Just a stab in the dark, but you’ve probably heard: There is a total solar eclipse today, August 21.

For the first time since 1979, the moon’s shadow will zip across the continental United States. The shadow will travel from Oregon to South Carolina in a swift 92 minutes. For those in the path of totality, total darkness will last only a couple of minutes. There and elsewhere in most of the United States, the moon will partially block the sun for around three hours.
If you don’t already have plans to travel to the 115-kilometer-or-so-wide path of totality, well, you’re probably too late. But here are some links to help you experience the eclipse, whether or not you’re able to see it in person.

The eclipse will be visible in all of North America — as well as in Central America and a small part of South America. Wondering what you’ll see where you live? Check out this interactive map from NASA or this cool tool from Vox.

Still need eclipse glasses? While many retailers have been sold out for days, some organizations are handing out free glasses at eclipse-watching events. Check your local TV/newspaper/radio stations’ newsfeeds for the latest. Make sure your glasses are safe.

No eclipse glasses? Never fear! You can still see the moon eclipsing the sun by making a pinhole projector or a box projector. Or just let sunlight shine through something that has holes, like a colander or Ritz Cracker (look at the ground to see the shape of the shadow the holes cast).

Watching with kids? Check out Growth Curve blogger Laura Sanders’ tips for protecting little ones’ eyes during the eclipse.
Which reminds me: Whatever you do, don’t look directly at the sun. Permanent damage to your eyes may result. If you’re in the path of totality, officials say it’s OK to look directly at the sun once the moon completely blocks it. But that’s very brief, so be prepared to quickly look away or shield your eyes once the moon slips out of total alignment.

Want to do more with your eclipse experience? It’s not too late to participate in a citizen science project.

Stuck indoors, or out of totality? Watch the livestream. NASA’s programming begins at noon Eastern on NASA TV, which you can watch at this link or right here:
Want some tunes to go along with it? The NASA interns made an eclipse playlist. There are also several Spotify playlists around, like this one from WXPN, this from the Washington Post and this one from the Boston Globe.

If all this excitement has you fancying a future in eclipse chasing, check out our interactive map of the next 15 total solar eclipses.

And let’s not forget that there will be a ton of science going on during the eclipse. Here are the big questions physicists and astronomers will seek to answer today.

Still want more? Follow us on Facebook and on Twitter for eclipse updates and RT’s of our correspondents in totality. Watch as the Science News team takes over the Society for Science & the Public’s Snapchat (Society4Science). And come back to Science News later today for a report from our astronomy writer, Lisa Grossman, who is spending the day in Casper, Wyo., with a research team that’s studying the sun’s wispy atmosphere, the corona.

Molecules are seriously chilling out. Scientists report the first cooling of molecules below a previously impassable milestone. The result, in which scientists cooled molecules down to tens of millionths of a degree, is a step toward reaching the ultracold temperatures already achievable with atoms, researchers report August 28 in Nature Physics.

Scientists regularly chill atoms to less than a millionth of a degree above absolute zero (‒273.15° Celsius), even reaching temperatures as low as 50 trillionths of a degree (SN: 5/16/15, p. 4). But molecules are more difficult to cool down, as they can spin and vibrate in a variety of ways, and that motion is a form of heat.
Previously, physicists have made ultracold molecules by convincing prechilled atoms to link up (SN: 12/20/08, p. 22), but the technique works for only a few kinds of molecules. Putting the freeze on already assembled molecules has allowed scientists to chill additional types but, until now, down to only a few hundreds of millionths of degrees.

Using lasers and magnetic fields, the scientists corralled and cooled molecules inside a device called a magneto-optical trap. In the trap, molecules of calcium monofluoride are slowed — and therefore cooled — when they absorb photons from a laser. But only so much cooling is possible with this method. To go beyond what’s called the Doppler limit, the researchers adapted a method used for cooling atoms, known as Sisyphus cooling. Two lasers pointed at one another create an electromagnetic field that acts like an endless hill the molecule must climb, thereby sapping its energy and heat. With these two techniques, the molecules reached a frigid 50 millionths of a degree above absolute zero.
As the art of laser cooling advanced in recent decades, ultracold atoms rapidly became a popular research topic. Now, predicts study coauthor Michael Tarbutt, a physicist at Imperial College London, cold molecule research is “going to explode in exactly the same way that it did for cold atoms.”
Cold molecules could be useful for a variety of scientific purposes: studying how chemical reactions occur, looking for hints of new fundamental particles or simulating complex quantum materials in which many particles interact at once.

“It’s a really exciting result,” says physicist David DeMille of Yale University, who was not involved with the research. “It turns out it’s harder in almost every way to apply laser cooling and trapping to molecules, but there are many, many motivations for doing that.”

Immune cells can turn certain invaders on themselves, forcing them to prematurely self-destruct, researchers have discovered.

In mice, when white blood cells in the lungs engulf spores of a common airborne fungus, these immune cells release an enzyme that sends the fungal cells into programmed cell death. That prevents the spores from setting up shop in the lungs and sparking a potentially deadly lung infection, the researchers report in the Sept. 8 Science.

Found naturally in soil and decaying organic matter, the fungus, Aspergillus fumigatus, releases airborne spores that are found in small doses in the air people breathe every day. The finding may help explain why most people can regularly inhale the spores and not get sick. In people with weakened immune systems, though, this natural defense system doesn’t work. This research could eventually lead to better treatments for these patients.
Programmed cell death is a natural part of a cell’s life cycle — a way for organisms to break down old cells and make way for new ones. “Research in the last couple of decades has shown that microbes can exploit [cell death] pathways to cause disease,” says study coauthor Tobias Hohl, an infectious disease researcher at Memorial Sloan Kettering Cancer Center in New York City. But this study shows that the tables can be turned. “Not only can microbes exploit this in hosts, but host cells can exploit these pathways to instruct certain microbes to kill themselves.”

“The idea that the host triggers the mechanism of [programmed cell death] as a way of defending against infection is very cool,” says Borna Mehrad, a pulmonologist at the University of Florida College of Medicine in Gainesville who wasn’t part of the study.

Hohl and colleagues identified a gene in A. fumigatus that puts the brakes on programmed cell death. The gene, AfBIR1, shares an ancestor with the human gene survivin, which also regulates cell death.

When the researchers amped up the activity of AfBIR1 in a strain of the fungus, half the mice infected with the spores died during the eight-day study period. (Mice infected with unmodified spores were fine.) Cues that would normally send fungal cells to their death didn’t register, so the fungus was able to grow in the mice’s lungs.

In another experiment, the scientists gave mice a drug called S12, which took away AfBIR1’s brake effect. As a result, the mice were able to fight off the infection. “Those two findings suggested to us that this fungal [cell death] pathway really is critical,” Hohl says.
Hohl did this research with a special variety of A. fumigatus that changes color when its suicide instructions kick in. That advance allowed the researchers to make observations that weren’t possible before, Mehrad says.

For instance, Hohl and his colleagues noticed that fungal cells being engulfed by neutrophils, a type of white blood cell, appeared to be undergoing programmed cell death. That suggested that neutrophil activity might set off fungal programmed cell death.

Neutrophils release an enzyme called NADPH oxidase, and mice deficient in the enzyme weren’t as good at fending off the fungus, Hohl found. That makes sense with clinical data in humans too. People with a genetic mutation that causes a deficiency in NADPH oxidase are particularly at risk for developing an Aspergillus infection, Hohl says. People who have fewer neutrophils, due to chemotherapy or HIV infection, for instance, also make less of the enzyme and are less able to resist a fungal infection.

Survival rates vary, but the U.S. Centers for Disease Control and Prevention estimates that 41 percent of organ transplant recipients who contract aspergillosis die within a year. Seventy-five percent of stem cell transplant recipients with the infection die in that same time frame. Someday, a version of S12 that’s modified to work in humans might be able to boost these patients’ defenses against A. fumigatus infections, Hohl suggests.

In the future, he wants to see whether the same mechanisms extend to other fungal species too.

The patient arrived at the hospital one hot night in Masi-Manimba, an agricultural town unfurled along the Democratic Republic of the Congo’s Lukula River.

He couldn’t speak, he couldn’t walk, he was conscious but “barely could make … gestures,” says Béatrice Kasita, a nurse who was there when he came in. She remembers his deformed posture, how his body curved into a fetal position.

He was also unusually drowsy — a telltale sign of his illness. The patient, a 27-year-old man, had been brought in by a medical team screening villagers for sleeping sickness, a deadly parasitic disease spread via the bite of a blood-feeding fly.
Since the first case report in the late 14th century, the illness has ebbed and flowed in sub-Saharan Africa. Across the continent, the predominant form of sleeping sickness shows up in about two dozen countries, most cases now occurring in the DRC. The disease is a nightmarish scourge that can maim the brain and ultimately kill. But today, cases hover near an all-time low. In 2021, the World Health Organization reported just 747 cases of the predominant form, down from more than 37,000 in 1998.

That precipitous plunge came out of decades of work, millions of screenings, spinal taps upon spinal taps, toxic treatments and the rapid rise of safer though often burdensome ones, countless IV infusions, long hospital days and nights, medicine lugged to remote villages, and communities on constant alert for sleeping sickness’s insidious symptoms.

Now, a promising drug has fanned hope for halting transmission of the disease. Called acoziborole, the drug is taken by mouth in just a single dose. Kasita’s patient, who arrived at the hospital in June 2017, was among the first to try it.

Her hospital is one of 10 clinical trial sites in the DRC and Guinea working to test the drug with the Drugs for Neglected Diseases initiative, or DNDi, a nonprofit organization based in Geneva. In a small trial reported last year, the drug appeared to be safe and effective. A larger trial is ongoing, with results expected by the end of this year.
If the findings hold up, the drug would be “a game changer,” says Emmanuel Bottieau, an infectious disease specialist at the Institute of Tropical Medicine in Antwerp, Belgium, who is not involved with the clinical trial. A single-dose medication is “really a dream for us, coming from such a long history of very difficult or toxic or cumbersome treatments.”

But he and others know that even a game-changing drug doesn’t guarantee a win. The dominant form of sleeping sickness is on a short list of neglected tropical diseases the WHO is targeting for elimination by 2030. That means bringing cases in certain areas down to zero knowing that some control efforts may still be required. Vastly harder to achieve is disease eradication, where cases worldwide stay parked at zero permanently. (To date, just a single human infectious disease — smallpox — has been eradicated.)
Even elimination is no easy task — and can get harder as you approach the finish line. “We are advancing very well,” says José Ramón Franco, a WHO medical officer based in Geneva, “but we [haven’t] reached the last mile.”

Still, tiptoeing along the edges of optimism, some, like Kasita, are finding moments to cheer. For the severely ill patient, her team initially wondered if acoziborole would work. “Are we really going to help him with this single-dose treatment?”

Two weeks later, he could stand, with some support, and had started speaking again, a radical recovery. Kasita smiles widely as she remembers it. Watching him heal “was a great pleasure,” she says.

The symptoms of sleeping sickness
About 400 kilometers to the west of Masi-Manimba, physician Wilfried Mutombo Kalonji is preparing to visit Kasita’s hospital. Afterward, he’ll hit up hospitals in Idiofa, Bagata and then Bandundu, three other acoziborole clinical trial sites in the DRC. To reach the sites, Mutombo will travel by boat, plane, car and motorbike. He’ll stay in both modern hotels and hotels without running water or electricity. Then, he’ll return home to Kinshasa, the DRC’s bustling capital. It’s a great and noisy city, he grins, with people playing music in the streets and “many, many, many traffic jams.”

In Kinshasa, Roi Baudouin hospital is one of the DNDi’s acoziborole trial sites. Mutombo has been organizing logistics and ensuring that each site has what it needs to treat and monitor patients. That includes generators for electricity, an internet connection, medical equipment and trained clinical trial staff.

Mutombo has worked with sleeping sickness patients since 2004. Two weeks after finishing his medical training in Kasaï province, he shipped out to Kasansa, becoming the only medical doctor in a village of about 11,000 people. In Kasansa, which lies in western DRC, north of the Angola border, sleeping sickness was then, and still remains, endemic.

The disease, also called human African trypanosomiasis, is caused by a single-celled, ruffle-edged parasite that worms its way into the brain. One subspecies, Trypanosoma brucei gambiense, causes the vast majority of cases and tends to plague western and central Africa. Another, T.b. rhodesiense occurs in the eastern and southern parts of the continent and causes a more rapid, acute illness with far fewer cases in people.
Both subspecies can ride in the guts and glands of tsetse flies, which often buzz near bodies of water; many of Mutombo’s patients in Kasansa were fishers or farmers. When the fly bites, the parasite enters the bloodstream. From there, it can get picked up again when other flies feed, shuttling from insects to humans in a disease-spreading cycle.

In the blood, T.b. gambiense sparks a slow-burning illness that can begin with a fever and, if left untreated, end with death. As the parasite multiplies, lymph nodes enlarge and the head, muscles and joints ache. Patients can also become intensely itchy, scratching hard enough to damage the skin, Kasita says.

When the parasite slips past the blood-brain barrier, patients enter the second stage of the disease. No one knows exactly where the parasite lodges in the brain, but neurological symptoms can vary. Doctors and nurses describe a range of distressing and bizarre behaviors. One common behavior gives the illness its name. Somehow, the parasite reverses people’s sleep/wake cycle. “They will sleep a lot during the day, and at night, they will be up, watching,” Kasita says.

Patients can also feel depressed and confused, neglect to care for themselves, hallucinate or experience logorrhea, words cascading from lips in nonsensical streams. In some infected people, personalities can swing like a wrecking ball. Jacques Pépin, an infectious disease specialist at the University of Sherbrooke in Canada, worked with sleeping sickness patients in the 1980s and remembers one who suddenly threw a large rock at his head.

Such outbursts can be scary for patients and families, says Antoine Tarral, a pharmacologist and infectious disease physician who works with Mutombo and led the DNDi’s sleeping sickness program for 10 years. Fear of the disease can prompt villages to reject infected individuals, he says.

Sleeping sickness carries a social stigma that makes people feel like outcasts, Mutombo agrees. “This disease is terrible.” When he first began treating patients, he says, “I was doing my best to make them feel like human beings.”

But for decades, available treatments were terrible, too.
Sleeping sickness has a history of terrible treatments
For most of treatment history, injected or intravenous drugs were the only option for sleeping sickness. They could cure patients, but only if doctors administered them in time. And when cases advanced to the second stage, medical staff had to switch tactics. For patients, that meant a spinal tap to confirm diagnosis followed by different drugs.

Until the late 2000s, the most-used treatment for advanced gambiense sleeping sickness was the highly toxic melarsoprol. The drug is derived from arsenic (and it’s still the leading treatment for advanced rhodesiense cases). Medical staff administered the drug for 10 days via daily intravenous infusions that burned entering patients’ veins, Mutombo says. The treatment could also be lethal, killing some 5 percent of patients.

Mutombo grows somber remembering two of his patients who died, young men he tried to cure in Kasansa. “That was a very bad experience,” he says. “When patients come to the hospital, they come to receive a treatment, not to die … [from] the drug we gave them.”

But doctors didn’t have a lot of options. Without melarsoprol, patients with serious cases faced near-certain death.

Not long after his patients died, Mutombo heard that the DNDi was launching a project on a new, less toxic treatment for advanced cases. He jumped at the chance, applied to be an investigator and joined the project in 2006. The new treatment, called NECT, combined eflornithine, an IV drug developed for cancer, with the oral drug nifurtimox. Eflornithine was already being used to treat sleeping sickness, but required dozens of infusions, and nifurtimox was a treatment for Chagas disease.

In 2009, after a clinical trial and the WHO’s endorsement, NECT took off, rocketing past melarsoprol or eflornithine alone as the first-line treatment for advanced sleeping sickness. But NECT had some logistical snafus, Mutombo says. It wasn’t easy to transport, for one. Treatment for four patients came in 40-kilogram packages that had to be trucked over bad roads into rural areas that lacked medical workers. “That was a problem with NECT,” Mutombo says. “It was effective, but it was heavy and needed trained staff.”

Less than a decade later, Mutombo, Tarral and their DNDi colleagues debuted an easier alternative. Fexinidazole, at long last, was a drug doctors could deliver exclusively via pills rather than an IV. It’s not perfect — it’s administered by a nurse, patients need to take it for 10 days and it’s not best for the most severe cases (for these, the WHO still recommends NECT). But easy-to-use oral drugs lower the burden on health systems, Mutombo says. Medical staff could more easily bring treatments to remote patients. And that brought scientists one step closer to sleeping sickness’s elimination.
A new drug could help bring cases to zero
Acoziborole, the drug now being tested in clinical trials, may be another big step in the right direction. Just one dose cured some 95 percent of patients with late-stage infections, Mutombo, Tarral and colleagues reported November 29 in the Lancet Infectious Diseases. That’s comparable to treatment with NECT. “Acoziborole is one solution to manage this disease,” Tarral says.

Not only does the drug seem to be effective, but “it’s given orally … and it needs to be given only once,” says the University of Sherbrooke’s Pépin, who was not involved with the trial but wrote an opinion piece that appeared alongside the new report.

Yet, as Pépin points out, the acoziborole study has some limitations. The scientists tested the drug in just 208 patients, so no one knows if serious adverse effects might occur in larger populations. And the study wasn’t performed like the classic gold-standard clinical trial, with patients randomly assigned into different groups receiving different interventions.

Tarral acknowledges these drawbacks, which he says were due to low participant numbers. The researchers included only people with video-confirmed parasitic infections, which required years of searching for patients across 10 hospitals in two different countries.

“It’s not the standard approach, but that was the only possible approach,” Pépin says. “They did what could be done with the number of cases that are occurring now.”

The study’s promising results spurred a new, larger trial that will include 1,200 participants. This time, the team is enrolling people with positive antibody blood tests even if the parasite’s presence hasn’t been confirmed. Many of these participants may not actually be sick, says Veerle Lejon, a scientist at the French National Research Institute for Sustainable Development in Montpellier who was not involved in developing the drug but is collaborating with the DNDi on evaluating sleeping sickness diagnostics.

What this trial will offer, she says, is a raft of new data that will help determine the drug’s safety.
The challenges of eliminating an infectious disease
Even if acoziborole gets the green light, stamping out sleeping sickness isn’t a sure bet.

Eliminating an infectious disease is a slippery task. Success can, paradoxically, churn out new challenges. When case numbers dip low enough, for instance, interest in the disease can wane. Donors move money to other public health priorities, and once-robust control programs wither.

That happened for sleeping sickness in the 1960s, the last time cases dropped. Over the next few decades, cases ratcheted up, and epidemics broke out in Angola, the DRC and South Sudan. “Control of the disease was neglected, and then slowly, the disease came back,” says WHO medical officer Franco.

A doubled-down effort to find cases and treat them with ever-improving drugs got sleeping sickness under control again, with case numbers cratering to their low point today. But that level of surveillance is not sustainable, Franco says.
Health care workers can also lose knowledge of how to recognize the disease as they encounter fewer and fewer infected individuals, says Jennifer Palmer, a medical anthropologist at the London School of Hygiene and Tropical Medicine. “The challenge is really in making sure that people are aware that sleeping sickness is still a problem,” she says. In a small study in South Sudan, reported in 2020, Palmer and colleagues found that lay people encouraging people in the community to get tested accounted for more than half of detected cases.

Still, getting patients tested and treated can depend on whether they’re able to safely travel to health facilities. With the threat of violence in South Sudan and armed conflict in eastern DRC, the fate of sleeping sickness may also be shaped by the whims of war.

Even if every infected person was promptly found and treated, the disease-causing parasite would likely linger in wild and domestic animals. Scientists have found T.b. gambiense, for instance, in dogs, pigs, goats and sheep. No one knows the role infected animals play in reigniting outbreaks in humans.

Though the road to elimination may still be rocky, the patients Kasita and others are treating in Masi-Manimba and beyond offer a lesson for those working on disease elimination: Don’t give up too soon. Maybe the world won’t reach zero sleeping sickness cases by 2030, Lejon says, “but I think we should really give it a try,” she says. “We have momentum at this moment to do it.”

Mutombo echoes her enthusiasm. In less than 20 years, new drugs have completely overhauled patient care, he says. “We’ve made a great change in less than one generation…. Now, we expect that elimination is within reach.”

Discoveries on the island of Borneo illustrate that cave art emerged in Southeast Asia as early as in Western Europe, and with comparable complexity, researchers say.

A limestone cave in eastern Borneo features a reddish-orange painting of a horned animal, possibly a type of wild cattle that may have been found on the island at the time. The painting dates to at least 40,000 years ago, concludes a team led by archaeologist Maxime Aubert of Griffith University in Southport, Australia. This creature represents the oldest known example of a painted figure anywhere in the world, the scientists report online November 7 in Nature.
The same cave walls contain two hand outlines framed in reddish orange pigment that were made at least 37,200 years ago and a similar hand stencil with a maximum age of 51,800 years.

Three nearby caves display instances of a second rock art style that appeared around 20,000 years ago, the investigators say. Examples include purple-hued, humanlike figures and hand stencils, some decorated with lines or dots. Painted lines link some hand stencils to others.

Age estimates rest on analyses of uranium in mineral deposits that had formed over and underneath parts of each cave painting. Scientists used known decay rates of radioactive uranium in these deposits to calculate maximum and minimum dates for the paintings.

Aubert’s group previously used this technique, called uranium-series dating, to calculate that people on the nearby Indonesian island of Sulawesi created hand stencils on cave walls nearly 40,000 years ago (SN: 11/15/14, p. 6).
“Cave art could have potentially been exported from Borneo to Sulawesi and all the way to Papua and Australia,” Aubert says. Australian cave paintings of humanlike figures resemble those found on Borneo, he says. But the ages of the Australian finds remain uncertain.

No Southeast Asian cave paintings have been found from when humans first arrived in the region, between 70,000 and 60,000 years ago. At that time and up to the end of the last Ice Age around 10,000 years ago, Borneo formed mainland Eurasia’s easternmost tip thanks to lowered sea levels.

Those first Southeast Asians may have created cave art that hasn’t been discovered, Aubert says. Or, small groups of early colonizers may not have painted on cave walls until their populations expanded, leading to more complex social and ritual behaviors. It’s also possible that another human migration from elsewhere in Asia brought rock art to Borneo roughly 50,000 years ago.
Whatever the case, “Western European and Southeast Asian cave art seem to first appear at about the same time and with remarkable similarities,” says archaeologist Sue O’Connor of Australian National University in Canberra, who did not participate in the new study.
Other investigators have used the uranium-series technique to date a painted red disk in a Spanish cave to at least 40,800 years ago (SN: 7/28/12, p. 15). Another report this year suggested that Neandertals painted abstract shapes and hand stencils on the walls of several Spanish caves at least 64,800 years ago (SN: 3/17/18, p. 6).

Aubert’s team has criticized that study, saying the researchers may have unintentionally dated mineral deposits that are much older than the artworks. If so, humans rather than Neandertals could have created the Spanish cave art.

Meanwhile, scientists who conducted the Neandertal cave art study express their own doubts about the reliability of dates for the Borneo paintings. Descriptions of sampled mineral deposits from the Borneo caves leave it unclear whether, for example, Aubert’s group dated the horned animal figure or adjacent paint remnants of some other, unidentified figure, says archaeologist João Zilhão of the University of Barcelona.

Zilhão and Neandertal paper coauthor Paul Pettitt of Durham University in England don’t doubt that cave painting emerged in Southeast Asia at least 40,000 years ago. But they and Aubert’s team disagree about how to collect mineral samples for dating rock art.

Losing one variety of gut bacteria may lead to type 2 diabetes as people age.

Old mice have less Akkermansia muciniphila bacteria than young mice do, researchers report November 14 in Science Translational Medicine. That loss triggers inflammation, which eventually leads cells to ignore signals from the hormone insulin. Such disregard for insulin’s message to take in glucose is known as insulin resistance and is a hallmark of type 2 diabetes.

Researchers have suspected that bacteria and other microbes in the gut are involved in aging, but how the microbes influence the process hasn’t been clear. Monica Bodogai of the U.S. National Institute on Aging in Baltimore and colleagues examined what happens to mice’s gut bacteria as the rodents age. The mice lose A. muciniphila, also called Akk, and other friendly microbes that help break down dietary fiber into short-chain fatty acids, such as butyrate and acetate. Those fatty acids signal bacteria and human cells to perform certain functions.
Losing Akk led to less butyrate production, Bodogai’s team found. In turn, loss of butyrate triggered a chain reaction of immune cell dysfunction that ended with mice’s cells ignoring the insulin.

Treating old mice and elderly rhesus macaques with an antibiotic called enrofloxacin increased the abundance of Akk in the animals’ guts and made cells respond to insulin again. Giving old animals butyrate had the same effect, suggesting that there may be multiple ways to head off insulin resistance in older people in the future.

For the first time, humans have built a set of pushy, destructive genes that infiltrated small populations of mosquitoes and drove them to extinction.

But before dancing sleeveless in the streets, let’s be clear. This extermination occurred in a lab in mosquito populations with less of the crazy genetic diversity that an extinction scheme would face in the wild. The new gene drive, constructed to speed the spread of a damaging genetic tweak to virtually all offspring, is a long way from practical use. Yet this test and other news from 2018 feed one of humankind’s most persistent dreams: wiping mosquitoes off the face of the Earth.

For the lab-based annihilation, medical geneticist Andrea Crisanti and colleagues at Imperial College London focused on one of the main malaria-spreading mosquitoes, Anopheles gambiae. The mosquitoes thrive in much of sub-Saharan Africa, where more than 400,000 people a year die from malaria, about 90 percent of the global total of malaria deaths.

To crash the lab population, the researchers put together genes for a molecular copy-and-paste tool called a CRISPR/Cas9 gene drive. The gene drive, which in this case targeted a mosquito gene called doublesex, is a pushy cheat. It copies itself into any normal doublesex gene it encounters, so that all eggs and sperm will carry the gene drive into the next generations. Female progeny with two altered doublesex genes develop more like males and, to people’s delight, can’t bite or reproduce.

In the test, researchers set up two enclosures, each mixing 150 males carrying the saboteur genes into a group of 450 normal mosquitoes, males and females. Extinction occurred in eight generations in one of the enclosures and in 12 in the other (SN: 10/27/18, p. 6).

This is the first time that a gene drive has forced a mosquito population to breed itself down to zero, says Omar Akbari of the University of California, San Diego, who has worked on other gene drives. However, he warns, “I believe resistance will be an issue in larger, diverse populations.” More variety in mosquito genes means more chances of some genetic quirk arising that counters the attacking gene drive.

But what if a gene drive could monkey-wrench a wild population, or maybe a whole species, all the way to extinction? Should people release such a thing? To make sense of this question, we humans will have to stop talking about “mosquitoes” as if they’re all alike. The more than 3,000 species vary considerably in what they bite and what ecosystem chores they do.

The big, iridescent adults of Toxorhynchites rutilus, for instance, can’t even drink blood. And snowmelt mosquitoes (Ochlerotatus communis) are pollinators of the blunt-leaved orchid (Platanthera obtusata), ecologist Ryo Okubo of the University of Washington in Seattle said at the 2018 meeting of the Society for Integrative and Comparative Biology.
Estimating what difference it would make ecologically if a whole mosquito species disappeared has stirred up plenty of speculation but not much data. “I got pretty fed up with the hand-waving,” says insect ecologist Tilly Collins of Imperial College London. So she and colleagues dug through existing literature to see what eats An. gambiae and whether other mosquitoes would flourish should their competitor vanish.

So far, extermination of this particular mosquito doesn’t look like an ecological catastrophe, Collins says. Prey information is far from perfect, but diets suggest that other kinds of mosquitoes could compensate for the loss. The species doesn’t seem to be any great prize anyway. “As adults, they are small, not juicy, and hard to catch,” she says. The little larvae, built like aquatic caterpillars with bulging “shoulders” just behind their heads, live mostly in small, temporary spots of water.
The closest the researchers came to finding a predator that might depend heavily on this particular mosquito was the little East African jumping spider Evarcha culicivora. It catches An. gambiae for about a third of its diet and likes the females fattened with a human blood meal. Yet even this connoisseur “will readily consume” an alternative mosquito species, the researchers noted in July in Medical and Veterinary Entomology.

Collins also thinks about the alternatives to using genetically engineered pests as pest controls. Her personal hunch is that saddling mosquitoes with gene drives to take down their own species is “likely to have fewer ecological risks than broad-spectrum use of pesticides that also kill other species and the beneficial insects.”

Gene drives aren’t the only choice for weaponizing live mosquitoes against their own kind. To pick just one example, a test this year using drones to spread radiation-sterilized male mosquitoes in Brazil improved the chances that the old radiation approach will be turned against an Aedes mosquito that can spread Zika, yellow fever and chikungunya.

Old ideas, oddly enough, may turn out to be an advantage for antimosquito technologies in this era of white-hot genetic innovation. Coaxing the various kinds of gene drives to work is hard enough, but getting citizens to sign off on their use may be even harder.

The monarch butterfly isn’t the only insect flying up and down North America in a mind-boggling annual migration. Tests show a big, shimmering dragonfly takes at least three generations to make one year’s migratory loop.

Ecologist Michael Hallworth and his colleagues pieced together the migration of the common green darner, described December 19 in Biology Letters, using data on forms of hydrogen in the insects’ wings, plus records of first arrivals spotted by citizen scientists.
The study reveals that a first generation of insects emerges in the southern United States, Mexico and the Caribbean from about February to May and migrates north. Some of those Anax junius reach New England and the upper Midwest as early as March, says Hallworth, of the Smithsonian Migratory Bird Center headquartered in Washington, D.C.

Those spring migrant darners lay eggs in ponds and other quiet waters in the north and eventually die in the region. This new generation migrates south from about July until late October, though they have never seen where they’re heading. Some of these darners fly south in the same year their parents arrived and some the next year, after overwintering as nymphs.

A third generation emerges around November and lives entirely in the south during winter. It’s their offspring that start the cycle again by swarming northward as temperatures warm in the spring. With a wingspan as wide as a hand, they devote their whole lives to flying hundreds of kilometers to repeat a journey their great-grandparents made.
Scientists knew that these dragonflies migrated. Dragonfly enthusiasts have spotted swarms of the green darners in spring and in fall. But which generations were doing what has been tricky to demonstrate. “Going in, we didn’t know what to expect,” Hallworth says.
Tracking devices that let researchers record animals’ movements for more than a week or two haven’t been miniaturized enough to help. The smallest still weigh about 0.3 grams, which would just about double a darner’s weight, Hallworth says. So researchers turned to chemical clues in darner tissues. Conservation biologist and study coauthor Kent McFarland succeeded at the delicate diplomacy of persuading museums to break off a pinhead-sized wing tip fragment from specimens spanning 140 years.

Researchers checked 800 museum and live-caught specimens for the proportion of a rare heavy form of hydrogen that occurs naturally. Dragonfly wings pick up their particular mix of hydrogen forms from the water where the aquatic youngsters grow up. Scientists have noticed that a form called hydrogen-2 grows rarer along a gradient from south to north in North America. Looking at a particular wing in the analysis, “I can’t give you a zip code” for a darner, Hallworth says. But he can tell the native southerners from Yankees.

An adult darner, regardless of where it was born, is “a green piece of lightning,” says McFarland, of the Vermont Center for Ecostudies in White River Junction. Darners maneuver fast enough to snap insect prey out of the air around ponds across North America. The front of an adult’s large head is “all eye,” he says, and trying to catch samples for the study was “like hitting a knuckleball.”

Although the darners’ north-south migration story is similar to that of monarchs (Danaus plexippus), there are differences, says evolutionary biologist Hugh Dingle of the University of California, Davis, who has long studied these butterflies. Monarchs move northward in the spring in stepwise generations, instead of one generation sweeping all the way to the top of its range.

Also, Dingle says, pockets of monarchs can buck the overall scheme. Research suggests that some of the monarchs in the upper Midwest do a whole round trip migration in a single generation. As researchers discover more details about green darners, he predicts, the current basic migration scheme will turn out to have its quirky exceptions, too.

The adolescent saber-toothed cat on a summertime hunt realized too late that she had made a terrible miscalculation.

Already the size of a modern-day tiger, with huge canine teeth, she had crept across grassy terrain to ambush a giant ground sloth bellowing in distress. Ready to pounce, the cat’s front paw sank into sticky ground. Pressing down with her other three paws to free herself, then struggling in what has been called “tar pit aerobics,” she became irrevocably mired alongside her prey.

Scenarios much like this played out repeatedly over at least the last 35,000 years at California’s Rancho La Brea tar pits. Entrapped herbivores, such as the sloth, attracted scavengers and predators — including dire wolves, vultures and saber-toothed Smilodon cats — to what looked like an easy meal. Eventually the animals would disappear into the muck, until paleontologists plucked their fossils from the ground in huge numbers over the last century.

Five million or so fossils have been found at the site. But “it’s not like there was this orgy of death going on,” says Christopher Shaw, a paleontologist and former collections manager at the La Brea Tar Pits and Museum in Los Angeles. He calculates that such an entrapment scenario, dooming 10 or so large mammals and birds, would have needed to occur only once per decade over 35,000 years to account for that bounty of fossils.

At La Brea, the collection of Smilodon fatalis fossils alone includes more than 166,000 bones, from an estimated 3,000 of the ill-fated prehistoric cats. Famed for their fearsome canines, which grew up to 18 centimeters long, S. fatalis weighed as much as 280 kilograms, bigger than most of today’s largest lions and tigers.
Fossils of S. fatalis, the second largest of three Smilodon species that roamed the Americas during the Pleistocene Epoch, have been found across the United States and in South America, west of the Andes as far south as Chile. And a recent study put S. fatalis in Alberta, Canada, about 1,000 kilometers north of its previously known range.

But the La Brea fossil site, unique in offering up so many specimens, is the source of the vast majority of knowledge about the species. There, fossils of dire wolves and saber-toothed cats together outnumber herbivores about 9-to-1, leading scientists to speculate that both predators may have formed prides or packs, similar to modern lions and wolves. Yet a small number of experts argue against cooperative behavior for Smilodon, reasoning that pack-living animals would have been too intelligent to get mired en masse.
New studies may help settle the debate about Smilodon’s sociality, and answer questions about how the cat lived and why it died out 10,000 to 12,000 years ago.

“We have an innate curiosity to understand what it was doing and why it went extinct,” says Larisa DeSantis, a vertebrate paleontologist at Vanderbilt University in Nashville. Now, she says, “we can answer these questions.”

DeSantis is studying microscopic wear on fossil teeth and chemical signatures in the enamel to reveal Smilodon’s diet. Other scientists are doing biomechanical studies of the skull, fangs and limbs to understand how the powerful cat captured and killed its prey. Some researchers are extracting DNA from fossils, while others are gathering data on the paleoclimate to try to piece together why Smilodon died out.

“It’s the T. rex of mammals … a big, scary predator,” says Ashley Reynolds, a paleontology Ph.D. student and fossil cat researcher at the University of Toronto. She presented the Alberta fossil find in October in Albuquerque at the Society of Vertebrate Paleontology conference. Explaining why Smilodon cats continue to excite researchers, she says, “They’re probably the baddest of all the cats that have ever existed.”
Safety in numbers
Whether Smilodon was a pack hunter has long been debated (SN: 10/28/17, p. 5) because living in groups is rare among large cats today. But an unusual number of healed injuries in the Smilodon bones at La Brea makes it unlikely that these cats were solitary, DeSantis and Shaw reported in November in Indianapolis at a meeting of the Geological Society of America.

More than 5,000 of the Smilodon bones at La Brea have marks of injury or illness: tooth decay, heavily worn arthritic joints, broken legs and dislocated elbows that would have occurred before the animals’ tar burial. Dramatic examples include crushed chests and spinal injuries, which the cats somehow survived. “You would actually wince to see these horribly, traumatically injured specimens,” says Shaw, who is also coeditor of the 2018 book Smilodon: The Iconic Sabertooth.

One particularly debilitating injury was a crippled pelvis, but evidence of new bone growth shows that the animal lived long enough for healing to occur. “There was a lot of infection, pain and smelly stuff, and just a really awful situation for this animal, but it survived well over a year,” Shaw says. “To me that indicates [the injured cat] was part of a group that helped it survive by letting it feed at kills and protecting it.”

Shaw and DeSantis looked at a series of specimens with what were probably agonizing maladies in the teeth and jaws, including fractured canines and massive infections that left animals with misshapen skulls.

“These animals probably couldn’t have gone out … to kill anything,” Shaw says. “You know how it is when you have a toothache. This is like that times 100.”
DeSantis compared microscopic pits and scratches on the surface of the teeth of injured animals with microwear on the teeth of seemingly healthy Smilodon cats. The injured cats’ dental surfaces indicated that the animals were eating softer foods, which would have been less painful to chew, “likely a higher proportion of flesh, fat and organs, as opposed to bone,” she says.

The findings are consistent with the interpretation that Smilodon was a group-living animal, she says, and that the cats “allowed each other access to food when [injured pack members] couldn’t necessarily take down their own prey.”

Reynolds agrees that the healed injuries are persuasive evidence that Smilodon lived in groups. “When you see an animal with really nasty injuries that healed somehow, it does make you wonder if they were cared for.”

Not everyone is convinced, however. Ecologist Christian Kiffner of the Center for Wildlife Management Studies in Karatu, Tanzania, has studied modern carnivores such as African lions and spotted hyenas. “Relatively long survival of Smilodon fatalis individuals after dental injuries had occurred does not necessarily provide airtight evidence for a specific social system in this species,” he says. “It is very, very difficult to use patterns in Pleistocene carnivore [fossil] assemblages to make inferences about behavior of an extinct species.”

Even if the saber-toothed cats did live in groups, the animals’ exact social structure remains an open question, Reynolds says. Modern lion prides have numerous females and several younger males led by an alpha male, with intense competition between male lions. As a result, males are much bigger than females, as the males must work hard to defend their positions.

Despite searching, scientists have not found obvious evidence of a size difference between the sexes in Smilodon; researchers can’t even tell which La Brea fossils are male or female. Size differences between the sexes, if they existed, may have been small.

“That lack of sexual dimorphism is odd,” says Blaire Van Valkenburgh, a UCLA paleontologist who studies fossil carnivores. Sex-related size differences are seen in many big cats today, most particularly lions. She thinks the lack of sexual dimorphism in Smilodon might hint at a different social structure. Perhaps males weren’t competing quite so intensely for access to females. Maybe there was no single alpha male preventing the majority of males from making a move.

Family affair
Perhaps Smilodon groups had an alpha female rather than an alpha male, or an alpha pair. Such is the case in modern wolves and coyotes, which have less pronounced size differences between sexes than lions do. The prehistoric cats “could have had extended family structures [similar to wolves] where uncles and aunts hung around, because it probably took a while to raise the young saber-toothed cats,” Van Valkenburgh suspects.

Kittens may have taken a long time, as long as 22 months, to get most of their adult teeth, she says. The upper canines took even longer, as much as three years or more, to reach their massive size, researchers reported in PLOS ONE in 2015. Modern lions, in contrast, typically have all of their adult teeth by 17 months, Van Valkenburgh says.

Smilodon kittens also probably went through a substantial learning curve before attempting to take down large prey. “It took longer for them to learn how to safely kill something without breaking their teeth or biting in the wrong place and hurting themselves,” Van Valkenburgh speculates.

Pack living would enable this slower development: “If you’re a social species, you can afford to grow at a slower rate than a nonsocial species because you have a family safety net,” Reynolds says. She is studying Smilodon fossils from Peru’s Talara tar pits for evidence of slow bone development using bone histology, examining thin cross sections under a microscope to determine such things as age and growth rate.
To understand how saber-toothed cats eventually took down prey, Van Valkenburgh joined paleobiologist Borja Figueirido of the University of Málaga in Spain and others. The group studied the biomechanics of Smilodon’s killing bite and how the animal used its sabers. That work, published in the October 22, 2018 Current Biology, adds to a consensus that the cat used its powerful forelimbs, which existed even in the youngsters (SN Online: 9/27/17), to pin prey before applying a lethal bite to the neck.

“The specialization of being a saber-toothed appears to have been partly to effectively take prey larger than yourself and to do that very quickly,” Van Valkenburgh says. With the prey tightly gripped, a Smilodon cat would position itself so that one or two really strong canine bites would rip open the pinned animal’s throat.

In contrast, lions suffocate prey — one lion may clamp its jaws around the neck, crushing the windpipe, while another uses its mouth to cover the victim’s nose and mouth. Using this slower method would have increased Smilodon’s chances of injuring or damaging those precious canine teeth.

Diverging senses
Smilodon and its extinct saber-toothed relatives are on a branch of the cat family tree that is far from today’s cats. Scientists think Smilodon’s branch diverged from the ancestors of all living cats about 20 million years ago. Given the evolutionary distance, researchers are still trying to determine how similar — or different — Smilodon was from its living feline cousins. A recent focus has been the cat’s sounds and senses.

At the October vertebrate paleontology conference, Shaw presented evidence that Smilodon may have roared, as do lions, tigers, leopards and their close relatives. The clues come from 150 La Brea fossils that were once part of the hyoid arch, or larynx, in the Smilodon throat. (Tar pits stand out for preserving tiny bones rarely found elsewhere.) The small fossils are very similar in shape and style to those of roaring cats. House cats and others that purr have a different arrangement of bones.
Smilodon may have “used this type of communication as an integral part of social behavior,” Shaw says. Roaring, however, is not a sure sign of pack living, Reynolds notes; most roaring cats today do not live in large groups.

How Smilodon’s sense of smell compared with living cats’ is something else researchers wonder about. To probe this part of the extinct animal’s biology, a team lead by Van Valkenburgh looked at Smilodon’s cribriform plate — a small, perforated bone inside the skull. Smell-sensing nerve cells pass through holes in the plate from the olfactory receptors in the nose to the brain. The size and number of holes are thought to correlate with the number of receptors and, therefore, the extent of an animal’s sense of smell.

To confirm this link, Van Valkenburgh’s team combined CT scans and 3-D images of skulls from 27 species of living mammals with information on the number of olfactory receptor genes. A CT scan of a skull revealed that Smilodon may have had slightly fewer olfactory receptor nerve cells than a domestic cat, the researchers reported at the paleontology conference. Smilodon’s sense of smell was perhaps 10 to 20 percent less keen than a modern lion’s, says Van Valkenburgh, whose team reported the findings in the March 14, 2018 Proceedings of the Royal Society B.

Smilodon “might have relied more heavily on their eyes and their ears,” she says. Perhaps, in an ancient evolutionary divergence, Smilodon’s level of reliance on smell went in a slightly different direction than in modern big cats.

Saber-toothed swan song
As the pieces of the Smilodon puzzle fall into place, perhaps the biggest remaining mystery is why the animal disappeared 10,000 to 12,000 years ago. Debate about the extinction of some of North America’s large mammal species swings between blaming humans and climate change (SN: 11/10/18, p. 28). While humans, who probably arrived on the continent more than 15,000 years ago, and Smilodon certainly knew one another in the Americas, they may not have overlapped at La Brea, Shaw says. The earliest evidence of people in the Los Angeles Basin is about 11,000 years ago, by which time Smilodon may or may not already have gone. Nevertheless, human hunting of large prey elsewhere in the Americas could have led to a scarcity of food for the big cats, he says.

One theory holds that Smilodon went through tough times at La Brea when lack of prey forced the saber-toothed cats to consume entire carcasses including bones. This has been posited as the reason for all those broken teeth among the La Brea fossils. But DeSantis isn’t convinced; she thinks breakages happened during scuffles with prey. She says dental microwear suggests that Smilodon was not eating great quantities of bone.
Some opportunistic carnivores, such as cougars, did eat bone and managed to survive to the modern day. Perhaps Smilodon couldn’t adapt to hunting smaller prey when larger herbivores disappeared, also around 10,000 to 12,000 years ago (SN: 11/24/18, p. 22).

“A lot of the large prey on the landscape go extinct,” DeSantis says. “You lose out on the horses, camels, giant ground sloths, mammoths and mastodon. That’s got to have had an impact.”

The challenge of dating fossils from the tar pits has been one hurdle to understanding exactly what was going on with Smilodon over time. Bones deposited over many thousands of years get jumbled by movement in the tar, for reasons experts don’t fully understand. Plus, the tar itself becomes embedded in each specimen, complicating carbon dating.

However, new methods of chemically pretreating fossils to remove the tar have made carbon dating much easier and cheaper — and a multi-institutional project is now dating hundreds of Smilodon and other bones. Researchers will soon be able to track changes in Smilodon over the 35,000 years of prehistory recorded at La Brea and correlate fossil changes to known changes in climate over that time.

“We’re going to have a much better handle,” Van Valkenburgh says, “on what was going on towards the end of their existence.”

This article appears in the March 30, 2019 issue of Science News with the headline, “The Baddest Cat of All: Fresh details say saber-toothed Smilodon helped injured pack members.”

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.”