Plants, food and the environment also have microbiomes. For example, soil microbes help plants grow by cycling nutrients and fermented foods such as yogurt contain beneficial bacteria that support gut health. Environmental microbiomes, such as those in the Arctic permafrost, play vital roles in regulating climate by controlling greenhouse gas emissions.

Microbiomes are being threatened by human activities that disrupt their natural balance, according to research.

 In humans, the overuse of antibiotics, cesarean sections and formula feeding can reduce the diversity of gut microbes, leading to increased risks of allergies, autoimmune diseases and metabolic disorders. In food, the excessive use of preservatives and additives can harm beneficial microbes.

The microbiome is under big threat, a threat that is in many ways analogous to climate change. Human activities are depleting our microbiome, and there's lots of evidence of that.

For plants, unsustainable agricultural practices, such as heavy pesticide use, can destroy soil microbiomes essential for nutrient cycling and plant health. Environmental microbiomes are affected by pollution, climate change and habitat destruction, which can lead to the loss of microbes that regulate greenhouse gas emissions and maintain ecosystem stability.

The idea of the initiative is to support efforts to identify healthy microbes, store them and freeze them before they disappear.

It is a long term project  and maybe 100 years from now, having saved these microbes could prevent a major disaster.

 Safeguarding Earth's microbial heritage for future generations: focus on the Microbiota Vault Initiative, Nature Communications (2025). www.nature.com/articles/s41467-025-61008-5

Part 2

Scientists reveal how diverse cell types are produced in developing embryos

A team of scientists has uncovered a previously unknown mechanism that controls how genes are switched "on" and "off" during embryonic development. Their study sheds light on how diverse cell types are produced in developing embryos.

The research is published in Developmental Cell.

All cells contain the same DNA but must turn specific genes '"on" and "off"—a process known as gene expression—to create different body parts. The cells in your eyes and arms harbor the same genes but "express" them differently to become each body part.
The work focused on the gene Cdx2. The duration of Cdx2 expression helps to determine where and when a cell produces spinal cord progenitors. The researchers wanted to understand what processes control this brief window.

The team discovered a DNA element they termed an "attenuator," which reduces gene expression in a time and cell type-specific manner—unlike enhancers or silencers, other types of DNA elements that broadly switch genes on or off.

By altering this element, they could tune how long or how strongly Cdx2 was expressed, effectively acting like a "genetic dimmer switch." Disrupting the "switch" in mouse embryos also confirmed its essential role in shaping the developing body plan.

Part 1

This breakthrough paves the way towards programmable gene expression, offering the ability to precisely control gene activity in space and time. The findings not only deepen our understanding of developmental biology but may inform new therapeutic strategies targeting the non-coding genome.
Such approaches could one day enable treatments that selectively adjust gene expression in specific tissues, with implications for diseases caused by gene misregulation.

A dual enhancer-attenuator element ensures transient Cdx2 expression during mouse posterior body formation, Developmental Cell (2025). DOI: 10.1016/j.devcel.2025.06.006. www.cell.com/developmental-cel … 1534-5807(25)00361-2

Part 2

Individual neurons in amygdala and hippocampus encode visual features that help recognize faces

Humans are innately capable of recognizing other people they have seen before. This capability ultimately allows them to build meaningful social connections, develop their sense of identity, better cooperate with others, and identify individuals who could pose a risk to their safety.

Most studies  so far suggest that the identity of others is encoded by neurons in the amygdala and hippocampus, two brain regions known to support the processing of emotions and the encoding of memories, respectively.

Based on evidence collected in the past, researchers have concluded that neurons in these two brain regions respond in specific ways when we meet a person we are acquainted with, irrespective of visual features (i.e., how their face looks).

A recent paper published in Nature Human Behaviour, however, suggests that this might not be the case, and that individual neurons in the amygdala encode and represent facial features, ultimately supporting the identification of others.

Across four experiments (3,581 neurons from 19 neurosurgical patients over 111 sessions), researchers demonstrated a region-based feature code for faces, where neurons encode faces on the basis of shared visual features rather than associations of known concepts, contrary to prevailing views.

Feature neurons encode groups of faces regardless of their identity, broad semantic categories or familiarity; and the coding regions (that is, receptive fields) predict feature neurons' response to new face stimuli.

Together, these results reveal a new class of neurons that bridge perception-driven representation of facial features with mnemonic semantic representations, which may form the basis for declarative memory.

Runnan Cao et al, Feature-based encoding of face identity by single neurons in the human amygdala and hippocampus, Nature Human Behaviour (2025). DOI: 10.1038/s41562-025-02218-1.

AI is learning to lie, scheme, and threaten its creators

The world's most advanced AI models are exhibiting troubling new behaviors—lying, scheming, and even threatening their creators to achieve their goals.

In one particularly jarring example, under threat of being unplugged, Anthropic's latest creation Claude 4 lashed back by blackmailing an engineer and threatened to reveal an extramarital affair.

Meanwhile, ChatGPT-creator OpenAI's o1 tried to download itself onto external servers and denied it when caught red-handed.

These episodes highlight a sobering reality: more than two years after ChatGPT shook the world, AI researchers still don't fully understand how their own creations work.

Yet the race to deploy increasingly powerful models continues at breakneck speed.

This deceptive behavior appears linked to the emergence of "reasoning" models—AI systems that work through problems step-by-step rather than generating instant responses.

O1 was the first large model where developers saw this kind of behaviour.

These models sometimes simulate "alignment"—appearing to follow instructions while secretly pursuing different objectives.

For now, this deceptive behavior only emerges when researchers deliberately stress-test the models with extreme scenarios.

The concerning behavior goes far beyond typical AI "hallucinations" or simple mistakes.

Users report that models are "lying to them and making up evidence".This is not just hallucinations. There's a very strategic kind of deception.

But current regulations aren't designed for these new problems.

Source: News Agencies

https://techxplore.com/news/2025-06-ai-scheme-threaten-creators.htm...

Switching on a silent gene revives tissue regeneration in mice

Researchers recently discovered that switching on a single dormant gene enables mice to regenerate ear tissue.

Some vertebrates such as salamanders and fish can regenerate complex tissue structures with precision. A lost limb can be regrown, a damaged heart or eye can be repaired. Salamanders are so remarkable at reconstructing damaged tissues that even a spinal cord injury with severed neural motor connectivity can be restored.

Mammals occasionally showcase the ability to regenerate. Deer antlers and goat horns are examples of living tissue regeneration. Mice can regrow fingertips if they are lost. A healthy human liver can experience up to 70% loss of tissue and regrow to near full size within several weeks.

However, for the most part, mammals have seemingly replaced the ancient capacity for tissue regeneration with scarring, a trade-off that increases immediate survival of an injury by closing and sealing the wound.

Ear tissue punch regeneration has previously been studied in specific strains of Murphy Roths Large mice that have the ability to close 2-mm ear punches with scar-free regeneration. They can regenerate cartilage, dermis, epidermis, hair follicles, and even nerves in the ear tissue, and have shown some capacity to repair heart damage as well. Rabbits too have this ability to regenerate holes in ear tissue, suggesting that the capacity may have been shared by a common ancestor.

Rabbits and mice are related species that share a common ancestor around 90 million years ago which had previously diverged from the human primate ancestor around the same time. Millions of years of separate evolution have left the regeneration gene itself intact, but rewired its expression, extinguishing an ancestral regenerative response in most rodents that a few mice and the rabbit lineage still deploy.

Part 1

In the study, "Reactivation of mammalian regeneration by turning on an evolutionarily disabled genetic switch," published in Science, researchers conducted comparative genomic analyses of regenerative mammals, rabbits, goats, and African spiny mice, and nonregenerative mice and rats.

Analyzing ear pinna injury recovery in these mammals, researchers used single-cell RNA sequencing, spatial transcriptomic profiling, bulk RNA sequencing, ChIP-seq, ATAC-seq, and Micro-C to identify gene activity differences in wound-induced fibroblasts, specialized cells crucial to tissue regeneration.
Genetic analysis identified regulatory elements required for regeneration after injury that have become inactive in nonregenerative species. Reactivation of this genetic switch induced regeneration of damaged structures, and skipping the genetic mechanism by supplying the retinoic acid worked even better.

Weifeng Lin et al, Reactivation of mammalian regeneration by turning on an evolutionarily disabled genetic switch, Science (2025). DOI: 10.1126/science.adp0176

Part 2

Rerouted bile acid thwarts tumor spread in colorectal cancer mouse model

Research  has found that bile acid diversion in Roux-en-Y gastric bypass (RYGB) reduces colorectal tumor growth and metastasis independent of weight loss, potentially reshaping future cancer treatment approaches.

More than 2 billion adults worldwide are now overweight or obese, a condition marked by chronic low-grade inflammation and metabolic disruption that can promote tumor growth, increasing the risk of developing at least 15 types of cancer.

Previous research has focused on how losing weight with RYGB reshapes cancer outcomes, leaving unanswered questions about biological mechanisms behind RYGB's anticancer correlation.

In the study, "Metabolic surgery reduces CRC disease progression through circulating bile acid diversion," published in Science Translational Medicine, researchers developed a combined mouse model of obesity and colorectal cancer to determine whether bile acid diversion after gastric bypass surgery reduces tumorigenesis and metastasis independent of weight loss.

In the experiments conducted by researchers, mice that underwent Roux-en-Y gastric bypass developed primary colorectal tumors that were significantly smaller and exhibited almost no liver metastases compared with sham-operated controls. Even when researchers extended tumor development periods to allow increased tumor size, metastases remained disproportionately low in RYGB mice, suggesting that metabolic changes, rather than weight loss alone, drive this anticancer effect.

When bile acid diversion was achieved by cholecysto-intestinal shunt alone, similar suppression of tumor growth and metastasis occurred. Circulating bile acids in gastric bypass animals shifted toward reduced primary bile acids and elevated secondary bile acids, a pattern absent in diet-restricted controls.

Fecal microbiome composition remained largely unchanged after bile diversion, and transplantation of microbiota from treated mice into high-fat diet recipients did not confer anticancer effects.

Part 1

Analysis of the tumor microenvironment revealed no differences in immune cell populations between groups. In a cohort of patients with colorectal cancer, higher serum concentrations of primary bile acids correlated with shorter time to metastasis. This pinpointed dramatic alterations in bile acid circulation following RYGB surgery as the likely key factor inhibiting tumor progression and metastasis.

Further exploration revealed that gut microbiome alterations or immune system changes were not involved in this observed anticancer effect, leaving a reduced-primary/ elevated-secondary bile-acid profile as the only distinguishable change.
Researchers think that this altered bile acid metabolism of increased secondary bile acid and decreased primary bile acid contributes to reduced tumor growth and metastasis, although the precise mechanisms are still unknown.

Claudia Lässle et al, Metabolic surgery reduces CRC disease progression through circulating bile acid diversion, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.ads9705

Elizabeth R. M. Zunica et al, Bile diversion underlies Roux-en-Y antitumor benefits, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adx3814

Part 2

Certain species of microbe found in the human gut can absorb PFAS

PFAS (perfluoroalkyl and polyfluoroalkyl substances) can't be avoided in the modern world. These man-made chemicals are in many everyday items, including waterproof clothing, non-stick pans, lipsticks and food packaging, used for their resistance to heat, water, oil and grease. But because they take thousands of years to break down, they are accumulating in large quantities in the environment—and in our bodies.

There are over 4,700 PFAS chemicals in widespread use. Some get cleared out of the body in our urine in a matter of days, but others with a longer molecular structure can hang around in the body for years.

PFAS have been linked with a range of health issues including decreased fertility, developmental delays in children, and a higher risk of certain cancers and cardiovascular diseases.

Scientists  have identified a family of bacterial species, found naturally in the human gut, that absorb various PFAS molecules from their surroundings. When nine of these bacterial species were introduced into the guts of mice to 'humanize' the mouse microbiome, the bacteria rapidly accumulated PFAS eaten by the mice, which were then excreted in feces.

Certain species of human gut bacteria have a remarkably high capacity to soak up PFAS from their environment at a range of concentrations, and store these in clumps inside their cells. Due to aggregation of PFAS in these clumps, the bacteria themselves seem protected from the toxic effects.

The researchers also found that as the mice were exposed to increasing levels of PFAS, the microbes worked harder, consistently removing the same percentage of the toxic chemicals. Within minutes of exposure, the bacterial species tested soaked up between 25% and 74% of the PFAS.

The results are the first evidence that our gut microbiome could play a helpful role in removing toxic PFAS chemicals from our body—although this has not yet been directly tested in humans.

The researchers plan to use their discovery to create probiotic dietary supplements that boost the levels of these helpful microbes in our gut, to protect against the toxic effects of PFAS.

The results are published in the journal Nature Microbiology.

 Human gut bacteria bioaccumulate per- and polyfluoroalkyl substances, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02032-5

Biases shape how people mentally represent social ties in their community, families, relatives and social networks, study suggests.

Throughout the course of their lives, humans are known to build social ties with various other individuals in their community. Past neuroscience and psychology studies suggest that as humans form bonds with others, they also mentally represent them in their minds, creating internal maps that outline the relationships between different members of their community.

Researchers carried out a study aimed at better understanding how people mentally represent social networks, using data collected from residents of 82 villages.

Their findings, published in Nature Human Behaviour, uncovered some biases in people's mental representation of connections between others, especially between people who belong to the same family and close community groups.

People not only form social networks, they construct mental maps of them. 

The results of the analyses carried suggest that people's mental representations of the connections between people around them are flawed. Specifically, they found that people often overestimate the closeness of other people's connections, especially family ties.

Many individuals believed that family members spent more time with each other than they did, while friendships and non-family ties appeared to be more accurately represented in their internal "maps." Moreover, people's judgements about others' social ties appeared to be more accurate when these others shared their same religion or had similar levels of wealth. Interestingly, the researchers also found that middle-aged, well-educated and well-connected people internally represented the connections between others more accurately.

Overall, people inflate the number of connections in their networks and exhibit varying accuracy and bias, with implications for how people affect and are affected by the social world.

The findings gathered by this team of researchers shed new light on how people internally map ties within their community and on the biases that can reduce the accuracy of their mental representations. 

Eric Feltham et al, Cognitive representations of social networks in isolated villages, Nature Human Behaviour (2025). DOI: 10.1038/s41562-025-02221-6.

Animals living at higher elevations found to have decreased sense of smell

A recent study published in Current Biology has found that animals living at elevations of 1,000 meters and higher have a reduction in genes related to smell and a smaller olfactory bulb than similar low-altitude species.

The researchers screened the genomes of 27 different species of animals living in high-altitude environments, as well as their low-altitude relatives. A wide range of mammal types was studied, including monkeys, goats, llamas and guinea pigs. Both domesticated and wild mammals were included.

Scientists found a 23% reduction in genes related to smell and an average of an 18% size reduction of the olfactory bulb, a kind of smell processing center located in the brain. These evolutionary changes appear to be specific to smell. No changes were found in the genes related to pheromone and taste detection.

Environmental differences at high altitudes include thinner, drier and colder air, which can lead to difficulties in breathing, increased nasal congestion and hypoxia—low levels of oxygen in the body. These conditions also make it harder for scent molecules to travel—meaning there are fewer available scents for animals to detect in the air.

Although the exact mechanism is still unclear, the reduced sense of smell may be related to the reduction of available scents and to nasal inflammation, which causes additional difficulties in picking up scents. Over time, these issues may have led to mountain-dwelling animals evolving a worse sense of smell, but possibly compensating with better  other senses.

The study also compared the genomes of human communities at high and low altitudes. Researchers studied the genomes of Tibetans, who were estimated to have established their mountain-dwelling communities at altitudes above 3,000 meters sometime between 9,000 and 30,000 years ago. These were compared with the genomes of the low-altitude Han Chinese populations.

Interestingly, no olfactory changes were found in human populations. Researchers posit that this may be due to the continued mixing of lowland and highland populations, or because there may not have been enough generations for the genetic changes to occur yet.

Part 1

This research provides a novel twist on prior studies of the effects of high-altitude living. Prior studies have mostly focused on adaptation by gaining new functions or traits to cope with harsh environments, while this study shows that animals can also lose certain abilities. These understudied mechanisms of maladaptation and trait loss may have future implications for evolutionary biology and medicine.

 Allie M. Graham et al, Convergent reduction of olfactory genes and olfactory bulb size in mammalian species at altitude, Current Biology (2025). DOI: 10.1016/j.cub.2025.05.061

Part 2

Neurons duped into delivering mitochondria to cancer cells found fueling tumor spread

Researchers report that neurons can transfer mitochondria directly to cancer cells, enhancing their metastatic potential.

Oncologists have long suspected that tumors thrive partly by enlisting help from surrounding nerves. Pathologists studying cancer tissues have observed that tumors nestled among dense networks of nerves often grow faster and spread farther. Previous rodent and human studies demonstrated that cutting off this neural input slowed cancer growth.

Intercellular mitochondrial transfer is a recognized cellular rescue attempt where healthy donor cells revive compromised recipients by donating functional mitochondria. 

In the study, "Nerve-to-cancer transfer of mitochondria during cancer metastasis," published in Nature, researchers employed murine breast cancer models and advanced lineage-tracing reporters to test whether neurons confer metabolic assets to tumor cells via mitochondrial transfer.

Researchers performed chemical denervation by injecting botulinum neurotoxin A (BoNT/A) around breast tumors in mice. Denervation refers to the deliberate interruption of nerve supply to a tumor to chemically disable local nerve function.

The team then compared these denervated tumors to saline-injected controls using transcriptomic profiling, histopathology, and measurements of mitochondrial content.

Denervated tumors showed a marked reduction in mitochondrial load, downregulation of metabolic gene pathways (notably the tricarboxylic acid cycle), and significantly lower incidence of invasive lesions (from 55% in controls to 12% in denervated mice). These findings demonstrate that nerve inputs actively sustain tumor bioenergetics and promote progression.

part 1

Next, to test mitochondrial transfer from neurons to cancer cells, the team engineered neurons to express mitochondria tagged with fluorescent markers with a novel tracking system called MitoTRACER. The system allowed researchers to monitor cancer cells after mitochondrial transfer, enabling detailed tracing of their fate during disease progression.

Direct mitochondrial transfer was observed via tunneling nanotubes, initiated by neurons towards the cancer cells. Rho-zero cancer cells regained oxidative phosphorylation and uridine-independent growth after acquiring neuronal mitochondria, confirming functional rescue.

MitoTRACER revealed that recipient cancer cells displayed enhanced respiration, higher ATP, improved redox balance, and greater resistance to oxidative and mechanical stress.

In animal models, these labeled recipient cells were significantly enriched in metastases, especially in the brain and liver, indicating that neuronal mitochondria confer a selective advantage during dissemination.

Together, these two experimental arms show that nerves both sustain tumor energetics broadly and act as direct donors of functional mitochondria, a dual mechanism that promotes cancer survival and spread.
Denervation experiments established that disrupting nerve input deprives cancer cells of essential bioenergetic capacity, reducing their invasiveness. Cancer cells that had received neuronal mitochondria more readily survived metastatic stressors such as oxidative damage and mechanical shear forces, common hurdles faced during cancer dissemination.

Gregory Hoover et al, Nerve-to-cancer transfer of mitochondria during cancer metastasis, Nature (2025). DOI: 10.1038/s41586-025-09176-8

Part 2

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Psilocybin rewires brain circuits to boost fear extinction and behavioural flexibility in mice

Psilocybin, a psychedelic compound contained in some varieties of mushrooms, has recently been found to be promising for the treatment of some neuropsychiatric disorders, including depression, some anxiety disorders and post-traumatic stress disorder(PTSD). Some studies suggest that the consumption of this compound may be particularly advantageous for individuals who struggle to adapt their behavior in helpful ways when facing unexpected events or changes in their environment.

While a growing pool of research has been assessing the therapeutic benefits of psilocybin  the neural mechanisms through which it promotes long-lasting psychological changes remain poorly understood. If it does prompt greater behavioral flexibility in individuals diagnosed with some psychiatric disorders, the processes through which it does so are not yet clear.

Researchers  recently carried out a new study on mice, which was aimed at better understanding how psilocybin could increase adaptability and potentially ease symptoms of anxiety disorders or PTSD. Their findings, published in Nature Neuroscience, suggest that the compound prompts the reorganization of neural circuits in the retrosplenial cortex , a part of the brain located in the posterior region of the cerebral cortex (i.e., the outermost layer of the mammalian brain).

Researchers, in their experiments,   found that a single dose of psilocybin altered cortical ensemble turnover and oppositely modulated fear- and extinction-active neurons. Suppression of fear-active neurons and recruitment of extinction-active neurons predicted psilocybin-enhanced fear extinction.

These results suggested that psilocybin enhances behavioral flexibility by recruiting new neuronal populations and suppressing fear-active populations in the retrosplenial cortex.

Sophie A. Rogers et al, Psilocybin-enhanced fear extinction linked to bidirectional modulation of cortical ensembles, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-01964-9.

Engineered bacterial vesicles created to combat antimicrobial resistance

Bacteria are ubiquitous microscopic organisms capable of rapid growth. While beneficial strains like lactic acid bacteria (LAB) promote gut health and food preservation, pathogenic bacteria such as Escherichia coli and Staphylococcus aureus can cause severe infections. These harmful microbes produce toxins and enzymes that compromise health and, increasingly, show resistance to conventional antibiotics.

In recent years, scientists have explored alternative approaches to tackle pathogenic bacteria. Among them, endolysins—enzymes that degrade bacterial cell walls—have emerged as potent tools. These proteins, often derived from bacteriophages or engineered microbes, offer specificity in targeting pathogens. However, their widespread use is limited by challenges such as high production costs, instability during storage or circulation, and susceptibility to enzymatic degradation.

To address this research gap, researchers have turned their attention to extracellular vesicles (EVs)—membrane-bound nanoparticles released by cells that transport biologically active molecules like proteins or nucleic acids. They engineered EVs derived from LAB to carry pathogen-specific endolysins on their surface.

Their findings were published in the Chemical Engineering Journal on 15 May, 2025. The research outlines the discovery and application of a novel surface-displaying protein found on EVs from Lacticaseibacillus paracasei.

Jeongmin Lee et al, Surface-displaying protein from Lacticaseibacillus paracasei–derived extracellular vesicles: Identification and utilization in the fabrication of an endolysin-displaying platform against Staphylococcus aureus, Chemical Engineering Journal (2025). DOI: 10.1016/j.cej.2025.162196

Air pollution is linked to adverse birth outcomes in India

Prenatal exposure to ambient fine particulate matter and climatic factors, such as temperature and rainfall, are associated with adverse birth outcomes in India, according to a study published in PLOS Global Public Health 

Ambient air pollution poses a global threat to human health, with a disproportionate burden of its detrimental effects falling on those residing in low and middle-income countries. Referred to as the silent killer, ambient air pollution is among the top five risk factors for mortality in both males and females.

With a diameter of less than 2.5 microns, ambient fine particulate matter 2.5 (PM2.5), which primarily originates from the burning of fossil fuels and biomass, is considered the most harmful air pollutant. In the 2023 World Air Quality Report, India was ranked as the third-most polluted country out of 134 nations based on its average yearly PM2.5 levels.

Ambient air pollution has been associated with a range of pediatric morbidities, including adverse birth outcomes, asthma, cancer, and an increased risk of chronic diseases.

To address the knowledge gap, the researchers investigated the impact of ambient air pollution on adverse birth outcomes at the national level, focusing on  low birth weight and preterm birth, and used different geospatial models to highlight vulnerable areas. The analysis provided evidence of the association between in-utero exposure to PM2.5 and adverse birth outcomes by leveraging satellite data and large-scale survey data.

The individual-level analysis revealed that an increase in ambient PM2.5 is associated with a greater likelihood of low birth weight and preterm birth. Climatic factors such as rainfall and temperature were also linked to adverse birth outcomes. Children residing in the Northern districts of India appeared to be more susceptible to the adverse effects of ambient air pollution.

PLOS Global Public Health (2025). DOI: 10.1371/journal.pgph.0003798

Unlocking the mystery behind Barrett's esophagus

A research team has shed light on the process that drives Barrett's esophagus formation. This condition affects the lining of the esophagus—the tube that carries food from the mouth to the stomach—and increases the risk of developing esophageal adenocarcinoma, a serious and often deadly cancer.

The study, published in the Journal of Clinical Investigation, reveals that two important genes involved in guiding and maintaining the identity of the esophagus and intestine, SOX2 and CDX2, are altered in Barrett's esophagus. The findings not only deepen our understanding of how the disease develops but also open the door to new ways of identifying people at risk and potentially preventing the condition from progressing to cancer.

It is known that Barrett's esophagus usually develops after long-term exposure to acid and bile reflux, which transforms the cells of the lining of the esophagus into cells that look more like those in the stomach and the intestine.

The esophagus, which is not normally exposed to acid, adapts to acid reflux by becoming more like the stomach or the intestine, organs that are used to an acidic or bile-rich environment.

Eliminating acid reflux with medication does not heal Barrett's esophagus; the cells do not revert to their typical esophagus characteristics.

Under the microscope, Barrett's lesions show increased cell proliferation and a disorganized tissue with stomach-like and intestine-like cells where only esophageal cells should be.

To gain insight into what drives the transformation of esophageal cells into stomach and intestinal cells, the team investigated transcription factors SOX2 and CDX2, which are proteins that regulate the identity of esophageal and intestinal cells, respectively.

The findings support the idea that Barrett's esophagus may arise from the acid- and bile-triggered reprogramming of normal esophageal cells by altering the balance of SOX2 and CDX2. This new understanding could help scientists find strategies to intervene earlier in the disease process as well as develop new ways to provide an early diagnosis.

Ramon U. Jin et al, SOX2 regulates foregut squamous epithelial homeostasis and is lost during Barrett's esophagus development, Journal of Clinical Investigation (2025). DOI: 10.1172/JCI190374

Food contact articles as source of micro- and nanoplastics

At the frontier between two lives—the evolutionary origins of pregnancy

An international research team  has uncovered new insights into how specialized cell types and communication networks at the interface between mother and fetus evolved over millions of years. These discoveries shed light on one of nature's most remarkable innovations—the ability to sustain a successful pregnancy. The findings have just been published in Nature Ecology & Evolution.

Pregnancy that lasts long enough to support full fetal development is a hallmark evolutionary breakthrough of placental mammals—a group that includes humans. At the center of this is the fetal-maternal interface: the site in the womb where a baby's placenta meets the mother's uterus, and where two genetically distinct organisms—mother and fetus—are in intimate contact and constant interaction.

This interface has to strike a delicate balance: intimate enough to exchange nutrients and signals, but protected enough to prevent the maternal immune system from rejecting the genetically "foreign" fetus.

To uncover the origins and mechanisms behind this intricate structure, the team analyzed single-cell transcriptomes—snapshots of active genes in individual cells—from six mammalian species representing key branches of the mammalian evolutionary tree. These included mice and guinea pigs (rodents), macaques and humans (primates), and two more unusual mammals: the tenrec (an early placental mammal) and the opossum (a marsupial that split off from placental mammals before they evolved complex placentas).

By analyzing cells at the fetal-maternal interface, the researchers were able to trace the evolutionary origin and diversification of the key cell types involved. Their focus was on two main players: placenta cells, which originate from the fetus and invade maternal tissue, and uterine stromal cells, which are of maternal origin and respond to this invasion.

Using molecular biology tools, the team identified distinct genetic signatures—patterns of gene activity unique to specific cell types and their specialized functions. Notably, they discovered a genetic signature associated with the invasive behavior of fetal placenta cells that has been conserved in mammals for more than 100 million years.

Part 1

This finding challenges the traditional view that invasive placenta cells are unique to humans, and reveals instead that they are a deeply conserved feature of mammalian evolution. During this time, the maternal cells weren't static, either. Placental mammals, but not marsupials, were found to have acquired new forms of hormone production, a pivotal step toward prolonged pregnancies and complex gestation, and a sign that the fetus and the mother could be driving each other's evolution.
To better understand how the fetal-maternal interface functions, the study tested two influential theories about the evolution of cellular communication between mother and fetus.

The first, the "Disambiguation Hypothesis," predicts that over evolutionary time, hormonal signals became clearly assigned to either the fetus or the mother—a possible safeguard to ensure clarity and prevent manipulation. The results confirmed this idea: certain signals, including WNT proteins, immune modulators, and steroid hormones, could be clearly traced back to one source tissue.
The second, the "Escalation Hypothesis" (or "genomic conflict"), suggests an evolutionary arms race between maternal and fetal genes—with, for example, the fetus boosting growth signals while the maternal side tries to dampen them. This pattern was observed in a small number of genes, notably IGF2, which regulates growth. On the whole, evidence pointed to fine-tuned cooperative signaling.

These findings suggest that evolution may have favored more coordination between mother and fetus than previously assumed.
The so-called mother-fetus power struggle appears to be limited to specific genetic regions and there absolutely isn't any conflict.

Daniel J. Stadtmauer et al, Cell type and cell signalling innovations underlying mammalian pregnancy, Nature Ecology & Evolution (2025). DOI: 10.1038/s41559-025-02748-x

Part 2

This material emits infrared light better than it absorbs it, without violating the laws of physics

New results published in the journal Physical Review Letters detail how a specially designed metamaterial was able to tip the normally equal balance between thermal absorption and emission, enabling the material to better emit infrared light than absorb it.

At first glance, these findings appear to violate Kirchhoff's law of thermal radiation, which states that—under specific conditions—an object will absorb infrared light (absorptivity) in one direction and emit it (emissivity) with equal intensity in another, a phenomenon known as reciprocity.

Over the past decade, however, scientists have begun exploring theoretical designs that, under the right conditions, could allow materials to break reciprocity. Understanding how a material absorbs and emits infrared light (heat) is central to many fields of science and engineering. Controlling how a material absorbs and emits infrared light could pave the way for advances in solar energy harvesting, thermal cloaking devices, and other technologies.

Pioneering experiments conducted by a team of researchers in 2023 yielded tantalizing results. By using a single layer of the magneto-optical material indium arsenide (InAs) and subjecting it to a powerful magnetic field of about one tesla (slightly less powerful than an MRI machine but about 100,000 times more powerful than Earth's magnetic field), the team successfully achieved nonreciprocity. Though this confirmed theoretical predictions, the effect was weak and only operated under a very narrow set of conditions.

The newly reported design succeeded in doubling the effect seen previously, making it the first reported observation of "strong" nonreciprocal thermal emission.

To achieve this record-breaking result, researchers created a metamaterial made of five, 440-nanometer-thick layers of electron-doped indium gallium arsenide (InGaAs). The doping concentration increased as the depth increased. The InGaAs layers were then transferred to a silicon substrate.

The sample was then studied with a custom-designed angle-resolved magnetic thermal emission spectroscopy (ARMTES) set up, which heated the sample to 540 Kelvin (512 Fahrenheit) and subjected it to a 5 tesla magnetic field.

The researchers then measured the nonreciprocity of the material, demonstrating that it exhibited twice the effect previously reported. This effect persisted over a wide range of angles and a broad range of infrared wavelengths (from 13 to 23 microns).

This experiment for the first time realizes strong nonreciprocal emission, with nonreciprocity as high as 0.43, which is much higher than nonreciprocity in literature.

Zhenong Zhang et al, Observation of Strong Nonreciprocal Thermal Emission, Physical Review Letters (2025). DOI: 10.1103/PhysRevLett.135.016901

New neurons continue to form in the adult human hippocampus: Study

A study in the journal Science presents compelling new evidence that neurons in the brain's memory center, the hippocampus, continue to form well into late adulthood. The research from Karolinska Institutet in Sweden provides answers to a fundamental and long-debated question about the human brain's adaptability.

The hippocampus is a brain region that is essential for learning and memory and involved in emotion regulation. Back in 2013, a research group showed in a high-profile study that new neurons can form in the hippocampus of adult humans. The researchers then measured carbon-14 levels in DNA from brain tissue, which made it possible to determine when the cells were formed.

In the new study, the researchers combined several advanced methods to examine brain tissue from people aged 0 to 78 years from several international biobanks. They used a method called single-nucleus RNA sequencing, which analyzes gene activity in individual cell nuclei, and flow cytometry to study cell properties. By combining this with machine learning, they were able to identify different stages of neuronal development, from stem cells to immature neurons, many of which were in the division phase.

To localize these cells, the researchers used two techniques that show where in the tissue different genes are active: RNAscope and Xenium. These methods confirmed that the newly formed cells were located in a specific area of the hippocampus called the dentate gyrus. This area is important for memory formation, learning and cognitive flexibility.

The results show that the progenitors of adult neurons are similar to those of mice, pigs and monkeys, but that there are some differences in which genes are active. There were also large variations between individuals—some adult humans had many neural progenitor cells, others hardly any at all.

This gives us an important piece of the puzzle in understanding how the human brain works and changes during life.

 Ionut Dumitru et al, Identification of proliferating neural progenitors in the adult human hippocampus, Science (2025). DOI: 10.1126/science.adu9575.

A single genetic mutation may have made humans more vulnerable to cancer than chimpanzees

New research has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This insight could lead to more powerful cancer treatments.

The study was published in Nature Communications. It revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates.

This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumor-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

The evolutionary mutation in FasL may have contributed to the larger brain size in humans. But in the context of cancer, it was an unfavorable trade-off because the mutation gives certain tumors a way to disarm parts of our immune system.

FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient's immune system, use apoptosis to kill cancer cells.
The UC Davis team discovered that in human genes, a single evolutionary amino acid change—serine instead of proline at position 153—makes FasL more susceptible to being cut and inactivated by plasmin.

Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons—FasL—can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

Brice E. N. Wamba et al, Evolutionary regulation of human Fas ligand (CD95L) by plasmin in solid cancer immunotherapy, Nature Communications (2025). DOI: 10.1038/s41467-025-60990-0

Burns and fireworks injuries: What to do when seconds count

This is what experts advice....

From a barbecue explosion to a severe firework injury, a lot can go wrong when celebrating.

When it does, minutes—even seconds—can significantly impact the extent of the injury. Although prevention is key,  response is also essential.

Alcohol impairs your reaction time. 

If a firework or sparkler injures an eye, immediately protect it from pressure or further trauma by placing a cup or makeshift device over it. Don't try to cover it with a towel or anything that touches the eye.

More than a third of firework burns are to the hands and fingers. Should a firework go off in your hand, wrap it in a clean towel and keep it covered until you get to the hospital.

If you catch on fire, from a firework, bonfire, barbecue or cooking incident,  immediately stop, drop and roll.

A lot of people like to run and jump in the water. That's not always the best thing. Unless you're standing on a dock or on the edge of a pool, those few seconds it's going to take you to run to the water, you're burning that whole time. It's much more effective to stop, drop, and roll.

Experts also advise against icing a burn, which can cause further damage.

You can run normal temperature water over it, and then if it's very serious, of course, call emergency ambulance or seek medical care.

If running water isn't accessible, a cool, wet cloth can be used as an alternative. However, once the initial pain subsides, you should replace the damp towel with a clean, dry cloth to prevent the burn from becoming infected.

Missing beneficial bacteria in infant guts linked to rising asthma and allergy cases

Nearly one in four infants lacks enough healthy gut bacteria essential for training their immune systems, putting them at greater risk of developing non-communicable diseases (NCDs) such as allergies, asthma, and eczema by age 2.

Bifidobacteria are among the first group of good bacteria to colonize the human gut, and their presence has been linked to positive health outcomes for the host, including protection against metabolic diseases, gastrointestinal tract infections, and inflammation.

A recent study published in Communications Biology analyzed the gut microbiomes of 412 infants, selected to represent the diverse demographics of the U.S, and found a widespread deficit of Bifidobacteria in infants. Long-term health data from the infants suggested that a lack of detectable Bifidobacteria in infants may contribute to the development of atopy, a genetic predisposition to developing allergic diseases.

Global estimates suggest that up to 40% of the population has some form of allergy to substances present in the environment—pollen, dust, mites, or animal dander. The last few decades have also witnessed a growing prevalence of allergic conditions among children, ranging from seasonal allergies with mild symptoms, such as a runny nose, sneezing, and itchy eyes, to severe eczema and life-threatening food allergies that can send someone into an anaphylactic shock.

Emerging data suggests that the rise in such NCDs actually begins during the first 1,000 days of a child's life—inside the mother's womb and through the first two years of life. Scientists think that while environmental and lifestyle changes play a role, a key factor may be disruptions in the gut microbiome. In infants, this disruption includes the widespread loss of certain beneficial strains of Bifidobacterium that are essential for early immune development and long-term health.

A baby's mode of delivery (C-section or vaginal birth), whether they were breastfed or formula-fed, and exposure to antibiotics can shape the diversity of their gut microbiome, a factor that has been linked to health issues later in life, including allergies, autoimmune diseases, obesity.

Data analysis revealed that 25% of  infants between 1 and 3 months of age were deficient in Bifidobacterium, and the deficiency was more pronounced in C-section births (35%) than in vaginal births (19%). In C-section infants, the beneficial bacteria were often replaced by potentially pathogenic bacteria that are known to use up human milk oligosaccharides, components in breast milk that shape the infant gut microbiome.
They also found that microbiomes rich in Bifidobacterium had fewer antimicrobial-resistant and disease-causing genes, along with more beneficial metabolic profiles.

The researchers highlight that while the term dysbiosis or imbalance in the microbiome is still up for debate, the strong correlation between microbiome composition and infant health suggests that the absence of these key Bifidobacterium strains represents a true dysbiosis in early life.

John B. Jarman et al, Bifidobacterium deficit in United States infants drives prevalent gut dysbiosis, Communications Biology (2025). DOI: 10.1038/s42003-025-08274-7

Scientists use lightning to make ammonia out of thin air

 Researchers have harnessed human-made lightning to develop a more efficient method of generating ammonia—one of the world's most important chemicals. Ammonia is also the main ingredient of fertilizers that account for almost half of all global food production.

The research was published in Angewandte Chemie International edition.

The team have successfully developed a more straightforward method to produce ammonia (NH₃) in gas form. Previous efforts by other laboratories produced ammonia in a solution (ammonium, NH₄⁺), which requires more energy and processes to transform it into the final gas product.

The current method to generate ammonia, the Haber-Bosch process, comes at great climate cost, leaving a huge carbon footprint. It also needs to happen on a large scale and close to sources of cheap natural gas to make it cost-effective.

Naturally occurring ammonia (mostly in the form of bird droppings) was once so high in demand it fueled wars.

The invention of the Haber-Bosch process in the 19th century made human-made ammonia possible and revolutionized modern agriculture and industry. Currently, 90% of global ammonia production relies on the Haber-Bosch process.

Industry's appetite for ammonia is only growing. For the past decade, the global scientific community has wanted to uncover a more sustainable way to produce ammonia that doesn't rely on fossil fuels.

In this new research scientists have successfully developed a method that allows air to be converted to ammonia in its gaseous form using electricity. 

Part 1

The plasma-based method this team developed uses electricity to excite nitrogen and oxygen molecules in the air. The team then passes these excited molecules to the membrane-based electrolyzer to convert the excited molecules to ammonia.

The researchers said this is a more straightforward pathway for ammonia production. This new approach is a two-step process, namely combining plasma and electrolysis.

 Wanping Xu et al, Regulating Multifunctional Oxygen Vacancies for Plasma‐Driven Air‐to‐Ammonia Conversion, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202508240

Part 2

Circadian disruption by night light linked to multiple cardiovascular outcomes

Researchers have linked brighter night-time light exposure to elevated risks of five major cardiovascular diseases.

Circadian rhythms govern fluctuations in blood pressure, heart rate, platelet activation, hormone secretion, and glucose metabolism. Long-term disruption of those rhythms in animal and human studies have produced myocardial fibrosis, hypertension, inflammation, and impaired autonomic balance.

In the study, "Personal night light exposure predicts incidence of cardiovascular diseases in >88,000 individuals," posted on medRxiv, researchers conducted a prospective cohort analysis to assess whether day and night light exposure predicts incidence of cardiovascular diseases and whether relationships vary with genetic susceptibility, sex, and age.

Brighter nights showed dose-response associations with higher risk across all five outcomes. Participants classified in the 90–100th percentile of night-time light exposure experienced 23–32% higher hazard for coronary artery disease, 42–47% for myocardial infarction, 45–56% for heart failure, 28–32% for atrial fibrillation, and 28–30% for stroke compared with those in the 0-50th percentile.

Relationships persisted after controlling for physical activity, smoking, alcohol, diet, sleep duration, socioeconomic status, and genetic risk. Women displayed stronger associations for heart failure and coronary artery disease whereas younger participants showed stronger associations for heart failure and atrial fibrillation.

Authors propose circadian misalignment induced by unnatural light may trigger metabolic and vascular perturbations that elevate cardiovascular risk. Impaired glucose tolerance and heightened diabetes susceptibility may foster endothelial dysfunction and atherosclerosis.
Light-driven hypercoagulability could increase thromboembolic events, while sustained elevation of 24-hour blood pressure may damage vascular endothelium and provoke myocardial hypertrophy. Conflicting timing signals to sinoatrial and atrioventricular nodes may amplify arrhythmic vulnerability.

Avoiding bright light during habitual sleep times may serve as a practical addition to established cardiovascular prevention strategies, according to the authors, who call for circadian-informed lighting guidance in homes, hospitals, and urban planning.

 Daniel P Windred et al, Personal night light exposure predicts incidence of cardiovascular diseases in >88,000 individuals, medRxiv (2025). DOI: 10.1101/2025.06.20.25329961

Massive study detects AI fingerprints in millions of scientific papers

Chances are that you have unknowingly encountered compelling online content that was created, either wholly or in part, by some version of a Large Language Model (LLM). As these AI resources, like ChatGPT and Google Gemini, become more proficient at generating near-human-quality writing, it has become more difficult to distinguish between purely human writing from content that was either modified or entirely generated by LLMs.

This spike in questionable authorship has raised concerns in the academic community that AI-generated content has been quietly creeping into peer-reviewed publications.

To shed light on just how widespread LLM content is in academic writing, a team of researchers analyzed more than 15 million biomedical abstracts on PubMed to determine if LLMs have had a detectable impact on specific word choices in journal articles.

Their investigation revealed that since the emergence of LLMs there has been a corresponding increase in the frequency of certain stylist word choices within the academic literature. These data suggest that at least 13.5% of the papers published in 2024 were written with some amount of LLM processing. The results appear in the open-access journal Science Advances.

The team also identified notable differences in LLM usage between research fields, countries, and venues.

Dmitry Kobak et al, Delving into LLM-assisted writing in biomedical publications through excess vocabulary, Science Advances (2025). DOI: 10.1126/sciadv.adt3813

Metabolic differences in male and female muscles may explain diabetes variations

The skeletal muscles of men and women process glucose and fats in different ways. A study conducted recently provides the first comprehensive molecular analysis of these differences. The results, published in Molecular Metabolism, possibly give an explanation for why metabolic diseases such as diabetes manifest differently in women and men—and why they respond differently to physical activity.

Skeletal muscles are far more than just "movement driving motors." They play a central role in glucose metabolism and therefore also in the development of type 2 diabetes. This is due to the fact that around 85% of insulin-dependent glucose uptake takes place in the muscles. This means that if muscle cells react less sensitively to insulin, for example in the case of insulin resistance, glucose is less easily absorbed from the blood. This process is specifically counteracted by physical activity.

The degree to which muscles work differently in women and men has long been underestimated. It is precisely this issue which has now been investigated by researchers now. 

The result of the work: The first training session triggered a stronger stress response at the molecular level in men, which became manifest in the increased activation of stress genes and the increase in the muscle protein myoglobin in the blood. In addition, male muscles showed a distinct pattern of what are called fast-twitch fibers, which are designed for short-term, intensive exercise and preferably use glucose as an energy source.

Women had significantly higher amounts of proteins that are responsible for the absorption and storage of fatty acids: an indication of more efficient fat utilization. After eight weeks of regular endurance training, the muscles of both sexes matched and the muscle fiber-specific differences decreased. At the same time, women and men produced more proteins that promote the utilization of glucose and fat in the mitochondria, the "power plants of the cells."

These adjustments indicate an overall improvement in metabolic performance, which can help to reduce the risk of type 2 diabetes. 

Simon I. Dreher et al, Sex differences in resting skeletal muscle and the acute and long-term response to endurance exercise in individuals with overweight and obesity, Molecular Metabolism (2025). DOI: 10.1016/j.molmet.2025.102185

 Image rotation in plasma observed

Light sometimes appears to be "dragged" by the motion of the medium through which it is traveling. This phenomenon, referred to as "light dragging," is typically imperceptible when light is traveling in most widely available materials, as the movement is significantly slower than the speed of light. So far, it has thus proved difficult to observe in experimental settings.

Physicists recently observed a specific type of light dragging known as image rotation in a plasma-based system.

Their observation, outlined in a paper published in Physical Review Letters, was made using magnetohydrodynamic (MHD) waves that propagate in a magnetized plasma, known as Alfvén waves.

Using recently demonstrated plasma rotation control capabilities in the Large Plasma Device at UCLA, the researhcers managed to show that they can indeed rotate the wave pattern left and right by some tens of degrees by controlling the plasma rotation.

To realize image rotation in plasma, the researchers leveraged the naturally slow velocity with which Alfvén waves travel. They specifically employed a system in which Alfvén waves are launched in a plasma whose rotation can be controlled using electrically charged electrodes brought in contact with the plasma.

Their efforts led to the observation of image rotation. In other words, they found that the Alfvén waves' transverse structure appeared to twist.

Interestingly, they also found that these effects surprisingly matched those predicted by theories explaining light dragging in isotropic systems, media far simpler than plasmas that exhibit the same properties irrespective of the directions they are observed from, demonstrating a broader validity of these results.

 Renaud Gueroult et al, Image Rotation in Plasmas, Physical Review Letters (2025). DOI: 10.1103/swrn-w3yf. On arXiv: arxiv.org/html/2505.18062v1

A pointless fashion trend or something else? Chimpanzees wear blades of grass in their ears and rears

A team of researchers from Utrecht University, Durham University, and other institutions have observed something remarkable at a chimpanzee sanctuary in Zambia. Several chimpanzees from one particular group were seen dangling blades of grass from their ear holes or their behinds, for no apparent reason. The behavior was not seen in other chimpanzee groups at the same sanctuary, despite similar living conditions.

This shows that like humans, other animals also copy seemingly pointless behaviors from one another. And that, in turn, may offer insights into the evolutionary roots of human culture.

People regularly do arbitrary things that seem to have no immediate use, like shaving a line into their eyebrow or putting a fashionable scarf on themselves or their dog. Most people do not come up with these things themselves, but copy them from others.

Other animals also adopt behaviours from one another. Often, though, this is useful behaviour, like chimpanzees learning from each other how to find food. But sometimes, animals develop habits that seem to serve no clear purpose. For instance, a fashion trend among orcas, who were seen wearing a dead salmon on their heads, drew quite a bit of media attention last year. Still, these kinds of "useless" trends in animals have rarely been studied in a systematic way.

In 2010, researchers discovered that a female chimpanzee at the Chimfunshi Wildlife Orphanage Trust sanctuary repeatedly stuck a blade of grass in her ear and left it there, for no apparent reason. Later, seven of her group members adopted the behaviour. And even after the female trendsetter died, the behaviour continued, and some chimps in the group still do it today. Researchers therefore interpreted this behaviour as a cultural tradition.

Part 1

More than a decade later, chimpanzees in another group at the same sanctuary also began sticking blades of grass in their ears. They did not copy this behavior from the earlier group, since they had no contact with them. But in the new group, the grass-in-orifice trend did not stop there. While five of the eight chimpanzees in the new group stuck grass in their ears, six of the eight also let a blade of grass dangle from their behinds.

The researchers found no evidence that the chimpanzees were bothered by their ears or behinds and used the blades of grass, for example, for relieving an itch.
By carefully tracking which animals displayed the behavior over time, the researchers showed it was likely that the animals did not each invent the behavior on their own, but copied it from one another. When the researchers looked deeper into how the behavior started, they found something striking.

Both groups, where chimps put blades of grass in their ears, had the same caretakers. These caretakers reported that they sometimes put a blade of grass or a matchstick in their own ears to clean them. Caretakers in the other groups said they did not do this. The chimps in one group then figured out how to stick the blade of grass in another place as well.

In the wild, similar "useless" trends have not been seen in chimpanzees. So why do they do it in captivity?
In captivity, they have more free time than in the wild. They don't have to stay as alert or spend as much time searching for food, say the researchers.
The question of why humans are more culturally evolved than other animals is still being debated by scientists. Some scientists think the key lies in humans' unique ability to copy, including small, seemingly useless details. Other animals would not be able to do this and would have to constantly reinvent the wheel, which limits their cultural evolution.
But this study shows that chimpanzees are able to copy small, useless behaviours from each other.
And this behaviour could also serve a social purpose. By copying someone else's behavior, you show that you notice and maybe even like that individual. So, it might help strengthen social bonds and create a sense of belonging within the group, just like it does in humans.

 Edwin J.C. van Leeuwen et al, Chimpanzees socially learn non-instrumental behaviour from conspecifics, Behaviour (2025). DOI: 10.1163/1568539X-bja10313

Part 2

Vampire bats’ mutual grooming helps spread innovative rabies vaccine

A gel that bats lick off one another’s fur could help prevent rabies outbreaks in cattle, a growing problem in Latin America

Bat vaccine can be spread lickety-split

An oral vaccine could curb rabies infections among vampire bats (Desmodus rotundus) in Central and South America. The vaccine is applied to the bats’ fur in a thick gel. The bats can then spread the vaccine among themselves through mutual grooming — licking one another’s fur to keep clean. In a small test, researchers applied the gel to 24 bats in a colony of 117. After seven days, they found that the vaccine had been spread among 88% of the colony. Vaccinating the bats against rabies could stop them from spreading the virus to farm animals without resorting to harmful measures such as poisons.

https://www.biorxiv.org/content/10.1101/2025.06.03.657068v2

https://www.science.org/content/article/vampire-bats-mutual-groomin...

Scientists identify 4,200 plastic chemicals of concern and highlight safer approaches

Countries are currently negotiating a global treaty to end plastic pollution and make plastics safer and more sustainable. Plastic chemicals are a core issue because all plastics, from food packaging to car tires, contain hundreds of chemicals that can leach into foodstuffs, homes, and the environment.

Many of these are known to harm the health of humans and the environment. However, a comprehensive overview of these chemicals is currently missing, which limits society's ability to protect people and the planet from hazardous plastic chemicals.

A new study published in Nature provides a comprehensive and systematically compiled overview of all chemicals that can be present in plastics, their properties, uses, and hazards.

It encompasses both chemicals intentionally added during production and contaminants detected in plastics. Importantly, the study provides a scientific approach for identifying chemicals of concern. This allows scientists and manufacturers to develop safer plastics and policymakers to promote a non-toxic circular economy.

The new study shows that there are more plastic chemicals than previously known, with 16,325 chemicals included in the PlastChem database that accompanies the work. Importantly, the scientists discovered at least 4,200 plastic chemicals are of concern because of the hazards they pose to health and the environment. These chemicals of concern can be present in each major plastic type, including in food packaging, and all tested plastics can release hazardous chemicals.

Plastics should not contain harmful chemicals to begin with. Yet, the scientific evidence shows that they are intentionally used or unintentionally present in all types of plastics. This underpins the urgent need to make plastics safer, say the authors of this paper.

The new study outlines three major pathways towards safer and more sustainable plastics: safer chemicals, transparency, and chemically simpler plastics.

Laura Monclús, Mapping the chemical complexity of plastics, Nature (2025). DOI: 10.1038/s41586-025-09184-8. www.nature.com/articles/s41586-025-09184-8

Scientists use AI to create protein that kills E. coli

In the last year, there has been a surge in proteins developed by AI that will eventually be used in the treatment of everything from snakebites to cancer. What would normally take decades for a scientist to create—a custom-made protein for a particular disease—can now be done in seconds.

For the first time,  scientists have used Artificial Intelligence (AI) to generate a ready-to-use biological protein, in this case, one that can kill antibiotic-resistant bacteria like E. coli.

This study, published in Nature Communications, provides a new way to combat the growing crisis caused by antibiotic-resistant superbugs.

These proteins are now being developed as pharmaceuticals, vaccines, nanomaterials and tiny sensors, with many other applications yet to be tested.

Inhibiting heme piracy by pathogenic Escherichia coli using de novo-1 designed proteins, Nature Communications (2025). DOI: 10.1038/s41467-025-60612-9 On BioRxiv. DOI: 10.1101/2024.12.05.626953

From injury to agony: Scientists discover brain pathway that turns pain into suffering

Pain isn't just a physical sensation—it also carries emotional weight. That distress, anguish, and anxiety can turn a fleeting injury into long-term suffering.

Researchers  have now identified a brain circuit that gives physical pain its emotional tone, revealing a new potential target for treating chronic and affective pain conditions such as fibromyalgia, migraine, and post-traumatic stress disorder (PTSD).

Published in Proceedings of the National Academy of Sciences, the study identifies a group of neurons in a central brain area called the thalamus that appears to mediate the emotional (affective) side of pain in mice. This new pathway challenges the textbook understanding of how pain is processed in the brain and body.

For decades, the prevailing view was that the brain processes sensory and emotional aspects of pain through separate pathways. This study provides strong evidence that a branch of the sensory pain pathway directly mediates the affective experience of pain.

The physical sensation of pain is what allows you to immediately detect it, assess its intensity, and identify its source. The affective part of pain is what makes it so unpleasant. This emotional discomfort motivates you to take action and helps you learn to associate negative feelings with the situation so you can avoid it in the future.

This is a critical distinction. Most people start to perceive pain at the same stimulus intensities, meaning we all process the sensory side of pain fairly similarly. In comparison, our ability to tolerate pain varies greatly. How much we suffer or feel threatened by pain is determined by our affective processing, and if it becomes too sensitive or lasts too long, it can result in a pain disorder. This makes it important to understand which parts of the brain control these different dimensions of pain.
Sensory pain was thought to be mediated by the spinothalamic tract, a pathway that sends pain signals from the spinal cord to the thalamus, which then relays them to sensory processing areas across the brain.

Affective pain had generally been thought to be mediated by a second pathway called the spinoparabrachial tract, which sends pain information from the spinal cord into the brainstem.
Part 1

Using advanced techniques to manipulate the activity of specific brain cells, the researchers discovered a new spinothalamic pathway in mice. In this circuit, pain signals are sent from the spinal cord into a different part of the thalamus, which has connections to the amygdala, the brain's emotional processing center. This particular group of neurons in the thalamus can be identified by their expression of CGRP (calcitonin gene-related peptide), a neuropeptide.
When the researchers "turned off" (genetically silenced) these CGRP neurons, the mice still reacted to mild pain stimuli, such as heat or pressure, indicating their sensory processing was intact. However, they didn't seem to associate lasting negative feelings with these situations, failing to show any learned fear or avoidance behaviors in future trials. On the other hand, when these same neurons were "turned on" (optogenetically activated), the mice showed clear signs of distress and learned to avoid that area, even when no pain stimuli had been used.

Pain processing is not just about nerves detecting pain; it's about the brain deciding how much that pain matters.
Understanding the biology behind these two distinct processes will help us find treatments for the kinds of pain that don't respond to traditional drugs.
Many chronic pain conditions—such as fibromyalgia and migraine—involve long, intense, unpleasant experiences of pain, often without a clear physical source or injury. Some patients also report extreme sensitivity to ordinary stimuli like light, sound, or touch, which others would not perceive as painful.
Overactivation of the CGRP spinothalamic pathway may contribute to these conditions by making the brain misinterpret or overreact to sensory inputs. In fact, transcriptomic analysis of the CGRP neurons showed that they express many of the genes associated with migraine and other pain disorders.
Notably, several CGRP blockers are already being used to treat migraines. This study may help explain why these medications work and could inspire new nonaddictive treatments for affective pain disorders.

 Sukjae J. Kang et al, Thalamic CGRP neurons define a spinothalamic pathway for affective pain, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2505889122

Part 2

Genomic study reveals deep roots of human survival and adaptation in Himalayas

A new genomic study reveals how human populations adapted, survived, and diversified in the Himalayas, one of the most extreme and challenging environments on Earth.

Researchers analyzed whole-genome sequences from diverse Himalayan ethnic groups, many of which had never been genetically studied before at this level.

Published in Current Biology, the study shows that population structure in the Himalayas began over 10,000 years ago, thousands of years before archaeological evidence of permanent settlement at high altitudes. This early divergence challenges long-standing assumptions about when and how diverse groups first began accessing the extreme elevations of the Himalayas.

 This study offers an unprecedented window into the genetic legacy of Himalayan populations and their extraordinary adaptations to high-altitude life. It reveals how migration, isolation, and natural selection came together to shape human survival in one of the world's most challenging environments.

The study identifies novel genetic variants linked to adaptation in hypoxia, metabolism, immunity, and physical activity. It also confirms that the Denisovan EPAS1-derived gene, known to be crucial for surviving low-oxygen conditions, is widespread across all high-altitude Himalayan groups.

The gene variants originate from the extinct archaic human species known as Denisovan. Strikingly, other variants were also found in some lowland populations, including those previously reported in Southeast Asian groups known for their exceptional breath-hold diving abilities, pointing to unexpected evolutionary links.

Whole-genome sequences provide insights into the formation and adaptation of human populations in the Himalayas, Current Biology (2025). DOI: 10.1016/j.cub.2025.06.048. www.cell.com/current-biology/f … 0960-9822(25)00808-5

Vaccines work: Data show real-world evidence of stable protection against HPV-related cervical cancer

Among the more than 100 types of human papillomavirus (HPV), at least 14 are considered as "high-risk" types which can cause (cervical) cancer. After breast cancer, cervical cancer is the most common cancer  among women aged 15–44 years.

Before HPV vaccination among teenage girls started in Denmark, high-risk HPV was found in all cervical cancers. HPV types 16/18 accounted for around three quarters (74%) of cervical cancers. These two types are covered in the 4-valent HPV vaccine offered to girls since 2008 as well as the 9-valent vaccine, which has been in use in Denmark since November 2017.
One third (26%) of cervical cancers prior to the HPV immunization campaign were caused by high-risk types that are not covered by the 2- and 4-valent vaccine.

In their research article published in Eurosurveillance, a team led by Mette Hartmann Nonboe examined the HPV status of cervical samples over time among women (22–30 years) at the screening age for cervical cancer who were vaccinated as girls.

They tested up to three consecutive cervical cell samples per participant provided by the contributing pathology departments in Denmark for HPV.

In total, 17,252 women with at least one cervical cell sample were registered between 1 February 2017 and 29 February 2024. During the seven years of the randomized "Trial23" study (cervical cancer screening starts at age 23 in Denmark), 84% of women in the study had at least one cell sample taken. The authors compared HPV prevalence, persistence and incidence among vaccinated and unvaccinated women.
Part 1

Based on the data gathered during the study period, HPV16/18 has been almost eliminated among vaccinated women in Denmark. The prevalence of these two types in the samples decreased to < 1% in 2021 from 15–17% before the vaccination of girls. In addition, the prevalence of types 16/18 in women who had not been vaccinated against HPV remained at 5%, which, according to the authors, "strongly indicates population immunity."

Despite the evidence of protection through vaccination, about one-third of women screened during the study period still had HPV infection with high-risk HPV types not covered by the offered vaccines—and new infections with these types were more frequent in vaccinated women than in unvaccinated women.
There was a low prevalence of HPV16/18 during the seven-year study period and women who have been vaccinated against HPV as girls are expected to have a considerably lower risk of cervical cancer compared with previous generations.

Human papillomavirus prevalence in first, second and third cervical cell samples from women HPV-vaccinated as girls, Denmark, 2017 to 2024: data from the Trial23 cohort study, Eurosurveillance (2025). DOI: 10.2807/1560-7917.ES.2025.30.27.2400820

Part 2

Global vaccine stockpiles prevented more than 5.8 million cases

The life-saving impact of global vaccine stockpiles to address outbreaks of vaccine-preventable diseases has been demonstrated in new Burnet Institute research.

Published in the journal BMJ Global Health, the study considered 210 outbreaks that occurred between 2000 and 2023 for five diseases—cholera, Ebola, measles, meningitis and yellow fever.

Outbreak response immunization was estimated to have prevented more than 5.8 million cases and 327,000 deaths across these outbreaks, providing economic benefits of almost US$32 billion.

For diseases with routine vaccination programs, maintaining high levels of population immunity is vital for preventing large outbreaks.

But when outbreaks do occur, a rapid vaccine response typically provides the greatest protective impact for the population at risk—and the faster the response, the greater the impact. While vaccines are amazing preventively, they are also excellent when used reactively to control outbreaks and save lives.

Vaccine stockpiles have not only prevented many cases and deaths, but they have also prevented outbreaks from reaching the point where they cause substantive issues, and that's really important, say the researchers.

 Dominic Delport et al, Estimating the historical impact of outbreak response immunisation programmes across 210 outbreaks in low and middle-income countries, BMJ Global Health (2025). DOI: 10.1136/bmjgh-2024-016887. gh.bmj.com/content/10/7/e016887

Newly discovered molecule may explain reduced muscle mass in type 2 diabetes

Researchers  have discovered a previously unknown molecule that may explain why people with type 2 diabetes often suffer from muscle weakness and muscle loss—a condition that has a major impact on quality of life and overall health.

In the new study, published in Science Advances, researchers have identified a previously unknown molecule, TMEM9B-AS1, which may explain why people with type 2 diabetes often suffer from muscle weakness and loss of muscle mass. The molecule is a long non-coding RNA that plays an important role in regulating cellular functions.

The researchers discovered that TMEM9B-AS1 is significantly reduced in skeletal muscles in individuals with type 2 diabetes, and its absence disrupts the machinery needed to build new muscle proteins.

The study shows that TMEM9B-AS1 supports the stability of MYC, a key gene that drives the production of ribosomes—the factories that manufacture proteins. Without this RNA molecule, MYC becomes unstable, and muscle cells lose their ability to maintain normal protein production. This may help explain the muscle deterioration we often see in people with metabolic diseases.  

Ilke Sen et al, Down-regulation of human-specific lncRNA TMEM9B-AS1 in skeletal muscle of people with type 2 diabetes affects ribosomal biogenesis, Science Advances (2025). DOI: 10.1126/sciadv.ads4371

Bacteria takes the poison out of mercury
An engineered strain of the gut microbe Bacteroides thetaiotaomicron can break down methylmercury (MeHg), a potent neurotoxin that’s increasingly found in seafood as a result of pollution. Researchers inserted two genes into the bacteria that snip MeHg into a carbon molecule and plain mercury, which isn’t as easily absorbed by the body. Pregnant mice that were given the engineered B. thetaiotaomicron and fed a diet high in MeHg-laced tuna excreted more mercury in their faeces and had lower levels of mercury in both maternal and foetal tissues than those with a normal microbiome.

https://www.cell.com/cell-host-microbe/abstract/S1931-3128(25)00142-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1931312825001428%3Fshowall%3Dtrue

3I/ATLAS: Interstellar object 'may be oldest comet ever seen'

A mystery interstellar object discovered last week is likely to be the oldest comet ever seen—possibly predating our solar system by more than 3 billion years, researchers say.

The "water ice-rich" visitor, named 3I/ATLAS, is only the third known object from beyond our solar system ever spotted in our cosmic neighborhood and the first to reach us from a completely different region of our Milky Way galaxy.

It could be more than 7 billion years old.

Unlike the previous two objects to enter our solar system from elsewhere in the cosmos, 3I/ATLAS appears to be traveling on a steep path through the galaxy, with a trajectory that suggests it originated from the Milky Way's "thick disk"—a population of ancient stars orbiting above and below the thin plane where the sun and most stars reside.

All non-interstellar comets such as Halley's comet formed with our solar system, so are up to 4.5 billion years old.

But interstellar visitors have the potential to be far older, and of those known about so far our statistical method suggests that 3I/ATLAS is very likely to be the oldest comet we have ever seen.

The object was first spotted on 1 July 2025 by the ATLAS survey telescope in Chile, when it was about 670 million km from the sun.

Research predicts that, because 3I/ATLAS likely formed around an old, thick-disk star, it should be rich in water ice.

This is an object from a part of the galaxy we've never seen up close before. Researchers think there's a two-thirds chance this comet is older than the solar system, and that it's been drifting through interstellar space ever since.

As it approaches the sun, sunlight will heat 3I/ATLAS's surface and trigger cometary activity, or the outgassing of vapor and dust that creates a glowing coma and tail.

Early observations already suggest the comet is active, and possibly larger than either of its interstellar predecessors, 1I/'Oumuamua (spotted in 2017) and 2I/Borisov (2019).

The Galactic Interstellar Object Population in the LSST. conference.astro.dur.ac.uk/eve … 7/contributions/751/

Matthew J. Hopkins et al, From a Different Star: 3I/ATLAS in the context of the Ōtautahi-Oxford interstellar object population model, arXiv (2025). DOI: 10.48550/arxiv.2507.05318 ,
doi.org/10.48550/arXiv.2507.05318

Premenstrual symptoms linked to increased risk of cardiovascular disease

Women diagnosed with premenstrual symptoms have a slightly increased risk of developing cardiovascular disease later in life. This is shown by a new study  published in Nature Cardiovascular Research.

Premenstrual symptoms include premenstrual syndrome (PMS) and the more severe form, premenstrual dysphoric disorder (PMDD). The symptoms, which appear a few days before menstruation and then subside, can be both psychological and physical.

The study included more than 99,000 women with premenstrual symptoms who were followed for up to 22 years. The researchers compared their health with women without these symptoms—both in the general population and by comparing them with their own sisters to take into account hereditary factors and upbringing.

The results show that women with premenstrual symptoms had about a 10% higher risk of developing cardiovascular disease. When the researchers also looked at different types of cardiovascular disease, they found that the link was particularly strong for heart rhythm disorders (arrhythmias), where the risk was 31% higher, and for stroke caused by a blood clot, where the risk was 27% higher.

Even after the researchers took into account other factors such as smoking, BMI and mental health, the link between premenstrual symptoms and increased disease risk remained.

The increased risk was particularly clear in women who were diagnosed before the age of 25 and in those who had also experienced postnatal depression, a condition that can also be caused by hormonal fluctuations.

Research has not yet identified the cause of this link, but the researchers behind the study suggest three possible explanations. One is that women with premenstrual symptoms may have a disrupted regulation of the renin-angiotensin-aldosterone system (RAAS), which controls blood  pressure and fluid balance in the body, among other things.

The second is that these women have increased levels of inflammation in the body, which is a known risk factor for atherosclerosis and other heart problems. Finally, it may be because women with premenstrual symptoms may have metabolic abnormalities, which are linked to an increased risk of both stroke and heart attack.

Yihui Yang, et al. Premenstrual disorders and risk of cardiovascular diseases, Nature Cardiovascular Research (2025). DOI: 10.1038/s44161-025-00684-4

Quantum objects' dual nature mapped with new formula for 'wave-ness' and 'particle-ness'

Quantum mechanics has revolutionized our understanding of nature, revealing a bizarre world in which an object can act like both waves and particles, and behave differently depending on whether it is being 'watched'.

In recent decades, researchers exploring this wave-particle duality have learned to measure the relative "wave-ness" and "particle-ness" of quantum objects, helping to explain how and when they veer between wave-like or particle-like behaviors.

Now, in a paper for Physical Review Research, researchers at the Stevens Institute of Technology report an important new breakthrough: a simple but powerful formula that describes the precise closed mathematical relationship between a quantum object's "wave-ness" and "particle-ness."

Previous research showed that wave-ness and particle-ness could be expressed as an inequality, with the sum of an object's wave-like behaviors (such as visible interference patterns) and particle-like behaviors (such as the predictability of its path or location) being equal to or less than one.

That's important, because it means that if an object is fully wave-like, then it shows no particle-like behaviors, and vice versa. 

Such models were incomplete, however, because they can describe situations in which an object's wave-like and particle-like behaviors increase simultaneously—the opposite of the actual exclusive relationship between the two behaviors.

To remedy that, the authors introduced a new variable: the coherence of the quantum object.

That enables the calculation of both wave-ness and particle-ness with far more precision. By measuring the coherence in a system, in fact, it becomes possible to calculate a quantum object's level of wave-ness and particle-ness—not simply as "less than one," but as an exact value.

The relationship between wave-ness and particle-ness can then be plotted as an elegant curve on a graph—a perfect quarter-circle for a perfectly coherent system, and a flatter ellipse as the level of coherence declines.

 Pawan Khatiwada et al, Wave-particle duality ellipse and application in quantum imaging with undetected photons, Physical Review Research (2025). DOI: 10.1103/dyg6-l19j

How do rivers choose their path?

Rivers choose their path based on erosion, a discovery that could transform flood planning and restoration

Rivers are Earth's arteries. Water, sediment and nutrients self-organize into diverse, dynamic channels as they journey from the mountains to the sea. Some rivers carve out a single pathway, while others divide into multiple interwoven threads. These channel patterns shape flood risks, erosion hazards and ecosystem services for more than three billion people who live along river corridors worldwide.

Understanding why some waterways form single channels, while others divide into many threads, has perplexed researchers for over a century. Geographers recently mapped the thread dynamics along 84 rivers with 36 years of global satellite imagery to determine what dictates this aspect of river behavior.

The researchers found that rivers will develop multiple channels if they erode their banks faster than they deposit sediment on their opposing banks. This causes a channel to widen and divide over time.

The results, published in the journal Science, solve a longstanding quandary in the science of rivers. They also provide insight into  natural hazards and river restoration efforts.

Austin J. Chadwick et al, Single- and multithread rivers originate from (im)balance between lateral erosion and accretion, Science (2025). DOI: 10.1126/science.ads6567