Why some cancers are worse than others
Cancers with tetraploid cells—cells containing four chromosome sets—are associated with more aggressive tumor growth and poorer prognosis, partly due to recruitment of supportive stromal cells. Tumors with smaller tetraploid cells exhibit faster growth, greater invasiveness, and higher drug tolerance, with smaller cell size correlating with worse outcomes across multiple cancer types.

Most normal cells in your body are diploid, meaning they have two copies of each chromosome—one set from each parent.

To stay healthy, a diploid cell divides to make more diploid cells. But occasionally, a dividing cell makes a mistake, which throws off the chromosome numbers. And then, like an error at a printing press, that mistake is replicated and starts to accumulate.

This is one of the ways diseases like cancer can form.
Why do tetraploid cells make things so much worse?
Researchers saw that the number of tetraploid cells actually diminished during tumour formation in mice, and yet tumour mass ballooned fast and large.

In a first-of-its-kind discovery, they found that this growth was driven by the recruitment of stromal cells—non-cancerous connective tissue cells that provide structural support.

The presence of even a small fraction of these tetraploid cells can promote the recruitment of extra non-cancerous cells that support further tumour progression.
The second investigation initially targeted the physiology of tetraploid cells.
When the researchers made human-derived cancer cells tetraploid and isolated single-cell clones, he noticed something unexpected: the cells from the first few clones differed in size.

They anticipated all the clones to be two times larger than regular diploid cells because of the extra material crammed inside—but some were 25% to 30% smaller than expected.

And the smaller clones happened to be more tumorigenic than the large clones.
The smaller clones are more aggressive. They grow faster, are more invasive, and more tolerant of common anti-cancer and stress-inducing drugs."

Later experiments in mice showed that tumours with smaller tetraploid cells often increased more rapidly. Moreover, results did not depend on cancer cell type—they saw the same behaviour in colorectal and breast cancer.
The same things were identified even in human cancer cells.

Cimini, Daniela, Oxidative stress and serum deprivation influence the evolution of newly formed tetraploid cells during tumorigenesis, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2522077123. doi.org/10.1073/pnas.2522077123

Mathew Bloomfield et al, Cell and Nuclear Size Is Associated with Chromosomal Instability and Tumorigenicity in Cancer Cells That Undergo Whole Genome Doubling, Cancer Research (2026). DOI: 10.1158/0008-5472.can-24-3718

Blood pressure swings over 24 hours tied to poorer brain health

Frequent changes in blood pressure could affect cognitive health and contribute to brain changes associated with dementia risk, according to new research

Greater variability in blood pressure over 24 hours is associated with poorer cognitive performance and increased evidence of vascular brain injury. These fluctuations, even when modest, correlate with cognitive deficits equivalent to several years of aging, suggesting that dynamic blood pressure changes may contribute to dementia risk beyond average blood pressure levels.
Higher average blood pressure over 24 hours was also associated with greater evidence of vascular brain injury.
Even a modest increase in blood pressure variability was linked to lower performance on cognitive tests, equivalent to roughly seven years of additional aging.

Most people think of blood pressure as a single number taken in a doctor's clinic, but blood pressure is dynamic.

"Blood pressure rises and falls across the day and night, and those fluctuations may carry important information about brain health."

Madeline Gibson et al, Association of 24-Hour Blood Pressure Variability With Cognition and Brain MRI Markers of Structural Change in Adults in Mid- to Late-Life, Neurology (2026). DOI: 10.1212/wnl.0000000000214935

Freud's century-old ideas are colliding with modern brain science in ways that could change how minds are treated
Freud’s psychoanalytic concepts and the modern predictive brain model both describe the mind as oriented toward stability and predictability, with parallels between projection and prediction processes. Both frameworks explain persistent mental disorders as rigid, maladaptive prediction models that reduce uncertainty but distort reality. Integrating these perspectives may enhance understanding and treatment of mental disorders by linking neurological mechanisms with subjective experience.

Erik Stänicke et al, Freud's Model of the Mind Within a Predictive Processing Neuroscientific Paradigm, Entropy (2026). DOI: 10.3390/e28030318

The first signs of human cremation may date back 100,000 years
Burned Homo sapiens bones from Ethiopia’s Afar Rift, dated to about 100,000 years ago, may represent the earliest evidence of human cremation. Undisturbed artifacts and fossils, including obsidian from distant sources, indicate complex behaviour, repeated short-term occupation, and long-distance movement. Local hydrological factors, rather than global climate, primarily shaped human adaptation in this region.
Significant fossils were found in the area, including remains of Homo sapiens individuals, among them bones that had been burned at high temperatures. This may indicate cremation and could represent the earliest known evidence of human cremation.

The remains also showed bite marks from predators and signs of sudden burial.

The study further shows that local hydrological factors—such as the flood cycles of the ancient Awash River—influenced human life more than global climate fluctuations.

Thousands of stone tools indicate that people repeatedly returned to the area for short periods on a seasonally flooding plain.

Artifacts documented at the site have remained in nearly undisturbed layers, giving researchers an unusually precise understanding of the spatial relationships between objects and fossils across a wide area.

This research helps us build a comprehensive understanding of how early Homo sapiens interacted with their environment.

Yonas Beyene et al, Halibee member archaeology: Middle Stone Age environment, technology, and postmortem modifications, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2534441123

How did we learn which plants are safe to eat? Food scientists explain
Humans identified edible and toxic plants through generations of observation, experimentation, and cultural knowledge, later enhanced by scientific analysis. Many plants contain natural toxins, but preparation methods such as soaking, cooking, and fermentation can reduce or eliminate harmful compounds. Modern science has further improved safety by breeding plant varieties with lower toxin levels. Toxicity often depends on dose and preparation, not just the presence of specific compounds.
==
Memory decline after menopause linked to loss of estrogen production in brain tissue
Loss of brain-derived estrogen in aging female mice disrupts the extracellular matrix (ECM) in the hippocampus, impairing memory and social function, while males are unaffected. These findings suggest that postmenopausal estrogen decline uniquely increases Alzheimer's disease risk in women by altering ECM biology, highlighting a potential therapeutic target beyond amyloid-focused treatments.

Loss of brain-derived estrogen is associated with sex- and age-dependent alterations in memory, affective behavior, and hippocampal extracellular matrix gene expression, Aging Cell (2026).

Magnet-guided soft robots could lead to safer treatment of life-threatening blood clots

Researchers have developed an AI-assisted technique and a robotic platform that may one day help surgeons perform safer, faster and less invasive procedures to treat conditions such as blood clots located deep inside a patient's neurovascular pathways.

The method relies on small, soft, flexible robots that can maneuver through the delicate and complicated pathways of the human body to find and remove potentially dangerous obstacles to blood flow. The robots are made of a biocompatible rubber-like composite that contains microparticles that allow them to be wirelessly guided by external magnets.
A magnetically guided, soft robotic platform using AI-assisted closed-loop control enables precise navigation and manipulation within simulated vascular environments, outperforming conventional catheter-based methods in accuracy, stability, and resistance to fluid disturbances. The system reduces tracking errors by up to 77% and minimizes control effort, indicating potential for safer, less invasive treatment of deep-seated blood clots.

Alireza Moezi et al, Robotic-assisted tracking control of magnetoactive soft continuum robots in magnetic gradients, Smart Materials and Structures (2026). DOI: 10.1088/1361-665x/ae2708

AI uncovers why squeezed tumors grow slower under physical pressure

Researchers have solved a long-standing mystery about why physical forces slow cancer growth—and the answer could reshape how the disease is treated.
Cancer cells are known to bypass many of the body's normal growth controls, but tumors still respond to mechanical pressure.

Mechanical pressure on tumors increases hydrostatic pressure, counteracting osmotic swelling required for cell growth and division, thereby inhibiting tumor expansion. AI-accelerated computational modeling and experimental validation with breast cancer spheroids confirm that physical confinement prevents cells from reaching the critical size needed for division, highlighting the tumor microenvironment's active role in growth regulation and implications for mechanotherapy and drug efficacy.
The research findings suggest that learning to harness the pressure of physical force on a tumor could open an entirely new role for treatments known as mechanotherapies in the fight against cancer.
The research highlighted how, for decades, scientists have noticed that tumor cells seem to respond to one thing that chemicals cannot easily override: physical pressure—put enough physical pressure on a tumor, and its growth slows down.
The key lies in how cells grow in the first place. Before a cell can divide, it has to get bigger. It does this by manufacturing complex biological molecules (proteins, lipids, and other building blocks) which draws water into the cell through osmosis, inflating it like a tiny balloon. Once the cell reaches a critical size, it can split in two. Under normal circumstances, this swelling process works smoothly.

But when a tumor becomes physically confined by the surrounding tissue pressing in on it, something disrupts that process. The external mechanical load creates high hydrostatic pressure that fights against the osmotic swelling from the inside. The result? Cells can no longer reach the size needed to trigger division. Growth stalls. In other words, the physical architecture of a tumor is not just a passive backdrop, it's an active participant in the disease.
The implications stretch well beyond explaining an interesting biological process. Many cancer drugs work by targeting cell division. If a tumor's mechanical environment is already suppressing growth, understanding that interaction could reveal why some drugs work better in certain tumor types or locations, and why others fail.

Irish Senthilkumar et al, Stress-dependent growth in breast cancer arises from a mechano-osmotic coupling and cell-sizing checkpoint, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2523159123

A severed piece of sea cucumber refused to die, and what happened next could transform medicine

In a new study, researchers documented the continued viability of amputated tissue from a sea cucumber for over three years in natural seawater. It's the first known report of the long-term survival—and continued growth—of discarded tissue outside of a highly controlled, sterilized environment.

The finding challenges assumptions of what's possible for tissue immortality and opens up exciting possibilities in the biomedical field. It could also be used as an experimental model for biological research that is more widely accessible, without the ethical and logistical challenges of many existing cell lines.

Since the mid-20th century, scientists have made significant breakthroughs with "immortal" cell lines, like the famous HeLa cells, that can be grown in a lab and proliferate indefinitely for long-term research.
In earlier studies, though, tissue cultures have only been maintained under "axenic" conditions that are tightly controlled, rigorously maintained, and lack any bacteria or other organisms. Even then, they have not demonstrated signs of actual healing and growth, nor retained the ability to move independently.

Many echinoderms, the phylum that includes sea cucumbers, are known to display impressive regeneration capacity and negligible cell aging. Lost tissue, though, was always assumed to eventually decay or die. Yet the researchers noticed that some discarded tissue from a tube foot of a sea cucumber hadn't decayed after a number of weeks. In fact, it seemed to be growing.

Part 1

The researchers ran a number of experiments in flowing seawater with tissue removed from the feet, main body, and tentacles of three individuals of Psolus fabricii, a cold-water species of sea cucumber.

They found evidence of diversifying cells, immune activity, and tissue reorganization in the explanted tissue. And in the absence of a mouth, the cells appeared to be getting nutrients by absorbing amino acids dissolved in the seawater. Even after three years, when the researchers stopped the experiments in order to publish, the tissue was still active. This ability to survive in a complex, stressful environment makes this cell line unique compared to other tissue cultures.
and the rich environment full of bacteria and all this organic matter was actually feeding them and allowing this tissue to heal and grow.
The implications for biomedical sciences and engineering are profound, with potential applications in everything from tissue regrowth to antimicrobial healing.

It also opens up new opportunities for biological research and education more broadly. The tissue they've preserved shows an unprecedented ability to maintain its structural integrity and complexity in culture. It can be grown more easily in the lab.

Sara Jobson, Natural tissue immortality: Indefinite survival of sea cucumber explants, Science Advances (2026). DOI: 10.1126/sciadv.aeb1394. www.science.org/doi/10.1126/sciadv.aeb1394

Part 2

Reconstructed 1.5‑billion‑year‑old protein network reveals hundreds of hidden disease‑linked genes

The cells inside every living thing are like microscopic cities with molecular machines that make energy, transport supplies from place to place, build structures and get rid of trash. Because these machines are so critical for the survival of an organism, versions of them have been passed down over more than a billion years of evolution. Molecular machines are made of proteins, which are produced with instructions stored in genes. And because these ancient molecular machines are so important for life, when one of the genes that helps build them breaks, it can lead to serious diseases in humans.
There was a huge range of diseases that we could predict pretty well, just using ancient protein complexes
Reconstruction of a 1.5-billion-year-old protein interactome identified hundreds of previously unrecognized human disease-associated genes, with about half of all human genes traceable to the Last Eukaryotic Common Ancestor (LECA). Experimental validation in animal models confirmed associations with three rare disorders, suggesting that ancient protein complexes can predict gene-disease links across eukaryotes.
This representation of protein networks, known as the protein interactome and published in Cell Genomics, is like a treasure map the researchers have used to dig up hundreds of genes that weren't previously known to be associated with human diseases. Using animal models and human patient data, they have already confirmed for the first time that three of these genes are connected to rare disorders. The work could potentially lead to new targets for treating a host of other diseases.

A protein interactome for the last eukaryotic common ancestor illuminates the biochemical basis of modern genetic diseases, Cell Genomics (2026). DOI: 10.1016/j.xgen.2026.101254. www.cell.com/cell-genomics/ful … 2666-979X(26)00116-3

Dying cells don't all release key inflammatory cytokine in the same way, research reveals

Researchers have uncovered a previously unrecognized mechanism controlling how dying cells release the inflammatory cytokine IL-33, a key driver of allergy, asthma, tissue inflammation, and cancer progression. The findings reveal that cells do not release IL-33 uniformly; instead, individual cells exhibit striking differences in release timing controlled by the membrane rupture protein NINJ1.

The research team discovered that IL-33 release frequently occurs only after catastrophic plasma membrane rupture mediated by NINJ1, rather than directly through Gasdermin pores as previously thought.

The study further demonstrated that the timing of IL-33 release differs dramatically depending on the type of cell death. During necroptosis, IL-33 is released almost instantaneously when membrane integrity collapses. In contrast, during apoptosis and pyroptosis, some cells released IL-33 immediately, whereas others waited tens of minutes before release.

This study reveals that inflammatory signal release is not a simple on/off event.

Even cells dying under the same conditions can release IL-33 with very different timing. They found that temporal regulation of NINJ1 activation is a key determinant of this heterogeneity.

The researchers also showed that deleting NINJ1 strongly suppressed IL-33 release across multiple cell types and cell death pathways. This highlights NINJ1 as a central executor of the release of damage-associated molecular patterns (DAMPs)—molecules released from dying cells that alert the immune system.

Because IL-33 plays critical roles in allergic disease, fibrosis, cancer, and immune activation, the findings may open new therapeutic avenues for controlling excessive inflammation by targeting membrane rupture mechanisms rather than upstream cytokine production alone.

Takumi Kanokogi et al, Temporal control of Ninj1 activation determines cell-to-cell heterogeneity in IL-33 release, Communications Biology (2026). DOI: 10.1038/s42003-026-10300-1

Gut microbes help shape how many calories you absorb from food

Food labels make calories seem simple. They show the number of calories per serving, which is calculated based on how much fat, carbohydrates and protein the food contains. But inside the body, digestion is far more complicated. Food passes through a living microbial ecosystem that can influence how many of those calories people actually absorb.

Digestion is not just a human process—it is a collaboration between our bodies and trillions of microbes living in the gut.
Gut microbes significantly influence the number of calories absorbed from food by fermenting undigested components in the colon, producing short-chain fatty acids that contribute to total energy intake. A new model, DAMM, more accurately estimates calorie absorption by accounting for both human and microbial metabolism, revealing that high-fiber diets result in fewer net absorbed calories despite increased microbial activity.
A new mathematical model developed by researchers takes a closer look at that hidden part of digestion. The model, called DAMM—for digestion, absorption and microbial metabolism—follows food through the digestive tract, estimating what the body absorbs directly, what reaches the colon and how gut microbes help process the remaining material into products that are either absorbed or excreted.
DAMM gives us a powerful new way to quantify how those microbial partners contribute to human health and energy balance, and also point at the importance of properly feeding our gut microbes.
The model could eventually help researchers better understand obesity, diabetes and other metabolic disorders by showing how different diets affect both the human body and the microbial community inside the colon.
part 1

For more than a century, scientists have relied on Atwater parameters to estimate the energy people get from food, measured in calories. The method multiplies the amount of protein, carbohydrates and fat in the food by the average metabolizable calories per gram of each.

The system is simple and useful, but it does not capture the microbial side of digestion, including how different diets feed gut microbes or how those microbes produce compounds such as short-chain fatty acids from fiber and other undigested food in the colon.

The new research builds on a controlled diet study that examined how the gut microbiome affects human energy balance. The gut microbiome is the vast community of bacteria and other microbes living in the digestive tract.
What is truly unique about the DAMM model is that it quantitatively links human metabolism to the metabolism of the microorganisms in the colon in a way that matches the results from the clinical study and provides fundamental insight into how the microbial community works in partnership with the human host.
DAMM starts by splitting a diet into the nutrients that make up the protein, carbohydrates and fat; then, it estimates how much usable energy of those components is absorbed in the upper digestive tract.

Next, it follows the material into the colon, where gut microbes break down the remaining food components that escaped earlier digestion. In the process, they produce short-chain fatty acids, which can be absorbed through the colon and used by the body as additional calories. The model also accounts for methane production by certain microbes known as methanogens.

That microbial contribution is meaningful. The model estimated that short-chain fatty acids absorbed from the colon contributed an average of about 140 calories per day, or roughly 7.4% of total usable energy. About 85% of usable energy came from the upper gastrointestinal tract, while about 15% came from the lower gastrointestinal tract, where microbial activity plays a central role.

When researchers tested DAMM against results from the controlled diet study, it came closer than the standard Atwater approach to estimating how many calories people actually absorbed from food. The standard method tended to underestimate absorbed calories, while DAMM produced estimates that more closely matched the study measurements.
The model also captured meaningful differences between the high- and low-fiber diets. The microbiome-enhancer diet delivered more fermentable material to the colon, where microbes could convert it into short-chain fatty acids.

Taylor L. Davis et al, Modeling the microbial contribution to human energy balance using the Digestion, Absorption, and Microbial Metabolism (DAMM) model, PLOS One (2026). DOI: 10.1371/journal.pone.0347668

Part 2

Why you wake up so tired after vivid dreams
Feeling tired after vivid dreams is typically due to waking during REM sleep, which disrupts deep, restorative sleep stages. Remembering dreams often indicates sleep fragmentation, reducing the brain's ability to clear adenosine and leading to fatigue. Dreaming itself does not cause tiredness; rather, it is the timing and frequency of awakenings that impact sleep quality.

original article.

Unprecedented view inside live stem cells reveals aging process and loss of regenerative capacity

Scientists have developed a powerful new technique that allows them to observe how individual cells manufacture proteins during aging, offering an unprecedented glimpse into the hidden molecular activity of stem cells in living tissue. As a result of the research, conducted at the Institute for Regenerative Medicine in Switzerland, scientists were able to observe aging unfold inside individual epidermal stem cells.

What scientists saw was the intricate choreography within stem cells and how those molecular dance steps slow and change with age. The team of  scientists has concluded that the process of aging reshapes how skin stem cells manufacture proteins. The findings are published in the journal Molecular Cell.

The study revealed that aging epidermal stem cells undergo distinct shifts in their protein-production capabilities, changes that could help explain declining regenerative capacity of these cells in older tissue.

Stem cells are characterized by two features: their ability to self-renew throughout life and to differentiate into other cell types. 

Because stem cells are essentially blank slates capable of morphing into any cell type, their biological role and fate differ significantly from other cell types. By tracking them through stages of life, it's possible to see how they impact processes such as inflammation and immunity, the team found.

Paradoxically, even during youth, stem cells are not high-energy cells that keep their ribosomes busy with the production of proteins. Instead, these workbenches in stem cells where proteins are constructed exist as relatively quiescent structures.

"Somatic stem cells are characterized by their low overall protein-synthesis rates, a feature implicated in driving their stemness. 

The term "stemness," refers to the cells' capacities for self-renewal and remaining unspecialized until needed.

Both of these functions are closely linked to their precise regulation of gene expression. Somatic stem cells exhibit a unique signature marked by high ribosome biogenesis and a low protein synthesis rate.

Clara Duré et al, In vivo single-cell ribosome profiling reveals cell-type-specific translational programs during aging, Molecular Cell (2026). DOI: 10.1016/j.molcel.2026.04.017

Pigeons navigate using magnetic sensors in their livers, say researchers

How pigeons fly hundreds of kilometers and still find their way home has long fascinated people. Now, researchers say a surprising answer may be hidden, not in the brain or eyes of birds, but in the liver.

Pigeons possess iron-rich macrophages in their livers that act as magnetic sensors, enabling detection of Earth's magnetic field for navigation. Removal of these cells disrupts magnetic-based homing, especially under overcast conditions, indicating their essential role. These macrophages are positioned near nerve fibers, suggesting a pathway for transmitting magnetic information to the brain.

A study published in Science suggests that special cells in the liver of pigeons can sense Earth's magnetic field, giving the birds an internal compass.

The special cells, known as "macrophages," are immune cells that break down old red blood cells. As part of this process, they accumulate iron, giving them quantum properties that may allow them to respond to magnetic fields. Without these cells intact, pigeons could not navigate home, the study shows.

To identify where magnetic cells are found in pigeons, the researchers used techniques known as "vibrating sample magnetometry" and "magnetic cell separation" to screen organs thought to be involved in magnetic sensing, including the eyes, beak, and brain. They also examined the liver and spleen.

They had some clues that the liver and spleen have magnetic properties, because they break down red blood cells and so store much iron in the body.
The results supported that idea. Of all the tissues examined, the liver showed the highest concentration of iron.

Iron is crystallized in oxide nanoparticles, making the cells superparamagnetic and reactive to magnetic fields. They found by far the strongest magnetic response in liver tissue.
Further analysis identified macrophages in the liver as the cells responsible.
To test if liver macrophages played a role in navigation, the ornithological team conducted experiments on pigeons that were trained to return from distances over twenty kilometers back to their aviary.
After the macrophages were removed, pigeons lost their sense of direction on overcast days when the sun was obscured. When the sun was visible, however, the pigeons successfully navigated home, likely using solar cues. Together, these results illustrate the mechanism behind how birds use magnetic sensing, in addition to the sun's orientation, for navigation.

With evidence that these cells influence navigation, the researchers then looked for how signals from the liver might be relayed. Electron microscopy showed that the iron-rich macrophages sit close to nerve fibers, suggesting a pathway for magnetic information to reach the brain.
These findings provide the first concrete evidence of how Earth's magnetic field can be perceived within the body and passed on to the brain to guide movement.
The study brings together known biological processes, including iron metabolism and how the immune and nervous systems communicate, into a clear answer to the fundamental question of how animals navigate.

Clivia Lisowski et al, Homing pigeon navigation relies on superparamagnetic macrophages under overcast conditions, Science (2026). DOI: 10.1126/science.ady2486. www.science.org/doi/10.1126/science.ady2486

Gut microbe found to worsen sepsis by triggering hyperinflammatory immune responses

Why do some people recover easily from bacterial infections while others rapidly deteriorate into life-threatening sepsis? According to a new study published in Nature Communications, the answer may lie not only in the invading pathogen itself, but also in the microorganisms already living inside the gut.
Sepsis is a severe condition in which the body's immune system overreacts to infection, causing widespread inflammation and organ damage. In many cases, the excessive immune response itself becomes more dangerous than the bacteria causing the infection.

Recent studies have suggested that gut microbiota play an important role in regulating baseline immune status and may influence susceptibility to infectious diseases.
Researchers has now identified a specific gut microbial group that can dramatically worsen sepsis by excessively sensitizing immune cells.
The researchers observed that even genetically identical mice showed strikingly different infection outcomes depending on the composition of their gut microbiota. When exposed to the same amount of pathogenic bacteria, some mice survived with relatively mild symptoms, whereas others rapidly deteriorated and showed significantly lower survival rates due to overwhelming immune activation.

Further analysis revealed that one key factor associated with severe disease was the enrichment of a gut bacterial family known as Muribaculaceae. Among these microbes, a bacterium called Sangeribacter muris KT1-3 was found to produce metabolites that placed immune cells into an excessively hypersensitive state.
As a result, when pathogens invaded the body, the immune system reacted far more aggressively than necessary, leading to uncontrolled inflammation and fatal sepsis.
To confirm that the gut microbiota itself was responsible for these effects, the team also performed fecal microbiota transplantation experiments. When gut microbes associated with severe infection were transferred into otherwise resistant mice, survival rates declined sharply. Conversely, transferring healthier microbial communities improved survival outcomes.

The study further demonstrated that tiny metabolites produced by specific gut microbes can prime immune cells beyond their normal activation threshold. This exaggerated immune sensitivity caused even relatively small external stimuli to trigger explosive inflammatory reactions, ultimately resulting in life-threatening sepsis.
These findings suggest that sepsis severity is determined not only by the virulence of invading pathogens but also by the composition of the gut microbial environment.
This study demonstrates that gut microbiota can fundamentally alter the intensity of immune responses and thereby determine infection outcomes.

Enrichment of specific gut microbes, particularly Muribaculaceae and Sangeribacter muris KT1-3, increases sepsis severity by producing metabolites that excessively sensitize immune cells, leading to hyperinflammatory responses and reduced survival. Fecal microbiota transplantation confirmed that gut microbial composition directly influences susceptibility to severe sepsis.

Seonghan Jang et al, A Muribaculaceae-enriched microbiota exacerbates TLR4-dependent Acinetobacter baumannii-induced hyperinflammatory sepsis, Nature Communications (2026). DOI: 10.1038/s41467-026-72435-3

Depression may not only be a consequence, but also a cause of rheumatoid arthritis

According to researchers not only inflammation, but also sleep disorders, depression, obesity, and smoking may sustain persistent rheumatic symptoms. In their publications in the journals Nature Reviews Rheumatology and The Lancet Rheumatology, they also proposed a model that can help identify and treat the true causes of symptoms in time.
Rheumatoid arthritis is a chronic autoimmune disease in which the immune system attacks the joints, causing pain, swelling, and stiffness. It affects tens of thousands of people in Hungary only. Most patients respond well to treatment, but 6%–28% belong to the so-called "difficult-to-treat" group because they do not achieve lasting remission despite therapy.
According to the publications in Nature Reviews Rheumatology and The Lancet Rheumatology, these factors may not only coexist with the disease but may also help maintain it.

For example, pain and depression may reduce physical activity, increase body weight, worsen sleep and mood—all of which can feed back into pain and everyday functioning, creating a difficult-to-break "vicious cycle."

The researchers not only identified these patterns but also developed a new model that could improve the treatment of such difficult-to-treat patients.

Depression, sleep disorders, obesity, and smoking can contribute to the persistence of difficult-to-treat rheumatoid arthritis, not merely coexist with it. These factors may sustain symptoms independently of inflammation, creating a self-perpetuating cycle. A new model emphasizes identifying and addressing these non-inflammatory contributors to improve patient outcomes and guide more effective, individualized treatment.

Lilla Gunkl-Tóth et al, Bridging the gap: combining treat-to-target and difficult-to-treat strategies in the management of rheumatoid arthritis, Nature Reviews Rheumatology (2026). DOI: 10.1038/s41584-026-01354-w

Wenhui Xie et al, Associated lifestyle factors and comorbidities of difficult-to-treat rheumatoid arthritis: a systematic review and meta-analysis, The Lancet Rheumatology (2026). DOI: 10.1016/s2665-9913(26)00041-x

Lilla Gunkl-Tóth et al, Lifestyle factors in difficult-to-treat rheumatoid arthritis, The Lancet Rheumatology (2026). DOI: 10.1016/s2665-9913(26)00108-6

Lab-grown brain-spinal cord model shows 'irreversible' nerve damage may be reversed
Lab-grown human brain-spinal cord organoid models revealed that axon regrowth capacity is lost during neuronal maturation but can be restored by blocking specific gene networks. The hormone drug lynestrenol significantly enhanced axon regeneration in damaged mature neurons, indicating that neuron-intrinsic barriers to repair are reversible and suggesting new therapeutic avenues for central nervous system injuries.

George M. Gibbons et al, A human corticospinal organoid-slice connectoid model informs enhancer strategies for post-injury axon regrowth, Cell Reports (2026). DOI: 10.1016/j.celrep.2026.117399

Oral inflammation may reach ovaries, speeding fertility decline, mouse study suggests
Chronic oral inflammation in mice induces systemic immune responses that reach the ovaries, elevating ovarian inflammatory cytokines, altering immune cell populations, and causing oxidative and DNA damage in oocytes. These changes impair follicle development, reduce oocyte quality, and significantly lower fertility, suggesting oral inflammation may accelerate reproductive aging and contribute to infertility.

P. Kles et al, Chronic Oral Inflammation Impairs Female Reproduction in a Murine Model, Journal of Dental Research (2026). DOI: 10.1177/00220345251412768

Why do you get so tired while driving?
Driving requires sustained attention and coordination across multiple brain regions, making it mentally demanding and prone to fatigue. Fatigue impairs attention, decision-making, and reaction time, increasing crash risk and the likelihood of microsleeps, which can be catastrophic. Risk factors include insufficient sleep, long driving periods, circadian disruption, dehydration, and stress. Regular breaks, adequate sleep, and hydration are essential for maintaining alertness while driving.

 original article.

AI can mass-produce finance research papers indistinguishable from human work, reports study
AI and large language models can rapidly generate large volumes of finance research papers that closely resemble human-authored work, including plausible hypotheses and theoretical justifications. This capability raises concerns about the scalability of HARKing, the integrity of scientific contribution, and increased strain on the peer-review system, suggesting a need for adaptation in academic standards and evaluation processes.

Robert Novy-Marx et al, Artificial Intelligence–Powered (Finance) Scholarship, Journal of Economic Literature (2026). DOI: 10.1257/jel.20251821

Ming Dynasty Surgeons Used Poison as an Anesthetic

Traces of red material crusted on ancient surgical tools may not be a record of pain, but rather the absence thereof.

Metal scissors and tweezers recovered from a Ming Dynasty tomb in Jiangyin County, China, retain what scientists think may be the earliest direct chemical evidence of surgical anesthesia – a substance used for painless medical treatment.

It's the first discovery of its kind and highlights the sophisticated medicine of the Ming Dynasty.

 That substance appears to be aconitine, a highly toxic compound derived from the group of plants that includes wolfsbane.

Its presence on the tools of a revered surgeon – Xia Quan, who lived around 1348 to 1411 and in whose tomb the tools were found in 1974 – implies a very high level of skill and precision.
Six centuries ago, a Ming Dynasty surgeon performed an operation with a pair of iron scissors and tweezers, and today researchers have read the traces of anesthetic medicine left on those instruments using a beam of laser light.
This is the first time humanity has found direct chemical evidence of anesthetics on ancient surgical tools, proving that our ancestors already knew how to safely alleviate patients' pain with highly toxic herbs.

https://www.cambridge.org/core/journals/antiquity/article/surgical-...

Tardigrades reveal extreme heat-blocking survival trick while in tun state

The tun state is a form of suspended animation used by tardigrades (water bears) to survive harsh environmental conditions. When faced with extreme drought, freezing, or radiation, they expel nearly all their water and curl into a dry, lifeless ball, dropping their metabolism to virtually zero.
A biological process that allows tardigrades to survive in extreme environments is anhydrobiosis. This is a reversible process via which the animals lose most of their body water and their metabolism temporarily stops, which in turn allows them to survive in dry environments. When tardigrades undergo this process, they curl up and enter what is known as a "tun" state.
Researchers at the Indian Institute of Science recently carried out a study aimed at better understanding how a species of tardigrade—called Paramacrobiotus sp. BLR strain—survives extreme heat while in the tun state. Their findings, published in the Journal of the Royal Society Interface, suggest that reductions in thermal conductivity are central to the survival of this species at high temperatures and under extreme heat.

Tardigrades in the tun state exhibit significantly reduced thermal conductivity, enabling survival at extreme temperatures up to 85°C, unlike their active counterparts. This physical adaptation limits heat flow, protecting internal cellular structures and contributing to their extremotolerance beyond known biochemical mechanisms.
Researchers found that active tardigrades did not survive high temperatures for one hour, even the lowest experimental temperature of 45°C. Instead, 90% of tardigrades in the tun state survived under the same conditions, and some of them were still alive after one hour at 85°C.
Interestingly, the researchers found that tardigrades in the tun state exhibited a higher thermal resistance and a reduced flow of heat through their bodies. In their paper, they propose that the observed lower thermal conductivity protects the animals' internal cellular structures and prevents heat-related damage.
The results of this study suggest that the ability to survive extreme temperatures is supported not just by biochemical, but also by physical processes.

Harikumar R. Suma et al, Thermal conductivity modulation as a mechanism of inducible thermotolerance in the eutardigrade Paramacrobiotus sp., Journal of the Royal Society Interface (2026). DOI: 10.1098/rsif.2025.1033

Humans reshape predator-prey rules across food webs, creating a challenging new world for wildlife

The relationship between predators and prey in the wild is underscored by an evolutionary arms race spanning millions of years, but new research has found modern human activity is reshaping the rules.
The review found that physical and behavioural traits of both predator and prey have been altered by human interference, and this has affected how they interact with each other.

Human activities such as selective hunting, fishing, habitat alteration, and pollution are altering the physical and behavioural traits of both predators and prey, disrupting established predator-prey interactions. These trait shifts can cascade through food webs, leading to population declines, food web restructuring, and potential local extinctions, fundamentally altering ecosystem function.
Predator–prey interactions underpin the evolution of entire ecosystems.
They influence everything from species abundance to vegetation and nutrient cycling—if we change how predators and prey interact, those effects can cascade through food webs and fundamentally alter ecosystems.

One of the key takeaways from the study was that changes in animal behavior and physiology weren't always obvious or immediate, but could have long-term consequences.

Trait shifts can build over time, leading to cascading effects like population declines, food web restructuring, or even local extinctions.
By understanding how human activities drive these changes, we can design better conservation strategies.

Eamonn I.F. Wooster et al, Human-induced trait shifts reshape predator–prey interactions, Trends in Ecology & Evolution (2026). DOI: 10.1016/j.tree.2026.01.005

What separates dreaming from deep sleep? Brain rhythm offers new clue to consciousness

Neuropsychology researchers have discovered a rhythm in the midbrain that could serve as a biophysiological signature for specific states of consciousness.
A rapid oscillation in the human thalamus, occurring at 20–45 Hz, is present only during wakefulness and REM sleep, but absent during non-REM sleep. This thalamic rhythm may serve as a biophysiological marker distinguishing conscious states from deep, unconscious sleep.
The thalamus is a deep-lying structure in the center of the brain which gathers and relays signals from many different areas of the brain. It functions like a gate for perception and attention and is thought to play a key role in supporting conscious states.
The researchers discovered a previously unknown rapid activity pattern in the human thalamus.
This rapid oscillation, in the frequency range of 20 to 45 Hertz, occurs exclusively during waking hours and REM sleep, the phase of sleep with rapid eye movements and intensive dreams. It is entirely absent in non-REM sleep, when eye movements are absent and consciousness is strongly reduced. In this sleep phase, the brain activity is dominated instead by slower oscillations.
The results show that the central thalamus plays an important role in regulating brain states. In the context of existing research, our results show that this small deep-lying brain structure could actively influence our states of consciousness.
These characteristic rhythm patterns can be reliably attributed to specific states and thus have the potential to serve as a measurable biological signature of states of consciousness.

Aditya Chowdhury et al, Thalamic oscillations distinguish natural states of consciousness in humans, Nature Human Behaviour (2026). DOI: 10.1038/s41562-026-02446-z

The left and right ventricles differ in their ability to withstand the effects of cardiac arrest, study finds
The right ventricle demonstrates greater resistance to ischemia and better preservation of electrical activity than the left ventricle during cardiac arrest caused by ventricular fibrillation. Electrical gradients between heart regions can be detected via surface ECG, which may help predict neurological recovery outcomes. These findings suggest potential for targeted therapies to improve left ventricular resistance during cardiac arrest.

https://medicalxpress.com/news/2026-05-left-ventricles-differ-abili...

CAR T moves beyond cancer, targeting autoimmune disease with immune system reset
CAR T cell therapy, originally developed for cancer, is being investigated for autoimmune diseases by targeting and eliminating pathogenic B cells, potentially resetting immune function. Early trials show promising symptom improvement and reduced need for other immunotherapies, but risks include severe inflammation, immunosuppression, and uncertain long-term effects such as secondary malignancies. Newer approaches aim to enhance safety and reduce costs, including mRNA-based CAR T and off-the-shelf donor cell therapies. Long-term efficacy and safety in autoimmunity remain under investigation.

Originally designed to target and wipe out cancer by reprogramming the patient's immune cells, CAR T is now being offered to patients in hundreds of clinical trials for autoimmune conditions like multiple sclerosis, lupus, Graves' disease, vasculitis and many others. The hope is that CAR T can duplicate the success it has demonstrated in a range of blood cancers by hunting down and eliminating cells that target the self in autoimmune diseases. This would essentially reset the body's defenses to a state like the one that existed before the disease took hold.
But along with CAR T's promise come risks, questions and challenges. There's uncertainty about how well it will work for autoimmunity and how long any benefits might last, as well as what long-term side effects might arise.
The basic premise of CAR T is to activate the power of key immune cells called T cells. T cells normally recognize other cells that have been infected by a virus or bacterium, or are otherwise abnormal, and either destroy them or recruit other parts of the immune system to do so.

In CAR T for cancer, scientists engineer those T cells to specifically hunt and destroy malignant cells. The technology got its start when cancer researchers figured out how to take out a patient's own T cells, insert DNA instructions for a "chimeric antigen receptor," or CAR, and put them back into the person's circulation. The CAR, which sits on the T cell's surface and latches on to a specific molecular partner on the surface of cancerous cells, activates the T cell to attack.

Today CAR T cells are most commonly programmed to attack B cells, another key immune player. B cells are normally responsible for making antibodies, but in certain blood cancers, they proliferate out of control. By giving T cells a CAR that recognizes one of a couple of molecules unique to the B cell surface, the cells are reprogrammed to find and eliminate those cancerous cells.

B cells are also the central problem in many autoimmune conditions: They mistakenly make antibodies against normal tissues instead of against invading pathogens. So as CAR T began to succeed against B cell cancers, it didn't take long for doctors to reason that CAR T therapy might also be able to wipe out bad B cells in people with autoimmunity.
A German team pioneered autoimmune CAR T in a woman with lupus, reporting positive results in 2021. Since then, that team and others have worked to translate the oncology success of CAR T to tackle a broad spectrum of autoimmune diseases.
Part 1

Despite such striking results, reprogramming the immune system is no simple matter. In early treatment of cancer patients, CAR T cells produced life-threatening side effects, as outlined in a 2026 article in the Annual Review of Medicine. As CAR T cells attack their targets, the associated inflammation can cause symptoms like high fevers and low blood pressure. If that inflammation reaches the brain, it can cause additional problems such as confusion and drowsiness.

Fortunately, physicians now have a decade's worth of experience recognizing and treating these problems. They're certainly reversible and don't cause long-term damage most of the time.
Physicians and patients also must contend with decreased immunity as both a side effect of the treatment and its desired outcome. In CAR T treatment, doctors typically use powerful chemotherapy drugs to temporarily reduce the body's immune cell population to make room for the new, engineered cells, leaving patients temporarily immunosuppressed. And if the treatment works, it will decimate B cell populations. Patients can be vulnerable to infections for up to a year after treatment.
These effects are manageable with preventive antibiotics, antivirals and vaccines. Patients also retain antibodies that their B cells made before the treatment, which provide residual protection for a few months. And for reasons that are not yet fully understood, CAR T seems to leave older B cells, which provide immune memory of past infections, intact in some cases. One study found that autoimmune patients treated with CAR T still made antibodies for diseases they'd been previously vaccinated against, like chicken pox and measles. These are signs that the treatment did not completely return the immune system to its factory settings.

When evaluating CAR T risk, it's important to consider that many existing treatments for autoimmune disease also suppress the immune system for as long as a person takes them, experts note.
Researchers are already working on second- and third-generation versions of CAR T that they expect to be safer for both cancer and autoimmunity.

Source: https://knowablemagazine.org/content/article/health-disease/2026/ca...

Part 2

AI is making journalistic language more repetitive and predictable—and it's a problem for all of us
Increased use of AI-generated text in journalism leads to more repetitive, predictable, and homogenized language, reducing linguistic diversity and innovation. This shift limits the press's traditional role in introducing new vocabulary and nuanced expression, potentially reinforcing existing biases and diminishing the public's capacity for precise communication and debate. Mixing synthetic and human-generated text can mitigate these effects, but large-scale replacement of human writing risks long-term decline in public language richness.

original article.

Wounds may trigger 'aged' cells within hours, reshaping how senescence starts
Cells can enter senescence within minutes to hours after injury, using pre-existing mRNA to rapidly produce p21 protein, independent of new gene transcription. This early senescence actively coordinates wound healing by releasing signaling molecules and guiding cell migration, but is beneficial only during a narrow time window and is eliminated after healing. Persistent senescent cells are linked to age-related diseases.

Karla Valdivieso et al, Transcription-independent induction of rapid-onset senescence is integral to healing, Nature Cell Biology (2026). DOI: 10.1038/s41556-026-01948-2

The Y chromosome is home to surprising jumping genes

The humble Y chromosome may be the smallest chromosome in the mammalian genome (and getting even smaller), but it is mighty: Genes on the Y chromosome are critical for fertility in males.

In a new study in the journal Current Biology, researchers have studied deer mice to outline how the Y chromosome defends itself against decay by acquiring gene families, holding its own to maintain fertility.
A gene family named Phf8y was identified on the Y chromosome of deer mice, originating from the X-linked Phf8 gene via transposable element-mediated duplication. This represents a rare case of a gene moving from the X chromosome to an autosome and then to the Y chromosome. Such gene acquisitions may help the Y chromosome maintain essential functions for male fertility and contribute to the evolutionary stability of sex ratios.

Autosomes are all of the chromosomes that aren't the sex chromosomes. However, the Y chromosome is often thought of as a place where genes go to die because its genes don't recombine.
In this study, researchers discovered a gene family, which they named Phf8y, that bucked this trend, hopping to the Y and duplicating itself.
It's a unique pattern that they didn't expect—having a gene move from the X chromosome to an autosome to the Y chromosome.
What's driving the process? In the production of sperm, the X chromosome from the maternal side and the Y chromosome from the paternal side result in a sperm cell that has either an X or Y chromosome.

During this period, the X serves as a sort of autosome for genes important for viability and spermatogenesis, Mueller explains.
But since males carry just one X, an alternative method arose evolutionarily to provide a way to back up important genes for creating sperm.
It's like having your own clone around who can jump in when you've gone on vacation.
There are genes that copy themselves, called transposable elements. They hide out in our genome and are activated on rare occasions. In fact, these so-called jumping genes make up half of the human genome.

The team discovered that the deer mouse Phf8y on the Y chromosome is derived from the X-linked Phf8, apparently having hijacked the transposable element machinery to make an extra copy of itself.

What Phf8y is doing is still a mystery.

The team speculates that this gene on the Y chromosome is involved in chromatin packing, or how DNA is packaged, and could confer an edge to Y-bearing sperm to compete with X-bearing sperm.

Previous studies in house mice have revealed genes that share similar features to Phf8y and are in an X–Y arms race.

Ivan F. Mier et al, An X-to-autosome-to-Y chromosome amplified retrogene family functions in spermatids, Current Biology (2026). DOI: 10.1016/j.cub.2026.04.045

some chikungunya virus infections may turn chronic

Chikungunya virus, which is transmitted to people by infected Aedes mosquitoes and characterized by high fever and intense joint swelling and pain, has made a resurgence in many countries around the world in recent years.

Researchers estimate that about half of people infected with chikungunya virus will progress to a chronic form of the disease and experience relapsing arthralgia and arthritis that can span years and currently has no treatment.
Chikungunya virus can persist in joint-associated macrophages, which act as reservoirs, leading to chronic joint pain and inflammation in about half of infected individuals. Advanced sequencing techniques identified these macrophages as harbouring viral RNA, and antiviral treatment targeting viral replication reduced chronic inflammation, indicating persistent infection in these cells drives chronic symptoms.

Kristen M. Zarrella et al, Chikungunya virus persists in joint-associated macrophages and promotes chronic disease in mice, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02303-9

One-time gene editing treatment lowers 'bad' cholesterol by up to 62%
A single infusion of the gene editing therapy VERVE-102 reduced LDL cholesterol by up to 62% in adults with inherited high cholesterol or premature coronary artery disease, with effects lasting up to 18 months. No serious adverse events were observed at the highest dose, and only mild, transient infusion reactions and liver test changes occurred. Larger studies are ongoing to confirm safety and efficacy.

Scott B. Vafai et al, In Vivo Base Editing of PCSK9 with VERVE-102 for Hypercholesterolemia, New England Journal of Medicine (2026). DOI: 10.1056/nejmoa2601283

A common food compound may hold the key to shutting down leaky gut damage

When the intestinal lining breaks down, harmful gut bacterial antigens can slip into the bloodstream alongside nutrients. This breach in the gut's protective barrier, known as "leaky gut," is more than a digestive issue—it's a sign of inflammatory bowel disease (IBD) and has been increasingly linked to a number of chronic conditions.
A team of researchers has uncovered a key mechanism underlying leaky gut and identified a promising and natural way to repair it. And a potential solution is already in many of the foods we eat every day.

In a study published in the journal Nature Communications, the team shares how phytic acid (or InsP6), a natural compound found in whole grains, beans, lentils, nuts, and seeds, plays an important role in maintaining the integrity of the intestinal barrier.

Phytic acid is something many people already consume daily, especially in plant-rich diets.It's beyond just a dietary component; it also functions as a biologically active molecule that supports gut health.
Phytic acid (InsP6), a compound found in whole grains, beans, lentils, nuts, and seeds, directly activates histone deacetylase 3 (HDAC3), a regulator essential for maintaining intestinal barrier integrity. This mechanism protects against gut barrier breakdown and inflammation associated with leaky gut and inflammatory bowel disease, suggesting potential for targeted supplementation therapies.

Sujan Chatterjee et al, Phytic acid (InsP6) activates HDAC3 epigenetic axis to maintain intestinal barrier function, Nature Communications (2026). DOI: 10.1038/s41467-026-68994-0

Exploding immune cells that kill surrounding tissue

 Scientists have discovered a new type of immune cell that kills surrounding cells via explosion—a cellular detonation so fast and complete that the cell vanishes within minutes, leaving no trace behind. This discovery comes from an unlikely source: planarian flatworms. These aquatic, slithering pancake versions of worms are famous for their ability to survive dismemberment and grow whole new organisms from the sliced-up segments of their formerly unified body. Understanding how these flatworms' immune systems have managed to endure for hundreds of millions of years could hold important insights for modern medicine.

In a new study published June 2 in Cell, the team describes the discovery and names these new cells "ruptoblasts" for their explosive response to a certain hormone.

A postdoctoral researcher first observed these cells while investigating the long-standing mystery in flatworm biology of whether or not they can tell the difference between their own tissues and those of another individual. To find out, she longitudinally sliced the flatworms and fused them together with a separate worm. Although adept at regrowing their own tissues, the researcher noted that these "Frankenstein" worms rejected halves of other worms, similar to how a human body may reject an organ transplant from a donor.

Unlike humans, however, a different cellular defense mechanism sprang into action.

It's this huge inflammatory response. Like there's a fire and an alarm goes off, and the cells just blow up.

Some mammalian cells and bacteria may also do an explosive sort of cell death, but the timescale is really long. They are exploding, but it's more like pores that slowly leak things out over the course of several hours. Ruptosis happens within seconds to minutes.

In a matchup against E. coli bacteria, human kidney cells, and mouse blood cells, ruptoblasts destroyed all three. Yet the authors noted that cell fatalities were limited to the immediate area of the explosion and did not trigger any sort of chain reaction or lingering toxicity. This localized effect holds promise for targeted treatments of bacterial infections or tumours.

Another characteristic that sets ruptoblasts apart from other immune cells, like T-cells or neutrophils, is the fact that they are glandular cells rather than hematopoietic cells, or blood cells produced in the bone marrow. The ruptoblasts seem to figure out a way to amplify their secretion machinery to suddenly and violently release cytotoxic substances in response to activin. A sharp increase in calcium from the endoplasmic reticulum within the ruptoblast helps facilitate the ruptosis.

In searching for these cells in other organisms,  the researchers discovered that they only appear in basal bilaterians like the flatworms, which points to these cells having early evolutionary origins.

The reason these cells were filtered out of modern vertebrate immune systems could be because vertebrates lack the ability to repair other cells after ruptosis occurs, unlike flatworms that are rich in stem cells.

Explosive cytotoxicity of ruptoblasts bridges hormone surveillance and immune defense, Cell (2026). DOI: 10.1016/j.cell.2026.05.008. www.cell.com/cell/fulltext/S0092-8674(26)00567-2

Cutting a photon in two creates an infinite swarm of particles
Attempting to split a single photon using a fast optical shutter does not yield two smaller photons but instead generates a quantum superposition containing infinitely many photons due to disturbances in the electromagnetic field's quantum fluctuations. Locally, the system appears unchanged, but globally, the quantum state becomes highly complex, illustrating the non-classical behaviour of quantum particles.

Isak Cecil Onsager Rukan et al, Truncated photon, Physical Review Letters (2026). DOI: 10.1103/94pm-hp34. On arXiv: arxiv.org/abs/2510.21636

====

Embryonic tissues can behave like fluids or solids to reshape cell fate signals Tissue rigidity in embryonic development is actively regulated by cell-cell adhesion, not cell density, enabling transitions between fluid-like and solid-like states. Increased adhesion induces tissue stiffening, which restricts morphogen diffusion, spatially localizing developmental signals such as Nodal and influencing cell fate. Morphogen signaling can also enhance local tissue rigidity, creating a feedback loop between mechanical and biochemical processes.

Rustarazo-Calvo, L., et al. Adhesion-driven rigidity transition decoupled from density-driven jamming triggers epithelial organization in embryonic tissues., Nature Physics (2026). DOI: 10.1038/s41567-026-03276-6

Camilla Autorino et al, Tissue rigidity phase transition shapes morphogen gradients, Nature Cell Biology (2026). DOI: 10.1038/s41556-026-01954-4

UN warns world to prepare for El Nino extreme weather

There is an 80% probability of El Niño developing between June and August, with a likelihood near or above 90% by November. El Niño is expected to cause above-normal global temperatures and increase the risk of extreme weather events, including drought, heavy rainfall, and heat waves. Climate change does not increase El Niño frequency or intensity but can amplify its impacts. Regional forecasts indicate drier and warmer conditions in parts of Africa, South Asia, and Central America.

News Agencies

A small amount of rare earth metal shapes the environmental impact of magnets
Dysprosium, though comprising only 1–8% of permanent magnets used in electric vehicles and wind turbines, accounts for up to 78% of their environmental impact and 44% of raw material costs due to energy- and chemical-intensive extraction and separation processes. Reducing dysprosium content through improved material efficiency or alternative technologies could significantly lower environmental and economic burdens while decreasing supply chain vulnerability.

Stellina Samuel et al, Mitigating the disproportionate environmental impacts and costs of dysprosium in Nd-Fe-B magnets through material efficiency, Sustainable Production and Consumption (2026). DOI: 10.1016/j.spc.2026.04.006

Single cell transforms into cannibalistic 'supergiant,' swallowing its clones whole

Researchers have discovered a microscopic organism that can transform into a cannibalistic "supergiant" that drastically changes size, shape, and behavior, and abandons filter-feeding to hunt and consume their genetically identical relatives.
Euplotes gigatrox, a newly identified ciliate, can transform from a filter-feeding cell into a larger, cannibalistic "supergiant" that preys on its clonal relatives. This transformation represents a distinct, transcriptionally regulated developmental stage, with altered morphology, behavior, and gene expression. Supergiant formation is rare, environmentally triggered, and may represent a bet-hedging strategy.
The work demonstrates how single-celled organisms are capable of complex, regulated development, which scientists have largely only studied in multicellular animals.
In clonal populations of these organisms where every cell shares the same DNA, a small number of cells can spontaneously develop into supergiants more than twice the length of normal cells, with a broader body shape and a larger mouth.

Rather than filter-feeding on bacteria as normal cells do, supergiants become raptorial predators, running over smaller clonal relatives to capture and swallow them whole at a rate of roughly one prey every 10 minutes.

Ben T. Larson et al, Regulated development of cannibalistic supergiant cells in the ciliate Euplotes gigatrox, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2606891123. On bioRxiv: www.biorxiv.org/content/10.110 … /2025.08.19.671124v2

The hum that only a few can perceive: Potential sources of a low-frequency sound

Some people occasionally hear a low buzzing or humming sound that doesn't have a clear source. An estimated 2–4% of the world's population hear this. Scientists have been trying to figure out for decades where this sound comes from.

Some people find the sound annoying but can live with it. Others can get sick from this low-frequency sound, which is often also experienced as a vibration.

The humming sound isn't easy to hear outdoors, but it often appears indoors—and is most noticeable when you've gone to sleep at night. If you look out the window to see if there is something with a motor in the neighborhood, there's nothing to see.

And others who are in the same place hear nothing.
The hum phenomenon, a persistent low-frequency sound perceived by 2–4% of people, has unclear origins and is reported globally, often in densely populated or coastal areas. Potential sources include human-made infrastructure, natural phenomena, and individual auditory sensitivity, but most cases are not linked to especially acute low-frequency hearing or measurable oto-acoustic emissions. Evidence suggests that for most individuals, the hum is a form of low-frequency tinnitus, while a minority may detect actual external sounds. Improved understanding of low-frequency auditory processing is needed to clarify the phenomenon’s mechanisms.
The phenomenon was first recorded and discussed in the city of Bristol, England in the mid-1970s. Suddenly, the Bristol Evening Post began receiving letter after letters from people who heard an inexplicable sound, and wondered where it came from.

One theory was that the humming sound came from large, industrial fans that were located inside the warehouse of a large department store. However, when the warehouse was closed down a few years later, people continued to hear the sound.

Since then, the sound has been recorded in several places in the United Kingdom, mainly in coastal cities such as Hythe, Plymouth, Southampton, Swansea, but also in London.

The sound is called the hum phenomenon, or simply the hum.
In the 1990s, it cropped up in the United States, first in the city of Taos, New Mexico and in the city of Kokomo, Indiana. The phenomenon has since been recorded worldwide: in Canada, Australia, New Zealand, South Africa and several European cities. The sound is typically reported in relatively densely populated areas.

A couple of years ago, people in the Oslo area also reported an unexplained humming sound, according to the Norwegian Broadcasting Corporation (NRK).
Part 1

Many different theories have been offered to explain the cause of the phenomenon; everything from acoustic pollution from human-made sources to sounds that nature itself makes—as well as conspiracy theories that the sound is produced by the CIA or even aliens.

There are many human sources of low-frequency sound. These can include ventilation systems, heat pumps, traffic noise, windmills and more. Examples of natural sources include the sounds of waves crashing along the coast and wind sweeping through the landscape.

The hum has attracted the interest of hearing and audiology researchers worldwide.
Other explanations for 'the hum'
Military aircraft and submarines
One theory that has been proposed is that the hum relates to sound waves from US military aircraft that use radio frequencies at the lowest end of the spectrum of sound frequencies to communicate with submarines. These aircraft operate at night, and their movements are top secret. The theory may also explain why many "hum sites" are located on the coast.

Amorous fish
The Scottish Association for Marine Science has suggested that the noise in the UK coastal town of Hythe could be caused by the mating call of schools of male plainfin midshipman fish (Porichthys notatus). Amorous male fish make loud sounds, sometimes for hours, to attract females.

Waves, volcanic eruptions, or lightning strikes
In 2015, French researchers suggested that the hum was caused by waves moving along the seafloor. When the waves collide with ridges on the continental shelves, it creates vibrations that are audible to some.

Other researchers have suggested that vibrations caused by volcanic eruptions and earthquakes could be the cause.

Yet another theory points to the lightning strikes that strike Earth every day. Lightning strikes build up a massive electromagnetic charge that creates a resonance between Earth's surface and the ionosphere—much like blowing air over the top of a bottle.

Sensitive brains
Dr. David Baguley, head of the audiology department at Addenbrooke's Hospital in England, has done extensive research into the phenomenon. He believes it is due to sensitive brains that can pick up ultra-low sound frequencies.

He pointed out that our sense of hearing is greatly affected if we experience a lot of stress, and the brain turns up the volume to detect threatening sounds.

Sounds that can be measured
The researchers tested two hypotheses.

One was that the hum can be measured, both from human-made infrastructure and industry and also from nature itself, which creates low-frequency sounds.

Part 2

These sounds have long wavelengths that can travel over great distances.

The first thing the researchers did was test whether the participants had particularly good hearing for low-frequency sounds that are actually known to exist.

Most did not, except for two participants who had better hearing than average at certain low frequencies.
It still means that the hypothesis of having especially good hearing for low-frequency sounds does not hold for most people.
There are differences in hearing thresholds (microstructures) that make it possible for some people to hear sensitively in a very narrow frequency range, for example between 50 and 51 Hertz. These nuances are not captured by conventional hearing tests.
The ear can produce sounds itself
The cochlea in the inner ear itself produces weak sounds with different frequencies, typically between about 500 and 5000 Hertz. These sounds have no function of their own, but are a by-product of a physiological sound amplification process.

Most of us don't hear these sounds. However, a few people can actually hear the sounds that the ear itself produces. And these sounds can be measured objectively
These particular sounds are called oto-acoustic emissions and can be detected by placing a sensitive microphone in the ear canal. In some people, these spontaneous oto-acoustic emissions can be experienced as troublesome tinnitus.

"One hypothesis was that the participants in our group could hear oto-acoustic emissions at low frequencies.
But… the answer was no.
Sounds that cannot be measured
"Then there are people who hear something that cannot be measured objectively.
Tinnitus or ringing in the ears is when you hear a sound in the ear or in the head, which is not caused by an external sound source.

Many people experience tinnitus, either permanently or for shorter periods. These individuals first experience the sounds in their ears as a sound coming from outside.

But as the sound persists, even when they move to other places, they gradually become aware that the source of the sound is not external.
based on what is known about hearing and the tests they conducted on study participants, the best explanation is twofold.

A few people who hear the hum actually have particularly good low-frequency hearing. However, for most people, it may be a form of tinnitus, meaning a sound that originates from inside the auditory system.
Based on the results, although the researchers haven't ruled out cases of physical external sound sources, they suggest that subjective tinnitus in the low-frequency range is often the cause of hearing pulsations of low-frequency sound perceptions.

Bonifaz Baumann et al, On the potential sources of a low-frequency sound percept that only a few can perceive, PLOS One (2026). DOI: 10.1371/journal.pone.0326818

Part 3

Ebola may have spread beyond Africa. How are health authorities responding?
The current Ebola outbreak, caused by the Bundibugyo strain, has resulted in over 900 suspected cases and 223 deaths in the DRC, with limited spread to Uganda and suspected but unconfirmed cases in Italy and Brazil. International health authorities have declared a public health emergency, implemented travel restrictions, and activated safety protocols. Vaccine development is being accelerated, but the risk of global spread remains low with current containment measures.

Similar to the West African outbreak, this latest Ebola outbreak has spread to other continents through travel.

Nine cases and one death have already been reported in Uganda, which shares a border with the DRC.

An American man who tested positive for Ebola while working in the DRC, is in a stable condition after being treated in Germany.

In Italy, authorities are monitoring a traveler who recently returned from the DRC to the city of Cagliari.

According to some reports, Brazilian authorities are investigating two suspected Ebola cases. They are believed to be two travelers, one who returned from the DRC to São Paulo and the other from Uganda to Rio de Janeiro.

Importantly, both suspected cases have been diagnosed with other illnesses. The São Paulo patient presented with fever and was later diagnosed with severe meningitis. The Rio de Janeiro patient tested positive for malaria after developing a cough, chills and diarrhea, but has since tested negative for Ebola.

So for now, no Ebola cases have been confirmed in Brazil. But these suspected cases have prompted the country to activate its Ebola safety protocols, including patient isolation, laboratory testing, and epidemiological investigations.

Meanwhile, several countries have imposed travel restrictions to prevent Ebola from reaching their shores.

original article.

Older brains work harder to stay upright, with nearly 50% longer delay

Aging is known to degrade sensory systems, posing a major challenge to balance control and resulting in an increased risk of falls.
Researchers  have shed light on the brain mechanisms underlying age-related changes in postural control. Using a novel approach, the researchers discovered that older brains must work significantly harder than younger ones to process sensory information and control movement, alongside a substantial processing delay.

Older adults exhibit significantly increased brain activity and nearly 50% longer processing delays when maintaining balance compared to younger individuals. This heightened neural effort is closely linked to greater postural instability and is not solely explained by vestibular decline, indicating that aging brains require more active control to maintain upright posture.

The study demonstrated that when older adults try to stay balanced, their brain activity syncs up closely with how much they wobble, especially in difficult balancing situations—and those who wobble the most have the highest brain activity.
This means that older adults have to actively maintain their balance, using parts of their brain to stay upright. Younger people, on the other hand, stay balanced automatically without having to think about it or use up mental energy.

Furthermore, it takes significantly longer for an older person's brain to process balance information, almost 50% longer. Interestingly, even though many older participants showed inner-ear decline, this wasn't the reason their brains were working so much harder.

Ultimately, this research helps us understand how the aging brain controls balance, and it opens the door for future studies in medicine and neuroscience to help predict and hopefully prevent fall risks in older adults.

Thomas Legrand et al, Aging increases the cortical resources allocated to static balance maintenance, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2524894123

Short videos may hinder learning by fragmenting attention and memory, study finds

Recent technological advances and the introduction of new digital media platforms have dramatically changed how people learn and source information about topics that interest them. Some recent studies have found that while browsing online or scrolling down social media platforms, users tend to spend under one minute on average on individual videos.

Short videos that summarize concepts have thus become increasingly popular among online content creators. More recently, they have also made their way into some educational settings, yet the extent to which they can support learning and help students memorize information remains unclear.

Researchers recently set out to assess the potential of short videos and longer videos as learning resources. Their findings, published in Communications Psychology, suggest that short videos are significantly less effective learning tools than longer videos, as people tend to rapidly forget the information presented in them.

The rapid rise of short videos, particularly social media-style formats characterized by rapid switching and fragmented content, has led to their increasing integration into learning environments, wrote the researchers in their paper, but  their efficacy and neurocognitive impact remain contentious.

The researchers carried out three separate experiments involving over 150 college students. 

The videos that participants watched were either 10 minutes long or spanned between 30 seconds and two and a half minutes. In addition, some participants were explicitly asked to memorize the content of the video, while others were not.

"Across three experiments, memory performance and forgetting rate were assessed under both incidental and intentional encoding conditions, and inter-subject correlation (ISC) analysis was employed to investigate neural response patterns during short video viewing," wrote the authors. "Behaviourally, participants learning with short videos showed significantly lower immediate memory accuracy across encoding conditions and exhibited a higher rate of forgetting when explicitly instructed to remember."

Notably, the study participants watched videos inside a functional magnetic resonance imaging (fMRI) scanner, a machine that maps activity in the brain by tracking changes in blood flow. The research team later analyzed the fMRI scans they collected and tried to uncover neural activity patterns associated with viewing short and long videos.

"At the neural level, ISC analyses revealed that short videos elicited reduced neural synchrony in key brain regions supporting visuospatial attention, episodic memory, and cognitive control, including the superior parietal lobule, precuneus, and middle occipital gyrus," wrote the researchers. "In contrast, short videos evoked higher synchrony in temporal and frontal regions associated with bottom-up attentional processing. Furthermore, functional connectivity analyses indicated that SVs weakened coupling between visual, attentional, and cognitive control networks."

Part 1

The results of the team's experiments suggest that when people watch short videos, they do not remember the information presented to them as well as they would when watching longer videos. In addition, the researchers found that while their study participants were watching short videos, brain regions involved in attention, episodic memory (i.e., memory of events or facts) and cognitive control (i.e., the control of mental functions) were less synchronized.

In contrast, they recorded a greater synchrony between brain regions linked to a focus on external stimuli. Collectively, these observations suggest that the disjointed and rapidly changing quality of short videos interferes with the deep processing of information, making it harder for viewers to memorize contained information or acquire new knowledge.
Together, these findings suggest that the fragmented and rapidly switching nature of typical social media short videos enhances bottom-up attentional capture at the expense of top-down cognitive processes critical for deep learning and long-term memory consolidation," wrote the authors. "This study provides converging neurobehavioral evidence suggesting that SVs viewing in social media contexts is associated with reduced neural synchronization and poorer memory performance."

Meiting Wei et al, Learning via short videos impairs memory accuracy and reduces brain synchrony, Communications Psychology (2026). DOI: 10.1038/s44271-026-00476-x

Part 2

Charred Bronze Age teeth unlock age at death despite cremation

Over 3,000 years ago, the people of Bronze Age Poland burned their dead and placed their ashes in urns, often destroying the intimate records of their lives preserved in their bones. Now, researchers have shown that some of these records can still be read, hidden in the charred roots of their teeth.
The new study, published in Scientific Reports, has shown that microscopic growth lines in teeth may offer a promising alternative to traditional methods, which are often too scrambled or destroyed to provide an age-at-death. Additionally, the researchers made a surprise discovery, finding that growth lines may also provide insights into a person's diet, environment, or some other part of daily life.

"Cremated human remains are often considered extremely difficult to study because fire changes the structure of bones and teeth so dramatically. Scientists now accepted this challenge.
As the tooth root grows, it leaves behind alternating dark and light lines that researchers can use to estimate age at death.
To test whether these lines persisted in ancient cremated remains, the team examined 62 tooth roots from across Poland's Lusatian Urnfield culture, which existed during the Late Bronze and Early Iron Age, roughly 3,300 to 2,500 years ago.

The name 'Urnfield' comes from the widespread practice of cremating the dead and burying their ashes in ceramic urns gathered in large cemeteries, sometimes containing hundreds or even thousands of graves.
For the Lusatian Urnfield culture, cremation was not just common, it was near universal. This makes intact bodies extremely rare, forcing researchers to rely on the broken and burned cremated bones, which often leave unanswered questions.
The researchers sliced the teeth into paper-thin sections for microscopic examination. They then had two researchers count the lines and compare them to surviving alternative age estimates. Not only did the tooth-based estimates align with traditional methods, but they also pinpointed the age to a much narrower timeframe.

Intriguingly, the researchers also noticed the line thickness varied. While previous researchers had suggested this may be the result of differences between males and females, the study authors found the width was likely related to geographic region.

It is possible these differences are related to different environments, diets, or other aspects of daily life that may have affected the teeth. However, the researchers are careful to note that the findings are preliminary.

Agata Hałuszko et al, Methodological validation and inter-site analysis in Late Bronze and Early Iron Age cremations using tooth cementum annulation counts, Scientific Reports (2026). DOI: 10.1038/s41598-026-51841-z

Even years after stroke, spinal cord stimulation could improve arm function

Researchers report the final outcomes of a pioneering pilot clinical trial using electrical stimulation of the spinal cord to improve arm and hand mobility in people with chronic stroke in Nature Medicine.
The study, which was primarily focused on investigating safety and preliminary efficacy, showed that seven participants with profound muscle weakness due to stroke experienced an average 32% increase in arm strength, along with improvement in overall arm mobility and reduction in muscle spasticity.

Importantly, the intervention required fewer than nine hours of movement-based training over four weeks and did not cause discomfort or serious adverse events.

The stimulation works mostly as an assistive technology—when it's on, people can move better. By stimulating the spinal cord, we can immediately allow residual connections between the brain and the spinal cord to work more efficiently, enabling better movement.
Stimulation sends targeted electrical signals to sensory nerve fibers in the spinal cord to enhance communication between the brain and weakened muscles. The same class of device has been used for decades to treat chronic pain, but this is the first time it has been used to restore arm function after stroke.
Researchers observed two distinct types of benefit. Over the four-week study period, all seven research participants experienced immediate improvements in strength when stimulation was turned on, regardless of how severe their impairment was at baseline. Additionally, spasticity—abnormal muscle stiffness caused by stroke-damaged nerve pathways—was reduced in all seven participants.
This approach is designed to rapidly help people move their arms better, even years after a stroke.

Spinal cord stimulation for upper limb motor function in people with chronic post-stroke hemiparesis: a feasibility trial, Nature Medicine (2026). DOI: 10.1038/s41591-026-04435-1

UN report warns AI could soon use 3% of world's electricity and more water than we need to drink

By 2030, AI could consume 3% of global electricity, emit carbon equivalent to the UK, and use more water for cooling than the annual global drinking water requirement. Efficiency improvements may not reduce total resource use due to increased demand, following the Jevons paradox. The report emphasizes the need for responsible AI governance, environmental disclosures, and integration of sustainability into AI development and policy.

original article.