Extraterrestrial life may be slipping past space missions, astrobiologists warn

Current astrobiological detection methods risk false-negative results, potentially missing existing extraterrestrial life due to preservation issues, detection limitations, and insufficiently targeted research strategies. Overlooking such evidence may deprioritize promising environments and lead to premature resource exploitation, risking irreversible loss of undiscovered life. Improved strategies integrating laboratory, modeling, fieldwork, and AI-driven pattern recognition are needed to minimize these risks.

False negatives in the search for extraterrestrial life, Nature Astronomy (2026). DOI: 10.1038/s41550-026-02863-0

How does gold keep its glitter? Researchers uncover why it resists tarnish

Gold has been prized for thousands of years for its enduring shine, but researchers have discovered that gold's resistance to tarnishing depends on more than its chemistry.

In a new study published in Physical Review Letters, researchers found that atoms on certain gold surfaces naturally rearrange themselves into protective patterns that dramatically suppress reactions with oxygen.

The discovery helps explain why gold jewelry and other gold objects can remain untarnished for centuries—and could also point the way toward designing more effective gold-based catalysts for industrial and energy-related applications.

Using computer simulations that predict how atoms and electrons behave, the researchers studied how oxygen molecules interact with two common gold surface structures. They found that without this atomic rearrangement, oxygen molecules could break apart and react with gold much more easily.

Instead, the rearranged surfaces suppress oxygen reactions by a factor of a billion to a trillion, essentially creating a protective atomic-scale barrier that helps gold stay shiny indefinitely.

The findings offer a new explanation for one of gold's best-known properties while also opening the door to potential advances in catalysis.

Anonymous, Role of reconstruction in the inertness of gold towards oxygen, Physical Review Letters (2026). DOI: 10.1103/g3bc-t1qv

Decades after Chernobyl disaster, this radioactive landscape has become one of wildlife's most unlikely strongholds
Today (May 22nd) we are celebrating the International Day for Biological Diversity 2026

The Chernobyl Exclusion Zone and adjacent protected areas, with minimal human activity, exhibit the highest mammal diversity and occupancy rates, including rare and endangered species. Large, strictly protected zones provide superior refuge for wildlife compared to smaller parks or unprotected areas, highlighting the significant positive impact of reduced human disturbance on biodiversity.

There are nearly 8 million species on our planet, yet around 15,000 of them are now threatened with extinction. Even more alarming is the speed at which this is happening. Species today are disappearing at a rate estimated to be 1,000 to 10,000 times higher than the natural extinction rate—in other words, the pace at which species would have vanished if humans weren't here.

It is well documented that human activities and changes in land use for agriculture, industrialization, and urbanization have destroyed several habitats, leading to a decline in biodiversity. Establishing protected areas is a sound way to protect vulnerable species and preserve biodiversity. Compared to unprotected regions, these special zones experience far less human disturbance, reducing stressors such as hunting, habitat loss, and human-animal interactions, allowing ecosystems to recover and thrive.
Some areas are deliberate PAs, while others are devoid of human establishments due to natural or man-made disasters such as the CEZ.

The researchers in this study explored a vast area of about 60,000 km² in northern Ukraine to see how different levels of PAs—CEZs, nature reserves, national parks, and areas with no legal protection—affected where large animals live. They set up 174 motion-sensing camera traps to capture images of wildlife residents in the area and analyzed the images using mathematical tools such as Bayesian occupancy models to estimate occupancy and detection probabilities.

The results revealed that the CEZ and its nearby natural reserve have transformed into an excellent refuge for endangered and shy wildlife. The number and variety of animals in the region were much higher than in smaller parks, owing to the region's strict human-entry rules.

Svitlana Kudrenko et al, The Chornobyl Exclusion Zone as a wildlife refuge: restricted human access shaped mammal recolonization, Proceedings of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rspb.2025.3151

Wildlife is watching us, too—and changing behaviour in response

Analysis of GPS-tracked movements of 37 bird and mammal species across the U.S., combined with mobile phone and satellite data, shows that over 65% of species alter their behaviour in response to human presence, with effects varying by species and habitat context. Some animals reduced their range to avoid humans, while others expanded it or exploited human-associated resources. These findings indicate that both habitat alteration and direct human presence influence wildlife, suggesting conservation strategies should address not only habitat loss but also the timing and intensity of human activity.

Ruth Y. Oliver et al, Interacting effects of human presence and landscape modification on birds and mammals, Science (2026). DOI: 10.1126/science.adq3396. www.science.org/doi/10.1126/science.adq3396

Why some antibiotics fail in the body—pH conditions can dramatically change how bacteria respond

When researchers test whether an antibiotic will work, they usually do so in a controlled laboratory environment. But when an infection happens inside the human body, things aren't so clean and tidy. New research found that even a slight change in acidity may dramatically shift how bacteria respond to treatment.
The study is centered around Klebsiella pneumoniae, a major cause of deadly infections and one of the world's most antibiotic-resistant pathogens.

Klebsiella pneumoniae exhibits up to 64-fold increased resistance to beta-lactam antibiotics under mildly acidic conditions (pH 5), due to the expression of alternative cell wall synthesis proteins (PBP2PARA, PBP3PARA, and PBP1b). Silencing these proteins reduces resistance, indicating their critical role in antibiotic survival at low pH. These findings highlight the need to assess antibiotic efficacy under physiologically relevant conditions.
Researchers set out to learn what happens to antibiotic resistance when K. pneumoniae grows in mildly acidic conditions like those found in parts of the human body during an active infection. What they found was that when grown at a pH of 5, the bacterium became up to 64 times more resistant to beta-lactam antibiotics, the most widely prescribed treatment for infections.

These beta-lactams work by shutting down the cell wall-building proteins in the bacterium known as PBPs. Without these, the bacterium can't properly construct its cell wall or divide, and it eventually dies. However, in addition to these PBPs made at neutral pH, it appears that K. pneumoniae has a reserve team ready to step up when conditions get acidic.
K. pneumoniae has a backup set of cell wall-building proteins that come online as the cell enters, in this case, an acidic environment.
PBP2PARA and PBP3PARA are duplicate copies of essential cell wall synthesis genes, and when conditions turn acidic, these alternate versions of cell building and division proteins are expressed.

This was surprising, given that past research on pathogen resistance had been done on a model organism, E. coli, which does not have a backup team of proteins. "This sets up a lot of implications for reevaluating and rethinking how we're assessing antibiotic resistance in pathogens.
Additionally, they identified another duplicate cell wall synthesis protein, PBP1b, whose activity appeared to be important for stress response during growth at low pH. These results suggest that these duplicate proteins may be important for helping the bacterium survive against antibiotic treatments under acidic conditions.
To confirm this, researchers silenced these proteins and they found that when these proteins weren't made, the cell lost much of its antibiotic resistance. PBP1b and PBP3PARA make the most impact on resistance, so their presence is most critical to the cell at low pH.

In the face of antibiotic resistance, these findings offer a warning and a potential path forward.

Sarah Beagle et al, Acid-dependent beta-lactam resistance in Klebsiella pneumoniae is mediated by paralogous class B PBPs and the class A PBP, PBP1b, mBio (2026). DOI: 10.1128/mbio.00092-26

Overpopulation can impair fertility. A new study explains why

Scientists have reported it for decades: overpopulation can impair reproduction. Crowded chickens lay fewer eggs. Crowded mice have smaller broods. In humans, several studies have associated increased population density with reduced fertility.

External factors, such as resource scarcity and social influences, undoubtedly play a role. But researchers have long suspected that intrinsic, biological mechanisms may also be at play as an evolutionary tool to keep populations in check.

New research, published this month in the journal Nature Communications, identifies one key mechanism. It found that overcrowded animals secrete a chemical messenger that can damage eggs, impair embryos and cause genetic mutations in offspring for generations to come.
Overcrowding in animals triggers secretion of a cysteine protease enzyme (CPR-4/Cathepsin B), which damages DNA in germ cells, increases genetic mutations, reduces fertility, and causes developmental defects in offspring. These mutations can be inherited across generations. Silencing the enzyme prevents these effects, indicating its central role in crowding-induced reproductive impairment. Implications for humans remain to be determined.

Bin Yu et al, Cathepsin B protease mediates high population density-induced mutagenesis to drive genome evolution and competitive growth, Nature Communications (2026). DOI: 10.1038/s41467-026-72521-6

Why energy fades with age: Missing membrane lipid may destabilize mitochondria

Why do cells age—and why do we lose our energy and vitality as we get older? This question is one of the central challenges of modern biomedicine. The focus is particularly on mitochondria—tiny cellular organelles long known as the cell's powerhouses but now understood as dynamic control centers that not only produce energy, but also coordinate cellular communication, adaptation, and many of the processes essential for life.
They supply us with the energy that our body needs for movement, growth, and repair processes. But as we age, these powerhouses begin to slow down. It has long been known that their function declines with age.
Age-related decline in cellular energy is linked to reduced phosphatidylcholine synthesis, leading to destabilized mitochondrial membranes and impaired mitochondrial network function. Supplementation with phosphatidylcholine or its precursor choline restores mitochondrial structure and energy production in aged cells, indicating that aspects of mitochondrial and systemic aging are modifiable through targeted metabolic interventions.
For a long time, it was assumed that genetic damage within the mitochondria themselves was primarily responsible. A study now published in Nature Communications by an international research team.
provides a surprising answer to this question: A key factor appears to be the imbalance in the structure of the mitochondrial network, which is caused by the absence of a major lipid in the membrane composition.

The focus is on phosphatidylcholine—a fundamental lipid that is a major component of biological membranes. It ensures that membranes remain flexible and can dynamically reorganize themselves. Precisely this property is crucial for so-called "mitochondrial fusion"—a process in which individual mitochondria merge into networks. These networks are necessary for cells to distribute key molecules—such as cellular energy equivalents, metabolic products, DNA, and signaling molecules—and facilitate their exchange, thereby preventing imbalances and replacing damaged components.

The study shows that the body's production of phosphatidylcholine declines with age, leading to increased fragmentation and dysfunction of mitochondrial membranes. When genes involved in phosphatidylcholine synthesis were deactivated in young worms, their mitochondria in the cells quickly began to look "aged."

The researchers were particularly fascinated by how closely these changes resembled the mitochondria typically observed in chronologically old organisms. Even more striking was the observation that the mitochondria regained a more youthful structure within just two days when the worms were fed phosphatidylcholine or its precursor, choline.

The most important finding of the study, however, lies in the reversibility of aging-associated failures: through a targeted increase in phosphatidylcholine levels—for example, via diet.

Tetiana Poliezhaieva et al, Aging-associated decline of phosphatidylcholine synthesis is a malleable trigger of natural mitochondrial aging, Nature Communications (2026). DOI: 10.1038/s41467-026-71508-7

part 2

Calcium and vitamin D supplements offer little to no meaningful benefit on fracture, fall prevention, review concludes

Calcium, vitamin D, or combined supplements offer little to no clinically meaningful benefit for fracture and fall prevention in most older people, finds an in-depth review of the latest evidence published by The BMJ.
Calcium, vitamin D, or combined supplementation provides little to no clinically meaningful benefit for preventing fractures or falls in most older adults, based on moderate to high certainty evidence from 69 randomized controlled trials. These findings suggest routine supplementation is not supported for fracture or fall prevention, and recommendations should be re-evaluated.

Calcium, vitamin D, or combined supplementation to prevent fractures and falls: systematic review and meta-analysis, The BMJ (2026). DOI: 10.1136/bmj-2025-088050

The Great Pyramid of Giza has survived 4,500 years of Egyptian earthquakes

The Great Pyramid of Giza in Egypt has survived more than 4,500 years. Earthquakes have repeatedly shaken the region, including the magnitude 5.8 Cairo earthquake in 1992, which dislodged some of the pyramid's outer casing stones. Yet the main body remained essentially intact.

The Great Pyramid of Giza exhibits natural vibration frequencies (2.0–2.6 Hz) distinct from the surrounding soil (0.6 Hz), reducing the risk of resonance during earthquakes. Structural features such as a broad base, low center of mass, and massive masonry contribute to its stability. While these characteristics enhance seismic resilience, there is no direct evidence they were intentionally designed for earthquake resistance.
What the research found
The researchers measured the pyramid's vibrations in ambient conditions. They found that its natural frequencies—the frequencies at which it "prefers" to vibrate—are mostly between about 2.0 and 2.6 hertz (cycles per second). The surrounding soil has a much lower dominant frequency, around 0.6 Hz.

If earthquake shaking matches a structure's natural frequency, the motion can be amplified. This is called resonance, and it can be catastrophic.

The study also reports reduced vibrations near the so-called relieving chambers above the King's Chamber. These chambers are understood to redirect the enormous weight of stone above, and may also affect how vibration energy moves through the pyramid.

These findings suggest some behavior that may be helpful during an earthquake, including a frequency mismatch between the pyramid and the soil. But they do not, by themselves, prove people intentionally built the pyramid to be resilient to earthquakes.
When shaking from an earthquake happens at a frequency that matches a structure's natural frequency, it can cause resonance.

So the measured difference matters. If the ground and the structure vibrate at different rates, the ground is less likely to feed energy efficiently into the structure.

But this addresses only one possible mechanism of earthquake damage. There are plenty of examples of structures performing poorly in earthquakes, even though there was a frequency mismatch to the soil below.
The pyramid may not have been intentionally designed for resilience in an earthquake. But its survival is not an accident, either.

From an engineering point of view, it has many favorable features: a broad base, low center of mass, tapering form, symmetrical plan, competent limestone foundation and massive masonry load path. It is squat, stiff and well-founded rather than tall, slender and flexible.

The safest conclusion is that the builders made excellent empirical engineering choices. Those choices may have been driven by construction experience, observation, structural necessity, or cultural intent. Their seismic benefits may be real without being the original purpose.

The Great Pyramid's survival is not magic, and it is not proof of ancient seismic design.

Mohamed ELGabry et al, Architectural and geotechnical aspects affecting earthquake resilience for the antique Egyptian Khufu pyramid, Scientific Reports (2026). DOI: 10.1038/s41598-026-49962-6

A father's obesity affects his children's metabolism

The scientific literature already contains robust evidence that obesity, whether maternal or paternal, can lead to metabolic changes in offspring that increase their risk of developing diseases. A new study published in the journal Nature Communications reveals the mechanism by which this "inheritance" is transmitted to the embryo by the father via the sperm.

Paternal obesity leads to increased levels of let-7 microRNAs in adipose tissue and sperm, which are transferred to the embryo and inhibit DICER enzyme production, causing mitochondrial dysfunction and persistent metabolic impairment in offspring, particularly males. Weight loss in obese fathers normalizes let-7 levels and prevents transmission of these metabolic defects, a finding validated in both mice and humans.

In experiments with mice, the authors observed that the offspring of obese males were born at a normal weight. However, as the days passed, they exhibited glucose intolerance and insulin resistance, which can lead to type 2 diabetes. This condition is called "silent metabolic dysfunction."

The good news is that when the parents lost weight, the "marks" left by obesity in the semen disappeared—a finding that was later validated in human analyses.

Chien Huang et al, Male obesity causes adipose mitochondrial dysfunction in F1 mouse progeny via a let-7-DICER axis, Nature Communications (2026). DOI: 10.1038/s41467-026-69686-5

Head Blows During Football Tied to Changes in Gut Microbiomes

Small head impacts that did not cause any symptoms were linked with microbial diversity shifts in athletes, offering clues into potential biomarkers for head trauma.
While scientists have previously shown that concussions in football players disrupt their gut microbiomes, researchers did not know whether non-concussive head impacts led to a similar effect.
Recently, the team of researchers found that non-concussive head impacts that did not cause any clinically detectable symptoms in six football players were correlated with changes in the gut microbiome. Their findings, published in PLoS One, offer early clues in identifying gut microbiome-associated biomarkers for assessing the severity of head trauma.

Pelland ZJ, et al. Non-concussive head impacts sustained during American football corr.... PLoS One. 2026;21(5):e0345651.

Bees get distracted just like us, hinting at their own awareness

Even tiny insects need to focus. In a recent study, honey bees—usually quick to learn which scent means sugar—completely flubbed the task when a flashing light joined the party. This surprisingly human-like breakdown suggests that these little buzzers might engage something like awareness when connecting cause and effect. 

Bees are famous for their smarts. Prior work has shown that honey bees can learn complex tasks, from recognizing faces to navigating mazes. In the lab, researchers often use classical conditioning to test bee memory: An odor (conditioned stimulus) is paired with sugar (unconditioned stimulus). If the two overlap in time (delay conditioning), bees learn quickly.

However, if the sugar arrives a few seconds after the smell ends (trace conditioning), the task becomes much harder. In fact, scientists have found that bees can learn delayed tasks easily, but trace tasks falter when attention is disrupted. In other words, linking a scent to a reward across a time gap seems to need something like attention or "awareness," much as it does in humans.

In the new study, researchers took this idea further by adding a twist called reversal learning. First, bees were trained to extend their proboscis (a feeding reflex) to odor A because it predicted sugar (A⁺), but not to odor B (B⁻). After a few trials, the rule was flipped: Now B would give sugar (B⁺) and A would not (A⁻). This tested flexibility—could the bee unlearn A⁺ and learn B⁺ instead?
The scientists ran this reversal task under two conditions: delay (scent and reward overlap) and trace (reward delayed). In both cases, bees eventually mastered the new rules, but those in the trace group learned more slowly and less reliably. This was expected: Bridging the gap in trace conditioning is tougher.

Part 1

Next, the team introduced a visual distractor, a simple flashing light, during the reversal phase. The effect was dramatic and different for each group. Delay-conditioned bees under the light started responding to both odors (an A⁺B⁺ pattern), as if they had stopped telling the scents apart. Trace-conditioned bees did the opposite: they responded to neither odor (an A⁻B⁻ pattern). In essence, the distraction caused one group to over-generalize and the other to freeze.

This split result is telling. In humans, losing awareness of the link between events can cause similar failures: either broad overreaction or blanking out, depending on the task.

The researchers explain, "Awareness of stimulus contingencies appears necessary for solving reversal learning under a trace-conditioning regime."

In other words, when the bee needs to link scent and reward across time, something like awareness is needed to keep track. The flashing light likely scrambled that process, so the bees' responses collapsed in opposite ways.
The way these bees behaved under distraction hints at more than automatic learning. As the authors state, "These findings provide evidence that bees engage awareness-like processes during trace reversal learning, highlighting cognitive processing in an insect."
That's a bold claim. It suggests that bees aren't just Pavlovian robots, but can flexibly apply attention when tasks demand it. Importantly, the experiment measured only reflexive feeding responses, not anything directly like a verbal report of awareness. Still, the binary failure patterns (respond to all vs. none) align with the idea that trace learning invokes something akin to consciousness.
Part 2

Of course, caution is needed. Bees can't tell us what they feel, and all we have are behavior scores. The scientists note they didn't record bee brain signals or thought patterns, so they stop short of claiming bees are "conscious" in our sense. And the proboscis extension (yes/no) is a simple measure—there might be subtle changes it missed. But the unexpectedly human-like breakdown under distraction strengthens the case that insects, at least, employ more than simple reflexes when they are learning tough tasks.

These results add fuel to debates on animal minds. If a bee shows "awareness-like" learning, does it have an inner experience? Even if it doesn't think as we do, the study reveals surprising flexibility in a tiny brain. In practical terms, a better understanding of bee cognition could help beekeepers and ecologists. For example, it suggests that environmental distractions (pesticides, lights, noise) might interfere with a bee's learning in the wild, affecting foraging or navigation. It also shows a model for designing AI and robots: even small neural networks can use attentional gating to solve temporal puzzles.

The study's authors emphasize that it's just a start. Future work could look at bee brain activity during such tasks or test other species to see how widespread these effects are.
For now, a striking quote from the paper stands out: "Our findings in honey bees echo [human] results: awareness of stimulus contingencies appears necessary for solving reversal learning under a trace-conditioning regime."

Catherine Macri et al, Attention, awareness and flexibility in honeybees: divergent effects of distraction on delay versus trace reversal learning, Proceedings of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rspb.2025.2891

Part 3

A distinct communication subspace in the brain turns goals into actions

Humans continuously adapt their actions and behaviours in response to changes in their surrounding environment. Past neuroscience studies suggest that this adaptation process relies on the brain's ability to translate abstract goals or rules into specific physical actions or behaviours, yet its neural underpinnings have not yet been clearly elucidated.

Adaptive behaviour relies on the ability to translate abstract rules and goals into actions suited to the current context.

Researchers  recently carried out a study aimed at better understanding how context-related mental representations in a region of the brain known as the prefrontal cortex (PFC) are transformed into movement plans, which are processed in the primary motor cortex (M1). Their findings, published in Nature Neuroscience, led to the identification of a distinct communication subspace that links the PFC and M1, through which contextual information that can inform the planning of actions is transmitted.

Neha Binish et al, A communication subspace relays context-dependent actions from human prefrontal to motor cortex, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02290-4.

The 700-million-year history of our blood cells

Almost all animal species—including humans—have blood cells, but between different species our blood tells different stories. The lineage and components of blood cells vary widely, and this variety is a testament to how animals have evolved to protect themselves from infectious diseases.
Comparative gene expression analysis across animal species indicates that blood cells originated approximately 700 million years ago, with macrophage-like cells as the earliest form, derived from single-celled ancestors. The evolutionary lineage shows mast cells, T cells, red blood cells, and B cells subsequently branching from these ancestral macrophages, reflecting the deep evolutionary history of blood cell differentiation.
Thanks to advances in hematology and immunology, we now have detailed knowledge of the components and functions of both human and mouse blood cells. However, their evolutionary history has remained largely unknown. This inspired a team of researchers to investigate when and how blood cells originated, and how they diversified. The work appears in Proceedings of the National Academy of Sciences.

The team began by developing a new analytic method to compare gene expression profiles across various cell lineages and animal species. With this, they were able to construct phylogenetic trees of cell lineages and estimate the evolutionary history of these lineages in animals. They also included unicellular organisms in their comparison in order to trace the origin of blood cells back to possible single-celled ancestors.
Among the various lineages of human blood cells the team observed, macrophages showed the most striking resemblance to unicellular organisms, suggesting that early blood cells were macrophage-like. They then traced the gene FOS—commonly expressed in blood cells across animal species—back to a single-celled ancestor that lived 700 million years ago, suggesting that the first blood cells emerged around the same time as the onset of multicellular animals.

This finding implies that early animals generated the first blood cells by repurposing genetic material inherited from single-celled progenitors. The team's analysis also revealed that mast cells branched off from the macrophages, and that prototypic T cells and red blood cells subsequently branched off from the mast cells. Furthermore, prototypic B cells branched off from the macrophages after the segregation of mast cells.
Ultimately, the scientists were able to reconstruct the family tree of blood cells over a 700-million-year span, revealing that evolutionary history has been imprinted in our bodies as differentiation pathways of these cells. This work illustrates that the blood and immune cells circulating in our bodies can be considered a successful extension of the legacy left to us by our single-celled predecessors.
The researchers expect that the method developed in this study could help unravel the evolutionary origins of diseases such as cancer, leading to a better understanding of mechanisms and the development of new treatments.

Animals have expanded the evolutionary legacy of unicellular ancestors in blood cells, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2528110123

Homo erectus may have left a genetic legacy in people today

Analysis of ancient tooth enamel proteins from East Asian Homo erectus fossils reveals a unique amino acid variant shared with Denisovans and present in modern Southeast Asian and Oceanian populations, indicating gene flow from H. erectus to Denisovans and subsequently to modern humans. These findings support a model of frequent interbreeding among archaic hominins, resulting in modern human genomes as mosaics of multiple ancestral lineages.

https://www.nature.com/articles/s41586-026-10478-8

Short exposures to common air pollutants have distinct impacts on lung function and brain activity, study shows
New research by a collaboration of scientists has revealed that common indoor and outdoor air pollutants can alter both brain and respiratory function within just four hours of exposure, offering key insights into how air pollution impacts brain health and may contribute to dementia risk.
Air pollution can influence the brain either directly, when harmful particles enter the brain, or indirectly, through inflammation in the lungs which then impacts the brain. Neurological diseases have been increasing for decades, and there is now a greater understanding that long-term exposure to elevated levels of air pollution is associated with dementia risk. While we often categorize air quality by the total amount of particulate matter, this new study demonstrates that the source of the pollution matters as much as the quantity.

Short-term exposure to different air pollution sources produces distinct effects on lung function and cognitive performance, even at identical particulate concentrations. Limonene-derived aerosols most strongly impaired lung function, while diesel exhaust and woodsmoke altered cognitive processing speed and executive function. These findings indicate that pollutant source and composition, not just total particulate matter, critically influence health impacts.
The findings published in npj Clean Air reveal that different pollutant sources produce varied health effects even at identical concentrations in the air. Recognizing these differences is essential for shaping public policy, improving clinical diagnoses and developing protective strategies. With an ever-growing aging population and increasing urbanization, the public-health imperative to mitigate neurological disease becomes increasingly urgent.
After 60 minutes of exposure, and a four-hour break, researchers assessed respiratory function alongside working memory, selective attention, socio-emotional processing, psychomotor speed and motor control.

Respiratory responses showed limonene had the greatest impact on lung function, followed by woodsmoke, diesel exhaust and finally cooking emissions.
Cognitive function was also found to be significantly influenced by pollutant sources. Diesel exhaust and woodsmoke improved processing speed; limonene-derived secondary organic aerosol enhanced working memory compared to cooking emissions; and diesel exhaust showed signs of impairing executive function. The team suggests that the presence of nitrogen oxides (NOX), known as vasodilators, may alter blood flow to the brain and contribute to these mixed cognitive effects.
Given that measurable effects were detectable after a brief 60-minute exposure, the findings suggest that prolonged exposure could have significant long-term consequences for brain health.

Thomas Faherty et al, Neurological and respiratory outcomes of the HIPTox controlled double-blind air pollution exposure trial, npj Clean Air (2026). DOI: 10.1038/s44407-026-00068-3

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.
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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.
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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...

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original article.