus. Instead of pooping, the pair regurgitated waste out of their mouths.
Next up is figuring out whether other arthropods also regenerate more than scientists thought, and how sea spiders do it, Brenneis says. “I would like to see how it works.”

A new smartwatch app alerts users who are deaf or hard of hearing of nearby sounds, such as microwave beeps or car horns.

“The main motivation [for the app] came from my own experience, and conversations that my colleagues and I have had with deaf and hard of hearing people over several years,” says Dhruv Jain, who presented the system, called SoundWatch, at the virtual ASSETS conference on October 28.

Jain, who is hard of hearing, uses SoundWatch at home to avoid sleeping through a smoke alarm. “On a nature walk, it’ll tell me that there’s birds chirping, or there might be a waterfall nearby,” he says. “Those sounds make me feel more present and connected to the world.”

Sound awareness apps for smartphones exist. But Jain prefers the immediacy of sound notifications on his wrist, rather than in his pocket — and surveys of people who are deaf or hard of hearing show he’s not alone.

The SoundWatch app pairs an Android smartwatch and phone. The watch records ambient noises and sends that data to the phone for processing. When the phone detects a sound of interest, the smartwatch vibrates and displays a notification.

Jain, a computer scientist at the University of Washington in Seattle, and colleagues designed the app to identify 20 noises. In experiments, SoundWatch correctly identified those 20 sounds 81.2 percent of the time. When set to listen only for urgent noises — a fire alarm, door knock or alarm clock — the app was 97.6 percent accurate. Eight deaf and hard of hearing people who used SoundWatch around a university campus gave the app broadly favorable reviews, but noted that the app misclassified some sounds in noisy outdoor settings.

Jain and colleagues are now working on a version of SoundWatch that users can train to recognize new sounds, such as their own house alarm, using just a few recordings.

November is beginning to feel a lot like last March.

In Europe, where the coronavirus was largely under control for much of the summer and fall, cases are skyrocketing nearly everywhere. Twenty countries, including the United Kingdom and France, have shuttered restaurants, introduced curfews or generally urged people to stay at home, though most schools and universities are staying open for now.

Cases are surging across the United States, too, where more than 100,000 new infections are being reported each day. Already in November, more than half of states have set records for the most cases in a week, and in places such as Minnesota, Utah and Wisconsin, some hospitals are nearing capacity. In North Dakota, nearly 1 in every 14 people has already contracted the coronavirus, with 2,254 cases reported November 8 alone in a state of 762,000 people.

To make matters worse, “the virus is going into its sweet spot at a time that we’re exhausted by it,” says Jeffrey Shaman, an infectious diseases epidemiologist at the Columbia University Mailman School of Public Health in New York City. That sweet spot is indoors, where people are spending more time as the weather in the Northern Hemisphere turns colder — and where the virus can spread more easily.

Despite such a grave outlook, experts say it’s still not too late to turn the tide.

Shutting down borders, businesses and schools are among the most drastic measures to do that. Worries over economic consequences may hold governments back from issuing widespread stay-at-home orders this time around, though.

U.S. President-elect Joe Biden, who unveiled a COVID-19 advisory board November 9, has proposed a multipronged plan for controlling the pandemic, including nationwide mask mandates and expanded testing. But Biden won’t take office until January 20, and President Donald Trump has repeatedly downplayed the surge in cases.

While getting a COVID-19 vaccine — or vaccines — is closer than ever (SN: 11/9/20), most experts agree that vaccines probably won’t be available to everybody until late spring or early summer.
That means getting through the winter will require falling back on the familiar public health tools of physical distancing, mask wearing, and testing and isolating infected people, Shaman says. But all of those measures fall short unless everyone is willing to follow the rules.

Living in this reality can be draining, acknowledges Aleksandra Zając, a doctor specializing in nuclear medicine in Warsaw. Doctors and patients alike are tired of not being able to leave their homes and having to wear a mask when they do, she says, but “as a doctor, I really see the need for all those restrictions.” People aren’t helpless against the virus, she says. “We still have some impact on what’s going on.”
Zając devised a calculator to help people learn how much wearing masks and goggles, regularly washing their hands and keeping distance from others might help protect them. Alone, none of those measures is perfect, but doing them all together can boost protection, like layering slices of Swiss cheese so that holes in one slice are covered by another slice. The Swiss cheese idea is not new, but it’s still relevant for stacking public health measures, Zając says. It goes for individual actions, too.

“One individual cannot do much” beyond protecting themselves, Zając says, “but if we sum up all the individuals together and they all follow the rules, I truly believe we can control this pandemic.”

Scientists know much more about the virus than they did in March, and that knowledge can help make the most of all the public health tools at our disposal.

Mask up
Dozens of studies have made it abundantly clear that wearing a mask is one of the most effective steps an individual can take to help curb the pandemic. Masks are especially crucial in lessening the risk of someone who doesn’t know they’re infected passing the virus to someone else (SN: 6/26/20).

Additionally, there’s a growing understanding among scientists that masks are good for the wearer too. The U.S. Centers for Disease Control and Prevention updated their scientific guidance on November 10 to acknowledge that cloth masks can reduce the number of infectious droplets inhaled by the wearer, which offers a degree of protection, especially when masks are multi-layered.

In a study published October 23 in Nature Medicine, scientists estimate that if 95 percent of people wore masks when outside their homes, nearly 130,000 deaths from COVID-19 might be averted in the United States between the end of September and the end of February 2021. If 85 percent of people wear masks, about 96,000 lives might be saved, the researchers calculate.

The debate over which kind of mask is best, however, has been spirited (SN: 8/12/20).

When it comes to ubiquitous cloth masks, only one randomized clinical trial in the world is testing their effectiveness in preventing COVID-19. That trial in Guinea-Bissau is giving all 66,000 expected participants advice about how to avoid respiratory illnesses. Half of those people will each also get two locally sewn cloth masks. The trial is expected to wrap up in November.

Some research on the prevention of other respiratory illnesses suggests that a cloth mask’s effectiveness depends on many factors, including wearing the mask properly over both the nose and mouth. Regular washing in hot water is also necessary, says Raina MacIntyre, a mask researcher at the University of New South Wales in Sydney.
In 2015, she and colleagues published in BMJ Open results of a trial conducted in Hanoi, Vietnam. Roughly 1,600 health care workers at 15 hospitals were assigned to either wear a medical mask at all times during their shift, to wear a two-layer cloth mask or to follow the hospital’s standard practice, which may or may not involve wearing a mask. The results weren’t encouraging. At the end of the five-week study, people in the cloth mask group had the highest rate of respiratory infections, such as colds — even higher than the group that wasn’t regularly wearing masks. The researchers concluded that health care workers shouldn’t wear cloth masks and opt instead for medical masks.

The trial was very controversial, MacIntyre says, “because the message was that cloth masks could be dangerous. That caused a lot of angst during the pandemic. In March and April, I had a lot of health workers in the U.S. and Europe contacting me and saying, ‘The hospital has run out of respirators. Is it better I wear no mask than wear a cloth mask?’”

That prompted MacIntyre and colleagues to examine unpublished data from the trial. Both surgical and cloth masks get contaminated with respiratory viruses, the researchers found. But surgical masks are disposable. If people didn’t wash their reusable cloth masks every day, the masks became more and more contaminated.

“If you washed your cloth mask in a washing machine with hot water, you were just as protected as wearing a surgical mask,” MacIntyre says. But workers who hand-washed their masks had double the risk of infection of those wearing a medical mask, the researchers reported September 28 in BMJ Open.
“The bottom line is, the washing is part of the protective effect of a cloth mask,” MacIntyre says. She recommends a daily wash in water at 60° to 90° Celsius, far hotter than anyone could stand to hand-wash. Shrinkage from hot water also tightens up pores in the mask, keeping the virus from slipping through easily.

Health care workers should also wear protective goggles to prevent rare cases of infection through the eye, MacIntyre says. But determining whether people going about their daily lives need goggles, face shields or other eye protection in addition to masks is a tricky bit of calculus, she says. “You have to look at community transmission rates. You have to look at where you’re actually going. Are you just going for a walk outside or are you going to a doctor’s surgery and are going to be sitting in an unventilated waiting room for two hours?”

The best most people can do is to take all the precautions they can, including avoiding large gatherings — especially indoors — wearing masks and keeping distance from people they don’t live with.

Fine-tuning lockdowns
Early in the pandemic, lockdowns and social distancing measures (of varying severity) enacted in many countries largely worked. Staying at home starved the virus of transmission opportunities, preventing over 500 million infections in six hard-hit countries, according to some experts (SN: 6/9/20).

Circumstances are different now. “I don’t think we’ll lock down at that scale again,” says Michael Osterholm, an epidemiologist at the University of Minnesota in Minneapolis and a member of Biden’s task force. Now that scientists have a better understanding of transmission, blanket lockdowns may not be needed. Instead, restrictions could focus on crowded, poorly ventilated spaces like restaurants and bars.

If cases continue to grow exponentially, however, stricter lockdowns may be the only tool left to prevent hospitals from being overwhelmed. But such measures are increasingly less palatable to many Americans, Osterholm says. “What the public will accept is key. If they won’t comply, it doesn’t really matter what you recommend or how you recommend it.”

Limits of lockdowns
Stay-at-home orders also don’t stop transmission within a household, where experts are learning that the virus can rapidly spread. In a sample of 101 homes with a positive coronavirus test, 53 percent of other people living in those homes became quickly infected, researchers reported in the Nov. 6 Morbidity and Mortality Weekly Report.

“We know that it’s really gatherings in close contact indoors that are riskiest,” says Alison Hill, an epidemiologist at Johns Hopkins University. “There’s no reason why if you’re in your own house or among family or friends to think that the disease can’t spread.” Isolating infected members of a household, wearing masks and improving ventilation can limit household transmission, she says.

And not everyone can stay home, which has contributed to inequities in who is getting sick in this pandemic.

In the United States, residents of poorer neighborhoods, often home to racial and ethnic minorities disproportionately affected by COVID-19 (SN:4/10/20), were less likely to stay at home during the early months of the pandemic than residents of richer neighborhoods. Cell phone mobility data suggest that this difference stems from work-related demands, according to a study published November 3 in Nature Human Behavior. Residents of the highest-income neighborhoods reduced days at work outside the home by 13.7 percent, compared with 6.6 percent for residents of lower-income neighborhoods, Jonathan Jay, a public health researcher at Boston University, and colleagues found.

Many residents of lower-income neighborhoods work jobs that can’t be done from home. But when there was a choice, people in these neighborhoods did limit their activities, Jay says. The data showed that people of all income groups reduced outings unrelated to work at roughly similar levels.

Policies like restricting evictions so people don’t fear losing their home if they miss work, expanding unemployment insurance and mandating paid sick leave could help these residents physically distance, Jay says.

Test and trace
Lockdowns by themselves will not end the pandemic. They are only supposed to be temporary measures that buy time for local and state health departments to beef up other infection-control strategies. Crucial among these are testing and contact tracing, a tried-and-true public health intervention whereby contacts of positive cases are quickly identified and instructed to quarantine (SN: 4/29/20).

“Contact tracing is really key when you have a disease that’s as fast-spreading as COVID-19,” because it breaks crucial chains of transmission, says Martial Ndeffo, an infectious diseases researcher at Texas A&M University in College Station.

Contact tracing and isolation is most powerful when cases are identified early in the course of infection, their contacts are traced and informed of their exposure quickly, and those contacts comply with requests to quarantine. Such a system requires broadly available testing and lots of contact tracers to do the detective work.
Otherwise, even with relatively small caseloads, contact tracing systems can’t keep up with a growing epidemic. At this point, most of the United States can’t keep up. In October, only three states and the District of Columbia had enough full-time contact tracers to deal with current caseloads, according to a survey conducted by NPR and the Johns Hopkins Center for Health Security. And as cases climb, even well-staffed systems could be overwhelmed.

“Given the number of cases in the U.S., it is unrealistic to think that most states have the resources and available staff to raise the army of contact tracers needed,” Ndeffo says. Biden’s COVID-19 response plan includes efforts to “mobilize at least 100,000 Americans across the country” to boost the contact tracing effort. Currently, there are just over 50,000 contact tracers nationwide.

Robust contact tracing systems work only if people comply with public health officials and share their contact history or quarantine if necessary. Yet only 58 percent of Americans would be likely to speak with a public health official who contacted them by phone or text message about the coronavirus outbreak, according to a Pew Research survey released October 30. “A substantial number of people do not comply with or provide adequate information needed for contact tracing to be effective,” Ndeffo says. Clearer and more consistent public health messaging could improve these numbers.

Time is of the essence
It’s important to act quickly to introduce social distancing measures when case counts begin to surge, as they are now in the United States and Europe, Shaman says, because outbreaks grow at exponential rates. “Exponential growth leads to a tsunami-like effect; it gets worse the longer you wait on it.”

He and colleagues simulated what would have happened had states done exactly what they did at the beginning of the U.S. epidemic in March, only earlier. Enacting social distancing and stay-at-home orders on March 1 instead of March 8 would have headed off about 600,000 confirmed cases and 32,000 deaths. Acting two weeks earlier would have avoided more than 1 million cases and about 60,000 deaths nationwide, Shaman and colleagues reported November 6 in Science Advances.

No one can turn back the clock. But countries including Vietnam, Taiwan, Singapore, New Zealand and Australia have shown that acting aggressively can curb the spread of the virus. “Going forward, the longer you delay in acting on this virus the more damage it does,” both to people who are infected and to the economy, Shaman says.

For instance, at the end of September, 89 counties in Tennessee eased or removed social distancing restrictions. But as COVID-19 cases rose, traffic to bars and restaurants decreased, researchers from Vanderbilt University in Nashville report. Cell phone mobility data as of October 21 suggest that business dropped once restrictions were lifted and was 24 percent below where it was during the same time in 2019. Those findings suggest that infection rates, not restrictions, have a bigger effect on people’s choices, the researchers conclude.

“If you don’t control the virus,” Shaman says, “you’re not going to have an economy.”