Most people are unaware of the environmental effects of sunscreen

UV filter compounds enter the marine environment directly or indirectly. Direct pathways include swimming or other water-based recreational activities, and indirect pathways include washing towels that have been used to dry sunscreen-coated skin, washing off residue during showering and even in urine.

Traditional sewage and water treatment technologies cannot effectively remove most UV filters, and organic UV filters have been reported in 95% of wastewater effluents and 86% of surface waters globally. They have also been detected in marine environments worldwide, from busy tourist locations to remote areas such as Antarctica and the Arctic, highlighting the extent of this contamination.

UV filter pollution has also been linked with agricultural practices, where recycled wastewater and sludge biosolids used as fertilizers can transfer UV filters onto crops and into runoff that eventually reaches rivers and coastal waters.

New research has revealed a striking gap in awareness about the environmental impacts of sunscreen, with more than half of people never having considered that the products they use to protect their skin from the sun's rays could be harmful once they enter the ocean.
That is despite extensive scientific evidence showing that sunscreen ingredients—particularly ultraviolet (UV) filters—can pose a number of risks to marine organisms, including fish, algae and coral reefs.

The research also showed that more than 8 out of 10 people were unaware of the existence of reef-safe sunscreen, an unregulated marketing term often used by brands to imply reduced harm to marine life, despite this not always being the case. This inconsistency is another issue explored within the study.
The researchers say their findings highlight a clear gap between scientific evidence and public awareness and have direct implications for future marine policy and regulation, product labeling and consumer guidance.

That, they add, is because public opinions are essential in encouraging manufacturers to develop choices that balance human and environmental safety.
A key piece of data is that 55% of participants had never considered that sunscreen may be harmful to the marine environment. This demonstrates just how vital clear and accessible communication is in bridging the gap between research and public awareness.
In the study, 281 participants voluntarily responded to a set of five questions on the topic, and 89% reported using sunscreen at some point within the year. However, 81% were unfamiliar with the term reef-safe, and 55% had never considered sunscreens harmful to the marine environment.
The researchers say these findings emphasize the need for clear public messaging and more transparent and regulated product information.

Anneliese A. Hodge et al, User habits and public perceptions of sunscreen pollution: A global review and case study of Britain's Ocean City, Marine Policy (2026). DOI: 10.1016/j.marpol.2026.107244

One million years without sex fails to erase stick insects' unused biological system
In Timema stick insects reproducing asexually for ~1 million years, X-chromosome dosage compensation remains functional in rare males. Its persistence despite prolonged absence of sexual reproduction indicates that sex-chromosome regulatory mechanisms may not rapidly decay after their original selective role is removed.

Darren J. Parker et al, Dosage compensation and meiotic sex chromosome inactivation are maintained under relaxed selection, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2531501123

Why a doctor saying 'it's normal' can backfire

A new study suggests that when physicians try to reassure patients by saying their symptoms are "normal," patients may infer that treatment isn't necessary—and become less inclined to seek it. Doctors may think they're saying "Don't panic." But many patients hear "Don't bother" instead.
Doctors use "normal," it seems, to mean common and well understood. Patients often interpret it as meaning acceptable—or not worth treating.
Published in Nature Human Behaviour, the findings of 14 experiments involving 9,371 participants and a wide range of health conditions, from menopause and migraines to dental pain, seasonal allergies and elevated blood glucose levels.

The findings come amid broader conversations about patients feeling dismissed in health care settings, sometimes described as "medical gaslighting." The study identifies a communication gap that may contribute to those experiences, even when doctors are trying to help.

The good news is that miscommunication isn't inevitable. The researchers also tested two simple ways to reduce it: pairing normalizing language with an explicit recommendation for treatment and explaining that "normal" was meant in a statistical, not normative or prescriptive, sense.

Both approaches helped close the communication gap.
The key takeaway for patients: If you're unsure what your doctor means when they say a symptom is "normal," don't assume it means treatment isn't recommended and you should just live with it. Ask.

Common symptoms can still deserve attention—and treatment.

Seyi Lawal et al, Reassurance through normalization inadvertently suppresses treatment, Nature Human Behaviour (2026). DOI: 10.1038/s41562-026-02542-0

Genome study reveals centromeres as one of the fastest-changing regions in human DNA
A centromere is a specific region on a chromosome that ensures that, when a cell divides, the chromosome separates accurately so each new cell receives the correct amount of genetic material. Despite their essential role, centromeres remain one of the last major blind spots in the human genome.

A recent study published in Nature set out to reveal what had been hidden inside human centromeres, using advanced long-read sequencing and custom-built computational tools to piece together 2,110 complete centromeres. The researchers sampled individuals from 28 population groups across five continents, then compared their centromeres with 5,747 assembled by the Human Pangenome Reference Consortium to trace how these regions differ and evolve.

They discovered 226 major centromere haplotypes—distinct genetic patterns—and 1,870 new genetic variants. By studying a four-generation family, they were able to follow centromeres as they changed from parent to child, tracking genetic changes across generations.
They discovered that centromeres mutated faster than any other part of the human genome, with certain chromosomes accumulating changes at up to 20 times the rate of others.

The kinetochore attachment site, the anchor point where the chromosome attaches to the cell machinery during division, mutated faster than any other part.
The results revealed that centromeres have far more genetic and structural diversity than previously appreciated. When a cell divides, it attaches each chromosome to a protein handle called a kinetochore. For years, scientists assumed there was only one handle per chromosome.

This sequencing found that some centromeres break that rule: Around 6% have two kinetochores, and about 1% have three. Even more importantly, these multi-handled centromeres run in families, passing from parents to children across generations.

While mapping centromeres, the researchers noticed something remarkable: On chromosomes 10 and 21, some people carried centromeres that were separated by more than a million years of evolution from the other modern versions.

Comparing these sequences with ancient genomes indicated that modern humans outside Africa might have inherited these unique centromeres from ancient human relatives through interbreeding with Neanderthals and Denisovans.
Based on the findings, the researchers proposed a kind of evolutionary tug-of-war between centromere DNA and its binding proteins. The anchor point mutates so often that they keep changing both the DNA sequence and the chemical markers that control how it's used, driving rapid evolution in these critical regions of our genome.

Shenghan Gao et al, A global view of human centromere variation and evolution, Nature (2026). DOI: 10.1038/s41586-026-10841-9

Female Brains Wake Up from Anesthesia Differently Than Male Brains
Ketamine anesthesia drives female-specific microglial activity in mice, offering insight about the anesthetic and highlighting the need to study sex as a biological variable.
All over the world, doctors perform more than 300 million surgeries each year. While some procedures require local anesthetics, other ones and people undergoing them go under general anesthesia .
While doctors must ensure that patients go under anesthesia for the procedure, it is equally important that they wake up after the surgery. Researchers have previously found that male and female animals respond differently to the general anesthetic ketamine, but they did not fully understand its underlying molecular basis.
Now, scientists found that sex differences in ketamine recovery arise due to distinct dynamics of neurons and immune cells called microglia in male and female brains. Their findings, published in Science Advances, offer a deeper understanding of ketamine anesthesia recovery and highlight the need to study sex as a biological variable.

https://www.science.org/doi/10.1126/sciadv.adz6517

Growing rice on the moon

The Moon's surface is a tough place to farm. It has no organic material, and the nitrogen sources that plants need, like ammonia and nitrate, are essentially absent.

Scientists in Japan have created a portable plasma device that can turn air into fertilizer, helping rice grow in simulated lunar soil.

It may sound like science fiction, but a team of researchers from Japan have made it possible to harvest fresh rice on lunar soil. 

The researchers developed a portable plasma device that converts ordinary air into nitrogen fertilizer, When applied to soil designed to simulate the Moon's surface, it neutralized the soil's harsh alkalinity and released trapped nutrients like calcium, magnesium and potassium. This enabled the researchers to grow rice seedlings in the lunar soil.

Beyond its off-world potential, the researchers note that their low-power, fossil-fuel-free technology could help make farming on Earth more sustainable too. 

https://www.nature.com/articles/s41526-026-00602-3

Too Cool To Care? Air Conditioning Weakens Climate Action Support: behavioural insulation

Study finds that the more people rely on air conditioning to stay cool, the less likely they are to support broader efforts to cool cities and cut energy use.
As global temperatures rise, air conditioning has become essential to protect people from extreme heat. But a new study has found that widespread reliance on private cooling may be creating a paradox in cities: the more effectively households cool themselves indoors, the less urgency they feel to support the broader climate measures needed to cool cities.
The study has found that households that depend heavily on air conditioning are less likely to adopt energy-saving habits or support community-wide heat mitigation strategies. The findings, published in Sustainable Cities and Society, describe this phenomenon as “behavioural insulation”, where effective indoor cooling dampens the perceived urgency to address heat through collective action.
Heat awareness does not always change behaviour

To explore how people respond to rising temperatures, the researchers analysed survey responses from 967 adults across 416 households in Singapore, together with spatial heat indicators and household electricity consumption records.

The results revealed a clear divide. People who felt more affected by heat were more likely to discuss climate issues and encourage others to act. But this rarely translated into lower household energy use. Those who relied most on air-conditioning tended to consume more electricity and were less likely to adopt energy-saving habits.

One of the key findings is that experiencing heat does not automatically translate into lower-energy behaviour or stronger collective climate action.
The researchers also observed that heavy air-conditioning users showed less support for public heat mitigation measures such as expanding urban greenery, increasing tree cover and improving neighbourhood shading, even while spending more on keeping their own homes cool.
According to the researchers, the findings point to something more systemic than individual indifference — a gradual shift in which widespread private cooling may weaken the behavioural conditions associated with support for collective climate action.
The researchers say they are not arguing against air-conditioning, as cooling is essential for comfort, health and wellbeing. Rather, they argue that cooling should be complemented by urban design strategies which include shading, greening, improved ventilation, reflective building materials and climate-sensitive planning, that reduce outdoor temperatures in the first place.

https://www.sciencedirect.com/science/article/pii/S2210670726003318...

Eye contact may help babies learn
Have you ever noticed how babies get hooked the moment someone makes eye contact with them? That eye contact is not only cute; it may also send a powerful message to a baby. For years, scientists have been investigating whether social messages like eye contact and baby talk do more than engage babies. They may help synchronize babies' brains with adult brain waves. But the biggest question remained: Does it actually help babies learn?
A new study, published in Nature Communications, offers an answer. Scientists found that 9-month-old infants were able to learn a novel language when the face in a video looked directly at them with fully visible eyes.

Using electroencephalography, or EEG, brain scanning, scientists detected a kind of "neural handshake" between the adult's and infant's brains, synchronized through eye contact.
The results showed how vital eye contact may be for babies' learning. When the person in the video made eye contact while their eyes were fully visible, the infants succeeded in learning the invented language. They recognized which combinations of sounds formed "words" and demonstrated this understanding by spending more time looking at novel sound combinations than ones they had heard before.
The findings provide support for a key assumption of developmental psychology: "Adults curate infants' information selection through ostensive marking of valuable content using social cues such as eye contact." In other words, adults not only provide information for infants but also help them select what to learn.

However, when the speaker's eyes were partly obscured by dark glasses or entirely covered by opaque ones, the babies did not learn. It was as if the switch for learning was off. This was not because they stopped paying attention; the babies looked at the screen for roughly the same amount of time whether the speaker's eyes were visible or not.

Although their eyes were glued to the screen, hiding the speaker's eyes appeared to "scramble" the message, and the participants did not acquire the new language.

The intriguing pattern held for all infants, regardless of whether they were from Singapore or the UK. Babies in both groups were selective learners only when learning from a speaker making visible eye contact.
Part 1

What made the visible-eyes videos different? To answer that question, researchers used EEG readings. The adult speaker's EEG readings were recorded in advance during video production, while the babies wore EEG caps as they watched the videos. Analyzing brain signals allowed researchers to determine the degree of matching between the adult's and baby's brain activity.

Researchers found that adult-to-infant neural coupling—the one-way matching of adult brain waves to infant brain waves—predicted the infants' ability to learn. Only adult→infant neural coupling, not the infants' own rhythmic brain activity, predicted learning ability.

"The key insight," the authors point out, "is that speaker-to-listener neural coupling is a better predictor of selective learning than infants' own neural activity." Statistical tests supported this: Once researchers accounted for the strength of adult-to-infant coupling, the direct effect of gaze on learning essentially vanished. In short, eye contact drove a brain-to-brain signal that explained the learning boost.

Wei Zhang et al, Adult-to-infant unidirectional neural coupling mediates selective social learning in infants from the United Kingdom and Singapore, Nature Communications (2026). DOI: 10.1038/s41467-026-75831-x

Part 2

What if there's a star inside a black hole?
A dark-matter halo with an exotic pressure–density relation can mathematically surround a neutron star with an event horizon while leaving the star nonsingular and structured inside. Such configurations exist only within a narrow halo-density range and require dark-matter densities far above expected astrophysical values, so they remain theoretical.

Chen Tan et al, A Neutron Star Hidden Inside a Black Hole, arXiv (2026). DOI: 10.48550/arxiv.2608.06224

Arthritis origins may begin before birth

Researchers have discovered that some joints may be more susceptible to inflammatory arthritis before birth, offering new insight into why rheumatoid arthritis attacks particular joints while sparing others.
"The embryonic origins of site-specific arthritis", published in Nature Immunology, provides new insight into one of the long-standing mysteries of rheumatoid arthritis: why inflammation targets certain joints while leaving others relatively unaffected.

Rheumatoid arthritis is an autoimmune disease that causes pain, swelling and stiffness when the immune system attacks the synovium, the tissue lining the joints. Over time, this inflammation can damage cartilage, bone and surrounding tissues.

The study compared two finger joints that differ in their susceptibility to rheumatoid arthritis. Researchers compared proximal interphalangeal (PIP) joints, which are commonly affected by the disease, and distal interphalangeal (DIP) joints near the fingertips, which are usually spared.

They found that the PIP joints contained larger synovial volumes and higher levels of PI16-positive (PI16+) fibroblasts, a specialized type of connective tissue cell. These differences were established before birth, suggesting that the tissues themselves may play an important role in determining where disease occurs.

The embryonic origins of site-specific arthritis. Credit: NDORMS

Part 1

For decades we have known that rheumatoid arthritis selectively targets particular joints, but one of the great unanswered questions is why?
These new findings suggest that the answer lies not only in the immune system but also in the tissues themselves. The cellular and structural characteristics established during development may help determine where inflammation takes hold later in life.
Researchers found that the developing joints were made up mainly of structural cells, including cartilage-forming cells and fibroblasts, rather than immune cells. They then investigated what drives these cells to develop into their different specialized forms.

One population that drew particular attention was the synovial lining fibroblasts. These cells produce substances that lubricate the joint to help protect and maintain smooth movement, yet they can also behave abnormally in arthritis. Further analysis suggested that the lining may come from two different sources, both the cartilage and surrounding joint fibroblasts.

The process appeared to be influenced by specific localized signals such as low oxygen levels. This may provide insights into the mechanisms driving their function and help identify ways to restore their normal protective role in disease.
The researchers found important differences between the PIP and DIP joints. A bespoke image analysis tool showed that PI16+ fibroblasts that were enriched in the PIP joints were specifically located around blood vessels and at sites where tendons and ligaments connect with surrounding tissue.

They also showed that PI16+ fibroblasts responded differently to inflammatory signals compared with other fibroblast populations. While PI16+ fibroblasts shared a common pro-inflammatory response with PI16- fibroblasts, they also displayed distinct changes in pathways linked to tissue organization and immune regulation.

The team also identified striking structural differences between the joints. Using high-resolution 3D imaging at Diamond Light Source at the Harwell Science and Innovation Campus, they found that the synovial tissue surrounding PIP joints was larger and organized differently from that seen in joints that are not usually affected by rheumatoid arthritis. Together, these cellular and structural differences may help explain why inflammation develops in some locations but not others.
Together, the findings suggest that the tendency of rheumatoid arthritis to affect particular joints may be shaped by tissue architecture established during development. Rather than being determined by immune activity alone, vulnerability to inflammation may depend on the local cellular and structural environment of each joint.

Sarah Davidson et al, The embryonic origins of site-specific arthritis, Nature Immunology (2026). DOI: 10.1038/s41590-026-02542-2

Female gut muscles reshape to meet the demands of reproduction, preclinical study suggests

Organs don't just grow in early life; they can change in response to physiological or environmental challenges in adulthood. Researchers have now identified an active role for the intestinal muscles in remodelling the gut after reproduction.
Reproduction remodels intestinal smooth muscle in female fruit flies and mice, elongating contractile filaments without increasing cell number and reducing contractility. In flies, mating lowers juvenile hormone receptor signalling in muscle, permitting growth, while epithelial growth is promoted by the same hormone. These changes may enhance nutrient absorption during reproduction.

Alessandro Mineo et al, The sex and reproductive plasticity of intestinal muscles instruct gut size, Cell (2026). DOI: 10.1016/j.cell.2026.07.024

A 236-million-year-old fossil challenges the story of mammalian live birth

Some cynodonts may have been giving birth to live young much sooner in evolutionary history than previously assumed. A new Frontiers in Mammal Science study has offered the first compelling evidence that cynodonts may have been viviparous—a reproductive mode characterized by live birth.

Researchers showed for the first time that live birth was present in at least one mammalian ancestor, Chiniquodon theotonicus, which lived approximately 236 million years ago. This implies that viviparity among early cynodonts originated in the mammalian lineage at least 95 to 90 million years earlier than previously thought.

Cynodonts thrived in the Triassic, a period of recovery and restructuring of ecosystems after one of the most devastating mass extinctions in life history. This meant high competition for resources and strong predatory pressures. Combined with a trend toward aridity and strong seasonality, embryos of viviparous species would be better protected than those of egg-laying species.

Until now, giving birth to live young was considered a relatively modern evolutionary acquisition in the mammalian lineage. The finding raises questions about which other traits believed to have appeared much later were already present among cynodonts, the researchers say.

Early Origin of Viviparity in the Mammalian Lineage, Frontiers in Mammal Science (2026). DOI: 10.3389/fmamm.2026.1845319

Nature's original bioplastic may have fed animals for hundreds of millions of years

Long before humans discovered biodegradable plastics, microorganisms had already invented their own. Many bacteria and archaea produce natural bioplastics called polyhydroxyalkanoates (PHAs), storing them inside their cells as reserves of carbon and energy.
Until now, scientists thought that only microorganisms themselves could break down these substances. Researchers at the Max Planck Institute for Marine Microbiology in Bremen, Germany, have now overturned that long-standing assumption.

In a study published in Nature Ecology & Evolution, they show that animals ranging from marine worms and starfish to terrestrial species, including earthworms, have enzymes capable of degrading microbial PHAs. The findings reveal a previously overlooked way in which microbial carbon can enter animal food webs.
Microbial PHAs occur naturally in soils, sediments and aquatic environments worldwide. They are produced whenever microorganisms store excess carbon for later use and are among the few naturally occurring plastics that are completely biodegradable. Because PHAs are increasingly manufactured as sustainable alternatives to conventional plastics, understanding how they are degraded in nature has become an important area of research.
The new findings suggest that animals, together with microorganisms, may contribute to the breakdown of these natural bioplastics. More fundamentally, they reveal that animals can exploit a microbial carbon reserve that had previously been thought to be inaccessible to them.

Animal degradation of microbial storage polyhydroxyalkanoates, Nature Ecology & Evolution (2026). DOI: 10.1038/s41559-026-03153-8

**

Fungal age remains elusive as underground networks continually grow, split and recycle
Fungal age is difficult to define because mycelial networks continually grow, recycle tissue and fragment into genetically identical units. Longevity likely varies among species and lifestyles, requiring genetic tracking, long-term experiments and microfluidic systems to characterize persistence and life cycles.

Exploring the concept of longevity in fungi, Trends in Microbiology (2026). DOI: 10.1016/j.tim.2026.07.001

Fridge-free vaccines

Scientists have successfully trialled vaccines that do not need to be refrigerated or frozen, which could slash the number of vaccine doses that are wasted each year. Sixty volunteers received a tetanus-diphtheria vaccine that had been kept as a dry powder for a year at room temperature before it was dissolved and injected. The jab was “safe and well tolerated” and gave “equivalent” immune responses to the conventional vaccine. The team will launch a larger trial of 160 people in the coming months.

https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(26)00369-X/fulltext?utm_source=Live+Audience&utm_campaign=e2b449d6f7-nature-briefing-translational-research-20260812&utm_medium=email&utm_term=0_-928f7c52f0-50323416

AI agents struggle to perform original scientific research

Among the many predictions about the future of artificial intelligence is that models will one day be able to conduct scientific research on their own, leaving humans out of the equation. Already, they can write code, run experiments and search scientific literature, but carrying out open-ended research would require a significant leap in ability.
In a paper posted on the arXiv preprint server, researchers tested AI's ability to conduct open-ended research and found that it came up short.
The study authors gave frontier agents (cutting-edge, state-of-the-art AI tools designed to carry out complex, multi-step tasks autonomously) six days to conduct research and write papers based on two then-unpublished AI conference submissions. This ensured they couldn't just find the answers online.

The agents had full access to the internet, dedicated computing power and approximately $3,000 in model-use credits, meaning they had a budget to conduct open-ended exploration and run experiments. The topics they had to research and write about were the structure and controllability of language-model personas and designing a detector for distribution shifts in tabular foundation models.

Once the six days were up, human researchers reviewed the AI-written papers and graded them as they would papers submitted to a top-tier AI conference.

The frontier agents did not do well at all. Both papers received unambiguous rejection scores (2/6 and 1/6 overall) from the expert human reviewers. Although the AI understood the research questions and proposed some directions that closely mirrored those of the original researchers, its scientific reasoning suffered from major flaws. Experimental designs were weak, and the agents handled negative feedback poorly, often adding caveats to existing findings rather than redesigning their studies.

They also managed their time poorly and spent less than half of their allocated API budget. Despite having time, they rushed through their work and submitted papers that fell far short of publishable standards.

The reviewers did not hold back on their assessments of the agents:

"The experiments and methodological choices were bizarre and hard to understand. The results seem clearly a result of post hoc choices."—David Africa, expert reviewer.
"Upon testing a few unsuccessful signals using a PFN's internals, going from there to 'there are no signals we can use that leverage a model's internals' is a huge leap, a kind of 'proof by example' fallacy that is highly non-scientific."—Viet Nguyen, expert reviewer.
While these results are a sobering reality check on AI's ability to perform scientific research, they do not mean models have no place in the lab. In the near term, they are more likely to serve as assistants handling routine tasks rather than being deeply involved in the process of discovery.

Peter Kirgis et al, Can AI agents conduct open-ended AI research? Early evidence from two case studies, arXiv (2026). DOI: 10.48550/arxiv.2607.27191

Curiosity has its own neural signal: Brain separates valuable information from water rewards in mice
Often, humans and other animals seek information that can help them complete tasks and attain desired rewards. In some cases, however, they seek information driven simply by curiosity and a desire to obtain knowledge for its own sake, even if it does not lead to external rewards. Scientists know this better.
Researchers recently created a new experimental paradigm for studying the neural processes associated with curiosity and the desire for knowledge in mice. This paradigm, outlined in a paper in Nature Neuroscience, allowed them to gain new insights into how the brain represents the value of information regardless of physical rewards.
Previous studies offered some initial clues about how the mammalian brain attributes value to information. However, the process through which it recognizes stimuli that can provide interesting information and represents their value has not yet been elucidated.

This is a higher-order process of cognition, since what is most valuable as information depends on what we already know, and we can't detect and know how good information is by physiological processes in our body, the way we can with food or many other better understood types of reward that motivate our actions.
Researchers offered thirsty mice the choice of poking their noses into two holes.
One hole revealed with a short puff of odor whether they would receive a water reward, and the other revealed nothing but, critically, offered them the exact same chance and amount of water. Prior to making their decision, the mice had to poke in a third hole that presented them with an odor that either directed them to the information- or non-information-providing hole or offered them the choice. In this way, the mice learned that individual odors each predicted a certain amount of information or water reward.
Interestingly, the researchers observed that the mice predominantly preferred poking their noses into the hole that gave them information. This occurred even if the information-providing hole contained less water than the other hole. These findings suggest that mice are often willing to exchange water (i.e., a reward) for information. This, in turn, implies that the mice attribute value to the information itself.
Part 1

As the mice were learning this behavioral task, the researchers recorded their brain activity using miniaturized microendoscopes. These are ultrathin, lightweight imaging devices that can measure activity in hundreds of neurons simultaneously. The team observed activation patterns in the orbitofrontal cortex (OFC), a brain region involved in evaluating decisions guided by reward value.
The researchers chose to look at the orbitofrontal cortex because it has been shown to represent the value of options when humans and other animals are making decisions and previous experiments using mice had shown that it represents reward value that is signaled by odors in particular.
To understand how the brain represents the prospect of obtaining information, the researchers compared cases in which, based on the odor they sniffed, the mice expected to receive information with trials in which the reward outcome would remain unknown.

They identified a representation of the predicted value of information in the mouse orbitofrontal cortex.
Approximately 20% of the cells in the OFC showed different neural activity in response to odors that predicted information versus those that predicted no information, and the magnitude of that activity difference scaled with the duration of time the mice had knowledge of the reward outcome. This indicates that they identified a representation of information value that depended on its resolution of uncertainty, which is intrinsic to information and cognition.
The team's findings suggest that the mouse brain processes a desire for knowledge and the drive for physiological rewards differently.

The representation of the predicted value of information was discernible across the neural population in a way that was orthogonal to the representation of the predicted water value, which they observed in response to separate odors in their experiments. Given that they observed this pattern in the OFC, a brain area intimately involved in generating representations of the world to guide decisions, the representation of information value could be a critical signal that allows animals to take actions to gain information and increase their knowledge of the world.
The researchers pursued neural processes underlying curiosity and the drive to seek knowledge, with the goal that their work will also be applicable to humans.
Understanding how we evaluate sources of information and how wanting to gain knowledge drives our behaviour would have important implications for helping people navigate our information-rich modern world, including through learning during childhood development.
Not only could a better understanding of curiosity, the drive to gain information, improve people's success in learning, given the pleasurable, rewarding nature of acquiring knowledge, it could offer us access to more joy and fulfillment—something we all could use.

Jennifer J. Bussell et al, Representations of the intrinsic value of information in mouse orbitofrontal cortex, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02377-y.

Part 2

Cells use a little-known molecule to protect themselves from iron overload

Iron is essential. Our cells need it to produce energy, carry oxygen throughout the body and power countless chemical reactions that sustain life. But this metal has a dark side. When too much of it is left free inside cells, it can trigger destructive reactions that break down DNA, proteins and even cell membranes.
Now researchers have discovered that cells rely on an unexpected protector against this threat: small molecules called polyamines.

The researchers' detailed findings, published in the journal Cell, reveal that polyamines act like storage lockers for iron, safely holding the metal in a nonreactive state until cells need it.
These findings solve a decades-old mystery about why cells maintain such extraordinarily high levels of polyamines and uncover a previously unknown defense mechanism that protects cells from toxic iron overload.

This work could also help scientists develop better cancer treatments by allowing iron overload to trigger cancer cell death. It could also offer new clues about diseases like early-onset Parkinson's disease, in which mutations affect polyamine levels within neurons.

Polyamines buffer labile iron to suppress ferroptosis, Cell (2026). DOI: 10.1016/j.cell.2026.07.040. www.cell.com/cell/fulltext/S0092-8674(26)00872-X

Organs age at different speeds: A blood test might soon tell which ones

Some people seem to age more slowly than others, looking and acting like 45 at 60. Others appear to have gotten ahead of the calendar. But why is that, and what is actually happening inside the body?
AI-based "tissue clocks" can estimate the biological age of human organs from histological images, researchers showed. By analyzing more than 25,000 tissue samples across 40 tissue types, their study reveals that organs age at different rates throughout life and that these changes can even be detected from blood samples. The findings, published in Nature Medicine, provide a new framework for understanding aging and may open new avenues for disease monitoring and early diagnosis.
the researchers turned to the Genotype-Tissue Expression Project (GTEx), which collected tissue samples from 983 individuals across 40 different tissue types, ranging from the brain and heart to the lung, pancreas, skin and intestine. These were transformed into high-resolution digital images of tissue slices, each revealing the microscopic architecture of the organ in question. The scale is staggering: 25,712 images, representing about 480 million individual image tiles, analyzed with state-of-the-art vision models.

They found that the architecture of organs keeps a silent diary of time: Even without explicitly teaching the AI about it, age turned out to be the single strongest factor shaping tissue appearance across all 40 tissue types. Building on this, the research team developed so-called "tissue clocks"—predictive models that estimate a person's biological age from the appearance of their tissue, for each organ independently.

These clocks achieved a mean prediction error of just 4.9 years and outperformed existing DNA-based aging estimates in capturing tissue-specific pathology. Importantly, the predicted biological age was strongly linked to known hallmarks of aging, including telomere shortening, tissue pathology and the number of chronic diseases an individual had.
Part 1

Our tissues carry a remarkably detailed record of the aging process.
By combining histology images with artificial intelligence, we can detect patterns of biological aging that are invisible to the human eye and begin to understand how aging unfolds differently across the body.
The analysis revealed that aging does not occur uniformly: Some tissues, such as the lung, kidney, pancreas and adrenal gland, showed signs of accelerated aging between the ages of 20 and 40. Others followed more complex trajectories, with peaks of accelerated aging appearing later in life. The uterus displayed a particularly striking shift around the age of menopause.

The researchers also identified strong links between tissue-specific aging and medical conditions or lifestyle-associated factors. For example, kidney failure was associated with accelerated aging signals in multiple tissues, while diabetes showed pronounced effects in the pancreas.

What stands out is how differently each organ ages, and how that shows up in tissue architecture.
Deep learning lets us read these spatial patterns, capturing aging as architectural remodelling, not just molecular drift. While the tissue clocks captured the normal pace of aging across organs, they also highlighted outliers—individuals whose tissues showed pronounced structural shifts ahead of their chronological age.
However, tissue samples cannot always be collected. By linking blood-based gene expression profiles with the histologically derived tissue age gaps of the same individuals, the researchers built predictors of tissue-specific biological age from blood samples alone.
These blood-based predictors successfully identified aging patterns linked to several diseases, including Alzheimer's disease, Crohn's disease, cystic fibrosis, vasculitis, diabetes and stroke. In Alzheimer's disease, for example, the strongest aging signal was detected specifically in the brain, whereas Crohn's disease showed accelerated aging across the gastrointestinal tract.

Histological aging signatures for monitoring tissue-specific aging and disease, Nature Medicine (2026). DOI: 10.1038/s41591-026-04566-5

Part 2

What are chalk streams and why are these rare rivers under threat?
Chalk streams are groundwater-fed rivers with clear, cool, mineral-rich water and stable flows; seasonal headwaters called winterbournes support specialised aquatic and terrestrial species. Their biodiversity is threatened by water abstraction, pollution, channel modification, drought and heat. Reducing pollution and restoring natural flows can improve resilience.

What happens when someone's chromosomes, sex hormones and body don't align?
Differences of sex development arise when chromosomes, gonads, hormone production, or hormone responsiveness diverge from typical pathways. Conditions such as congenital adrenal hyperplasia, androgen insensitivity, 5-alpha-reductase deficiency, and sex-chromosome variations can affect anatomy, puberty, fertility, and health. Individualized specialist care, clear information, and psychological support are important.

original article.

Boiling Liquid Does Something in Near-Zero Gravity
Out in deep, dark depths of space, electronics and fuel can still get hot – very hot.

As plans are made for longer missions and more advanced tech systems, one of the key areas scientists want to understand better is what happens to ultra-cold, cryogenic liquids when they boil.

These liquids are used as rocket fuel and to cool electronics, for example, but at the moment, we don't know enough about their boiling behavior in microgravity.

A new study investigating just that, in a series of airborne experiments, has turned up some surprising results. The findings are published in npj Microgravity

We know boiling liquids behave strangely in space; we've seen it happen before.
With less gravity, convection doesn't circulate heat through liquids as readily. And bubbles don't detach from surfaces as easily; they are less buoyant, so they don't float up as they do on Earth.
So it might reasonably be assumed that low gravity would also reduce the cooling capacity of those space bubbles because they can't carry heat away as fast.

But the researchers found the opposite: reduced gravity improved heat removal under certain conditions.

That is, until a heat threshold was exceeded and boiling became unstable.
Researcher s found that bubbles started forming sooner, and heat transfer was improved under near-zero-gravity conditions. The researchers think it's because in microgravity, the bubbles stick closer to the heated surface, which improves heat removal efficiency.
Their hypothesis is that bubbles stop floating away, so they linger on the surface.
When bubbles are on the surface, there is a small liquid gap between the bubble and the heater, and that liquid layer is so thin that it can improve heat transfer.
While that sounds beneficial, the cooling systems reached their limit faster in the simulated space conditions.

The maximum amount of heat that the liquid nitrogen coolant could handle dropped by 65 percent in microgravity compared to the lab tests.

Part 1

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Essentially, the lingering bubbles begin to link together, dry out the surface faster, and cause the cooling mechanism to collapse. Reduced gravity is an advantage for heat transfer, right up until it isn't.

There are limitations to consider here: only nitrogen was tested, and on short parabolic flights.

However, the data gathered will be useful for future modeling as researchers devise equipment for more efficient, safer space travel.

https://www.nature.com/articles/s41526-026-00631-y

Part 2

A Common Plastic Increases Risk of Fatty Liver Disease

One of the world's most common plastics – used in food packaging, plastic wraps, storage containers, and takeaway cups – may be partially responsible for your risk of fatty liver disease.

The disease, as we know it today, was first described in 1980.

But physicians have known since the 19th century that fatty infiltration of the liver is somehow related to diet, long before formal studies began.

A new study in mice suggests modern food conveniences might be adding to the problem.
People often aren't aware they have fatty liver disease (the non-alcoholic kind) until it is detected incidentally when they get a scan for some other condition.

When people do experience symptoms, they may present with fatigue, feeling generally unwell, and discomfort under the right side of their ribs.

Excess fat builds up in the liver cells, which can eventually lead to inflammation, then fibrosis (an accumulation of scar tissue), and even cirrhosis (serious damage), if untreated.
You're more at risk for fatty liver disease if you're carrying extra weight, especially around the middle.

Other risk factors include high blood fat levels (LDL cholesterol or triglycerides), type 2 diabetes or prediabetes, and high blood pressure.
All of these risk factors involve food and metabolism, but a new study in mice shows there may be an important aspect of people's diets that has been overlooked: exposure to microplastics, specifically polyethylene.

It's one of the most important plastics for food convenience: it packages takeaways, cling-wraps leftovers, stops your single-use cup from dissolving in your hand.

And, compared to many other polymers, polyethylene has kind of been considered a lesser concern.
Studies suggest that microscopic polyethylene can trigger signs of fatty liver disease, even with a standard diet. Regardless of diet, the addition of microplastics appeared to exacerbate the condition – even among the mice who ate a relatively healthy diet.
Part 1

Levels of ALT, an enzyme indicative of poor liver health, and liver triglycerides were higher in both groups of mice in the experiments whose diets were laced with microplastics than in animals fed the same corresponding diet without polyethylene.

The same went for liver cell inflammation and ballooning, and steatosis (fat buildup in the liver).
Genes encoding proteins PPAR-alpha (which regulates liver fat production) and Annexin A2 (which, in the liver, is involved with tissue repair) were both in overdrive in the microplastics-affected livers.

https://www.science.org/doi/10.1126/sciadv.aec8681

Part 2

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Faecal transplant soothes peanut allergy
Six people with a severe peanut allergy can tolerate the nut after a transplant of gut bacteria from the stool of people without the allergy. Four months after the transplant, five participants could eat 600 milligrams or more of peanut protein — the equivalent of about two and a half peanuts — without triggering a severe immune response. The potential of this type of therapy to have a lasting benefit is really, really exciting, because available treatments for food allergies are limited and short-lived.

https://www.science.org/doi/10.1126/scitranslmed.aee3263

Taking screenshots makes you more likely to forget information

Snapping a photo or taking a screenshot to remember something? According to recent cognitive research, the practice may make you more likely to forget.

Research has consistently shown that if you take photographs or screenshots during an experience, your memory of the information or event is degraded.

Taking photos or screenshots can impair memory for captured information, particularly when images are not later reviewed. Across seven experiments, capture showed no memory benefit and was associated with poorer recall and source memory. Divided attention, cognitive offloading, and attentional disengagement may contribute.

Known as the photo-taking impairment effect, the phenomenon occurs for material that the picture-taker doesn't review afterward. According to other research, using photographs to retrieve and review memories may benefit long-term retention.
However, many of us take more photos and screenshots than we can use—about 20 photos a day, with about 2,000 photos stored on the average smartphone, according to estimates.

Unless you are actively reviewing those images as cues for elaborative memory retrieval, it is unlikely to benefit you.

Another study suggests that our memory isn't impaired when photographs are captured automatically using a wearable clip camera. This indicates that there's something about the act of taking a photo or capturing a screenshot that impairs memory, rather than the knowledge that something is being saved.
One possible mechanism behind digital amnesia is divided attention: The act of capturing an experience takes away cognitive resources that would otherwise be dedicated to encoding the information in memory. While divided attention plays a role, it's unlikely to be the main source of memory impairment. People show a comparable deficit when extra time is provided to view artwork before or after taking a photograph and when the capture task is made less difficult, which should minimize its effects.

Another possibility is cognitive offloading, in which we do not allocate cognitive resources to remember information if it's stored externally. Offloading allows us to redirect those conserved cognitive resources toward aspects of an experience that weren't captured or toward unrelated tasks.

Individuals should only employ the strategy if the information is reliably saved and accessible. However, research has shown that memory remained impaired even when picture-takers knew their images would be immediately deleted. With screenshots in particular, people were less likely to remember whether they captured an image or viewed a piece of art, and had worse memory for the art itself when it was captured.

A third hypothesis is attentional disengagement, in which the act of taking a photograph or screenshot causes us to unconsciously distance ourselves from the experience.
This unconscious detachment may be sparked by a longstanding association between capturing images and the ability to offload information.
Part 1

A better option for remembering information: Break out a pen and paper. Writing something down—for example, taking notes during a lecture—forces us to process and organize the information into manageable bullet points and draw connections. Known as "desirable difficulty," the mental effort in this kind of processing may make us more likely to remember the information.

However, it's not foolproof; sometimes, writing something down can lead to cognitive offloading—such as forgetting a friend's birthday after we add it to our calendar and set reminders. Like the phone numbers in your contact list, you may no longer be able to remember the specific information.

Screenshotting can potentially supplement your memory if you take only a few intentional shots and review them later—similar to how a calendar reminder can support your memory of an upcoming event. But taking frequent screenshots and letting them accumulate unreviewed has the opposite effect, research shows.
The results of the current study suggest that we are likely harming our memory for information and experiences with the press of a button, and that this impairment may even extend beyond what is captured.

Sophia P. Fabrizio et al, Digital amnesia: The aftermath of a screenshot, Memory & Cognition (2026). DOI: 10.3758/s13421-026-01921-2

Part 2

Scientists have designed a functioning virus from scratch using AI. What you need to know
AI-generated genomes for the bacteriophage ΦX174 produced 16 functional phages among 285 synthesized designs, demonstrating that sequence models can generate viable viral genomes based on existing biological patterns. The system remains limited to a simple bacteriophage; clinical phage applications and biosecurity require further validation and oversight.

original article.

Can vitamin C cure a cold? How a Nobel Prize winner convinced us it could
Vitamin C does not prevent colds in the general population or help when started after symptoms begin. Regular supplementation may modestly reduce severe symptom duration and severity, with greater effects in athletes and military personnel. High doses can cause gastrointestinal effects, kidney-stone risk, increased iron absorption, and drug interactions.

original article.

Male Neanderthal pelvises resemble those of modern females, challenging decades-old assumptions
A new study published in Scientific Reports offers an explanation for one of the striking differences between men and women: the evolutionary development of the modern human pelvis.
By comparing Neanderthal pelvises with those of modern humans, the researchers reached a surprising conclusion: The unusual structure of the pelvis may not be that of the Neanderthal, as has been assumed for decades, but rather that of the modern human male.
According to the researchers, the male pelvis evolved into a unique biomechanical shock-absorbing mechanism that stores energy and makes long-distance walking more efficient.
The study is based on a comparison of two nearly complete male Neanderthal pelvises, one from Kebara Cave in Israel and the other from the Sima de los Huesos site in Spain, with dozens of modern human pelvises.

Surprisingly, despite their large size and robust construction, the Neanderthal pelvises were found to resemble those of modern human females in most measurements and proportions rather than those of modern human males.

During every step of bipedal walking, the body's center of mass drops downward. This drop strains the joints and requires energy to raise the body again in preparation for the next step.

According to the new model, the distinctive geometry of the male pelvis enables the thigh muscles to cushion the drop of the body's center of mass, store potential energy during the step and then release that energy immediately afterward—effectively "springing" the body upward into the next step.

In this way, the pelvis functions as a natural shock absorber and energy-return system. It may reduce energy expenditure, improve walking efficiency and thereby provide a significant advantage during long-distance travel on foot. The change in the position of the hip joints also required additional structural adaptations, including the thickening of the pubic bone and deepening of the anterior portion of the pelvis to withstand the new mechanical loads.
Modern human females, by contrast, could not adopt the full suite of these modifications. According to the researchers, the constraints imposed by childbirth require a relatively shallow pelvis and a sufficiently wide birth canal. As a result, the female pelvis remains closer to the ancestral configuration—the same general configuration found in male Neanderthals.
Part 1

The findings of the study change the way we understand the evolution of the human pelvis. It is not the Neanderthal pelvis that is the anomaly requiring explanation. Rather, it is the pelvis of the modern human male. The mechanism that evolved within the human male represents the evolutionary innovation.

The researchers note that the study presents a new biomechanical model that may explain a substantial part of the human pelvis's sexual dimorphism, the anatomical differences between females and males.

Yoel Rak et al, Neandertal pelvis reveals specialized walking apparatus in human males, Scientific Reports (2026). DOI: 10.1038/s41598-026-59915-8

Part 2

Restoring a missing slice of sunshine to indoor light may help prevent myopia

Myopia, or nearsightedness, develops when the eye grows too long from front to back. This prevents images from focusing directly on the retina in the back of the eye, causing distant objects to appear blurry.

Myopia usually begins in childhood and can progress through adolescence. Beyond the need for glasses or contact lenses, high myopia increases the risk of vision-threatening complications later in life, including retinal detachment, glaucoma and macular degeneration.

Research has already shown that the more time children spend playing with screens indoors instead of outdoors, the more likely they are to develop myopia. In fact, some experts predict that nearly 5 billion people (or 50% of the world's population) will be nearsighted by 2050.
Now, a new study led by vision researchers  suggests that myopia can be prevented with improved indoor lighting.

Details were published online Aug. 18, 2026, in Cell Reports Medicine.

The research focuses on indigo light—a short-wavelength light that is abundant in sunlight but poorly represented in standard white LED lighting. In experiments involving tree shrews—an animal model with a human-like visual system—the team demonstrated that exposure to indigo light completely prevented nearsightedness from developing.
The study used tree shrews because their eyes share anatomical and optical features with human eyes.
Part 1

The team used these animals in a series of tests that exposed them to different wavelengths of light while using a biometer to measure eye shape and axial length and an autorefractor to measure refractive changes over time.

Earlier work in mice suggested that violet light near 380 nanometers could suppress myopia and revealed that opsin 5 (OPN5), a light-sensing receptor, was required for this response. But that wavelength did not work in tree shrews because, as in humans, the ocular lens blocks most light below about 400 nanometers.

Human lenses, and now we know tree shrew lenses, don't transmit a lot of light in the ultraviolet spectrum.
The findings support a broader idea that modern indoor life has changed the lighting environment in ways that affect children's eye development. Standard white LEDs typically have a peak around 450 nanometers and emit substantial longer-wavelength light that supports vision. But they provide little of the indigo light that appears to stimulate nonvisual opsins—light-sensitive pathways involved in biological processes beyond image formation.
We evolved outside in the full-spectrum light provided by our sun. When we live inside, we don't get all the wavelengths the eye needs for normal refractive development, and so we get myopia. That's the basic message of this research paper.
One way to prevent myopia would be to encourage children to spend much more time outside, where their eyes can focus across a wider range of near and distant objects while their growing bodies are bathed in full-spectrum sunlight. But reversing the course of our increasingly technical culture appears unlikely.

Another way to prevent myopia would be to improve lighting systems.

Prevention of myopia in a near-primate by supplemental indigo light suggests a hypothesis for the myopia boom, Cell Reports Medicine (2026). DOI: 10.1016/j.xcrm.2026.102999. www.cell.com/cell-reports-medi … 2666-3791(26)00416-7

Part 2

A new mathematical tool to uncover 'who eats whom' in nature

Understanding "who eats whom" is the key to keeping our oceans alive—and our dinner plates full. However, this invisible network that makes up the food chain can unravel with the pull of just one thread. Overfish one species, and its predators starve. Cut off a tiny prey species, and the entire food chain collapses—including us.
The intricacies of this web have remained a mystery because traditional ecological research is almost forensic, incredibly slow and strictly limited to the number of species scientists can physically collect during fieldwork. To find a better way, marine scientists had to look outside the ocean entirely and delve into an unexpected specialty: mathematics.
New research published in Methods in Ecology and Evolution on Aug. 6, 2026, blends marine science and engineering mathematics to solve the "impossible" problem of this chaotic web. The resulting algorithm reconstructed invisible ocean networks with 80% accuracy, essentially turning the invisible visible.
The algorithm reconstructed invisible ocean networks with more than 80% accuracy. Even better, its calculations of the percentage of each prey that predators ate had an error rate of less than 5%. Even when fed "noisy" or imperfect field data, the system remained perfectly steady.

Ettore Barbieri et al, The superposition method for the reconstruction of food webs, Methods in Ecology and Evolution (2026). DOI: 10.1111/2041-210x.70376

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Link between whale calls and special relativity

For a more precise and consistent way to detect the presence of whales, oceanographers rarely rely on sight.
Sound from a fin whale can be heard from 100 kilometers (62 miles) away underwater with a single hydrophone. Because those calls travel so far, we can use them to pinpoint where an animal is by comparing when its sound reaches receivers spread across the seafloor.
But there's a catch: If they were trying to track a nearby whale using just standard physics, they'd probably place the animal in the wrong spot—off by hundreds of meters.

In a paper recently published in the journal Physical Review E, researchers offer a potential explanation for why this occurs: The humble whale call is, improbably, tangled up with the same speed limits Einstein deduced from the universe. Their findings could improve whale tracking for conservationists.
When a whale calls, the sound doesn't take a single path to each receiver. Some of the sound travels directly to a receiver, while some of it ricochets off the ocean surface first, arriving fashionably late.
That delay can put the two signals out of phase, causing them to interfere with one another and shifting when sound appears to arrive at a receiver.
The researchers stumbled onto this while refining a computer program meant to calculate the correct speed of sound for his whale-tracking equations. The results were surprising.

The first time, they got a number that was around 1,000 meters per second, well below the roughly 1,500 meters per second that sound normally travels in seawater. And then, further on, they got values that were sometimes 3,000 meters per second.

After examining the software for a few hours, they discovered that the behaviour wasn't a coding error, but a physical effect caused when a receiver picked up both the direct signal and its reflected echo when a whale was near the ocean's surface.
Physicists call this "temporal interference," the same phenomenon that causes TV broadcasts at your home antenna to fade out because two paths arrive out of phase or out of sync. The interference can also shift the peak of the energy earlier and break the speed limit.

What appears to speed up is not the signal carrying information but the position of the signal's strongest peak. That crucial distinction is the reason their finding aligns with Einstein's theory.

For more than a century, physicists have known that waves can sometimes appear to travel faster than light when their shape changes. But the information encoded in those waves still cannot travel faster than light—the central principle of Einstein's theory of special relativity.

John L. Spiesberger et al, Supersonic and superluminal energy and speed of information via temporal interference in a dispersionless environment, Physical Review E (2026). DOI: 10.1103/1mth-rs2j. On arXiv: arxiv.org/abs/2510.20060

Why do we get sleepy? How neurons control sleep drive

Why does staying awake inevitably make us sleepy? Researchers have identified neuronal populations in the brains of mice that become activated during prolonged wakefulness and are crucial for sleep drive. Their findings provide new insights into how the brain generates the need for sleep.
After a long day or a sleepless night, the urge to sleep becomes almost impossible to resist. This increasing sleep pressure, also known as sleep drive, ensures that prolonged wakefulness is followed by deeper and longer recovery sleep. As sleep is essential for survival, scientists have long been investigating how the brain keeps track of time spent awake and translates it into the need for sleep.
They now have identified specific neurons that are crucial for this balanced relationship between sleep and wakefulness. This is an important missing piece of the puzzle in understanding why we become sleepy.
To identify the brain regions involved, the researchers compared brain activation patterns in mice during normal sleep-wake cycles, sleep deprivation and recovery sleep. This highlighted specific brain areas that reflected time spent awake. Within one of these regions, they further identified two distinct neuronal populations that influence sleep drive: GABAergic and serotonergic neurons in the brainstem. The activation of both neuronal populations increased the longer the animals stayed awake and declined again after sleep onset.

The researchers next asked whether these neuronal populations merely reflect wakefulness or actively generate a compensatory response to sleep. When both populations were artificially activated, mice slept longer and more deeply, displaying a form of recovery sleep that normally follows prolonged wakefulness. In contrast, inhibiting these neurons strongly reduced sleep and allowed animals to maintain alert wakefulness.
These neurons do not simply signal that an animal has been awake. The experiments show that they are crucial to promote sleep, and that they may be key components of the neural circuitry that generates sleep drive. The findings therefore provide one of the clearest demonstrations to date that specific wake-active neurons increase the drive to sleep rather than merely responding to wakefulness.
Further experiments showed that long-term inhibition of the two neuronal populations substantially reduced the need for sleep, with mice sleeping approximately 70% less than usual. Unexpectedly, most of these animals did not exhibit some of the severe behavioural impairments that typically accompany sleep deprivation. In other words, these neurons appear to determine not only how much the animals sleep but also how strongly their need for sleep builds over time.
Understanding how the brain generates sleep drive would provide entirely new opportunities for sleep research.

William Joo et al, Wake-activated neuronal populations that regulate sleep drive., Nature (2026). DOI: 10.1038/s41586-026-10928-3

Is the laundry still damp, or just cold? Why your skin can't tell the difference

Humans lack dedicated wetness receptors; perceived wetness arises from integrated cold, friction, pressure, and contextual sensory signals. Cold dry laundry can mimic dampness because both activate cold receptors. Rubbing, squeezing, visual inspection, or warming fabric can improve discrimination.

original article.

A new transmissible cancer in bullhead catfish
Genomic analysis showed melanoma tumours in brown bullhead catfish are clonally related to each other rather than to their hosts, indicating a transmissible cancer, brown bullhead transmissible melanoma. Historical reports suggest similar lesions may be longstanding and widespread, but their relationship to this disease is unconfirmed.

transmissible cancer.

original article.

Why does salmonella cause serious illness in some people but not others?
Salmonella usually remains in the gut, but some strains can survive within immune cells and spread to the bloodstream, potentially causing sepsis. Severe invasive disease depends on bacterial type and strain, infectious dose, age, immune status and underlying conditions. Hospitalization data may overrepresent severe cases and cannot alone establish unusual strain virulence.

original article.

A smarter antibody could skip the fetus
Researchers have engineered a possible way around the risk some antibody drugs pose in pregnancy. These drugs, used against cancer, autoimmune disease and migraines, are hard to use safely in pregnancy because they are actively carried to the fetus via a receptor called FcRn. But the process has a quirk: mouse models and human tissue showed that the receptor binds to both IgG antibodies — which are used in the majority of approved antibody therapies — and albumin, but only shuttles the antibody across the placenta. By fusing therapeutic antibodies to albumin, the team made drugs that reached the fetus far less and reduced adverse events in mice.

https://www.science.org/doi/10.1126/sciimmunol.aee5151?utm_source=L...

https://www.genengnews.com/topics/drug-discovery/albumin-fused-anti...

Dark energy and quantum gravity may be deeply intertwined

For close to a century, physicists have pursued a way to unite gravity with quantum mechanics. Known as quantum gravity, this goal has remained frustratingly out of reach so far. Similarly elusive is the force of dark energy, which is believed to be driving the universe's accelerating expansion.
But through new research published in Physical Review D, physicists have proposed a new explanation suggesting that these two phenomena might not be separate at all. Instead, dark energy could be a natural side effect of quantum gravity, acting on the geometry of space itself.
Gravity and quantum mechanics shape the universe on vastly different scales: While quantum mechanics concerns the realm of subatomic particles, gravity shapes structures as large as galactic clusters and cosmic filaments.

Individually, both of these theories have been tested to extraordinary precision through decades of painstaking experiments. However, the extreme conditions where both should apply at once, such as inside a black hole, have remained far beyond what any experiment can reach.
In his study, physicists took a different approach: suggesting that we can't pin down both the size and expansion rate of the universe at the same time with perfect accuracy. This limitation is built into the fundamental uncertainty that governs the quantum world: When applied to the universe as a whole, it subtly changes the equations that describe how cosmic expansion should behave over time. This built-in uncertainty could then produce exactly the kind of accelerating expansion that cosmologists currently attribute to dark energy.

Depending on the exact mathematical details, this macroscopic imprint of quantum gravity could also replace the singularity at the instant of the Big Bang, which cosmologists have long struggled to explain. Rather than relying on a point of infinite density, their proposal suggests that the Big Bang followed a gentler rebound from a previously contracting universe.
If this idea is correct, it could provide a far cleaner explanation for the origins of dark energy. In contrast to many existing theories, this would mean that the phenomenon doesn't need to be explained by some hidden particle or exotic field waiting to be discovered: Instead, it is a property of space itself, hiding in plain sight in our observations of the universe.

Savvas M. Koushiappas, Cosmological uncertainty relation and late-universe acceleration, Physical Review D (2026). DOI: 10.1103/zgnd-h2xv. On arXiv: arxiv.org/abs/2604.27771

Simple mouth rinse may help detect stomach and colorectal cancer signals
It's widely understood that the microbiome—especially microbes found in the mouth and the gut—can have a profound effect on health. In a study published in the journal Cell Host & Microbe on Aug. 20, researchers report that by analyzing the makeup of oral microbes, they may be able to detect signals associated with gastric (stomach) and colorectal cancer. These findings could lead to the development of new, less invasive screening tests for gastrointestinal cancers.
Many species of microbes associated with the mouth are also present in the gut and may flourish there. These observations made the researchers

wonder whether oral microbes reach and persist in the gastrointestinal tract differently in people with cancer.
To conduct the study, the researchers recruited 507 volunteers to donate both oral and fecal samples, using a highly standardized collection process. The cohort included 129 healthy individuals; 215 people with metabolic disorders such as metabolic syndrome, hypertension, hyperlipidemia and type 2 diabetes; 77 people with gastric cancer; and 86 people with colorectal cancer. For the volunteers with cancer, samples were collected before the start of any treatment.

The team used gene sequencing to create what they called a mouth-to-feces (MF) index, which measures the extent to which identical microbial sequence variants are found in oral and fecal samples from the same person. They then evaluated how well the MF index could distinguish cancer patients from healthy individuals. The analysis revealed distinct signatures in people with gastric or colorectal cancer.

The findings were more nuanced than a simple cancer-versus-healthy comparison. The MF index was significantly elevated in patients with gastric or colorectal cancer but not in people with metabolic disorders. After accounting for alcohol consumption, regular exercise and BMI, the association remained robust for both gastric and colorectal cancers.
The team also compared the signatures found in the cancer patients with results from fecal occult blood tests, a standard colorectal cancer screening tool that analyzes stool samples. They found higher sensitivity with the oral samples, which were collected by a simple mouth rinse.

"It was notable that cancer-related information could be recovered from oral samples alone," say the researchers. Although only a small fraction of oral bacterial variants were also detected in the gut, models built using only these oral features could distinguish patients with cancer from healthy individuals across several independent cohorts.
In the longer term, combining microbial patterns with genetics, lifestyle and clinical outcomes may help explain why oral microbes persist more readily in some people than in others and may improve individualized risk prediction.

Mouth-to-gut microbial transmission signatures enable robust, non-invasive diagnosis of gastrointestinal cancers, Cell Host & Microbe (2026). DOI: 10.1016/j.chom.2026.07.007. www.cell.com/cell-host-microbe … 1931-3128(26)00308-2

Why immune responses to vaccines vary from person to person

Vaccines protect most people from serious illness, but the strength of that protection can vary considerably from one person to another. A new study helps us understand why.
Before a vaccine ever enters the body, the immune system may already hold clues to how strongly it will respond. In blood samples from more than 4,000 people, researchers measured antibodies against 185 antigens—targets recognized by the immune system, including those from common viruses and bacteria as well as targets associated with autoimmune diseases.

They then used artificial intelligence to analyze patterns in samples collected before and after COVID-19 vaccination, identifying antibody signatures that helped distinguish strong vaccine responders from weak ones.

The research opens a possible path toward more personalized vaccination strategies.
What this study found is that certain biomarkers, when analyzed with AI, can predict who is likely to respond well to a vaccine, even before they receive it. This suggests that some people may be more immune-ready than others.
Usually, scientists evaluate vaccine response after the shot by measuring whether the immune system produces antibodies against the target. Here, the researchers asked a different question: Could patterns already present in the blood predict the response before vaccination?

Age, sex, genetics, prior illnesses and underlying health conditions have all been linked to how strongly people respond to vaccines. People with immune-compromising conditions are often at higher risk of weaker responses. But even within these groups, outcomes can differ sharply.

The new approach is one of the first to use a broad, pre-vaccine antibody "fingerprint" to assess immune readiness. Unlike some prediction methods that rely on genetic analyses, this strategy uses antibody patterns in blood, which may be easier to adapt for clinical use.
Part 1

To test whether that antibody fingerprint could reveal vaccine readiness, the researchers analyzed antibody responses to 185 antigens. These included SARS-CoV-2, the virus that causes COVID-19, other common viruses and bacteria, and targets associated with autoimmune diseases.

The study included 8,687 samples from 4,089 participants, spanning healthy volunteers and people with conditions or treatments linked to immune suppression, such as HIV, multiple myeloma, solid organ malignancy, autoimmune disease, inflammatory bowel disease and solid organ transplantation.

The researchers found that several immunosuppressed groups were more likely to have blunted responses to COVID-19 vaccination. But those categories were imperfect predictors. Some immunosuppressed participants mounted strong responses, while about 5% to 6% of healthy participants had weak responses.
The study found that higher levels of certain preexisting antibodies, including antibodies to common microbes such as Staphylococcus aureus, RSV and human respirovirus 3, were associated with stronger COVID-19 vaccine responses.

The researchers describe these as "sentinel" antibodies because they may indicate a person's baseline immune readiness. They are not necessarily fighting the vaccine target directly. Instead, they may reflect how responsive the antibody-producing arm of the immune system is likely to be.

The researchers then asked whether the full antibody fingerprint, not just a few individual markers, could help identify people likely to have weak vaccine responses. Their deep-learning model analyzed patterns across the antibody panel, combining many measurements into a broader immune profile.

The study highlights a key strength of AI in health research: its ability to find subtle, predictive patterns in millions of biological data points that might otherwise remain hidden. The approach suggests that vaccine readiness may be better understood by looking at the immune system as a whole, rather than focusing only on a single disease or a single antibody.

The work also highlights the value of newer technologies that can measure large numbers of antibody responses at once. Instead of asking whether someone has antibodies to one pathogen, the method can scan a wider immune landscape, capturing patterns formed by many previous encounters with viruses, bacteria and other immune targets.
Sentinel antibody profiling could help guide vaccine testing, vaccine development and clinical care for people at risk of weak immune responses.

The approach might eventually help doctors identify patients who need additional vaccine doses, closer follow-up or alternative protective measures. It could also help researchers better understand why some people respond well to vaccination while others do not.

Pre-vaccine sentinel antibodies predict blunted vaccine responses, Cell Press Blue (2026). DOI: 10.1016/j.cpblue.2026.100088. www.cell.com/cell-press-blue/f … 3051-3839(26)00086-1

Part 2

Too much RNA can starve cells of energy, study finds

Why do you feel very weak after viral infections?

A new study by researchers has uncovered a previously unknown consequence of viral infection: Too much RNA inside a cell can disrupt its ability to produce energy.
Published in the journal Proceedings of the National Academy of Sciences, the study found that when excess RNA builds up inside cells during poxvirus infection, it can impair mitochondria—the structures responsible for generating most of a cell's energy—reducing the cell's ability to function normally.

The discovery could have broad implications for understanding viral infections, age-related diseases and RNA-based therapeutics, including mRNA vaccines, because excess RNA can accumulate in each of these conditions.
Scientists have long known that RNA degradation helps control protein production and remove defective RNA. This new study reveals another important role: It helps cells maintain the energy they need to function properly.
The findings suggest that RNA degradation serves a broader purpose than scientists once realized. In addition to controlling protein production, supporting RNA quality control and helping cells regulate immune responses, it also helps protect the cell's ability to generate energy.

RNA exists in many forms. Messenger RNA (mRNA) carries the genetic instructions cells use to make proteins, which help cells perform their normal functions. Another form, double-stranded RNA (dsRNA), is commonly produced during viral infections and alerts the immune system that something is wrong.

During viral infection, viruses can produce large amounts of RNA. If cells cannot break down the excess RNA quickly enough, the buildup can damage mitochondria and reduce the cell's ability to generate energy.

While scientists already knew that excess dsRNA can trigger immune responses and that cells need to control dsRNA levels, the effects of mRNA came as a surprise.

mRNA is a normal component of our cells, but it seems like with many good things, if we get too much, that can become a problem for the cell. When too much RNA builds up, including mRNA, it can damage the mitochondria and interfere with the cell's ability to produce energy.
Viruses rely entirely on host cells for energy and protein production, but producing too much viral RNA can overwhelm the very cells viruses depend on to survive.
poxviruses—the family of viruses that includes smallpox and mpox—appear to use RNA cleanup systems to degrade RNAs and keep infected cells functioning long enough for the virus to continue replicating.

If the cell is not healthy, the virus would not replicate well. The virus needs to keep RNA levels balanced inside the cell.
The team also found that mitochondrial impairment occurred before major immune responses were activated and did not depend on the immune system's usual response to infection, further supporting the idea that RNA itself contributes to the damage.
Researchers think the negatively charged RNA may accumulate around mitochondria and disrupt the electrical balance needed for energy production, although how it happens is unknown.
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