In the summer of 1518, people in Strasbourg couldn’t seem to stop dancing—some even danced themselves to death.

It all started with one woman, who stepped into the street and began moving uncontrollably. Soon, dozens of other residents followed suit, overcome with the inexplicable urge to hop, jerk, and sway. Within weeks, the outbreak had spread throughout the city, leaving officials, physicians, and religious leaders scrambling to figure out what was happening—and, more importantly, how to make it stop.

Five centuries later, the dancing plague of 1518 remains one of history’s strangest medical mysteries. Historical records confirm that a bizarre episode turned a medieval city into a very unwilling dance floor that summer, but exactly why it happened remains a matter of debate. 

A bizarre outbreak takes hold

The dancing plague began on July 14, 1518, when a woman named Frau Troffea started dancing in Strasbourg, then part of the Holy Roman Empire and now a city in northeastern France. Though her husband begged her to stop, Troffea kept moving as day faded to night, while a crowd of onlookers gathered around to watch. Eventually, she collapsed and fell asleep, but when she awoke the next morning, she resumed her solitary jig. 

Troffea’s uncontrollable dancing, known as choreomania, seemed to be contagious. Dozens of other people were soon gyrating in the streets of Strasbourg and, by late August, as many as 400 individuals had succumbed.

At the time, the leading theory was that St. Vitus, a fourth-century Sicilian martyr believed to punish sinners by making them dance, had cursed the afflicted. Then, once St. Vitus decided his victims had suffered enough, he would relieve them of the curse.

City leaders determined that the best course of action was to keep the dancers dancing, so they cleared the outdoor grain market, built a stage, and hired musicians. They didn’t explain their rationale in any known, surviving documents, so historians don’t know exactly why they did this. But John Waller, associate professor of the history of medicine at Michigan State University and the author of The Dancing Plague: The Strange, True Story of an Extraordinary Illness, suspects they had two reasons: They believed dancing could help people purge physical impurities from their bodies, and they viewed it as a form of penance. 

“If people were believed to have been cursed by God or a saint for some kind of immorality, well, dancing was associated with hedonism and that was fundamentally immoral,” he tells Popular Science. “A way of basically punishing oneself would be to dance to the point of exhaustion and pain and potentially even death. It would make sense with that potential framework.” In other words, from the leaders’ perspective, if dancing was their punishment, let them be punished.

Dancing themselves to death

Regardless of their motives, the authorities’ decision had “very, very clear consequences,” he says. It was a hot summer, and the dancers were likely under the full glare of the sun. They weren’t eating or drinking much, and they weren’t resting. 

“This is certainly going to be extremely dangerous for a large number of people, particularly anybody with any kind of susceptibility to heart attack or stroke,” says Waller.

The historical records are murky on exactly how many people died—one writer claimed as many as 15 per day, at least for a time—but it was enough to make city leaders completely change course. 

“They essentially banned dancing, except for some people in the privacy of their own homes, and then instituted a program of penance and prayer,” says Waller. “They clearly realized that what they’d been doing before was causing harm and I suspect they got the impression that it was making things worse.”

Eventually, the authorities transported the remaining dancers to a shrine dedicated to St. Vitus about 30 miles away, where religious leaders went to work praying and leaving offerings. As days and weeks passed, the dancers overcame their choreomania and returned to their normal lives—traumatized and tired, but otherwise fine.

The dancing plague of 1518 wasn’t the only such incident of its kind. Numerous other outbreaks of uncontrollable dancing occurred in western Europe between the late 1300s and mid-1500s—and Waller thinks it’s no coincidence that many were clustered along the Rhine River and its tributaries. 

“Rivers are very good for, obviously, transporting trade goods, but they’re also very good for spreading ideas,” he says. “From the headwaters in Switzerland all the way down to where the Rhine flows into the North Sea, you’ve got this belief in a saint who curses with a dance.”

Theories behind the dancing

Now that we have the benefit of hindsight, what might explain the dancing plague of 1518 and others like it? One theory is that the dancers were sickened by ergot, a fungus that can contaminate grain. Another holds venomous spiders bit the afflicted. Demonic possession, epilepsy, typhus, and encephalitis—brain inflammation caused by an infection or autoimmune response—have also been put forward as possible explanations.

But after considering all the evidence, Waller thinks there’s only one plausible theory that truly makes sense. He suspects the dancers of Strasbourg were all victims of mass hysteria, also known as mass psychogenic illness, brought on by intense psychological distress. 

The years leading up to 1518 were rough, particularly for the lower classes, with failed crops, bad weather, economic issues, social unrest, religious tensions, and illnesses like smallpox, leprosy, and syphilis taking a toll on peoples’ psyches. They were hungry, anxious, sad, scared, and worried that God had abandoned them. 

Waller suspects the people living in Strasbourg simply reached their breaking point, then entered into a trance-like state that rendered them largely insensitive to their extreme fatigue and sore feet. They danced, Waller argues, rather than weeping, fighting, praying, or engaging in some other behavior because of their belief in St. Vitus and his dancing curse.

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Modern takeaways 

Given the period-specific cultural and religious underpinnings, could something like the dancing plague of 1518 happen today? 

Waller shares several modern examples of mass psychogenic illness that, although they don’t involve dancing, he finds to be similar in nature. More than 300 students in Blackburn, England, suffered from a mysterious fainting fit in 1956, for example, and hundreds of people succumbed to alternating fits of laughing and sobbing in East Africa in 1962. In 2007, students at a Catholic boarding school near Mexico City came down with a mysterious sickness that made walking difficult. A year later, 20 female students in Tanzania suffered a mass fainting episode during their final-year national examinations.

And although the dancing plague of 1518 took place more than 500 years ago, Waller says we can still learn plenty from it. For him, the most important takeaway is “the way in which our expression of severe distress can be culturally conditioned and channeled.” 

When Waller initially started researching the dancing plague of 1518, it was such a “wild phenomenon” that his inclination was to think “as strange as the past can be, this was simply too strange to have actually happened,” he says. But as he dug deeper—and, more importantly, began to understand the context within which it arose—it started to make more and more sense. 

In other words, he says, it reminds us that psychological distress is not expressed in a vacuum. The culture, beliefs, and circumstances around us can shape how our inner turmoil manifests—and, in some cases, how it spreads from one person to another. 

In That Time When, Popular Science tells the weirdest, most surprising, and little-known stories that shaped science, engineering, and innovation.

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Tattoos are pretty permanent decisions, and laser removal is often described as more painful than actually getting them in the first place. But what about a design that can only be seen when you want to see it? Engineers at the University of Colorado Boulder are working on a new type of tattoo ink to answer that question. Their dye is specifically concocted to physically alter depending on exposure to visible or ultraviolet (UV) light.

The team described their invention in a study published earlier this month in the journal Matter & Light, and they didn’t only demonstrate the capabilities in the lab on silicone and pig skin. One of its creators, Carson Bruns, has already tattooed himself with the ink.

“[It’s] almost a tradition,” the study co-author recently told Nature.

Bruns, a nanoscientist at UC Boulder, previously developed a now-commercialized tattoo product called “Magic Ink” that turns magenta depending on its exposure to UV light. To highlight its efficacy, Bruns gave himself “solar freckles” as a method to track his exposure to sunlight. In similar fashion, he recently completed a similar session on his leg using the disappearing ink.

The formula currently comes in three colors—yellow, blue, and magenta—and essentially relies on the same principles behind transition lenses and some textiles. Each dye is composed of tiny spheres of acrylic glass. These beads contain photochromes, which are chemical compounds engineered to absorb specific light wavelength photons. In this case, the photochomic dye’s spheres begin in their original color, but then flatten into transparency after absorbing corresponding light photons exposed to UV rays. The dye remains this way until it absorbs visible light photons, which destroys the chemical bond and allows the spheres to return to their original shape.

Aside from the lab tests, Bruns tattooed his own leg over about 12 months using various dye combinations, all of which responded as intended to UV and visible light exposure. The ink also remained effective for over two years—but the team’s intention is go beyond a nifty parlor trick. Future ink iterations may be particularly useful in medical procedures, such as temporary markings to help maintain accuracy during direct radiotherapy sessions. For now, however, the photochromic tattoo dyes remain for laboratory (and Bruns’) use only until further safety assessments are completed.

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Excerpted from PENELOPE by Paul Bochner. Copyright © 2026 by Paul Bochner. Published in the United States by Crown, an imprint of the Crown Publishing Group, a division of Penguin Random House LLC. 

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On the evening of March 18, as it was growing dark, I went to the window, not knowing what was drawing me. Next to the house stood a shadow, ghost-like, shrunken, at one with the dusk, almost translucent, and I recognized The Girl with the Broken Foot.

I walked out into the falling wet snow, slowly approaching her, and she allowed me to come close. Nine months old, she was the size of a fawn half that age. Starkly emaciated, her body seemed to be collapsing inward, her head held low. Literal hunger and a deeper starvation were palpable. She bore the haunted look of terminal solitude seen in souls driven to the margins of society, among the liv-ing, yet apart. She seemed so frail that I couldn’t imagine she would live more than another day or two.

Going inside and returning with a bowl of apples, I cut them into pieces and placed a few on the ground between us. She was raven-ously hungry and I gave her a few more apples, and still more, until she had eaten a total of eight. After she had finished eating, she stayed with me. We stood about a foot apart. She showed no fear of me, a fact which I would later come to recognize as meaningful. The moment had the compelling quality which has been present at the onset of many enduring connections in my life, of being un-bound by linear time.

“I am watching over you,” I said softly. “If you come here, I will take care of you. You are not alone.”

It was fully dark when we parted, having been together for an hour. I expected that she would recede into the woods, yet the next morning she was sleeping against the house, directly beneath the window closest to where I sit all day to work. Save for the wall separating us, she could not have gotten any closer to me.

When I went around to the front of the house, she struggled to her feet and approached. In the morning light, I was better able to assess the state of her health. Months of solitary survival had taken a severe toll. Her body seemed hollowed, her ribs and pelvis sharply visible beneath her skin, and it felt a miracle that she was alive. On her right flank was a hemispherical mass the size of a cantaloupe, which I took to be a tumor, yet it had an open, running wound at its center, which she periodically craned her neck to lick. Her eyes were running and had congealed masses at their inner corners.

I bent to get a look at her injured foot. From not being walked on, the backward-facing cloven hoof had grown to an abnormal length and was curling upward. The wrist, which unnaturally bore her weight, had a flattened forward surface, an oval about two inches across, worn raw, without hair or skin, only pale pink–grey flesh, which, at its center, appeared to have been further abraded to the bone. Her right front foot, forced to compensate, was splayed and rockered, her right scapula protruded, and her front quarters were substantially lower than her hips.

I again placed apple pieces on the ground between us. I spoke very gently to her, saying, “You are the best one of all the deer. You are the most beautiful. You are good.” I continued to talk to her while she ate her apples, and when she had taken all she could, she returned to her resting spot under the window. I went inside to work, keeping periodic watch, pleased that she seemed to have claimed a place. But in a few minutes, from around the corner of the house came the twins, followed by their mother who immediately and ag-gressively charged at her. The Girl with the Broken Foot lurched upright and hobbled down the embankment, across the road and into the woods.

She was once again alone, but a step had been taken. Since the previous evening, things had changed. Even before her second feed-ing she had recognized me on sight. She had approached and had again allowed me near.

Although I had seen her fewer than half a dozen times in the preceding months, from the night of our first connection, she began to come to the house every day. She slowly gained strength and I would watch for her and thrill to the sight of her slow approach. It was our private time. We stood together, and I placed her food on the ground between us. After she ate, she would stare into my eyes for long periods, seemingly entranced. I told her stories. I sang softly to her. I told her she was my beauty.

So began our journey, and one of the greatest loves I have ever known.

About the Author

Paul Bochner began his professional life early, as a working musician through his mid-teens in Los Angeles, then moving to Montreal at the invitation of the National Film Board of Canada. He has won several international awards for his films and is the recipient of a Guggenheim Fellowship in painting. He has written for The New Yorker and The Atlantic.

The post The remarkable bond between a man and a deer appeared first on Popular Science.

You would think, post-COVID, that we would all understand the importance of frequent and thorough handwashing. And yet, spend any time in a public restroom and you’ll see an alarming number of people who still see it as optional. 

We know it can help curb the spread of illness when you’re sick, but on an average day, just how gross is it to not wash your hands? 

“Your hands have a microbial flora that is always present. These are mostly good bacteria that help protect your skin,” Allison Pappas, PhD, Director of Business Development at Gillson Sciences, tells Popular Science. “On unwashed hands, your normal flora is going to be the most abundant group of inhabitants and they’re nothing to worry about. If you’re not washing your hands, they won’t become overgrown by deadly bacteria. However, your hands will accumulate an increasing number of pathogenic bacteria and viruses from your environment.”

Pappas explains that eating a sandwich or wiping your nose after exposure to these pathogenic bacteria are quick ways to then introduce those germs into your body. She describes it as a “tug-of-war,” with germs pulling one way and handwashing your only way to tug in the opposite direction. There are also physical characteristics that come into play as well. People with longer fingernails or rough, coarse skin give bacteria more places to hide. And it’s not always visible. As Pappas puts it: “Your hands can look clean but be utterly disgusting from a microbial perspective.” 

According to the Center for Disease Control (CDC), germs like Salmonella, E. coli, and norovirus that cause diarrhea, as well as some respiratory infections like adenovirus and hand-foot-mouth disease can all be present on unwashed hands. Why? Because there might be…wait for it…invisible poop. 

“It’s extremely gross, but assume you’ve got poop on your hands,” says Pappas. “That sounds crazy, but studies have found fecal bacteria on children’s hands and toys and on the hands of 28 percent of commuters in the UK. Even if you don’t have a child and don’t commute via subways, you’re still touching all the same door handles and common utensils as the people who do. That poop is transferring to your hands, you just can’t see it.” 

So how gross is not washing your hands? It’s “you have poop on your hands” gross. 

“Yeah,” says Pappas, “Please wash your hands.”

What is the right way to wash your hands?

Recent studies suggest that most people wash their hands too briefly to actually kill germs. So, if you want to avoid getting sick and spreading illness, it’s time to forget everything you thought you knew, and follow these instructions for proper hygiene:

1. Wet your hands with water at a comfortable temperature. You can’t actually get the water hot enough to kill microbes without burning your skin, so just do what feels nice. The CDC actually recommends shutting the tap off while you lather your soap to conserve water.
2. Lather your hands with soap. Don’t worry about buying something with anti-microbial ingredients; research shows that outside of a hospital setting, these additives don’t provide a significant benefit, and their use contributes to the rise of antibiotic resistance.
3. Make sure you lather the backs of your hands, between your fingers, and under your nails, as dangerous microbes can lurk on any part of your skin.
4. Continue scrubbing for 20-30 seconds before you start rinsing. It’s longer than you think. One study showed that most adults lather for just six seconds. Try singing “Happy Birthday” twice in your head (or out loud, if you’re feeling fun) to help keep time.
5. Turn the tap back on and rinse. The CDC notes there’s little evidence that using a paper towel to turn the tap on and off after washing will improve your health.
6. Dry your hands with a clean towel if possible, or with an air dryer. The CDC says that wet hands more easily transfer microbes. Plus, you don’t want to walk around with clammy hands all day.

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Mark Wahlberg, who once sank money into a gym chain that got kicked off the NYSE, is now building his own, and he promises you’ll get a cold plunge, a blood panel and a protein muffin without needing a trust fund.

New research points to a "possibly overlooked mechanism" for how microplastics can harm people's health.

Your eyes really can betray your thoughts, but don’t get too self-conscious about it. Researchers in Japan believe that the subtle signs our eyeballs make are more useful to neuroscientists than the interrogation room. Based on their findings recently published in the journal iScience, examining the difference physiological responses from “inner” versus “overt” speech may help us better understand everything from linguistic development in children to the efficacy of silent pep talks.

To learn more, a team at the University of Tsukuba in Honshu enlisted dozens of volunteers for a series of simple counting exercises. After observing the participants at rest while thinking about nothing in particular for a control, researchers then asked them to count sequentially (1, 2, 3…), in number-subject combinations (one dog, two dogs…), and in specific intervals (1, 3, 5…). They also completed each task both silently and aloud. In each phase, the team carefully monitored their pupil dilation.

The results were subtle, but striking. Participants’ pupils dilated during each overt speech task, but this same muscle movement depended across each inner speech directive. Pupils constricted while volunteers silently counted sequentially, dilated for interval counting, and didn’t change at all for number-subject counting. But regardless of the inner speech task, pupil size changes were always smaller than they were during overt speech.

“The results of the present study do not support the initial assumption that inner and overt speech produce equivalent pupillary responses,” the team summarized. “Across the three experiments, overt speech consistently elicited pupil dilation, whereas inner speech did not.”

This collective data indicates that our inner speech isn’t simply the nonverbal counterpart to talking aloud. Instead, it’s a form of communication that appears to correspond to lower levels of brain arousal. If true, measuring pupil dilation may become a valuable tool when attempting to assess internal language and thinking. This could be particularly useful for studying language development in young children and infants who can’t properly describe their experiences to adults yet.

The post Your eyes dilate depending on your thoughts appeared first on Popular Science.

Intero Biosystems beat out 199 other Startup Battlefield companies to take home the $100,000 grand prize at TechCrunch Disrupt 2026.

In the mid-1970s, Linnda Caporael was a college student facing a seemingly mundane decision. 

A science major at U.C. Santa Barbara, she needed a humanities course to graduate. The course she chose, on women in American history, came with a term paper, and she had to pick a topic.

Caporael’s first choice—Lydia Wardell, a Quaker woman who protested Puritan persecution by walking naked into a meeting house in the 1660s—was intriguing, but already taken. So Caporael instead settled on her second choice: Ann Putnam, one of the accusers in the 1692 Salem witch trials. In doing so, Caporael reshaped the way millions of people view a nearly 300-year-old chapter of American history. 

Caporael’s paper introduced the theory that the visions, convulsions, and distress the “afflicted” girls reported might not have been supernatural after all. Instead, she proposed, they could be explained by ergot, a fungus that grows on rye grain and produces a hallucinogenic toxin. In other words, blame moldy bread. 

The ergot theory, despite being debunked within a year of being published, has continued to spread and thrive like fungus on rye. As recently as 2023, comedian-turned-podcasting-juggernaut Joe Rogan discussed the theory enthusiastically on his show, effectively reanimating a story that seems destined to never fully die.

“It’s sexy,” says historian Margo Burns about the enduring appeal of Caporael’s ergot theory. “It’s about drugs. It’s about witches. It’s about killing people. Also, we like to think that when there’s an unjust sentence or execution, there’s someone or something to blame.”

Burns, a Salem scholar who has spent years tracing how the ergot theory took hold and persisted, says she rarely gets through a talk on the trials without someone in the audience bringing up moldy bread.

How a term paper went viral

The fact that a single undergraduate college paper could have such a lasting and wide-ranging impact on our understanding of the Salem witch trials seems bizarre, but it can be explained in part by a thoroughly modern phenomenon: virality. Although the World Wide Web was still decades away, Caporael’s paper found a way to spread fast through newspaper wire services.

After she started graduate school, Caporael submitted the paper to Science, which, to her surprise, published it in April 1976. That alone might have kept the theory confined within academic circles. Instead, newspaper editors saw a story with mass appeal.

“Editors and newspapers just grabbed it, saying, ‘Oh, here’s a human interest thing,’” Burns says. “And when they put it in their papers, like The Washington Post, The New York Times, The Boston Globe, it got syndicated. And the syndication of those articles went through the whole country and Canada within a matter of weeks.”

Caporael, who had explored the topic through the lens of the scientific method, wasn’t claiming to know what had happened at Salem. At the suggestion of a pre-med friend, she began looking into ergot poisoning as a possible explanation, not a definitive answer. 

According to Burns, who has spoken with Caporael directly, she was only testing whether ergot could be ruled out. Working from the limited sources available to her, Caporael determined that she couldn’t rule it out. Even then, though, she called her own findings “suggestive,” not conclusive.

But that nuance didn’t survive exposure to the public, which in 1976 was already fixated on LSD and what it might do to young people. The press coverage essentially retrofitted 1692 with the anxieties of 1976, recasting the Salem girls as teenagers on a bad trip.

“You give that to the American public, which doesn’t understand there’s a difference between scientific inquiry and historical storytelling, and it’s just so compelling,” Burns says.

Debunked, but far from dead

Not all the viral attention was positive, though. Within that same year, researcher Nicholas Spanos and graduate student Jack Gottlieb published a rebuttal in Science, dismantling Caporael’s argument point by point. By their reckoning, various aspects of the Salem girls’ symptoms did not add up. 

“There are a couple of different kinds of ergot poisoning, and one of them is gangrenous, so people’s fingers would start rotting,” Burns says. “And they would have gastrointestinal problems, and we don’t have any instances in the records that either of those things happened.”

The problems for the theory didn’t end there. Ergot poisoning was thought to hit hardest among people with vitamin A deficiencies, but Salem’s residents had dairy cows and the sea nearby, and likely plenty of vitamin A. (Ironically, Burns notes, that the vitamin A argument was itself based on a discredited 1930s source that relied on circumstantial evidence and has never been replicated.) And while whole families ate from the same supply of rye, usually only one or two people per household fell ill.

The rebuttal, though methodical and logical, was little more than a momentary speed bump for the runaway popularity of the psychedelic bread story. In fact, it may have helped. 

Arguing with a claim, however insubstantial, implies that it’s worth arguing about, and a formal rebuttal in Science can make a student’s term paper look like one side of a valid scientific debate.

“It’s really hard to refute something,” Burns says. “If anything, it just sort of nails it and makes it more permanent.”

“They were eating their own”

Whatever was causing young women in Salem to convulse, the atrocities that followed are much harder to grasp. By the time the panic ended, 152 people had been formally accused, 19 had been hanged, and one man, Giles Corey, had been pressed to death with stones for refusing to stand trial. Several more died in jail.

“The people who were responsible were the adults in the room,” Burns says.

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To the modern eye, this looks like lunacy. To most people in 1692, though, witchcraft wasn’t superstition. It was an accepted fact, part of an invisible world in which Satan and his agents wreaked havoc on everyday life. Conflict with Indigenous peoples on the Maine frontier had sent traumatized refugees into the region, relating horror stories of attacks on their homes. Many colonists thought Satan engineered those attacks, too.

In a way, the people of Salem did exactly what Americans would do nearly 300 years later, when the psychedelic era latched onto the ergot theory: They explained strange behavior through the lens of what frightened them most.

In such a charged social climate, suspicion could fall on just about anyone, and it did. The accused weren’t just outcasts, Burns says. Many were fully covenanted members of the Puritan church.

“We’re not talking about going after ‘The Other,’” she says. “They were eating their own.”

Someone to blame

Burns knows the cost of Salem’s betrayals about as well as anyone. An associate editor of Records of the Salem Witch-Hunt, the definitive collection of the trials’ legal records, she is also the 10th-generation great-granddaughter of Rebecca Nurse, who was hanged on the charge of witchcraft in 1692.

Nurse, a respected member of the church in Salem Town, was tried and found not guilty. But Chief Justice William Stoughton refused to accept the verdict. He sent the jury back to reconsider a remark Nurse had made when confessed witches Deliverance Hobbs and her daughter, Abigail, were brought in to testify against her: She had said the two were “of our company.” Nurse meant that they had been jailed together, but the court heard that they were fellow witches. 

When jurors asked her what she meant, the courtroom was in such an uproar that Nurse didn’t hear the question. At the time, failing to answer an accusation was treated as a confession, and the jury returned a guilty verdict. In a later appeal, Nurse wrote that she was “something hard of hearing, and full of grief,” and didn’t realize she was being asked to explain herself.

It was the kind of injustice no mere fungus could cause.

“[Chief Justice] Stoughton was singularly, individually responsible for her execution,” Burns says.

The question of who is to blame is rarely so straightforward, though. Which might be part of the ergot theory’s appeal; it offers “one silver bullet” that tidily explains everything.

“There are just so many reasons that all came together,” Burns says.

But when pressed on why she thinks it happened, she offers an answer that’s part joke, part harsh reality: “People are mean.”

In That Time When, Popular Science tells the weirdest, most surprising, and little-known stories that shaped science, engineering, and innovation.

The post In 1976, a college paper blamed the Salem witch trials on moldy bread. It wasn’t true. appeared first on Popular Science.

The Ojai Raptor Center released the final necropsy results for Jackie, an internet-famous bald eagle mother who was in their care this summer. Jackie was brought into the bird rehabilitation center weak and dehydrated following an altercation with another eagle in July. 

Officially designated as Patient 26-519, Jackie’s necropsy revealed a “complex and unusual disease process involving severe, chronic inflammation and ulceration of the stomach, persistent internal bleeding, anemia and secondary bacterial sepsis.” She was also diagnosed with Highly Pathogenic Avian Influenza (HPAI) commonly called bird flu, which was behind severe stomach ulceration. Raptors (eagles, hawks, falcons, owls, etc.) are highly susceptible to the virus 

All of these medical complications developed over time and ultimately contributed to her death on August 10.

“These findings have helped connect many of the pieces we were seeing throughout her hospitalization and provided a better understanding of the challenges she faced,” the Ojai Raptor Center wrote. “We are grateful to the many veterinary specialists, laboratories, wildlife agencies and partner organizations who worked alongside our team to understand her illness and provide her with the best possible care. Caring for her was an extraordinary privilege for our entire team.”

The full report can be read in Jackie’s veterinary medical journal. The necropsy was preformed by veterinary pathologists at the San Diego Zoo Wildlife Alliance.

Friends of Big Bear Valley (FOBBV), the non-profit organization that runs the live cameras where viewers from all over the world watched Jackie and her partner Shadow, said that they will follow up with their thoughts once their team has had time to process the report.

“The story of the Big Bear bald eagle reflects the powerful connection people feel to these iconic birds,” California Department of Fish and Wildlife Director Meghan Hertel added. “We’re grateful to everyone who cared for her and worked to support her well-being.  Understanding the results of these tests is an important part of learning from this case and can help inform the care and treatment of other eagles and wildlife in the future.”

Jackie’s story

Jackie was born, raised, and lived in Big Bear Valley in Southern California. Prior to the 2011-2012 nesting season, no bald eagle chicks were known to have ever hatched in Big Bear Valley. Then came Jackie, named after a forest ranger and born to parents Ricky and Lucy in 2012. 

During the 2016-2017 nesting season, Jackie took over a nest where Friends of Big Bear Valley (FOBBV) had a camera stationed. In 2018, she had two chicks named Stormy and Big Bear Baby (or BBB) with her first mate, Mr. B. 

Her long-time partner Shadow entered the picture in summer 2018. He showed up at the nest and would not leave. FOBBV called the new male Shadow because he appeared so determined to stay in the nest, and the team initially believed he was one of Jackie’s siblings, also named Shadow. The eagle’s plumage indicated he was one year older than the other Shadow and not Jackie’s sibling, but the name stuck. 

Shadow continued to hold his ground and Mr. B gave up and eventually left. Jackie then accepted Shadow as her new mate.

Wildlife cameras documented Jackie and Shadow’s life together, offering viewers a direct look into the brutality and beauty of nature. The pair successfully raised chicks in 2019 (Cookie and Simba) and 2022 (Spirit). The pair’s eggs failed to hatch in 2023 and 2024. In 2025, Jackie laid three eggs that all hatched in early March. However, a strong snowstorm dumped up to two feet of snow and battered the nest with strong wind and only two of the chicks (Sunny and Gizmo) survived.  

In January, Jackie laid two eggs in the nest, but ravens destroyed them. She later laid two more eggs that hatched in April and named Luna and Sandy. The name Sandy is in honor of FOBBV’s former executive director Sandy Steers who died from cancer in February. 

Jackie’s injury and death

On July 17, Jackie was found injured on the ground near Dana Point Park, California. Cell phone video from a witness confirmed that she had an altercation with two other subadult eagles. She successfully fended off the other eagles by turning over and using her talons, but could not fly far away. 

She was transferred to the Ojai Raptor Center, where she was diagnosed with severe anemia. Her anemia worsened during the first week of August, the Ojai Raptor Center said that she was in unstable condition on August 9. Her packed cell volume (PCV) fell below percent, before rising to nine percent.  

On July 17, Jackie was found injured on the ground near Dana Point Park, California. Cell phone video from a witness confirmed that she had an altercation with two other subadult eagles. She successfully fended off the other eagles by turning over and using her talons, but could not fly far away. 

She was transferred to the Ojai Raptor Center for care, where she was diagnosed with severe anemia. Her anemia worsened during the first week of August, the Ojai Raptor Center said that she was in unstable condition on August 9. Her packed cell volume (PCV) fell below percent, before rising to nine percent. 

Jackie died early in the morning on August 10. The necropsy did not reveal a single cause of death, and instead pointed to several factors including severe anemia, blood clots in her wing and one kidney, and liver and lung abnormalities.

Jackie’s resilience inspired millions of people around the world. To honor her memory, FOBBV accepts donations to support its conservation efforts in the area.  Supporters can also donate to Ojai Raptor Center’s Bald Eagle Recovery Campaign. 

The post Jackie the bald eagle’s final cause of death revealed appeared first on Popular Science.

Thanks to some medieval human teeth, archaeologists have pinpointed when lead production first expanded across Europe during the Middle Ages. By examining dental enamel collected from graves located in central England, researchers now know the post-Roman society started mining and smelting again during the mid-7th century. As the team explains in a study published today in the journal Antiquity, the consequences of exposure to the toxic were stark—but distributed unequally among locals.

Humanity’s complicated relationship with lead dates back over 9,000 years, and our environmental exposure to the toxic metal is traceable as far as two million years ago. Lead was instrumental in prehistoric smelting advancements, and its invaluable properties paved technological progress all the way through the Industrial Revolution. However, lead is now known to cause various early developmental issues and its uses are dwindling, but tracing our reliance on the material helps contextualize and understand a society’s historical arc.

Researching these metals also isn’t easy. From the 16th to 19th centuries, manufacturers constantly re-smelted lead waste from ancient Rome and medieval England, which destroyed any discernible way to examine its prior origins and uses. Archaeologists including University of Nottingham’s Christopher Loveluck knew of another way to trace lead production in the Derbyshire Peak District, one of Europe’s largest providers of the metal during the Middle Ages

“The team is delighted to have finally confirmed definitively the date by which the early medieval lead industry was established in the Peak District…through evidence provided by the people themselves,” Loveluck said in the study’s accompanying announcement.

Archaeologists analyzed teeth from bodies buried in three Peak District cemeteries dating back to between 650 and 1500 CE. More specifically, they focused on tooth enamel. The external protective layer finishes forming during childhood, meaning any prior lead exposure stays embedded in the enamel for the rest of an individual’s life. Loveluck and his colleagues discovered that by the 7th century, the Derbyshire children’s lead levels were the same, if not higher, than those of children who lived in industrialized cities during the mid-18th and 19th centuries. By the mid-8th century, the growing lead industry had even begun to seep into surrounding regions like Castleton.

Teeth samples showed lead exposure reached its highest levels during the late 12th and early 13th centuries, which aligns with previous historical and environmental data. While the metal’s presence was ubiquitous among the population, it wasn’t necessarily the same across class or gender. High status gravesites included weapons and other personal items with lower lead concentrations than those seen in the graves of poorer residents. This implies that while the upper class owned lead-imbued possessions, they were higher quality objects. Meanwhile, working class families employed in mines and factories routinely exposed their children to larger amounts of lead.

There is also evidence that suggests women were especially at risk during this era. Three women who died between 17 and 25 years old showed particularly increased lead quantities in their tooth enamel. Overall, most of the men survived to middle or old age, while women often died during young adulthood.

“Our results indicate that in these mining communities, girls and boys alike were raised in dangerously polluted home environments,” said Castleton excavation co-director and study co-author Anna Bloxam. “This exposure…perhaps contributed to higher rates of premature death among women of child-bearing age.”

Lead contamination is still a serious issue today, although overall conditions have improved greatly since medieval England. Still, the underlying problems of environmental degradation and socio-economic vulnerabilities remain relevant today.

“This study has enabled us, for the first time…to look more deeply into the profound impact lead production had on individuals and the communities they lived in,” added University of Sheffield historian and study co-author Colin Merrony.

The post Human teeth pinpoint when lead began poisoning medieval town appeared first on Popular Science.

Wandering around Milan, you come across two kinds of power: the kind you can observe and the kind you can only feel. That first one is obvious, all incense-soaked architecture and ascendant liturgies. The second, though, is more understated in pauses, glances, murmured blessings, and other hushed, huddled choreography. 

Pinnacles and pulpits look down on the penitent holding their rosaries. Beyond the gargoyles’ gaze, an equally adorned set of transformation seekers do the same to the so-last-season. Because, wandering around Milan, you come across another kind of power both manifested and metaphysical: the power of fashion.

It’s July 2025, and I’m in Milan at the invitation of EssilorLuxottica. I’m here to learn how the world’s largest eyewear company designs frames and lenses that help everybody, from the fashionable to the far-sighted, see and be seen. And where else but the Italian capital of fashion? Here, at the intersection of spirit and spirituality, faith and fit, this vertically integrated multinational predicts and produces trends years before they hit retail. But more interesting even than shapes and shades are the developments in microelectronics and med-tech that turn frames into smart systems, into something powerful you can witness and wear. 

[Disclosure: EssilorLuxottica provided travel accommodations during the creation of this story.]

Our tour begins at the Oakley Milano flagship, a two-story space styled like a brutalist bunker that cloisters current attire alongside retired accessories from the ’90s and early aughts, displayed like relics in a cathedral. Oakley is just one of EssilorLuxottica’s many, many proprietary brands, licensed luxury labels, and, with the Oakley HSTN and Vanguard Performance AI models, a part of the company’s push to take smart glasses from concept to category. 

We see the Prizm Interactive Wall, where we compare simulations of different Oakley lenses. Placed on a platform, a screen shows how a lens’s selective wavelength tuning and “noisy” light filtering boost specific colors and contrast, whether you’re on a shady trail or out to sea. Then there’s the Performance Chamber. A stationary bike sits in a simulator where you pedal through adjustable wind and lighting conditions to experience how different eyewear (and helmets) ride.

The next stop on our photopic pilgrimage is the Luxottica Digital Factory and its Tortona Experience Center, a striking building full of workspaces and high-end industry showrooms. Here, in the Zona Tortona design district, we work our way back to the future, to where teams study economics, demographics, technology, fashion, and interior design to inform storylines that won’t hit retail for 18–24 months.

Nina Esteves, senior trend & foresight manager at EssilorLuxottica, walks us through the future of frames, where AI and 3D printing widen structural possibilities to far more far-out. At the extreme, they’re alien eyes, or maybe that’s alienized. And, temporarily, that’s how I feel. I feel like Andy Sachs just starting at Runway, out of my element but eager to dive into the deep end of fashion.

I see magma hues and intentionally ruined chrome finishes. I see the renewal of ovals and chunky curves, informed by international datasets of face-shape fittings (it pays to own thousands of LensCrafters and Sunglass Hut locations, etc.). I see what (under)tones of green, clear, and white will become neo-neutrals. I see how cat-eyes become more sci-fi. Slowly, I start to understand the curve as silhouettes and innovation cascade from runway to bargain bin.

We’re in a period when plain-lens and barely-there frames are expression, not just function. They may be interchangeable, worn like earrings. And tinted lenses are similar. For those looking to occupy both worlds, the company’s Transitions lenses use reactive molecules that adapt to light, forming complex shapes to block UV from the sun and filter blue light from our screens.

When I was growing up, these eyepieces were slowly shifting, tobacco-brown photochromics. But these ain’t your grandpa’s glasses. The clustered cones embedded in Transitions Gen S come in eight hues, snap to dark sunglasses in around 25 seconds, and reverse back to clear in under 2 minutes. You can blend or clash tones with your frames without sacrificing clarity. An XTRActive variant even has dynamic polarization.

[EssilorLuxottica’s push is for Transitions to go from “must-wear” to “love-wear.” I’m convinced enough by the demonstration that they’re not the nerdy, never-quite-clear, high-school science teacher vibe of my youth that I get a pair when I return home. And, as someone unwilling to use contacts and too cheap … OK, lazy … to buy prescription sunglasses for decades, I can say they’ve been a revelation. Better late than never.] 

And Transitions aren’t the only lens technology that has improved exponentially. Progressive lenses have dumped the “bifocals” stigma. They’ve become a far more seamless way to address stress you may not even know is affecting you, according to Today show style editor and Varilux lenses brand partner Bobbie Thomas. She spent months with nausea, vertigo, and headaches. Doctors suspected hormonal causes, but it turned out to be presbyopia.

About 2.1 billion people have presbyopia, an age-related loss of near vision; this number is projected to reach 4 billion by 2050, according to Essilor market reports and United Nations internal analysis. Plus, digital life is accelerating that. With 60 percent of our cerebral cortex involved in vision, good vision is associated with feelings of connection and community and therefore with good mental health, according to Sebastien Fricker, manager of the vision and perception modeling team. 

With this in mind, Essilor develops digital twins, which are virtual replicas of individual wearers based on their prescription, pupillary distance measurements, age, morphology, lifestyle, head and eye movements, and more. These are used to test various Varilux progressive lenses through simulation, model how a real brain perceives sharpness and distortion over time, and determine what works best and what needs refinement. And IRL, when getting fitted for the XR Series, an “Eye-Ruler” measures Near Vision Behavior (NVB) and considers posture, how you hold your device, and how your gaze shifts. Then behavioral AI predicts head and eye movement to align the lenses with how you actually view the world. 

[I’m a presbyope who had a terrible, multi-day ordeal adapting to progressives in my mid-40s. So I was reluctant to give a new pair a go. But while I was getting Transitions, I took the leap to Varilux XR, and now I have no obvious lines or disorienting “swim effect.” According to Essilor, citing a 2005 study, you make more than 100,000 eye movements a day in every direction, and standard progressive lenses are designed primarily for linear eye movements. With Varilux XR, you get what you pay for, which is a natural per-eye positioning of near, intermediate, and far focal zones, plus sharpness in motion.]

Of course, lenses, for all the chemistry and careful cutting that goes into them, are relatively easy to drop into a traditional frame, whether it’s an A$AP Rocky Wayfarer Puffer or some kind of titanium wisp with a granny chain swinging off it like a thurible. Their transformative power is something you can see. What’s introduced next is felt more than seen. 

We demo the Ray-Ban Meta, learning about the layers of delicate circuitry in its arms and the challenge of fitting components that must stay linear onto a face, which is anything but flat. A few steps away, however, is something even more interesting to me: Nuance Audio glasses, first introduced in April 2025 at around a grand without prescription lenses (thousands less than traditional hearing aids). They’re basically an over-the-counter hearing aid disguised as something I’d already have on my face, and the only prescription required is for lenses, if you need them.

A rep puts a neckband speaker on another journalist and hits play to emit restaurant chatter and clatter. Then a different voice talks over it, conversational, not loud, and the response is middling. “I don’t really understand everything,” the wearer admits. So the rep switches the glasses on, frontal mode kicks in, and the glasses amplify whoever you face within a 30-degree cone, aimed like a laser pointing from your nose. Alternately, a 360-degree mode can handle the street for more encompassing awareness. Other features include four pre-configured amplification settings that target different levels of hearing loss, plus background noise reduction.

“I’m hearing her a lot more clearly,” the participant declares. Meanwhile, I’ve found something I want to hear more about.

I admit it: I’m the guy who fails the “restaurant test.” I sometimes struggle to navigate low-light, high-noise spaces. Varilux XR lenses have somewhat helped cut down on menu-reading challenges and peering over my frames at things held mere inches from my face, but I still have a hard time hearing anyone at the table who’s not immediately next to or across from me. If my eyes are a window to my health, and at least some of the world around me, then my ears are a door to the room where my sanity comes and goes … and sometimes it feels like it’s swinging shut. 

I mean, it’s my own fault. As a former professional music critic and would-be superstar DJ, I stood in front of line arrays for many, many years before I took earplugs seriously. Between that and turning 50, I’ve lost some top end, what my audiologist calls “the women and children range,” much to the chagrin of my wife. So I know exactly why I tilt my head “like a dog that just heard the word ‘treat,’” as the wife I find harder to hear so lovingly puts it. I’m trying to catch consonants along with visual cues to help cut through the static. And it’s mentally exhausting, to the point that sometimes I’ll just check out when out and about.

This makes me more interested in being part of the conversation on mild to moderate hearing loss and removing the stigma of hearing aids, or even hearables. So, eight months after Milan, I’m even more interested in attending SWITCH, EssilorLuxottica’s first-ever summit for about 1,000 vision-care professionals from more than 30 countries, held in Orlando in March 2026. 

Among conversations on myopia management, neuroscience, and emerging oculomics, I gravitate to the gear. According to a presentation by Dr. Charlotte Yeh, about 73 million Americans have hearing loss, which is 1 in 5 (that number goes up to 1 in 3 if you count people, like me, who have “hidden hearing loss” … where you mostly struggle with speech in noisy places but don’t have serious measurable loss). Fewer than a third of those act on it, often waiting 7 to 10 years. Untreated loss can lead to loneliness and also contribute to dementia, according to a 2024 Lancet Commission.

One of those people with untreated hearing loss is Frank Lynch, and his daughter, actress Jane Lynch, explains what’s at stake and how hearables can help. In her keynote, she describes her father going from someone who would burst into impromptu songs to someone who laughed half a beat behind. Then his TV got louder and louder, and saying “What?” in response to conversations got more and more frequent. Finally, he seemed to be disappearing, there but not there. Yet Frank didn’t want traditional hearing aids because he didn’t want to appear weak or vulnerable. So, when Jane started noticing her own issues with background noise getting in the way, you guessed it, in restaurants, she embraced the opportunity to do something about her hidden hearing loss when introduced to the “adorable” Nuance Audio glasses. “Getting help for hearing loss is not a surrender,” Lynch says.

It wasn’t just Lynch who ended up with a pair. Another went to her friend Janice, who spent a dinner saying they were a “game changer,” while another went to Lynch’s spouse. That’s three people embracing a solution, and more people who might be tempted to upgrade. Announced at SWITCH and recently released at retail, Nuance Audio Plus is the next generation of the company’s hearing glasses, starting at $829 and now available in three styles and five colors, with improved audio and amplification, battery life, and switches/controls. 

You see, adorable isn’t as simple to engineer when electronics are involved. All those PCBs and batteries and other components are flat and add weight, the enemy of all-day wear. That’s why the arms of Nuance Audio glasses and Meta models typically have a thickened profile, to house and hide the deliberate directional microphones that listen and the speakers that aim sound toward your ears. [Admittedly, the Meta Gen. 3 frames, with aviator and cat-eye styles, are a few millimeters smaller, but …]

Still, the team strives for connected devices to “be beautiful glasses first,” says Matteo Battiston, EssilorLuxottica’s chief design officer, talking to me between sessions.

It’s been a slow process to adapt the technology for the most wearers, though. For someone like me, with a -6.25 prescription, physics is fighting back. You design a frame like they design a car, without knowing which wheels will go on it, says Battiston. And not all wheels fit all wheel wells. Similarly, a prescription as thick as mine adds weight and must share space with microphones and motherboards that can’t be bent as the lenses get pushed in.

However, Alex Himel, Meta’s vice president of wearables, says that the most engaged users wear connected glasses with prescription or Transitions lenses. One of the company’s answers is another SWITCH debut: Ray-Ban Meta Optics. It’s a little easier with Nuance, which doesn’t have the cameras in the end piece, etc. For Ray-Ban, however, they made lighter frames that support what the company calls its widest prescription range. The hinges have an additional 10 degrees of rotation, the nose pads are swappable, and the temple tips adjust a bit. Not to the extent of traditional acetate, where opticians use heat to make things malleable, but with more flexibility than before.

Back at the Nuance Audio booth, I think about another feature they might want to put on the spec sheet: better table manners. Testing out a pair of Nuance at a dinner, I found I’m no longer half-nodding but rather making full eye contact. I’m reengaged. 

When I first arrived in Milan, I felt like I was wearing a metaphorical lumpy blue sweater, sure that the trend table wouldn’t have much to do with me. But even if I’m not the most fashion-forward, I loved learning how the frames, lenses, and electronics-laden eyewear I ended up wearing were curated long before I chose them. And the shade of cerulean that mattered most as it trickled down to me was whatever was being said at the far end of the table. Miranda Priestly never has to raise her voice; the room leans in. Well, I got tired of leaning in. Now I can sit back and still catch the … nuance.

The post I went from Milan to Orlando to learn whether glasses that change your look can change your outlook appeared first on Popular Science.

Squid skin behaves a bit like a large, 10-armed human ear. While scientists at Case Western Reserve University were probing these enigmatic cephalopods, they discovered that squid have significantly more hair cells than was previously known. 

Hair cells are cells with bundles of hair-like protrusions, and researchers already knew that squid had  them on their heads and arms. Now, it looks like the invertebrates have hundreds more of them all over their bodies, with potential insight for understanding human hearing. 

“Squid are cephalopods with a diverse population of hair cells on the surface of their bodies, which may yield insights not only into how these fascinating animals detect water movement to survive, but also into how hearing and deafness occur in humans,” Brian McDermott, a biologist and co-author of a quid study recently published in the journal Current Biology, said in a statement. That’s because these squid hairs are similar to those inside the human ear, which enables us to hear things. 

McDermott (who investigates hair cells) and his colleagues used an imaging technique called light sheet microscopy to probe the cells. During this process, a thin sheet of light lights up one plane of a specimen at a time and researchers can produce detailed 3D images while minimizing tissue damage. Their work also included the first full-body mapping of lateral lines (features made up of hair cell clusters) on squid.

Understanding these hairs have implications for our own ears. Human hearing involves sound vibrations moving to a snail-shaped organ in the inner ear called a cochlea. The cochlea is filled with thousands of hair cells, each of which has a collection of small hair-like features called stereocilia, or cilia. The length of cilia depends on where they are found. If they are in areas where low pitches are detected, the cilia are longer. If they are in high-pitch areas, the cilia are shorter. This positioning helps orient each cell to a specific sound frequency. 

When the sound vibrations reach the cochlea, the cilia move. The hair cells then transmit the signals to the brain via the nervous system, where the messages are turned into meaningful sounds. Marine animals such as squid and octopuses feature similar cilia bundles on their bodies. Their survival appears to depend on detecting various frequencies of water movement, akin to how human ears pick up on sound pitches. 

In other words, squid skin appears to behave like a human ear. This new research even suggests that squids regulate the length of the hair bundles to tune the hair cells to various frequencies, similarly to human ears. The hair bundles in fish lateral lines, on the other hand, are all the same length. So by studying squids, researchers could learn more about human hearing. 

“Often, when a child is born deaf or a hearing person loses their hearing, it is the hair bundle that has been damaged,” McDermott concluded. “So, studying the squid’s hair bundle holds promise for understanding how hearing loss occurs.”

The post Squid are covered in little hairs like the ones in your ear appeared first on Popular Science.

Typical brains function smoothly, with neurons (nerve cells) firing rhythmically like predictable weather patterns. 

But in epileptic brains, a sunny day can suddenly turn dark and stormy. Neurons will just be trucking along, operating in the controlled and routine way that keeps a body’s mental and physical functions stable when, all of a sudden, they freak out, pulsing with an electrochemical intensity that causes confusion and uncontrollable jerking. 

The broken doll movement and unexpected mental interruptions of epileptic seizures have probably always been unsettling. Some cultures have explained their onset as the consequence of religious sin, others as divine intervention or a sign of sacredness.

To the ancient Romans, epilepsy was a contagious disease caused by evil spirits or demonic possession, and there was only one way to cure it—with the blood of a gladiator.

How blood became an epilepsy cure

Ancient Rome wasn’t the first place epilepsy was treated with human blood. There’s evidence of its use in ancient Greece, Egypt, Mesopotamia, and elsewhere. But the Romans were the first to look to the blood of a warrior for a cure, according to “Between Horror and Hope: Gladiator’s Blood as a Cure for Epileptics in Ancient Medicine,” an article by Ferdinand Peter Moog and Axel Karenberg published in the Journal of the History of Neurosciences in 2003.

Drinking the “hot blood from the throat of a gladiator” is first recommended in the Book on Medicine in 40 C.E. and, over the next 500 years, Roman doctors experimented with exactly how to administer the cure: three spoonfuls a day for 30 days, sucking directly from a bleeding wound, filling a cup with the dripping blood of the slaughtered. 

In the sixth century, one physician’s method was to burn a rag soaked in the blood of a swordsman and mix its ashes with wine. “With seven doses you will free the patient of epilepsy,” he wrote. “Often applied with excellent results.”

Gladiator blood was a magical cure

For a remedy to have such staying power over such a long period of time is unusual. When that remedy is drinking the blood of a gladiator, Moog, senior lecturer at the Institute for the History of Medicine and Medical Ethics at the University of Cologne in Germany, tells Popular Science, it suggests a strong undercurrent of magical thinking. 

“Magic is not logic,” he explains. “People are healed by those things and procedures they expect to be healed from.”

Gladiators weren’t exactly average Romans. In the early days of the republic, their death in combat had religious associations, with fallen gladiators believed to be offerings to the gods or escorts for the dead into the next world. Even as gladiatorial combat later lost its religious connotations, the dramatic circumstances of the contestants’ deaths still made their blood a potent epileptic cure.

Belief in the remedy likely had something to do with what Moog and Karenberg describe as “the illusion of therapeutic effectiveness.” Since the symptoms of some forms of epilepsy affect only children before disappearing completely around puberty, a child who consumed gladiator blood while still symptomatic would appear to anyone unfamiliar with the disorder as having been cured by it.

Blood from the decapitated worked just fine, too

When gladiatorial combat was outlawed in the Roman Empire around 400 C.E., physicians were forced to look for an alternative treatment for epileptic patients. They found it in the blood of those executed by decapitation. 

“The blood of the decapitated was the blood of ‘noble’ criminals, and this might have been important when searching for a substitute for gladiator’s blood,” says Moog. It seems not to have been the legendary strength and virility of the gladiator that imbued a person’s blood with healing power, then, but the way they died—by the blade of a sword (or later a guillotine).

There was a practical element to using blood from an execution too, Moog continues. “In the case, for example, of a hanging, you’d have to hurt the body of the executed yourself. And wounding a corpse was in many cultures regarded as a bad thing.” 

The blood spilled by decapitation, on the other hand, “was easy to get.”

The new twist on the old remedy apparently proved just as enduring as the original. The blood of the executed was a “miracle cure” for epilepsy all the way until the 20th-century invention of anti-epileptic pharmaceuticals. 

In That Time When, Popular Science tells the weirdest, most surprising, and little-known stories that shaped science, engineering, and innovation.

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The post Ancient Romans thought drinking gladiator blood could cure epilepsy appeared first on Popular Science.

Human T cell leukemia virus type 1, the first human retrovirus ever identified, infects an estimated 5 to 10 million people worldwide, a figure extrapolated from surveys covering only about one-seventh of the global population. The virus inserts a DNA copy of its RNA genome into the chromosomes of host T cells, establishing a lifelong infection that can drive a spectrum of diseases, including adult T cell leukemia/lymphoma, HTLV-1-associated myelopathy, and HTLV-1-associated uveitis, a chronic inflammation inside the eye that is particularly common in endemic regions such as Japan. Despite the scale of the problem, coordinated global action has been slow; the World Health Organization only published technical reports aimed at reducing HTLV-1-related morbidity and mortality in 2021, and no broadly effective intervention has emerged in decades of research.

Current treatment for the ocular disease relies heavily on corticosteroids, delivered as topical drops, injections into the eye, or oral prednisone. This approach has serious shortcomings. Studies indicate that 30 to 60 percent of patients with HTLV-1-associated uveitis experience recurrent episodes, and long-term steroid exposure can trigger cataracts, glaucoma, macular edema, epiretinal membranes, retinal degeneration, optic nerve atrophy, and bullous keratopathy. Most importantly, corticosteroids suppress inflammation without reducing the number of virus-infected cells or halting disease progression. Newer molecular targeted agents, including the anti-CCR4 antibody mogamulizumab and the immunomodulatory drug lenalidomide, have been explored, but treatment-related inflammation and adverse effects remain significant obstacles. This therapeutic gap motivated a team led by Yaru Zou and Koju Kamoi of Tokyo Medical and Dental University to investigate whether an epigenetic drug already approved for blood cancer could address the root of the ocular inflammation.

The drug in question is valemetostat, marketed as EZHARMIA, a dual inhibitor of the enzymes EZH1 and EZH2 that was approved in 2022 for adult T cell leukemia/lymphoma. Both enzymes are the catalytic components of polycomb repressive complex 2, a molecular machine that silences genes by adding three methyl groups to lysine 27 on histone H3, producing the repressive chromatin mark known as H3K27me3. Previous work had shown that EZH1 and EZH2 are overexpressed, and H3K27me3 deposition increased, in ATL cells and in cells expressing the viral oncoprotein Tax. Dual EZH1/2 inhibitors have also been reported to curb the spontaneous proliferation and exaggerated immune responses of HTLV-1-infected cells in patients with HTLV-1-associated myelopathy. What remained unknown was whether such inhibition could benefit the inflamed eye.

To find out, the researchers built a series of laboratory models centered on ARPE-19 cells, a human retinal pigment epithelial cell line chosen because the retinal pigment epithelium forms the outer blood-retinal barrier and governs retinal immune homeostasis. They exposed these ocular cells to three kinds of T cells: MT-2 cells, which carry transcriptionally active HTLV-1 and express the viral protein Tax; TL-Om1 cells, an ATL-derived line in which the virus is largely silent and Tax is low or absent; and Jurkat cells, which are uninfected and served as controls. In parallel, they treated the T cell lines themselves. Western blotting and quantitative PCR revealed that HTLV-1 infection drove significant upregulation of both EZH1 and EZH2, along with elevated H3K27me3, in infected retinal pigment epithelial cells and in MT-2 cells, with EZH1 protein rising roughly 2.5-fold in infected ocular cells and six-fold in MT-2 cells. This was the first demonstration that HTLV-1 infection induces polycomb-mediated epigenetic changes in retinal cells.

The team then treated the models with valemetostat at 0.01, 0.1, and 1 micromolar for 96 hours, concentrations selected in preliminary experiments because they harmed infected T cells while leaving normal ocular cells, including primary human trabecular meshwork cells, unaffected below 10 micromolar. The results were strikingly dependent on the model. In co-cultures of retinal cells with Tax-positive MT-2 cells, and in retinal cells directly infected with HTLV-1, the drug produced modest but statistically significant reductions in cell viability at the highest dose, accompanied by small increases in late-stage apoptosis. No such effects appeared in co-cultures with TL-Om1 or Jurkat cells. Crucially, the absolute magnitude of apoptosis remained limited, typically only 1 to 3 percent above baseline, indicating that valemetostat is not broadly toxic to retinal cells, an important safety consideration given their role in maintaining vision.

The virological findings were equally nuanced. Valemetostat did not significantly reduce the HTLV-1 proviral load in co-culture systems or in directly infected retinal pigment epithelial cells. However, in MT-2 cells themselves, 1 micromolar valemetostat significantly lowered proviral load and suppressed the messenger RNA levels of both Tax and HBZ, the two hallmark transcripts of the virus. Because MT-2 cells represent the transcriptionally active, highly infectious state of HTLV-1, while TL-Om1 represents latency, the results suggest that the drug’s antiviral effect is gated by the transcriptional status of the infected cell. Within the four-day treatment window, the authors conclude, valemetostat’s benefit to the ocular environment is likely indirect, acting primarily by quieting the most virally active cells rather than by eradicating provirus everywhere.

The most clinically relevant effects emerged in the inflammatory readouts. HTLV-1-infected T cells recovered from the eyes of patients with uveitis are known to secrete copious interleukin-6, interleukin-8, and interleukin-10, all implicated in disease. In the new study, valemetostat produced a dose-dependent increase in the anti-inflammatory cytokine IL-10 in MT-2-containing conditions, significant at 1 micromolar in the co-culture system and across all doses in MT-2 cells. This fits a mechanistic expectation: blocking EZH1/2 removes H3K27me3 marks that repress the IL-10 gene, and prior genetic studies showed that loss of EZH2 directly activates IL-10 transcription in several CD4-positive T cell subsets. Meanwhile, pro-inflammatory signals fell in a context-dependent pattern. IL-12p70 and the chemokine CXCL-10 dropped in co-cultures, IL-6 and IL-8 declined mainly in MT-2 cells, and CCL-2 fell at low doses in the MT-2 co-culture, whereas the chemokine CCL-5 was unchanged in every model.

The drug’s influence on NF-kappaB, the central inflammatory pathway that Tax hijacks to drive both viral replication and cytokine production, was more subdued. Valemetostat modestly reduced NF-kappaB p65 phosphorylation in the MT-2 co-culture at the lowest dose and slightly decreased the nuclear-to-cytoplasmic ratio of p65 in retinal cells stimulated with TNF-alpha, but it did not abolish nuclear translocation. The authors attribute this to the overwhelming strength of Tax-driven NF-kappaB activation, which a 96-hour course of EZH1/2 inhibition may be insufficient to counteract, and to the fact that NF-kappaB and cytokine networks are regulated by many factors beyond polycomb complexes. Immunofluorescence confirmed that valemetostat significantly lowered H3K27me3 in retinal cells exposed to MT-2 cells or directly infected, but not in cells co-cultured with TL-Om1 or Jurkat cells, again underscoring the model dependence of the epigenetic response.

The study also carries a cautionary note about IL-10. Although the cytokine is anti-inflammatory, it can promote the survival of HTLV-1-infected T cells and facilitate immune evasion by impairing dendritic cell antigen presentation and downregulating MHC class I molecules, and patients with aggressive ATL often show abnormally elevated IL-10. The authors therefore suggest that combining EZH1/2 inhibition with IL-10 pathway blockade could prove more effective, noting evidence that IL-10 neutralization sensitizes ATL cells to standard therapies. In the TL-Om1 model of ATL-related ocular infiltration, valemetostat failed to reduce H3K27me3, proviral load, or NF-kappaB activation within the malignant cells, yet it suppressed TL-Om1-induced CXCL10 secretion and induced dose-dependent apoptosis, pointing to a benefit mediated through the inflammatory microenvironment rather than direct tumor killing.

The authors are candid about the limitations. The work relied entirely on in vitro co-cultures and established cell lines, which cannot reproduce the blood-retinal barrier, retinal architecture, or local immune regulation of a living eye, and the intraocular pharmacokinetics of valemetostat after systemic administration remain undefined. Sex as a biological variable could not be assessed because donor-defined primary cells were not used. Even so, the findings establish a proof of concept that an approved epigenetic therapy can counteract HTLV-1-induced chromatin changes in retinal cells, dampen viral transcription in the most active infected cells, and reshape the cytokine milieu that sustains uveitis. Longer treatment studies, in vivo models, and patient-derived systems will be needed to determine whether these modest, context-dependent effects can be translated into a genuine steroid-sparing therapy for one of the most burdensome manifestations of a virus that medicine has long neglected.

Subject of Research: EZH1/2-targeted epigenetic therapy with valemetostat for HTLV-1-associated uveitis

Article Title: Dual impact of EZH1/2-targeted therapy in HTLV-1-associated inflammation: Direct and indirect mechanisms

Article References: Zou, Y., Kamoi, K., Yang, M., Zong, Y., Zhang, J., & Ohno-Matsui, K. (2026). Dual impact of EZH1/2-targeted therapy in HTLV-1-associated inflammation: Direct and indirect mechanisms. iScience, 29(11), Article 117775. https://doi.org/10.1016/j.isci.2026.117775

Image Credits: AI Generated

DOI: 10.1016/j.isci.2026.117775

Keywords: HTLV-1, valemetostat, EZH1, EZH2, H3K27me3, uveitis, epigenetics, PRC2, Tax, IL-10, NF-kappaB, retinal pigment epithelium

Frost is one of the most punishing adversaries of tea cultivation. A single cold snap can scorch tender leaves, derail an entire season’s harvest, and degrade the delicate chemistry that gives tea its value. For growers and breeders, however, judging how badly a field has been damaged has long been a stubbornly subjective exercise: visual ratings lump continuous injury into crude categories, and laboratory assays destroy the very tissue they measure. A new study published in Plant Methods by Zhengtong He of Shihezi University, Zhiwei Chen of the Tea Research Institute of Shandong Academy of Agricultural Sciences, and colleagues offers a way out, pairing hyperspectral imaging with a purpose-built deep learning model to read frost damage directly from the way leaves reflect light.

The core problem the team confronted is that frost injury is not a binary event but a continuum. Leaves exposed to sub-zero temperatures suffer a cascade of overlapping stresses: photosynthetic pigments degrade, the machinery of photosynthesis falters, and cell membranes and walls break down. Any single measurement captures only a sliver of that cascade. To capture the whole picture, the researchers collected hyperspectral data together with eight key physicochemical indicators from tea plants growing across natural frost damage gradients in the field, rather than in the artificial conditions of a growth chamber. From these multidimensional physiological responses they constructed a composite measure, the tea cold stress response index, or TCSRI, which expresses frost damage severity as a continuous value instead of a coarse visual class.

Building TCSRI is a meaningful advance in itself. Traditional frost assessment often relies on ordinal scales, where an observer assigns a score of mild, moderate, or severe. Such scales throw away information and make it difficult to track recovery or compare cultivars with fine precision. By integrating several physiological dimensions into one index, the team created a target variable that reflects the plant’s actual internal state. The challenge then became predicting that index, and the individual chemical indicators behind it, from spectral data alone, without touching or destroying a single leaf.

Hyperspectral sensing is well suited to this task in principle. Across hundreds of narrow wavelength bands, plant leaves encode a wealth of information: chlorophyll absorption in the visible range, water and structural features in the near infrared. But the data are high-dimensional, with far more spectral channels than samples, a regime that invites overfitting, especially in field studies where collecting ground-truth measurements is laborious. Conventional chemometric approaches, from partial least squares regression to standard machine learning pipelines, often struggle to separate genuine physiological signals from noise, sensor drift, and the confounding effects of leaf surface properties and illumination variation.

The researchers’ answer is a model they call STAMPformer, short for spectral-prior-guided multi-view attention pooling. Its architecture reflects a deliberate design philosophy: rather than letting a neural network rediscover everything from scratch, the model is steered by what spectroscopists already know about how plants respond to stress. At its front end, a parameter-free attention convolution extraction module jointly models both the raw reflectance spectra and their first-order derivatives. Derivative spectra are a classic spectral prior: they accentuate subtle local features such as absorption peaks and shoulders that are easily drowned out in raw reflectance, while suppressing broad baseline drift and noise. By processing both views together, the module sharpens the local spectral signatures that carry physiological meaning.

On top of this extraction stage sits the second innovation, a multi-view attention pooling module. Deep networks processing spectral sequences produce long streams of features, but not all wavelengths matter equally for a given prediction. The pooling module adaptively aggregates sequence features drawn from different feature subspaces, learning to amplify the responses that are most diagnostic of cold stress and to down-weight the rest. This attention mechanism acts like a learned spotlight, and because it operates across multiple subspaces, it can capture complementary patterns that a single attention head might miss. The result is a compact representation tailored to the prediction task at hand, whether that is estimating a specific chemical indicator or the composite TCSRI.

The performance numbers are striking. Across all nine prediction tasks, spanning the eight physicochemical indicators and the TCSRI itself, STAMPformer achieved coefficients of determination above 0.87 and ratios of performance to deviation above 2.80, thresholds generally regarded as indicating reliable quantitative prediction. In other words, from a leaf’s reflectance fingerprint alone, the model could reconstruct the plant’s internal frost-stress state with an accuracy that approaches laboratory measurement, while remaining entirely non-destructive. The team did not stop at headline metrics. Ablation experiments systematically removed each proposed module to confirm that both the attention convolution extraction and the multi-view pooling contributed measurably to the gains, and paired statistical tests across multiple random seeds ensured the improvements were not artifacts of a lucky initialization.

Interpretability was a further priority, and here the study delivers something rarer than raw accuracy. Applying SHAP analysis, a technique that attributes each prediction to the contributions of individual input features, the researchers identified the wavelengths the model relied on most heavily. These key spectral regions correspond to physiologically meaningful processes: pigment degradation, photosynthetic impairment, and the disruption of cellular structure. That alignment between machine attention and plant biology matters on two fronts. It gives spectroscopists confidence that the model has learned genuine stress signatures rather than spurious correlations, and it hands plant physiologists a data-driven map of which parts of the spectrum track which facets of cold injury, potentially guiding future sensor design and breeding assays.

Crucially, the model also proved itself on data it had never seen. Independent external validation, using samples not involved in training, demonstrated that STAMPformer’s predictive ability generalizes beyond its original dataset, addressing one of the most common failure modes of machine learning in agricultural sensing. For a field where models are often tuned and tested on the same plots, this external check is an important credibility marker, suggesting the framework could be deployed across different farms, seasons, and frost events rather than remaining a laboratory curiosity.

The practical implications reach well beyond tea. An accurate, non-destructive, continuous measure of cold damage opens the door to rapid post-frost field surveys, letting growers quantify losses within hours instead of waiting for symptoms to develop or sending samples to a lab. For breeders screening for cold-tolerant germplasm, a spectral readout of TCSRI could accelerate the evaluation of hundreds of candidate lines without destructive sampling. And in the emerging vision of the smart tea garden, where drones and handheld spectrometers roam the rows, a model like STAMPformer could feed real-time frost maps into irrigation, shading, and recovery-management decisions. The authors frame their work as supporting frost monitoring, cold-tolerant germplasm evaluation, and intelligent garden management, and the architecture’s reliance on general spectral priors rather than tea-specific tricks suggests the approach could be adapted to other crops facing abiotic stress. As climate variability makes late-season frosts increasingly erratic, tools that turn light reflected from a leaf into a precise physiological diagnosis may become as essential to the tea garden as the thermometer.

Subject of Research: Hyperspectral deep learning prediction of continuous frost damage severity in tea plants

Article Title: STAMPformer: spectral-prior-guided multi-view attention learning for hyperspectral prediction of continuous frost damage severity in field-grown tea plants

Article References: He, Z., Chen, Z., Ding, Z., Wang, Z., Zhang, F., Zhao, Y., & Dong, C. (2026). STAMPformer: spectral-prior-guided multi-view attention learning for hyperspectral prediction of continuous frost damage severity in field-grown tea plants. Plant Methods. https://doi.org/10.1186/s13007-026-01597-4

Image Credits: AI Generated

DOI: 10.1186/s13007-026-01597-4

Keywords: tea plant, frost damage, hyperspectral imaging, deep learning, attention mechanism, cold stress index, non-destructive prediction, SHAP analysis, precision agriculture, spectral priors, plant physiology, smart farming

Nearly 100 patients discussed their maladies with a Google bot, called AMIE, before meeting with physicians.