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The holiday onslaught is upon us. For some families with children, the crush of holiday gifts — while wonderful and thoughtful in many ways — can become nearly unmanageable, cluttering both rooms and minds.

This year, I’m striving for simplicity as I pick a few key presents for my girls. I will probably fail. But it’s a good goal, and one that has some new science to back it. Toddlers play longer and more creatively with toys when there are fewer toys around, researchers report November 27 in Infant Behavior and Development.
Researchers led by occupational therapist Alexia Metz at the University of Toledo in Ohio were curious about whether the number of toys would affect how the children played, including how many toys they played with and how long they spent with each toy. The researchers also wondered about children’s creativity, such as the ability to imagine a bucket as a drum or a hat.

In the experiment, 36 children ages 18 to 30 months visited a laboratory playroom twice while cameras caught how they played. On one visit, the room held four toys. On the other visit, the room held 16 toys.

When in the playroom with 16 toys, children played with more toys and spent less time with each one over a 15-minute session, the researchers found. When the same kids were in a room with four toys, they stuck with each toy longer, exploring other toys less over the 15 minutes.

What’s more, the quality of the children’s play seemed to be better when fewer toys were available. The researchers noted more creative uses of the toys when only four were present versus 16.
Metz and colleagues noticed that initial attempts to play with a toy were often superficial and simple. But if a kid’s interest stuck, those early pokes and bangs turned into more sophisticated manners of playing. This type of sustained engagement might help children learn to focus their attention, a skill Metz likened to a “muscle that they have to exercise.” This attentional workout might not happen if kids are perpetually exposed to lots of distracting toys.

The toys used in the study didn’t include electronic devices such as tablets. Only one of the four toys and only four of the 16 toys used batteries. Noisy toys may have their own troubles. They can cut down on parent-child conversations, scientists have found. It’s possible that electronics such as televisions or tablets would have even greater allure than other toys.

Nor do the researchers know what would happen if the study had been done in kids’ houses and with their own toys. It’s possible that the novelty of the new place and the new toys influenced the toddlers’ behavior. (As everyone knows, the toys at a friend’s house are way better than the toys a kid has at home, even when they are literally the exact same toy.)

The results don’t pinpoint the optimal number of toys for optimal child development, Metz says. “It’s a little preliminary to say this is good and that is bad,” she says. But she points out that many kids are not in danger of having too few toys. In fact, the average number of toys the kids in the study had was 87. Five families didn’t even provide toy counts, instead answering “a lot.”

“Because of the sheer abundance of toys, there’s no harm in bringing out a few at a time,” Metz says.

That’s an idea that I’ve seen floating around, and I like it. I’ve already started packing some of my kids’ toys out of sight, with the idea to switch the selection every so often (or more likely, never). Another recommendation I’ve seen is to immediately hide away some of the new presents, which aren’t likely to be missed in the holiday pandemonium, and break them out months later when the kids need a thrill.

If more nerve cells mean more smarts, then dogs beat cats, paws down, a new study on carnivores shows. That harsh reality may shock some friends of felines, but scientists say the real surprises are inside the brains of less popular carnivores. Raccoon brains are packed with nerve cells, for instance, while brown bear brains are sorely lacking.

By comparing the numbers of nerve cells, or neurons, among eight species of carnivores (ferret, banded mongoose, raccoon, cat, dog, hyena, lion and brown bear), researchers now have a better understanding of how different-sized brains are built. This neural accounting, described in an upcoming Frontiers in Neuroanatomy paper, may ultimately help reveal how brain features relate to intelligence.
For now, the multispecies tally raises more questions than it answers, says zoologist Sarah Benson-Amram of the University of Wyoming in Laramie. “It shows us that there’s a lot more out there that we need to study to really be able to understand the evolution of brain size and how it relates to cognition,” she says.

Neuroscientist Suzana Herculano-Houzel of Vanderbilt University in Nashville and colleagues gathered brains from the different species of carnivores. For each animal, the researchers whipped up batches of “brain soup,” tissue dissolved in a detergent. Using a molecule that attaches selectively to neurons in this slurry, researchers could count the number of neurons in each bit of brain real estate.

For most animals, the team found the expected numbers of neurons, given a certain brain size. Those expectations came in part from work on other mammals’ brains. That research showed that with the exception of primates (which pack in lots of neurons without growing bigger brains), there’s a predictable relationship between the size of the cerebral cortex — the wrinkly outer layer of the brain that’s involved in thinking, learning and remembering — and the number of neurons contained inside it.

Story continues below interactive graphic
Feeling brainy
Comparing brain size and number of nerve cells in the cerebral cortex among several animal species revealed some surprises. Golden retrievers, for example, have many more nerve cells than cats, and brown bears have an unexpectedly low number of nerve cells given the relatively large size of their brain. Raccoons have a surprising number of nerve cells considering their small noggin. It’s too early, however, to say how neuron number relates to animal intelligence.

Tap or click the graph below for more information.

But some of the larger carnivores with correspondingly larger cortices had surprisingly few neurons. In fact, a golden retriever — with 623 million neurons packed into its doggy cortex —topped both lions and bears, the team found. (For scale, humans have roughly 16.3 billion neurons in the cortex.)

The brown bear is especially lacking. Despite being about 10 times bigger than a cat’s cortex, the bear’s cortex contained roughly the same number of neurons, about 250 million. “It’s just flat out missing 80 percent of the neurons that you would expect,” Herculano-Houzel says. She suspects that there’s a limit to how much food a big predator can catch and eat, especially one that hibernates. That caloric limit might also cap the number of energetically expensive neurons.

Another exception — but in the opposite direction — was the raccoon, which has a cat-sized brain but a doglike neuron number, a finding that fits the nocturnal mammal’s reputation as a clever problem-solver. Benson-Amram cautions that it’s not clear how these neuron numbers relate to potential intelligence. Raccoons are very dexterous, she says, and it’s possible that a beefed-up brain region that handles touch, part of the cortex, could account for the neuron number.

Herculano-Houzel expected large predators such as lions to have lots of neurons. “We went into this study with the expectation that being a predator would require smarts,” she says. But in many cases, a predator didn’t seem to have more neurons than its prey. A lion, for instance, has about 545 million neurons in its cerebral cortex, while a blesbok antelope, which has a slightly smaller cortex, has about 571 million, the researchers previously found.

It’s too early to say how neuron number relates to animal intelligence. By counting neurons, “we’ve figured out one side of that equation,” Herculano-Houzel says. Those counts still need to be linked to animals’ thinking abilities.

Some studies, including one by Benson-Amram, have found correlations between brain size, neuron number and problem-solving skills across species. But finding ways to measure intelligence across different species is challenging, she says. “I find it to be a really fun puzzle, but it’s a big challenge to think, ‘Are we asking the right questions?’”

The hardy souls who manage to push shorts season into December might feel some kinship with the thirteen-lined ground squirrel.

The critter hibernates all winter, but even when awake, it’s less sensitive to cold than its nonhibernating relatives, a new study finds. That cold tolerance is linked to changes in a specific cold-sensing protein in the sensory nerve cells of the ground squirrels and another hibernator, the Syrian hamster, researchers report in the Dec. 19 Cell Reports. The altered protein may be an adaptation that helps the animals drift into hibernation.
In experiments, mice, which don’t hibernate, strongly preferred to hang out on a hot plate that was 30° Celsius versus one that was cooler. Syrian hamsters (Mesocricetus auratus) and the ground squirrels (Ictidomys tridecemlineatus), however, didn’t seem to notice the chill until plate temperatures dipped below 10° Celsius, notes study coauthor Elena Gracheva, a neurophysiologist at Yale University.

Further work revealed that a cold-sensing protein called TRPM8 wasn’t as easily activated by cold in the squirrels and hamsters as in rats. Found in the sensory nerve cells of vertebrates, TRPM8 typically sends a sensation of cold to the brain when activated by low temperatures. It’s what makes your fingertips feel chilly when you’re holding a glass of ice water. It’s also responsible for the cooling sensation in your mouth after you chew gum made with menthol.

The researchers looked at the gene that contains the instructions to make the TRPM8 protein in ground squirrels and switched up parts of it to find regions responsible for tolerance to cold. The adaptation could be pinned on six amino acid changes in one section of the squirrel gene, the team found. Cutting-and-pasting the rat version of this gene fragment into the squirrel gene led to a protein that was once again cold-sensitive. Hamster TRPM8 proteins also lost their cold tolerance with slightly different genetic tweaks in the same region of the gene.

The fact that it’s possible to make a previously cold-resistant protein sensitive to cold by transferring in a snippet of genetic instructions from a different species is “really quite striking,” says David McKemy, a neurobiologist at the University of Southern California in Los Angeles.
As anyone who’s lain awake shivering in a subpar sleeping bag knows, falling asleep while cold is really hard. Hibernation is different than sleep, Gracheva emphasizes, but the squirrels and hamsters’ tolerance to cold may help them transition from an active, awake state to hibernation. If an animal feels chilly, its body will expend a lot of energy trying to warm up — and that’ll work against the physiological changes needed to enter hibernation. For example, while hibernating, small mammals like the ground squirrel slow their pulse and breathing and can lower their core body temperature to just a few degrees above freezing.

Modifications to TRPM8 probably aren’t the only factors that help ground squirrels ignore the cold, Gracheva says, especially as the thermometer drops even closer to freezing. “We think this is only part of the mechanism.”

Scientists also aren’t sure exactly how TRPM8 gets activated by cold in the first place. A detailed view of TRPM8’s structure, obtained using cryo-electron microscopy, was published by a different research group online December 7 in Science. “This is a big breakthrough. We were waiting for this structure for a long period of time,” Gracheva says. Going forward, she and colleagues hope that knowing the protein’s structure will help them link genetic adaptations for cold tolerance in TRPM8 with specific structural changes in the protein.

Cold weather often brings with it hot takes on so-called man flu. That’s the phenomenon in which the flu hits men harder than women — or, depending on who you ask, when men exaggerate regular cold symptoms into flu symptoms. In time for the 2017–2018 flu season, one researcher has examined the scientific evidence for and against man flu.

“The concept of man flu, as commonly defined, is potentially unjust,” Kyle Sue, a clinician at Memorial University of Newfoundland in St. John’s, Canada, writes December 11 in BMJ. Motivated by his own memorable bout of flu, he says, Sue began looking into man flu research and summarizes the work in a review article that’s part of BMJ’s Christmas issue, which traditionally features humorous takes on legitimate research.
There might be a reason men come across as wimps. In the United States, more men than women died from flu-related causes from 2007 to 2010 across several age groups, researchers reported in the American Journal of Epidemiology in 2013. An analysis of data on the 2004 to 2010 flu seasons in Hong Kong found that in children and adults, males were more likely to be hospitalized for the flu than females.

Sue isn’t the first to make a case for man flu. A prevailing explanation for men’s susceptibility says that women have higher levels of the hormone estradiol, which can boost the immune system, while men have higher levels of testosterone, which can sometimes suppress the immune system. However, these hormones interact with the immune system in other ways as well.

“There is some evidence that men make weaker immune responses to some viruses than women, but how this happens and whether it is seen across all viruses is still unclear to me,” notes John Upham, professor of respiratory medicine at Queensland University in Australia.

Sue’s review also cites evidence that women respond better to some flu shots than men do. Sex differences in immune response could have real consequences when it comes to vaccine choice, Upham says.
It’s also unclear what the evolutionary drivers for immune differences between the sexes might be. And studies of how the male and female immune systems respond differently all come with caveats, Sue notes: Such studies are often in mice rather than humans, have limited data or don’t account for health differences such as smoking habits and tendency to go to the doctor. Upham adds that studying differences in flu cases among men in Western versus non-Western societies could reveal the degree to which learned behavior plays a role in “man flu.”

As much as he’d like to help out his half of the species, Sue says, “we cannot yet conclude that this phenomenon is real, but the current evidence is suggestive that it may be.” Not surprising, his review has met just as much skepticism as previous man flu treatises.

Regardless of the possibility that men may be immunologically weaker than women, Sue says, both flu-stricken men and women alike “could benefit from resting in a safe, comfortable place with a recliner and TV.”

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.”

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 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.”

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.”

The oldest known fossils of pollen-laden insects are of earwig-like ground-dwellers that lived in what is now Russia about 280 million years ago, researchers report. Their finding pushes back the fossil record of insects transporting pollen from one plant to another, a key aspect of modern-day pollination, by about 120 million years.

The insects — from a pollen-eating genus named Tillyardembia first described in 1937 — were typically about 1.5 centimeters long, says Alexander Khramov, a paleoentomologist at the Borissiak Paleontological Institute in Moscow. Flimsy wings probably kept the creatures mostly on the forest floor, he says, leaving them to climb trees to find and consume their pollen.

Recently, Khramov and his colleagues scrutinized 425 fossils of Tillyardembia in the institute’s collection. Six had clumps of pollen grains trapped on their heads, legs, thoraxes or abdomens, the team reports February 28 in Biology Letters. A proportion that small isn’t surprising, Khramov says, because the fossils were preserved in what started out as fine-grained sediments. The early stages of fossilization in such material would tend to wash away pollen from the insects’ remains.
The pollen-laden insects had only a couple of types of pollen trapped on them, the team found, suggesting that the critters were very selective in the tree species they visited. “That sort of specialization is in line with potential pollinators,” says Michael Engel, a paleoentomologist at the University of Kansas in Lawrence who was not involved in the study. “There’s probably vast amounts of such specialization that occurred even before Tillyardembia, we just don’t have evidence of it yet.”

Further study of these fossils might reveal if Tillyardembia had evolved special pollen-trapping hairs or other such structures on their bodies or heads, says Conrad Labandeira, a paleoecologist at the National Museum of Natural History in Washington, D.C., also not part of the study. It would also be interesting, he says, to see if something about the pollen helped it stick to the insects. If the pollen grains had structures that enabled them to clump more readily, for example, then those same features may have helped them grab Velcro-like onto any hairlike structures on the insects’ bodies.

Fungi may help some tree-killer beetles turn a tree’s natural defense system against itself.

The Eurasian spruce bark beetle (Ips typographus) has massacred millions of conifers in forests across Europe. Now, research suggests that fungi associated with these bark beetles are key players in the insect’s hostile takeovers. These fungi warp the chemical defenses of host trees to create an aroma that attracts beetles to burrow, researchers report February 21 in PLOS Biology.

This fungi-made perfume might explain why bark beetles tend to swarm the same tree. As climate change makes Europe’s forests more vulnerable to insect invasions, understanding this relationship could help scientists develop new countermeasures to ward off beetle attacks.
Bark beetles are a type of insect found around the world that feed and breed inside trees (SN: 12/17/10). In recent years, several bark beetle species have aggressively attacked forests from North America to Australia, leaving ominous strands of dead trees in their wake.

But trees aren’t defenseless. Conifers — which include pine and fir trees — are veritable chemical weapons factories. The evergreen smell of Christmas trees and alpine forests comes from airborne varieties of these chemicals. But while they may smell delightful, these chemicals’ main purpose is to trap and poison invaders.

Or at least, that’s what they’re meant to do.

“Conifers are full of resin and other stuff that should do horrible things to insects,” says Jonathan Gershenzon, a chemical ecologist at the Max Planck Institute for Chemical Ecology in Jena, Germany. “But bark beetles don’t seem to mind at all.”

This ability of bark beetles to overcome the powerful defense system of conifers has led some scientists to wonder if fungi might be helping. Fungi break down compounds in their environment for food and protection (SN: 11/30/21). And some type of fungi — including some species in the genus Grosmannia — are always found in association with Eurasian spruce bark beetles.
Gershenzon and his colleagues compared the chemicals released by spruce bark infested with Grosmannia and other fungi to the chemical profile of uninfected trees. The presence of the fungi fundamentally changed the chemical profile of spruce trees, the team found. More than half the airborne chemicals — made by fungi breaking down monoterpenes and other chemicals that are likely part of the tree defense system — were unique to infected trees after 12 days.

This is surprising because researchers had previously assumed that invading fungi hardly changed the chemical profile of trees, says Jonathan Cale, a fungal ecologist at the University of Northern British Columbia in Prince George, Canada, who was not involved with the research.
Later experiments revealed that bark beetles can detect many of these fungi-made chemicals. The team tested this by attaching tiny electrodes on bark beetles’ heads and detecting electrical activity when the chemicals wafted passed their antennae. What’s more, the smell of these chemicals combined with beetle pheromones led the insects to burrow at higher rates than the smell of pheromones alone.

The study suggests that these fungi-made chemicals can help beetles tell where to feed and breed, possibly by advertising that the fungi has taken down some of the tree’s defenses. The attractive nature of the chemicals could also explain the beetle’s swarming behavior, which drives the death of healthy adult trees.

But while the fungi aroma might doom trees, it could also lead to the beetles’ demise. Beetle traps in Europe currently use only beetle pheromones to attract their victims. Combining pheromones with fungi-derived chemicals might be the secret to entice more beetles into traps, making them more effective.

The results present “an exciting direction for developing new tools to manage destructive bark beetle outbreaks” for other beetle species as well, Cale says. In North America, mild winters and drought have put conifer forests at greater risk from mountain pine beetle (Dendroctonus pendersoae) attacks. Finding and using fungi-derived chemicals might be one way to fend off the worst of the bark beetle invasions in years to come.