Biology

tiny-chips-hitch-a-ride-on-immune-cells-to-sites-of-inflammation

Tiny chips hitch a ride on immune cells to sites of inflammation


Tiny chips can be powered by infrared light if they’re near the brain’s surface.

An immune cell chemically linked to a CMOS chip. Credit: Yadav, et al.

Standard brain implants use electrodes that penetrate the gray matter to stimulate and record the activity of neurons. These typically need to be put in place via a surgical procedure. To go around that need, a team of researchers led by Deblina Sarkar, an electrical engineer and MIT assistant professor, developed microscopic electronic devices hybridized with living cells. Those cells can be injected into the circulatory system with a standard syringe and will travel the bloodstream before implanting themselves in target brain areas.

“In the first two years of working on this technology at MIT, we’ve got 35 grant proposals rejected in a row,” Sarkar says. “Comments we got from the reviewers were that our idea was very impactful, but it was impossible.” She acknowledges that the proposal sounded like something you can find in science fiction novels. But after more than six years of research, she and her colleagues have pulled it off.

Nanobot problems

In 2022, when Sarkar and her colleagues gathered initial data and got some promising results with their cell-electronics hybrids, the team proposed the project for the National Institutes of Health Director’s New Innovator Award. For the first time, after 35 rejections, it made it through peer review. “We got the highest impact score ever,” Sarkar says.

The reason for that score was that her technology solved three extremely difficult problems. The first, obviously, was making functional electronic devices smaller than cells that can circulate in our blood.

“Previous explorations, which had not seen a lot of success, relied on putting magnetic particles inside the bloodstream and then guiding them with magnetic fields,” Sarkar explains. “But there is a difference between electronics and particles.” Electronics made using CMOS technology (which we use for making computer processors) can generate electrical power from incoming light in the same way as photovoltaics, as well as perform computations necessary for more intelligent applications like sensing. Particles, on the other hand, can only be used to stimulate cells to an extent.

If they ever reach those cells, of course, which was the second problem. “Controlling the devices with magnetic fields means you need to go into a machine the size of an MRI,” Sarkar says. Once the subject is in the machine, an operator looks at where the devices are and tries to move them to where they need to be using nothing but magnetic fields. Sarkar said that it’s tough to do anything other than move the particles in straight lines, which is a poor match for our very complex vasculature.

The solution her team found was fusing the electronics with monocytes, immune cells that can home in on inflammation in our bodies. The idea was that the monocytes would carry the electronics through the bloodstream using the cells’ chemical homing mechanism. This also solved the third problem: crossing the blood-brain barrier that protects the brain from pathogens and toxins. Electronics alone could not get through it; monocytes could.

The challenge was making all these ideas work.

Clicking together

Sarkar’s team built electronic devices made of biocompatible polymer and metallic layers fabricated on silicon wafers using a standard CMOS process. “We made the devices this small with lithography, the technique used in making transistors for chips in our computers,” Sarkar explains. They were roughly 200 nanometers thick and 10 microns in diameter—that kept them subcellular, since a monocyte cell usually measures between 12 and 18 microns. The devices were activated and powered by infrared light at a wavelength that could penetrate several centimeters into the brain.

Once the devices were manufactured and taken off the wafer, the next thing to figure out was attaching them to monocytes.

To do this, the team covered the surfaces of the electronic devices with dibezocyclooctyne, a very reactive molecule that can easily link to other chemicals, especially nitrogen compounds called azides. Then Sarkar and her colleagues chemically modified monocytes to place azides on their surfaces. This way, the electronics and cells could quickly snap together, almost like Lego blocks (this approach, called click chemistry, got the 2022 Nobel Prize in chemistry).

The resulting solution of cell-electronics hybrids was designed to be biocompatible and could be injected into the circulatory system. This is why Sarkar called her concept “circulatronics.”

Of course, Sarkar’s “circulatronic” hybrids fall a bit short of sci-fi fantasies, in that they aren’t exactly literal nanobots. But they may be the closest thing we’ve created so far.

Artificial neurons

To test these hybrids in live mice, the researchers prepared a fluorescent version to make them easier to track. Mice were anesthetized first, and the team artificially created inflammation at a specific location in their brains, around the ventrolateral thalamic nucleus. Then the hybrids were injected into the veins of the mice. After roughly 72 hours, the time scientists expected would be needed for the monocytes to reach the inflammation, Sarkar and her colleagues started running tests.

It turned out that most of the injected hybrids reached their destination in one piece—the electronics mostly remained attached to the monocytes. The team’s measurements suggest that around 14,000 hybrids managed to successfully implant themselves near the neurons in the target area of the brain. Then, in response to infrared irradiation, they caused significant neuronal activation, comparable to traditional electrodes implanted via surgery.

The real strength of the hybrids, Sarkar thinks, is the way they can be tuned to specific diseases. “We chose monocytes for this experiment because inflammation spots in the brain are usually the target in many neurodegenerative diseases,” Sarkar says. Depending on the application, though, the hybrids’ performance can be adjusted by manipulating their electronic and cellular components. “We have already tested using mesenchymal stem cells for the Alzheimer’s, or T cells and other neural stem cells for tumors,” Sarkar explains.

She went on to say that her technology one day may help with placing the implants in brain regions that today cannot be safely reached through surgery. “There is a brain cancer called glioblastoma that forms diffused tumor sites. Another example is DIPG [a form of glioma], which is a terminal brain cancer in children that develops in a region where surgery is impossible,” she adds.

But in the more distant future, the hybrids can find applications beyond targeting diseases. Most of the studies that have relied on data from brain implants were limited to participants who suffered from severe brain disorders. The implants were put in their brains for therapeutic reasons, and participating in research projects was something they just agreed to do on the side.

Because the electronics in Sarkar’s hybrids can be designed to fully degrade after a set time, the team thinks this could potentially enable them to gather brain implant data from healthy people—the implants would do their job for the duration of the study and be gone once it’s done. Unless we want them to stay, that is.

“The ease of application can make the implants feasible in brain-computer interfaces designed for healthy people,” Sarkar argues. “Also, the electrodes can be made to work as artificial neurons. In principle, we could enhance ourselves—increase our neuronal density.”

First, though, the team wants to put the hybrids through a testing campaign on larger animals and then get them FDA-approved for clinical trials. Through Cahira Technologies, an MIT spinoff company founded to take the “circulatronics” technology to the market, Sarkar wants to make this happen within the next three years.

Nature Biotechnology, 2025. DOI: 10.1038/s41587-025-02809-3

Photo of Jacek Krywko

Jacek Krywko is a freelance science and technology writer who covers space exploration, artificial intelligence research, computer science, and all sorts of engineering wizardry.

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some-stinkbugs’-legs-carry-a-mobile-fungal-garden

Some stinkbugs’ legs carry a mobile fungal garden

Many insect species hear using tympanal organs, membranes roughly resembling our eardrums but located on their legs. Grasshoppers, mantises, and moths all have them, and for decades, we thought that female stinkbugs of the Dinidoridae family have them, too, although located a bit unusually on their hind rather than front legs.

Suspecting that they use their hind leg tympanal organs to listen to male courtship songs, a team of Japanese researchers took a closer look at the organs in Megymenum gracilicorne, a Dinidoridae stinkbug species native to Japan. They discovered that these “tympanal organs” were not what they seemed. They’re actually mobile fungal nurseries of a kind we’ve never seen before.

Portable gardens

Dinidoridae is a small stinkbug family that lives exclusively in Asia. The bug did attract some scientific attention, but not nearly as much as its larger relatives like Pentatomidae. Prior work looking specifically into organs growing on the hind legs of Dinidoridae females was thus somewhat limited. “Most research relied on taxonomic and morphological approaches. Some taxonomists did describe that female Dinidoridae stinkbugs have an enlarged part on the hind legs that looks like the tympanal organ you can find, for example, in crickets,” said Takema Fukatsu, an evolutionary biologist at the National Institute of Advanced Industrial Science and Technology in Tokyo.

Based on that appearance, these parts were classified as tympanal organs—the case was closed, and it stayed closed until Fukatsu’s team started examining them more closely. Most insects have tympanal organs on their front legs, not hind legs, or on abdominal segments. The initial goal of Fukatsu’s study was to figure out what impact this unusual position has on Dinidoridae females’ ability to hear sounds.

Early on in the study, it turned out that whatever Dinidoridae females have on their hind legs, they are not tympanal organs. “We found no tympanal membrane and no sensory neurons, so the enlarged parts on the hind legs had nothing to do with hearing,” Fukatsu explained. Instead, the organ had thousands of small pores filled with benign filamentous fungi. The pores were connected to secretory cells that released substances that Fukatsu’s team hypothesized were nutrients enabling the fungi to grow.

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neural-network-finds-an-enzyme-that-can-break-down-polyurethane

Neural network finds an enzyme that can break down polyurethane

You’ll often hear plastic pollution referred to as a problem. But the reality is that it’s multiple problems. Depending on the properties we need, we form plastics out of different polymers, each of which is held together by a distinct type of chemical bond. So the method we use to break down one type of polymer may be incompatible with the chemistry of another.

That problem is why, even though we’ve had success finding enzymes that break down common plastics like polyesters and PET, they’re only partial solutions to plastic waste. However, researchers aren’t sitting back and basking in the triumph of partial solutions, and they’ve now got very sophisticated protein design tools to help them out.

That’s the story behind a completely new enzyme that researchers developed to break down polyurethane, the polymer commonly used to make foam cushioning, among other things. The new enzyme is compatible with an industrial-style recycling process that breaks the polymer down into its basic building blocks, which can be used to form fresh polyurethane.

Breaking down polyurethane

Image of a set of chemical bonds. From left to right there is an X, then a single bond to an oxygen, then a single bond to an oxygen that's double-bonded to carbon, then a single bond to a nitrogen, then a single bond to another X.

The basics of the chemical bonds that link polyurethanes. The rest of the polymer is represented by X’s here.

The new paper that describes the development of this enzyme lays out the scale of the problem: In 2024, we made 22 million metric tons of polyurethane. The urethane bond that defines these involves a nitrogen bonded to a carbon that in turn is bonded to two oxygens, one of which links into the rest of the polymer. The rest of the polymer, linked by these bonds, can be fairly complex and often contains ringed structures related to benzene.

Digesting polyurethanes is challenging. Individual polymer chains are often extensively cross-linked, and the bulky structures can make it difficult for enzymes to get at the bonds they can digest. A chemical called diethylene glycol can partially break these molecules down, but only at elevated temperatures. And it leaves behind a complicated mess of chemicals that can’t be fed back into any useful reactions. Instead, it’s typically incinerated as hazardous waste.

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why-imperfection-could-be-key-to-turing-patterns-in-nature

Why imperfection could be key to Turing patterns in nature

In essence, it’s a type of symmetry breaking. Any two processes that act as activator and inhibitor will produce periodic patterns and can be modeled using Turing’s diffusion function. The challenge is moving from Turing’s admittedly simplified model to pinpointing the precise mechanisms serving in the activator and inhibitor roles.

This is especially challenging in biology. Per the authors of this latest paper, the classical approach to a Turing mechanism balances reaction and diffusion using a single length scale, but biological patterns often incorporate multiscale structures, grain-like textures, or certain inherent imperfections. And the resulting patterns are often much blurrier than those found in nature.

Can you say “diffusiopherosis”?

Simulated hexagon and stripe patterns obtained by diffusiophoretic assembly of two types of cells on top of the chemical patterns. Credit: Siamak Mirfendereski and Ankur Gupta/CU Boulder

In 2023, UCB biochemical engineers Ankur Gupta and Benjamin Alessio developed a new model that added diffusiopherosis into the mix. It’s a process by which colloids are transported via differences in solute concentration gradients—the same process by which soap diffuses out of laundry in water, dragging particles of dirt out of the fabric. Gupta and Alessio successfully used their new model to simulate the distinctive hexagon pattern (alternating purple and black) on the ornate boxfish, native to Australia, achieving much sharper outlines than the model originally proposed by Turing.

The problem was that the simulations produced patterns that were too perfect: hexagons that were all the same size and shape and an identical distance apart. Animal patterns in nature, by contrast, are never perfectly uniform. So Gupta and his UCB co-author on this latest paper, Siamak Mirfendereski, figured out how to tweak the model to get the pattern outputs they desired. All they had to do was define specific sizes for individual cells. For instance, larger cells create thicker outlines, and when they cluster, they produce broader patterns. And sometimes the cells jam up and break up a stripe. Their revised simulations produced patterns and textures very similar to those found in nature.

“Imperfections are everywhere in nature,” said Gupta. “We proposed a simple idea that can explain how cells assemble to create these variations. We are drawing inspiration from the imperfect beauty of [a] natural system and hope to harness these imperfections for new kinds of functionality in the future.” Possible future applications include “smart” camouflage fabrics that can change color to better blend with the surrounding environment, or more effective targeted drug delivery systems.

Matter, 2025. DOI: 10.1016/j.matt.2025.102513 (About DOIs).

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dna-analysis-reveals-likely-pathogens-that-killed-napoleon’s-army

DNA analysis reveals likely pathogens that killed Napoleon’s army

State-of-the-art methodologies

Painting of Napoleon's army.

Rascovan and his co-authors note in their paper that the 2006 study relied upon outdated PCR-based technologies for its DNA analysis. As for the virus family detected in the Kalingrad dental pulp, they argue that those viruses are both ubiquitous and usually asymptomatic in humans—and thus are unlikely to be the primary culprits for the diseases that wiped out the French army. So Rascovan’s team decided to use current state-of-the-art DNA methodologies to re-analyze a different set of remains of Napoleonic soldiers who died in Vilnius.

“In most ancient human remains, pathogen DNA is extremely fragmented and only present in very low quantities, which makes it very difficult to obtain whole genomes,” said Rascovan. “So we need methods capable of unambiguously identifying infectious agents from these weak signals, and sometimes even pinpointing lineages, to explore the pathogenic diversity of the past.”

An 1812 report from one of Napoleon’s physicians, J.R.L. de Kirckhoff, specifically noted typhus, dysentery, and diarrhea after the soldiers arrived in Vilnius, which he attributed to large barrels of salted beets the starving troops consumed, “greatly upsetting us and strongly irritating the intestinal tract.” Rascovan et al. note that such symptoms could accompany any number of conditions or diseases common to 19th-century Europe. “Even today, two centuries later, it would still be impossible to perform a differential diagnosis between typhus, typhoid, or paratyphoid fever based solely on the symptoms or the testimonies of survivors,” the authors wrote.

Imperial Guard button discovered during excavation

Imperial Guard button discovered during excavation. Credit: UMR 6578 Aix-Marseille Université, CNRS, EFS

Over 3,200 individual remains, almost all men between the ages of 20 and 50, were excavated from the mass grave at Vilnius. Rascovan et al. focused on 13 teeth from 13 different individuals. To compensate for the degraded nature of the 200-year-old genome fragments, co-authors at the University of Tartu in Estonia helped develop a multistep authentication method to more accurately identify pathogens in the samples. In some cases, they were even able to identify a specific lineage.

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clinical-trial-of-a-technique-that-could-give-everyone-the-best-antibodies

Clinical trial of a technique that could give everyone the best antibodies


If we ID the DNA for a great antibody, anyone can now make it.

One of the things that emerging diseases, including the COVID and Zika pandemics, have taught us is that it’s tough to keep up with infectious diseases in the modern world. Things like air travel can allow a virus to spread faster than our ability to develop therapies. But that doesn’t mean biotech has stood still; companies have been developing technologies that could allow us to rapidly respond to future threats.

There are a lot of ideas out there. But this week saw some early clinical trial results of one technique that could be useful for a range of infectious diseases. We’ll go over the results as a way to illustrate the sort of thinking that’s going on, along with the technologies we have available to pursue the resulting ideas.

The best antibodies

Any emerging disease leaves a mass of antibodies in its wake—those made by people in response to infections and vaccines, those made by lab animals we use to study the infectious agent, and so on. Some of these only have a weak affinity for the disease-causing agent, but some of them turn out to be what are called “broadly neutralizing.” These stick with high affinity not only to the original pathogen, but most or all of its variants, and possibly some related viruses.

Once an antibody latches on to a pathogen, broadly neutralizing antibodies inactivate it (as their name implies). This is typically because these antibodies bind to a site that’s necessary for a protein’s function. For example, broadly neutralizing antibodies to HIV bind to the proteins that help this virus enter immune cells.

Unfortunately, not everyone develops broadly neutralizing antibodies, and certainly doesn’t do so in time to prevent infections. And we haven’t figured out a way of designing vaccinations that ensure their generation. So we’re often found ourselves stuck with knowing what antibodies we’d like to see people making while having no way of ensuring that they do.

One of the options we’ve developed is to just mass-produce broadly neutralizing antibodies and inject them into people. This has been approved for use against Ebola and provided an early treatment during the COVID pandemic. This approach has some practical limitations, though. For starters, the antibodies have a finite life span in the bloodstream, so injections may need to be repeated. In addition, making and purifying enough antibodies in bulk isn’t the easiest thing in the world, and they generally need to be kept refrigerated during the distribution, limiting the areas where they can be used.

So, a number of companies have been looking at an alternative: getting people to make their own. This could potentially lead to longer-lived protection, even ensuring the antibodies are present to block future infections if the DNA survives long enough.

Genes and volts

Once you identify cells that produce broadly neutralizing antibodies, it’s relatively simple to clone those genes and put them into a chunk of DNA that will ensure that they’ll be produced by any human cell. If we could get that DNA into a person’s cells, broadly neutralizing antibodies are the result. And a number of approaches have been tried to handle that “if.” Most of them have inserted the genes needed to make the antibodies into a harmless, non-infectious virus, and then injected that virus into volunteers. Unfortunately, these viruses have tended to set off a separate immune response, which causes more significant side effects and may limit how often this approach can be used.

This brings us to the technique being used here. In this case, the researchers placed the antibody genes in a circular loop of DNA called a plasmid. This is enough to ensure that the DNA doesn’t get digested immediately and to get the antibody genes made into proteins. But it does nothing to help get the DNA inside of cells.

The research team, a mixture of people from a biotech company and academic labs, used a commercial injection setup that mixes the injection of the DNA with short pulses of electricity. The electricity disrupts the cell membrane, allowing the plasmid DNA to make it inside cells. Based on animal testing, doing this in muscle cells is enough to turn the muscles into factories producing lots of broadly neutralizing antibodies.

The new study was meant to test the safety of doing that in humans. The team recruited 44 participants, testing various doses of two antibody-producing plasmids and injection schedules. All but four of the subjects completed the study; three of those who dropped out had all been testing a routine with the electric pulses happening very quickly, which turned out to be unpleasant. Fortunately, it didn’t seem to make any difference to the production of antibodies.

While there were a lot of adverse reactions, most of these were associated with the injection itself: muscle pain at the site, a scab forming afterward, and a reddening of the skin. The worst problem appeared to be a single case of moderate muscle pain that persisted for a couple of days.

In all but one volunteer, the injection resulted in stable production of the two antibodies for at least 72 weeks following the injection; the single exception only made one of the two. That’s “at least” 72 weeks because that’s when they stopped testing—there was no indication that levels were dropping at this point. Injecting more DNA led to more variability in the amount of antibody produced, but that amount quickly maxed out. More total injections also boosted the level of antibody production. But even the minimal procedure—two injections of the lowest concentration tested—resulted in significant and stable antibodies.

And, as expected, these antibodies blocked the virus they were directed against: SARS-CoV-2.

The caveats

This approach seems to work—we can seemingly get anybody to make broadly neutralizing antibodies for months at a time. What’s the hitch? For starters, this isn’t necessarily great for a rapidly emerging pandemic. It takes a while to identify broadly neutralizing antibodies after a pathogen is identified. And, while it’s simple to ship DNA around the world to where it will be needed, injection setups that also produce the small electric pulses are not exactly standard equipment even in industrialized countries, much less the Global South.

Then there’s the issue of whether this really is a longer-term fix. Widespread use of broadly neutralizing antibodies will create a strong selective pressure for the evolution of variants that the antibody can no longer bind to. That may not always be a problem—broadly neutralizing antibodies generally bind to parts of proteins that are absolutely essential for the proteins’ function, and so it may not be possible to change those while maintaining the function. But that’s unlikely to always be the case.

In the end, however, social acceptance may end up being the biggest problem. People had an utter freakout over unfounded conspiracies that the RNA of COVID vaccines would somehow lead to permanent genetic changes. Presumably, having DNA that’s stable for months would be even harder for some segments of the public to swallow.

Nature Medicine, 2025. DOI: 10.1038/s41591-025-03969-0 (About DOIs).

Photo of John Timmer

John is Ars Technica’s science editor. He has a Bachelor of Arts in Biochemistry from Columbia University, and a Ph.D. in Molecular and Cell Biology from the University of California, Berkeley. When physically separated from his keyboard, he tends to seek out a bicycle, or a scenic location for communing with his hiking boots.

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bats-eat-the-birds-they-pluck-from-the-sky-while-on-the-wing

Bats eat the birds they pluck from the sky while on the wing

There are three species of bats that eat birds. We know that because we have found feathers and other avian remains in their feces. What we didn’t know was how exactly they hunt birds, which are quite a bit heavier, faster, and stronger than the insects bats usually dine on.

To find out, Elena Tena, a biologist at Doñana Biological Station in Seville, Spain, and her colleagues attached ultra-light sensors to Nyctalus Iasiopterus, the largest bats in Europe. What they found was jaw-droppingly brutal.

Inconspicuous interceptors

Nyctalus Iasiopterus, otherwise known as greater noctule bats, have a wingspan of about 45 centimeters. They have reddish-brown or chestnut fur with a slightly paler underside, and usually weigh around 40 to 60 grams. Despite that minimal weight, they are the largest of the three bat species known to eat birds, so the key challenge in getting a glimpse into the way they hunt was finding sensors light enough to not impede the bats’ flight.

Cameras, which are the usual go-to sensor, were out of the question. “Bats hunt at night, so you’d need night vision cameras, which together with batteries are too heavy for a bat to carry. Our sensors had to weigh below 10 percent of the weight of the bat—four to six grams,” Tena explained.

Tena and her team explored several alternative approaches throughout the last decade, including watching the bats from the ground or using military-grade radars. But even then, catching the hunting bats red-handed remained impossible.

In recent years, the technology and miniaturization finally caught up with Tena’s needs, and the team found the right sensors for the job and attached them to 14 greater noctule bats over the course of two years. The tags used in the study weighed around four grams, could run for several hours, and registered sound, altitude, and acceleration. This gave Tena and her colleagues a detailed picture of the bats’ behavior in the night sky. The recordings included both ambient environmental sounds and the ultra-frequency bursts bats use for echolocation. Combining altitude with accelerometer readouts enabled scientists to trace the bats’ movements through all their fast-paced turns, dives, and maneuvers.

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dinosaurs-may-have-flourished-right-up-to-when-the-asteroid-hit

Dinosaurs may have flourished right up to when the asteroid hit

That seemingly changes as of now, with new argon dating of strata from the Naashoibito Member in the San Juan Basin of present-day New Mexico. Many dinosaur fossils have been obtained from this region, and we know the site differs from the sort of ecosystem found at Hell Creek. But it was previously thought to date back closer to a million years before the mass extinction. The new dates, plus the alignment of magnetic field reversals, tell us that the ecosystem was a contemporary of the one in Hell Creek, and dates to the last few hundred thousand years prior to the mass extinction.

Diverse ecosystems

The fossils at Naashoibito have revealed an ecosystem we now label the “Alamo Wash local fauna.” And they’re fairly distinct from the ones found in Wyoming, despite being just 1,500 kilometers further south. Analyzing the species present using ecological measures, the researchers found that dinosaurs formed two “bioprovinces” in the late Cretaceous—essentially, there were distinct ecosystems present in the northern and southern areas.

This doesn’t seem to be an artifact of the sites, as mammalian fossils seem to reflect a single community across both areas near the mass extinction, but had distinct ecologies both earlier and after. The researchers propose that temperature differences were the key drivers of the distinction, something that may have had less of an impact on mammals, which are generally better at controlling their own temperatures.

Overall, the researchers conclude that, rather than being dominated by a small number of major species, “dinosaurs were thriving in New Mexico until the end of the Cretaceous.”

While this speaks directly to the idea that limited diversity may have primed the dinosaurs for extinction, it also may have implications for the impact of the contemporaneous eruptions in the Deccan Traps. If these were having a major global impact, then it’s a bit unlikely that dinosaurs would be thriving anywhere.

Even with the new data, however, our picture is still limited to the ecosystems present on the North American continent. We do have fossils from elsewhere, but they’re not exactly dated. There are some indications of dinosaurs in the late Cretaceous in Europe and South America, but we don’t have a clear picture of the ecosystems in which they were found. So, while these findings help clarify the diversity of dinosaurs in the time leading up to their extinction, there’s still a lot left to learn.

Science, 2025. DOI: 10.1126/science.adw3282 (About DOIs).

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termite-farmers-fine-tune-their-weed-control

Termite farmers fine-tune their weed control

Odontotermes obesus is one of the termite species that grows fungi, called Termitomyces, in their mounds. Workers collect dead leaves, wood, and grass to stack them in underground fungus gardens called combs. There, the fungi break down the tough plant fibers, making them accessible for the termites in an elaborate form of symbiotic agriculture.

Like any other agriculturalist, however, the termites face a challenge: weeds. “There have been numerous studies suggesting the termites must have some kind of fixed response—that they always do the same exact thing when they detect weed infestation,” says Rhitoban Raychoudhury, a professor of biological sciences at the Indian Institute of Science Education, “but that was not the case.” In a new Science study, Raychoudhury’s team discovered that termites have pretty advanced, surprisingly human-like gardening practices.

Going blind

Termites do not look like particularly good gardeners at first glance. They are effectively blind, which is not that surprising considering they spend most of their life in complete darkness working in endless corridors of their mounds. But termites make up for their lack of sight with other senses. “They can detect the environment based on advanced olfactory reception and touch, and I think this is what they use to identify the weeds in their gardens,” Raychoudhury says. To learn how termites react once they detect a weed infestation, his team collected some Odontotermes obesus and challenged them with different gardening problems.

The experimental setup was quite simple. The team placed some autoclaved soil sourced from termite mounds into glass Petri dishes. On this soil, Raychoudhury and his colleagues placed two fungus combs in each dish. The first piece acted as a control and was a fresh, uninfected comb with Termitomyces. “Besides acting as a control, it was also there to make sure the termites have the food because it is very hard for them to survive outside their mounds,” Raychoudhury explains. The second piece was intentionally contaminated with Pseudoxylaria, a filamentous fungal weed that often takes over Termitomyces habitats in termite colonies.

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the-neurons-that-let-us-see-what-isn’t-there

The neurons that let us see what isn’t there

Earlier work had hinted at such cells, but Shin and colleagues show systematically that they’re not rare oddballs—they’re a well-defined, functionally important subpopulation. “What we didn’t know is that these neurons drive local pattern completion within primary visual cortex,” says Shin. “We showed that those cells are causally involved in this pattern completion process that we speculate is likely involved in the perceptual process of illusory contours,” adds Adesnik.

Behavioral tests still to come

That doesn’t mean the mice “saw” the illusory contours when the neurons were artificially activated. “We didn’t actually measure behavior in this study,” says Adesnik. “It was about the neural representation.” All we can say at this point is that the IC-encoders could induce neural activity patterns that matched what imaging shows during normal perception of illusory contours.

“It’s possible that the mice weren’t seeing them,” admits Shin, “because the technique has involved a relatively small number of neurons, for technical limitations. But in the future, one could expand the number of neurons and also introduce behavioral tests.”

That’s the next frontier, Adesnik says: “What we would do is photo-stimulate these neurons and see if we can generate an animal’s behavioral response even without any stimulus on the screen.” Right now, optogenetics can only drive a small number of neurons, and IC-encoders are relatively rare and scattered. “For now, we have only stimulated a small number of these detectors, mainly because of technical limitations. IC-encoders are a rare population, probably distributed through the layers [of the visual system], but we could imagine an experiment where we recruit three, four, five, maybe even 10 times as many neurons,” he says. “In this case, I think we might be able to start getting behavioral responses. We’d definitely very much like to do this test.”

Nature Neuroscience, 2025. DOI: 10.1038/s41593-025-02055-5

Federica Sgorbissa is a science journalist; she writes about neuroscience and cognitive science for Italian and international outlets.

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world-famous-primatologist-jane-goodall-dead-at-91

World-famous primatologist Jane Goodall dead at 91

A sculpture of Jane Goodall and David Greybeard outside the Field Museum of Natural History in Chicago

A sculpture of Jane Goodall and David Greybeard outside the Field Museum of Natural History in Chicago Credit: Geary/CC0

David Greybeard’s behavior also challenged the long-held assumption that chimpanzees were vegetarians. Goodall found that chimps would hunt and eat smaller primates like colobus monkeys as well, sometimes sharing the carcass with other troop members. She also recorded evidence of strong bonds between mothers and infants, altruism, compassion, and aggression and violence. For instance, dominant females would sometimes kill the infants of rival females, and from 1974 to 1978, there was a violent conflict between two communities of chimpanzees that became known as the Gombe Chimpanzee War.

Almost human

One of the more colorful chimps Goodall studied was named Frodo, who grew up to be an alpha male with a temperament very unlike his literary namesake. “As an infant, Frodo proved mischievous, disrupting Jane Goodall’s efforts to record data on mother-infant relationships by grabbing at her notebooks and binoculars,” anthropologist Michael Wilson of the University of Minnesota in Saint Paul recalled on his blog when Frodo died from renal failure in 2013. “As he grew older, Frodo developed a habit of throwing rocks, charging at, hitting, and knocking over human researchers and tourists.” Frodo attacked Wilson twice on Wilson’s first trip to Gombe, even beating Goodall herself in 1989, although he eventually lost his alpha status and “mellowed considerably” in his later years, per Wilson.

Goodall became so renowned around the world that she even featured in one of Gary Larson’s Far Side cartoons, in which two chimps are shown grooming when one finds a blonde hair on the other. “Conducting a little more ‘research’ with that Jane Goodall tramp?” the caption read. The JGI was not amused, sending Larson a letter (without Goodall’s knowledge) calling the cartoon an “atrocity,” but their objections were not shared by Goodall herself, who thought the cartoon was very funny when she heard of it. Goodall even wrote a preface to The Far Side Gallery 5. Larson, for his part, visited Goodall’s research facility in Tanzania in 1988, where he experienced Frodo’s alpha aggressiveness firsthand.

A young Jane Goodall in the field.

A young Jane Goodall in the field. Credit: YouTube/Jane Goodall Institute

Goodall founded the JGI in 1977 and authored more than 27 books, most notably My Friends, the Wild Chimpanzees (1967), In the Shadow of Man (1971), and Through a Window (1990). There was some initial controversy around her 2014 book Seeds of Hope, co-written with Gail Hudson, when portions were found to have been plagiarized from online sources; the publisher postponed publication so that Goodall could revise the book and add 57 pages of endnotes. (She blamed her “chaotic note-taking” for the issue.) National Geographic released a full-length documentary last year about her life’s work, drawing from over 100 hours of previously unseen archival footage.

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150 million-year-old pterosaur cold case has finally been solved

Smyth thinks that so few adults show up on the fossil record in this region not only because they were more likely to survive, but also because those that couldn’t were not buried as quickly. Carcasses would float on the water anywhere from days to weeks. As they decomposed, parts would fall to the lagoon bottom. Juveniles were small enough to be swept under and buried quickly by sediments that would preserve them.

Cause of death

The humerus fractures found in Lucky I and Lucky II were especially significant because forelimb injuries are the most common among existing flying vertebrates. The humerus attaches the wing to the body and bears most flight stress, which makes it more prone to trauma. Most humerus fractures happen in flight as opposed to being the result of a sudden impact with a tree or cliff. And these fractures were the only skeletal trauma seen in any of the juvenile pterosaur specimens from Solnhofen.

Evidence suggesting the injuries to the two fledgling pterosaurs happened before death includes the displacement of bones while they were still in flight (something recognizable from storm deaths of extant birds and bats) and the smooth edges of the break, which happens in life, as opposed to the jagged edges of postmortem breaks. There were also no visible signs of healing.

Storms disproportionately affected flying creatures at Solnhofen, which were often taken down by intense winds. Many of Solnhofen’s fossilized vertebrates were pterosaurs and other winged species such as bird ancestor Arachaeopteryx. Flying invertebrates were also doomed.

Even marine invertebrates and fish were threatened by storm conditions, which churned the lagoons and brought deep waters with higher salt levels and low oxygen to the surface. Anything that sank to the bottom was exceptionally preserved because of these same conditions, which were too harsh for scavengers and paused decomposition. Mud kicked up by the storms also helped with the fossilization process by quickly covering these organisms and providing further protection from the elements.

“The same storm events responsible for the burial of these individuals also transported the pterosaurs into the lagoonal basins and were likely the primary cause of their injury and death,” Smyth concluded.

Although Lucky I and Lucky II were decidedly unlucky, the exquisite preservation of their skeletons that shows how they died has finally allowed researchers to solve a case that went cold for over a hundred thousand years.

Current Biology, 2025. DOI: 10.1016/j.cub.2025.08.006

150 million-year-old pterosaur cold case has finally been solved Read More »