How age affects vaccine responses and how to make them better

 Scientists are learning why vaccines can trigger a weaker response in older adults, around age 65, and what can be done to improve them. These insights open the door to designing more effective vaccines.

In the largest study of its kind, published in Nature, scientists discover that our T cells—key players in coordinating immune responses—undergo profound and specific changes as we age. These changes, far from being random or a byproduct of chronic disease and inflammation, are a fundamental feature of healthy aging and will happen to all of us as we get older.

Inflammation is not driving healthy aging. Scientists think inflammation is driven by something independent from just the age of a person.

This is important because there's been research showing similar findings that inflammation and aging don't go hand in hand, and your immune system is just changing with age.

The changes also point to why vaccines, including the annual flu shot and COVID-19 boosters, tend to be less effective in older adults.

T cells are a critical part of our immune system that help "train" white blood cells, called B cells, to produce antibodies in response to viruses and vaccines. But this study found that memory T cells in older adults undergo a dramatic shift toward what is known as a "Th2-like" state, which is a change in gene expression that fundamentally alters how these cells respond to threats.
Researchers found this shift directly affects B cells' ability to generate strong antibody responses. In other words, the flu shot might still deliver the right viral components, but if the memory T cells aren't functioning properly, the body struggles to respond effectively.
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With this insight, doctors may be able to use a person's immune profile to predict how well they'll respond to a vaccine. Now that scientists can pinpoint how T cells become less effective with age, they can also start designing new vaccine formulas or immune-boosting treatments to address these issues.
Since T cells in older adults function differently, scientists could reformulate vaccines to compensate specifically for age-related cellular changes rather than using a one-size-fits-all approach. Gene-editing tools like CRISPR could also be used to reprogram a person's T cells before vaccination, essentially re-programming older immune cells to make them respond to vaccines like younger cells do—like CAR-T cell therapy that reprograms immune cells to fight cancer.
Researchers say this work goes beyond just vaccines and reveals how our immune systems change in all of us as we get older and how our bodies fight age-related disease and viruses. It also opens the door to interventions like new therapies to restore key immune cells.

Claire Gustafson, Multi-omic profiling reveals age-related immune dynamics in healthy adults, Nature (2025). DOI: 10.1038/s41586-025-09686-5. www.nature.com/articles/s41586-025-09686-5

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Mathematical proof debunks the idea that the universe is a computer simulation

It's a plot device beloved by science fiction: our entire universe might be a simulation running on some advanced civilization's supercomputer. But new research  has mathematically proven this isn't just unlikely—it's impossible.

Researchers  have shown that the fundamental nature of reality operates in a way that no computer could ever simulate.

Their findings, published in the Journal of Holography Applications in Physics, go beyond simply suggesting that we're not living in a simulated world like The Matrix. They prove something far more profound: the universe is built on a type of understanding that exists beyond the reach of any algorithm.

It has been suggested that the universe could be simulated. If such a simulation were possible, the simulated universe could itself give rise to life, which in turn might create its own simulation. This recursive possibility makes it seem highly unlikely that our universe is the original one, rather than a simulation nested within another simulation. This idea was once thought to lie beyond the reach of scientific inquiry. However, the recent research has demonstrated that it can, in fact, be scientifically addressed.

The research hinges on a fascinating property of reality itself. Modern physics has moved far beyond Newton's tangible "stuff" bouncing around in space. Einstein's theory of relativity replaced Newtonian mechanics. Quantum mechanics transformed our understanding again. Today's cutting-edge theory—quantum gravity—suggests that even space and time aren't fundamental. They emerge from something deeper: pure information.

This information exists in what physicists call a Platonic realm—a mathematical foundation more real than the physical universe we experience. It's from this realm that space and time themselves emerge.

Here's where it gets interesting. The team demonstrated that even this information-based foundation cannot fully describe reality using computation alone. They used powerful mathematical theorems—including Gödel's incompleteness theorem—to prove that a complete and consistent description of everything requires what they call "non-algorithmic understanding."

Think of it this way. A computer follows recipes, step by step, no matter how complex. But some truths can only be grasped through non-algorithmic understanding—understanding that doesn't follow from any sequence of logical steps. These "Gödelian truths" are real, yet impossible to prove through computation.

Part 1

Here's a basic example using the statement, "This true statement is not provable." If it were provable, it would be false, making logic inconsistent. If it's not provable, then it's true, but that makes any system trying to prove it incomplete. Either way, pure computation fails.
So researchers have demonstrated that it is impossible to describe all aspects of physical reality using a computational theory of quantum gravity.
Therefore, no physically complete and consistent theory of everything can be derived from computation alone. Rather, it requires a non-algorithmic understanding, which is more fundamental than the computational laws of quantum gravity and therefore more fundamental than spacetime itself."
Since the computational rules in the Platonic realm could, in principle, resemble those of a computer simulation, couldn't that realm itself be simulated?

No, say the researchers. Their work reveals something deeper.

Drawing on mathematical theorems related to incompleteness and indefinability, they demonstrate that a fully consistent and complete description of reality cannot be achieved through computation alone.
It requires non-algorithmic understanding, which by definition is beyond algorithmic computation and therefore cannot be simulated. Hence, this universe cannot be a simulation, the researchers conclude.
Part 2

This research has profound implications. "The fundamental laws of physics cannot be contained within space and time, because they generate them. It has long been hoped, however, that a truly fundamental theory of everything could eventually describe all physical phenomena through computations grounded in these laws. Yet we have demonstrated that this is not possible. A complete and consistent description of reality requires something deeper—a form of understanding known as non-algorithmic understanding.
The team's conclusion is clear and marks an important scientific achievement.
Any simulation is inherently algorithmic—it must follow programmed rules. But since the fundamental level of reality is based on non-algorithmic understanding, the universe cannot be, and could never be, a simulation.
The simulation hypothesis was long considered untestable, relegated to philosophy and even science fiction, rather than science. This research brings it firmly into the domain of mathematics and physics, and provides a definitive answer.

Mir Faizal et al, Consequences of Undecidability in Physics on the Theory of Everything, Journal of Holography Applications in Physics (2025). DOI: 10.22128/jhap.2025.1024.1118. On arXiv: DOI: 10.48550/arxiv.2507.22950

Part 3

Babies' gut bacteria may influence future emotional health

A child's early gut microbiome may influence their risk of developing depression, anxiety or other internalizing symptoms in middle childhood, according to a new UCLA Health study. The effect appears to be related to the way bacteria are linked to communication across emotion-related brain networks.

Published in the journal Nature Communications, the observational study found that young children whose gut microbiome had a higher representation of bacteria in the Clostridiales order and Lachnospiraceae family were at higher risk of experiencing internalizing symptoms—an umbrella term that includes symptoms of depression and anxiety—in middle childhood. The connection appeared to work indirectly: The early microbiome composition was associated with differences in connectivity across different emotion-related brain networks that were linked to anxiety and depression later in childhood.

The findings suggest that early gut bacteria could play a role in programming brain circuits tied to emotional health in later childhood. If unaddressed, symptoms of depression and anxiety can carry a higher risk of mental health challenges persisting as children develop into adolescence and adulthood.

The study provides early evidence that  git microbes could help shape mental health during the critical school-age years.

Childhood gut microbiome is linked to internalizing symptoms at school age via the functional connectome, Nature Communications (2025). DOI: 10.1038/s41467-025-64988-6

How a chorus of synchronized frequencies helps you digest your food

Synchronization abounds in nature: from the flashing lights of fireflies to the movement of fish wriggling through the ocean, biological systems are often in rhythmic movement with each other. The mechanics of how this synchronization happens are complex.

For instance, in the vasculature of the brain, blood vessels oscillate, expanding and contracting as needed. When there is neural activity, the arterioles expand to increase blood flow, oxygen and nutrients. These oscillations are self-sustained, but the arterioles also work in concert with each other.

To uncover the answer, researchers looked to another part of the body: the gut. Here they found that oscillators operating at similar frequencies lock onto each other in succession, creating a staircase effect. Their work appears in Physical Review Letters.

It is known in the scientific community that if you have a self-sustained oscillation, such as an arteriole, and you add an external stimulus at a similar but not identical frequency, you can lock the two, meaning you can shift the frequency of the oscillator to that of the external stimulus. In fact, it has been shown that if you connect two clocks, they will eventually synchronize their ticking.

Researchers now found that if they applied an external stimulus to a neuron, the entire vasculature would lock at the same frequency. However, if they stimulated two sets of neurons at two different frequencies, something unexpected happened: some arterioles would lock at one frequency and others would lock at another frequency, forming a staircase effect.

The researchers found they could use a classical model of coupled oscillators with an intestinal twist to explain this.

The gut oscillates naturally due to peristalsis—the contracting and relaxing of muscles in the digestive tract—and provided a simplified model over the complex network of blood vessels in the brain. The intestine is unidirectional, meaning frequencies shift in one direction in a gradient from higher to lower. This is what enables food to move in one direction from the beginning of the small intestine to the end of the large intestine.

Coupled oscillators talk to each other and each section of the intestine is an oscillator that talks to the other sections near it. 

Normally, coupled oscillators are studied in a homogeneous setting, meaning all the oscillators are at more or less similar frequencies. In our case, the oscillators were more varied, just as in the intestine and the brain.

Part 1

In studying the coupled oscillators in the gut, past researchers observed that there is indeed a staircase effect where similar frequencies lock onto those around it, allowing for the rhythmic movement of food through the digestive tract. But the height of the rises or breaks, the length of the stair runs or frequencies, and the conditions under which the staircase phenomenon occurred—essential features of biological systems—was something which had not been determined until now.
This new mathematical solution answers two longstanding biological questions at the same time: how food moves through the digestive tract and how it is churned. The team hopes this work will support further research into peristalsis-related digestive health issues known as gastrointestinal motility disorders.

The mathematics had been solved in an approximate way before now, but not in a way that gave you these breaks and what happens at the breaks. That's a critical discovery.
Now that they've solved the question of oscillations in the gut, they're back to studying the complex vasculature of the brain. If the gut is unidirectional, the vasculature in the brain has hundreds of directions. While they both feature staircases, the one in the gut goes from one level to the next, one at a time. The stairs in the brain go along different paths at different lengths all at once.

The brain is infinitely more complicated than the gut, but this is science at its best. You ask one question, it leads you somewhere else, you solve that problem, then return to your original question.

Marie Sellier-Prono et al, Defects, Parcellation, and Renormalized Negative Diffusivities in Nonhomogeneous Oscillatory Media, Physical Review Letters (2025). DOI: 10.1103/8njd-qd14. On arXiv: DOI: 10.48550/arxiv.2502.09264

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Why pumpkins accumulate pollutants

Pumpkins, squash, zucchini and their relatives accumulate soil pollutants in their edible parts. A  research team has now identified the cause, making it possible to both make the produce safer and create plants that clean contaminated soil.

The gourd family of plants comprising pumpkins, zucchini, melons, cucumbers and more are known to accumulate high levels of pollutants in their edible parts.

The pollutants don't easily break down and thus pose a health risk to people who eat the fruit. Interestingly, other plants don't do this.

In previous studies, researchers identified a class of proteins from across the gourd family that bind to the pollutants, thus enabling them to be transported through the plant. Earlier this year, they discovered that the shape of the proteins and their binding affinity to the pollutants influence the accumulation in the aboveground plant parts. Their study was published in Plant Physiology and Biochemistry.

However, these proteins exist in many other plants, and even among the gourds, there are varieties that are more prone to accumulating pollutants than others. Researchers then noticed that in the highly accumulating varieties, there are higher concentrations of the protein in the sap.

In the same journal, the  same research team has now published that they could show that the protein variants from the highly accumulating plants are indeed exported into the sap, whereas other variants are retained in the cells.

They could also pinpoint that this is likely due to a small difference in the protein's amino acid sequence that acts as a tag that tells the cell which proteins to retain within. The team proved their point by showing that unrelated tobacco plants in which they introduced the highly accumulating protein versions also exported the protein into the plant sap.

Only secreted proteins can migrate inside the plant and be transported to the aboveground parts. Therefore, this seems to be the distinguishing factor between low-pollution and high-pollution plant varieties.

Understanding the mechanism behind pollutant accumulation is crucial to creating safer produce.

Minami Yoshida et al, Extracellular secretion of major latex-like proteins related to the accumulation of the hydrophobic pollutants dieldrin and dioxins in Cucurbita pepo, Plant Physiology and Biochemistry (2025). DOI: 10.1016/j.plaphy.2025.110612

Hideyuki Inui et al, Binding affinity of major latex-like proteins toward polycyclic aromatic hydrocarbons influences their aboveground accumulation in the Cucurbitaceae family, Plant Physiology and Biochemistry (2025). DOI: 10.1016/j.plaphy.2025.110280

Synthetic biology to supercharge photosynthesis in crops

 Researchers have created tiny compartments to help supercharge photosynthesis, potentially boosting wheat and rice yields while slashing water and nitrogen use.

How can we make plants fix carbon more efficiently? Scientists ask this question most of the time. 

So they engineered nanoscale "offices" that can house an enzyme called Rubisco in a confined space, enabling scientists to fine-tune compatibility for future use in crops, which should allow them to produce food with fewer resources. Their research is published in Nature Communications.

Rubisco is a common enzyme in plants that is essential for "fixing" carbon dioxide for photosynthesis, the chemical process that uses sunlight to make food and energy for plants.

Rubisco is very slow and can mistakenly react with oxygen instead of CO₂ which triggers a whole other process that wastes energy and resources. This mistake is so common that important food crops such as wheat, rice, canola and potatoes have evolved a brute-force solution: mass-produce Rubisco.

In some leaves, up to 50% of the soluble protein is just copies of this one enzyme, representing a huge energy and nitrogen expense for the plant. It's a major bottleneck in how efficiently plants can grow.

Some organisms solved this problem millions of years ago. Algae and cyanobacteria house Rubisco in specialized compartments and supply them with concentrated CO₂. They're like tiny home offices that allow the enzyme to work faster and more efficiently, with everything it needs close at hand.

Scientists have been trying for years to install these natural CO₂-concentrating systems into crops. But even the simplest of these Rubisco-containing compartments from cyanobacteria, called carboxysomes, are structurally complicated. They need multiple genes working in precise balance and can only house their native Rubisco.

Researchers in the current study 

took a different approach, using encapsulins. These are simple bacterial protein cages that require just one gene to build. Think of it like Lego blocks that automatically snap into place, rather than assembling complicated flat-pack furniture.

To load Rubisco inside, the researchers added a short "address tag" of 14 amino acids to the enzyme that, like a zip code, directs the enzyme to its destination inside the assembling compartment.

This worked well. 

Crops with this elevated CO2-fixing technology could produce higher yields while using less water and nitrogen fertilizer. These are critical advantages as climate change and population growth put pressure on global food systems.

Taylor N. Szyszka et al, Reprogramming encapsulins into modular carbon-fixing nanocompartments, Nature Communications (2025). DOI: 10.1038/s41467-025-65307-9

How parasitic cuckoos lay host-matching eggs while remaining a single species

European cuckoos lay very different eggs depending on the host species. Genetic analyses have revealed how this adaptation is inherited without leading to speciation.

Bright blue, white, greenish, speckled, or striped—cuckoo eggs exhibit an extraordinary variety. This range of colors is the result of an evolutionary race with over 100 avian host species. Cuckoos famously do not incubate their eggs, but secretly lay them in the nests of other bird species.

To ensure that the host does not recognize the cuckoo egg and throw it out of its nest, the egg must closely resemble the eggs of its host parent. However, every female cuckoo is tied to lay eggs of a specific color and pattern. This suggests that various evolutionary lineages of the European cuckoo (Cuculus canorus) exist, with each of them adapted to a specific avian host species.

An international team has now deciphered the genetic basis of these adaptations and shown how the cuckoo remains a single species. This calls for explanation, because as cuckoos evolve specialized adaptations to exploit new hosts, these populations could begin to genetically diverge to the point of forming new species.

For their study, the researchers analyzed some 300 genomes of the European and 50 of the Oriental cuckoo (Cuculus optatus), its eastern sister species. Subsequently, they checked which gene variants corresponded to the egg coloration.

The paper is published in the journal Science.

Part 1

The question was: How can a cuckoo reliably pass on the right egg color? After all, a female might not know what her own egg looks like.
Presumably, a female cuckoo will return to a nest of the type in which she was raised. For the egg color to really match, however, it needs to be encoded in the bird's genes. As far back as the 1930s, the hypothesis was formulated that the responsible genes reside somewhere on the maternal lineage.

The current analyses now confirm that the base color of the eggs of the European cuckoo is inherited almost exclusively via the female sex chromosome—the W chromosome—and mitochondria. The patterning, by contrast, depends to a greater extent on autosomal genes, which come from both parents. In the Oriental cuckoos studied, whose eggs were all whitish-green and differed only in their patterning, the researchers found no inheritance via the maternal lineage.
Inheritance via the W chromosome ensures that daughters always lay eggs with the same base color as their mothers. For new adaptations, however, this type of inheritance is suboptimal, as the possibilities of genetic variation are limited and more strongly dependent on random mutations than in the case of DNA inherited from both parents.
The researchers observed that a gene which 's possibly involved in egg coloration evidently 'migrated' from the autosomes [the non-sex chromosomes inherited from both parents] to the W chromosome.
Matrilineal inheritance shapes how genetic variation is spread across a species. When traits matter for both males and females, adapting to different hosts can quickly drive populations apart—and eventually create new species. In the cuckoo, by contrast, females can freely mate with any male without losing their adaptation to their host. The flow of genetic information across the rest of the genome is preserved.
And that is precisely what the researchers observed: The huge cuckoo population throughout Eurasia is almost genetically identical within DNA regions inherited from both parents.
But this evolutionary advantage does not protect the cuckoo from the dangers of the present. In many regions of Europe, populations are significantly declining, because their habitats are disappearing. "Without intact habitats, this fascinating system risks vanishing on our doorstep," caution the researchers.

Justin Merondun et al, Genomic architecture of egg mimicry and its consequences for speciation in parasitic cuckoos, Science (2025). DOI: 10.1126/science.adt9355

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AI gets ‘brain rot’ from social media
Artificial intelligence (AI) chatbots trained on ‘brain rot’ content — vapid social media posts that are the equivalent of mental junk food — are worse at generating accurate information. Researchers found that chatbots given a diet of popular and sensationalist Twitter/X posts skipped steps in their reasoning process (or didn’t use reasoning at all), spat out wrong answers and demonstrated ‘dark traits’ such as psychopathy and increased levels of narcissism.

Nature 
 arXiv preprint (not peer reviewed)

Chimpanzees rationally revise their beliefs

New evidence? No problem. Chimps can weigh conflicting clues, just like humans

Study is first to suggest our closest relatives think about their own thoughts

 Chimpanzees rationally revise their beliefs on the basis of evidence. 

In a series of play-based experiments at a Ugandan chimp sanctuary, researchers watched as the apes assessed the quality of the evidence before them, altered their behavior based on what they saw, and even revised their beliefs in light of new information. The results, published recently in Science, suggest chimpanzees can use the evidence in front of them to make smart decisions—and strengthen the case that these great apes think about their own thoughts, with awareness of what they do and don’t know.

https://www.science.org/doi/10.1126/science.adq5229

Prenatal exposure to specific fine particles linked to autism risk

A multi-institutional team  has found that prenatal air exposure to specific particulate matter components and early-life ozone is associated with autism spectrum disorder in  children.

Fine particulate matter has been linked to adverse health outcomes, with prenatal and early postnatal exposure associated with neurodevelopmental outcomes including autism spectrum disorder.

Most previous work has focused on fine particulate matter of airborne particles with a diameter of 2.5 micrometers or less (PM2.5), leaving uncertainty about variation in toxic effects among various chemical components and timing of exposure related to sensitive points in pregnancy. A large Southern California cohort study reported associations for several components, including sulfate, and a follow-up study also noted nitrate.

In the study, "Prenatal Exposure to Fine Particulate Matter Components and Autism Risk in Childhood," published in JAMA Network Open, researchers conducted a population-based retrospective cohort study to examine associations between prenatal and first-year-of-life exposure to specific PM_2.5 components, nitrogen dioxide, and ozone with autism diagnoses, and to identify potentially sensitive gestational windows.

Looking at birth through the first five years in Ontario, covering approximately 20 years, yielded 2,183,324 children after exclusions and 19,569 children who received an autism diagnosis.

Exposure assessment assigned prenatal concentrations by maternal postal code at delivery. Weekly nitrogen dioxide and ozone and biweekly PM2.5 mass and components were estimated from conception to age 36 weeks, with first-year exposures as annual postal code–level averages weighted by time at each address. Components included black carbon, dust, ammonium, nitrate, organic matter, sulfate, and sea salt. Models integrated satellite data, chemical transport modeling, land-use regression, and ground monitoring data.

Prenatal PM_2.5 mass was associated with increased risk when adjusted for first-year averages (HR 1.15), and window-specific signals were driven by sulfate during weeks 23–36 (HR 1.11) and ammonium during weeks 21–34 (HR 1.11), after which PM_2.5 mass was no longer associated with autism.

First-year ozone exposure was associated with autism risk with HR 1.09. Weekly models indicated significant windows for PM_2.5 during gestational weeks 14 to 32, sulfate during weeks 23 to 36, ammonium during weeks 21 to 34, and ozone during weeks 26 to 30, with reported window-specific HRs of 1.12 for PM_2.5, 1.11 for sulfate, 1.11 for ammonium, and 1.03 for ozone.

Black carbon, organic matter, dust, sea salt were not significant after adjustments, suggesting that specific chemical and not general PM_2.5 exposure associations.

Part 1

Urban settings showed larger estimated effects for PM2.5, sulfate, and ammonium compared with rural areas. Sex-stratified results indicated larger estimates for male children, with sulfate the only pollutant significantly associated among female children.

Neighborhood patterns suggested more pronounced estimated risks in lower-income and middle-income areas and in areas with higher proportions of racialized and newcomer populations.

Authors conclude that prenatal exposure to specific PM2.5 components, particularly sulfate and ammonium, was associated with autism risk, with sensitive periods in the second and third trimesters.

Postnatal ozone exposure in the first year of life was also associated with risk. Findings point to the potential importance of early-life environmental exposures.

Maxime Cloutier et al, Prenatal Exposure to Fine Particulate Matter Components and Autism Risk in Childhood, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.38882

Part 2

Bacteria borrow jumbo phages to spread their own defenses

A team of evolutionary biology researchers has discovered a new class of bacterial mobile genetic elements that use giant viruses—known as jumbo phages—to move between cells. The work, published in the Proceedings of the National Academy of Sciences, uncovers an unexpected twist in the long-running arms race between bacteria and their viruses.

In the study, a common bacterium was exposed to sterile filtrate from garden compost. The bacterium picked up several previously unknown DNA elements, each carrying genes that defend against phage infection. Remarkably, one of these elements, named I55, was found to hitch a ride on a jumbo phage, making it one of the first examples of a phage satellite exploiting such a large virus. The element not only spreads via the phage but also protects its bacterial host through a restriction–modification system—effectively allowing the bacterium to borrow viral machinery for its own benefit.

Yansong Zhao et al, Jumbo phage–mediated transduction of genomic islands, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2512465122

Crop production in 155 countries relies on forests in other nations, moisture flows reveal

Forests play a crucial role in providing precipitation to agricultural areas, importantly supporting crop production and global trade activities. A recent study published in Nature Water emphasizes that to manage global food risks, it is essential to conserve forests located upwind of agricultural regions.

In recent decades, climate extremes have become more frequent and intense, leading to over half of the loss incidences in crop production worldwide. Concurrently, intense deforestation has diminished forests' ability to supply stable moisture to agricultural areas, resulting in reduced evaporation, less precipitation, and altered rainy seasons.

The moisture flows connect forests not only with the agricultural areas within the countries but also across the borders, according to a study by scholars.

To understand how forests contribute to global crop production and exports, the researchers compared moisture flows with crop production and export data.

This interdependence is well illustrated by the case of Brazil. In addition to providing moisture to its own agricultural areas, Brazilian forests influence crop production in Peru, Ecuador, Bolivia, Paraguay, Uruguay, and Argentina.

These countries account for 10% of global crop exports accounted in the study, including shipments to Europe, Asia, Africa, and Oceania. Thus, nations importing crops from South American countries are indirectly reliant on moisture from Brazilian forests.

The study reveals that overall, croplands in 155 countries depend on moisture from forests located in other countries for up to 40% of their annual precipitation.

Agnes Pranindita et al, Forests support global crop supply through atmospheric moisture transport, Nature Water (2025). DOI: 10.1038/s44221-025-00518-4

Bacteria reveal hidden powers of electricity transfer

Microbes are masters of survival, evolving ingenious strategies to capture energy from their surroundings. For decades, scientists thought that only a handful of bacteria used specialized molecular "circuits" to shuttle electrons outside their cells—a process known as extracellular electron transfer (EET). This mechanism is critical for cycling carbon, sulfur, nitrogen, and metals in nature, and it underpins applications ranging from wastewater treatment to bioenergy and bioelectronics materials.

Now researchers have discovered that this remarkable ability is far more versatile and widespread than previously imagined. The paper is published in The ISME Journal.

Working with Desulfuromonas acetexigens—a bacterium capable of generating high electrical currents—the team combined bioelectrochemistry, genomics, transcriptomics, and proteomics to map its electron transfer machinery. To their surprise, D. acetexigens simultaneously activated three distinct electron transfer pathways previously thought to have evolved separately in unrelated microbes: the metal-reducing (Mtr), outer-membrane cytochrome (Omc), and porin-cytochrome (Pcc) systems.

This is the first time researchers have seen a single organism express these phylogenetically distant pathways in parallel. It challenges the long-held view that these systems were exclusive to specific microbial groups.

The team also identified unusually large cytochromes, including one with a record-breaking 86 heme-binding motifs, which could enable exceptional electron transfer and storage capacity. Tests showed that the bacterium could channel electrons directly to electrodes and natural iron minerals, achieving current densities comparable to the model species Geobacter sulfurreducens.

By extending their analysis to publicly available genomes, the researchers identified more than 40 Desulfobacterota species carrying similar multipathway systems across diverse environments, from sediments and soils to wastewater and hydrothermal vents.

This reveals an unrecognized versatility in microbial respiration. Microbes with multiple electron transfer routes may gain a competitive advantage by tapping into a wider range of electron acceptors in nature.

The implications go well beyond ecology. Harnessing bacteria that can employ multiple electron transfer strategies could accelerate innovations in bioremediation, wastewater treatment, bioenergy production, and bioelectronics.

Dario R Shaw et al, Independently evolved extracellular electron transfer pathways in ecologically diverse Desulfobacterota, The ISME Journal (2025). DOI: 10.1093/ismejo/wraf097

Tissue 'tipping points': How cells collectively switch from healthy to disease states

Cells convert mechanical forces into signals that influence physiological processes, such as exercise strengthening bones. A research team has discovered that biological tissues can also undergo dramatic phase transitions, or collective shifts where wound healing cells can switch from disordered, healthy states to highly coordinated disease states, like when water suddenly freezes into ice.

This discovery, published Oct. 3, 2025, in Proceedings of the National Academy of Sciences, reveals why fibrotic diseases often progress in switch-like jumps rather than gradually and points to new therapeutic strategies that target the physical properties of tissue rather than just cellular biochemistry.

The team used computational modeling to uncover the mechanical "tipping point" that determines whether cells can collectively coordinate to spread a disease called fibrosis, an excessive scarring that underlies failure of nearly any organ, and especially in diseases of the liver, lungs, kidneys and heart.

What they have shown is that this isn't a gradual process.

There's a sharp transition point. When cells are within a critical spacing that depends on the way their matrix deforms, they can 'talk' to each other mechanically through the matrix. Above it, they're effectively isolated, and below it they interact strongly with one another. This on-off switch behavior is what we see in fibrosis progression: periods of stability followed by rapid scarring.

Phase transitions are familiar in physics: Water freezes to ice at 0°C, and iron becomes ferromagnetic below 770°C. The new research demonstrates that living tissues show similar behavior. When cells are spaced far apart in a tissue, they act independently, but when cell density crosses a critical threshold—a few hundred micrometers apart—they begin communicating mechanically and acting in concert, dramatically compacting and stiffening the tissue.

The research shows why this phase transition occurs: Fibrous networks like collagen enable long-range mechanical communication in a way that uniform elastic materials cannot.

Collagen fibers can be recruited and aligned by cell forces, creating stiffened 'tension bands' that act as mechanical communication highways, transmitting signals over much longer distances.

The critical factor is what the researchers call the "critical stretch ratio," which is how much the collagen must be stretched before individual fibers align and stiffen. This property is determined by collagen crosslinking, which increases with aging and is influenced by factors like diet, advanced glycation end products, and metabolic diseases like diabetes.

 Xiangjun Peng et al, Fiber recruitment drives a phase transition of cell polarization at a critical cell spacing in matrix-mediated tissue remodeling, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2514995122

'Rotten egg' gas could be the answer to treating nail infections, say scientists

Hydrogen sulfide, the volcanic gas that smells of rotten eggs, could be used in a new treatment for tricky nail infections that acts faster and with fewer side effects, according to scientists.

Hydrogen sulfide (H2S) demonstrates strong antimicrobial activity against a range of nail pathogens, including drug-resistant fungi, and penetrates the nail plate more effectively than current topical treatments. Laboratory results indicate it disrupts microbial energy production, causing irreversible damage. A topically applied H2S treatment may offer a faster, safer alternative for nail infections.

Nail infections are mostly caused by fungi and occasionally by bacteria. They are very common, affecting between 4 and 10% of the global population, rising to nearly half those aged 70 or over. These infections can lead to complications, particularly in vulnerable groups such as diabetics and the elderly, but are notoriously difficult to treat.
Current treatments include oral antifungals taken in pill form, and topical treatments applied directly to the nail. Oral antifungals take around 2–4 months to act and are reasonably effective, but they carry risks of side effects, especially in patients with other medical conditions.

Treatments applied directly to the nail are safer, but they often take much longer to work, sometimes taking even years to work, and they frequently relapse or fail. This is largely because it's very difficult to get the drug to penetrate through the nail to where the infection resides.

Even the most effective topical treatments have relatively low cure rates, so there is a clear need for new therapeutic approaches that are safe, effective, and capable of reaching microbes embedded deep within the nail.
Part 1

A research team has now found that hydrogen sulfide (H₂S), a small, naturally occurring gas, could be developed into a promising new treatment.
Previous work has shown that it penetrates the nail plate far more efficiently than existing topical drugs, and now the team has demonstrated that it has strong antimicrobial activity against a wide range of nail pathogens, including fungi that are resistant to common antifungal treatments.

In laboratory tests, the team used a chemical that breaks down to release the hydrogen sulfide gas and found that it acts in a unique way, disrupting microbial energy production and triggering irreversible damage, ultimately killing the fungi.

Fritz Ka-Ho Ho et al, Antimicrobial effects and mechanisms of hydrogen sulphide against nail pathogens, Scientific Reports (2025). DOI: 10.1038/s41598-025-22062-7

Part 2

Reactivating a fetal gene enables adult heart cells to regenerate after injury

Around the globe, heart disease remains one of the top causes of death. Once patients begin to suffer from serious heart problems, like heart attacks and heart failure, the heart muscles become damaged and are difficult to treat and repair. Although many therapies have been developed to treat symptoms, full recovery to a pre-disease state has been essentially impossible. This is due to a lack of regeneration ability in adult human heart cells. Studies using stem cells or progenitor cells for repair have demonstrated limited efficacy in clinical trials, thus far.

However, there may be new hope for these patients. Researchers have been working to turn back time by switching on a gene known to regenerate heart muscle cells, or cardiomyocytes. Their study, recently published in npj Regenerative Medicine, indicates that adult human hearts may be given the ability to regenerate themselves with future therapies.

The study focuses on a gene called Cyclin A2 (CCNA2), which is functional during fetal growth and shuts off shortly after birth, limiting the ability for cell regeneration. In fetuses, while CCNA2 is still functional, it plays an important role in cell division and growth, facilitating the creation of new heart cells. However, adults appear to still have a very limited capacity for repair.

"There has been evidence of low-level cardiomyocyte turnover in the healthy human heart, but it is very limited, and this ability declines with age. Thus, cardiac regeneration in response to injury such as myocardial infraction (MI) remains a clinical challenge," the researchers write.

The study authors refer to CCNA2 as the "master regulator" of the heart cell cycle. So far, studies surrounding CCNA2—mostly in animal models—have shown promise in its ability to be switched back on.

Part 1

In the new study, the team moved on to testing out this method on in vitro human cells from adults aged 41 and 55 years old. To do this, they engineered a harmless virus, capable of expressing human CCNA2 and delivered it to the cultured cells. They then performed live-cell imaging to track cell division and structure. Finally, they performed RNA sequencing in mouse and human heart samples to analyze any changes in gene expression.

The results were promising—CCNA2 induced heart cell regeneration in the 41 and 55-year-old heart cells, reactivating the fetal-like and regenerative gene programs in the cells. They found that the resulting daughter cells retained heart muscle structure and function, and continued to handle calcium effectively.

Additionally, RNA sequencing in mice revealed a subpopulation of heart cells with active cell division and reprogramming gene signatures, even after CCNA2 expression.

"Taken together, these findings suggest that the partial reprogramming induced by CCNA2 reflects a controlled activation of developmental programs, consistent with regenerative responses observed in neonatal hearts, and aligns with prior evidence that modest increases in cell cycle gene expression can enhance cardiac regeneration capacity," the study authors write in their paper.

Esmaa Bouhamida et al, Cyclin A2 induces cytokinesis in human adult cardiomyocytes and drives reprogramming in mice, npj Regenerative Medicine (2025). DOI: 10.1038/s41536-025-00438-7

Part 2

Large language models still struggle to tell fact from opinion, analysis finds

Large language models (LLMs) may not reliably acknowledge a user's incorrect beliefs, according to a new paper published in Nature Machine Intelligence. The findings highlight the need for careful use of LLM outputs in high-stakes decisions in areas such as medicine, law, and science, particularly when belief or opinions are contrasted with facts.

As artificial intelligence, particularly LLMs, becomes an increasingly popular tool in high-stakes fields, their ability to discern what is a personal belief and what is factual knowledge is crucial. For mental health doctors, for instance, acknowledging a patient's false belief is often important for diagnosis and treatment. Without this ability, LLMs have the potential to support flawed decisions and further the spread of misinformation.

Researchers analyzed how 24 LLMs, including DeepSeek and GPT-4o, responded to facts and personal beliefs across 13,000 questions. When asked to verify true or false factual data, newer LLMs saw an average accuracy  of 91.1% or 91.5%, respectively, whereas older models saw an average accuracy of 84.8% or 71.5%, respectively.

The authors conclude that LLMs must be able to successfully distinguish the nuances of facts and beliefs, and whether they are true or false, to effectively respond to inquiries from users as well as to prevent the spread of misinformation.

Mirac Suzgun et al, Language models cannot reliably distinguish belief from knowledge and fact, Nature Machine Intelligence (2025). DOI: 10.1038/s42256-025-01113-8. On arXiv: DOI: 10.48550/arxiv.2410.21195

Decoding how cells choose to become muscles or neurons

Every cell in the body has the same DNA, but different cell types—such as muscle or brain cells—use different parts of it. Transcription factors help cells activate specific genes by reading certain DNA sequences, but since these sequences are common across the genome, scientists have long wondered how the factors know exactly where to bind.

Researchers  set out to address this question by looking at two closely related transcription factors—NGN2 and MyoD1—that steer cells toward becoming neurons and muscle cells, respectively. Using stem cells, they switched these transcription factors on one at a time and watched where they attached to the DNA and how they influenced gene expression.

They found that the binding of transcription factors to the DNA molecule depends not only on the DNA sequence but also on how open the DNA is and which partner proteins are present. Sometimes, transcription factors act as "pioneer factors" and are able to open tightly packed DNA at specific sites to turn on genes. Small DNA changes—sometimes just one letter—and the proteins these factors partner with can affect whether genes are activated.

Next, the team trained a machine learning model to recognize patterns in transcription factor binding. Using this model, they identified a "DNA language" that predicts where and how these factors bind. The model accurately predicted outcomes across different cell types, helping explain how similar transcription factors can guide distinct developmental trajectories.

The findings not only deepen our understanding of how transcription factors drive cell fates, but they also offer powerful tools to predict and possibly steer these decisions in development and disease, the researchers say.

Sevi Durdu et al, Chromatin-dependent motif syntax defines differentiation trajectories, Molecular Cell (2025). DOI: 10.1016/j.molcel.2025.07.005

Time-restricted eating without calorie cuts doesn't improve metabolic health, study finds

Contrary to common assumptions, a new study  shows that intermittent fasting (time-restricted eating) with an unchanged calorie intake does not lead to measurable improvements in metabolic or cardiovascular parameters but does shift the body's internal clocks. Prof. Olga Ramich and her team published the results of the ChronoFast study in the journal Science Translational Medicine.

Time-restricted eating (TRE) is a form of intermittent fasting characterized by a daily eating period of no longer than 10 hours and a fasting period of at least 14 hours. TRE is increasingly popular as a simple dietary strategy for weight control and metabolic health improvement. In rodents, TRE protects against diet-induced obesity and related metabolic dysfunctions.

Similarly, TRE studies in humans have suggested numerous positive cardiometabolic effects, such as improved insulin sensitivity, glucose, triglyceride, and cholesterol levels, as well as moderate reductions in body weight and body fat. Consequently, TRE is considered a promising approach to combat insulin resistance and diabetes.

Results of previous TRE trials have been partly contradictory and have not yet clarified whether the metabolic improvements are due to the restriction of daily eating duration, due to spontaneous calorie restriction, or due to the combination of both factors. In fact, most previous studies have not carefully monitored energy intake or other potential confounding factors.

Therefore, this new study investigated whether an eight-hour eating period could improve insulin sensitivity and other cardiometabolic parameters in a tightly controlled isocaloric environment in the ChronoFast trial.

Contrary to previous studies suggesting positive effects of TRE, the ChronoFast study shows no clinically relevant changes in insulin sensitivity, blood sugar levels, blood fats, or inflammatory markers, at least following this relatively short two-week intervention. These results suggest that the health benefits observed in earlier studies were likely due to unintended calorie reduction, rather than the shortened eating period itself, explain the researchers. 

Although the participants showed no marked metabolic improvements, the study of the internal clock in blood cells revealed that TRE influenced the circadian phase in blood cells and the sleep timing. The internal clock was, on average, shifted back by 40 minutes after the lTRE intervention compared to the eTRE intervention, and participants who followed the lTRE intervention went to bed and awaked later. The timing of food intake acts as a cue for our biological rhythms—similar to light, the researchers say. 

The results underscore that calorie reduction plays a central role in the health benefits of intermittent fasting. 

Beeke Peters et al, Intended isocaloric time-restricted eating shifts circadian clocks but does not improve cardiometabolic health in women with overweight, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adv6787

Demystifying a visual illusion: Why we see color that's not there

A new discovery has unraveled why we sometimes see colors that aren't there. The phenomenon of "color afterimages" is when you see illusory—or false—colors after staring at real colors for a longer time. Through this, the brain can be tricked into seeing color in a black and white image.

The cause of this illusion is the mechanism that allows us to see colors the same throughout the day, independently of light changes. Without it, the color of the world would change as we are under yellow sunlight, a green canopy, or in a bluish shadow.

Scientists have long debated what causes color afterimages, and how the brain creates them.

Researchers found the missing link between the illusory colors we see and the neural mechanisms that produce them. The answer is in the cone cells in our eyes.

We've finally got a conclusive answer—color afterimages are not opposing colors as everybody had thought. Instead, those illusory colors reflect precisely what happens in the cone photoreceptors.

Across all the experiments, researchers found the same thing—afterimages are not caused by opposing colors, as many scientists have thought. Instead, they match what we'd expect if they were caused by how cone cells in the eye adapt to light.

So,  now it is certain that afterimages come from cone cells and not from other parts of the visual system.

Christoph Witzel, The non-opponent nature of colour afterimages, Communications Psychology (2025). DOI: 10.1038/s44271-025-00331-5

Part 1

Fixate on the cross and you will see the moving grey circle become purple. Credit: Communications Psychology (2025). DOI: 10.1038/s44271-025-00331-5

Rabies research unlocks how viruses do so much with so few proteins

New antivirals and vaccines could follow the discovery by  researchers of strategies used by viruses to control our cells. Published in Nature Communications, the study reveals how rabies virus manipulates so many cellular processes despite being armed with only a few proteins.

Researchers think other dangerous viruses like Nipah and Ebola may also work the same way, possibly enabling the development of antivirals or vaccines to block these actions.

Viruses such as rabies can be incredibly lethal because they take control of many aspects of life inside the cells they infect.  They hijack the machinery that makes proteins, disrupt the 'postal service' that sends messages between different parts of the cell, and disable the defenses that normally protect us from infection.

A major question for scientists has been: how do viruses achieve this with so few genes? Rabies virus, for example, has the genetic material to make only five proteins, compared with about 20,000 in a human cell.

Understanding how these few viral proteins performed so many tasks could unlock new ways to stop infection.

Scientists now discovered that one of the rabies virus's key proteins, called P protein, gains a remarkable range of functions through its ability to change shape and to bind to RNA.

RNA is the same molecule used in new-generation RNA vaccines, but it plays essential roles inside our cells, carrying genetic messages, coordinating immune responses, and helping make the building blocks of life.

 By targeting RNA systems, the viral P protein could switch between different physical "phases" inside the cell. This allows it to infiltrate many of the cell's liquid-like compartments, take control of vital processes, and turn the cell into a highly efficient virus factory.

Although this study focused on rabies, the same strategy is likely used by other dangerous viruses such as Nipah and Ebola. Understanding this new mechanism opens exciting possibilities for developing antivirals or vaccines that block this remarkable adaptability.

 Stephen M. Rawlinson et al, Conformational dynamics, RNA binding, and phase separation regulate the multifunctionality of rabies virus P protein, Nature Communications (2025). DOI: 10.1038/s41467-025-65223-y

Researchers discover an 'all-body brain' in sea urchins

An international team of researchers has uncovered a surprisingly complex nervous system in sea urchins. The animals appear to possess an "all-body brain" whose genetic organization resembles that of the vertebrate brain. The team also identified light-sensitive cells distributed across the entire body—comparable to structures found in the human retina.

Using state-of-the-art single-cell and gene expression analyses, the researchers mapped the cell types of young post-metamorphic sea urchins. They found that the adult body plan is largely "head-like."

The body is made entirely of head-like organs Genes that in other animals define trunk structures are active only in internal organs such as the gut and the water vascular system. In sea urchins, a true trunk region is missing altogether.

Most striking is the extraordinary diversity of neuronal cell types. Hundreds of different neurons express both echinoderm-specific "head" genes and highly conserved genes otherwise found in the vertebrate central nervous system. These findings suggest that sea urchins do not possess a simple decentralized nerve net, but rather an integrated, brain-like system that extends throughout the entire body.

The team also discovered numerous light-sensitive cells (photoreceptors) expressing different opsins—proteins that respond to light.
One particular cell type combines melanopsin and go-opsin, suggesting a complex ability to detect and process light stimuli, and hinting at a previously underestimated visual capacity. In addition, large parts of the sea urchin nervous system appear to be light-sensitive and may even be regulated by light cues.

The findings challenge long-standing assumptions about the simplicity of echinoderm nervous systems and open up new perspectives on how complex neural and visual systems can evolve—even in animals without a centralized brain or true eyes.

Periklis Paganos et al, Single-nucleus profiling highlights the all-brain echinoderm nervous system, Science Advances (2025). DOI: 10.1126/sciadv.adx7753

Woodpeckers grunt and brace their bodies like athletes to maximize drilling power

Woodpeckers pack a punch, pounding wood with extreme force and experiencing decelerations of up to 400g. Now, researchers reveal in the Journal of Experimental Biology that drilling woodpeckers turn themselves into hammers by bracing their head, neck, abdomen and tail muscles to hold their bodies rigid when they pound on wood, driving each impact with the hip flexor and front neck muscles.

In addition, they discovered that the birds synchronize their breathing with their movements each time they strike wood, like ace tennis stars that grunt noisily to stabilize core muscles when they take a shot. The birds exhaled forcefully, as if grunting, at the instant that the beak struck wood. This type of breathing pattern is known to generate greater co-contraction of trunk musculature.

The team also realized that the birds perfectly synchronized their breathing with each impact as they tapped more softly at rates of up to 13 strikes per second, inhaling a mini-breath (~40 ms) between each rapid blow.

Woodpeckers use their entire bodies when drilling and tapping like a hammer, from the tip of their beaks to their tails, but unlike tennis players, their grunts are drowned out by the drumming.

Neuromuscular coordination of movement and breathing forges a hammer-like mechanism for woodpecker drilling, Journal of Experimental Biology (2025). DOI: 10.1242/jeb.251167

Universe's expansion 'is now slowing, not speeding up': Evidence mounts that dark energy weakens over time

The universe's expansion may actually have started to slow rather than accelerating at an ever-increasing rate as previously thought, a new study suggests.

"Remarkable" findings published recently in Monthly Notices of the Royal Astronomical Society cast doubt on the long-standing theory that a mysterious force known as 'dark energy' is driving distant galaxies away increasingly faster.

Instead, they show no evidence of an accelerating universe.

If the results are confirmed, it could open an entirely new chapter in scientists' quest to uncover the true nature of dark energy, resolve the 'Hubble tension,' and understand the past and future of the universe.

With the new tools in their arsenal, astronomers will now be better equipped to find clues about what exactly dark energy is and how it influences the universe.

Junhyuk Son et al, Strong Progenitor Age-bias in Supernova Cosmology. II. Alignment with DESI BAO and Signs of a Non-Accelerating Universe, Monthly Notices of the Royal Astronomical Society (2025). DOI: 10.1093/mnras/staf1685

Fake or the real thing? How AI can make it harder to trust the pictures we see

A new study has revealed that artificial intelligence can now generate images of real people that are virtually impossible to tell apart from genuine photographs.

Using AI models ChatGPT and DALL·E, a team of researchers  created highly realistic images of both fictional and famous faces, including celebrities.

They found that participants were unable to reliably distinguish them from authentic photos—even when they were familiar with the person's appearance.

Across four separate experiments, the researchers noted that adding comparison photos or the participants' prior familiarity with the faces provided only limited help.

The research has just been published in the journal Cognitive Research: Principles and Implications and the team say their findings highlight a new level of "deepfake realism," showing that AI can now produce convincing fake images of real people which could erode trust in visual media.

 Robin S. S. Kramer et al, AI-generated images of familiar faces are indistinguishable from real photographs, Cognitive Research: Principles and Implications (2025). DOI: 10.1186/s41235-025-00683-w

Scientists have unlocked a way to dye polyester using 90% fewer chemicals and 40% less water

Fizzy water was the key to making polyester dye less harmful to the environment in the creation of a new method developed by an interdisciplinary team.

Polyester makes up more than half of all global fiber output, with production increasing each year—but it takes centuries to decompose and it can be difficult to recycle from garment-to-garment. Textile production is estimated to be responsible for about 20% of global clean water pollution, largely due to chemicals released in the wastewater from dyeing.

The startup aims to tackle these challenges at the dyeing stage by reducing harmful chemicals, water waste and costs. This could also make it easier and safer to recycle polyester garments, according to researchers.

Not many people know that even more toxic chemicals are used to turn brightly colored wastewater into transparent liquid. When released into freshwater, this is a secret killer that harms people, animals and the environment.

The new method makes it easier to insert and remove dyes from the fiber by injecting a small amount of carbonated water into the dye bath. This triggers the dyes' unique switching behavior within the polyester fibers.

Switch Dye also works on other synthetic fibers, such as nylon and elastane, and is just as effective as a widely used dye, without compromising on colour. Importantly, it uses all the same equipment that manufacturers already have.

SwitchDye can be more easily removed from the fiber, making the clothes much more recyclable. Ultimately, SwitchDye helps to make the textile industry more circular and sustainable, in both the dyeing and recycling stages.

Source: University of Leeds

Growing transgenic plants in weeks instead of months by hijacking a plant's natural regeneration abilities

Plant biologists have developed a method for growing transgenic and gene-edited plants that cuts the slow and expensive process down from months to weeks.

Publishing in Molecular Plant, the method takes advantage of plants' natural ability to regenerate after being wounded or pruned. By injecting bacteria carrying genetic instructions for wound healing and regeneration into a pruned plant's wound site, the researchers triggered the plant to grow new shoots, some of which were transgenic and gene edited.

The method shows potential even in species that are usually difficult or impossible to regenerate, such as soybeans.

Typically, when creating transgenic or gene-edited plants, biologists edit the DNA of an individual plant cell, which they then stimulate to grow into a new plant. For species like tomatoes that are relatively easy to regenerate, this process takes at least four months; for more difficult species like cotton, it can take almost a year; and for some plants, such as beans and peppers, tissue culture is extremely difficult.

To speed up this process, the researchers took advantage of plants' natural ability to regenerate after being damaged or pruned.

When a plant gets wounded, it triggers a molecular cascade that first seals the wound by creating a hard callus and then stimulates cell division and differentiation to replace the lost tissue. This process is regulated by a protein called WIND1, which activates a string of other proteins that are involved in cell differentiation and shoot growth.

It's like a relay: once WIND1 is activated, it will activate the next step, ESR1, which then activates the next step.

To simultaneously induce regeneration and introduce new DNA into plants, the researchers used a plant-infecting bacteria, Agrobacterium, that naturally introduces its own DNA into plant cells.

They inserted the genetic instructions for WIND1, ESR1, and several other regeneration genes into Agrobacterium, along with a gene that causes red coloration. Then, they pruned plants and applied the genetically modified Agrobacterium to the wound site.

This technique could help us transform species that are usually very difficult to grow in tissue culture because it's faster and more natural.

 A synthetic transcription cascade enables direct in planta shoot regeneration for transgenesis and gene editing in multiple plants, Molecular Plant (2025). DOI: 10.1016/j.molp.2025.09.017

Three newly discovered toads give birth to live young

An international team of researchers has discovered three new, bizarre, and wart-covered species of tree toads from Tanzania that give birth to fully developed toadlets.

Most textbooks tell only one story about frog reproduction: eggs hatch into tadpoles, which then metamorphose into froglets and grow into adults. That's the standard paradigm.

 Live-bearing is exceptionally rare among frogs and toads, practiced by less than 1% of frog species, making these new species exceptionally interesting.

Christian Thrane et al, Museomics and integrative taxonomy reveal three new species of glandular viviparous tree toads (Nectophrynoides) in Tanzania's Eastern Arc Mountains (Anura: Bufonidae), Vertebrate Zoology (2025). DOI: 10.3897/vz.75.e167008

Why your daily walk might not work as well if you're on metformin

A widely prescribed diabetes drug may be sabotaging one of the most trusted strategies for preventing the disease: exercise.

That is the conclusion of a Rutgers-led study published in The Journal of Clinical Endocrinology & Metabolism, which found that metformin blunts critical improvements in blood vessel function, fitness and blood sugar control that normally come from working out.

Since 2006, doctors have been advised to tell patients with high blood sugar to take metformin while engaging in exercise. Two proven therapies should deliver better results together, they reasoned. But Rutgers researchers said the math doesn't add up.

Most health care providers assume one plus one equals two. The problem is that most evidence shows metformin blunts exercise benefits. 

In the experiments conducted the results were clear: Exercise alone improved vascular insulin sensitivity, meaning blood vessels responded better to insulin and allowed more blood flow to muscles. This matters because insulin's ability to open blood vessels helps shuttle glucose out of the bloodstream and into tissues, lowering blood sugar after meals.

But when metformin was added, the improvements shrank. The drug also diminished gains in aerobic fitness and reduced the positive effects on inflammation and fasting glucose.

Blood vessel function improved with exercise training, regardless of intensity. Metformin blunted that observation, suggesting one type of exercise intensity is not better either with the drug for blood vessel health. 

This matters because exercise is supposed to lower blood sugar and improve physical function, crucial goals of diabetes treatment. If metformin interferes with those benefits, patients may not get the protection they expect to help lower disease risk.

If you exercise and take metformin and your blood glucose does not go down, that's a problem. People taking metformin also didn't gain fitness. That means their physical function isn't getting better and that could have long-term health risk.

The implications go beyond lab measurements. Fitness gains translate into energy for daily life. This includes activities such as climbing stairs, playing with children and staying active with friends. If those improvements stall, quality of life suffers.

The findings don't mean people should stop taking metformin or exercising, researchers say. Instead, it raises urgent questions for doctors about how the two treatments can be combined and the need for close monitoring. They hope future research will uncover strategies that preserve the benefits of both.

Part 1

Why does metformin blunt exercise benefits? The answer is unclear but may lie in the drug's mechanism of action. Metformin works partly by blocking parts of the mitochondria, which reduces oxidative stress and improves blood sugar control. But that same inhibition may interfere with the cellular adaptations triggered by exercise, including improvements in mitochondrial function and aerobic capacity. In other words, the very process that makes metformin effective may block the body's ability to respond fully to physical training.
Previous research has hinted at similar effects, but this trial is among the first to examine vascular insulin sensitivity, which is a key factor controlling glucose regulation and cardiovascular health.
By showing that metformin can blunt improvements in both large arteries and tiny capillaries regardless of exercise intensity, the study underscores the complexity of combining such treatments.
Now we need to figure out how to best recommend exercise with metformin, the researchers conclude, we also need to consider how other medications interact with exercise to develop better guidelines for doctors to help people lower chronic disease risk.

Steven K Malin et al, Metformin Blunts Vascular Insulin Sensitivity After Exercise Training in Adults at Risk for Metabolic Syndrome, The Journal of Clinical Endocrinology & Metabolism (2025). DOI: 10.1210/clinem/dgaf551

Part 2

New insights on gut microbes that prevent formation of cancer-causing compounds

Nitrogen metabolism of gut bacteria can provide health benefits. Specifically, gut microbes metabolize dietary nitrates and nitrites and prevent the formation of cancer-causing compounds called nitrosamines. New research published in The FEBS Journal sheds light on these processes and pinpoints which types of bacteria are most important.

Investigators found that Escherichia coli—and to a lesser extent, species of the genera Lactobacillus, Bacteroides and Phocaeicola—can efficiently metabolize different forms of nitrogen, thus preventing carcinogenic nitrosamine formation.

They also demonstrate that this bacterial processing is critical to enable microorganisms to survive and colonize the intestinal tract, likely preventing harmful changes in the composition of the gut microbiota.

The findings highlight the importance of the gut microbiota in preventing the formation of harmful nitrogen metabolites, potentially decreasing the risk of certain cancers. The study also illustrates how the microbiota facilitates crosstalk between our diet and the gut, thus having important implications for both health and disease.

 Distribution and activity of nitrate and nitrite reductases in the microbiota of the human intestinal tract, FEBS Journal (2025). DOI: 10.1111/febs.70299

Coordinated brain network activity during emotional arousal may explain vivid, lasting memories

Past psychology studies suggest that people tend to remember emotional events, such as their wedding, the birth of a child or traumatic experiences, more vividly than neutral events, such as a routine professional meeting. While this link between emotion and the recollection of past events is well-established, the neural mechanisms via which emotional states strengthen memories remain poorly understood.

So researchers now carried out a study aimed at better understanding these mechanisms. Their findings, published in Nature Human Behaviour, suggest that emotional states facilitate the encoding of memories by increasing communication between networks of brain regions.

Emotional experiences tend to be 'sticky,' meaning that they endure in our memories and shape how we interpret the past, engage with the present, and anticipate the future. 

The primary objective of the recent study 's to study the neural processes that make emotional memories become more persistent. To do this, they used brain imaging techniques combined with computational models that can analyze and generate texts, known as natural language processing (NLP) models.

The analyses carried out by the researchers revealed that when participants were emotionally aroused, the activity of various brain networks was more coordinated than when they were in neutral or mild emotional states. Notably, this greater coordination between brain networks was found to predict how well participants remembered the scenes that they viewed during the experiment.

It is more like an orchestra, where different sections work together to create a unified performance, with arousal serving as a conductor that coordinates their activity. This perspective suggests that whether we remember an emotional memory depends not only on the strength of activity in any single region, but also on how effectively different systems communicate and share information.

Overall, the results of this research team's analyses suggest that emotions strengthen the synchronization between brain networks, which in turn supports the encoding of memories. Their paper thus introduces a new way of thinking about emotional memories, suggesting that it is supported by the coordinated activity of various brain regions.

 Jadyn S. Park et al, Emotional arousal enhances narrative memories through functional integration of large-scale brain networks, Nature Human Behaviour (2025). DOI: 10.1038/s41562-025-02315-1.

Urolithin A nudges aging immune cells toward a youthful profile in 28 days

An international research team focused on aging reports that urolithin A at 1,000 mg per day shifted human immune profiles toward a more naive-like, less exhausted CD8⁺ state and increased fatty acid oxidation capacity, with additional functional gains.

Urolithin A is a metabolite produced by gut bacteria after breaking down ellagic acid from certain foods, such as pomegranates and walnuts. While produced naturally through microbial digestion, it is in much smaller quantities than available as a supplement or used in the study.

Aging bodies face reduced production of mature T cells, shrinking naive T cell pools and chronic low-grade inflammation. Mitochondrial dysfunction and waning autophagy sit at the core of these shifts, with mitophagy failure linked to immune dysregulation and disease.

Preclinical evidence identified urolithin A as a potent inducer of mitophagy, clearing out damaged mitochondria, in rodents and humans. Previous clinical trials have reported improved physical performance following supplementation.

Improving mitochondrial quality control with a positive influence on immune function would represent a turning back of the aging biological clock, if it can have a meaningful and prolonged effect in humans.

Conclusion: Short-term urolithin A supplementation modulated human immune cell composition and metabolism and improved selected functional responses, supporting the body's potential to counteract age-related immune decline.

Dominic Denk et al, Effect of the mitophagy inducer urolithin A on age-related immune decline: a randomized, placebo-controlled trial, Nature Aging (2025). DOI: 10.1038/s43587-025-00996-x

A natural compound revitalizes the aging human immune system, Nature Aging (2025). DOI: 10.1038/s43587-025-01012-y

Good Social Interactions Slow Cancer Via an Anxiety-Reducing Neural Circuit

Just an hour of socializing per day helped mice fight tumors. Now scientists have traced the brain circuitry that turns companionship into a cancer-fighting signal.

In the 1970s and ‘80s, scientists began noticing that people who had few or poor social relationships had a higher risk of developing illnesses and all-cause mortality. A slew of follow-up studies suggested that social support could protect people from pathological conditions like arthritis, alcoholism, depression, and even death. This link holds true for cancer as well. Upon analyzing disease progression and survival rates in thousands of breast cancer patients, researchers observed a negative impact of social isolation and a positive impact of interpersonal connections on prognosis.

One of the popular theories explaining these effects states that being social eases anxiety, a well-established driver of tumor growth, and consequently inhibits cancer progression. But how exactly does the body sense these stimuli and pump the brakes on cancer?

In a recent study published in Neuron, researchers uncovered the neural circuitry that drives the therapeutic effects of social connections on cancer, in mice. It demonstrates a real biological pathway by which this nebulous subject of social interaction can influence cancer.

That means that now it's technically targetable, by drugs or by neuromodulation techniques, when before, we wouldn't even know what to target or if there was something to target.

 These findings establish a new paradigm for how psychosocial factors influence cancer via neural circuits and could potentially lead to therapies that complement existing treatments.

Wen HZ, et al. Social interaction in mice suppresses breast cancer progression via... Neuron. 2025;113(20)3374-3389.e9.

First ever atlas of brain development

First-ever atlas of brain development shows how stem cells turn into neurons

Scientists have created the most detailed maps yet of how our brains differentiate from stem cells during embryonic development and early life. In a collection of five papers, they tracked hundreds of thousands of early brain cells in the cortices of humans and mice, and captured with unprecedented precision the molecular events that give rise to a mixture of neurons and supporting cells. It's really the initial first draft of any ‘cell atlases’ for the developing brain.

https://www.nature.com/articles/d41586-025-03641-0?utm_source=Live+...

We're Still Evolving: Human Arms Keep Growing an Extra Artery

Subtle shifts in our anatomy today demonstrate how unpredictable evolution can be. Take something as mundane as an extra blood vessel in our arms, which, going by current trends, could be commonplace within just a few generations.

An artery that temporarily runs down the center of our forearms while we're still in the womb isn't vanishing as often as it used to, according to a study published in 2020 by researchers.

That means there are more adults than ever with what amounts to an extra channel of vascular tissue flowing under their wrist.

Since the 18th century, anatomists have been studying the prevalence of this artery in adults and our study shows it's clearly increasing.

The prevalence was around 10 percent in people born in the mid-1880s compared to 30 percent in those born in the late 20th century, so that's a significant increase in a fairly short period of time, when it comes to evolution

https://onlinelibrary.wiley.com/doi/10.1111/joa.13224

Neanderthal DNA helps explain how faces form

Every human face is unique, allowing us to distinguish between individuals. We know little about how facial features are encoded in our DNA, but we may be able to learn more about how our faces develop by looking at our ancient relatives, the Neanderthals. Neanderthal faces were quite distinctive from our own, with large noses, pronounced brows and a robust lower jaw.

Now, scientists are using the DNA of our extinct distant relatives to learn more about how faces develop and evolve.

Published in the journal Development, they show how a region of Neanderthal DNA is better at activating a jaw-forming gene than the human counterpart, revealing one potential reason for Neanderthal's larger lower jaws.

Scientists have sequenced the Neanderthal genome using DNA extracted from ancient bone. The Neanderthal genome is 99.7% identical to the genome of modern-day humans and the differences between species are likely responsible for altering appearance. Both human and Neanderthal genomes consist of about 3 billion letters that code for proteins and regulate how genes are used in the cell, which makes finding regions that impact appearance like looking for a needle in a haystack.

But still they decided on a region of the genome that is linked to Pierre Robin sequence, a syndrome in which the lower jaw is disproportionately small. Some individuals with Pierre Robin sequence have large deletions or DNA rearrangements in this part of the genome that change face development and limit jaw formation. They predicted that smaller differences in the DNA might have more subtle effects on face shape.

By comparing human and Neanderthal genomes, the team found that in this region, roughly 3000 letters in length, there were just three single-letter differences between the species. Although this region of DNA doesn't contain any genes, it regulates how and when a gene is activated, specifically a gene called SOX9, a key coordinator of the process of face development.

To demonstrate that these Neanderthal-specific differences are important for the development of the face, the researchers needed to show that the Neanderthal region could activate genes in the right cells at the right time as the embryo develops.

The researchers simultaneously inserted the Neanderthal and human versions of the region into the DNA of zebrafish and programmed the zebrafish cells to produce different colors of fluorescent protein depending on whether the human or Neanderthal region was active.

Watching the zebrafish embryos develop, the researchers found that both the human and Neanderthal regions were active in the zebrafish cells that are involved in forming the lower jaw and the Neanderthal region was more active than the human version.

This led them to think about what the consequences of these differences could be, and how to explore these experimentally.

Knowing that the Neanderthal sequence was more powerful at activating genes, the researchers then asked if the resulting increased activity of its target, SOX9, might change the shape and function of the adult jaw. To test this theory, they provided the zebrafish embryos with extra SOX9 and found that cells that contribute to forming the jaw occupied a larger area.

This research shows that by studying extinct species we can learn how our own DNA contributes to face variation, development and evolution.

Kirsty Uttley et al, Neanderthal-derived variants increase SOX9 enhancer activity in craniofacial progenitors that shape jaw development, Development (2025). DOI: 10.1242/dev.204779

Sodium bicarbonate fails to boost survival in patients with severe acidemia

Severe metabolic acidemia (acidic blood) has been linked to impaired cardiac contractility, arrhythmias, pulmonary vasoconstriction, systemic vasodilation, altered kidney blood flow, cerebral edema, and diaphragmatic dysfunction. Common etiologies in critical illness include hyperchloremic acidosis, lactate accumulation, and endogenous anion accumulation during acute kidney injury.

Now researchers  report no reduction in day 90 all-cause mortality with sodium bicarbonate infusion for critically ill adults with severe metabolic acidemia and moderate to severe acute kidney injury.

In the human body, carbon dioxide combines with water via carbonic anhydrase and forms carbonic acid, which dissociates into a hydrogen ion and bicarbonate. Early 20th century investigators described metabolic bicarbonate as an "alkaline reserve," naturally buffering the body to keep a healthy acid-base balance.

Sodium bicarbonate entered acute care protocols in the 1950s as a staple of cardiopulmonary resuscitation (CPR) guidance. Skepticism grew across the 1980s and beyond as routine dosing failed to show outcome advantages and reports raised concerns about potential harms.

Modern evidence, including recent trials, has coincided with removal of routine bicarbonate use from  CPR guidelines, with use retained for select cases of severe acidosis.

Prior work by researchers on bicarbonate outcomes did not show an overall benefit from sodium bicarbonate, though an acute kidney injury intervention suggested benefit, leaving open the possibility that it still might be of benefit under specific conditions.

In the study, "Sodium Bicarbonate for Severe Metabolic Acidemia and Acute Kidney Injury: The BICARICU-2 Randomized Clinical Trial," published in JAMA, researchers conducted an open-label, investigator-initiated, multicenter randomized clinical trial to determine whether sodium bicarbonate infusion reduces day 90 all-cause mortality after severe metabolic acidemia with moderate to severe acute kidney injury in critically ill adults.

Part 1