How a common herbicide affects honeybee brains and behaviour

Exposure to glyphosate, a widely used herbicide, reduces honeybee foraging by 13% and alters brain neurochemistry, even at sublethal levels. These changes may compromise colony stability, pollination effectiveness, and honey production, indicating that glyphosate poses a greater risk to honeybee health than previously recognized.

Laura C. McHenry et al, Sublethal glyphosate exposure reduces honey bee foraging and alters the balance of biogenic amines in the brain, Journal of Experimental Biology (2025). DOI: 10.1242/jeb.250124

Bacteria are weaving forever chemicals directly into their cell membranes, study finds
Bacteria can incorporate polyfluoroalkyl carboxylates, a type of PFAS, directly into their cell membrane lipids. This process demonstrates a biological interaction with these persistent environmental contaminants and suggests a potential microbial role in PFAS transformation, though complete degradation and disposal remain unresolved challenges.

Yongchao Xie et al, Bacteria covalently incorporate polyfluoroalkyl carboxylates into membrane lipids, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02301-x

AI makes rewilding look tame—and misses its messy reality
AI-generated images of rewilded British landscapes tend to depict sanitized, orderly scenes lacking ecological complexity, messiness, and controversial species. These images often exclude humans, decay, and less charismatic wildlife, reflecting the sanitized visuals promoted by environmental organizations. Accurate, ecologically rich depictions require highly specific prompts, limiting their accessibility to non-experts.

original article.

New study finds eye focuses using color signals, not just sharpness

The human eye functions like an exceptionally precise, high-end camera, one with a resolution of around 576 megapixels. What makes it intriguing is that although our eyes can focus on light at only one wavelength at a time, the result isn't fragmented or blurry. What we see feels seamlessly sharp and rich in details. This raises the question of which color it chooses to focus on when the scene we are looking at has multiple colors. A recent study published in Science Advances presents a mechanism that guides the choice.

The researchers discovered that the eye chooses its focus to maximize the quality of signals in specific neural pathways called color-opponent channels. These channels are neural pathways that combine signals from the three types of cone photoreceptors—long, medium, and short—into distinct patterns for color processing. These combinations create three channels: red–green, blue–yellow, and finally black–white, which represents brightness. Each channel operates in opposition, meaning that the two colors in a pair, such as red and green, cannot be perceived simultaneously.

This new discovery challenges the leading theory on which color the eyes choose to focus on.

In the real world, objects are almost never perfectly in focus, and the eyes constantly adjust to see objects clearly at different distances via a process called accommodation. This lack of focus is because visible light is made up of many different wavelengths, and each one bends slightly differently as it passes through the eye. Short wavelengths, such as blue light, focus closer to the lens; while longer ones, such as red light, focus farther away. Since the retina sits at a fixed distance behind the lens, not all wavelengths can be in focus at once, which creates a multi-colored blur known as longitudinal chromatic aberration (LCA).

Previously scientists thought that the eyes' choice of colour on which to focus hinged on achieving the best possible visual acuity—our ability to see fine details. The idea was that this mechanism worked by maximizing luminance contrast, enhancing the overall brightness and clarity of an image. However, this new discovery challenges that long-held notion.

The new study questions the prevailing theory, suggesting that brightness and contrast alone don't fully explain how the eye focuses on colored objects. There must be color-processing mechanisms at play too. To test this, the researchers used a combination of specialized hardware, personalized eye mapping, and computer simulations.

The results showed that the human eye doesn't just focus on light to make images as sharp and bright as possible, as scientists long thought. Instead, the eye picks which color on which to focus based on what allows the brain's color-processing pathways to work most efficiently.

The team also found that instead of focusing on extreme wavelengths like blue, the eye often chooses a middle wavelength like greenish-yellow as a compromise. This approach keeps the main image sharp while leaving the blue areas slightly blurry, resulting in a stronger, clearer signal for the brain to process.

Benjamin M. Chin et al, Focusing on color: How the eye chooses which wavelength to see best, Science Advances (2026). DOI: 10.1126/sciadv.aea5693

Virus from seafood is linked to a persistent eye disease in humans
A virus that typically infects marine animals, such as shrimp and fish, has jumped to humans and is causing chronic eye disease in some people, according to a study published in the journal Nature Microbiology. In recent years, the number of people in China with a condition called persistent ocular hypertension viral anterior uveitis (POH-VAU) has been increasing with no clear explanation as to why. Symptoms include extremely elevated eye pressure and inflammation.
Researchers suspected that covert mortality nodavirus (CMNV) might be the cause since patients with the condition consistently tested negative for common eye viruses such as herpes or shingles. And earlier investigations had identified unknown virus particles in the eye tissue of a few patients that looked similar in shape and size to CMNV.

To investigate further, scientists in China recruited 70 people diagnosed with the condition between January 2022 and April 2025.

The team examined patient tissue removed during eye surgery with electron microscopes and saw similar virus particles about 25 nanometers in size. No CMNV-like particles were found in the control group of healthy volunteers. To confirm the virus's identity, they used a special gold-labeled antibody that only binds to CMNV. Sequencing its genetic material revealed a 98.96% match to the version found in aquatic animals.

"This study reveals that an aquatic animal virus is associated with an emerging human disease," wrote the scientists in their paper.
The researchers interviewed the patients about their lives, and nearly three-quarters were either handling raw seafood without gloves or were eating raw aquatic animals. "Frequent unprotected processing of aquatic animals and consumption of raw aquatic animals were commonly reported exposure events," added the team.

To confirm that the virus was actually causing the disease rather than merely being present, the team conducted cell culture studies and infected mice with the virus. These rodents developed the characteristic symptoms of the condition seen in human patients, such as elevated intraocular pressure.
This is the first study to show that a virus originating from aquatic animals can be associated with a specific eye disease in humans. And it may not just be a problem in China.

As part of their study, the researchers conducted a global survey to see how far the viruses had spread. CMNV was found in 49 species, including crabs and mollusks, across Asia, Africa, Europe, Antarctica and the Americas.

Shuang Liu et al, An emerging human eye disease is associated with aquatic virus zoonotic infection, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02266-x

Fabian H. Leendertz et al, Aquatic virus transmission to humans, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02306-6

How microbes survive in the plastisphere
Microbes inhabiting the plastisphere—biofilms on ocean plastic—possess larger genomes with more functional gene copies than marine plankton, enabling enhanced nutrient uptake, carbon utilization, UV protection, and alternative energy use. These adaptations support survival in nutrient-poor, high-UV environments and may create eutrophic niches, potentially impacting ocean ecosystem health.

Stefan Lips et al, Metagenomic analyses of the plastisphere reveals a common functional potential across oceans, Environmental Pollution (2026). DOI: 10.1016/j.envpol.2026.127830

15 years after the eradication of rinderpest, lessons still ring true

Permanently wiping out a disease is tricky business. Polio, measles, mumps—all have effective vaccines, yet they persist in certain pockets around the world. To date, the World Health Organization considers just two viruses as successfully eradicated: smallpox and rinderpest.

Rinderpest, a highly contagious cattle disease, was officially eradicated in 2011, marking it as one of only two viruses eliminated globally. Success was achieved through a combination of technological advances, such as a heat-stable vaccine, and community-based strategies, including participatory epidemiology and targeted vaccination in remote areas. These approaches remain vital for controlling current and future animal diseases.
Rinderpest, a German word meaning "cattle plague," can be traced back as early as the Roman Empire. In the centuries when the virus was active, it ran through herds from Europe into Asia and Africa. When the disease struck, it often killed the entire herd.

The disease was so economically devastating that it's recognized as the cause of several historic famines. In the 18th century, rinderpest killed 200 million cows in Europe.

Part 1

In the 19th century—after colonialism spread the disease—rinderpest culled about 90% of plow oxen in Ethiopia. Rinderpest itself has no effect on human health, but the resulting famine killed one-third of Ethiopia's population.
"Without cattle to plow fields and fertilize crops with dung, the once-fertile Ethiopian lands became a graveyard
Attempts to develop a vaccine, which began as early as the 18th century, provided some protection, but not a full cure. It wasn't until the middle of the 20th century that the first effective vaccines were introduced. Shortly after, the U.N. Food and Agriculture Organization began a worldwide campaign to inoculate animals, shipping vaccines and brokering meetings between countries to discuss collaborative vaccination campaigns.

Soon, the number of global rinderpest infections fell precipitously, but occasional outbreaks continued.
Complete eradication remained out of reach until a technological breakthrough—along with what Mariner and other researchers have called "social innovations"—made it possible.

Most vaccines require refrigeration, and the rinderpest vaccine was no exception. But in many places where the disease was common—rural areas with cattle ranching—refrigerated shipping was expensive and complex.

It was extremely challenging to keep the vaccine cold while traveling to isolated areas then.
It required refrigeration facilities, ice machines, cold boxes, and fleets of vehicles. They needed an easier way to deliver the vaccine.
In the 1980s, researchers earned grant funding to experiment with ways to make a vaccine that did not require refrigeration. His team worked for two years and eventually developed a method to freeze-dry the vaccine. As a result, it could stay effective at temperatures as high as 98 degrees Fahrenheit and could last 30 days without refrigeration.

That innovation made it possible to deliver vaccines to a wider array of far-flung places, but it didn't necessarily make it easier.
So, the scientists engaged in a more targeted and strategic approach and went directly to those remote areas. Researchers helped train people in these communities to provide the vaccine and relied on their knowledge to decide how and when to distribute it. These efforts increased vaccination in herds that had been missed during previous campaigns. Locals then monitored for signs of disease after vaccination occurred.
The successful eradication, then, relied on both science and collaboration, and a tool called participatory epidemiology, which incorporates both researchers and stakeholders.

The elimination of rinderpest has had an enormous impact on the lives of people and their animals.

https://now.tufts.edu/2019/07/18/world-without-rinderpest

Part 2

AI uncovers hidden immune defenses inside bacteria

Researchers have discovered thousands of new proteins that protect bacteria from virus attacks using an AI system called DefensePredictor. What would usually take months of lab work can now be narrowed down to promising candidates in minutes.

Bacteria are under constant attack from viruses called bacteriophages. One of their most powerful defenses is CRISPR-Cas, a system that cuts up viral DNA to stop an infection and is now a valuable biotechnology tool for precisely editing genes in a lab.

Traditional methods of finding these defenses are long and laborious, equivalent to looking for a needle in a haystack. They involve searching for nearby known defensive genes and manually testing thousands of DNA fragments. But now, AI can take the strain.

To develop their machine learning tool, the scientists trained it on 17,000 different bacterial genomes, as they describe in a paper published in the journal Science. Because genes contain instructions for making proteins, the system identifies the proteins encoded in each genome and analyzes them using a protein language model called ESM2. It can distinguish between a normal protein and a defensive one by examining specific characteristics, such as gene length, nearby genes and patterns in the DNA sequences surrounding each gene.

To further refine DefensePredictor, the team trained it on 15,000 proteins already known to fight viruses and 186,000 normal proteins that perform everyday tasks. By comparing these two groups, the AI learned to rapidly distinguish defensive proteins from non-defensive ones.

Next came the system's big test. DefensePredictor scanned 69 diverse E. coli strains and identified 624 protein clusters as defensive. This included more than 100 that had no previously known connection to bacterial immune systems. The researchers then cloned 94 of these predicted systems into E. coli cells and exposed them to 24 different phages. Nearly 45% protected the bacteria from infection.

The results demonstrate that DefensePredictor is a powerful tool for discovering new prokaryotic immune systems

The researchers have released DefensePredictor as a resource for the global scientific community and will continue to refine it as new data arrives.

Peter C. DeWeirdt et al, DefensePredictor: A machine learning model to discover prokaryotic immune systems, Science (2026). DOI: 10.1126/science.adv7924

Cell-by-cell analysis offers clues to pregnancy risks

The biological connection between a pregnant woman and her developing baby has been mapped in unprecedented detail by  scientists, revealing new cell types and insights into conditions such as preeclampsia, preterm birth, and miscarriage.

Using advanced single-cell and spatial tools, the researchers analyzed about 200,000 individual cells and compared them with nearly 1 million cells in their original positions within the uterine and placental tissue. This enabled them to identify different cell types, track how they develop, and see how they are linked to pregnancy complications.

This work gives us a much clearer picture of this critical region than ever before.

The maternal-fetal interface is a temporary but essential structure composed of uterine and placental cells that forms about a week after fertilization and lasts throughout pregnancy. It supports fetal growth while maintaining the mother's health. Its complexity has long limited scientists' ability to study how healthy pregnancies develop and why complications arise.

By examining this tissue cell by cell across pregnancy, we can begin to understand both normal development and what may go wrong, say the researchers. 

Part 1

The atlas revealed a previously unknown maternal cell type located where fetal placental cells first enter the uterus. These cells appear to regulate how deeply placental cells invade uterine tissue, a process that is essential for establishing blood flow to the fetus.

The researchers found that these cells carry a cannabinoid receptor. Exposure to cannabinoid molecules caused them to further restrict placental cell invasion.

Population studies have linked cannabis use during pregnancy to poorer outcomes. This cell type may help explain the biological basis of that association.
To understand how complications arise, the team integrated genetic data from more than 10,000 patients. They mapped genetic risk signals for conditions including preterm birth, preeclampsia, and miscarriage onto regulatory regions of DNA that control gene activity. This approach allowed the researchers to identify the specific cell types and states most strongly associated with each condition.
The team then focused on preeclampsia, a potentially life-threatening disorder marked by sudden high blood pressure. They found that the most affected cell types are involved in remodeling the mother's uterine blood vessels, a process required to supply adequate blood to the placenta.

The findings suggest that preeclampsia may result from disrupted communication between maternal and fetal cells that normally coordinate this process.

Having established a detailed map of healthy pregnancies, the researchers plan to study complicated pregnancies to identify potential targets for treatment.

Single-cell spatiotemporal dissection of the human maternal–fetal interface, Nature (2026). DOI: 10.1038/s41586-026-10316-x. www.nature.com/articles/s41586-026-10316-x

Part 2

Some common IBS treatments are linked to a higher risk of death, say study

IBS is a chronic gastrointestinal condition.  There is no cure, but dietary modifications, behavioural therapy, and medications can help manage symptoms.

A large, long-term study led by Cedars-Sinai Health Sciences University investigators suggests that some medications commonly prescribed to treat irritable bowel syndrome (IBS)—including antidepressants—may be associated with a small but measurable increase in the risk of death. The findings, published in Communications Medicine, are based on nearly two decades' worth of electronic health records from more than 650,000 U.S. adults with IBS, making it the largest real-world study to examine the long-term safety of IBS treatments.

The study does not establish that these medications directly cause death; rather, the observed associations may reflect higher rates of adverse outcomes, such as cardiovascular events, falls, and stroke, which were more frequent among exposed patients.

Researchers emphasized that while the increase in risk is significant and may sound concerning, the overall risk to any individual patient is small.

"IBS patients should not panic, but they do need to understand and weigh the small but meaningful risks when considering long-term treatments," the researchers  stress.

Association of pharmacotherapy with all-cause mortality among patients with irritable bowel syndrome, Communications Medicine (2026). DOI: 10.1038/s43856-026-01498-6

**

Human-altered mountains drive most fatal landslides worldwide, analysis finds

A new study reveals that most fatal landslides occur in human-transformed environments. Conducted by an international team of researchers, the study provides a global overview of how human pressure modulates landslide occurrences. The paper is published in the journal Science Advances.

The most important finding of the study is that land-use-land-cover change has a substantially greater influence on landslide fatalities than physical factors such as topography and precipitation, especially in low- and lower-middle-income nations.

Landslides are among the most destructive hazards, typically killing over 4,500 people and causing $20 billion in damage annually. The starting point for this research was a critical global question: Why are landslides deadlier in certain regions than others with comparable terrain and climate?

As populations exposed to hazards in mountain areas have doubled since 1975, it's important to understand that human alterations to the land surface—such as clear-cutting, agricultural transition, and road construction—are drastically destabilizing hill slopes. This study highlights how increasing human-made pressure on nature exacerbates the vulnerability of socioeconomically disadvantaged people.

The researchers focused on mountainous landmasses across 46 countries, categorized by national income levels. They addressed a massive dataset comprising approximately 60 years of land-use-land-cover changes and 45 years of population dynamics. The team introduced a new metric, the total land-use-land-cover change, to quantify overall human alterations, integrating this with topography, precipitation, and exposure models.

The findings are striking: While high-income nations altered only 7% of their mountainscapes, low-income countries changed 50% of the mountain land cover of their countries. Such changes could include deforestation, and expansion of farmland and infrastructure.

In countries like Haiti, Sri Lanka, and El Salvador, this land-use-land-cover change correlates with a surge in fatal landslides and death tolls. However, this correlation weakens in wealthy nations such as Switzerland, Japan, and Italy, which experience fewer fatalities despite landslide-prone topography and climates.

Economically disadvantaged countries often also face substantial population pressures, unlike wealthier nations. These pressures lead to the rapid clearing of fragile mountainous areas for farming, informal housing, and basic infrastructure needs, the researchers say.

The authors of the study thus clearly demonstrate that minimal human intervention in land use in mountainous regions reduces the risk of fatal landslides.

Seçkin Fidan, Wealth and land cover change govern landslide fatalities on world's mountains, Science Advances (2026). DOI: 10.1126/sciadv.aec2739. www.science.org/doi/10.1126/sciadv.aec2739

City animals act in the same brazen ways around the world

Urban animals worldwide exhibit similar bold, opportunistic behaviours, such as food-stealing and reduced fear of humans, due to shared city environments and selective pressures favouring these traits. This behavioural homogenization is accompanied by a loss of behavioural and genetic diversity, reducing species' resilience to environmental change and complicating conservation efforts. The trend also increases potential for human-wildlife conflict and loss of unique, socially learned behaviours.

original article.

Loss of microbiota alters the profile of cells that protect the intestinal wall, experiments reveal

Research by scientists has made significant progress in understanding the relationship between gut microbiota and intestinal cells. The study, published in the journal Gut Microbes, showed how microbiota and the compounds it produces, such as butyrate, influence the functioning of cells that line the large intestine. This intestinal layer is in close contact with bacteria and produces mucus that contributes to its barrier function, helping to prevent bacteria from entering the body.
Loss of gut microbiota increases the abundance of a dual-function intestinal epithelial cell capable of both mucus secretion and nutrient absorption, a process regulated by microbiota-derived butyrate and its receptor GPR109A. This cell population expands in conditions of dysbiosis or aging, indicating adaptive epithelial plasticity and altered barrier function.
Among the findings is a description of the dual function of a cell that was previously thought to be exclusively mucus-secreting. The researchers discovered that the cell also absorbs nutrients and that its abundance in the epithelium is regulated by signals from the gut microbiota. The number of these cells increases when the gut microbiota is reduced.

The abundance of this cell is regulated by the production of butyrate—a compound resulting from the fermentation of dietary fiber—and its receptor, GPR109A. The more butyrate produced, the fewer of these cells there are.

This study paves the way for a better understanding of the role of microbiota and its metabolites in conditions such as inflammatory bowel disease and in developing treatments. Furthermore, the study demonstrates how the integrity of the intestinal wall can change, particularly in older individuals.
When the microbiota is reduced, the large intestine—which under normal conditions prioritizes mucus production—begins to express characteristics linked to nutrient absorption typically associated with the small intestine. We still don't know why this happens, but this change may be related to the expansion of dual-function cells and represent an adaptive response to the decrease in bacteria in this portion of the intestine, say the researchers.

Matheus de T. Moroti et al, Historical shifts, geographic biases, and biological constraints shape mammal species discovery, Journal of Systematics and Evolution (2026). DOI: 10.1111/jse.70040

Can drugs skip the blood-brain barrier?
Researchers have skipped the blood-brain barrier altogether by injecting drug-loaded nanoparticles into the space between skull bone layers. Immune cells then ferried these nanoparticles into the brain. In a randomized study of 20 stroke patients, clinical outcomes were better in the group where treatment was also injected through the skull, compared to the standard of care. The ability to skip the blood-brain barrier in its entirety could be massively useful for treating many brain-based disorders, but there’s a lot more work in store, writes medicinal chemist Derek Lowe.

https://www.sciencedirect.com/science/article/pii/S0092867425014217...

"Ghost Murmur"

Mammal ancestors laid eggs

A remarkable new discovery is shedding light on one of the greatest survival stories in Earth's history, and answering a decades-old scientific mystery. Lystrosaurus, a hardy, plant-eating mammal ancestor, rose to prominence in the wake of the End-Permian Mass Extinction some 252 million years ago, the most devastating extinction event our planet has ever experienced.

While countless species vanished, Lystrosaurus not only survived but thrived in a world marked by extreme environmental instability, intense heat, and prolonged droughts.

Now, groundbreaking research published in PLOS ONE reveals a discovery that transforms our understanding of this iconic survivor. An international research team has identified, for the first time, an egg containing an embryo of Lystrosaurus, dating back approximately 250 million years.

This extraordinary fossil represents the first-ever egg discovered from a mammal ancestor, finally answering a long-standing question: Did the ancestors of mammals lay eggs?

The answer is yes!

The researchers suggest these eggs were likely soft-shelled, explaining why they have remained elusive for so long. Unlike the hard, mineralized eggs of dinosaurs, which fossilize readily, soft-shelled eggs rarely preserve, making this find exceptionally rare. But the implications go far beyond reproduction.

The study reveals that Lystrosaurus laid relatively large eggs for its body size.

Part 1

In modern animals, larger eggs typically contain more yolk, providing all the nutrients an embryo needs to develop independently, without parental feeding after hatching.

This strongly suggests that Lystrosaurus did not produce milk for its young, unlike modern mammals. Large eggs also offer another crucial advantage: they are more resistant to drying out. In the harsh, drought-prone environment following the extinction, this would have been a critical survival trait.

The findings further suggest that Lystrosaurus hatchlings were likely precocial, born at an advanced stage of development. These young animals would have been capable of feeding themselves, escaping predators, and reaching reproductive maturity quickly.

In other words, Lystrosaurus succeeded by living fast and reproducing early.
In a world on the brink, this strategy proved unstoppable. This discovery not only provides the first direct evidence of egg-laying in mammal ancestors but also offers a powerful explanation for how Lystrosaurus came to dominate post-extinction ecosystems.

PLOS One (2026). DOI: 10.1371/journal.pone.0345016

Part 2

The 4 Minutes That Will Decide if Artemis II Astronauts Survive

One DNA letter can trigger complete sex reversal

Researchers have discovered that changing just one letter in DNA can completely alter sex development in mice. In the new study, published in Nature Communications, a single-letter insertion in a non-coding regulatory region caused XX mice, which would normally develop as females, to develop instead as males with testis and male genitalia.

The finding is especially striking because the mutation was not made in a gene itself, but in a distant stretch of DNA that helps control a key developmental gene. The study highlights the major role of the non-coding genome—the 98% of DNA that does not make proteins but helps regulate when and how genes are turned on and off.
This is a remarkable finding because such a tiny change—just one DNA letter out of approximately 2.8 billion—was enough to produce a dramatic developmental outcome. It shows that non-coding DNA can have a profound effect on development and disease.

The mutation was introduced into a regulatory element known as Enh13, which controls the activity of Sox9, a gene essential for testis development. For ovaries to develop normally, Sox9 must be kept turned off. The researchers found that Enh13 acts as a kind of molecular battle site/switch: in males, factors that promote testis development bind to it and activate Sox9 whereas in females, factors that promote ovary development bind to it and repress Sox9.

When the researchers introduced the mutation using CRISPER genome editing, that female repression failed. As a result, Sox9 was activated in XX mice, and testis developed, leading to complete internal and external male development.

The team created several mouse models with very small mutations in Enh13, including a one-base-pair insertion and a three-base-pair deletion. Both mutations caused XX mice to develop testis. The researchers then used cell-line reporter assays to understand how the mutation disrupted the normal regulatory mechanism.

Nature Communications (2026). DOI: 10.1038/s41467-026-71328-9

Why amphibians regenerate limbs but mammals cannot

Some animals can regrow lost body parts. Salamanders and frog tadpoles can rebuild entire limbs after amputation. Mammals cannot. For decades, biologists have tried to understand why. Now a research  team has discovered that oxygen plays a crucial role in limb regeneration. By comparing amputated limbs from frog tadpoles and embryonic mice, the researchers found that the way cells sense oxygen determines whether regeneration can even begin. The study is published in Science.

Limb regeneration begins with wound healing. After amputation, cells at the injury site must rapidly seal the wound and switch into regenerative cell types. In amphibians, this process runs smoothly. In mammals, it stalls early. Wound closure is slow and scar formation takes over, blocking regeneration.

One key difference lies in the environment. Amphibian larvae develop in water, where oxygen levels are lower than in the air. Moreover, many regeneration-competent species live in aquatic environments. Meanwhile, mammalian tissues are typically exposed to higher oxygen levels after injury.

What is unclear is whether this difference has played a direct role in regeneration or is merely a consequence of lifestyle.

The researchers amputated developing limbs from frog tadpoles and mouse embryos and cultured them outside the body under controlled oxygen conditions. Oxygen levels were lowered to match aquatic environments or raised to levels close to air.

They tracked how cells responded by measuring wound closure, cell movement, gene activity, metabolism, and epigenetic states, including changes to DNA packaging. The work focused on HIF1A, a protein that acts as a cellular oxygen sensor. When oxygen is low, HIF1A becomes stable and activates programs that set the stage for wound healing and regeneration.

Lowering oxygen levels had a clear effect on the limbs of mouse embryos. Under reduced oxygen, mouse cells closed wounds faster and showed signs of entering a regenerative program. Stabilizing HIF1A produced similar effects, even when oxygen levels remained high.

Low oxygen also changed cell behavior, with skin cells becoming more mobile and altering their mechanical properties. Metabolism shifted toward glycolysis, a process that takes place in low-oxygen states. At the same time, chemical marks on DNA-associated proteins shifted to favor the activation of regeneration-related genes.

Frog tadpoles behaved differently. Their limbs regenerated efficiently across a wide range of oxygen levels, including levels well above those normally found in air. Molecular analysis showed that their cells maintain stable HIF1A activity even when oxygen increases, due to low expression of genes that normally shut this pathway down.

By comparing frogs, axolotls, mice, and human datasets, the team found a consistent pattern. Regeneration-competent amphibians show reduced oxygen-sensing capacity, allowing regenerative programs to be initiated and sustained. Mammals show the opposite pattern. Their cells respond strongly to oxygen and switch regenerative programs off soon after injury.
The results suggest that mammalian limbs retain latent regenerative potential at early stages, depending on how cells respond to environmental signals such as oxygen. This means that adjusting oxygen-sensing pathways might one day improve wound healing or regenerative responses in humans.

Species-specific oxygen sensing governs the initiation of vertebrate limb regeneration, Science (2026). DOI: 10.1126/science.adw8526

Part 2

CAR-T therapy drives remission in patient with three autoimmune diseases

For the first time, scientists have used a modern cell therapy called CAR-T to treat a patient with three different life-threatening autoimmune diseases that had resisted years of treatment. The patient, who once required daily blood infusions, has been in remission without needing additional treatment for a year since the CAR-T therapy. The case report, published in Med, suggests that CAR-T therapies can help treat complex and severe autoimmune diseases.
After being sick for more than a decade, the patient is now in treatment-free remission and able to return to an almost normal life. This therapy significantly improved her quality of life.

CD19 CAR-T therapy induces remission in refractory autoimmune hemolytic anemia with ITP and antiphospholipid syndrome, Med (2026). DOI: 10.1016/j.medj.2026.101075

A 1.9 billion-year-old bedrock will soon house the world's first permanent nuclear waste site
Finland's Onkalo facility will be the world's first permanent deep geological repository for spent nuclear fuel, designed to isolate 6,500 tons of radioactive waste in stable bedrock for hundreds of thousands of years. The approach uses copper canisters and bentonite clay to contain radioactivity until it decays to safe levels, but uncertainties remain regarding long-term canister corrosion and future risks. Deep underground storage is considered safer than above-ground alternatives, though challenges persist in ensuring information preservation and minimizing risks to future generations.

-finland-spent-nuclear-future-ge...

Wildlife trade increases pathogen transmission: What 40 years of data say about spillover
Analysis of 40 years of wildlife trade data shows that traded wild mammals are 1.5 times more likely to share pathogens with humans than non-traded species, with risk increasing for illegally or live-traded animals. Each decade a species is present in trade adds, on average, one additional shared pathogen. These findings underscore the need for enhanced biosurveillance and reduced wildlife trade to limit zoonotic disease emergence.
Hedgehogs, elephants, pangolins, bears or fennec foxes: many wild species are sold as pets, hunting trophies, for traditional medicine, biomedical research, or for their meat or fur. These practices, whether legal or illegal, concern one-quarter of all mammal species. Now a study quantifies the impact of wildlife trade on the exchange of germs and parasites between animals and humans. The work, titled "Wildlife trade drives animal-to-human pathogen transmission over 40 years," appears in Science.
The team combined forty years of legal and illegal wildlife import-export data with compilations of host–pathogen relationships. Their analyses, led to the following result: Wild mammals that are traded are 1.5 times more likely to share infectious agents with humans than those that are not involved in trade.

In other words, these species have a 50% higher probability of sharing at least one virus, bacterium, fungus or parasite with us. That is not all: the risk is even higher when species are traded illegally or alive (for example as exotic pets).
The most striking finding, according to the research team, is that "the length of time an animal has been present in trade plays a key role: On average, a species shares one additional pathogen with humans for every ten-year period spent on the market.
The results of the study highlight the need to improve biosurveillance of animals and animal-derived products in order to detect infectious agents and assess their potential for transmission to humans.

Jérôme M. W. Gippet, Wildlife trade drives animal-to-human pathogen transmission over 40 years, Science (2026). DOI: 10.1126/science.adw5518. www.science.org/doi/10.1126/science.adw5518

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

Non-coding genes cause diabetes in babies, study reveals

Bi-allelic variants in the non-coding RNA genes RNU4ATAC and RNU6ATAC were identified as causes of syndromic monogenic autoimmune neonatal diabetes in 19 children. These mutations disrupt splicing and affect the expression of approximately 800 genes, many involved in immune function, highlighting the pathogenic potential of non-coding genomic regions in rare autoimmune diabetes.

Matthew B. Johnson et al, Bi-allelic variants in the non-protein-coding minor spliceosome components RNU6ATAC and RNU4ATAC cause syndromic monogenic autoimmune diabetes, The American Journal of Human Genetics (2026). DOI: 10.1016/j.ajhg.2026.02.017

People use the same neurons to see and imagine objects, study shows

Why can images of things we have seen seem so real when we later recall them from memory? A new study led by Cedars-Sinai Health Sciences University investigators sheds light on the answer. The research shows that the same brain neurons are activated when we imagine something and when we perceive something. The research, led by Cedars-Sinai, is the first to provide a detailed understanding of the shared mechanism that underlies visual perception and creation of mental images in the human brain. It was published in the journal Science.
Visual perception and imagination activate overlapping populations of neurons in the human fusiform gyrus, with about 40% of visually responsive neurons reactivating during mental imagery using the same neural code as during perception. This shared neural mechanism underlies the vividness of visual imagination and may inform understanding of psychiatric disorders involving altered mental imagery.
We generate a mental image of an object that we have seen before by reactivating the brain cells we used to see it in the first place.
The new study revealed the code that we use to re-create the images.
The findings provide a biological basis for visual imagination, a process that is also critical for creative arts.

"Further insight into this neural process has the potential to open pathways toward developing new therapies for post-traumatic stress disorder, obsessive-compulsive disorder, and other mental conditions that involve uncontrolled vivid imagery.
To conduct the study, investigators asked 16 adults with epilepsy, who had electrodes temporarily implanted in their brains for diagnosing their seizures, to view a series of images of faces and objects.

After viewing them, a subset of the participants were asked to imagine those same images from memory. Meanwhile, researchers recorded the electrical activity of hundreds of individual neurons in each participant's brain.

When the patients viewed the images, neurons were activated in their fusiform gyrus, an area of the brain essential for high-level visual processing, particularly for faces. For 80% of the visually responsive neurons recorded in the study, the researchers uncovered the aspects of the images they reacted to, thereby revealing their neural code.
When the patients later imagined the images, about 40% of these neurons reactivated using the same code, thereby recreating the pattern of activity that occurred during the initial viewing of the images.

V. S. Wadia et al, A shared code for perceiving and imagining objects in human ventral temporal cortex, Science (2026). DOI: 10.1126/science.adt8343. www.science.org/doi/10.1126/science.adt8343

Artemis Re-Entry | NASA Most Dangerous 20 Minutes

Moon Joy, Courtesy of NASA's Artemis II Astronauts

Orbital Mechanics

Baby's body clock begins to synchronize with local time while still in utero, study shows

Humans and most other organisms have internal biological clocks that track the daily cycle of sunrise and sunset. These clocks help time our sleep, metabolism and other essential body functions over the course of a day, creating daily patterns called circadian rhythms. Research shows that when these rhythms are disrupted—by jet lag, lack of sleep or irregular work schedules—people can suffer long-term negative health effects.

Scientists who study daily rhythms have long wondered about when the mammalian circadian clock starts ticking and synchronizes to local time. In a new study published in the Journal of Biological Rhythms, researchers reported that a mother helps to set the biological clock for her babies while they are still in the womb.

Disrupting circadian rhythms during pregnancy can affect how sleep and daily rhythms develop in infants, and these early disruptions are linked to a higher risk of mood disorders such as anxiety and depression later in life.

Understanding when the fetal clock begins to function helps us identify sensitive developmental windows when circadian disruption may have lasting effects and how those effects might be prevented or corrected.

In mouse models researchers  found clear day-night rhythms in the pups that synchronized to the mother's rest-activity cycle during the last week of pregnancy, equivalent to the third trimester in humans. This suggests that the clock machinery forms early in development and receives entraining cues from mom later.

Importantly, they found daily rhythms across the placenta from the mother to the baby before the fetus can sense light.

The researchers found that circadian synchronization of the pups to the mother coincided with when glucocorticoid hormones from the mother cross the placenta, potentially acting as timing signals for the fetal clock. These stress-related hormones normally rise and fall over the course of the day under the control of the mother's internal clock.

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Synthetic glucocorticoids are routinely given to pregnant women at risk of preterm birth, often without considering the time of day when these hormones naturally fluctuate. The authors found that giving these steroids daily to the mother accelerated the synchronization to local time of the daily rhythms in the pups. These findings may be important when considering how and when doctors administer medications to treat pregnancy conditions.

During the study, the researchers also observed a strong association between failure to develop circadian clock gene activity in the fetuses and failure to deliver. It is not clear yet whether the absence of rhythms contributes to developmental problems or simply reflects them. But the observation suggests that circadian clock activity may be closely linked to healthy fetal development.
The findings also highlight the importance of maintaining stable circadian rhythms during pregnancy. Over 80% of the world's population is exposed to artificial light at night that can disrupt daily rhythms, and this includes pregnant people.
Understanding when and how the body clock starts ticking helps scientists identify sensitive developmental windows when circadian disruption may have lasting effects. This knowledge could help guide medical treatments, inform clinical practices and shape public health policies aimed at protecting neonatal circadian health during pregnancy.

K. L. Nikhil et al, Fetoplacental Circadian Rhythms Develop and Then Synchronize to the Mother In Utero, Journal of Biological Rhythms (2026). DOI: 10.1177/07487304261435435

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Five warning signs that rivers are polluted—even when they look clean
Key indicators of river pollution, even when water appears clean, include the presence of sewage fungus, algal blooms, unusual water coloration or murkiness, persistent white foam with chemical odors, and signs of aquatic life distress or absence. Many pollutants are invisible, and these signs may overlap with natural phenomena, so additional context and caution are necessary for accurate assessment.

original article.

Negative effects of artificial sweeteners may pass on to next generation, study suggests
In mice, consumption of sucralose and stevia altered gut microbiome composition, reduced beneficial short-chain fatty acids, and changed gene expression related to inflammation and metabolism, with some effects persisting across generations. Sucralose produced more pronounced and lasting metabolic and microbiome disruptions than stevia. These findings suggest potential transgenerational metabolic impacts of artificial sweeteners.
Health organizations are starting to raise concerns about the potential long-term impacts of artificial sweeteners, which taste sweet but—unlike sugar—contain no calories, suggesting they could interfere with energy metabolism and increase the eventual risk of diabetes or cardiovascular disease.
Now a new study in mice indicates that the popular sweeteners sucralose and stevia have negative effects on the gut microbiome and gene expression, potentially compromising metabolic health, which can be transmitted between generations.
The scientists found that different sweeteners produced different effects, which changed over time.

In the first generation, only the male offspring of sucralose-consuming mice showed signs of impaired glucose tolerance, but by the second generation, elevated fasting blood sugar was detected in male descendants of sucralose-consuming mice and female descendants of stevia-consuming mice.

Both groups of mice that ate sweeteners had more diverse fecal microbiomes but lower concentrations of short-chain fatty acids, suggesting the bacteria were producing fewer beneficial metabolites; both succeeding generations also had lower concentrations of short-chain fatty acids.

Sucralose-consuming mice were more seriously and more persistently affected by changes to the fecal microbiome, with more pathogenic species and fewer beneficial species of bacteria in their feces.

Similarly, sucralose appears to kick-start the expression of genes linked to inflammation and dampen the expression of genes linked to metabolism for two generations after consumption. Stevia also impacts gene expression, but its effects are smaller and are not passed on for more than one generation.

Artificial and Natural Non-Nutritive Sweeteners Drive Divergent Gut and Genetic Responses Across Generations, Frontiers in Nutrition (2026). DOI: 10.3389/fnut.2026.1694149

Women's immune systems show bigger age-related changes than men's

Immunological aging exhibits distinct sex-specific patterns, with women showing more pronounced age-related changes, including increased inflammatory immune cells, potentially explaining higher autoimmune disease prevalence and postmenopausal inflammatory pathologies. In men, immune aging changes are less extensive but include increased pre-leukemia blood cells, correlating with higher blood cancer rates in older men. These findings highlight the importance of considering biological sex in precision medicine for aging and immune health.
Statistics show clear differences in the population's immune system according to sex: men are more susceptible to infections and cancers, while women have stronger immune responses, which translate, for example, into better responses to vaccines. Even so, with a more reactive immune system, the probability of the body attacking itself also increases, causing 80% of autoimmune disease development to occur in women.
In this context, understanding the aging of the immune system is key since, with age, the composition of immune cells changes and their protective functions deteriorate, causing a greater susceptibility to diseases.
A new study published this week in Nature Aging demonstrated, for the first time, that immunological aging follows different dynamics between men and women, identifying the cells and genes responsible for the process, and providing a molecular explanation for the differences that previously were only observed globally in the population.
The results reveal that women present more pronounced changes in the immune system with age, with an increase in inflammatory immune cells. This finding could help explain why autoimmune diseases are mainly developed by women, especially at advanced ages, as well as the worsening of certain inflammatory pathologies after menopause.
On the other hand, the changes associated with immune system aging observed in men are globally less extensive, but an increase in certain blood cells presenting pre-leukemia alterations was observed, a fact that could explain why some blood cancers are more frequent in older men.
Finding these patterns was possible thanks to the analysis of blood samples from nearly 1,000 people of different ages covering the entire adult life, combined with a technology capable of analyzing each cell individually, called single-cell RNA sequencing. In total, the researchers analyzed the activity of 20,000 genes in more than one million blood cells, which allowed them to identify how the immune system changes over the years and detect clear differences between sexes.

Maria Sopena-Rios et al, Single-cell analysis of the human immune system reveals sex-specific dynamics of immunosenescence, Nature Aging (2026). DOI: 10.1038/s43587-026-01099-x

Epigenetic changes at birth are associated with an infant's microbiome and neurodevelopment
Epigenetic patterns at birth influence the development of the infant gut microbiome during the first year and are associated with later neurodevelopmental signs, including ASD and ADHD. Specific gut microbes, such as Lachnospira pectinoschiza and Parabacteroides distasonis, may mitigate the risk of these neurodevelopmental conditions in children with certain epigenetic profiles.
The gut microbiome and epigenetics—molecular switches that turn genes on or off—are intertwined, and both contribute to neurodevelopment, finds a study published in Cell Press Blue. The researchers showed that epigenetic changes present at birth can impact how an infant's gut microbiome develops during their first year.
They also identified specific epigenetic changes and gut microbes that were associated with signs of autism spectrum disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) when the children were three years old.

Certain bacteria seem to offer protection, which is exciting because it suggests there could be ways to support a child's development through diet or probiotics in the future.
Early life biology matters:
The first years of life are critical for brain development and immune system maturation. Though previous studies have shown that both early epigenetic changes and gut microbiome development can impact health in later life, little is known about how these two systems interact.
Researchers discovered a kind of conversation happening: a baby's epigenetic setting at birth can influence their risk for neurodevelopmental disorders, but the presence of certain 'good' bacteria in their gut can step in and modify the risk.
The researchers characterized DNA methylation patterns—a type of epigenetic change—from the umbilical cord blood of 571 infants. They paired this information with gut microbiome data collected from 969 infants at 2, 6, and 12 months of age, and from their parents during the third trimester of pregnancy.

When the children reached 36 months of age, the researchers used a behavioral questionnaire to assess their neurodevelopment and investigate links between the microbiome, epigenome, and early signs of ASD and ADHD.
They found that an infant's epigenome at birth was associated with birth mode, length of gestation, having older siblings, and maternal allergies, but it was not affected by their parents' gut microbiomes.

Microbiome development, on the other hand, was associated with birth mode, antibiotics, having older siblings, and breastfeeding. Infants who were born by cesarean section showed different patterns of DNA methylation for several genes involved in immune responses and brain development.
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The team also showed that an infant's epigenome at birth impacted how their microbiome developed during their first year. Specifically, infants developed less diverse gut microbiomes at 12 months of age when they showed higher rates of DNA methylation in immune genes involved in recognizing pathogens.

The behavioral survey revealed that signs of ASD and ADHD in 3-year-olds were associated with specific epigenetic patterns and the presence of certain gut microbes.

However, other microbial species seemed to mitigate these effects: infants with epigenetic patterns associated with ASD or ADHD were less likely to show signs of the disorders if they acquired Lachnospira pectinoschiza and Parabacteroides distasonis, respectively, during their first year.

Epigenome–microbiome interplay in early life associates with infants' neurodevelopmental outcomes, Cell Press Blue (2026). DOI: 10.1016/j.cpblue.2026.100009. www.cell.com/cell-press-blue/f … 3051-3839(26)00007-1

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Too young for the MMR shot, babies become 'sitting ducks' in measles outbreaks
Infants too young for measles vaccination are highly vulnerable during outbreaks, relying on herd immunity, which requires ≥95% community vaccination coverage. Declining vaccination rates and increased exemptions have eroded this protection, leading to significant outbreaks and increased risk of severe illness or death in infants. Legislative efforts to restrict vaccine requirements may further reduce coverage and increase disease spread.
Source: News agencies

How the US Will Blockade Iran in the Strait of Hormuz

Why do some stars in the galactic center survive while others are destroyed?
Strong internal magnetic fields in compact stars near the galactic center can suppress the accretion of stellar material onto nascent black holes, slowing or halting their growth and allowing the stars to survive. This mechanism, termed magnetically arrested transmutation, explains the survival of magnetars and highly magnetized white dwarfs, while stars with weaker magnetic fields are more likely to be destroyed.
The center of our galaxy is an extreme place. Surrounding the supermassive black hole Sagittarius A, stars are packed densely into a region where gravity, radiation, and dark matter all interact in complex ways. It is a natural laboratory for testing some of the deepest ideas about astrophysics.
Compact stars—such as neutron stars and white dwarfs—are expected to accumulate dark matter over time, especially in such dense environments. Under the right conditions, this accumulation can trigger the formation of a tiny black hole at the very center of the star.

Once formed, the black hole should begin to grow by accreting the surrounding stellar material. The expected outcome is dramatic: The star is gradually consumed from within and eventually collapses entirely into a black hole.

If this picture were complete, many compact stars in the galactic center should already have been destroyed. But observations suggest otherwise.
Some stars clearly survive. Others appear to be missing. This uneven outcome raises a fundamental question: What determines whether a star lives or dies in such an environment?

One particularly intriguing clue comes from the magnetar PSR J1745-2900, located remarkably close to Sagittarius A*. Magnetars are neutron stars with extremely strong magnetic fields, and this object is both highly magnetized and stable. Its survival is not easy to reconcile with the expectation of rapid destruction driven by internal black hole growth.

At the same time, there is evidence for an overabundance of strongly magnetized white dwarfs near the galactic center.

In contrast, ordinary pulsars—neutron stars with comparatively weaker magnetic fields—appear to be underrepresented, a long-standing issue often referred to as the "missing pulsar problem."

Taken together, these observations suggest that not all stars share the same fate. Something must be influencing the outcome.
A natural candidate is magnetism.

Compact stars can host some of the strongest magnetic fields in the universe. In many astrophysical environments, magnetic fields are known to regulate how matter moves, especially in accretion processes. They can channel, redistribute, or even suppress the flow of matter onto compact objects. This raises an important possibility: Could magnetic fields also influence the growth of a black hole forming inside a star?

In recent work, this possibility was explored in detail. The findings are published in The European Physical Journal C.
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The central idea is that if a small black hole forms at the core of a strongly magnetized star, it does not grow in isolation. Instead, it is embedded in a medium where magnetic forces are significant. These fields can exert pressure and tension that oppose the inward flow of matter toward the black hole.

As a result, the accretion process—the mechanism that drives black hole growth—can be substantially reduced.
In this picture, the black hole may still form, but its growth is effectively slowed or even halted. Instead of a runaway process in which the star is inevitably consumed, the system becomes regulated. The star could survive for much longer timescales, potentially remaining observable.

This mechanism is referred to as magnetically arrested transmutation (MAT).

MAT provides a natural way to understand the contrasting observations in the galactic center. Stars with strong internal magnetic fields, such as magnetars or highly magnetized white dwarfs, may be protected from rapid destruction.

Their magnetic fields act as a barrier that limits the growth of any black hole forming inside them. On the other hand, stars with weaker magnetic fields may lack this protection, making them more vulnerable to being consumed from within.

In this way, magnetic fields may effectively decide the fate of compact stars in extreme environments.

H. A. Adarsha et al, Magnetically arrested transmutation of a compact star, The European Physical Journal C (2026). DOI: 10.1140/epjc/s10052-026-15515-4

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Ribosomal DNA may help explain human size differences

The ribosome is the most basic yet essential part of life on Earth. In humans, ribosomes are made up of about 80 proteins and four types of RNA. To keep up with the high demand for protein-making structures in cells, our bodies carry hundreds of copies of the instructions for making them in the form of rDNA. The number of these copies varies considerably between individuals, ranging from around 200 to 600 copies per human genome.

Ribosomal RNA (rRNA), made from many copies of ribosomal DNA (rDNA), is the core component that powers ribosomes—protein-building machines in our body. It helps build proteins by linking amino acids together, and can also fine-tune this process by interacting with other proteins and messenger RNA (mRNA). For a long time, scientists assumed ribosomes were more or less identical within a species. A new study in Cell Genomics is challenging that idea.

The work shows that rDNA can vary quite a bit, not just between species, but even from one person to another, and these small genetic differences can subtly change the shape of ribosomes, which may influence diversity in human size traits such as height and weight.

Recent studies reveal that rDNA can vary not only in how many copies people have, but also in its sequence, with small changes such as single-letter differences and insertions or deletions. 

Researchers discovered a cluster of genetic variations in a region of 28S rRNA called expansion segment 15L (ES15L) that is strongly linked to body size traits such as height, weight, and birth weight. These genetic differences are not just passive markers built into the ribosomes and could change their physical shape and structure. These effects appeared to be independent of the number of rDNA copies a person has.

This study uncovers a previously overlooked source of genetic variation that shapes human traits such as height and weight, while also highlighting the ribosome as an unexpected contributor to human diversity. 

Francisco Rodriguez-Algarra et al, Germline sequence variation within the ribosomal DNA is associated with human complex traits, Cell Genomics (2026). DOI: 10.1016/j.xgen.2026.101213

Nature might have a universal rhythm

Animal communication can look wildly different—flashing lights, chirping calls, croaking songs and elaborate dances. But new research suggests many of these signals share a surprising feature: They repeat at nearly the same tempo.

In a new study, scientists found that communication signals across a wide range of species tend to repeat at about 2 hertz, or roughly two beats per second.

The researchers propose this tempo might reflect a shared biological constraint. Animal brains, including humans, may be naturally tuned to process signals arriving at that pace. In other words, two beats per second may be a rhythmic "sweet spot" that enables brains to detect signals more easily and process communication more efficiently.

Understanding this potentially universal tempo could help scientists better interpret animal signaling and social behaviour across species. The findings also hint that human perception of rhythms, including beats in popular music and the cadence of speech, may arise from the same neural timing principles found throughout nature.

The study grew out of the researchers' project to understand how synchrony arises in nature. 

 They noticed that the flashing of the fireflies and the chirping of the nearby crickets were in sync with each other and they thought that it was crazy that these two unrelated species would interact in such a way.

After analyzing their own recordings, the team concluded that the species were not synchronizing with one another. Instead, they were sending independent signals at very similar tempos—around two-to-three pulses per second.

To investigate whether the firefly-cricket coincidence reflected a broader pattern, they analyzed previously published studies of animal communication across a wide range of species. These rhythmic signals included: firefly flashes, cricket chirps, frog calls, birds' mating displays, sound and light pulses from fish and vocals and gestures from mammals.

Despite enormous differences in body sizes, habitats and communication methods, the team found that many species repeat signals within a narrow range of roughly 0.5 to 4 hertz (1 to 4 beats per second). The pattern spans animals that communicate through sound, light or movement, suggesting a common underlying principle.

Earlier biophysicists noted that the biophysics of a single neuron operates at the same rhythm. Neurons require time to integrate information before firing again. Because of this biological constraint, neural circuits tend to respond most strongly to signals arriving every few hundred milliseconds—roughly two times per second.

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To test this idea, the team built computer models of simple neural circuits and examined how they responded to signals at different tempos. According to the models, the circuits respond most strongly to signals within the same 2 hertz range observed across animal communication. That means communication signals may have evolved to match the rhythms that brains process most easily.

Musicologists have long noted that popular songs cluster around 120 beats per minute, which is exactly 2 hertz. That rhythm fits our body.

Guy Amichay et al, A widespread animal communication tempo may resonate with the receiver's brain, PLOS Biology (2026). DOI: 10.1371/journal.pbio.3003735

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Birds that put more energy into parenthood age faster and die younger, research shows

In a new study, appearing in Proceedings of the Royal Society B: Biological Sciences, scientists selectively bred Japanese quails into two groups: laying either relatively large or small eggs. As the quails don't do much "parenting" after eggs hatch, mothers' main contribution is the resources they transfer to their eggs (chicks from larger eggs are more likely to survive).

After five to six generations of selective breeding, females bred to lay larger eggs aged faster and died about 20% younger than females bred for small eggs.

The findings of the study support a fundamental evolutionary theory: that high "investment" in offspring unavoidably leads to faster aging and a shorter life.

All living things have limited energy and resources, and face trade-offs between competing priorities.

Artificial selection for increased reproductive effort accelerates actuarial senescence and reduces lifespan in a precocial bird., Proceedings of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rspb.2025.2908

Scientists develop 'light switch' for the love hormone

Researchers have developed a molecular "light switch" for the so-called love hormone oxytocin, offering new insights into how social behaviour, partnership bonding, emotions, and mental health are wired in the brain.
A light used at a specific wavelength releases neuropeptides, enabling researchers to observe their effects on individual synapses, neurons, and neuronal circuits.

Oxytocin plays a key role in social connections, including trust, bonding, parenting, emotional regulation, empathy, learning and memory. Changes in oxytocin signaling are also linked to conditions including autism, anxiety, depression, addiction, post-traumatic stress disorder, schizophrenia and psychotic disorders.
A molecular light-activated probe enables precise, localized release of oxytocin and vasopressin in the brain, allowing real-time observation of their effects on specific neurons and circuits. This approach overcomes previous limitations in studying neuropeptide signalling, facilitating detailed investigation of social behaviour mechanisms and potential development of targeted therapies.

Konstantin Raabe et al, Photocaged Oxytocin and Vasopressin Probes to Decipher Neuropeptide Signalling With High Spatiotemporal Resolution, Angewandte Chemie International Edition (2026). DOI: 10.1002/anie.202513373

Popular AI chatbots are confidently dispensing medical misinformation, analysis shows

Fifty percent of medical responses from five popular AI chatbots were problematic, with 20% highly problematic and 30% somewhat problematic, especially for open-ended prompts. Chatbots performed best on vaccines and cancer, worst on stem cells, athletic performance, and nutrition, and often provided confident but inaccurate or incomplete information with poor reference quality and difficult readability.

Generative artificial intelligence-driven chatbots and medical misinformation: an accuracy, referencing and readability audit, BMJ Open (2026). DOI: 10.1136/bmjopen-2025-112695