Microplastics found to change gut microbiome in first human-sample study

New research presented at UEG Week 2025 shows that microplastics—plastic particles smaller than 5 mm commonly found in the environment—can alter the human gut microbiome, with some changes resembling patterns linked to depression and colorectal cancer.

The study used stool samples from five healthy volunteers to grow ex vivo gut microbiome cultures. These cultures were then exposed to five common microplastic types—polystyrene, polypropylene, low-density polyethylene, poly(methyl methacrylate) and polyethylene terephthalate

—at concentrations reflecting estimated human exposure, as well as higher doses to investigate potential dose-dependent effects.

While total and viable bacterial cell counts remained largely unchanged, microplastic-treated cultures showed a consistent and significant increase in acidity (lower pH levels) compared to controls, indicating altered microbial metabolic activity.

Further analysis revealed microplastic-specific shifts in bacterial composition, with certain bacterial groups increasing or decreasing depending on the microplastic type. Changes were observed across several bacterial families, including Lachnospiraceae, Oscillospiraceae, Enterobacteriaceae and Ruminococcaceae, with the majority occurring within the phylum Bacillota—a key group of gut bacteria important for digestion and overall gut health.

These shifts in bacterial composition were accompanied by changes in the chemicals produced by the bacteria, some of which corresponded with the observed decreases in pH. Certain microplastic types altered levels of valeric acid and 5-aminopentanoic acid, while others affected lysine or lactic acid, highlighting the complexity of microplastic-microbiome interactions.

Importantly, some of these microplastic-induced changes in microbial composition reflected patterns previously linked to diseases such as depression and colorectal cancer, underscoring the potential implications of microplastic exposure for disease risk.

Pacher-Deutsch, C et al. Microplastic-induced alterations in gut microbiome and metabolism: Insights from an ex vivo bioreactor model. Presented at UEG Week 2025; 7 October 2025; Berlin, Germany.

Many newborn baby deaths linked to preventable or treatable factors

A new study has identified the most critical risk factors linked to neonatal deaths worldwide, providing comprehensive evidence to help guide global efforts to save newborn lives.

Researchers reviewed more than 60 studies published in the past 35 years, covering more than 50 risk factors for neonatal mortality—defined as a baby dying in the first 28 days of life.

The paper, "Risk factors for neonatal mortality: an umbrella review of systematic reviews and meta-analyses," is published in eClinicalMedicine.

It found strong evidence of conditions and factors that significantly increase the likelihood of neonatal mortality, covering maternal health and lifestyle factors (obesity, prenatal opioid exposure, anemia, bleeding disorders), socioeconomic and environmental factors (maternal age, low occupational status, arsenic exposure), neonatal factors (preterm birth, delayed breastfeeding, low birthweight) and protective factors (antenatal care, health facility delivery).

Babies born with low birthweight face more than 15 times the risk of dying compared to those born at a healthy weight, babies born preterm face up to seven times higher risk, delaying breastfeeding by more than 24 hours after birth increases the risk by 60% to 70%, while mothers who receive antenatal care can reduce the risk of losing their baby by up to 85%.

These are staggering numbers, but they are also clear, actionable areas where change could save countless lives, the researchers say.

These are preventable and treatable issues—if we get this right, the impact will be profound across the globe.

Bereket Kefale et al, Risk factors for neonatal mortality: an umbrella review of systematic reviews and meta-analyses, eClinicalMedicine (2025). DOI: 10.1016/j.eclinm.2025.103525

Three scientists win Nobel Prize in chemistry for the development of metal-organic frameworks

Three scientists won the Nobel Prize in chemistry this week for their development of new molecular structures that can trap vast quantities of gas inside, laying the groundwork to potentially suck greenhouse gases out of the atmosphere or harvest moisture from desert environments.

Heiner Linke, chairperson of the committee that made the award, compared the structures called metal-organic frameworks to the seemingly bottomless magical handbag carried by Hermione Granger in the "Harry Potter" series. Another example might be Mary Poppins' enchanted carpet bag. These containers look small from the outside but are able to hold surprisingly large quantities within.

The committee said Susumu Kitagawa, Richard Robson and Omar M. Yaghi were honored for "groundbreaking discoveries" that "may contribute to solving some of humankind's greatest challenges," from pollution to water scarcity.

The chemists worked separately but added to each other's breakthroughs over decades, beginning with Robson's work in the 1980s.

The scientists were able to devise stable atomic structures that preserved holes of specific sizes that allowed gas or liquid to flow in and out. The holes can be customized to match the size of specific molecules that scientists or engineers want to hold in place, such as water, carbon dioxide or methane.

That level of control is quite rare in chemistry.

A relatively small amount of the structure—which combines metal nodes and organic rods, somewhat like the interchangeable building pieces in Tinker Toys—creates many organized holes and a huge amount of surface area inside.

Why the work matters

Today researchers around the world are exploring possibilities that include using the frameworks to remove greenhouse gases from the atmosphere and pollution from industrial sites. Another possibility is to use them to harvest moisture from desert air, perhaps to one day provide clean drinking water in arid environments.

Scientists are also investigating using the structures for targeted drug delivery. The idea is to load them with medicine that may be slowly released inside the body. It could be a better way to deliver low doses continually.

The research "could be really, really valuable" in many industries.

Nobel committee announcement:

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry 2025 to

Susumu Kitagawa, Kyoto University, Japan

Richard Robson, University of Melbourne, Australia

Omar M. Yaghi, University of California, Berkeley, U.S.

"for the development of metal-organic frameworks"

Their molecular architecture contains rooms for chemistry

The Nobel Prize laureates in chemistry 2025 have created molecular constructions with large spaces through which gases and other chemicals can flow. These constructions, metal-organic frameworks, can be used to harvest water from desert air, capture carbon dioxide, store toxic gases or catalyze chemical reactions.

https://www.nobelprize.org/prizes/chemistry/2025/press-release/

New type of diabetes discovered in babies

Advanced DNA sequencing technologies and a new model of stem cell research have enabled an international team to discover a new type of diabetes in babies.

The researchers established that mutations in the TMEM167A gene are responsible for a rare form of neonatal diabetes.

Some babies develop diabetes before the age of six months. In over 85% of cases, this is due to a genetic mutation in their DNA. Research  found that in six children with additional neurological disorders such as epilepsy and microcephaly identified alterations in a single gene: TMEM167A.

To understand its role, the researchers  used stem cells differentiated into pancreatic beta cells and gene-editing techniques (CRISPR). They found that when the TMEM167A gene is altered, insulin-producing cells can no longer fulfill their role. They then activate stress mechanisms that lead to their death.

This discovery shows that the TMEM167A gene is essential for the proper functioning of insulin-producing beta cells, but also for neurons, whereas it seems dispensable for other cell types. These results contribute to a better understanding of the crucial steps involved in insulin production and could shed light on research into other forms of diabetes, a disease which today affects almost 589 million people worldwide.

Enrico Virgilio et al, Recessive TMEM167A variants cause neonatal diabetes, microcephaly and epilepsy syndrome, Journal of Clinical Investigation (2025). DOI: 10.1172/jci195756

Novel blood test for chronic fatigue achieves 96% accuracy

Scientists  have developed a high accuracy blood test to diagnose chronic fatigue syndrome, also known as myalgic encephalomyelitis (ME/CFS).

The debilitating long-term illness affects millions worldwide but is poorly understood and has long lacked reliable diagnostic tools.

With 96% accuracy, the new test offers new hope for those living with the condition—which is often misunderstood and misdiagnosed. It is hoped that the breakthrough could pave the way for a similar blood test to diagnose long COVID.

Chronic fatigue syndrome is not a genetic disease you're born with. That's why using EpiSwitch 'epigenetic' markers—which can change during a person's life, unlike a fixed genetic code—was key to reaching this high level of accuracy.

The team discovered a unique pattern that appears consistently in people with ME/CFS that is not seen in healthy people.

The researchers also found signs of immune system and inflammation pathways involved in the disease, which may help guide future treatments and identify patients more likely to respond to specific therapies.

'Development and validation of blood-based diagnostic biomarkers for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) using EpiSwitch® 3-dimensional genomic regulatory immuno-genetic profiling, Journal of Translational Medicine (2025). translational-medicine.biomedc … 6/s12967-025-07203-w

Schizophrenia is linked to iron and myelin deficits in the brain, neuroimaging study finds

Schizophrenia is a severe and debilitating psychiatric disorder characterized by hallucinations, disorganized speech and thought patterns, false beliefs about the world or oneself, difficulties concentrating and other symptoms impacting people's daily functioning. While schizophrenia has been the topic of numerous research studies, its biological and neural underpinnings have not yet been fully elucidated.

While some past brain imaging studies suggest that schizophrenia is associated with abnormal levels of iron and myelin in the brain, the results collected so far are conflicting. Iron is a metal known to contribute to healthy brain function, while myelin is a fatty substance that forms a sheath around nerve fibers, protecting them and supporting their conduction of electrical signals.

Researchers  recently set out to further explore the possibility that schizophrenia is linked to abnormal levels of iron and myelin in the brain. Their findings, published in Molecular Psychiatry, uncovered potential new biomarkers of schizophrenia that could improve the understanding of its underlying brain mechanisms.

Iron is essential for many neuronal processes but excess causes oxidative damage, so brain levels are kept in a delicate balance. Iron-sensitive MRI studies focusing on schizophrenia have yielded conflicting results, with both increases and decreases reported. As myelin—which increases brain signal transmission—influences iron-sensitive MRI, myelin variation could complicate interpretation.

Researchers  examined the brains of 85 individuals diagnosed with schizophrenia and 86 matching control subjects. To study the brains of the study participants, they used iron-sensitive and myelin-sensitive magnetic resonance imaging (MRI), imaging techniques that allow researchers to detect iron and myelin levels in specific regions of the brain.

The researchers' results suggested iron and myelin anomalies that affected specific regions in the brains of individuals diagnosed with schizophrenia, including the caudate, putamen, and globus pallidus. Their findings are aligned with those of some earlier studies and could help to paint a clearer picture of disease pathophysiology.

They found that patients with schizophrenia had lower magnetic susceptibility, higher mean diffusivity, and lower magnetic susceptibility anisotropy, suggesting that both iron and myelin brain levels are lower in schizophrenia.

This was most significant in regions rich in oligodendrocytes. As oligodendrocytes utilize iron to synthesize myelin, this links oligodendrocyte dysfunction to schizophrenia, highlighting the mechanism underlying this as an important research area.

Luke J. Vano et al, The role of low subcortical iron, white matter myelin, and oligodendrocytes in schizophrenia: a quantitative susceptibility mapping and diffusion tensor imaging study, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03195-7.

Nanoparticle vaccine prevents multiple cancers and stops metastasis in mice

A new study by researchers demonstrates that their nanoparticle-based vaccine can effectively prevent melanoma, pancreatic and triple-negative breast cancer in mice. Not only did up to 88% of the vaccinated mice remain tumor-free (depending on the cancer), but the vaccine reduced—and in some cases completely prevented—the cancer's spread.

By engineering these nanoparticles to activate the immune system via multi-pathway activation that combines with cancer-specific antigens, they could prevent tumor growth with remarkable survival rates.

The first test paired their nanoparticle system with well-characterized melanoma peptides (called an antigen, similar to how a flu shot typically contains parts of the inactivated flu virus). The formulation activated immune cells called T cells, priming them to recognize and attack this type of cancer. Three weeks later, the mice were exposed to melanoma cells.

Eighty percent of these "super adjuvant" vaccinated mice remained tumor-free and survived until the completion of the study (250 days). In comparison, all of the mice vaccinated with traditional vaccine systems, non-nanoparticle formulations or unvaccinated mice developed tumors; none survived longer than 35 days.

The vaccine also protected against the spread of cancer to the lungs. When exposed to melanoma cells systemically, which mimics how cancer metastasizes, none of the nanoparticle-vaccinated mice developed lung tumors, while all of the other mice did.

The tumor-specific T-cell responses that the researchers are able to generate—that is really the key behind the survival benefit. 

There is really intense immune activation when you treat innate immune cells with this formulation, which triggers these cells to present antigens and prime tumor-killing T cells. This robust T-cell response is possible because of the particular nanoparticle design of the vaccine.

The researchers say that their design offers a platform approach that could be used across multiple cancer types.

"Super adjuvant" nanoparticles for platform cancer vaccination, Cell Reports Medicine (2025). DOI: 10.1016/j.xcrm.2025.102415. www.cell.com/cell-reports-medi … 2666-3791(25)00488-4

Certain dietary fatty acids can supercharge cancer-fighting immune cells

A research team has discovered that certain dietary fatty acids can supercharge the human immune system's ability to fight cancer. The team found that a healthy fatty acid found in olive oil and nuts, called oleic acid (OA), enhances the power of immune γδ-T cells, specialized cells known for their cancer-fighting properties.

Conversely, they found that another fatty acid, called palmitic acid (PA), commonly found in palm oil and fatty meats, diminishes the ability of these immune cells to attack tumors.

Their study, published in the journal Signal Transduction and Targeted Therapy, offers an innovative approach using dietary OA supplementation to strengthen the antitumor immunity of γδ-T cells.

Dietary fatty acids are essential for health, helping with growth and body functions. They may also play a role in cancer prevention and treatment, but understanding how they affect cancer is challenging because of the complexity of people's diets and the lack of detailed studies.
Recently, scientists have learned that fatty acids can influence the immune system, especially in how it fights cancer. Specialized immune cells, called γδ-T cells, are particularly good at attacking tumors. These cells, once activated, have helped some lung and liver cancer patients live longer.
However, this therapy is not effective for all patients, partly because the variation of metabolic status, such as fatty acid metabolism, can influence its efficacy in the patients.

The research team identified a correlation between PA and OA levels and the efficacy of cancer therapies. The research suggests that dietary fatty acid supplementation, particularly with foods rich in OA, such as olive oil and avocados, could enhance γδ-T cell immunosurveillance, leading to more effective cancer treatments.

The team also discovered that another fatty acid, called PA, can weaken these immune cells and how OA can counteract this.

The results indicate that cancer patients should avoid PA and consider OA supplementation in their diets to improve clinical outcomes of γδ-T cell-based cancer therapies.

By analyzing blood samples, the researchers confirmed that the levels of these fatty acids are linked to the outcome of cancer immunotherapy.

Part 1

For cancer patients, this discovery suggests simple changes, like eating more foods rich in OA (such as olive oil, avocados and nuts) and cutting back on PA (found in processed foods, palm oil and fatty meats), could improve the effectiveness of cancer treatments. The study also points to novel strategies, like combining dietary changes with specific drugs to further boost the immune system.

Yanmei Zhang et al, Oleic acid restores the impaired antitumor immunity of γδ-T cells induced by palmitic acid, Signal Transduction and Targeted Therapy (2025). DOI: 10.1038/s41392-025-02295-8

Part 2

Study suggests air pollution can contribute to obesity and diabetes

Long-term exposure to fine air pollution can impair metabolic health by disrupting the normal function of brown fat in mice. A study co-led by the University of Zurich shows that this occurs through complex changes in gene regulation driven by epigenetic mechanisms. The results demonstrate how environmental pollutants contribute to the development of insulin resistance and metabolic diseases.

There is growing evidence that air pollution is not just harmful to our lungs and heart, but also plays a significant role in the development of metabolic disorders like insulin resistance and type 2 diabetes.

For their investigation, the researchers exposed laboratory mice to either filtered air or concentrated PM2.5 for six hours a day, five days a week, over a period of 24 weeks. This setup was designed to closely mimic chronic urban exposure in humans.
Particular attention was paid to brown adipose tissue, a special type of fat that helps the body generate heat and burn calories, and therefore plays a key role in energy balance and glucose metabolism. After the exposure period of about five months, the mice that had inhaled PM2.5 showed signs of disrupted metabolism, including impaired insulin sensitivity.

Further examination revealed that the function of brown fat had been significantly altered. In particular, they found that the expression of important genes in brown adipose tissue which regulate its ability to produce heat, process lipids and handle oxidative stress were disturbed. These changes were accompanied by increased fat accumulation and signs of tissue damage and fibrosis within the tissue.

Part 1

The researchers then examined the underlying mechanisms driving these changes. They found that air pollution had triggered significant changes in the regulation of DNA in brown fat cells.

This included modifications in DNA methylation patterns and changes in how accessible certain genes were for being turned on or off—a process known as chromatin remodeling. These epigenetic changes affect how cells function by regulating gene activity without altering the genetic code itself.

Two enzymes were identified as main drivers of this process: HDAC9 and KDM2B. These enzymes are involved in modifying histones, the proteins around which DNA is wrapped. They were found to bind to specific regions of the DNA in brown fat cells of the mice exposed to PM2.5, leading to a reduction in key chemical tags, or methyl groups, that normally promote gene activity.

When these enzymes were experimentally suppressed, brown fat function improved, whereas increasing their activity led to further declines in metabolism.
The study shows that long-term exposure to fine air pollution can impair metabolic health by disrupting the normal function of brown fat. This occurs through complex changes in gene regulation controlled by epigenetic mechanisms.

Rengasamy Palanivel et al, Air pollution modulates brown adipose tissue function through epigenetic regulation by HDAC9 and KDM2B, JCI Insight (2025). DOI: 10.1172/jci.insight.187023

Part 2

Blood cancer: Scientists reprogram cancer cell death to trigger immune system

The aim of immunotherapy strategies is to leverage cells in the patient's own immune system to destroy tumor cells. Using a preclinical model, scientists successfully stimulated an effective anti-tumor immune response by reprogramming the death of malignant B cells. They demonstrated an effective triple-therapy approach for treating forms of blood cancer such as certain lymphomas and leukemias which affect B cells. The study was published on August 15 in the journal Science Advances. 

Immunotherapy strategies represent a major breakthrough in cancer treatment. They aim to harness the patient's immune system so that their own cells can recognize and specifically eliminate tumor cells. Immune cells can act like sentinels, scanning the body and identifying all residual tumor cells to reduce the risk of relapse. Various novel immunotherapy strategies are emerging, one of which makes use of a cell death mechanism known as necroptosis. Unlike apoptosis, which results in silent cell death, necroptosis releases warning signals that attract and stimulate immune cells so that they can kill any remaining tumor cells.

Scientists set out to explore the effectiveness of this necroptosis-based immunotherapy strategy on hematological malignancies. They began by observing that necroptosis cannot be easily induced in malignant B cells because of the absence of the MLKL protein.

To overcome this hurdle, the scientists combined administration of three drugs already used in clinical practice. They confirmed induction of necroptosis and observed a strong immune response leading to the complete elimination of leukemia in a preclinical model. 

The triple therapy they used forces cancer cells to die in a way that activates the immune system.

The results were observed in preclinical models using an innovative intravital imaging technique. The scientists were able to monitor the interactions between immune cells and cancer cells in real time for the different types of cell death induced.

"This novel immunotherapy strategy, successfully tested in preclinical models, turns tumor cells into triggers for the immune system, pointing to a potential therapeutic avenue for certain cancers, such as lymphomas or leukemias affecting B cell.

Ruby Alonso et al, Reprogramming RIPK3-induced cell death in malignant B cells promotes immune-mediated tumor control, Science Advances (2025). DOI: 10.1126/sciadv.adv0871

Menstrual cycle found to affect women's reaction time, but not as much as being active

Women performed best on cognitive tests during ovulation but physical activity level had a stronger influence on brain function, according to a new study .

The study, published in Sports Medicine–Open, explored how the different phases of the menstrual cycle and physical activity level affected performance on a range of cognitive tests designed to mimic mental processes used in team sports and everyday life, such as the accurate timing of movements, attention, and reaction time.

Researchers found that women had the fastest reaction times and made the fewest errors on the day of ovulation, when the ovaries release an egg ready to be fertilized (and when women's fertility is at its peak).

But while cognitive performance fluctuated across the menstrual cycle, much greater differences were observed between those who were active and those who weren't. Compared to active participants, inactive participants had reaction times on average around 70 milliseconds slower and made around three times as many impulsive errors, regardless of cycle phase.

The researchers say the findings are particularly relevant to women's sport, where slightly quicker reaction times of around 20 milliseconds may make the difference between sustaining or avoiding an injury like concussion. Previous research on elite athletes has suggested injuries are more common at certain points during the menstrual cycle, and the authors say that these changes in cognition might partially explain this occurrence.

However, while a difference of 20 milliseconds is likely to be inconsequential in everyday life, the much larger difference between active and inactive groups is more significant, where 70 milliseconds could determine whether we regain balance after tripping over an obstacle or not.

Menstrual cycle and athletic status interact to influence symptoms, mood, and cognition in females, Sports Medicine–Open (2025). DOI: 10.1186/s40798-025-00924-8

Easter Island's statues actually 'walked,' and physics backs it up

For years, researchers have puzzled over how the ancient people of Rapa Nui did the seemingly impossible and moved their iconic moai statues. Using a combination of physics, 3D modeling and on-the-ground experiments, a research team has confirmed that the statues actually walked—with a little rope and remarkably few people.

Studying nearly 1,000 moai statues, they found that the people of Rapa Nui likely used rope and "walked" the giant statues in a zig-zag motion along carefully designed roads. The paper is published in the Journal of Archaeological Science.

They 

 had previously demonstrated via experimental evidence that the large statues "walked" from their quarry to ceremonial platforms using an upright, rocking motion, challenging a theory that the statues were moved lying prone on wooden devices.

"Once you get it moving, it isn't hard at all—people are pulling with one arm. It conserves energy, and it moves really quickly," they say.

The hard part is getting it rocking in the first place. The question is, if it's really large, what would it take? Are the things that we saw experimentally consistent with what we would expect from a physics perspective?"

To explore how a larger statue might move, the team created high-resolution 3D models of the moai and identified distinctive design features—wide D-shaped bases and a forward lean—that would make them more likely to be moved in a rocking, zig-zagging motion.

Putting their theory to the test, the team built a 4.35-ton replica moai with the distinct "forward-lean" design. With just 18 people, the team was able to transport the moai 100 meters in just 40 minutes, a marked improvement over previous vertical transport attempts.

The physics makes sense, say the researchers, "What we saw experimentally actually works. And as it gets bigger, it still works. All the attributes that we see about moving gigantic ones only get more and more consistent the bigger and bigger they get, because it becomes the only way you could move it."

Adding to the support for this theory are the roads of Rapa Nui. Measuring 4.5 meters wide with a concave cross-section, the roads were ideal for stabilizing the statues as they moved forward.

 Carl P. Lipo et al, The walking moai hypothesis: Archaeological evidence, experimental validation, and response to critics, Journal of Archaeological Science (2025). DOI: 10.1016/j.jas.2025.106383

First device based on 'optical thermodynamics' can route light without switches

A team of researchers  has created a new breakthrough in photonics: the design of the first optical device that follows the emerging framework of optical thermodynamics.

The work, reported in Nature Photonics, introduces a fundamentally new way of routing light in nonlinear systems—meaning systems that do not require switches, external control, or digital addressing. Instead, light naturally finds its way through the device, guided by simple thermodynamic principles.

Universal routing is a familiar engineering concept. In mechanics, a manifold valve directs inputs to a chosen outlet. In digital electronics, a Wi-Fi router at home or an Ethernet switch in a data center directs information from many input channels to the correct output port, ensuring that each stream of data reaches its intended destination.

When it comes to light, the same problem is far more challenging, however. Conventional optical routers rely on complex arrays of switches and electronic control to toggle pathways. These approaches add technical difficulty, while limiting speed and performance.

The photonics team has now shown that there is another way. The idea can be likened to a marble maze that arranges itself.

Normally, you'd have to lift barriers and guide a marble step-by-step to make sure it reaches its destination—the right hole. In the team's device, however, the maze is built so that no matter where you drop the marble, it will roll on its own toward the right place—no guiding hands needed. And this is exactly how light behaves: it finds the correct path naturally, by following the principles of thermodynamics.

Party 1

Chaos tamed by thermodynamics : Nonlinear multimode optical systems are often dismissed as chaotic and unpredictable. Their intricate interplay of modes has made them among the hardest systems to simulate—let alone design for practical use. Yet, precisely because they are not constrained by the rules of linear optics, they harbor rich and unexplored physical phenomena.

Recognizing that light in these systems undergoes a process akin to reaching thermal equilibrium—similar to how gases reach equilibrium through molecular collisions—the researchers developed a comprehensive theory of "optical thermodynamics." This framework captures how light behaves in nonlinear lattices using analogs of familiar thermodynamic processes such as expansion, compression, and even phase transitions.
The team's demonstration in Nature Photonics marks the first device designed with this new theory. Rather than actively steering the signal, the system is engineered so that the light routes itself.

The principle is directly inspired by thermodynamics. Just as a gas undergoing what's known as a Joule-Thomson expansion redistributes its pressure and temperature before naturally reaching thermal equilibrium, light in the new device experiences a two-step process: first an optical analog of expansion, then thermal equilibrium. The result is a self-organized flow of photons into the designated output channel—without any need for external switches.

Hediyeh M. Dinani et al, Universal routing of light via optical thermodynamics, Nature Photonics (2025). DOI: 10.1038/s41566-025-01756-4

Part 2

Women Have Twice as Many Depression Genes as Men, Says  Study

Women are genetically at higher risk of clinical depression than men, Australian researchers found in a study published last week that could change how the disorder is treated.
Billed as one of the largest-ever studies of its kind, scientists pored through the DNA of almost 200,000 people with depression to pinpoint shared genetic "flags".

Women had almost twice as many of these genetic markers linked to depression as men, according to the study.
The genetic component to depression is larger in females compared to males. Around 13,000 genetic markers were linked with depression in women, the researchers found, compared with 7,000 markers in men.

Some of these genetic changes could alter biological pathways linked to metabolism or hormone production.

https://www.nature.com/articles/s41467-025-63236-1

Living in an unequal society impacts the structure of children's brains, study finds

The distribution of wealth between different people living in specific geographical regions has changed substantially over the past decades, with some segments of the population benefiting most from economic growth than others. In some parts of the United States, the United Kingdom and various European countries, the distribution of wealth has become increasingly uneven.

An uneven wealth distribution essentially means that there is significant disparity in the income and resources of the general population, with some people earning good salaries and others living in the same place struggling to meet their basic needs. This inequality is typically measured with a value ranging from 0 to 1, known as the Gini coefficient, where 0 represents perfect equality and 1 extreme inequality.

Researchers  recently carried out a study aimed at exploring the possible impact of living in a society where wealth is unevenly distributed on the brain's development in late childhood and pre-adolescence. Their findings, published in Nature Mental Health, suggest that living in places with a high income inequality is associated with differences in the structure of some brain regions, which could in turn predict the emergence of mental health disorders.

As part of their study, the researchers analyzed data from the ABCD dataset, which was collected from over 8,000 9–10-year-old children living across 17 U.S. states, along with Gini coefficients for these states. The data they analyzed included magnetic resonance imaging (MRI) scans showing the thickness, surface area and volume of specific regions of the children's brain, as well as functional magnetic resonance imaging (fMRI) scans showing the connections between 12 key regions in their brains.

In their analyses, the researchers controlled for other factors that might be influencing the development of the children's brains, such as their family's income, education, health care access and incarceration rates in their home state. In addition, they looked at the children's reported mental health 18 months after the brain scans were collected.

The results of the analyses  suggest that living in an unequal society is associated with a thinner cortex (i.e., the brain's outer layer), as well as significant differences in the surface area of various brain regions. In addition, the communication between some brain networks appeared to be altered in children living in places marked by higher income inequality.

The differences observed by the researchers could partly explain the relationship they found between state-wide inequality and children's mental health, particularly the emergence of disorders in children living in unequal environments.

 Divyangana Rakesh et al, Macroeconomic income inequality, brain structure and function, and mental health, Nature Mental Health (2025). DOI: 10.1038/s44220-025-00508-1.

DNA repair mechanisms help explain why naked mole-rats live a long life

Naked mole-rats are one of nature's most extraordinary creatures. These burrowing rodents can live for up to 37 years, around ten times longer than relatives of a similar size. But what is the secret to their extreme longevity? How are they able to delay the decay and decline that befalls other rodents? The answer, at least in part, is due to a switch in a common protein that boosts DNA repair, according to new research published in the journal Science.

One of the main causes of aging in all animals, including humans, is the accumulation of damaged DNA, our genetic instruction manual. When this damage is not fixed, it leads to defective cells, damaged proteins and eventually a breakdown in the body's functions.

To understand how the naked mole-rat is so resistant to DNA damage, a study focused on a common protein called cGAS (cyclic GMP-AMP synthase). In most mammals, cGAS interferes with DNA repair, but the researchers suspected it may have evolved a different function in the long-living rats.

Researchers compared the cGAS protein in naked mole-rats to that of humans and mice and identified four changes in amino acids (building blocks of cGAS) that flip the protein's function so that it enhances a cell's ability to repair damaged DNA.

To test this, the scientists inserted the mole-rat's unique cGAS into human and mouse cells in the lab. The result was a significant boost in the cells' ability to repair their DNA and a reduction in cellular aging. Then, they engineered fruit flies to produce naked mole-rat cGAS and found that they lived around ten days longer than a control group of fruit flies that couldn't produce cGAS. Finally, they used gene therapy to give the naked mole-rat cGAS to mice. These treated rodents were less frail, had less gray hair and there were fewer old, worn out cells in different organs than mice that didn't receive the gene.

"This alteration confers naked mole-rat cGAS with a greater capacity to stabilize the genome, counteract cellular senescence   and organ aging, and promote extended life span and health span," commented the researchers.

Yu Chen et al, A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging, Science (2025). DOI: 10.1126/science.adp5056

Atrial fibrillation after bypass found in nearly half of patients

Investigators  report a higher-than-expected one-year incidence of new-onset atrial fibrillation after coronary artery bypass grafting, paired with very low burden beyond 30 days.

Postoperative atrial fibrillation (AF) ranks among the most frequent early complications after cardiac surgery with reported incidence near 30%, tying into longer hospital stays, higher costs, discomfort, and observational links to thromboembolic stroke, heart failure, and recurrence.

North American guidelines state that 60 days of oral anticoagulation is reasonable with later reassessment, and European guidance advises that long-term anticoagulation should be considered in patients with new-onset AF after cardiac surgery.

Previous large cohort studies leaned on brief in-hospital telemetry and intermittent checks after discharge, leaving incidence, burden, and recurrence insufficiently characterized and prompting calls for long-term continuous monitoring.

In the study, "Long-Term Continuous Monitoring of New-Onset Atrial Fibrillation After Coronary Artery Bypass Grafting," published in JAMA, researchers conducted a prospective multicenter cohort study to test whether one-year AF incidence after coronary artery bypass grafting (CABG) exceeds prior literature and to assess AF burden.

Part 1

Enrollment involved 198 adults at two academic cardiac surgery centers in Germany, all undergoing first-time isolated CABG for three-vessel or left main disease, without prior arrhythmias, monitored for one year after implant of a device during surgery.

Patients were followed through continuous rhythm surveillance using an insertable cardiac monitor placed at skin closure. AF was defined as device-detected and adjudicated episodes lasting at least two minutes.

Within one year, 95 of 198 patients developed new-onset AF, yielding a cumulative incidence of 48% with a 95% CI of 41%–55%. Standard monitoring identified a 34% cumulative incidence with a 95% CI of 27%–41% and Gray's test P = .01 versus continuous monitoring. Sensitivity analyses using longer episode thresholds produced cumulative incidences of 46% at four minutes, 45% at six minutes, and 44% at 12 minutes.

Across the cohort with new-onset AF, median AF burden over the first year measured 0.07%, corresponding to 370 minutes. Early postoperative days carried the most arrhythmia time, with median burden of 3.65% on days 1–7, 0.04% on days 8–30, and 0% on days 31–365. A total of 2,053 episodes, accounting for 2,522 hours, were recorded, with a median episode length of six minutes and a median time-to-incident episode of 3.3 days. Asymptomatic presentations comprised 63% of episodes, and 67% were not captured by standard monitoring.

Among 95 patients with AF, 73 patients had incident episodes within seven days and 90 within 30 days, and 45% of accumulated AF time occurred within the first seven days and 77% within 30 days.

Recurrent AF later than 30 days appeared in 19 of 90 patients with incident episodes prior to 30 days, totaling 554 episodes with a median length of four minutes. Asymptomatic recurrences comprised 43% of these later episodes, and 3% were detected by standard monitoring.

The authors conclude that continuous monitoring uncovers substantially more AF than standard surveillance, while measured burden remains very low after 30 days.
Their findings question routine long-term oral anticoagulation after new-onset AF following CABG and support reassessment at 30 days when treatment is initiated.

Florian E. M. Herrmann et al, Long-Term Continuous Monitoring of New-Onset Atrial Fibrillation After Coronary Artery Bypass Grafting, JAMA (2025). DOI: 10.1001/jama.2025.14891

Gregory M. Marcus, Is There Really Something Different About Postoperative Atrial Fibrillation After Cardiac Surgery?, JAMA (2025). DOI: 10.1001/jama.2025.15275

Part 2

Rare Earth Elements: 17 Minerals More Valuable Than Gold in Today’s Tech World

Seafood unfairly singled out in microplastics debate, researchers say

Seafood has received disproportionate attention in media coverage about microplastics, despite evidence that fish and shellfish are not the main source of human exposure, according to a new scientific review.

Researchers found that more than 70% of scientific and media coverage on microplastics in food has focused on seafood, contributing to the public perception that eating fish is the biggest risk.

This misperception has real consequences, as some consumers report reducing consumption of seafood because of concerns over microplastics exposure, and thereby miss out on the health benefits of seafood consumption. The findings are reported in the journal Environmental Science & Technology Letters.

In reality, people are far more exposed to microplastics from indoor air and dust.

A previous study reported that the presence of microplastics in mussels collected from the environment was lower than the amount of microplastics that falls on a plate of mussels during dinner time in a typical household.

Seafood, including mussels and oysters and finfish like salmon and cod, may contribute 1–10 microplastic particles per day, which is consistent with other foods, like salt, honey and chicken.

Ingestion from bottled water is estimated at 10 to 100 particles per day, and exposure from indoor air accounts for considerably higher exposure—100 to 1,000 particles per day.

There is minimal evidence that they pose a health risk. The evidence we do have indicates that plastic particles readily pass through the digestive tract and exit the body.

While there are perceptions that toxic substances associated with plastic particles may pose health risks, evidence indicates concentrations are actually exceedingly low compared to other sources of exposure.

Theodore B. Henry et al, Examining Misconceptions about Plastic-Particle Exposure from Ingestion of Seafood and Risk to Human Health, Environmental Science & Technology Letters (2025). DOI: 10.1021/acs.estlett.5c00551

The migration period has started. Millions of birds are migrating now.

But birds face a variety of threats during migration—collisions with windows, communications towers and wind turbines; light pollution that disorients them; habitat loss or degradation in their migration stopover areas; human disturbance while feeding at stopover areas; predators; and storms.

Artificial light is one of the biggest dangers for birds traveling at night. It can confuse or attract them toward buildings, where they may crash into windows.

Birds collide with windows when they can't see them or, even worse, are attracted to them because of reflections of plants or the sky.This happens during the day, as well as at night during migration when lights disorient birds or if fog is causing them to fly low.

That's why people have an important role to play, say experts. The three most important things you can do for birds this time of year are to keep cats indoors, turn your lights off and use window mitigation.

Turn off unnecessary outdoor lighting at night or use motion sensors and timers so lights are only on when needed. If you must leave a light on, use warm-colored lights with shields that face downward.

Homeowners can also help reduce window collisions by: Placing bird feeders within three feet of windows or more than 30 feet away

Using window screens, UV tape or hanging cords to make glass visible

Closing blinds to limit reflections

Leaving fallen logs or stick piles in yards to give birds shelter as they stop to rest.

Enjoy these visitors as they pass through. But feed responsibly! Clean your feeders regularly, follow window guidance, and keep your cats indoors.

Nanoplastics detected in farm animal cells: Study warns of possible human consequences

Scientists at the Research Institute for Farm Animal Biology (FBN) in Dummerstorf and the University of Udine have detected the uptake of nanoplastics in farm animal cell cultures. The results provide evidence of potential risks to animal health, meat production and also human food safety.

Plastic bags, packaging, yogurt lids—items that are carelessly thrown away decompose over years into tiny plastic particles. They end up in soil, waterways and ultimately in our food chain. Although numerous studies have already shown that microplastics can harm marine animals, birds and insects, the effects of nanoplastics on livestock have hardly been researched to date.

Unlike microplastics (1 µm–5 mm), there are currently few adequate methods for detecting nanoplastics (< 1 µm) in humans and animals. However, researchers assume that these small particles can also accumulate in tissue.

In a new study, researchers have demonstrated the uptake of nanoplastic particles made of polystyrene into cultured cells from cattle and pigs. This absorption led to changes that could impair the cell function and health of the animals in the long term.

The study examined granulosa cells from cattle, which play an important role in reproduction, and myoblasts from pigs, which are used to form muscle tissue. Even low concentrations led to microscopically visible accumulations. These could impair the fertility of the animals and their products.
Farm animals are part of the human food chain. Direct health risks to consumers cannot be inferred at present. Nevertheless, the researchers urge for more detailed investigations into the long-term consequences of microplastics and nanoplastics.

Francesca Corte Pause et al, Exploring the influence of polystyrene-nanoplastics on two distinct in vitro systems in farm animals: A pilot study, Science of The Total Environment (2025). DOI: 10.1016/j.scitotenv.2025.179378

Do plastics have toxic effects on the heart? Higher exposure linked to changes in heart rhythms

We've all heard warnings about BPA—a chemical found in plastics and personal care products. Studies show that nearly millions of people around the world have detectable levels of BPA in their bodies. Now, new research has revealed this everyday exposure is tied to changes in the heart's electrical system.

Phenols are a wide variety of chemicals. The best-known example is BPA.

BPA can be found in water bottles, food can linings, cash register receipts, eyeglass lenses, even baby bottles and makeup. These are environmental phenols—chemicals in products we touch every day.

 So researchers studied 600 people. Urine tests and EKGs found higher exposure was linked to changes in heart rhythms.

The electrical conduction literally keeps us alive. If it gets altered in any way, you could die immediately, say cardiologists.

Healthy individuals should not be affected by this. But if you find a person that's genetically predisposed, that is older, these can lead to potential changes.

https://www.uc.edu/news/articles/2025/10/do-plastics-have-toxic-eff...

Rewriting the rules of genetics: Study reveals gene boundaries are dynamic, not fixed

Molecular biologists have long thought that the beginning of a gene launched the process of transcription—the process by which a segment of DNA is copied into RNA and then RNA helps make the proteins that cells need to function.

But a new study published in Science by researchers challenges that understanding, revealing that the beginning and end of genes are not fixed points, but move together—reshaping how cells build proteins and adapt through evolution.

This work rewrites a textbook idea: the beginning of a gene doesn't just launch transcription—it helps decide where it stops and what protein you ultimately make. 

For years, we taught that a gene's 'start' only decides where transcription begins. We now show the start also helps set the finish line—gene beginnings control gene endings, say the researchers  of this new work.

The discovery offers a promising new strategy for targeting cancer and neurological disorders, as well as developmental delays and aging. When gene transcription is disrupted or misregulated, protein production can become abnormal, potentially causing tumor growth.

The understanding that the beginning and ends of genes are connected could allow physicians to redirect gene expression—restoring healthy protein variants and suppressing harmful ones, without altering the underlying DNA sequence.

Misplacing a start or an end isn't a small mistake—it can flip a protein's domain structure and change its function, too. In cancer, that flip can mean turning a tumor suppressor into an oncogene. An oncogene is a mutated gene that has the potential to cause cancer by promoting uncontrolled cell growth and division.

These new findings show that controlling where a gene begins is a powerful way to control where it ends—and, ultimately, what a cell can do. 

Ezequiel Calvo-Roitberg et al, mRNA initiation and termination are spatially coordinated, Science (2025). DOI: 10.1126/science.ado8279

Flipping the switch on sperm motility offers new hope for male infertility

Infertility affects about one in six couples, and male factors account for roughly half of all cases—often because sperm don't swim well. Researchers have uncovered a key component of the "switch" that keeps the movement signal strong, offering a promising new avenue for both diagnosis and treatment. When this switch is absent, sperm slow down, and fertilization fails. By restoring that signal in the lab, the team rescued swimming and achieved healthy births in mice.

The study has been published in Proceedings of the National Academy of Sciences.

For sperm to successfully fertilize an egg, they must be able to swim, a process driven by their tail. This movement is activated by an essential signaling molecule called cyclic AMP (cAMP). While it was known that an enzyme named soluble adenylyl cyclase (sAC) produces cAMP inside sperm, the precise mechanism controlling this enzyme's stability and function remained largely a mystery.

The study focused on a protein with a previously unknown function, TMEM217, which is produced specifically in the testes. They engineered mice that could not produce TMEM217 and found that the males were completely infertile, with sperm that were almost entirely immotile. Further investigation revealed that TMEM217 partners with another protein, SLC9C1, to form a stable complex.

This complex is crucial for maintaining the presence of the sAC in mature sperm. Without TMEM217, SLC9C1 is lost and sAC is markedly reduced, causing cAMP levels to plummet and sperm motility to fail.  

In a significant breakthrough, the team took the immotile sperm from these mice and treated them with a cAMP analog—a molecule that mimics cAMP. This treatment successfully restored the sperm's movement and enabled them to fertilize eggs in vitro, leading to the birth of healthy pups.

The study has revealed a fundamental "switch" in sperm, providing a deeper understanding of sperm motility regulation. The discovery of the TMEM217-SLC9C1-sAC axis offers a new target for diagnosing unexplained cases of male infertility.

Formation of a complex between TMEM217 and the sodium-proton exchanger SLC9C1 is crucial for mouse sperm motility and male fertility, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2516573122

New lab-grown human embryo model produces blood cells

Scientists have used human stem cells to create three-dimensional embryo-like structures that replicate certain aspects of very early human development—including the production of blood stem cells. The findings are published in the journal Cell Reports.

Human blood stem cells, also known as hematopoietic stem cells, are immature cells that can develop into any type of blood cell, including red blood cells that carry oxygen and various types of white blood cells crucial to the immune system.

The embryo-like structures, which the scientists have named "hematoids," are self-organizing and start producing blood after around two weeks of development in the lab—mimicking the development process in human embryos.

The structures differ from real human embryos in many ways, and cannot develop into them because they lack several embryonic tissues, as well as the supporting yolk sac and placenta needed for further development.

Hematoids hold exciting potential for a better understanding of blood formation during early human development, simulating blood disorders like leukemia, and for producing long-lasting blood stem cells for transplants.

The human stem cells used to derive hematoids can be created from any cell in the body. This means the approach also holds great potential for personalized medicine in the future, by allowing the production of blood that is fully compatible with a patient's own body.

A post-implantation model of human embryo development includes a definitive hematopoietic niche, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116373. www.cell.com/cell-reports/full … 2211-1247(25)01144-1

A neural basis for flocking

When animals move together in flocks, herds, or schools, neural dynamics in their brain become synchronized through shared ways of representing space, a new study by researchers  suggests. The findings challenge the conventional view of how collective motion arises in nature.

Flocking animals, such as hundreds of birds sweeping across the sky in unison, are a mesmerizing sight. But how does their collective motion—seen in many species, from swarming locusts to schooling fish and flocking birds—arise?

Researchers have developed a novel theoretical framework that integrates neurobiological principles to upend long-held assumptions about how flocking behavior emerges in nature.

In a recent article published in Nature Communications they demonstrate that flocking does not require individuals to rely on rigid behavioral rules, as is typically assumed. Instead, it can arise naturally from a simple and widespread neural architecture found across the animal kingdom: the ring attractor network.

In the new model, flocking arises because neural activity in each animal becomes linked through perception: Every individual processes its surroundings using a ring attractor—a circular network of neurons that tracks the direction toward perceived objects in space. This way, the animal can maintain bearings toward others relative to stable features in the environment. The researchers found that when many such individuals interact, their neural dynamics synchronize, giving rise to spontaneous alignment and collective movement.

This means that coordinated motion can emerge directly from navigational processes in the brain, challenging decades of theory.

The new framework shows that collective motion emerges when individuals represent the directions of others relative to stable features in their surroundings—a world-centered, or allocentric, perspective. This mechanism underlies what the authors describe as "allocentric flocking."

Mohammad Salahshour et al, Allocentric flocking, Nature Communications (2025). DOI: 10.1038/s41467-025-64676-5

Mom's voice boosts language-center development in preemies' brains, study finds

Hearing the sound of their mother's voice promotes development of language pathways in a premature baby's brain, according to a new  study.

During the study, which is published in Frontiers in Human Neuroscience, hospitalized preemies regularly heard recordings of their mothers reading to them. At the end of the study, MRI brain scans showed that a key language pathway was more mature than that of preemies in a control group who did not hear the recordings. It is the first randomized controlled trial of such an intervention in early development.

This is the first causal evidence that a speech experience is contributing to brain development at this very young age.

Premature babies—born at least three weeks early—often spend weeks or months in the hospital, typically going home around their original due dates. During hospitalization, they hear less maternal speech than if they had continued to develop in utero.

Parents can't usually stay at the hospital around the clock; they may have older children to care for or jobs they must return to, for example. Preemies are at risk for language delays, and scientists have suspected that reduced early-life exposure to the sounds of speech contributes to the problem.

The researchers decided to boost preemies' exposure to their mom's voices during hospitalization. They did this by playing recordings of the mothers speaking, a total of two hours and 40 minutes a day, for a few weeks at the end of the babies' hospital stays.

Babies were exposed to this intervention for a relatively short time. In spite of that, researchers saw very measurable differences in their language tracts. It's powerful that something fairly small seems to make a big difference.

Part 1

Fetal hearing begins to develop a little more than halfway through pregnancy, around 24 weeks into what is normally a 40-week gestation period. As the fetus grows, the uterus expands and the uterine wall thins.

Late in pregnancy, more sounds, including the mother's conversations, reach the fetus. At birth, full-term newborns recognize their mother's voice and prefer the sounds of their parents' native language to other languages, prior research has shown.

These factors suggest that listening to Mom's voice contributes to brain maturation in the latter half of a full-term pregnancy.

So in their work the researchers realized that by supplementing the sounds that premature babies hear in the hospital so they resemble what they would have heard in the womb, they had a unique opportunity to possibly improve brain development at this stage of life.

 Listening to Mom in the Neonatal Intensive Care Unit: A randomized trial of increased maternal speech exposure on white matter connectivity in infants born preterm, Frontiers in Human Neuroscience (2025). DOI: 10.3389/fnhum.2025.1673471

Part 2

Men’s brains shrink more with age
Men’s brains shrink more as they age than women’s brains do, which could scupper the theory that age-related brain changes explain why women are more frequently diagnosed with Alzheimer’s disease than men. Using more than 12,500 brain scans from 4,726 people, researchers found that men experienced a greater reduction in volume across more regions of the brain over time than women did. This suggests that sex differences in brain volume don’t play a part in the development of Alzheimer’s, but “just looking at age-related changes in brain atrophy is unlikely to explain the complexities behind [the disease]”, say neurophysiologists.

 Proceedings of the National Academy of Sciences paper

https://www.pnas.org/doi/10.1073/pnas.2510486122

https://www.nature.com/articles/d41586-025-03353-5?utm_source=Live+...

A rare variety of wheat with three ovaries—gene discovery could triple production

Researchers discovered the gene that makes a rare form of wheat grow three ovaries per flower instead of one. Since each ovary can potentially develop into a grain of wheat, the gene could help farmers grow much more wheat per acre. Their work is published in the journal Proceedings of the National Academy of Sciences.

The special trait of growing three ovaries per flower was initially discovered in a spontaneously occurring mutant of common bread wheat. But it wasn't clear what genetic changes led to the new trait. The UMD team created a highly detailed map of the multi-ovary wheat's DNA and compared it to regular wheat.

They discovered that the normally dormant gene WUSCHEL-D1 (WUS-D1) was "switched on" in the multi-ovary wheat.
When WUS-D1 is active early in flower development, it enlarges the flower-building tissues, enabling them to produce extra female parts like pistils or ovaries.

If breeders can control or mimic this genetic trick of activating WUS-D1, they could design new wheat varieties that grow more kernels per plant. Even small gains in the number of kernels per plant can translate into huge increases in food supply at the global scale.

Pinpointing the genetic basis of this trait offers a path for breeders to incorporate it into new wheat varieties, potentially increasing the number of grains per spike and overall yield, say the researchers. By employing a gene editing toolkit, scientists can now focus on further improving this trait for enhancing wheat yield. This discovery provides an exciting route to develop cost-effective hybrid wheat.

The discovery of WUS-D1 could also lead to the development of similar multi-ovary varieties of other grain crops.

 Adam Schoen et al, WUSCHEL-D1upregulation enhances grain number by inducing formation of multiovary-producing florets in wheat, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2510889122

Electric charge connects jumping worm to aerial prey

A tiny worm that leaps high into the air—up to 25 times its body length—to attach to flying insects uses static electricity to perform this astounding feat, scientists have found.

The journal PNAS published the work on the nematode Steinernema carpocapsae, a parasitic roundworm. 

Researchers identified the electrostatic mechanism this worm uses to hit its target, and we've shown the importance of this mechanism for the worm's survival. Higher voltage, combined with a tiny breath of wind, greatly boosts the odds of a jumping worm connecting to a flying insect.

They conducted the experiments, including the use of high-speed microscopy techniques to film the parasitic worm—whose length is about the diameter of a needle point—as it leaped onto electrically charged fruit flies.

The researchers showed how a charge of a few hundred volts, similar to that generated by an insect's wings beating the air, initiates an opposite charge in the worm, creating an attractive force. They identified electrostatic induction as the charging mechanism driving this process.

Using physics, scientists learned something new and interesting about an adaptive strategy in an organism.

Ranjiangshang Ran et al, Electrostatics facilitate midair host attachment in parasitic jumping nematodes, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503555122

Differences in coexistence create new species

A simple change in species composition can impact the course of evolution: A research team shows that the presence of just one other fish species is enough to drive the emergence of new species in sticklebacks.

It has long been assumed that adaptation to different habitats plays an important role in the evolution of new species. Yet how important this influence truly is—particularly during the initial stages of the speciation process—and which ecological differences are most critical remain major questions in evolutionary research.

For the current study, the research team studied populations of threespine stickleback—small fish about the size of a finger—from lakes in western Canada. These lakes formed after glaciers from the last ice age melted less than 12,000 years ago and were then colonized by sticklebacks from the sea. While many of these lakes are environmentally similar, they differ in one aspect: in some, another fish species, the prickly sculpin, lives alongside sticklebacks, while in other lakes sculpins are absent.

This seemingly simple ecological difference—living with or without sculpins—has repeatedly pushed sticklebacks down distinct evolutionary paths: in lakes with sculpins, sticklebacks have evolved into slimmer open-water forms, while in sculpin-free lakes they have become stockier bottom-feeding specialists.

 Marius Roesti et al, A species interaction kick-starts ecological speciation in allopatry, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2506625122

Human cells activate self-destruction when viruses disrupt RNA production, study shows

Viruses are masters at taking over our cells: They disable our defenses and hijack the cellular machinery in order to multiply successfully. For example, the herpes simplex virus 1, which causes blister-like skin rashes, and influenza viruses specifically block a crucial step in gene activity in which the production of RNA molecules is completed—known as transcription termination. The blockade results in unnaturally long RNA molecules that cannot be translated into proteins. This suppresses the antiviral defense in the cells and creates optimal conditions for the viruses to multiply.

A new study published in Nature now shows that human cells are not helpless against this viral sabotage. They recognize the disruption of transcription termination as an alarm signal, activate a "self-destruction program" and sacrifice themselves—even before the virus can multiply in them. This enables them to nip the spread of the infection in the bud.

Researchers discovered that the unnaturally long RNA molecules adopt a special structure: They twist into left-turning double strands, known as Z-RNAs. These unusual RNA forms are recognized by the cellular protein ZBP1. And then the controlled cell death begins.

It is particularly noteworthy that Z-RNAs form primarily in those sections of these unnaturally long RNA molecules that originate, among other things, from remnants of previous viral infections. These otherwise silent areas of our genome are only transcribed into RNA due to the virus-related disruption of transcription termination.

Our cells therefore use these genetic remnants of ancient viral infections to detect and ward off current viral attacks.

Evolution has thus turned the tables: what once began as a viral invasion now serves as an alarm signal for the antiviral immune defense. This discovery impressively demonstrates how closely virus and host have been intertwined over millions of years—and how our cells can transform viral sabotage into highly effective protective strategies.

 Chaoran Yin et al, Host cell Z-RNAs activate ZBP1 during virus infections, Nature (2025). DOI: 10.1038/s41586-025-09705-5

Scientists turned off moths' sex signals—this could be the key to greener pest control

A single "sexy" gene could help us combat one of the world's most destructive fruit pests. By deleting the gene that lets female moths produce their mating scent, researchers  created an "unsexy" moth—and showed one way to turn insect attraction into a powerful pest control tool.

You've probably seen moths flittering around a bright lamppost on a balmy summer night. Those same insects, in their larval form, are the worms that burrow into your apples and peaches, making them serious pests in agriculture.
Moths are usually controlled with chemical pesticides, but pests evolve resistance and these sprays also harm bees and other pollinators. We need new and more sustainable methods to protect important crops targeted by moth larvae, like apples, maize, tomatoes and rice.

In a new study published in the Journal of Chemical Ecology, researchers have demonstrated a way to unravel sexual communication in insects and provide a more sustainable alternative to pesticides. Yes, now  we can stop moths by using their natural instincts against them.

Marie Inger Dam et al, Sex pheromone biosynthesis in the Oriental fruit moth Grapholita molesta involves Δ8 desaturation, Insect Biochemistry and Molecular Biology (2025). DOI: 10.1016/j.ibmb.2025.104307

Why women's brains face higher risk: Scientists pinpoint X-chromosome gene behind MS and Alzheimer's

New research has identified a sex-chromosome linked gene that drives inflammation in the female brain, offering insight into why women are disproportionately affected by conditions such as Alzheimer's disease and multiple sclerosis as well as offering a potential target for intervention.

The study, published in the journal Science Translational Medicine, used a mouse model of multiple sclerosis to identify a gene on the X chromosome that drives inflammation in brain immune cells, known as microglia. Because females have two X chromosomes, as opposed to only one in males, they get a "double dose" of inflammation, which plays a major role in aging, Alzheimer's disease and multiple sclerosis.

When the gene, known as Kdm6a, and its associated protein were deactivated, the multiple sclerosis-like disease and neuropathology were both ameliorated with high significance in female mice.

Multiple sclerosis and Alzheimer's disease each affect women more often than men, about two to three times as often. Also, two-thirds of healthy women have 'brain fog' during menopause. These new findings explain why and point to a new treatment to target this.

When researchers genetically "knocked out" the gene Kdm6a in brain immune cells, the inflammatory molecules shifted from being activated to a resting state. Additionally, they  performed a pharmacologic "knock down" of the protein made by this gene using metformin. Metformin is widely used as a treatment for diabetes but is currently being researched for potential anti-aging properties.

While these interventions were highly significant in female mice, their effect was almost undetectable in males.

This is consistent with there being 'more to block' in females due to having two copies of the X-linked gene.

It's also why females are more likely to get MS and AD than males. This has implications for the clinic. Women may respond differently to metformin treatment than men.

The findings may also have implications for explaining a connection to brain fog in healthy women during menopause.

Sex chromosomes and sex hormones achieve a balance through evolution. There is a selection bias to do so. Females have a balance between X chromosome-driven inflammation that can be good to fight infections at child-bearing ages. This is held in check by estrogen, which is anti-inflammatory and neuroprotective. As women age, menopause causes loss of estrogen, unleashing the proinflammatory and neurodegenerative effects of this X chromosome in brain immune cells.

Yuichiro Itoh et al, Microglia-specific deletion of the X-chromosomal gene Kdm6a reverses the disease-associated microglia translatome in female mice, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adq3401. www.science.org/doi/10.1126/scitranslmed.adq3401

'Jump-scare' science: Study elucidates how the brain responds to fear

In haunted houses across the US this month, threatening figures will jump out of the shadows, prompting visitors—wide-eyed and heart racing—to instinctively freeze and flee.

Evolutionarily speaking, this "innate threat response" is key to survival, helping a wide variety of animal species escape predators. But when stuck in overdrive it can cause problems for humans.

A  research team has identified a novel brain circuit responsible for orchestrating this threat response. Known as the interpeduncular nucleus (IPN), this dense cluster of specialized neurons not only jump-starts that freeze-and-flee reaction, but dials it down when animals learn there's no real danger.

In people with anxiety or post-traumatic stress disorder (PTSD), this circuit may be broken, researchers say.

The findings could help explain why some people have a greater appetite for risk than others and lead to new therapies for psychiatric disorders.

The brain's threat system is like an alarm. It needs to sound when danger is real, but it needs to shut off when it's not. This new study shows how the brain learns to fine-tune those responses through experience, helping us adapt to the world.

 Elora W. Williams et al, Interpeduncular GABAergic neuron function controls threat processing and innate defensive adaptive learning, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03131-9

**

Preventing overhydration: Study uncovers a neural circuit that prompts mice to stop drinking

Identifying the neural mechanisms that support the regulation of vital physiological processes, such as drinking, eating and sleeping, is a long-standing goal within the neuroscience research community. As the disruption of these processes can severely impact people's health and everyday functioning, uncovering their neural and biological underpinnings is of the utmost importance.

New insights gathered by neuroscientists could ultimately inform the development of more effective interventions designed to regulate vital physiological processes. Thirst and hunger are known to be regulated by homeostatic processes, biological processes that allow the body to maintain internal stability.

Yet drinking behaviour can also be anticipatory, which means that animals and humans often adjust their actions (i.e., stop drinking) before the concentration of substances in the blood changes in response to drinking water. The mechanisms through which the brain predicts when it is the right time to stop drinking remain poorly understood.

Researchers  recently carried out a study involving mice aimed at shedding new light on these mechanisms. Their findings, published in Nature Neuroscience, led to the identification of a neural pathway that reduces neural activity in specific regions of the mouse brain, signaling that the body has received enough water.

Drinking behaviour is not only homeostatically regulated but also rapidly adjusted before any changes in blood osmolality occur, known as anticipatory thirst satiation.

Homeostatic and anticipatory signals converge in the subfornical organ (SFO); however, the neural pathways conveying peripheral information to the SFO before changes in blood composition are incompletely understood till now.

Researchers now  reveal an inhibitory pathway from the medial septum (MS) to the SFO that is involved in the control of anticipatory drinking behaviour in mice.

As part of their experiments, researchers observed the drinking behavior of adult mice, while recording their neural activity. This led to the discovery of a neural pathway connecting the MS, a small region in the mouse brain that contributes to the synchronization of brain circuits, and the SFO, a region implicated in the monitoring of bodily fluids.

"MS γ-aminobutyric acid (GABA)ergic neurons encode water-satiation signals by integrating cues from the oral cavity and tracking gastrointestinal signals," wrote the authors in their research paper. "These neurons receive inputs from the parabrachial nucleus and relay to SFOCaMKII neurons, forming a bottom-up pathway with activity that prevents overhydration. Disruption of this circuit leads to excessive water intake and hyponatremia."

Essentially, the researchers found that after a mouse starts drinking, GABAergic neurons in the MS become active and receive signals from the parabrachial nucleus, a brain region that processes signals originating from the mouth and gut. These GABAergic neurons then send inhibitory signals to neurons in the SFO, which in turn modulate the feeling of thirst.

Part 1

Interestingly, when the team disrupted this pathway's activity, they found that mice no longer stopped drinking and developed hyponatremia. This is a condition characterized by overhydration and an abnormally low concentration of sodium in the blood.

This recent study gathered new valuable insight into how the mouse brain prevents overhydration, signaling that it is time to stop drinking.

Lingyu Xu et al, A bottom-up septal inhibitory circuit mediates anticipatory control of drinking, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02056-4.

Part 2

The way we talk to chatbots affects their accuracy, new research reveals

Whether we're seeking customer support, looking for recommendations, or simply asking a quick question, AI chatbots are designed to give us the answers we're looking for. But there's more going on beneath the surface. Every time we chat with them, they are learning from us to improve their understanding and responses. And the type of language we use, whether formal or informal, directly affects the quality of their answers, according to new research.

In general, people naturally adapt their conversation style to the person they are speaking with. 

The researchers compared thousands of messages people sent to human agents with those sent to AI chatbots, focusing on features like grammar, vocabulary and politeness. They found that people were 14.5% more polite and formal and 5.3% more grammatically fluent when chatting with humans than when talking with AI, based on analysis by the Claude 3.5 Sonnet model.

Next, they trained an AI model called Mistral 7B on about 13,000 real chats between people, then tested how well it understood more than 1,300 messages people had sent to chatbots. To broaden the AI's exposure, they also created blunt and polite rewrites of those messages to simulate different communication styles.

It turns out that chatbots trained on a diverse mix of message styles, including real and fake messages, were 2.9% better at understanding user intent than AI trained solely on original human conversations. The researchers also tried to improve Mistral AI's understanding by rewriting informal messages at the last minute to be more formal, but this led to a drop in understanding by almost 2%.

So the best way to make chatbots smarter is to train them on a range of communication styles, as the researchers state in their paper published on the arXiv preprint server. "Training-time exposure to diverse linguistic variation is more effective than inference-time normalization. Models must learn to interpret diverse communication styles during training, rather than rely on brittle post-hoc transformations that risk semantic distortion."

Fulei Zhang et al, Mind the Gap: Linguistic Divergence and Adaptation Strategies in Human-LLM Assistant vs. Human-Human Interactions, arXiv (2025). DOI: 10.48550/arxiv.2510.02645

Men experience more brain atrophy with age despite women's higher Alzheimer's risk

Many women complained to me that their husbands "behaved strangely" as they got older and older. 

It seems they complained more, got irritated and angry more, understood situations less, grumbled a lot, ... and the descriptions take a strange turn as they go on describing them.

Now we have an explanation for such behaviours.

Women are far more likely than men to end up with Alzheimer's disease (AD). This may, at least partially, be due to women's longer average lifespans, but many scientists think there is probably more to the story. It would be easy to surmise that the increased risk is also related to differences in the way men's and women's brains change as they age. 

Now, a new study, published in Proceedings of the National Academy of Sciences, indicates that it's men who experience greater decline in more regions of the brian as they age. Researchers involved in the study analyzed 12,638 brain MRIs from 4,726 cognitively healthy participants (at least two scans per person) from the ages of 17–95 to find how age-related changes occurred and whether they differed between men and women.

The results showed that men experienced declines in cortical thickness and surface area in many regions of the brain and a decline in subcortical structures in older age. Meanwhile, women showed greater decline only in a few regions and more ventricular expansion in older adults. So, while differences in brain aging between the sexes are apparent, the cause of increased AD prevalence in women is still a bit mysterious.

These findings suggest that the higher prevalence of AD diagnoses in women likely stems from factors beyond differential rates of age-related brain atrophy," the study authors write.

One factor that might be to blame is genetics, particularly the APOE ε4 allele, which may affect protein accumulation in the brain and work differently in men and women. Other factors might include differences in hormonal changes, diagnosis patterns, and sociocultural influences.

Survival bias may also skew the results in AD studies, as more men may have been diagnosed with AD if their average lifespans matched women's more closely. In this particular study, participants were also more educated on average, which is a protective factor for AD—leading to a potential representativity bias.

When the researchers corrected for life expectancy, they say some of the differences did clear up for men and additional differences cropped up in women.

"The interpretation of these sex differences is complicated by our life expectancy analyses, which removed several cortical decline effects in men while revealing effects in women, including greater hippocampal decline. Whether this reflects the removal of proximity-to-death artifacts or elimination of biological aging differences cannot be determined, and these findings should be interpreted with caution, especially considering representativity bias in our sample with potentially healthier men," the authors explain.

Anne Ravndal et al, Sex differences in healthy brain aging are unlikely to explain higher Alzheimer's disease prevalence in women, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2510486122

Disconnected cerebral hemisphere in epilepsy patients shows sleep-like state during wakefulness

Sleep-like slow-wave patterns persist for years in surgically disconnected neural tissue of awake epilepsy patients, according to a study published in PLOS Biology.

The presence of slow waves in the isolated hemisphere impairs consciousness; however, whether they serve any functional or plastic role remains unclear.

Hemispherotomy is a surgical procedure used to treat severe cases of epilepsy in children. The goal of this procedure is to achieve maximal disconnection of the diseased neural tissue, potentially encompassing an entire hemisphere, from the rest of the brain to prevent the spread of seizures.

The disconnected cortex—the outer layer of neural tissue in the brain—is not surgically removed and has a preserved vascular supply. Because it is isolated from sensory and motor pathways, it cannot be evaluated behaviorally, leaving open the question of whether it retains internal states consistent with some form of awareness. More broadly, the activity patterns that large portions of the disconnected cortex can sustain in awake humans remain poorly understood.

Researchers recently tried to investigate these things.

They  used electroencephalography (EEG) to measure activity in the isolated cortex during wakefulness before and up to three years after surgery in 10 pediatric patients, focusing on non-epileptic background activity. Following surgery, prominent slow waves appeared over the disconnected cortex. This is novel evidence that this pattern can last for months and years after complete cortical disconnection. The persistence of slow waves raises the question of whether they play any functional role or merely reflect a regression to a default mode of cortical activity.

The pronounced broad-band EEG slowing resembled patterns observed in conditions such as deep non-rapid eye movement (NREM) sleep, general anesthesia, and the vegetative state. The findings indicate absent or reduced likelihood of dream-like experiences in the isolated cortex. Overall, the EEG evidence is compatible with a state of absent or reduced awareness.

According to the researchers, any inference about the presence or absence of consciousness, based solely on the brain's physical properties such as prominent EEG slow waves, should be approached with caution, particularly in neural structures that are not behaviorally accessible. The slowing observed at the scalp level should be further characterized with intracranial recordings in cases in which clinical outcomes require postoperative invasive monitoring.

Michele A. Colombo et al, Hemispherotomy leads to persistent sleep-likslow waves in the isolated cortex of awake humans, PLOS Biology (2025). DOI: 10.1371/journal.pbio.3003060

How to STOP A Dog Attack BEFORE It Happens!

Older fathers linked to more new gene mutations in puppies, study finds

An international study has shown how and when entirely new gene mutations, known as de novo mutations, originate in dogs. A key finding is that higher paternal age increases the number of de novo mutations in puppies. Maternal age also has an effect.

The study analyzed 390 parent–offspring trios. Trio denotes a design where the genomes of the puppy and both parents are sequenced. This enables accurately identifying gene mutations that do not occur in either parent's genome—mutations that have taken place in the sperm, the ovum or soon after conception. While these rare mutations are the basis of evolution, they can also predispose their carriers to hereditary diseases.

The results, published in Genome Biology, also show why dogs differ from humans in certain genomic regions and what the findings mean for canine health and breeding.

Shao-Jie Zhang et al, Determinants of de novo mutations in extended pedigrees of 43 dog breeds, Genome Biology (2025). DOI: 10.1186/s13059-025-03804-2

What happens when the cell's 'antenna' malfunctions?

Researchers have uncovered the molecular mechanisms responsible for regulating a structure that plays a critical role in how cells communicate with their environment. Their new study has been published in Communications Biology.

Found on the surface of almost every cell, the primary cilium is a tiny antenna-like projection that enables the cell to sense environmental signals. Through this structure, cells regulate essential processes such as growth, development, and adaptation. For healthy functioning, primary cilia must maintain the correct length, stability, and morphology.

The research highlights the role of DYRK kinases, a family of enzymes that regulate intracellular processes. The findings  show that these kinases are essential for maintaining the length, stability, and shape of primary cilia.

When DYRK kinases malfunction, cilia may become abnormally long, structurally deformed, or unstable. In such cases, the cell loses its ability to properly sense and process external signals.

This discovery not only advances our understanding of fundamental cell biology but also provides new perspectives on health conditions linked to ciliary dysfunction, such as developmental disorders, kidney diseases, and vision loss. Moreover, it may open new avenues for addressing complex diseases in the future by uncovering potential targets for therapeutic intervention.

 Melis D. Arslanhan et al, Kinase activity of DYRK family members is required for regulating primary cilium length, stability and morphology, Communications Biology (2025). DOI: 10.1038/s42003-025-08373-5

'Wetware': Scientists use human mini-brains to power computers

Wetware (brain), a term drawn from the computer-related idea of hardware or software, but applied to biological life forms.

'Wetware': Scientists use human mini-brains to power computers

Ten universities around the world are conducting experiments using FinalSpark's organoids -- the small company's website even has a live feed of the neurons at work.

Inside a lab in the picturesque Swiss town of Vevey, a scientist gives tiny clumps of human brain cells the nutrient-rich fluid they need to stay alive.

It is vital these mini-brains remain healthy, because they are serving as rudimentary computer processors—and, unlike your laptop, once they die, they cannot be rebooted.

This new field of research, called biocomputing or "wetware," aims to harness the evolutionarily honed yet still mysterious computing power of the human brain.

The scientists think that that processors using brain cells will one day replace the chips powering the artificial intelligence boom.

The supercomputers behind AI tools like ChatGPT currently use silicon semiconductors to simulate the neurons and networks of the human brain. Instead of trying to mimic, these scientists are using the real thing.

Among other potential advantages, biocomputing could help address the skyrocketing energy demands of AI, which have already threatened climate emissions targets and led some tech giants to resort to nuclear power.

Biological neurons are one million times more energy efficient than artificial neurons, these scientists say. They can also be endlessly reproduced in the lab, unlike the massively in-demand AI chips made by companies like behemoth Nvidia.

But for now, wetware's computing power is a very long way from competing with the hardware that runs the world.

Source: News agencies

https://www.newindianexpress.com/lifestyle/tech/2025/Oct/17/wetware...'Wetware'%3A%20Scientists%20use%20human%20mini%2Dbrains%20to%20power%20computers