The next flu drug could come from frog mucus. It’s not as crazy as it sounds: For decades, scientists have searched for new antiviral drugs by mining proteins that animals produce to protect themselves from microbes. In lab tests, proteins found in amphibian secretions can defend against HIV, herpes and now the flu.

David Holthausen of Emory University in Atlanta and colleagues sampled slime from the skin of Hydrophylax bahuvistara, a recently discovered frog species from southern India. They tested the influenza-fighting ability of 32 slime peptides. Four showed promise, but three proved toxic to mammals.
The fourth peptide, however, was safe and showed a propensity for fighting off the flu. When exposed to four H3N2 and eight H1N1 strains, this peptide, dubbed urumin, inhibited H3N2 viruses to a degree but was particularly adept at killing H1N1 viruses, which are more common among humans. The frog slime protein even cut viral numbers in a set of seven drug-resistant strains and protected mice during flu infections. Urumin blows up flu virus particles by targeting the stalk region of the hemagglutinin protein in H1 varieties, the team found. With further development, urumin could form the basis of future influenza drugs, the researchers write in the April 18 Immunity.

Fascination with faces is nature, not nurture, suggests a new study of third-trimester fetuses.

Scientists have long known that babies like looking at faces more than other objects. But research published online June 8 in Current Biology offers evidence that this preference develops before birth. In the first-ever study of prenatal visual perception, fetuses were more likely to move their heads to track facelike configurations of light projected into the womb than nonfacelike shapes.

Past research has shown that newborns pay special attention to faces, even if a “face” is stripped down to its bare essentials — for instance, a triangle of three dots: two up top for eyes, one below for a mouth or nose. This preoccupation with faces is considered crucial to social development.
“The basic tendency to pick out a face as being different from other things in your environment, and then to actually look at it, is the first step to learning who the important people are in your world,” says Scott Johnson, a developmental psychologist at UCLA who was not involved in the study.

Using a 4-D ultrasound, the researchers watched how 34-week-old fetuses reacted to seeing facelike triangles compared with seeing triangles with one dot above and two below. They projected triangles of red light in both configurations through a mother’s abdomen into the fetus’s peripheral vision. Then, they slid the light across the mom’s belly, away from the fetus’s line of sight, to see if it would turn its head to continue looking at the image.
The researchers showed 39 fetuses each type of triangle five times. Of the 195 times a facelike triangle was projected, fetuses turned their heads 40 times. In contrast, the nonfacelike triangles elicited only 14 head turns, says study coauthor Vincent Reid of Lancaster University in England. The finding suggests that fetuses share newborns’ predisposition for looking at facelike shapes, the researchers conclude.
Psychologist Melanie Spence of the University of Texas at Dallas, who was not involved in the work, says it’s a leap to draw too many similarities between the visual perceptions of fetuses and newborns. Although the triangle images mimic facelike ones used to test newborns, they aren’t the same, she notes. Scientists typically show babies faces in black and white, with head-shaped borders.

Still, Johnson says evidence that a fundamental aspect of facial perception may be hardwired into humans’ visual system is “very, very exciting.” The new study’s method of projecting images into the womb and watching the fetus’s reaction also “opens up all kinds of new doors to understand human development,” Johnson says. A similar light projection and 4-D ultrasound technique might be used to see whether fetuses can distinguish between different quantities in the same way that babies can.

A protein made by the fetus may lead to preeclampsia in moms.

People born to mothers who had the prenatal disorder were more likely to have certain DNA variations near a gene known to influence blood vessels. The results, published online June 19 in Nature Genetics, point to that gene as a possible preeclampsia culprit, and may help scientists develop ways to stop or prevent the pregnancy complication. Preeclampsia, which is marked by a dangerous spike in blood pressure, affects about 5 percent of pregnancies and is estimated to kill over 70,000 women a year globally.
Scientists have known that preeclampsia can run in families, but the genetics of the fetus hadn’t been scrutinized. “Over the years, people have looked at mothers’ genes,” says geneticist Linda Morgan of the University of Nottingham in England. “This is the first large study to look at babies’ genes.”

Morgan and colleagues compared DNA variations in 2,658 babies, children and adults born to mothers who had preeclampsia with those in more than 300,000 people. (This large group probably included some people born to mothers with the condition, but the vast majority were not.)

A genome-wide association study (GWAS), a technique used to comb through DNA looking for genetic variations that may be linked to a disorder, pinpointed a spot on chromosome 13, near a gene called FLT1. That gene is involved with blood vessel formation, an intricate process for the placenta as it grows into the inside wall of the uterus and merges the baby’s blood supply to the mother’s. The same genetic hot spot turned up in tests of a second group of offspring from mothers who had preeclampsia, Morgan and colleagues report. Another DNA variation near the gene also showed a link to the disorder.

Identifying FLT1 “makes a lot of sense,” says Ananth Karumanchi, a vascular biologist at Beth Israel Deaconess Medical Center in Boston, who was not involved in the study. Earlier experiments by Karumanchi and others suggest that the gene plays a role in preeclampsia.

Preeclampsia is kicked off by the placenta, an organ grown mostly from fetal cells that helps provide nutrients to the fetus. And though the details are unclear, some scientists suspect that unhealthy placentas start to pump out too much Flt-1 protein. A version of the protein called sFlt-1 can then slip into a mother’s bloodstream, where it may damage blood vessels in a way that leads to high blood pressure.
The GWAS results can’t explain the bulk of preeclampsia cases. A fetus carrying a single copy of one of the troublesome variants near FLT1 raised a mother’s risk of preeclampsia by about 20 percent, the analysis suggests. Other risk factors are known to be much stronger, Morgan says, including previous high blood pressure, former preeclampsia diagnoses or carrying twins.

Karumanchi says that the genetic results might not be strong enough on their own to make the case that the gene is involved. But other work points to FLT1. “We feel it’s the right target,” he says.

In Europe, a preliminary clinical trial is testing a filtration method that removes excess sFlt-1 protein from the blood of women with signs of preeclampsia. So far, about 20 women have undergone the procedure, says nephrologist Ravi Thadhani of Massachusetts General Hospital in Boston. Early results are “quite encouraging,” he says, and he hopes to expand the study soon.

[Millions of diabetics] could be indebted to a strain of diabetic mice being bred in Bar Harbor, Maine. In diabetes research, “this mouse is the best working model to date,” one of its discoverers, Dr. Katharine P. Hummel, says.… A satisfactory animal subject had eluded diabetes researchers, until the mouse was found. — Science News, August 12, 1967

Update
Hummel’s diabetic mice are still used in research to mimic type 2 diabetes in humans, which is linked to obesity. In the mid-1990s, researchers found that the diabetic mice carry a mutation in the leptin receptor gene, which prevents the hormone leptin from signaling fullness and triggering other metabolic processes. In people, however, the disease is more complicated. More than 40 genetic variants are associated with susceptibility to type 2 diabetes. Unlike the mouse mutation, none of those variants guarantee a person will develop the disease.

Across Europe, rivers aren’t flooding when they used to.

Long-term changes in temperature and precipitation are making some rivers flood days, weeks or even months earlier than they did 50 years ago, and pushing flooding in other areas much later, researchers report August 11 in Science. Those changes could impact people, wildlife and farms near rivers.

Previous studies have shown that climate change is likely to increase the severity and frequency of coastal floods, but it can be tricky to concretely link river flooding to climate change, says Günter Blöschl, a hydrologist at the Vienna University of Technology who led the study.
Coastal flooding is worsened largely by one overriding variable that can be tracked: sea level rise. But river flooding is affected by a complex set of factors, says Rob Moore, a policy analyst at the Natural Resources Defense Council in Chicago who specializes in water issues. Both the timing and quantity of precipitation matter, as does the type of soil and whether it’s dry or already waterlogged when rain hits. What’s more, changes in land use around a river or engineering projects such as dams that change river flow can also affect flood risk — but aren’t necessarily related to the climate.
So instead of tracking the size or frequency of river floods, the researchers examined the seasonal timing of those floods. That measurement is less impacted by factors that have nothing to do with climate. Blöschl worked with researchers from 38 countries to analyze hydrological data collected at 4,262 sites across Europe from 1960 to 2010.

Flood season shifted as much as 13 days earlier or nine days later per decade, the researchers found. Over the entire study period, that shift added up to floods in some regions occurring, in the most extreme cases, as much as 65 days earlier or 45 days later. The biggest changes were in Western Europe, where a quarter of the monitoring sites recorded flood timing shifts of more than 36 days over the 50-year period. Elsewhere, effects were more moderate, though still measurable: In northeastern Europe and the area around the North Sea, for instance, more than half of the stations showed shifts of more than 8 days.
The effect varies substantially by region because not all parts of Europe experience the same sorts of floods, says Blöschl. In southern Sweden and the Baltics, floods are mostly driven by snowmelt. Warmer local temperatures make the snow melt earlier in the spring, shifting flood season up, too. In southern England, on the other hand, heavy autumn rains saturate the soil, and subsequent winter deluges can cause flooding. Flood season there is driven by when the soil gets too waterlogged to take in more moisture.

The study shows that flood timing has changed, but does not address specific consequences. It’s clear, though, that off-season flooding could have far-reaching effects, especially if these trends continue. Animals that rely on river conditions at a certain time of year in order to breed or find food could be affected by surprise floods. Out-of-season floods or unexpected dry spells could damage crops.

Plus, people are less prepared when big floods happen off-season, says Moore. While a comprehensive study like this one hasn’t been done in the United States, floods are occurring at unusual times here, too, he notes. Moore cites devastating floods that swelled the upper Mississippi River to a record size in December 2015 — not the time of year when the river is expected to overflow its banks. That flooding, combined with tornadoes spurred by the same storm system, killed more than 50 people and caused almost $2 billion in damage.

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.

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.