A draft of the poppy’s genetic instruction book is providing clues to how the plant evolved to produce molecules such as morphine.

Scientists pieced together the genome of the opium poppy (Papaver somniferum). Then, they identified a cluster of 15 close-together genes that help the plant synthesize a group of chemically related compounds that includes powerful painkillers like morphine as well as other molecules with potential medical properties (SN: 6/10/17, p. 22).

A group of genes that help poppy plants produce some of these molecules, collectively known as benzylisoquinoline alkaloids, have been clustered together for tens of millions of years, researchers report online August 30 in Science. But the plant’s morphine production evolved more recently. Around 7.8 million years ago, the plant copied its entire genome. Some of the resulting surplus genes evolved new roles helping poppies produce morphine, because the plant already had at least one other copy of those genes carrying out their original jobs.

It wasn’t a one-step process, though. An even earlier gene duplication event caused two genes to fuse into one. That hybrid gene is responsible for a key shape-shift in alkaloid precursors, directing those molecules down the chemical pathway toward morphinelike compounds instead of other benzylisoquinoline alkaloids (SN Online: 6/25/15).

Jocelyn Bell Burnell first noticed the strange, repeating blip in 1967. A University of Cambridge graduate student at the time, she had been reviewing data from a radio telescope she had helped build near campus. Persistent tracking revealed the signal’s source to be something entirely unknown up to that point — a pulsar, or a rapidly spinning stellar corpse that sweeps beams of radio waves across the sky like a lighthouse.

A half-century later on September 6, Bell Burnell was awarded the $3 million Special Breakthrough Prize in Fundamental Physics. The prize has been given only three times before: to British physicist Stephen Hawking for discovering a type of radiation from black holes in 1974, the CERN team that discovered the Higgs boson in 2012, and the LIGO collaboration that in 2016 found gravitational waves.

But before any of those discoveries, Bell Burnell’s pulsar find was revolutionizing astrophysics. It led to precise tests of Einstein’s theory of gravity, the first observations of exoplanets and the 1974 Nobel Prize in physics — from which Bell Burnell was famously excluded. Now 75 years old, Bell Burnell is giving back, donating her prize to create scholarships for underrepresented minorities in physics and astronomy.

Science News caught up with Bell Burnell to chat about aliens, impostor syndrome and how being an outsider can be a boon in scientific research. The following answers have been edited for length and clarity.
SN: What did the first pulsar data look like to you?
J.B.B.: It was an anomaly, and it was a very small anomaly. Typically it took up about 5 millimeters of my long rolls of chart paper, out of half a kilometer. I was being very, very thorough, very careful. I kept poking at it to try and understand what it was.

SN: You called the first signal LGM-1, for Little Green Man 1. Did you really think it might be a signal from aliens?
J.B.B.: That was a bit of a joke, which I now rather regret. But we did check it out. My advisor Tony [Hewish] argued that, if it were little green men as we nicknamed them, they’d probably be on a planet going round their sun. As their planet moved, we would see what’s called Doppler shift. The spacing between pulses would change as their planet moved. We looked for that, but we couldn’t find any such motion.

SN: At what point did you realize that pulsars were going to be a big deal?
J.B.B.: Quite late in the process. I’d found all four that I was going to find. The first paper announcing the results was to be published a day or two later [on February 24, 1968, in Nature]. My thesis advisor, Tony Hewish, gave a talk in Cambridge, and gave it a very titillating title. Everybody came, and the excitement was palpable.

SN: What have pulsars taught us since then?
J.B.B.: We’ve learned a lot about extreme physics, because pulsars are really, really extreme. They are the remains of stars after the star has expired in a violent explosion. They’re about 10 miles across, but they weigh as much as the sun, a thousand million million million million tons. That’s four millions. Very small, very heavy, very peculiar composition.

We’re using pulsars to test some of Einstein’s theories. His ideas are standing up very well, which is interesting (SN: 2/3/18, p. 7). And we’re developing ideas, looking very far ahead, for using these things as navigation beacons, when we start traveling through the galaxy in spaceships (SN: 2/3/18, p. 7).
SN: What do you wish you’d been told about being a woman in astronomy when you were younger?
J.B.B.: I think it wasn’t what people would tell me, it would be having more women around. Because there were so few women in Cambridge, I rarely got the chance to mix with other women. I would have liked a bit of that.

SN: Do you credit your discovery at all to being in the minority?
J.B.B.: Yes, I do. I was, I reckon, suffering from impostor syndrome in Cambridge, although we didn’t have that name at that time. Cambridge is in the southeast of England, and it’s a very confident, suave type of society. As you may guess from my accent, I don’t come from the southeast of England. I’m from the north and western parts of Britain.

I was both geographically out of place, and as a woman out of place. I thought, wow, they’re all terribly clever. I’m not so bright. They’ve made a mistake. They’re going to find out their mistake, and they’re going to throw me out.

But I said to myself, I’m not going to waste this opportunity. Until they throw me out, I will work my very hardest, so that when they throw me out, I won’t have a guilty conscience…. I think a lot of other people would have overlooked that little anomaly that I chased up.

SN: How did you feel about not being included on the 1974 Nobel Prize?
J.B.B.: At that stage, the image people had of science was of a senior man, and it always was a man, with a fleet of younger people working for him. And if the project went well, the man got praise. If the project went badly, the man got the blame. The younger people working under him were isolated from all of that. It seemed to me to be part of that pattern of doing things.

I think the Nobel Prize is still fairly male orientated. The world is now making strenuous efforts to be more inclusive. Prizes like the Nobel tend to go to the most senior people, so that will reflect how the society was when they were young and active. It’s going to be some time until changes percolate to the senior prizes.

SN: How do you feel now, winning the Breakthrough Prize?
J.B.B.: Oh, it’s fantastic, amazing! I was speechless when I was told about it. And as you may guess, I’m not often speechless.

SN: Why did you decide to donate the money to diversity initiatives?
J.B.B.: I’ve been conscious that diverse bodies are often more successful, more flexible, more robust. I’d like to see more diversity in science, and I’d like more people who often don’t get the chance to do research given the chance to do research. That’s my thinking.

SN: What other diversity initiatives have you been involved in?
J.B.B.: This is not the first. I’ve been one of a small group of senior women that set up a project in the United Kingdom called Athena SWAN, that encourages universities to be women-friendly places…. And if they’re women-friendly, they’re probably fair for everybody, not just women.

Bite a mouse in the back of the neck and don’t let go. Now shake your head at a frenzied 11 turns per second, as if saying “No, no, no, no, no!”

You have just imitated a hunting loggerhead shrike (Lanius ludovicianus), already considered one of North America’s more ghoulish songbirds for the way it impales its prey carcasses on thorns and barbed wire.

Once the shrike hoists its prey onto some prong, the bird will tug it downward “so it’s on there to stay,” says vertebrate biologist Diego Sustaita. He has witnessed a shrike, about the size of a mockingbird, steadying a skewered frog like a kabob for the grill. A bird might dig in right away, keep the meal for later or just let it sit around and demonstrate sex appeal (SN Online: 12/13/13).
Shrikes eat a lot of hefty insects, mixing in rodents, lizards, snakes and even small birds. The limit may be close to the shrike’s own weight. A 1987 paper reported on a shrike killing a cardinal not quite two grams lighter than its own weight and then struggling to lift off with its prize. Recently, Sustaita got a rare chance to study how the loggerheads kill their prey to begin with.

Conservation managers breed one loggerhead subspecies on San Clemente Island. That’s about 120 kilometers west of where Sustaita works at California State University San Marcos. Sustaita set up cameras around a caged feeding arena and filmed shrikes, beak open, lunging to catch dinner. “They’re aiming for the prey’s neck,” he says.
That’s a very shrikey thing. Falcons and hawks attack with their talons, but shrikes evolved on the songbird branch of the bird tree — without such powerful grips. Instead, shrikes land on their feet and attack with their hooked bills. “The bite happens at the same time the feet hit the ground,” Sustaita says. If the mouse somehow dodges, the shrike pounces again, “feet first, mouth agape.”

Reading several decades of gruesome shrike papers, Sustaita first believed the real killing power came from the bird’s bill, with bumps on the side, wedging itself between neck vertebrae and biting into the spine. Shrikes definitely bite, but based on videos, he now proposes that shaking may help immobilize, or even kill, prey.

Sustaita and colleagues discovered that the San Clemente shrikes fling their mouse prey with a ferocity that reached six times the acceleration due to Earth’s gravity, or about what a person’s head would feel in a car crash at 2 to 10 miles per hour, the researchers report September 5 in Biology Letters. “Not superfast,” he acknowledges, but enough to give a person whiplash.

In a small mouse, such shaking looks more damaging. Video analysis showed that the mouse’s body and head were twisting at different speeds. “Buckling,” Sustaita calls it. Just how much damage twisting does versus the neck bite remains unclear. But there’s a whole other question: How does a shrike manage not to shake its own brain to mush?

The language we learn growing up seems to leave a lasting, biological imprint on our brains.

German and Arabic native speakers have different connection strengths in specific parts of the brain’s language circuit, researchers report February 19 in NeuroImage, hinting that the cognitive demands of our native languages physically shape the brain. The new study, based on nearly 100 brain scans, is one of the first in which scientists have identified these kinds of structural wiring differences in a large group of monolingual adults.
“The specific difficulties [of each language] leave distinct traces in the brain,” says neuroscientist Alfred Anwander of the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, Germany. “So we are not the same if we learn to speak one language, or if we learn another.”

Every human language expresses itself using a different set of tricks. Some use rich systems of suffixes and prefixes to build enormous, dense words. Others change how words sound or how they are arranged within phrases to create meaning. Our brains process these tricks in a constellation of brain regions connected by white matter. This tissue routes long, cablelike nerve cells from one part of the brain to another and speeds up communication between them. Wiring brain regions together this way is part of how we learn: The more often we use a connection, the more robust it becomes.

Different parts of the brain’s language circuit have different jobs. But while the large-scale structure of this circuit is universal, every language has “its own difficulties,” which might result in different white matter networks, Anwander says.

He and his team recruited 94 healthy volunteers who spoke one of two unrelated native languages — German or Levantine Arabic — for structural MRI brain scans. The Arabic speakers had arrived recently in Germany as refugees and didn’t yet speak German. They tended to have stronger connections across their left and right hemispheres, the scans revealed, whereas the German speakers had a denser network of connections within the left hemisphere.

“This corresponds to the specific difficulties in the respective languages,” Anwander says.
For instance, the complexity of Arabic’s roots — trios of consonants that buddy up with vowel patterns to produce words — might demand extra effort from parts of the brain involved in parsing sounds and words. A common example of this kind of root is k-t-b, which forms words related to writing like kitaab (book), taktub (you or she writes) and maktab (office). Arabic text is also written right to left, which the researchers speculate might demand more communication between the hemispheres.

German, for its part, has a complex and flexible word order that allows the language to create subtle shades of meaning just by shuffling around words within a phrase. While an English speaker can’t rearrange the words woman, ball and dog in the sentence “the woman gave the dog a ball” without garbling the core meaning, it’s possible to do exactly that in German. This could explain the German speakers’ denser white matter networks within parts of the left hemisphere that parse word order.

Still, it’s possible that the Arabic speakers’ recent arrival in Germany could have tweaked their white matter networks too, says Zhenghan Qi, a cognitive neuroscientist at Northeastern University in Boston who was not part of the study.

Just one month of learning a new language, she says, can lead to more engagement of the brain’s right hemisphere and greater interaction between the two hemispheres. Examining MRI scans of Arabic speakers living in their home countries or tracking brain changes as people learn new languages would help separate the effects of language learning from those of native language, Qi says.

While the new study focused just on the language circuit, parts of that circuit handle more than just language, Qi says. And language learning “might also change nonlinguistic regions of the brain,” so it’s possible that people with different language experiences might process nonlanguage information differently too, she says.

It’s still controversial whether language-associated white matter rewiring affects more than just language, Anwander says. But at least within the language circuit, the new results hint that our mother tongues are far more than just the words we happened to grow up with — they are quite literally a part of us.

What pollution does to you — Science News, March 31, 1973

Scientists described the results of their attempts to correlate pollution levels with various complaints of patients…. As expected, when smog increased, so did incidence of eye irritation, pulmonary disorders and nosebleeds…. Finally, for reasons not yet understood, more patients complained of animal bites on days when the air contained more suspended particulate matter.

Update
The harms of air pollution go beyond irritated eyes, lungs and noses. Researchers have linked exposure to dirty air with an increased risk for heart disease, diabetes, and dementia (SN: 9/19/17), and have found associations with violent behavior.

Air pollution appears to lead to more aggressive behavior in other animals too. For example, the risk of dogs biting people goes up on smoggy days, an analysis of nearly 70,000 U.S. cases found. More bites occurred with increasing ground-level ozone, which occurs when pollutants chemically react in sunlight (SN: 12/8/21), scientists reported in December on the preprint server Research Square. The dogs’ aggression may be due to a stress response or brain impacts from the ozone exposure, the researchers suggest.

Listen carefully, and a plant may tell you it’s thirsty.

Dry tomato and tobacco plants emit distinct ultrasonic clicks, scientists report March 30 in Cell. The noises sound something like a kid stomping on bubble wrap and also popped off when scientists snipped the plants’ stems.

When evolutionary biologist Lilach Hadany gives talks about her team’s results, she says, people tell her, “‘You cut the tomato and it screams.’” But that is jumping to a conclusion her team has not yet reached. “Screaming” assumes the plant is intentionally making the noise, Hadany says. In the new study, “we’ve shown only that plants emit informative sounds.”
Intentional or not, detecting those sounds could be a step forward for agriculture, potentially offering a new way to monitor water stress in plants, the study’s authors propose. If microphones in fields or greenhouses picked up certain clicks, farmers would know their crops were getting dry.

Previous work had suggested that some plants produce vibrations and ultrasonic emissions. But those experiments used sensors connected directly to the plant, says Alexandre Ponomarenko, a physicist at the biotech company NETRI in Lyon, France, who has detected sounds made by slices of pine trees in the lab. Hadany’s team tried something new.

She and her colleagues at Tel Aviv University set up ultrasonic microphones next to, but not touching, living plants. The team wanted to find out if the plants could generate airborne sounds — vibrations that travel through the air.

The researchers first detected the horticultural hiccups coming from plants set up on tables in the lab. But the team couldn’t be sure that something else wasn’t making the noises. So the researchers ordered sound-dampening acoustic boxes and tucked them in the basement away from the lab’s hustle and bustle. Inside the hushed boxes, thirsty tomato plants emitted about 35 ultrasonic clicks per hour, the team found. Tomato plants cut at the stem were slightly less noisy, and tobacco plants clicked even less. Plants not water-stressed or chopped kept mostly quiet.
The plants’ short sounds were about as loud as a typical conversation, but too high-pitched for humans to hear (though dogs’ ears might perk up). And each plant species had a recognizable “voice.” A machine learning algorithm the team created could tell the difference between clicks from tomato plants and tobacco plants. It could also pick out thirsty and hydrated plants.

The algorithm could even differentiate between plants when they sat in a noisy greenhouse, filled with the sounds of people talking and building renovations next door.
Hadany doesn’t know exactly what’s causing the emitted sounds; it could simply be bubbles forming and popping within the plants’ water-carrying tissues. The sounds might be akin to “someone’s creaking joints,” says Tom Bennett, a plant biologist at the University of Leeds in England who was not involved with the research (SN: 3/29/18). “It doesn’t mean that they’re crying for help.”

Still, it’s possible that other organisms eavesdrop on the noises, he says, something Hadany’s team is currently investigating. She is curious whether other plants or insects like moths, some of which can hear in the ultrasonic range, are tuning in. It’s possible moths, as well as mice and other mammals, could detect the noises as far as five meters away, the team suggests.

And tomato and tobacco weren’t the only plants that prattled. Similar sounds came from wheat, corn, Cabernet Sauvignon grapevines and pincushion cactus. “It is happening in so many different plants that grow in so many different environments,” says Ravishankar Palanivelu, a plant developmental biologist at the University of Arizona in Tucson who did not work on the study. “It seems like this is not a random thing.”

He doesn’t know if the sounds have any evolutionary significance, but, Palanivelu says, he thinks the study’s results will certainly generate some noise.

A fungus that recently evolved to infect humans is spreading rapidly in health care facilities in the United States and becoming harder to treat, a study from the U.S. Centers for Disease Control and Prevention finds.

Candida auris infections were first detected in the United States in 2013. Each year since, the number of people infected — though still small — has increased dramatically. In 2016, the fungus sickened 53 people. In 2021, the deadly fungus infected 1,471 people, nearly twice the 756 cases from the year before, researchers report March 21 in Annals of Internal Medicine. What’s more, the team found, the fungus is becoming resistant to antifungal drugs.
The rise of cases and antifungal resistance is “concerning,” says microbiologist and immunologist Arturo Casadevall, who studies fungal infections. “You worry because [the study] is telling you what could be a harbinger of things to come.” Casadevall, of Johns Hopkins Bloomberg School of Public Health, was not involved in the CDC study.

In tests of people at high risk of infection, researchers also found 4,041 individuals who carried the fungus in 2021 but were not sick at the time. A small percentage of carriers may later get sick from the fungus, says Meghan Lyman, a medical epidemiologist in the CDC’s Mycotic Diseases Branch in Atlanta, possibly developing bloodstream infections that carry a high risk of death.

Starting in 2012, C. auris infections popped up suddenly in hospitals on three continents, probably evolving to grow at human body temperature as a result of climate change (SN: 7/26/19). The fungus, typically detected through blood or urine tests, usually infects people in health care settings such as hospitals, rehabilitation facilities and long-term care homes. Because people who get infected are often already sick, it can be hard to tell whether symptoms such as fevers are from the existing illness or an infection.
Those most at risk of infection include people who are ill; those who have catheters, breathing or feeding tubes or other invasive medical devices; and those who have repeated or long stays in health care facilities. Healthy people are usually not infected but can spread the fungus to others by contact with contaminated surfaces, including gowns and gloves worn by health care workers, Lyman says.

Growing drug resistance
Infections can be treated with antifungal drugs. But Lyman and colleagues found that the fungus is becoming resistant to an important class of such medications called echinocandins. These drugs are used as both the first line and the last line of defense against C. auris, says Casadevall.

Before 2020, six people were known to have echinocandin-resistant infections and four other people had infections resistant to all three class of existing antifungal drugs. That resistance developed during treatment using echinocandin. None of those cases passed the resistant strain to others. But in 2021, 19 people were diagnosed with echinocandin-resistant infections and seven with infections resistant to multiple drugs.

More concerning, one outbreak in Washington, D.C., and another in Texas suggested people could transmit the drug-resistant infections to each other. “Patients who had never been on echinocandins were getting these resistant strains,” Lyman says.

Some health care facilities have been able to identify cases early and prevent outbreaks. “We’re obviously very concerned,” Lyman says, “but we are encouraged by these facilities that have had success at containing it.” Using those facilities’ infection control measures may help limit cases of C. auris, she says, as well as reducing spread other fungal, bacterial and viral pathogens.

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.”

Uracil, a building block of life, has been found on the asteroid Ryugu.

Yasuhiro Oba and colleagues discovered the precursor to life in samples collected from the asteroid and returned to Earth by Japan’s Hayabusa2 spacecraft, the team reports March 21 in Nature Communications.

“The detection of uracil in the Ryugu sample is very important to clearly demonstrate that it is really present in extraterrestrial environments,” says Oba, an astrochemist at Hokkaido University in Sapporo, Japan.
Uracil had been previously detected in samples from meteorites, including a rare class called CI-chondrites, which are abundant in organic compounds. But those meteorites landed on Earth, leaving open the possibility they had been contaminated by humans or Earth’s atmosphere. Because the Ryugu samples were collected in space, they are the purest bits of the solar system scientists have studied to date (SN: 6/9/22). That means the team could rule out the influence of terrestrial biology.

Oba’s team was given only about 10 milligrams of the Ryugu sample for its analysis. As a result, the researchers were not confident they would be able to detect any building blocks, even though they’d been able to previously detect uracil and other nucleobases in meteorites (SN: 4/26/22).

Nucleobases are biological building blocks that form the structure of RNA, which is essential to protein creation in all living cells. One origin-of-life theory suggests RNA predated DNA and proteins and that ancient organisms relied on RNA for the chemical reactions associated with life (SN: 4/4/04).
The team used hot water to extract organic material from the Ryugu samples, followed by acid to further break chemical bonds and separate out uracil and other smaller molecules.

Laura Rodriguez, a prebiotic chemist at the Lunar and Planetary Institute in Houston, who was not involved in the study, says this method leaves the possibility that the uracil was separated from a longer chain of molecules in the process. “I think it’d be interesting in future work to look at more complex molecules rather than just the nucleobases,” Rodriguez says.

She says she’s seen in her research that the nucleobases can form bonds to create more complex structures, such as a possible precursor to the nucleic acid which may lead to RNA formation. “My question is, are those more complex structures also forming in the asteroids?”

Oba says his team plans to analyze samples from NASA’s OSIRIS-REX mission, which grabbed a bit of asteroid Bennu in 2020 and will return it to Earth this fall (SN: 10/21/20).

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.