Shocking stories tell tale of London Zoo’s founding

When Tommy the chimpanzee first came to London’s zoo in the fall of 1835, he was dressed in an old white shirt.

Keepers gave him a new frock and a sailor hat and set him up in a cozy spot in the kitchen to weather the winter. Visitors flocked to get a look at the little ape roaming around the keepers’ lodge, curled up in the cook’s lap or tugging on her skirt like a toddler. Tommy was a hit — the zoo’s latest star.
Six months later, he was dead.

Tommy’s sorrowful story comes near the middle of Isobel Charman’s latest book, The Zoo, a tale of the founding of the Gardens of the Zoological Society of London, known today as the London Zoo. The book lays out a grand saga of human ambition and audacity, but it’s the animals’ stories — their lives and deaths and hardships — that catch hold of readers and don’t let go.

Charman, a writer and documentary producer, resurrects almost three decades of history, beginning in 1824, when the zoo was still just a fantastical idea: a public menagerie of animals “that would allow naturalists to observe the creatures scientifically.”

It was a long, hard path to that lofty dream, though: In the zoo’s early years, exotic creatures were nearly impossible to keep alive. Charman unloads a numbing litany of animal misery that batters the reader like a boxer working over a speed bag. Kangaroos hurl themselves at fences, monkeys attack each other in cramped, dark cages and an elephant named Jack breaks a tusk while smashing up his den. Charman’s parade of horrors boggles the mind, as does the sheer number of animals carted from all corners of the world to the cold, wet enclosures of the zoo.

Her story is an incredible piece of detective work, told through the eyes of many key players and famous figures, including Charles Darwin. Charman plumbs details from newspaper articles, diaries, census records and weather reports to craft a narrative of the time. She portrays a London that’s gritty, grimy and cold, where some aspects of science and medicine seem stuck in the Dark Ages. Doctors still used leeches to bleed patients, and no one had a clue how to care for zoo animals.
Zoo workers certainly tried — applying liniment to sores on a lion’s legs, prescribing opium for a sick puma and treating a constipated llama with purgatives. But nothing seemed to stop the endless conveyor belt that brought living animals in and carried dead ones out. Back then, caring for zoo animals was mostly a matter of trial and error, Charman writes. What seems laughably obvious now — animals need shelter in winter, cakes and buns aren’t proper food for elephants — took zookeepers years to figure out.

Over time the zoo adapted, making gradual changes that eventually improved the lives of its inhabitants. It seemed to morph, finally, from mostly “a playground of the privileged,” as Charman calls it, to a reliable place for scientific study, where curious people could learn about the “wild and wonderful” creatures within.

One of those people was Darwin, whose ideas about human origins clicked into place after he spent time with Jenny the orangutan. Her teasing relationship with her keeper, apparent understanding of language and utter likeness to people helped convince Darwin that humankind was just another branch on the tree of life, Charman writes.
Darwin’s work on the subject wouldn’t be published for decades, but in the meantime, the zoo’s early improvements seemed to have stuck. Over 30 years after Tommy the chimpanzee died in his keeper’s arms, a hippopotamus gave birth to “the first captive-bred hippo to be reared by its mother,” Charman notes. The baby hippo not only survived — she lived for 36 years.

Readers may wonder how standards for animal treatment have changed over time. But Charman sticks to history, rather than examining contrasts to modern zoos. Still, what she offers is gripping enough on its own: a bold, no-holds-barred look at one zoo’s beginning. It was impressive, no doubt. But it wasn’t pretty.

Random mutations play large role in cancer, study finds

Researchers have identified new enemies in the war on cancer: ones that are already inside cells and that no one can avoid.

Random mistakes made as stem cells divide are responsible for about two-thirds of the mutations in cancer cells, researchers from Johns Hopkins University report in the March 24 Science. Across all cancer types, environment and lifestyle factors, such as smoking and obesity, contribute 29 percent of cancer mutations, and 5 percent are inherited.
That finding challenges the common wisdom that cancer is the product of heredity and the environment. “There’s a third cause and this cause of mutations is a major cause,” says cancer geneticist Bert Vogelstein.

Such random mutations build up over time and help explain why cancer strikes older people more often. Knowing that the enemy will strike from within even when people protect themselves against external threats indicates that early cancer detection and treatment deserve greater attention than they have previously gotten, Vogelstein says.

Vogelstein and biomathematician Cristian Tomasetti proposed in 2015 that random mutations are the reason some organs are more prone to cancer than others. For instance, stem cells are constantly renewing the intestinal lining of the colon, which develops tumors more often than the brain, where cell division is uncommon. That report was controversial because it was interpreted as saying that most cancers are the result of “bad luck.” The analysis didn’t include breast and prostate cancers. Factoring in those common cancers might change the results, some scientists said. And because the researchers looked at only cancer within the United States, critics charged that the finding might not hold up when considering places around the world where different environmental factors, such as infections, affect cancer development.

In the new study, Vogelstein, Tomasetti and Hopkins colleague Lu Li examined data from 69 countries about 17 types of cancer, this time including breast and prostate. Again, the researchers found a strong link between cancer and tissues with lots of dividing stem cells. The team also used DNA data and epidemiological studies to calculate the proportions of mutations in cancer cells caused by heredity or environmental and lifestyle factors. Remaining mutations were attributed to random errors — including typos, insertions or deletions of genes, epigenetic changes (alterations of chemical tags on DNA or proteins that affect gene activity) and gene rearrangements. Such errors unavoidably happen when cells divide.
Usually cancer results after a cell accumulates many mutations. Some people will have accumulated a variety of cancer-associated mutations but won’t get cancer until some final insult goads the cell into becoming malignant (SN: 12/26/15, p. 28). For some tumors, all the mutations may be the hit-and-miss result of cell division mistakes. There’s no way to evade those cancers, Vogelstein says. Other malignancies may spring up as a result of different combinations of heritable, environmental and random mutations. Lung cancer and other tumor types that are strongly associated with environmentally caused mutations could be eluded by avoiding the carcinogen, even when most of the mutations that spur cancer growth arise from random mistakes, Tomasetti says.

“They are venturing into new territory,” says Giovanni Parmigiani, a biostatistician at the Harvard T.H. Chan School of Public Health. Tomasetti, Li and Vogelstein are the first to rigorously estimate the contribution of environment, heredity and DNA-copying errors to cancer, he says. “Perhaps the estimates will improve in the future, but theirs seems like a very solid starting point.”

Now that the Hopkins researchers have pointed it out, the relationship between dividing cells and cancer seems obvious, says biological physicist Bartlomiej Waclaw of the University of Edinburgh. “I don’t think that the existence of this correlation is surprising,” he says. “What’s surprising is that it’s not stronger.”

Some tissues develop cancers more or less often than other tissues with a similar number of cell divisions, Waclaw and Martin Nowak of Harvard University pointed out in a commentary on the Hopkins study, published in the same issue of Science. That suggests some organs are better at nipping cancer in the bud. Discovering how those tissues avoid cancer could lead to new ways to prevent tumors elsewhere in the body, Waclaw suggests.

Other researchers say the Hopkins team is guilty of faulty reasoning. “They are assuming that just because tissues which have high stem cell turnover also have high cancer rates, that one is causing the other,” says cancer researcher Anne McTiernan of the Fred Hutchinson Cancer Research Center in Seattle. “In this new paper, they’ve added data from other countries but haven’t gotten away from this biased thinking.”

Tomasetti and colleagues based their calculations on data from Cancer Research UK that suggest that 42 percent of cancers are preventable. Preventable cancers are ones for which people could avoid a risk factor, such as unprotected sun exposure or tanning bed use, or take positive steps to lower cancer risks, such as exercising regularly and eating fruits and vegetables. But those estimates may not be accurate, McTiernan says. “In reality, it’s very difficult to measure environmental exposures, so our estimates of preventability are likely very underestimated.”

To attribute so many cancer mutations to chance seems to negate public health messages, Waclaw says, and some people may find the calculation that 66 percent of cancer-associated mutations are unavoidable disturbing because they spend a lot of time trying to prevent cancer. “It’s important to consider the randomness, or bad luck, that comes with cellular division,” he says.

In fact, Tomasetti and Vogelstein stress that their findings are compatible with cancer-prevention recommendations. Avoiding smoking, tanning beds, obesity and other known carcinogens can prevent the “environmental” mutations that combine with inherited and random mutations to tip cells into cancer. Without those final straws loaded from environmental exposures, tumors may be averted or greatly delayed.

People with cancer may be able to take some comfort from the study, says Elaine Mardis, a cancer genomicist at the Nationwide Children’s Hospital in Columbus, Ohio. “Perhaps the positive message here is that, other than known risk factors, such as smoking, radiation exposure and obesity, there is a component of cancer that is simply a consequence of being human.”

Language heard, but never spoken, by young babies bestows a hidden benefit

The way babies learn to speak is nothing short of breathtaking. Their brains are learning the differences between sounds, rehearsing mouth movements and mastering vocabulary by putting words into meaningful context. It’s a lot to fit in between naps and diaper changes.

A recent study shows just how durable this early language learning is. Dutch-speaking adults who were adopted from South Korea as preverbal babies held on to latent Korean language skills, researchers report online January 18 in Royal Society Open Science. In the first months of their lives, these people had already laid down the foundation for speaking Korean — a foundation that persisted for decades undetected, only revealing itself later in careful laboratory tests.

Researchers tested how well people could learn to identify and speak tricky Korean sounds. “For Korean listeners, these sounds are easy to distinguish, but for second-language learners they are very difficult to master,” says study coauthor Mirjam Broersma, a psycholinguist of Radboud University in Nijmegen, Netherlands. For instance, a native Dutch speaker would listen to three distinct Korean sounds and hear only the same “t” sound.

Broersma and her colleagues compared the language-absorbing skills of a group of 29 native Dutch speakers to 29 South Korea-born Dutch speakers. Half of the adoptees moved to the Netherlands when they were older than 17 months — ages at which the kids had probably begun talking. The other half were adopted as preverbal babies younger than 6 months. As a group, the South Korea-born adults outperformed the native-born Dutch adults, more easily learning both to recognize and speak the Korean sounds.

This advantage held when the researchers looked at only adults who had been adopted before turning 6 months old. “Even those who were only 3 to 5 months old at the time of adoption already knew a lot about the sounds of their birth language, enough even to help them relearn those sounds decades later,” Broersma says.

Uncovering this latent skill decades after it had been imprinted in babies younger than 6 months was thrilling, Broersma says. Many researchers had assumed that infants start to learn the sounds of their first language later, around 6 to 8 months after birth. “Our results show that that assumption must have been wrong,” she says.

It’s possible that some of these language skills were acquired during pregnancy, as other studies have hinted. Because the current study didn’t include babies who were adopted immediately after birth, the results can’t say whether language heard during gestation would have had an influence on later language skills. Still, the results suggest that babies start picking up language as soon as they possibly can.

Hidden hoard hints at how ancient elites protected the family treasures

BOSTON — Long before anyone opened a bank account or rented a safe deposit box, wealth protection demanded a bit of guile and a broken beer jug. A 3,100-year-old jewelry stash was discovered in just such a vessel, unearthed from an ancient settlement in Israel called Megiddo in 2010. Now the find is providing clues to how affluent folk hoarded their valuables at a time when fortunes rested on fancy metalwork, not money.

At the fortress city of Megiddo, a high-ranking Canaanite family stashed jewelry in a beer jug and hid it in a courtyard’s corner under a bowl, possibly under a veil of cloth, Eran Arie of the Israel Museum in Jerusalem, said November 17 at the annual meeting of the American Schools of Oriental Research.
The hoard’s owners removed the jug’s neck and inserted a bundle of 35 silver items, including earrings and a bracelet, which were wrapped in two linen cloths. Other valuables were then added to the jug, including around 1,300 beads of silver and electrum — an alloy of gold and silver — that had probably been threaded into an elaborate necklace. There were 10 additional pieces of electrum jewelry, including a pair of basket-shaped earrings, each displaying a carved, long-legged bird.
A Canaanite city palace stood only about 30 meters from the Iron Age building that housed the courtyard, Arie said. Due to the lesser building’s strategic location, its inhabitants must have held key government positions, he proposed. “For the family that lived there, the hoard represented the lion’s share of their wealth.” Those family members presumably fled around the time the structure that held the jewelry hoard was destroyed in a catastrophic event, possibly a battle.
The Megiddo hoard was hidden but not buried, giving its owners quick access to their valuables. But no one ever retrieved the treasure. “We will never know why no one returned to claim this hoard,” Arie said.

False alarms may be a necessary part of earthquake early warnings

Earthquake warning systems face a tough trade-off: To give enough time to take cover or shut down emergency systems, alerts may need to go out before it’s clear how strong the quake will be. And that raises the risk of false alarms, undermining confidence in any warning system.

A new study aims to quantify the best-case scenario for warning time from a hypothetical earthquake early warning system. The result? There is no magic formula for deciding when to issue an alert, the researchers report online March 21 in Science Advances.
“We have a choice when issuing earthquake warnings,” says study leader Sarah Minson, a seismologist at the U.S. Geological Survey, or USGS, in Menlo Park, Calif. “You have to think about your relative risk appetite: What is the cost of taking action versus the cost of the damage you’re trying to prevent?”

For locations far from a large quake’s origin, waiting for clear signs of risk before sending an alert may mean waiting too long for people to be able to take protective action. But for those tasked with managing critical infrastructure, such as airports, trains or nuclear power plants, an early warning even if false may be preferable to an alert coming too late (SN: 4/19/14, p. 16).

Alerts issued by earthquake early warning systems, called EEWs, are based on several parameters: the depth and location of the quake’s origin, its estimated magnitude and the ground properties, such as the types of soil and rock that seismic waves would travel through.

“The trick to earthquake early warning systems is that it’s a misnomer,” Minson says. Such systems don’t warn that a quake is imminent. Instead, they alert people that a quake has already happened, giving them precious seconds — perhaps a minute or two — to prepare for imminent ground shaking.
Estimating magnitude turns out to be a sticking point. It is impossible to distinguish a powerful earthquake in its earliest stages from a small, weak quake, according to a 2016 study by a team of researchers that included Men-Andrin Meier, a seismologist at Caltech who also coauthors the new study. Estimating magnitude for larger quakes also takes more time, because the rupture of the fault lasts perhaps several seconds longer – a significant chunk of time when it comes to EEW. And there is a trade-off in terms of distance: For locations farther away, there is less certainty the shaking will reach that far.
In the new study, Minson, Meier and colleagues used standard ground-motion prediction equations to calculate the minimum quake magnitude that would produce shaking at any distance. Then, they calculated how quickly an EEW could estimate whether the quake would exceed that minimum magnitude to qualify for an alert. Finally, the team estimated how long it would take for the shaking to strike a location. Ultimately, they determined, EEW holds the greatest benefit for users who are willing to take action early, even with the risk of false alarms. The team hopes its paper provides a framework to help emergency response managers make those decisions.

EEWs are already in operation around the world, from Mexico to Japan. USGS, in collaboration with researchers and universities, has been developing the ShakeAlert system for the earthquake-prone U.S. West Coast. It is expected be rolled out this year, although plans for future expansion may be in jeopardy: President Trump’s proposed 2019 budget cuts the USGS program’s $8.2 million in funding. It’s unclear whether Congress will spare those funds.

The value of any alert system will ultimately depend on whether it fulfills its objective — getting people to take cover swiftly in order to save lives. “More than half of injuries from past earthquakes are associated with things falling on people,” says Richard Allen, a seismologist at the University of California, Berkeley who was not involved in the new study. “A few seconds of warning can more than halve the number of injuries.”

But the researchers acknowledge there is a danger in issuing too many false alarms. People may become complacent and ignore future warnings. “We are playing a precautionary game,” Minson says. “It’s a warning system, not a guarantee.”

These transparent fish turn rainbow with white light. Now, we know why

The ghost catfish transforms from glassy to glam when white light passes through its mostly transparent body. Now, scientists know why.

The fish’s iridescence comes from light bending as it travels through microscopic striped structures in the animal’s muscles, researchers report March 13 in the Proceedings of the National Academy of Sciences.

Many fishes with iridescent flair have tiny crystals in their skin or scales that reflect light (SN: 4/6/21). But the ghost catfish (Kryptopterus vitreolus) and other transparent aquatic species, like eel larvae and icefishes, lack such structures to explain their luster.

The ghost catfish’s see-through body caught the eye of physicist Qibin Zhao when he was in an aquarium store. The roughly 5-centimeter-long freshwater fish is a popular ornamental species. “I was standing in front of the tank and staring at the fish,” says Zhao, of Shanghai Jiao Tong University. “And then I saw the iridescence.”

To investigate the fish’s colorful properties, Zhao and colleagues first examined the fish under different lighting conditions. The researchers determined its iridescence arose from light passing through the fish rather than reflecting off it. By using a white light laser to illuminate the animal’s muscles and skin separately, the team found that the muscles generated the multicolored sheen.
The researchers then characterized the muscles’ properties by analyzing how X-rays scatter when traveling through the tissue and by looking at it with an electron microscope. The team identified sarcomeres — regularly spaced, banded structures, each roughly 2 micrometers long, that run along the length of muscle fibers — as the source of the iridescence.

The sarcomeres’ repeating bands, comprised of proteins that overlap by varying amounts, bend white light in a way that separates and enhances its different wavelengths. The collective diffraction of light produces an array of colors. When the fish contracts and relaxes its muscles to swim, the sarcomeres slightly change in length, causing a shifting rainbow effect.
The purpose of the ghost catfish’s iridescence is a little unclear, says Heok Hee Ng, an independent ichthyologist in Singapore who was not involved in the new study. Ghost catfish live in murky water and seldom rely on sight, he says. But the iridescence might help them visually coordinate movements when traveling in schools, or it could help them blend in with shimmering water to hide from land predators, like some birds, he adds.

Regardless of function, Ng is excited to see scientists exploring the ghost catfish’s unusual characteristics.

“Fishes actually have quite a number of these interesting structures that serve them in many ways,” he says. “And a lot of these structures are very poorly studied.”

Chia seedlings verify Alan Turing’s ideas about patterns in nature

LAS VEGAS – Chia seeds sprouted in trays have experimentally confirmed a mathematical model proposed by computer scientist and polymath Alan Turing decades ago. The model describes how patterns might emerge in desert vegetation, leopard spots and zebra stripes.

These and other blotchy and stripy features in nature are examples of what are called Turing patterns, so named because in 1952, Turing presented equations for how simple interactions between competing factors can lead to surprisingly complex surface patterns. In the case of arid regions, the competition for moisture among plants would drive the intricate distribution of vegetation.
But proving that Turing’s model explains patterns in the real world has been challenging (SN: 10/21/15). It wasn’t clear whether Turing’s idea is really behind natural distributions of vegetation. It could be that the idea is a mathematical just-so story that happens to produce similar shapes in a computer, says physicist Flavio Fenton of Georgia Tech in Atlanta.

In research presented at the American Physical Society meeting, Brendan D’Aquino, who studied in Fenton’s lab during the summer of 2022, described an experiment that seems to confirm that Turing’s model truly underlies patterns in vegetation.

The team grew chia seeds in even layers in trays and then adjusted the available moisture. In essence, the researchers were experimentally tweaking the factors that appear in the Turing equations. Sure enough, patterns resembling those seen in natural environments emerged. The patterns also strongly resembled computer simulations of the Turing model.
“In previous studies,” said D’Aquino, who is an undergraduate computer science student at Northeastern University, “people kind of retroactively fit models to observe Turing patterns that they found in the world. But here we were actually able to show that changing the relevant parameters in the model produces experimental results that we would expect.”

Although Turing patterns have been produced in some chemistry experiments and other artificial systems, the team believes this is the first time that experiments with living vegetation have verified Turing’s mathematical insight.

In mice, anxiety isn’t all in the head. It can start in the heart

When you’re stressed and anxious, you might feel your heart race. Is your heart racing because you’re afraid? Or does your speeding heart itself contribute to your anxiety? Both could be true, a new study in mice suggests.

By artificially increasing the heart rates of mice, scientists were able to increase anxiety-like behaviors — ones that the team then calmed by turning off a particular part of the brain. The study, published in the March 9 Nature, shows that in high-risk contexts, a racing heart could go to your head and increase anxiety. The findings could offer a new angle for studying and, potentially, treating anxiety disorders.
The idea that body sensations might contribute to emotions in the brain goes back at least to one of the founders of psychology, William James, says Karl Deisseroth, a neuroscientist at Stanford University. In James’ 1890 book The Principles of Psychology, he put forward the idea that emotion follows what the body experiences. “We feel sorry because we cry, angry because we strike, afraid because we tremble,” James wrote.

The brain certainly can sense internal body signals, a phenomenon called interoception. But whether those sensations — like a racing heart — can contribute to emotion is difficult to prove, says Anna Beyeler, a neuroscientist at the French National Institute of Health and Medical Research in Bordeaux. She studies brain circuitry related to emotion and wrote a commentary on the new study but was not involved in the research. “I’m sure a lot of people have thought of doing these experiments, but no one really had the tools,” she says.

Deisseroth has spent his career developing those tools. He is one of the scientists who developed optogenetics — a technique that uses viruses to modify the genes of specific cells to respond to bursts of light (SN: 6/18/21; SN: 1/15/10). Scientists can use the flip of a light switch to activate or suppress the activity of those cells.
In the new study, Deisseroth and his colleagues used a light attached to a tiny vest over a mouse’s genetically engineered heart to change the animal’s heart rate. When the light was off, a mouse’s heart pumped at about 600 beats per minute. But when the team turned on a light that flashed at 900 beats per minutes, the mouse’s heartbeat followed suit. “It’s a nice reasonable acceleration, [one a mouse] would encounter in a time of stress or fear,” Deisseroth explains.

When the mice felt their hearts racing, they showed anxiety-like behavior. In risky scenarios — like open areas where a little mouse might be someone’s lunch — the rodents slunk along the walls and lurked in darker corners. When pressing a lever for water that could sometimes be coupled with a mild shock, mice with normal heart rates still pressed without hesitation. But mice with racing hearts decided they’d rather go thirsty.

“Everybody was expecting that, but it’s the first time that it has been clearly demonstrated,” Beyeler says.
The researchers also scanned the animals’ brains to find areas that might be processing the increased heart rate. One of the biggest signals, Deisseroth says, came from the posterior insula (SN: 4/25/16). “The insula was interesting because it’s highly connected with interoceptive circuitry,” he explains. “When we saw that signal, [our] interest was definitely piqued.”

Using more optogenetics, the team reduced activity in the posterior insula, which decreased the mice’s anxiety-like behaviors. The animals’ hearts still raced, but they behaved more normally, spending some time in open areas of mazes and pressing levers for water without fear.
A lot of people are very excited about the work, says Wen Chen, the branch chief of basic medicine research for complementary and integrative health at the National Center for Complementary and Integrative Health in Bethesda, Md. “No matter what kind of meetings I go into, in the last two days, everybody brought up this paper,” says Chen, who wasn’t involved in the research.

The next step, Deisseroth says, is to look at other parts of the body that might affect anxiety. “We can feel it in our gut sometimes, or we can feel it in our neck or shoulders,” he says. Using optogenetics to tense a mouse’s muscles, or give them tummy butterflies, might reveal other pathways that produce fearful or anxiety-like behaviors.

Understanding the link between heart and head could eventually factor into how doctors treat panic and anxiety, Beyeler says. But the path between the lab and the clinic, she notes, is much more convoluted than that of the heart to the head.

An antibody injection could one day help people with endometriosis

An experimental treatment for endometriosis, a painful gynecological disease that affects some 190 million people worldwide, may one day offer new hope for easing symptoms.

Monthly antibody injections reversed telltale signs of endometriosis in monkeys, researchers report February 22 in Science Translational Medicine. The antibody targets IL-8, a molecule that whips up inflammation inside the scattered, sometimes bleeding lesions that mark the disease. After neutralizing IL-8, those hallmark lesions shrink, the team found.

The new treatment is “pretty potent,” says Philippa Saunders, a reproductive scientist at the University of Edinburgh who was not involved with work. The study’s authors haven’t reported a cure, she points out, but their antibody does seem to have an impact. “I think it’s really very promising,” she says.

Many scientists think endometriosis occurs when bits of the uterine lining — the endometrium — slough off during menstruation. Instead of exiting via the vagina, they voyage in the other direction: up through the fallopian tubes. Those bits of tissue then trespass through the body, sprouting lesions where they land. They’ll glom onto the ovaries, fallopian tubes, bladder and other spots outside of the uterus and take on a life of their own, Saunders says.
The lesions can grow nerve cells, form tough nubs of tissue and even bleed during menstrual cycles. They can also kick off chronic bouts of pelvic pain. If you have endometriosis, you can experience “pain when you urinate, pain when you defecate, pain when you have sex, pain when you move around,” Saunders says. People with the disease can also struggle with infertility and depression, she adds. “It’s really nasty.”
Once diagnosed, patients face a dearth of treatment options — there’s no cure, only therapies to alleviate symptoms. Surgery to remove lesions can help, but symptoms often come back.

The disease affects at least 10 percent of girls, women and transgender men in their reproductive years, Saunders says. And people typically suffer for years — about eight on average — before a diagnosis. “Doctors consider menstrual pelvic pain a very common thing,” says Ayako Nishimoto-Kakiuchi, a pharmacologist at Chugai Pharmaceutical Co. Ltd. in Tokyo. Endometriosis “is underestimated in the clinic,” she says. “I strongly believe that this disease has been understudied.”

Hormonal drugs that stop ovulation and menstruation can also offer relief, says Serdar Bulun, a reproductive endocrinologist at Northwestern University Feinberg School of Medicine in Chicago not involved with the new study. But those drugs come with side effects and aren’t ideal for people trying to become pregnant. “I see these patients day in and day out,” he says. “I see how much they suffer, and I feel like we are not doing enough.”

Nishimoto-Kakiuchi’s team engineered an antibody that grabs onto the inflammatory factor IL-8, a protein that scientists have previously fingered as one potential culprit in the disease. The antibody acts like a garbage collector, Nishimoto-Kakiuchi says. It grabs IL-8, delivers it to the cell’s waste disposal machinery, and then heads out to snare more IL-8.

The team tested the antibody in cynomolgus monkeys that were surgically modified to have the disease. (Endometriosis rarely shows up spontaneously in these monkeys, the scientists discovered previously after screening more than 600 females.) The team treated 11 monkeys with the antibody injection once a month for six months. In these animals, lesions shriveled and the adhesive tissue that glues them to the body thinned out, too. Before this study, Nishimoto-Kakiuchi says, the team didn’t think such signs of endometriosis were reversible.
Her company has now started a Phase I clinical trial to test the safety of therapy in humans. The treatment is one of several endometriosis therapies scientists are testing (SN: 7/19/19) . Other trials will test new hormonal drugs, robot-assisted surgery and behavioral interventions.

Doctors need new options to help people with the disease, Saunders says. “There’s a huge unmet clinical need.”

Half of all active satellites are now from SpaceX. Here’s why that may be a problem

SpaceX’s rapidly growing fleet of Starlink internet satellites now make up half of all active satellites in Earth orbit.

On February 27, the aerospace company launched 21 new satellites to join its broadband internet Starlink fleet. That brought the total number of active Starlink satellites to 3,660, or about 50 percent of the nearly 7,300 active satellites in orbit, according to analysis by astronomer Jonathan McDowell using data from SpaceX and the U.S. Space Force.
“These big low-orbit internet constellations have come from nowhere in 2019, to dominating the space environment in 2023,” says McDowell, of the Harvard-Smithsonian Center for Astrophysics in Cambridge, Mass. “It really is a massive shift and a massive industrialization of low orbit.”

SpaceX has been launching Starlink satellites since 2019 with the goal of bringing broadband internet to remote parts of the globe. And for just as long, astronomers have been warning that the bright satellites could mess up their view of the cosmos by leaving streaks on telescope images as they glide past (SN: 3/12/20).

Even the Hubble Space Telescope, which orbits more than 500 kilometers above the Earth’s surface, is vulnerable to these satellite streaks, as well as those from other satellite constellations. From 2002 to 2021, the percentage of Hubble images affected by light from low-orbit satellites increased by about 50 percent, astronomer Sandor Kruk of the Max-Planck Institute for Extraterrestrial Physics in Garching, Germany, and colleagues report March 2 in Nature Astronomy.

The number of images partially blocked by satellites is still small, the team found, rising from nearly 3 percent of images taken between 2002 and 2005 to just over 4 percent between 2018 and 2021 for one of Hubble’s cameras. But there are already thousands more Starlink satellites now than there were in 2021.

“The fraction of [Hubble] images crossed by satellites is currently small with a negligible impact on science,” Kruk and colleagues write. “However, the number of satellites and space debris will only increase in the future.” The team predicts that by the 2030s, the probability of a satellite crossing Hubble’s field of view any time it takes an image will be between 20 and 50 percent.
The sudden jump in Starlink satellites also poses a problem for space traffic, says astronomer Samantha Lawler of the University of Regina in Canada. Starlink satellites all orbit at a similar distance from Earth, just above 500 kilometers.

“Starlink is the densest patch of space that has ever existed,” Lawler says. The satellites are constantly navigating out of each other’s way to avoid collisions (SN: 2/12/09). And it’s a popular orbital altitude — Hubble is there, and so is the International Space Station and the Chinese space station.
“If there is some kind of collision [between Starlinks], some kind of mishap, it could immediately affect human lives,” Lawler says.

SpaceX launches Starlink satellites roughly once per week — it launched 51 more on March 3. And they’re not the only company launching constellations of internet satellites. By the 2030s, there could be 100,000 satellites crowding low Earth orbit.

So far, there are no international regulations to curb the number of satellites a private company can launch or to limit which orbits they can occupy.

“The speed of commercial development is much faster than the speed of regulation change,” McDowell says. “There needs to be an overhaul of space traffic management and space regulation generally to cope with these massive commercial projects.”