Scientists observe Einstein's gravity in the quantum world

An international team has observed a long-predicted effect of gravity on a falling quantum object for the first time. The result shows that a fundamental principle at the heart of Einstein's theory of gravity remains consistent with the behaviour of matter in the quantum world.
For more than a century, physicists have relied on two extraordinarily successful descriptions of nature. Quantum mechanics explains the strange behavior of atoms and other tiny objects. Einstein's theory of gravity explains how objects fall and how gravity shapes the universe. Yet physicists still do not fully understand how the two fit together.

Now, an international team has performed an experiment that probes the point where they meet. In the study, the researchers observed a distinctive change in the quantum properties of atoms as they fell under gravity. Crucially, the effect they measured is the same one predicted when Einstein's equivalence principle, a cornerstone of his theory of gravity, is applied to a quantum object.

The equivalence principle states that for an observer in free fall, gravity should locally disappear. Someone falling freely in an elevator, for example, would experience weightlessness. While this theory has survived extraordinarily precise tests involving ordinary matter, it was unclear how it could be experimentally tested with quantum objects, which can behave as waves and effectively travel along more than one path.
Although previous experiments have used quantum particles to measure gravity, the researchers say this is the first direct measurement of the predicted quantum phase of a freely falling object.

Observation of the quantum phase of free fall and the consistency with the equivalence principle, Science Advances (2026). DOI: 10.1126/sciadv.aec8045

When biology inspires mathematics: Hidden symmetries explain why widely used evolutionary methods can give false answers
Why do some groups of organisms contain thousands of species while others have only a handful? Evolutionary biologists have spent decades trying to answer this question using mathematical models that estimate how biological traits and environmental factors influence the formation and extinction of species.
These models have become a cornerstone of modern biology and have been used in more than 1,000 scientific studies. Yet the models carry a known weakness: They can sometimes lead scientists to the wrong conclusions. For years, no one fully found out why.
Several years ago, researchers found that many evolutionary models can generate exactly the same observations even when they rest on entirely different assumptions about evolutionary history. This meant that scientists could unknowingly reach different conclusions that were all equally consistent with the same data. Whether the same ambiguity also affected the more sophisticated models used to study how traits shape biodiversity remained unclear because their mathematics was too complex to analyze directly.
Sergei Tarasov at the Finnish Museum of Natural History and Josef Uyeda at Virginia Tech approached the problem from a different angle. Their path to the solution started with a simple but unusual question: Imagine three apples—one red, one light green and one dark green. Should the two green apples be grouped together or treated as different colors? The researchers ran into the same classification puzzle while studying beetle anatomy.

Searching for an answer led them to lumpability, a mathematical concept introduced in the 1960s that defines when different states of a Markov model can be safely grouped together without changing how a system behaves. Building on it, they unexpectedly discovered a new way of representing Markov models, one of the most fundamental classes of stochastic models used across science.

They showed that every discrete-state Markov model can be rewritten as an equivalent hidden-state model, a decomposition they call Hidden Expansion. Although the rewritten model looks larger, it is built from simple, identical mathematical components. This representation exposed previously hidden mathematical symmetries and turned an intractable problem into a solvable one.
This mathematical property had gone unnoticed despite decades of research on Markov models.
Part 1

The new decomposition allowed the researchers to answer the question that had resisted mathematical analysis for years. They showed that the same hidden symmetries also affect the sophisticated models used to study biodiversity and that the misleading conclusions these models sometimes produce are not isolated statistical mistakes. Instead, they stem from a deeper mathematical ambiguity built into the models themselves.
Scientific discoveries often begin with advances in mathematics that later transform biology. This study followed the opposite path. A biological question about how to represent anatomical traits of beetles led to a new mathematical discovery, which in turn solved a long-standing problem in evolutionary biology.

It's a wonderful example of biology and mathematics driving each other forward.

Sergei Tarasov et al, Unidentifiability and false-positive inference in state-dependent diversification models, Nature Communications (2026). DOI: 10.1038/s41467-026-75829-5

Part 2

Scientists discover how fructose may help drive obesity
High-fructose corn syrup is just one of many food additives linked to obesity. It is typically found in sweetened beverages and processed foods and is added to enhance flavour and sweetness.
But exactly how it it contributes to weight gain and obesity ?
New research
suggests the calories the sweetener contains are not the only drivers of these body changes. It could also be due to how fructose is processed, which may alter the intestine's physical structure and affect fat absorption. Details of the work are published in a paper in Science Advances.

The scientists wanted to study the gut specifically because the small intestine is the first place in the body that processes dietary fructose. They designed a series of controlled experiments in mice to examine a highly active form of a fructose-processing enzyme called Ketohexokinase-C.

For up to 12 weeks, the mice were given drinking water containing a high concentration of high-fructose corn syrup. Meanwhile, a control group of normal mice was given the exact same high-fructose diet, while another set of mice received normal drinking water without added sugar.

Throughout the study, the research team tracked the animals' body weight, fat mass and blood sugar levels. They also measured fat absorption. To do this, they gave the mice a dose of soybean oil and monitored how much fat entered their bloodstream versus how much passed into their waste.

According to the paper, mice lacking intestinal Ketohexokinase-C consumed the same total number of calories as normal mice but put on significantly less weight, stayed leaner and showed better glucose tolerance and lower fasting insulin levels.

Because the modified mice lacked Ketohexokinase-C in their intestinal cells, fructose was not broken down normally in the small intestine. Consequently, it traveled further down the digestive tract, where it altered the gut microbiome.

This, in turn, lowered the number of immune cells in the gut wall, which caused fat-absorbing tubes in the intestine (lacteals) to shrink. Because shorter fat tubes couldn't absorb as much dietary fat into the body, more of it passed straight out in their feces.

To confirm this, the researchers transplanted the altered gut bacteria into normal mice. They too developed shorter fat tubes and stopped absorbing as much fat.
"We found an unexpected role of small intestinal fructose catabolism [the biological breakdown of fructose for energy] in modulating gut microbiome, ileum-specific lacteal growth, dietary fat absorption, and eventually whole-body metabolic fitness," wrote the team in their paper.

Part 1

If this intestinal process is the same in humans, it could help explain why diets high in both sugar and fat may be particularly harmful and point to new ways to tackle obesity by targeting fructose metabolism, for example, with drugs that inhibit Ketohexokinase.

"This previously unappreciated link between intestinal fructose catabolism and dietary lipid absorption may explain the synergistically stronger effects of a diet enriched with both fat and fructose."

Miranda L. Lopez et al, Intestinal fructose catabolism promotes obesity and insulin resistance via ileal lacteal remodeling, Science Advances (2026). DOI: 10.1126/sciadv.aec0481

Part 2

To promote climate action, emotion may matter more than information

Every year, public authorities and nongovernmental organizations spend millions on communication campaigns designed to encourage people to take action on climate change. But which strategies work best? Should campaigns rely on fear or positive messages, prioritize facts or appeal to emotions, and focus on words or visuals?
Across 71 studies involving 216,000 participants, most climate communication strategies increased pro-climate intentions, behaviours, or policy support. Emotionally engaging storytelling, awe, moral framing, and images outperformed factual information alone. Individual or collective responsibility messages showed little benefit and may provoke reactance.

The strategies reviewed encompassed 15 different approaches, ranging from providing factual information to fill knowledge gaps to appealing to emotions—for example, by evoking a sense of wonder or awe at the beauty of nature. They also included approaches based on the principle of bounded rationality, which are designed to facilitate decision-making by highlighting specific aspects of climate change, such as its health or financial consequences.

Research shows that almost all of these strategies are likely to have a positive effect on people's intentions and behaviours, as well as on their support for climate policies. Only strategies based on individual and collective responsibility—with messages such as 'success depends largely on you'—appear to have little or no effect. They may even foster reactance.
But not all effective strategies are equally effective. "Campaigns that evoke a strong emotional response—particularly through storytelling or by inspiring a sense of wonder at the beauty of nature—are significantly more effective than simply presenting facts and scientific evidence. Messages that draw on moral, ethical or even religious considerations, highlighting our connection to something greater than ourselves that we have a responsibility to preserve, also achieve better results.
The researchers also found that messages are more effective when they include images.

Despite these differences, the fact that almost all of these strategies can have a positive effect is encouraging.
This is particularly encouraging given that the studies reviewed mainly measured the effects of messages to which people were exposed only once. Yet we know that repeated exposure can strengthen their impact. At a time when the scientific evidence is well established and the challenge is to turn knowledge into action, there is considerable scope to improve climate communication.

Mario Herberz et al, A systematic review and meta-analysis of communication strategies to promote climate action, Journal of Environmental Psychology (2026). DOI: 10.1016/j.jenvp.2026.103176

UN report finds 1.5°C warming limit likely to be exceeded by 2030

For more than a decade, the world has been trying to limit global warming to 1.5°C.

That's no longer possible, according to a new United Nations report. We will likely pass 1.5°C in 2030. That's not good news for anyone

Global warming is likely to exceed 1.5°C around 2030, increasing risks of extreme events, sea-level rise, ecosystem loss and potentially irreversible climate tipping points. Rapid emission cuts could limit peak warming and enable a later decline through carbon removal, but current policies remain insufficient.

original article.

How cells teach themselves to move together

Scientists have long wondered how cells organized into sheets begin to move together to form organs, especially when the sheets form closed, sphere-like surfaces and tissues with no edges to direct motion. Researchers used a combination of live imaging, genetic experiments and mathematical modelling to understand how cells in the fruit fly egg chamber synchronize their movement.
In fruit fly egg chambers, epithelial cells initiate collective rotation through feedback between cell motion and protein polarization. Movement polarizes a protein rearward, promoting aligned motion in neighbouring cells via mechanical coupling. Support-tissue forces initiate long-axis rotation, while chamber elongation stabilizes its direction.
Researchers found that cells can spontaneously organize and rotate together through a self-reinforcing mechanism in which a specific protein helps individual cells align their movement.

Once the cells start moving, that motion polarizes the protein to the back of the cell, which promotes further movement by the cells behind it in the same direction. Mechanical connections between adjacent support cells and the global egg chamber geometry mediate the coordination of cell movements.

Epithelial cells that form surfaces in the body undergo collective migrations while tissues are developing, during the closing of wounds, the spread of cancers or the constant turnover of things like your intestinal lining. But when there are closed surfaces, there are no external cues that tell the cells which way to go. So, this is a self-organized process.
The study, published in PNAS, also explains why the egg chamber always rotates around its long axis. Initially, this is caused by the physical forces through which the egg chamber interacts with nearby support tissues. As the egg chamber grows and becomes more oval-shaped, its own geometry helps stabilize the rotation axis.

This work holds potential implications for understanding both normal development and diseases in which collective cell movement goes awry.

Sierra Schwabach et al, Initiation of rotational collective migration in Drosophila through tissue geometry and mechanochemical feedback, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2528342123

Is this the first glimpse of dark matter?
A single data point from a dark-matter detector in the United States could be the first discovery of the elusive particle we call dark matter. The LUX-ZEPLIN experiment at the Sanford Underground Research Facility in South Dakota contains 10 tonnes of liquid xenon. It seeks evidence of a candidate particle called a WIMP (weakly interacting massive particle) by looking for flashes created when such a particle collides with the nucleus of just one xenon atom. If the finding can be backed up with more data, it could mean that the material that seems to make up most of the mass of the Universe has finally been discovered.

https://lz.lbl.gov/wp-content/uploads/sites/6/2026/08/LZ_Preprint_2...

https://www.nature.com/articles/d41586-026-01985-9?utm_source=Live+...

Diabetes drug metformin could be repurposed to help slow aging mechanisms

Over the past few years, a new field of science has been gaining momentum: geroscience. Instead of treating age-related diseases one by one, geroscience asks a bigger question: What if we could target the biological drivers of aging itself? Researchers are uncovering the common mechanisms that fuel aging and multiple chronic diseases, hoping to slow these processes and help people stay healthier for longer.

Metformin, a widely prescribed, safe and inexpensive drug for type 2 diabetes, is a first-line treatment that lowers blood sugar and improves the body's response to insulin. The drug appears to trick cells into sensing an energy shortage, similar to what happens during fasting or dieting. This activates a key cellular energy sensor called AMPK, which helps trigger cellular waste cleanup and supports cellular repair. Now, a recent review suggests metformin might also help counter some effects of aging.

Researchers compiled decades of global research, from cellular and molecular studies to animal and human studies, to provide a comprehensive, unified picture of how metformin might affect aging and longevity. The collective data indicated that metformin acts as a geroprotective agent that can target the biological root causes of aging and potentially improve health span.

Metformin's anti-aging effects are evident across species. Male monkeys treated for 40 months saw their tissues become biologically younger, with their brains alone reversing by nearly 6 years—a leap equivalent to 18 years in human terms. A similar pattern was seen in humans, where observational data indicate that people taking metformin had biological ages up to 3.43 years younger, with people with diabetes taking the drug living as much as 15% longer than their peers without diabetes.
A large body of evidence indicates that people prescribed metformin to manage blood sugar levels also had fewer cardiovascular events and showed lower rates of cognitive decline. Because developing new drugs takes years, researchers shifted their focus toward investigating whether metformin could be repurposed to slow the effects of aging.
Part 1

Instead of treating just one disease, metformin acts on multiple biological root causes of aging at the same time. It can trigger autophagy, the cell's cleanup system, helping clear cellular waste while supporting DNA stability. As we age, the chemical tags on our DNA called methylation begin to shift, affecting how genes are regulated. Metformin slows abnormal changes in DNA by stabilizing an enzyme called TET2, helping preserve a more youthful genetic profile. Its effects also reach the gut and its microbiome, where it can boost beneficial, mucus-protecting bacteria and the production of short-chain fatty acids. This is promising news, as previous studies have found that a healthy gut microbiome can lower age-related inflammation throughout the body.

In microscopic worms called C. elegans, metformin extended lifespan by 36% to 40% by putting the animals into a state similar to calorie restriction. In mice, across different models, metformin increased average lifespan by 5.8% to 20.1% and delayed the onset of certain tumours.

Jarra Manneh et al, Metformin at the convergence of aging and longevity, Aging (2026). DOI: 10.18632/aging.206407

Part 2

Healthy aging shaped by more varied biology than previously thought

Molecular changes in aging are far more unique than previously thought, meaning two healthy individuals of identical age can experience significantly different aging journeys.
A new study is the most comprehensive molecular study of aging to date. It demonstrates for the first time that genetic factors and environmental influences continuously interact across a person's lifespan.

The study, published in Science, observed how multiple genetic variants shape how an individual ages.

Notably, researchers found different courses of change among participants with a gene linked to cardiac aging (CXCL9). They also found that levels of the tumour suppressor gene tumour protein p53 (TP53) declined in certain individuals as they grew older, potentially altering their risk of cancer.

Such biological shifts can indicate distinct environmental exposures or reveal an underlying genetic predisposition to disease. Pinpointing individuals at higher risk offers future opportunities for earlier targeted health care interventions.

Importantly, the research also highlights correlations between environmental exposures, such as shifting blood levels of PFAS, commonly referred to as "forever chemicals," and evolving molecular profiles over time. This highlights how public health measures targeting environmental risks can affect the molecular level.

Molecular aging involves the steady accumulation of cellular damage alongside chemical changes in key molecules like DNA, proteins and lipids. Over time, this progression drives a gradual deterioration of tissue function, heightened physical vulnerability and a higher risk of age-related conditions, including cancer as well as cardiometabolic and neurodegenerative disorders.

Understanding how aging happens at the molecular level is vital to preventing or even reversing a range of age-related diseases—as well as increasing longevity.
Rather than there being a single molecular roadmap of aging, this study shows that people follow distinct biological journeys. Two healthy people of the same age can be aging in surprisingly different ways at the molecular level. That raises the possibility of much more personalized approaches to predicting disease risk and maintaining health as we grow older.
Over eight years, the team repeatedly measured blood RNA levels, the activity levels of around 16,000 genes and hundreds of metabolites in the same 335 individuals from TwinsUK during the study, creating one of the most detailed long-term multi-omic studies of healthy aging to date. They found that some study participants had markedly different, and sometimes opposite, molecular changes.

Aging patterns were not uniform across the immune system, which is key to the aging process—molecular changes over time differed between innate and adaptive immune cells. Innate immune cells are the fast, first line of defense you are born with, while adaptive immunity is a slower immune response that builds memory over time.
These findings suggest that human aging at the molecular level is not a uniform process, but one that is dynamic and environment-dependent.

Longitudinal dynamics of gene expression and metabolomics in an ageing population cohort, Science (2026). DOI: 10.1126/science.aed6452

Brain scans reveal new link between progesterone and women's mood

The influence of the hormone progesterone on mood is well known. Now, researchers have shown how higher levels of progesterone during the menstrual cycle are linked to less distinct patterns of activity in areas of the brain involved in controlling emotions.
The study, published in Psychological Medicine, explored how natural levels of the ovarian hormones estradiol and progesterone influence parts of the brain involved in emotion control and whether this could help explain differences in mood.

Emotion control is the ability to regulate behaviour in response to emotional information, particularly when automatic emotional responses need to be overridden. For example, if someone needed to ask an unfriendly person for help, their instinct might be to avoid them—emotion control would help overcome that impulse and approach them anyway.
Analysis of MRI scan data from study participants revealed that when progesterone levels were higher, there was a less clear distinction between "easy" and "difficult" emotional situations in the brain scans. This suggests that the brain would be less able to distinguish between different emotional situations in real life.

In contrast, participants whose brain scans had a clearer distinction between "easy" and "difficult" emotional situations tended to report better mood in the preceding week.

This brain mechanism accounted for roughly 7% of the variation in mood scores.
The researchers found that higher progesterone levels were linked to brain activity patterns that made it harder to tell different emotion control situations apart, which also corresponded with lower mood in participants.

This suggests that if the brain can tell different emotional situations apart more clearly, it may be better at regulating emotion in daily life.

Endogenous progesterone blurs frontostriatal representations of emotion control in healthy young women, Psychological Medicine (2026). DOI: 10.1017/S0033291726105315

Cancer cells release antioxidants to prevent immune cells from destroying them

Molecules called reactive oxygen species, which include so-called "free radicals," have long been viewed as damaging by-products of our body's metabolism—a reason antioxidant supplements have been considered a potential way to reduce cancer risk.
Now, scientists have discovered that certain immune cells depend on these molecules to activate and destroy cancer cells and that tumours exploit this dependency by releasing natural antioxidants to shut down the immune attack.
Our immune system keeps us healthy by hunting down and destroying harmful material, including invading bacteria and viruses, as well as cancer cells. It does so by deploying a number of different types of immune cells, including specialized cells known as T cells. These T cells hunt down and destroy tumor cells, but they need small amounts of reactive oxygen species to activate and switch on their killing ability.
Researchers analyzed the fluid surrounding cells within tumours grown in mice and found that cancers chemically 'smother' T cells, stopping their activation and preventing them from destroying cancer cells. Tumours do this by releasing large amounts of a protein that is a natural antioxidant, Peroxiredoxin 1 (PRDX1), which mops up reactive oxygen species and deprives T cells of the activating signals they need to kill cancer cells.

Next, the team used CRISPR gene-editing technology to create mouse cancer cells that could no longer make the antioxidant protein. They found that removing the cancer cells' capacity to produce the antioxidant promoted immune-cell activity and limited tumor growth.

Finally, the team looked for the same mechanism in people. They analyzed published data on the proteins released by human cancer cell lines, examined gene activity across thousands of human tumours, and isolated the fluid surrounding tumours removed from patients. All three approaches pointed the same way: Human cancers also release PRDX1 into their surroundings, where it can strip away the reactive oxygen species that T cells depend on.
Now that the researchers found a new way by which cancers shut down the immune system, we can block this process and make tumours that don't respond to some immunotherapies start responding to treatment. That tells us this is a pathway worth targeting therapeutically, and there are several ways we might be able to achieve this.
The findings also carry broader implications. Several large randomized clinical trials have found that antioxidant supplements fail to reduce cancer risk and, in some cases, worsen outcomes.

The discovery that T cells depend on reactive oxygen species to fight tumours may help explain why: Antioxidants could inadvertently blunt the immune system's ability to attack cancer.

Tumor-derived antioxidants suppress immunity by depriving T cells of reactive oxygen species, Science (2026). DOI: 10.1126/science.adz8203

Patients diagnosed with lung cancer found to have more microplastic in their lungs

People with lung cancer are more likely to have microplastics in their lungs and to have larger quantities of microplastics in their lungs, according to research that has been presented at the European Respiratory Society (ERS) Congress in Barcelona, Spain.
Among 100 patients undergoing bronchoscopy, microplastics were detected in 70%, with higher detection frequency and burden in those later diagnosed with lung cancer. Polypropylene and polyethylene predominated. The observational results show an association but cannot determine whether microplastics contribute to cancer or are retained differently by diseased lungs.
Researchers say their study adds to evidence that microplastics are entering our bodies via the air we breathe and suggests that there may be a link between microplastics and lung disease.
Across all samples, the researchers identified a total of 232 microplastic particles. Overall, 70% of patients had detectable microplastics in at least one sample (either the lung wash, tissue or both). When the lung wash and tissue samples from each patient were analyzed together, patients with lung cancer were more likely to have detectable microplastics and had a higher overall microplastic burden than those without cancer.

Patients with lung cancer were also more likely to have detectable microplastics in their lung wash samples (66% versus 46%) and had a higher microplastic burden than patients without lung cancer.

When the researchers compared the lung wash and tissue samples from the same individual, they found that patients with more microplastic in their lung wash tended to have less in the corresponding tissue sample, and vice versa. Because lung wash samples collect particles from the airspaces whereas tissue samples capture particles embedded within the lung itself, this finding suggests that microplastics may not be distributed evenly throughout the lung and that different regions may retain particles differently.

Analysis of the microplastics showed that polypropylene and polyethylene were the most common types of plastic. These are widely used in everyday products such as packaging, textiles, household materials and consumer goods.
This adds to the growing evidence that reducing environmental plastic pollution may have benefits that extend beyond ecosystems and into human health.

‘High respiratory microplastic burden across paired airway and tissue samples in patients with lung cancer’ by Ilias E. Dimeas et al. was presented in session at European Respiratory Society Congress 2026 on Thursday 3rd September.

Scientists studying cockroach milk and nose-blowing win Ig Nobel prizes for quirky science

Ten research teams were honoured this week at a satirical science awards ceremony that was hosted outside the U.S. for the first time due to travel concerns.
Ig Nobel prizes recognized unconventional work on cockroach milk, nose blowing, kissing evolution, and soil decomposition measured using buried underwear. The ceremony moved to Zurich because of travel and visa concerns, with future events planned across Europe.
Researchers who studied milk from cockroaches and analyzed soil health using underwear received Ig Nobel prizes celebrating unusual and imaginative contributions to science.
Another research team buried 1,000 pairs of underwear in more than 25 countries to study how critters in the soil helped them decompose.

Could damaged sperm be causing miscarriages?

Local neural wiring may set the brain's range of activity patterns

The human brain contains billions of neurons, specialized nerve cells that receive, transmit and process information through electrical and chemical signals. Human thoughts, sensory perceptions and behaviors are known to emerge not from the activity of individual neurons but from collective patterns of activity distributed across different neuron populations.

One way to characterize the collective activity of neurons is to measure its dimensionality, or, in other words, the number of independent activity patterns (i.e., degrees of freedom) exhibited by a specific neuronal population. High-dimensional activity can encompass various distinct activity patterns, while low-dimensional activity is restricted to a smaller range of possible patterns.

A new study  published in Nature Neuroscience, suggest that the collective activity of cortical networks is strongly influenced by the structure of neural circuits. As a result, local neural wiring could shape the breadth of activity states available to the brain.

The brain contains an astronomical number of neurons, but it is their collective activity that underlies brain function. The number of degrees of freedom that this activity explores (its dimensionality) is therefore a fundamental signature of neural dynamics. However, it is not known what controls dimensionality in the biological brain.

Researchers analyzed neural activity recordings collected in the mouse visual cortex using Neuropixels. These are tiny probes that can be used to monitor the electrical  activity of hundreds of neurons at once.

"Through analysis of high-density Neuropixels recordings, here, we argue that areas across the mouse cortex predominantly operate in a sensitive regime that gives recurrent synaptic networks a strong role in regulating dimensionality," the authors wrote. "This control is expressed across time, as cortical activity transitions among states with different dimensionalities. Moreover, this control is mediated through highly tractable features of synaptic networks (network motifs)."

The researchers tried to determine how many independent activity patterns were required to describe the collective activity of neurons in the mouse visual cortex. They also tracked this dimensionality over time to shed light on whether cortical activity remained in a single state or shifted between states with different dimensionalities.

The researchers also analyzed a dataset that contained physiological measurements of synaptic connections among more than 32,000 pairs of neurons in mouse and human cortical tissue. This allowed them to investigate whether network motifs predicted to affect dimensionality were prevalent in both species.

"Analyzing a massive synaptic physiology dataset, we find that motifs impacting dimensionality are prevalent in both mouse and human brains," the authors wrote. "Thus, local circuitry scales up systematically to help control the degrees of freedom that brain networks may explore and exploit."

Part 1

The results of the team's analyses suggest that interconnected neural circuits in the mouse cortex play a key role in regulating the dimensionality of neural activity. In other words, these local circuits help control how many different patterns of activity a group of neurons can exhibit at a given time.

The researchers also found that the dimensionality of cortical activity was not fixed. Over time, they observed shifts between states that involved different numbers of distinct activity patterns.

David Dahmen et al, Strong and localized recurrence controls the dimensionality of neural activity across brain areas, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02395-w.

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part 2

Aging blocks the retina's ability to regrow lost neurons, a first-of-its-kind study finds
Aging markedly reduces transcription factor–driven glial-to-neuron reprogramming in the retina. Reduced cellular plasticity and age-associated inflammation, potentially worsened by barrier dysfunction, contribute to this limitation. Anti-inflammatory steroids partially restored regeneration in aged tissue.

Jugasmita Deka et al, Aging limits neuronal regeneration from glia in the mouse retina, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2612369123

CRISPR gene-editing therapy safely and continuously lowers cholesterol and triglycerides, first-in-human trial shows

A first-in-human clinical trial has shown that a one-time infusion of a gene-editing therapy using CRISPR-Cas9 was effective and safe in reducing LDL ("bad") cholesterol and triglycerides in people with medication-resistant lipid disorders through one year of follow-up across all doses.
In a 15-participant phase I trial, one-time CRISPR-Cas9 therapy targeting hepatic ANGPTL3 lowered LDL cholesterol by 52.5% and triglycerides by 47.8% at 12 months at the highest dose. No treatment-related serious adverse events occurred during one-year follow-up; longer-term safety monitoring is planned.

Luke J. Laffin et al, Durability of CRISPR-Cas9 Gene Editing Targeting ANGPTL3 with CTX310, New England Journal of Medicine (2026). DOI: 10.1056/nejmc2609825

Immune therapy engineered inside the body
Sixteen people with autoimmune conditions have had their symptoms relieved by a treatment that produces disease-fighting immune cells inside their bodies. Researchers used a modified virus to deliver the genetic instructions for making chimeric antigen receptors (CARs) on participants’ T cells. These CAR T cells target antibodies produced by other immune cells, which attack the body’s own healthy tissue in autoimmune diseases. The findings are a proof of concept for in vivo CAR-T-cell therapy, says clinician-researcher David Simon, which is cheaper and faster to produce than is lab-made CAR-T.

https://www.nejm.org/doi/10.1056/NEJMc2603114

https://www.nature.com/articles/d41586-026-02765-1?utm_source=Live+...

Lakes aren't just storing water—they're changing the carbon cycle

Lakes may look like picturesque stopping points along a river or stream, but they can have a big influence on what happens to carbon as it moves through a landscape. New research suggests that the more lake-rich a network of streams is, the more carbon is released into the atmosphere rather than carried downstream.

The finding, published in Geophysical Research Letters, comes from researchers who studied 32 connected stream-and-lake networks in northern Sweden, measuring how much carbon was released into the atmosphere and how much continued downstream. They found that networks with 10 times more lake surface area had almost twice the carbon emissions.

The results highlight a part of the carbon cycle that may have been overlooked by scientists. Rather than treating lakes and streams as separate pieces of the landscape, the researchers argue that they need to be considered together as connected networks.
Streams and rivers constantly pick up carbon from the land around them and carry it downstream toward larger rivers and eventually the ocean. However, some is transformed into gases, including carbon dioxide, and escapes from the water into the atmosphere.

How much carbon each route takes depends partly on how long the water stays within the aquatic network. A fast-flowing stream can carry carbon downstream relatively quickly, while a lake can slow the journey considerably, giving chemical and biological processes more time to act on the carbon.

The researchers call the length of time water remains within a stream-and-lake network its "network residence time." In the Swedish networks they studied, this varied enormously, from just 42 minutes to as long as 29 years. Lakes accounted for almost all of this residence time.

To investigate what this means for the carbon cycle, the team repeatedly sampled the networks during four different periods: spring snowmelt, early summer, late-summer low flow and autumn high flow. They measured carbon dioxide emissions across more than 360 sections of streams and from 42 lakes, while also estimating how much dissolved carbon was being transported downstream.

The pattern was striking. Networks with 10 times more aquatic surface area had approximately 35 times longer residence times and 1.8 times higher carbon emissions relative to downstream carbon export.

One likely explanation is that keeping carbon in the water longer gives microbes more opportunity to break down dissolved organic carbon. This process can ultimately produce carbon dioxide, which can then escape from the water into the atmosphere.

The researchers caution, however, that they did not directly measure all of the processes responsible for the pattern.
Part 1

The balance between carbon emissions and downstream export also changed substantially with the seasons. Carbon emissions relative to downstream export were lowest in spring and autumn and highest during summer.

This was particularly important because the summer measurements coincided with warmer, relatively dry conditions and lower stream flow. When less water is moving through a network, carbon can spend longer in the system, while warmer temperatures can also speed up processes that transform dissolved organic carbon.

The team found that the effect of lake-rich networks remained across the different environmental conditions they measured, including an unusually dry summer. Together, this suggests that both the amount of water in a network and how that water is distributed between lakes and streams can influence what happens to carbon.
The findings do not mean that lakes are simply replacing streams as the main source of carbon emissions. In fact, the study found that streams produced more carbon emissions overall. But in lake-rich networks, a greater proportion of the carbon was released into the atmosphere rather than exported downstream.

F. Alriksson et al, Lakes Amplify Carbon Emissions Relative to Downstream Export in Aquatic Networks, Geophysical Research Letters (2026). DOI: 10.1029/2025gl120340.

Part 2

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Can dogs sniff cancer? AI joins the hunt

When rescue dog Chloe is not tumbling across the grass on a farm outside India's tech capital, Bengaluru, she is learning to sniff human breath for cancer with a little help from AI.
Fitted with a 3D-printed helmet and harness packed with sensors, Chloe is part of experimental efforts to use dogs' extraordinary sense of smell to develop a noninvasive test for the disease.

A growing body of global research suggests dogs can be trained to detect cancer and other human illnesses, from Parkinson's to COVID-19.

The Bengaluru-based startup Dognosis is using AI to analyze dogs' brain activity, respiration and body language—turning their reaction to scent into data.

In an hour, they can do thousands of sniffs. Each sniff can evaluate a sample.
Dognosis hopes to launch commercially next year, which it says would make it the third company of its kind, after firms from Germany and Israel.

Early detection can make a crucial difference to cancer survival rates, but in India many patients are diagnosed only after the disease has advanced.

Dog sniffs could provide an easy and affordable first layer of screening to be deployed at scale, finding potential cases for further testing.

As it chases commercial approval, Dognosis—backed by venture-capital firms including Accel India—is collaborating with government medical institutions for its research.

Chloe, a Labrador mix, is one of 15 dogs being coached by the startup, clad in customized data-gathering helmets.

Research suggests diseases can alter the chemicals released by the body, creating distinctive odors.

Dogs have around 300 million scent receptors, compared to about five million in humans.

The testing method is simple: A patient breathes into a cotton mask for about 10 minutes, and the mask is then sealed in a bag and taken to the lab. Patients do not meet the dogs.

A recent Dognosis study of more than 1,500 participants, involving six hospitals in Karnataka state, was published in the Journal of Clinical Oncology.

The company said it achieved an accuracy rate of more than 90% across seven major types of cancer and now plans to test in real-world programs.

https://ascopubs.org/doi/10.1200/JCO-25-02310

The heart, lungs and brain work together to shape experience

People speak of "butterflies in the stomach," a "racing heart," being "choked up" or needing to "catch breath." Language routinely treats emotion and thought as though they inhabit the body. But why are events of the mind felt in the heart or stomach?
In a new paper published in Neuroscience of Consciousness, a UCSB-led team gets to the heart of an enduring question: Are you your brain or your body? Their answer points to what happens between them.

The brain is not simply receiving messages from the body. The heartbeat, breath and gastric rhythm are regular, predictable signals around which groups of neurons can organize, determining when they become more or less receptive to information. They are the drumbeats that keep our proverbial orchestra together.

Neuroscience has often treated consciousness as something produced by the brain alone. An emerging body of research expands that view, suggesting that conscious experience is shaped through a continuous, rhythmic dialogue between the brain and body.

The heart beats, the lungs breathe and the brain produces waves. Rhythm permeates the body. Just as musicians coordinate while playing different parts, brain rhythms can become organized by slower bodily cycles.

This coordination may help align neural processes involved in perception, emotion and the sense of self with the body's ongoing regulation of its internal state.

Consider the breath. People tend to inhale just before beginning the next trial of a cognitive task and exhale as they prepare to respond. Memory can also fluctuate with the breath: People are better at recognizing previously seen pictures when those pictures reappear during an inhale rather than an exhale.

Frightening images can gain faster access to awareness while the heart is contracting, whereas neutral stimuli—including sights, sounds, touch and even pain—may be processed less strongly during that same phase.

What matters, then, may not be any one signal alone, but the relationship between them. Two people could have similar heart rates, for example, while differing substantially in how strongly cardiac signals influence brain activity. Measuring this relationship may reveal differences that neither signal shows on its own.

The researchers note that the value of this coordination does not follow a simple "more is better" rule. Both unusually weak and unusually strong bodily influences on brain activity have been associated with adverse states. Healthy functioning may instead depend on the brain and body remaining coordinated within a Goldilocks zone—connected enough for bodily signals to inform experience, but not so strongly that they dominate it.

There is a popular intuition that mental illness is not solely mental, just as bodily dysfunction is not confined to the body.

Anxiety-related conditions can involve bodily signals becoming unusually salient and difficult to ignore. Depression may show a different pattern, including reduced sensitivity to some bodily signals and a diminished sense of connection to the body.

Other disorders may involve atypical timing, strength or flexibility in the exchange between brain and body. Across these conditions, the issue may lie not in the brain or body alone, but in how the two coordinate.
Part 1

The framework points toward an expanded view of consciousness. Many cognitive processes that characterize conscious experience—including perception, emotion, bodily awareness and the sense of self—are shaped in part by signals from within the body.

The findings also complicate the familiar image of a brain in a vat. This science-fiction brain, kept alive but severed from its body, might still generate neural activity. Yet it would be cut off from the recurring bodily signals that help give experience its visceral character and anchor it to a living self.

So, are you your brain or your body? Researchers of this new study suggest the question may be a false choice: Conscious experience emerges through the ongoing relationship between the two.

Asa Young et al, I sync, therefore I am: brain–body synchrony in typical and disordered consciousness, Neuroscience of Consciousness (2026). DOI: 10.1093/nc/niag028

Part 2

Atherosclerosis may meet key criteria for autoimmune disease, evidence suggests

In autoimmune diseases, the immune system turns against the body through pathogenic high-affinity B cells or T cells, leading to severe organ damage. Multiple sclerosis (nervous system paralysis), type 1 diabetes (a strong risk factor for atherosclerosis requiring lifelong treatment) and rheumatoid arthritis (debilitating, excruciating joint deformities) are examples of clinically important autoimmune diseases.
Despite decades of international research efforts, no such defining criteria have been documented for atherosclerosis. Research by an international consortium now reports in Nature Cardiovascular Research that, according to its findings, atherosclerosis satisfies crucial defining criteria of an autoimmune disease.

The current research identifies high-affinity autoreactive antibodies that, following adoptive transfer into mice, accelerate atherosclerosis. One of the autoantibodies is directed against histone 2B.

Following vaccination of the mice with histone 2B, atherosclerosis severity increased. The experimental data in mice were substantiated in a clinical trial involving 495 patients from the general population who were recruited in Guangzhou.
This new data are likely to have transformative power because they characterize atherosclerosis as an autoimmune disease. They have fundamental and far-reaching implications for future research, as they allow the development of new types of diagnostics and immunotherapeutics before the development of myocardial infarcts and strokes.

Chuankai Zhang et al, Artery tertiary lymphoid organs encode a pathogenic high-affinity autoantibody−autoantigen pair in atherosclerosis, Nature Cardiovascular Research (2026). DOI: 10.1038/s44161-026-00864-w

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Soft back belts ease everyday low back pain, 12-week trial suggests
For many in the workforce, spending hours at a computer is an unavoidable part of daily life. Sitting for prolonged periods in the same position can contribute to low back pain (LBP), which affects up to 80% of people over their lifetime and remains a leading cause of disability worldwide. A group of French researchers decided to find out whether wearing a soft, flexible lower-back support belt can help people with common, unexplained lower back pain feel better and move more easily.
The study, across 17 medical centers in France, followed 168 adults ages 18–75 with unexplained low back pain lasting 1–6 months. Adding a soft lower-back belt to standard care made a difference in their recovery.

On a standard disability scale, patients who wore the belt improved by 10 points, compared with 5.3 points for those who received usual care alone. Some 60.5% of patients in the belt group reached a level of improvement considered clinically meaningful, compared with 40.5% in the usual-care group.

Laurent Grange et al, Lumbar Belt for Nonspecific Low Back Pain, JAMA Network Open (2026). DOI: 10.1001/jamanetworkopen.2026.29793

How dense breast tissue may lead to cancer
Stiff, fibrotic breast tissue activates STAT3 signaling, recruiting macrophages. In stiff environments, macrophages generate reactive oxygen species that form diffusible aldehydes, causing DNA damage in nearby breast cells. Higher stiffness, macrophage abundance, aldehydes, and DNA damage were associated with more advanced disease.

Mary-Kate Hayward et al, Tissue tension fosters macrophage-driven lipid peroxidation-induced DNA damage, Cancer Cell (2026). DOI: 10.1016/j.ccell.2026.03.022

Eating a handful of nuts each day is linked with lower risk of high blood pressure, research shows
A meta-analysis of 143,000 participants linked daily consumption of 30–35 g of nuts with a 26% lower hypertension risk versus no nut intake. Evidence is observational and cannot establish causality; benefits may reflect broader plant-rich diets and healthier lifestyles. Unsalted nuts may be preferable because sodium raises blood pressure.

What students gain and lose as AI chatbots take over parts of university teaching
AI tools can provide timely, accessible feedback, tutoring, practice, and language support while enabling institutions to set boundaries on student AI use. Risks include inaccuracies, biased simplification, environmental costs, and limited governance. Replacing educators may also reduce reciprocal recognition, adaptive teaching, and students’ sense that their intellectual development is seriously judged.

Thomas Corbin et al, Hybrid reading practices: how GenAI summarisers can support rather than replace reading, Studies in Higher Education (2026). DOI: 10.1080/03075079.2026.2708138

Almost half of farmers are being poisoned
There are more than 400 million cases of unintentional, acute pesticide poisoning every year, finds a new estimate — meaning that an estimated 46% of farmers worldwide are being poisoned. The analysis suggests there are 11,000 pesticide-related deaths annually, with nearly 60% of these in India. And that’s not taking into account long-term health impacts that are not immediately felt, such as a possible link with Parkinson’s disease.

https://www.frontiersin.org/journals/public-health/articles/10.3389...

Bunsen burners make poor air-cleansers

Bunsen burners’ reputation for sterilizing workplaces flames out

Bunsen burners, long used to cleanse airspaces and surfaces in labs of bacteria-laden particles, aren’t actually very effective at doing so, and might even make contamination worse. Researchers seeded the air above lab benches with the bacterium Gordonia rubripertincta and opened two Petri dishes — one near a lit Bunsen burner and one near an unlit one. They found that in several trials of differently sized burners, bacterial levels in dishes beside lit burners were as high as or higher than the other ones.

https://journals.asm.org/doi/10.1128/spectrum.01028-26

https://www.nature.com/articles/d41586-026-02758-0?utm_source=Live+...

Xanthelasma and its association with developing major cardio-cerebrovascular events

A Warning Sign of Heart Attack And Stroke May Show Up on Your Face

Atherosclerosis, the accumulation of fatty plaques in the arteries that causes restricted blood flow, is responsible for most heart attacks and strokes – but it often builds up slowly and silently, without symptoms, before causing a major medical emergency.

That's why researchers are looking for warning signs of atherosclerosis that might help doctors spot it earlier.

A new study, published in Atherosclerosis, looks at a condition called xanthelasma, where yellow patches appear around the eyes.

Those patches puff up when immune cells called macrophages get stuffed with cholesterol and other fats. The condition is often (but not always) associated with higher cholesterol in the blood, too.

As fatty clumps also play a role in atherosclerosis, researchers thought there might be a link.
A few studies have supported the association between xanthelasma and an increased risk of cardiovascular events, while others debate that it may not be an independent risk factor once traditional risk factors are accounted for.
The study analyzed health data from 17,925 people diagnosed with xanthelasma and the same number of matched controls – people with presbyopia, a condition that leads to farsightedness, chosen because it would have involved an eye examination, ensuring the controls didn't have xanthelasma.
Across the first year of data, 1 percent of those with xanthelasma (178 patients) suffered a heart attack compared to 0.35 percent (or 63) of the controls.

For strokes, the respective figures were 0.95 percent and 0.3 percent, and for transient ischemic attack (TIA) or a 'mini-stroke', it was 0.6 percent and 0.19 percent.
Those are all low percentages, but the risk was several times larger for the xanthelasma group.

The gap between the two groups narrowed slightly over time, but at the 5- and 10-year time points, the risk was still substantially higher for those with xanthelasma.

Xanthelasma is associated with higher short- and long-term incidence of MACCEs up to 10 years, highlighting its value as a clinical marker for cardiocerebrovascular risk stratification and preventive management," write the researchers.

Incidence rates of these cardiac events were similar in the xanthelasma group whether or not they had abnormally high levels of fat in their blood – suggesting this isn't the only underlying factor at play.

While the pale, puffy patches that characterize xanthelasma are seen as harmless in themselves, the findings are more evidence that they could signify something else, and perhaps future cardiovascular problems.
This new study study suggests that xanthelasma can be considered as a risk factor for future MACCEs.
Xanthelasma patches are easy for doctors to spot, and for these people at least, may be a useful warning sign so that lifestyle changes or medications could be put in place early – before MACCEs are triggered.

https://www.atherosclerosis-journal.com/article/S0021-9150(26)00013-4/fulltext

A Mold Living in Your Gut May Help Protect Against Radiation Damage

Mold isn't typically something you want growing inside your body.

But in the case of Mucor racemosus, there may be compelling reasons to make an exception.

That's because this symbiotic fungus that lives inside the human gut appears capable of protecting us from radiation, according to a new study in PNAS.

It might sound a bit hard to believe, but this isn't the first time we've seen fungi doing weird things with radiation.

We know that there are different kinds of radiation-resistant fungi, including species that survive being blasted with up to 200 times the fatal human dose of X-rays.

There's also the funky world of radiotrophic fungi, which use radiation as an energy source – like the bizarre fungus living its best life in the radioactive remains of the Chernobyl Nuclear Power Plant.

M. racemosus has a different kind of parlor trick for radiation, but it's no less impressive.
In their research, a team of scientists found the fungus can confer protection from radiation to its host through a couple of different mechanisms, suggesting M. racemosus may be a beneficial presence in the gut.

In experiments with mice exposed to radiation, the researchers found that animals administered M. racemosus experienced less weight loss, inflammation, and oxidative stress than control mice that weren't given a fungal dose, suggesting M. racemosus provided the treated animals with a radioprotective effect.

This radioprotective effect was boosted when the researchers preadapted the fungus to the oxygen-poor conditions of the gut.

https://www.pnas.org/doi/10.1073/pnas.2608386123

We saw the results, we looked at ourselves, we said, 'this can't be correct'!

Arctic Rivers Are Breaking The Rules of Erosion

And scientists formed a new theory around Arctic erosion

Arctic landscapes are eroding much faster than previously thought, according to new SFU research. Fueled by climate change and extreme weather events, Arctic erosion is leading to the creation of new river systems as ice in frozen riverbeds melts. Earth scientists previously believed that the ice acted as a sort of glue, holding the landscape together and slowing down erosion. But surprising new findings suggest thawing ice in the ground can actually increase erosion rates up to 10 times compared to unfrozen rivers. SFU researchers explain how they carried out their research and what impact it could have.

https://www.nature.com/articles/s43247-026-03468-1

Newly mapped brain circuit offers clues to how slow nasal breathing eases anxiety

A slow breath in and out does the trick for many people when calming their nerves and dealing with anxiety, a disorder that affects millions of people worldwide. Pranayama, Taoism and meditation have long used slow nasal breathing to ease a negative mood. How this simple act works its magic, however, has been tickling the gray cells of scientists curious to unravel the biological pathways behind it. Now, scientists may have found a clue.

A recent study published in the Proceedings of the National Academy of Sciences discovered a nose-to-brain circuit that may help explain how the rhythm of nasal breathing can influence anxiety.

Researchers mapped a specific neural highway running directly from the nose into the brain's emotional network. This circuit begins with olfactory sensory neurons in the nasal cavity and continues to mitral cells in the olfactory bulb, the brain's smell-processing center. It then connects to a specific type of neuron, parvalbumin-positive interneurons (PV⁺), in a nearby brain region called the perirhinal cortex, which in turn links to the amygdala, the brain's fear and anxiety hub.

The frequency of nasal stimulation appeared to steer anxiety in different directions. Slow, low-frequency stimulation eased anxiety and boosted high-gamma brain waves in the perirhinal cortex, while faster stimulation had the opposite effect, increasing anxiety.
Breathing happens largely on autopilot, with the brainstem setting its rhythm. The breath, however, also sends information back to the brain. The same nasal neurons that detect odours can sense the movement of air, and the rhythm of that airflow can synchronize activity in brain regions involved in emotion. Humans have used slow breathing for ages to influence emotional states, even without conscious control.
Despite its widespread use, researchers didn't know whether simply changing the pace of this nasal sensory signal could directly shift anxiety, nor had they pinpointed the exact brain pathway connecting nasal airflow to emotional states. In this study, researchers identified that missing link, exposing the brain pathway that could explain why slow, deliberate breathing feels so calming.
Part 1

The researchers mapped a specific four-step neural highway originating at olfactory sensory neurons in the nose and ending at glutamatergic neurons in the amygdala that translate physical air movement in the nose into emotional states.
They found that the speed of sensory signals from nasal airflow can directly push anxiety in opposite directions. Slow airflow at 2 Hz acted as a calming signal, reducing anxiety-like behavior in the mice, while fast airflow at 7 Hz had the opposite effect, increasing anxiety-like behavior. Airflow at 4 Hz, meanwhile, produced no significant change in anxiety.

Slow nasal stimulation activates PV⁺ interneurons in the perirhinal cortex, which in turn inhibit anxiety-promoting glutamatergic neurons in the basolateral amygdala. When the researchers silenced the connection between the olfactory bulb and the perirhinal cortex, this breathing-dependent control of anxiety disappeared completely.
Mice that received two hours of slow 2 Hz nasal airflow daily for two weeks showed restored normal high-gamma brain wave activity and reduced anxiety-like behaviors. These calming effects held strong for at least a week after the treatment stopped.

Together, these findings offer a more detailed view of how the nose and brain communicate, a pathway explaining how slow breathing calms anxiety. With anxiety disorders affecting more people worldwide than any other mental disorder, understanding this connection could open the door to effective, noninvasive ways of dealing with the issue.

Xinsong Guo et al, A nose-to-brain circuit underlies anxiety regulation by nasal afferent frequency in mice, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2603853123

**

Part 2

The 'costly son' hypothesis: Why bigger sons may make births riskier across species

A new comparative review, published in The Anatomical Record, examines factors that may lead to birth complications among humans and other mammals. The study suggests that faetal sex may play an important role in risky births in humans and several other species.
It's often thought that human childbirth is unusually difficult among mammals. The idea is that an evolutionary "obstetrical dilemma" arose because of our bipedal pelvic anatomy and increasing brain size over time. Larger babies passing through a narrow birth canal can increase the chance of obstructed labour, affecting mortality for both the baby and mother. Yet difficult births, including cases in which a faetus is too large for the birth canal, occur across many placental mammals.

Some research has suggested that the obstetrical dilemma was solved by relatively earlier births, but other studies found no evidence that humans have shorter gestations than other apes, even after controlling for body size. Furthermore, researchers involved in the new study say there is a maximum fetus size compatible with safe delivery, and when it is exceeded, obstructed birth results. In other words, birth size and weight are known to be associated with difficult delivery.

The new study suggests, however, that because male babies also tend to be larger, male births tend to be riskier. The team says this pattern is not restricted to humans.

"Most taxa, including humans, displayed a bias toward larger male fetuses. Fetal sex has nonetheless not been incorporated in evolutionary perspectives of childbirth, perhaps because it is often assumed that the sex of each baby is determined at random, since most mothers are likely to produce both sons and daughters," the study authors write.

"Every mother has the potential to gestate both offspring through the reproductive career. Hence, it might be assumed that selection has acted on offspring size in general to resolve the obstetrical dilemma. As we show, however, the risks of birth complications are not equal for sons and daughters."

Researchers compiled sex-specific birth-weight data for 140 placental mammal species across 11 mammal orders and compared sex differences among newborns with adult body-size differences and developmental style. They then searched for reports of difficult birth by offspring sex.

This analysis led the authors to propose the "costly son" hypothesis, which states that larger male offspring may raise birth risks for both mothers and babies. They found that male newborns were more often larger than female newborns across many species. In humans, boys are, on average, heavier by around 3% to 4%, have bodies that are around 1% to 1.7% longer and have bigger heads at birth.

In particular, larger male newborns were common in species in which adult males are larger than adult females. Species with male-biased adult size differences were about six times more likely to have larger male newborns than species in which adult females are larger.

The team says evidence from humans, livestock and some other mammals suggests male fetuses are more prone to difficult births (referred to as dystocia), especially when newborns are relatively large compared with the mother. They note that data on birth complications by offspring sex are scarce outside humans and domesticated animals, leading to a focus on humans and domesticated animals rather than wild animals.

"Where sufficient evidence exists—principally in precocial domesticated species and some other ungulates—larger male fetuses are associated with an elevated risk of dystocia. In several primate species where dystocia is reported, male neonates have larger average anatomical dimensions than females," the researchers write.

Part 1

"Therefore, we expect greater risk of obstructed labor, likely cephalopelvic disproportion, with male offspring in several taxa, but it has not yet directly been shown. We cautiously interpret this as support for the 'costly son' hypothesis: male offspring disproportionately contribute to fetopelvic disproportion and obstructed labor owing to their larger average size at birth."

The researchers also point out that the results identify a small average shift in risk for male births, not a prediction for any individual pregnancy. Because this is a comparative review and analysis, it doesn't prove that fetal sex directly causes difficult birth, but it does provide a testable prediction.
Evolutionarily speaking, larger sons often have more offspring because of male-male competition, and thus more grandchildren for the mother, ultimately meaning reproductive "success." The Trivers–Willard hypothesis used this argument to explain why mothers might be more likely to produce sons or daughters, depending on their physical condition. The mother expends more energy on large male babies, and on male babies in general. This increases birth risk but also increases the chance of reproductive success later on.

The study authors explain, "In humans, male fetal sex imposes a double burden on mothers, combining increased obstetric risk with elevated metabolic investment. Mothers of sons expend more energy during pregnancy and lactation, and this higher energetic investment contributes to enhanced fetal growth and larger birth size. In turn, this increased size elevates the risk of obstructed labor and adverse birth outcomes."

The new study does not find that mothers are more or less likely to produce sons or daughters, but the researchers do say that younger mothers seem to produce smaller newborns to partition energetic resources, regardless of sex. They also say it remains unknown whether females can adaptively adjust offspring sex to mitigate obstetric risk. Future work could systematically test whether younger or first-time mothers adjust offspring sex ratios or mainly produce smaller babies.

Nicole D. S. Grunstra et al, The "costly son" hypothesis: Sons exacerbate obstetrical dilemmas in humans and other mammals, The Anatomical Record (2026). DOI: 10.1002/ar.70331

Part 2

Could quantum protocols make electronic voting more secure?
Photon-based GHZ entanglement enabled proof-of-principle quantum voting protocols that anonymously encode votes and permit public result verification without a trusted central authority. Demonstrations involved up to 16 candidates and small voter groups. Scalability, efficiency, remote deployment, and resilience to real-world threats remain unresolved.

Nicolas Laurent-Puig et al, Experimental Quantum Electronic Voting, Physical Review Letters (2026). DOI: 10.1103/scjl-5ygh

F. Joseph Marcellino et al, Experimental Quantum Voting Using Photonic Greenberger-Horne-Zeilinger States, Physical Review Letters (2026). DOI: 10.1103/jlvb-t2xl. On arXiv: arxiv.org/abs/2512.03659

Does thin air slow the mind? New research on skiers' mental reactions

In mogul skiing, a fraction of a second can make all the difference. A momentary lapse in attention, a misjudged turn or a delayed decision can turn a smooth sequence into a mistake or even a disaster.

This is of particular concern to the coaches at Ski Acro Québec, the provincial governing body for freestyle skiing. During high-altitude training camps in Tignes in the French Alps, they noticed a marked increase in fatigue among their athletes, ages 16–21.

To understand why, they turned to Giorgio Varesco, a postdoctoral researcher at Université de Montréal's Centre for Advanced Research in Sleep Medicine, working under Guido Simonelli, a professor in the Department of Medicine.

Together with François Bieuzen and Nicolas Bourrel of the Institut national du sport du Québec, Varesco launched a study in 2025 to explore the interplay between sleep, fatigue and athletic performance. A key aim was to develop simple, field-ready methods for measuring cognitive fatigue—right on the mountain.

At 3,500 m, where oxygen saturation fell to 88%, young elite skiers showed slower reactions (363 to 375 ms) and increased errors (one to three) on brief mobile cognitive tests of attention and inhibitory control. Altitude-related cognitive fatigue may reflect hypoxia, sleep disruption, travel stress and training load.
In a controlled laboratory environment, assessing cognitive function is relatively straightforward. Researchers have access to a wide array of instruments and ample time to run tests.

On a European glacier, however, conditions are far from ideal. Equipment must be flown in and operated under often-challenging conditions. Tools need to be compact, rugged, user-friendly and, above all, fast. Athletes aren't keen to spend an hour a day on a battery of cognitive tests when they're there to train.

In a recent study published in the journal PLOS One, Varesco and his team used tablet- and smartphone-based tests that deliver reliable measurements of cognitive performance and fatigue-related decline while keeping time demands to a minimum.

They focused on two cognitive functions essential to elite performance: inhibitory control (the ability to override automatic impulses and distractions) and sustained attention.

Early results are encouraging, even with very short test durations. The tests were able to show that, in young elite athletes, cognitive performance declines at an altitude of 3,500 meters (11,500 feet), where blood oxygen saturation drops to 88%. Exposure to this altitude increased reaction times from 363 to 375 milliseconds and more than doubled error rates, from one to three mistakes.
Part 1

Ultimately, the results of this study could pave the way for incorporating cognitive assessments into routine athlete monitoring. Coaches could then better detect early signs of overtraining or altitude-related strain, which can increase the risk of technical errors and injury.

"The brain is also a key factor in athletic performance," said Varesco. "Even in sports that seem primarily physical, athletes must constantly make decisions: adjusting pace, reading the environment, reacting to the unexpected or following their coach's instructions. In mogul skiing, where movements follow one another at high speed, a split-second lapse in attention can have serious consequences."

A reliable, rapid cognitive test could allow coaches to gauge an athlete's cognitive readiness before or even during a training session, helping them decide when to dial back the intensity or steer clear of high-risk situations.
In Tignes, athletes sleep at 2,000 meters (6,600 feet) and train at elevations up to 3,400 meters (11,200 feet). While these are not considered extreme altitudes, they are enough to trigger a series of physiological adaptations.

The rarefied atmosphere is the obvious culprit, but according to Varesco, the story is more complicated than that. The body is reacting to more than just reduced oxygen supply to the brain.

Upon arrival at high altitude, the body activates a host of adaptive mechanisms, particularly in the cardiovascular and respiratory systems. Changes also occur in brain function and neurotransmitter regulation. All of these adjustments can affect sleep, performance and cognitive function.

"During some phases of sleep, breathing can become less regular and blood oxygen levels can fluctuate more," said Varesco. "We've observed that these fluctuations are more pronounced at the beginning of stays at high altitude, before the body gradually acclimatizes."

Poor sleep quality, in turn, affects the next day's performance. Fatigue at altitude is rarely due to a single factor. Altitude, travel, jet lag, stress and the accumulation of training sessions can all contribute.

Giorgio Varesco et al, Assessment of cognitive performance and fatigability in elite athletes: Short and portable protocols for field monitoring under hypoxia, PLOS One (2026). DOI: 10.1371/journal.pone.0353673

Part 2

Anemia in pregnancy linked to differences in babies' brain development

Maternal anemia during pregnancy was associated with ~4% smaller infant total brain volume and reduced putamen, caudate, and corpus callosum volumes by 12 months. Corpus callosum differences increased to 6% by 24 months, including among predominantly mild anemia exposures. Portable low-field MRI detected these differences comparably to conventional MRI.

The observed differences in regional brain volumes were still evident despite most of the mothers in this cohort having only mild anemia. The researchers say these findings identify antenatal maternal anemia as a strong risk factor for altered child brain structure and highlight the importance of preventing and treating anemia before and during pregnancy.

Jessica E Ringshaw et al, Antenatal maternal anaemia and infant brain structure: high-field (3 T) and ultra-low-field (64 mT) MRI findings from South Africa, Brain Communications (2026). DOI: 10.1093/braincomms/fcag318

Engineered antibodies offer broad protection against deadly cobra toxins

Each snake species produces a distinct cocktail of toxins that attack nerves, blood or tissues, making it difficult to develop a unified treatment. Current animal-derived antivenoms also have drawbacks, such as batch-to-batch variability, side effects and limited species coverage. Their production is costly and outdated, relying on venom milking and animal immunization, with low yields of active antibodies.

A research team has developed a recombinant, nanobody-based antivenom that offers broad protection against venom from geographically diverse cobra and king cobra species in India. The study is published in Science Translational Medicine
A five-nanobody recombinant cocktail neutralized neurotoxic venoms from diverse Indian cobra and king cobra species in mice. It prevented toxin–receptor binding and protected animals, including when administered 30 minutes after envenomation. Recombinant production could reduce reliance on animal-derived antivenoms and enable region-specific formulations.
Antibodies are usually Y-shaped, with both heavy- and light-chain proteins. The researchers used a portion at the tip of the Y shape, which is made up of heavy-chain proteins that can specifically bind to venom toxins.
They isolated a cocktail of five such antibody fragments, called nanobodies, that could bind to toxins in the various cobra species they tested. They found that this cocktail could neutralize venom activity and prevent the venom from binding to its target receptor.

The team then tested the antibody cocktail in mice injected with venom and found that it protected the animals against toxins from spectacled cobras, monocled cobras and both Indian king cobra species. It was also able to save mice from death even 30 minutes after venom injection.

Unlike conventional antivenoms, these recombinant antibodies can be manufactured using microbial and humanized expression systems without repeatedly immunizing animals such as horses. Additional antibody components can be added to expand protection to other medically important snakes, allowing future recombinant antivenoms to be tailored for different regions or species.
This work provides a blueprint for how recombinant antivenoms can be tailored to different regions of the world by targeting the toxin families that drive disease in local snake species.

Arpan Samanta et al, Oligoclonal nanobody-based recombinant antivenom protects mice challenged with venom from cobras and king cobras from India, Science Translational Medicine (2026). DOI: 10.1126/scitranslmed.aed4290

Mimicry: A fake spider at the tip of this snake's tail helps it lure birds

Lots of animals use mimicry to survive. Some copy the appearance of threatening predators, and others have evolved to resemble plants or rocks so they can blend into the background and avoid being attacked. But a viper from Iran has found an even stranger strategy. The tip of this snake's tail looks like a spider, complete with a bulbous body and long dangling legs. And when a bird swoops in to try to eat this "spider," the snake springs into action and eats the bird.

A spider-tailed horned viper. Credit: Omid Mozaffari.

The elusive spider-tailed horned viper is a relatively recently discovered species, and until now, scientists only knew what the outside of this snake's unusual tail looked like. But in a new study published in the journal The Anatomical Record, researchers used XCT scanners to get a glimpse of the inner workings of this snake's spidery tail—and found that its tail bones are bizarrely normal.

Scientists first collected a specimen of this snake in 1968, and when they brought it back to the Field Museum, people thought that it had some sort of deformity at the tip of its tail, like a tumour. It sat on the shelves of the museum for decades, but it wasn't until another specimen with a similar tail was found in 2003 that people revisited it.

In 2006, scientists described the snake as a new species, Pseudocerastes urarachnoides, the spider-tailed horned viper. When the researchers described the species, they used the specimen in the Field Museum's collections as the holotype, the specimen that serves as a standard-bearer for the physical characteristics of the species.

Soon after, researchers captured a video of the snake using the spider-like appendage at the tip of its tail to lure in birds and eat them.

Vertebral morphology and intracolumnar variation of the iconic and bizarre viperid snake Pseudocerastes urarachnoides (Serpentes, Viperidae), The Anatomical Record (2026). DOI: 10.1002/ar.70308

The brain keeps its options straight at decision time

A new study by neuroscientists shows how the brain encodes information throughout the decision-making process to keep options clearly in mind and ensure that chosen and unchosen options are remembered.
The key, the researchers show in the journal iScience, is that the brain convenes ensembles to produce coordinated patterns of electrical activity that distinctly represent and sort options, both during consideration and after a choice.

It keeps different neural ensembles, different thoughts, distinct from one another, preventing interference between them.

The brain doesn't just hold information statically. Throughout the decision process, the brain flexibly reorganizes information representation to meet the changing task demands.
The researchers found that the neurons acted in functional ensembles whose collective activity clearly indicated decision-related information, including the distinct target directions and their assigned values.
The researchers' key finding was that before the values were assigned and a decision was made, the neural ensemble patterns consistently represented options based on their order of presentation. For example, on the graphs, each "target 1" plane was nicely parallel with the others. Similarly, each "target 2" plane was parallel with its brethren, but the target 2s were more orthogonal, or more perpendicular, to the target 1s, showing that they were represented as entirely distinct from one another.

Then, after the decision, new ensembles provided new representations. Now the "chosen" options, whether they had been presented first or second, had parallel representations. The unchosen targets were also represented as parallel with one another, but as orthogonal to the chosen ones.

In other words, before the decision, the brain convened ensembles of neurons to distinguish targets by their presentation order and then, after the decision, gathered ensembles to sort them by whether they were chosen. This consistent way of representing chosen options, Li and Miller wrote, could aid decision-making by essentially packaging it for downstream circuits responsible for converting the decision into action (in this case, directing the animal's gaze in the chosen target direction).

"The observed alignment of chosen target representations could allow downstream areas to read out the location of the chosen target with a single decoder, regardless of its initial presentation order," the authors wrote, in their research paper based on this study.
Notably, the researchers also found that from round to round of the game, individual neurons could often be recruited into different ensembles. A neuron that in one round seemed "selective" for option 2 could end up being selective for option 1 in the next. The ensembles were therefore not permanent circuits of specialized neurons, but instead were assembled ad hoc among multifunctional neurons.

In another study, they have found that the brain uses brain waves to rapidly and flexibly accomplish this goal of ensemble recruitment.
Another clear implication of the data is that the brain maintained distinct memories of each option, whether it was chosen or not. This could be important for assigning credit down the line to facilitate learning. For instance, remembering that choosing target 2 in round 3 earned a reward.

"Our results illustrate the dynamic subspace reorganization supporting option maintenance and selection in economic decisions," the authors wrote.

Huidi Li et al, Neural subspace reorganization reflects value-based decision-making, iScience (2026). DOI: 10.1016/j.isci.2026.117492

Shrinking Planet
Even planets develop wrinkles as they age. As the planet Mercury shrinks, more “wrinkles” (in the form of hills and ridges) emerge, and scientists are trying to measure them. A new study focused on the planet’s surface roughness, such as craters and debris, and found that particularly rough areas have made the wrinkles harder to see. The analysis revealed that the planet has shrunk up to 14.5 miles in its history, 30 percent more than scientists previously thought.
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Drinking very hot tea and coffee is linked to a greater risk of esophageal cancer

A study of almost 1 million tea and coffee drinkers has linked very hot drinks to a threefold greater risk of developing one type of esophageal cancer.
This isn't the first time hot beverages have been linked to cancer. Earlier studies in Asia, Africa, South America and the Middle East found an association, but there has been far less evidence from Western populations. However, this research showed that temperatures typical of U.K. drinking habits were also linked to an increased risk.
But how much difference could everyday drinking habits actually make? To find out, scientists turned to a vast health data set. Researchers analyzed data from 977,282 adults who were asked about their hot drink consumption habits, whether they preferred their drinks warm, hot or very hot, and how many cups of tea and coffee they drank daily.

They then tracked participants' health data through NHS (National Health Service) records for more than a decade. In particular, they were on the lookout for new diagnoses of esophageal cancer while taking into account lifestyle factors like smoking, alcohol intake and body weight.

During the study period, 2,348 participants developed esophageal cancer, which affects the esophagus, the tube connecting the mouth to the stomach. However, the data revealed an important difference. When the team separated the cases and looked at the different types of esophageal cancer, they found that higher drink temperatures were not linked to them equally, as they write in their paper published in the International Journal of Cancer.

Drinking very hot beverages, as opposed to warm beverages, was linked to a threefold higher risk of squamous cell carcinoma (SCC), a type of esophageal cancer that forms in the thin, flat cells lining the inside of the esophagus. People who preferred their drinks hot also faced an elevated risk, though not nearly as steep as those who preferred them very hot.

But temperature wasn't the only thing that mattered. The number of drinks consumed daily was also a factor. People who drank six or more cups of tea or coffee a day saw their risk of SCC jump significantly compared with those who drank fewer cups. The association was similar regardless of whether people primarily drank tea or coffee, suggesting that the risk came from the temperature of the liquid rather than any specific ingredient.
Because the cancer risk was linked to temperature, the scientists offer straightforward advice. "These findings suggest that reducing drink temperature in populations where tea and coffee are frequently consumed could offer an important means of SCC prevention."

Keren Papier et al, Hot Drinks and Oesophageal Cancer: Prospective Analyses in Around 1 Million UK Adults, International Journal of Cancer (2026). DOI: 10.1002/ijc.70654

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