Fish oil supplements may not prevent Alzheimer's-related decline, clinical trial suggests
A two-year randomized, placebo-controlled trial in 365 older adults at elevated Alzheimer’s risk found that 2,000 mg/day DHA increased cerebrospinal fluid DHA by 17% but did not improve cognition or memory, nor prevent hippocampal atrophy. Results do not support high-dose fish oil supplements for Alzheimer’s prevention; broader lifestyle measures remain primary for risk reduction.

eBioMedicine (2026). www.thelancet.com/journals/EBI … (26)00198-2/fulltext

Nonsurgical procedure provides lasting relief for knee pain, finds study

Osteoarthritis is the most common form of arthritis. It causes inflammation, stiffness, reduced mobility and sensory nerve pain. According to the World Health Organization, knee osteoarthritis affects more than 365 million adults worldwide and is one of the leading contributors to disability.

Embolization of abnormal blood vessels using rapidly resorbable gelatin-based microspheres is safe and provides significant, lasting pain relief and functional improvement for patients with osteoarthritis-related knee pain, according to a new study published in Radiology.
Genicular artery embolization (GAE) is an emerging minimally invasive treatment that targets abnormal blood vessels using superselective embolization.

In an osteoarthritic knee, these abnormal vessels build up around the joint and drive inflammation and pain. During GAE, an interventional radiologist guides a thin catheter directly to each affected vessel and injects tiny particles to block it, calming the inflammation and easing the pain without surgery.
In their trials, researchers noticed a significant drop in pain and a significant increase in function, including sports and recreation and daily activity.
"Most importantly, their quality of life significantly increased."
Genicular artery embolization with rapidly resorbable gelatin microspheres in 194 patients with knee osteoarthritis was technically successful in all 239 procedures, with only mild, self-limited adverse events in 6.7%. Pain scores decreased from 7 to 3 over 12 months, functional and quality-of-life scores improved beyond clinically important thresholds in 80%, indicating durable, clinically meaningful benefit.

Florian Nima Fleckenstein et al, Genicular Artery Embolization Using Rapidly Resorbable Gelatin-based Microspheres for Osteoarthritis-related Knee Pain, Radiology (2026). DOI: 10.1148/radiol.253312 , pubs.rsna.org/doi/10.1148/radiol.253312

Jumping gene caught moving between species in first direct observation

Genes are not passed on exclusively from parents to their offspring. Some are mobile and can also jump to other species, as researchers have now shown. The direct observation of a jumping gene provides the first evidence that such genes can transfer from one species to another—from predator to prey. The study is published in the journal Scientific Reports.

Jumping genes are parasites in the genetic material of bacteria, plants, animals and humans. They are released into the cell as small RNA molecules from ribonucleic acid (RNA) and possess complex mechanisms for inserting themselves into other parts of the genetic material within the cell, thereby often conferring new properties on the cell and accelerating evolution. There are also jumping genes that free themselves from the RNA using an RNA enzyme. These ribozymes, or self-splicing introns, are a special group of jumping genes.

It is more difficult for a gene to jump into another cell or another species. Phylogenetic analyses of genes show that such jumps have taken place. Until now, it had been assumed that, for this to happen, the jumping genes traveled as 'hitchhikers' in the genomes of plasmids or viruses. Now,  researchers have made  this surprising observation.

Mobile self-splicing intron RNA from the predatory bacterium Candidatus Velamenicoccus archaeovorus was directly visualized in both predator cells and dead Methanothrix soehngenii cells, demonstrating horizontal transfer from predator to prey. The intron persists as stable circular RNA, indicating a plasmid- and virus-independent route for interspecies gene transfer that can accelerate microbial evolution.

Jana Kizina et al, Mobile intron RNA from a bacterial predator accumulates in dead archaeal cells, Scientific Reports (2026). DOI: 10.1038/s41598-026-51721-6

Mars-like conditions fail to kill some Earth pathogens, experiments suggest

Microorganisms from our planet could survive on celestial bodies where water is present, such as Mars. That is the conclusion of researchers after experiments with simulated space conditions. Our immune system reacts less effectively to pathogens that have undergone such a simulated space journey.
Earth extremophiles, especially yeasts, withstand simulated lunar, Martian, and icy moon conditions via enhanced DNA repair and protective responses. Human pathogens such as Klebsiella pneumoniae survive Mars-like exposure, become smaller, and elicit weaker immune cell responses. Simulated lunar and Martian regolith damage lung barriers and promote infection more than terrestrial sand.
Researchers also studied several well-known human pathogens, such as the bacterium Klebsiella pneumoniae, which can cause pneumonia. They observed that these pathogens shrank after a simulated trip to Mars, yet survived it. In laboratory experiments, immune cells from human blood responded less strongly to these shrunken pathogens.

This is important news for astronauts, who already face declining health in space and must therefore be extra cautious about infections. Space travel places heavy strain on the immune system because of the lack of a normal day-night rhythm, poor diet, disrupted gut function, DNA damage from radiation, limited social interaction and confinement in a small space.
In addition, astronauts must be wary of dust (regolith) from the moon and Mars.
Material from Mars, and even more so from our moon, damages the protective layer of the lungs and causes infections. Earth material usually does not.

Tommaso Zaccaria, Dissertation title: Life beyond Earth: microbial survival and immune health in space. Supervisors: Prof. Dr. M.G. Netea and Prof. Dr. M.I. de Jonge. Co supervisors: Dr. P. Rettberg and Dr. K. Beblo Vranesevic (both German Aerospace Center, Germany).

Spontaneous and voluntary laughter come from two different brain regions, researchers reveal
Laughter is a universal social signal that connects us with others.
In a review published in Trends in Neurosciences, researchers analyze reports from medical procedures in which the brain is electrically stimulated in awake patients. Laughter can be an unintentional byproduct of these stimulations, allowing scientists to pinpoint laughter-evoking brain areas.

By examining these reports and other clinical and animal studies, the authors describe two distinct networks in the brain for laughter: one that elicits spontaneous outbursts, and another that produces voluntary, conversational laughter.

Researchers have long observed two types of laughter in healthy humans.

Spontaneous, involuntary and sometimes uncontrollable laughter can be associated with certain types of seizure disorders, mood disorders, Alzheimer's disease and schizophrenia.
The second kind is volitional laughter. That's most of the laughter you encounter. It's timed incredibly precisely. If you look at people having a conversation, they will laugh together at the end of a sentence and then breathe together.

When people are talking to each other, volitional laughter starts and stops really quickly. This type of coordination points to a degree of control that is lacking in spontaneous laughter.

To tease apart the brain circuitry underlying these two types of laughter, the team turned to reports of presurgical brain stimulation in epilepsy patients. During these procedures, clinicians identify brain regions to target for surgery by electrically stimulating parts of the brain while patients are awake. These probes often unintentionally evoke laughter, and patients are able to describe their feelings in real time.

The authors analyzed these reports, along with other clinical and animal studies, to propose two distinct networks underlying spontaneous and voluntary laughter.

The spontaneous network consists of brain regions involved in motor control and emotional regulation, including the pregenual anterior cingulate cortex, nucleus accumbens and the temporal pole. Stimulating these regions produces laughter accompanied by enhanced mood, euphoria and mirth.

The voluntary network comprises areas involved purely in motor control of laughing and smiling, such as the rolandic operculum, globus pallidus and presupplementary motor area. Stimulation of these regions evokes laughter without positive emotions.

The authors suggest that the spontaneous network is a more evolutionarily ancient pathway that arose in animal "rough-and-tumble" play, with laughter-like vocalizations serving as a signal to prevent aggression and promote social bonding. This hypothesis is consistent with recent discoveries that several mammalian species produce laughter-like vocalizations during social interactions.

The voluntary network, on the other hand, overlaps with brain regions that produce speech, supporting the idea that it controls more purpose-driven, conversational laughter.

The neural basis of laughter, Trends in Neurosciences (2026). DOI: 10.1016/j.tins.2026.05.002

Discovery of 3 severe pneumonia subtypes could lead to tailored treatments

Pneumonia is the most common infectious cause of death worldwide, responsible for an estimated 2.5 million deaths a year. In severe cases, patients may need to be admitted to an ICU and given mechanical ventilation. Severe pneumonia accounts for six in 10 infections managed in intensive care, and spread of the infection within ICUs is a significant concern.
Severe pneumonia is usually diagnosed through a combination of symptoms, imaging and blood tests. Symptoms typically include fever or hypothermia, low oxygen levels, breathing difficulties and confusion.

Doctors have long struggled to understand why patients whose condition looks similar clinically can have very different recoveries. Some respond quickly to treatment, while others remain critically ill for weeks or even die.
Researchers have now shown that severe pneumonia has three different subtypes, helping explain why some patients in intensive care units (ICUs) recover from their illness faster than others, while for other patients the disease can be life-threatening.
Their findings could in future help inform tailored treatments, allowing individual patients to receive the most appropriate therapies.
Even though doctors are able to treat the initial infection, many patients with severe pneumonia still struggle to come off the ventilator and can develop lung failure. Therapies to tackle inflammation in the lungs have had mixed results in clinical trials—some suggest they are beneficial, others that they're harmful.
The current approach of classifying patients by their clinical syndromes—sepsis, acute respiratory distress syndrome and so on—without looking at the underlying biology risks missing what's key. Instead of asking 'Does this patient have pneumonia?' doctors should be asking 'What's the inflammatory pattern in this patient's lungs to correctly treat them?'"

Instead of relying only on blood tests or scans, however, the Cambridge team analyzed immune cells, inflammatory signals and gene activity in fluid taken from the lungs of the patients. They discovered that there are three distinct biological types—or "pneumotypes"—of severe pneumonia, none of which could be reliably detected using standard blood tests, even though they were strongly linked to how patients recovered.
Part 1

The most common pneumotype—accounting for almost half (49%) of cases—was characterized by immune suppression, significant damage to the lining of the lungs and bleeding in the alveoli (tiny air sacs within the lungs). There were fewer signs of inflammation, which may explain why treatments targeting inflammation can fail or even harm some patients.

The second pneumotype—accounting for just under a quarter (23%) of cases—was characterized by a balanced immune response and active repair of damage to the lungs. Patients were most likely to recover faster from this pneumotype and require the shortest time on the ventilator, even though they initially looked just as ill as the others.

Patients with the most dangerous pneumotype—the one that most resembles "classic" pneumonia—spent the longest on mechanical ventilation and had prolonged critical illness. They had severe and persistent inflammation, with a flood of immature immune cells in the lung. This group may be most likely to respond to anti-inflammatory therapies, the research team said.
Severe pneumonia is not a single disease, but several biologically distinct conditions that happen to look alike. This helps explain why 'one-size-fits-all' treatments—including some immune-modulating drugs—have often failed in clinical trials.

The tests used to determine the pneumotypes are too complex to enable rapid classification, but the researchers hope to develop a simplified tool that could help them stratify the patients and ultimately offer tailored treatments.

Pulmonary inflammation in severe pneumonia is characterised by compartmentalised and mechanistically distinct sub-phenotypes, Nature Communications (2026). DOI: 10.1038/s41467-026-74190-x

Scientists design a clay that can prevent fruits and vegetables from rotting too quickly
Chemically modified natural clay with enlarged pore structures can strongly adsorb and retain ethylene gas, slowing fruit and vegetable ripening without added toxicity. The work clarifies the physicochemical mechanisms governing ethylene uptake, enabling optimization for industrial food packaging. Potential applications include ethylene-scavenging pads to reduce food waste and improve flavour.

K. Kovalchuk et al, Disentangling interlayer confinement and pore surface adsorption in functionalized smectites for tunable ethylene gas capture, Applied Surface Science Advances (2026). DOI: 10.1016/j.apsadv.2026.101010

Contact lenses can repair themselves with just one hour of UV light exposure

A methacrylate hydrogel cross-linked with disulfide bonds and coated with an antibacterial, anti-scratch layer enables self-healing contact lenses. UV exposure at 365 nm for 1 hour induces disulfide exchange, efficiently repairing scratches with minimal loss of transparency. The coated lenses show soft-contact-like water retention and high abrasion resistance, but require further stability and regulatory evaluation.

Jung-Hyun Choi et al, Room-Temperature UV-Induced Self-Healing Hydrogels with Antifouling and Antiscratch Surfaces for Soft Contact Lenses, ACS Applied Polymer Materials (2026). DOI: 10.1021/acsapm.5c04803

White barn owls may use moonlight to startle prey
Male barn owls with white plumage orient flights toward the moon and preferentially hunt in brighter, unshaded areas, increasing exposure of their bright feathers to prey. Dive-level capture probability is similar across colors and light levels, but white males capture more prey per hour on bright nights, supporting a startle rather than background-matching function of whiteness.

Kim Schalcher et al, Barn owl color morphs hunt differently in moonlight, Current Biology (2026). DOI: 10.1016/j.cub.2026.05.020

Hope for spinal injuries as pigs walk again after experimental gel treatment for severed spinal cords

In humans and other mammals, spinal cord injuries can be devastating, leading to permanent loss of movement, sensation and bladder control. When severed axons (the long fibers that carry messages between nerve cells) cannot regrow, a dense scar forms, preventing nerve signals from passing the injury site.

But the situation is different for some primitive invertebrates, which can rapidly reconnect severed nerves by fusing them. Inspired by this natural phenomenon, scientists report that they have successfully reconnected severed spinal cords in pigs, enabling them to walk again.

When a spinal cord is completely cut, the two severed ends naturally pull away from each other. In microscopic roundworms, for example, the nerve ends automatically find each other and fuse together. The researchers realized that to recreate a natural fusion process like this, they needed a material to fill the empty space and hold the two ends together.
As they detail in a paper published in the journal PLOS One, they engineered a fusogen-based gel designed to weld damaged nerve membranes back together. It contains a chemical used in medicine, polyethylene glycol, and a biological polymer, chitosan.

Pigs with complete spinal cord transections treated with a polyethylene glycol–chitosan fusogen gel showed rapid sensory recovery, restoration of bladder control by day 5, and independent walking by day 60, unlike untreated controls. Histology indicated reduced scarring and nerve fibers crossing the lesion, consistent with axonal fusion–mediated neurorepair.

Given the rapid clinical improvement observed, the therapeutic effects ... cannot be attributed solely to axonal regeneration ... This points to immediate neurorepair mechanisms, namely axonal fusion, being the primary driver of the initial recovery.
While this pig study is a significant advance, human clinical trials are likely still a long way off, as larger animal studies will be needed first. However, the research has demonstrated that damaged nerve fibers may reconnect after spinal injury, giving hope for future spinal treatments, as the researchers note.

Michael Lebenstein-Gumovski et al, Fusogen-induced recovery of spinal cord function and morphology after complete transection, PLOS One (2026). DOI: 10.1371/journal.pone.0349579

Vitamin D and calcium supplements may not protect against bone fractures, large new study suggests
Calcium or vitamin D supplements alone show little to no reduction in fractures or falls in adults, and combined supplementation yields only very small, clinically marginal benefits. The findings question routine supplementation for community-dwelling adults without deficiency or osteoporosis. Evidence more strongly supports weight-bearing exercise, balance training, and overall lifestyle measures for fracture and fall prevention.

original article.

Exposure to bright evening light linked to higher risk of age-related eye disease

The eye does more than help us see. It also plays a key role in setting our internal body clock, and, as a result, the amount and timing of light exposure may influence how the eye ages over time. Age-related eye diseases (AREDs), such as macular degeneration, cataracts and glaucoma, are a group of conditions that commonly develop in older adults and can lead to significant vision loss.

Many of these conditions share biological processes, including long-term inflammation, oxidative stress and disruptions in cellular energy production.

Every sunrise and sunset sends the body a signal, keeping the circadian clock running on a roughly 24-hour cycle. This clock evolved so organisms could adapt to Earth's daily rotation, syncing their biology to the pattern of day and night. Artificial lighting has freed human societies from relying on the sun to go about daily life, extending activity well into the night, but this convenience comes with a trade-off.
Researchers found that exposure to bright artificial light in the evening, especially between 8 p.m. and 11:30 p.m., may significantly increase the risk of developing serious eye diseases later in life. Those exposed to light levels above 1000 lux during these hours showed a notably higher likelihood of conditions such as age-related macular degeneration (AMD), cataracts and glaucoma.

It is not your living room lamp one needs to worry about, as standard indoor lighting, usually between 100 and 500 lux, stays safely within range. The real risk comes from extreme evening brightness from modern high-brightness screens and electronic displays, or occupational lighting in high-precision fields.

Researchers already knew there is a critical evening transition window when the body's internal clock is especially sensitive to light. However, there was limited real-world data linking specific light levels during this period to the development of actual eye diseases.

In this study, the researchers followed a database of 82,826 participants from the UK Biobank. Anyone who already had eye diseases was excluded to specifically track new cases that developed over time.
Part 1

After the week of light monitoring, the researchers followed the participants' health for an average of nearly eight years. The data pointed to a clear vulnerability threshold for eye health: average exposure to evening light exceeding 1,000 lux. In individuals consistently exposed to light above this level in the evening, the risk of developing major eye diseases rose sharply.

They observed a 31% higher risk of age-related macular degeneration, an 18% higher risk of cataracts and a 47% higher risk of primary open-angle glaucoma. The more time a person spent in bright light, the higher the risk.

Researchers suggest that this damage might be linked to disrupted circadian rhythms and exposure to blue light from modern LEDs, which can trigger oxidative stress and even cause photochemical damage in the delicate cells of the lens and retina.

Since high-intensity evening light is a modifiable risk factor, health care professionals can help people protect their long-term vision by choosing circadian-safe lighting, like dimming screens and using lower-intensity lights before bed.

Xiaoqian Wu et al, Association of high-intensity evening light exposure with risk of incident age-related macular degeneration, cataract, and glaucoma: a prospective cohort study of 82,826 participants, GeroScience (2026). DOI: 10.1007/s11357-026-02307-7

Part 2

Uneven cerebellum aging may partly explain why some older adults stay mentally sharp

The name "cerebellum" comes from Latin and means "little brain." While it is smaller than the rest of the brain, it contains most of the brain's neurons and coordinates a variety of functions and processes in the brain and body. These include balance, posture and fine motor skills like typing or writing.

Scientists may have discovered a new role for the cerebellum, the part of the brain that sits at the base of the skull. A new paper published in the journal Nature Neuroscience reports that different parts of the cerebellum change at different rates with age, which may be linked to differences in cognitive abilities and memory in later life. This may help explain why some people stay sharper as they get older.
The team analyzed brain scans and cognitive test scores from more than 700 healthy U.S. individuals whose data had been collected as part of the Human Connectome Project. Then they mapped out 11 separate sections on the digital scans and calculated how the volume of each region changed with age.

The scientists discovered that the cerebellum does not age evenly. Regions at the back, which are more connected to higher-order thinking networks, show faster shrinking than front regions involved in basic movement.
"We show a spatially heterogeneous pattern of aging in which specific association and motor-related regions show steeper relationships with age than other lobules," the authors wrote in their paper.

The data also revealed that people with a larger cerebellum scored higher on memory and thinking tests as they aged than people with a smaller cerebellum.

The research team saw a similar trend in a pool of about 47,000 adults in the UK Biobank and Alzheimer's Disease Neuroimaging Initiative. However, in people with Alzheimer's, it appears that support from the cerebellum has its limits as the disease progresses. "This supports a threshold-reserve model, in which the cerebellum helps sustain cognition until pathology becomes widespread."

The researchers cannot say for certain whether a larger cerebellum directly causes better cognition in old age. They have shown a link or association, not a true cause-and-effect relationship. Also, their findings might not apply to everyone globally because most of the study data came from white individuals with high levels of education.

Federico d'Oleire Uquillas et al, Cerebellar aging is spatially heterogeneous and supports cognitive resilience in later life, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02289-x

Why pollution affects some asthma patients more than others

For many people with asthma, air-quality advisories are harbingers of worsening symptoms. But the extent to which pollution exacerbates asthma varies widely from person to person.
In a study published in eBioMedicine, researchers identified biological pathways that begin to uncover this mystery, showing how air-pollution exposure interacts with a person's genes.

The study—which is among the largest and most comprehensive of its kind to date—could eventually lead to new avenues for asthma drug development, as well as potential new biomarkers and public health interventions targeted to those who are most vulnerable to pollution-exacerbated asthma.
Asthma severity responses to PM2.5 vary due to genetic differences in oxidative stress–related pathways. Whole-genome, exposure, and airway transcriptomic data identified variants in seven genes, including OXSR1, PXDN, and TPO, that alter pollution-induced RNA responses and are associated with lower lung function. These pathways suggest potential targets for precision diagnostics and interventions.

Using data from nearly 1,000 adults with asthma the analysis included a combination of whole-genome sequencing, air-pollution exposure data and gene-expression profiling. Among the thousands of genes in the human genome, the team focused on about 450 genes that control oxidative stress, a process in which highly reactive molecules can damage cells and tissues.
Those stresses on cells can translate into serious physiologic effects, like worsening lung function or asthma exacerbations.
The team focused on how these genes interacted with the environmental stress of exposure to fine particulate matter known as PM2.5. These microscopic particles, with a diameter less than that of a human hair (less than 2.5 microns), are small enough to penetrate deep into the lungs and are widely considered one of the most harmful components of air pollution.
A clear relationship emerged.

In these individuals who were living with asthma, the higher their exposure to this particulate matter, the lower their lung function overall.
The researchers found that the most vulnerable patients carried variants in seven oxidative stress–related genes that shape how the body responds to cellular damage from pollution. These genetic variants appear to influence how airway cells respond to the PM2.5 exposure, with some variants enhancing protection from PM2.5, while others appear to worsen the damage.

Individuals with less common variants in two specific genes, called OXSR1 and PXDN, had disproportionately worse lung function due to lower protective RNA responses to pollution. Those with a specific variant in another gene, called TPO, had worse lung function as well, but for them, it was due to stronger RNA responses.

The molecular pathways described in the study could point to targets for new therapies—and open the door to much more.

A cross-sectional study of oxidative stress pathway genotypes and their interactions with environmental pollutant levels identifies associations with gene expression and lung function, eBioMedicine (2026). DOI: 10.1016/j.ebiom.2026.106334

A species of gut bacteria could ease anxiety and diarrhea-predominant IBS

Irritable bowel syndrome (IBS) is a condition characterized by abdominal pain, bloating and changes in bowel movements, estimated to affect between 10% and 15% of people worldwide. Past studies suggest that in many cases this condition is accompanied by anxiety, an emotional state marked by worry, fear and/or overthinking about specific life events.
While IBS and anxiety are known to often occur together, the biological processes linking the two have not yet been fully elucidated. One possibility is that bacteria and other microorganisms living in the digestive tract, broadly referred to as gut microbiota, contribute to these biological processes.
Researchers carried out a study aimed at shedding more light on the biological mechanisms linking a type of IBS called diarrhea-predominant IBS (IBS-D), which is associated with frequent loose stools, with anxiety.

Their paper, published in Translational Psychiatry, suggests that a species of gut-inhabiting bacteria called Phocaeicola vulgatus could contribute to easing anxiety associated with IBS-D.
The researchers also carried out a series of genetic analyses on their mouse model of IBS to further explore the effects of the Phocaeicola vulgatus bacteria. The results of these analyses confirmed that the bacteria protected the mouse brain from anxiety.

Finally, giving live Phocaeicola vulgatus to mice eased anxiety by calming brain inflammation and repairing damaged neurons in the amygdala.

Jiacheng Wu et al, Phocaeicola vulgatus improves anxiety-like behavior by ameliorating amygdala neuroinflammation and the neurite impairment in IBS, Translational Psychiatry (2026). DOI: 10.1038/s41398-026-04142-y.

Poor metabolic health can age the brain even in young people, finds new large-scale study
Two people of very different ages can have a similar level of biological aging in their brains. Such an occurrence is possible because aging and metabolic health follow two distinct pathways that influence brain health. While it is known that the brain changes as we get older, a recent study analyzing more than 3,000 brain scans found that metabolic issues affect the brain through a different biological pathway than aging does.
The researchers found that the two axes operate independently of one another, meaning a person can be relatively young yet experience brain changes associated with poor metabolic health. These changes, driven by metabolic factors, were also linked to real-world cognitive performance.

People with poorer metabolic health generally struggled more with tasks that required cognitive flexibility, or the ability to shift between competing demands. The association was strongest in females.

The aging axis affects the brain by eroding its structural integrity. This includes thinning of the brain's outer layer and vascular dysfunction, which slows the flow of blood through the brain's vessels. The metabolic axis works differently. Instead of one main driver, it has an army of factors, including body weight, blood pressure and cholesterol, all acting together.

Their shared effect is a drop in cerebral perfusion, that is, less blood actually reaching the brain.

Asa Farahani et al, Aging and metabolism contribute separately to brain–body health, PLOS Biology (2026). DOI: 10.1371/journal.pbio.3003856

The universe should look the same in all directions at large scales, but DESI data suggest otherwise

Earlier this year, the Dark Energy Spectroscopic Instrument (DESI) completed observations that mapped 47 million galaxies across 11 billion light-years, allowing astronomers to better evaluate the large-scale structure of the visible universe. After studying these data, astronomers say the universe may not look the same in all directions. Their results, published in Nature, contradict a fundamental assumption in modern cosmology.
At the scale of a single galaxy or local groups of galaxies, the universe clearly appears to be anisotropic, meaning the structure is different depending on which direction you look. In one direction, there may be more void space, while another direction may have a cluster of galaxies.

However, the cosmological principle says that at larger scales, the universe consists of matter that is more or less distributed evenly in all directions. This is based on the Copernican principle, which states that there should be no "special observers" in the universe, meaning that at large scales, the universe should look the same from anywhere else in the universe.

For example, if you imagine the universe as a piece of cloth and zoom in to the scale of the individual fibers, you can clearly see areas of empty space and filament-like fibers that connect to make a larger structure. Yet when you zoom out to much larger scales, the cloth appears to be the same everywhere, with evenly distributed materials.
Research focusing on cosmic background radiation has provided some support for the cosmological principle, but other studies have shown that anisotropic structure still exists at scales of tens to hundreds of megaparsecs. However, the statistical significance of these studies is uncertain.
The authors of the new study say that past anisotropy probes tested for preferred directions instead of evaluating more general directional structure.
They found that galaxy samples from DESI show persistent anisotropic structure in galaxy distribution out to roughly gigaparsec scales, meaning galaxies were clumping together more than they should at scales far larger than those previously examined. Taking previous studies suggesting anisotropy at megaparsec scales as an example, this study indicates anisotropy still exists at scales 1,000 times larger.

"These results provide direct evidence that directional coherence persists to larger scales than predicted in the standard framework, challenging the assumption of large-scale isotropy," the study authors write.

Francesco Sylos Labini et al, Detection of anisotropic cosmic structures on a gigaparsec scale, Nature (2026). DOI: 10.1038/s41586-026-10702-5

Scientists find molecular-level evidence for two structures in liquid water

A study published in Nature Physics provides new molecular-level evidence from simulations that liquid water is not a single uniform substance, but a constantly shifting mixture of two distinct microscopic structures.
The idea that water might exist in two distinct structural states is not new. For decades, scientists have theorized that liquid water is composed of two interconvertible local structures—one denser and more disordered, the other less dense and more ordered.

This "two-state model" has been invoked to explain water's many anomalous properties, including why it becomes easier to compress as it cools and why it reaches maximum density at 4°C (39°F) rather than at its freezing point. But the model has remained controversial because direct molecular-level evidence for the two structures has been elusive.
Central to the two-state model is a hypothesized phenomenon known as the liquid-liquid phase transition (LLPT). The idea is that in the deeply supercooled regime, water splits into two macroscopically distinct liquid phases: a high-density liquid and a low-density liquid.
The boundary between them is thought to terminate at a "second critical point." This deeply supercooled region is so hard to study experimentally because water crystallizes rapidly. Much of the evidence for the LLPT has therefore come from computational studies.

Previously, a 2025 Nature Physics study made progress by using a deep neural network to map the location of this critical point.

"According to the two-state hypothesis, liquid water can be viewed as a mixture of two distinct structures, A and B. But no one has ever seen a genuine 'pure A' or 'pure B' liquid water. Indeed, due to the lack of direct molecular-level evidence, this model has been a subject of debate.
The problem is not just experimental, according to the researchers. Even in simulations, traditional methods that measure local density and energy differences between molecules failed to cleanly separate the two structures. What was needed was a way to let the data reveal the hidden molecular fingerprint of each structure—without any human assumptions about what that fingerprint should look like.
Part 1

To find this fingerprint, the team turned to an unsupervised deep learning approach—one that could extract hidden structural information from the data without any predefined assumptions about what the two structures should look like.

It is practically impossible for humans to intuitively guess or manually construct such complex, nonlinear, and nearly orthogonal physical parameters.
so the researchers took AIs help.
By using AI the researchers effectively rotated their viewing angle of the data, searching for the configuration at which the two structures—if they existed—would reveal themselves most clearly.
When the model found the optimal configuration, two distinct clusters emerged, suggesting two local structures: Structure A, denser and more disordered, and Structure B, less dense and more ordered. The simulations found these patterns across a broad range of temperatures and pressures, including some close to room-temperature conditions.
But the study revealed something beyond support for the existence of the two structures. The way Structure A and Structure B interconvert depends on where the system sits in the phase diagram. In the high-density liquid phase, the interconversion proceeds via an "upper semi-loop" pathway through a single transition state. In the low-density liquid phase, it follows a different "lower semi-loop" pathway through a different transition state.

Near the liquid-liquid phase boundary, where the two liquid phases compete most intensely, these two pathways combine into a complex three-dimensional "full-loop" reaction pathway involving three transition states. As the system moves away from the boundary and one phase begins to dominate, this full loop degenerates back into a simpler single-pathway semi-loop.

The transformation between Structure A and Structure B is not a simple 'back-and-forth' process. The interconversion pathways of the two structures are different under different states of water. This microscopic dynamic process is extremely difficult to identify using traditional theoretical methods.
The findings provide strong molecular-level evidence for the two-state model of water, with the bimodal feature in the data offering a structural signature of the two distinct local states.

Liwen Li et al, Evidence for the generic existence of two local structures in liquid water, Nature Physics (2026). DOI: 10.1038/s41567-026-03301-8.

Part 2

Did gravitational tides cause Earth's extinctions?
The article discusses a hypothesis that close passages of planetary-mass or dwarf-planet objects could generate strong gravitational tides, triggering giant tsunamis, enhanced volcanism, climate shifts, and redirected impactors, collectively driving some mass extinctions over the past 600 Myr. Correlations with geological and orbital anomalies are noted, but mass, frequency, and detailed evidence for such flybys remain highly uncertain.

Daniele Fargion, Mass Extinctions by Gravitational Tides, arXiv (2026). DOI: 10.48550/arxiv.2606.17105

What happens when environmental change outpaces life's ability to adapt?

When an animal's environment changes faster than the animal can adapt, its chances of survival can flatline. The same is true for populations and even entire species. Now, scientists have found that this connection between evolutionary adaptation and the pace of environmental change holds up at the global scale as well—and can determine life's susceptibility to mass extinction. The researchers have developed a theoretical model of this phenomenon, which they present in a paper published recently in Physical Review Letters.

A mathematical model links mass extinction severity to a mismatch between rates of global environmental change and biological adaptation. Using carbon-cycle proxies and extinction data from 27 events over 450 Myr, mass die-offs occur when environmental change exceeds most taxa’s adaptive capacity. Modern CO₂-driven change approaches these critical rate thresholds.

The team compared the model with available data from past major mass extinctions, including how fast the global environment changed at the time of each event. The model successfully predicted the severity of most mass extinctions in Earth's history, or the fraction of life that was unable to adapt and therefore went extinct.

Interestingly, the researchers found that the range of adaptation rates across animal groups is broadly similar to the range of rates at which the environment can change.
What we're beginning to see is a certain level of organization, and ways in which life behaves that are consistent with the ways in which the environment behaves.
It may be that life has evolved so that its range of adaptabilities matches the range of stresses that it meets.
For their new study, the researchers looked to test the rate-mismatch hypothesis at the global scale. They wanted to see whether mass extinction events in history could be explained by a mismatch between the rate of global environmental change and the rate at which life around the world can adapt.

To do so, at least in theory, they would have to compare two sources of data: the rates at which the global environment has changed over time and the rates at which different groups of organisms adapt to environmental change. The first can be found in geological records, which scientists have used extensively to infer how Earth's climate changed through history. The second, however, is almost impossible to record.
It is generally understood in evolutionary theory that a species can successfully adapt only when multiple conditions are met. For instance, there must be variation in the population. These variations must be heritable, some variations must enable an organism to adapt better than others, and the organisms that adapt better should leave more offspring. If all these conditions are met, the entire species should be able to adapt to a given environmental change. However, if any one condition fails, the population will go extinct.
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in this case, the probability of a species successfully adapting multiplies with every condition that it meets. And it turns out that this pattern can be described mathematically as a very simple, bell-shaped curve. Such a curve essentially describes what fraction of the world's animals can adapt at given rates, from the slowest to the fastest adapters, and how this fraction changes nonlinearly with the rate of adaptation. This curve generally shows that most animal groups can adapt at intermediate rates, while fewer animal groups adapt at the slowest and fastest rates.

After establishing this general pattern of adaptation rates, the researchers looked to see how this pattern compares with recorded rates of environmental change, and how these two rates match, or don't match, at times of mass extinction.

To do so, they considered paleontological and geochemical data from 27 episodes over the last 450 million years in which the carbon cycle experienced significant change—a measure that is generally understood to reflect global environmental change. They then compared rates of environmental change with the fraction of animal groups that went extinct during each episode—numbers that were established previously in a well-regarded study by paleobiologist John Alroy.
In the end, researchers observed that, for almost every mass extinction event in the last 450 million years, there was a mismatch in the rates at which the environment changed and at which animals could adapt; mass extinctions occurred when a significant fraction of animals could not adapt fast enough to match the changing environment. Their results confirm that the rate-mismatch hypothesis applies at the global scale.
Moreover, this mismatch in rates could predict the severity of extinction events, or the fraction of animal life that went extinct given the rate at which the environment changed.

In the case of the end-Permian extinction, it's likely that the rapid acidification of the ocean outpaced organisms' ability to evolve adequate protections, leading to the extinction of more than 80% of the world's marine species.

The team's work focuses on applying the new model to past extinction events. But the work could also provide a framework for understanding modern extinction risk.
Carbon dioxide levels in the ocean are increasing today at a rate which, when appropriately re-scaled, is similar to rates of carbon-cycle change that are just lower than those associated with major extinction events in the past.
It suggests that modern environmental change may be approaching rates beyond which adaptation becomes increasingly difficult.

Daniel H. Rothman et al, Relating Rates of Global Change, Evolutionary Adaptation, and Extinction, Physical Review Letters (2026). DOI: 10.1103/62jn-xgqy

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How we see colour revealed at the molecular level

To understand how we detect light and perceive colours, we need to know the exact structure of light-sensitive molecules in our eyes.

A global team now has cracked a decades-old mystery, revealing the atomic structures of the molecules in our eyes that allow us to see colours. 

Our perception of colour is mainly determined by the relative excitation of red-, green- and blue-sensitive cone photoreceptor cells found inside our retinas that contain these molecules.

There are three versions of the molecules, called cone opsins, with each converting red, green or blue light into chemical signals.

Revealing the atomic structures for each of the molecules in their light-activated state shows how they work inside cone cells to trigger signals that are ultimately sent to the brain. ?The results reveal fundamental differences between the cone opsins when they enter their active state after being hit with light.

Like how a high shutter speed lets a camera capture sharper images, having color-detecting molecules in our eyes that turn on and off quickly is thought to allow us to see sharp detail and color in motion accurately in daylight.

All three cone opsins contain the same light-sensitive vitamin A-derived molecule, with red, green and blue opsins binding to this molecule, called retinaldehyde, differently.

The red and green opsins appear to use very different placement of chemical electronic charges around the retinaldehyde. This difference explains how they shut off faster than the blue opsin, and much faster than the rod pigment.

In the long term, this development could help scientists discover better treatments for some vision disorders, such as cone dystrophies and altered colour vision.

Qi Peng et al, Cryo–electron microscopy structures of human cone visual pigments, Science (2026). DOI: 10.1126/science.adz8141

Concussion symptom history linked to increased odds of tinnitus

Greater concussion symptom history is associated with increased odds of tinnitus, and associations with cognition, depression, and anxiety are larger among those with tinnitus, according to a study published online June 19 inSports Medicine Open.

In former professional American football players, greater self-reported concussion symptom history was associated with higher odds of tinnitus (odds ratio 2.90 for highest vs lowest quintile). Tinnitus did not mediate associations between concussion history and neurobehavioral outcomes, but individuals with tinnitus showed stronger associations with perceived cognitive problems, depression, and anxiety.

Niki A. Konstantinides et al, Associations Between Football-Related Exposures, Head Injury, Tinnitus, and Neuropsychological Health Outcomes Among Professional American-Style Football Players, Sports Medicine—Open (2026). DOI: 10.1186/s40798-026-01053-6

Ovaries start second job after menopause

After the ovaries ramp down their reproductive role, releasing eggs and sex hormones, they might become more important to the immune system. Evidence from people and mice suggest that genes and proteins associated with immune activity are more active and prevalent in postreproductive ovaries — though it’s unclear whether it's a beneficial change.

Researchers found signs of reproductive function, including markers associated with egg and steroid production, diminished with age among the mice they tested. But the analyses of post-reproductive ovaries also revealed various kinds of immune cells at higher levels than what’s typical in younger mice. Older ovaries also showed greater activity of genes that encode different pro-inflammatory compounds, immune molecules that could be secreted into the bloodstream and travel to other parts of the body.

Whether older ovaries actually carry out any immune signalling or simply become an unintended reservoir for immune cells remains unclear. The new mouse study is interesting because it provides a potential idea as to what the post-reproductive ovary might be doing. The ovary might become a site where immune cells … come and get changed in some way that would potentially have systemic effects.

The finding could help explain why women tend to be less healthy than men as they age, even though they live longer.

The postreproductive ovary could secrete molecules that predispose people to chronic inflammation in their menopausal years. 

https://academic.oup.com/molehr/advance-article/doi/10.1093/molehr/...

Large MRI analysis uncovers brain-region thinning tied to depression

Major depressive disorder (MDD) is a psychiatric condition characterized by persistent feelings of sadness, a loss of interest in everyday activities, altered sleeping and/or eating patterns, low energy, and difficulty concentrating on tasks. While it is one of the most widespread mental health disorders worldwide, its unique neural and brain-related signatures have not yet been fully uncovered.

Recent studies have been trying to uncover differences in the structure of the brain associated with specific mental health disorders. This has mainly been done by analyzing brain scans collected from psychiatric patients using magnetic resonance imaging (MRI), a medical imaging technique that collects detailed images of specific organs using strong magnetic fields and radio waves.

Researchers recently performed a large-scale analysis of MRI scans collected from individuals diagnosed with depression and from people with no known mental health disorders. The results of their analysis, published in Nature Mental Health, unveiled differences in the structure of specific brain regions associated with depression, which appear to vary based on age, treatment stage, and medication use.

The researchers analyzed MRI brain scans collected from 5,736 patients with MDD and 6,538 individuals with no known psychiatric conditions. These scans were collected by 64 independent research groups worldwide as part of two international research projects.

The analyses show significantly lower cortical thickness in patients with MDD in multiple brain regions, including the inferior parietal, lateral occipital, superior parietal, medial and lateral orbitofrontal, anterior and posterior cingulate, and precentral gyri, with cortical surface area showing no significant differences.

The team found that people with depression exhibited thinner cortical layers across various brain regions, but no significant differences in these regions' surface area. These observed differences appeared to be more pronounced in adult patients who were having an acute depressive episode. In contrast, adolescents with depression did not present any significant differences in brain structure compared with adolescents with no mental health disorders.

The researchers also observed slightly more prominent cortical thinning in the brains of patients who were taking antidepressant medications, such as selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs). Nonetheless, the effects of antidepressant use on people's brain structure appeared to be subtle and modest in size.

Chao-Gan Yan et al, Vertex-wise cortical abnormalities in major depressive disorder from 64 cohorts from the DIRECT and ENIGMA MDD consortia, Nature Mental Health (2026). DOI: 10.1038/s44220-026-00667-9.

Giant exoplanet may hold a magnetic grip on its host star

Within their planetary systems, stars are continuously shaping their orbiting planets through gravity, radiation and magnetic forces. So far, this relationship has appeared to be a one-way street.
But through new research published in Science, an international research team has found compelling evidence that the dynamic can run in reverse: A giant exoplanet orbiting very close to its star appears to be leaving a measurable magnetic imprint on the star itself.
The ways in which stars influence their planets are varied and powerful. Gravitationally, a star can distort a planet's orbit over time, stretching it or locking its rotation into step with its orbit. Radiatively, the intense light and high-energy particles streaming from a star can erode a planet's atmosphere, gradually stripping away lighter gases.

Magnetically, the star's field pervades the surrounding space, interacting with any magnetic field the planet itself possesses. In most cases, the star so thoroughly dominates these interactions that any influence the planet might exert in return is negligible.

For their study, the team focused on a red dwarf star called GJ 436, located about 30 light-years from Earth and roughly half the mass of our sun. It is orbited by a single known planet: a world around the size of Neptune and four times the mass of Earth. The exoplanet also completes a full orbit every 2.6 days, placing it extraordinarily close to its host star.

The researchers analyzed 18 years of high-resolution spectroscopic observations of the star, tracking specific emission signatures from hydrogen and calcium in its outer atmospheric layer. Since these signatures are sensitive to the star's magnetic environment, they are an especially useful indicator of activity.
Remarkably, the team found periodic fluctuations in these signals that matched the planet's orbital period—suggesting the planet was somehow triggering a rhythmic response in the star. This signal wasn't always present, however. During periods of high stellar activity, it was drowned out, and during very quiet periods, there was too little background activity for the planet's influence to enhance. But at intermediate activity levels, a clear periodic pattern emerged.

To explain this unusual pattern, the team modeled a physical connection between the magnetic field lines of the planet and star, which funnel energy into the star's outer atmosphere. Accounting for the star's rotation and the planet's tilted, eccentric orbit, this model was able to reproduce the observations and placed the planet's magnetic field strength as comparable to Jupiter's.
The findings present the possibility of an entirely new type of relationship between exoplanets and their host stars.

D. Revilla et al, Constraining an exoplanet's magnetic field using star-planet interactions, Science (2026). DOI: 10.1126/science.adv3075

Coastal and estuarine carbon removal technique may backfire when pushed too far

The ocean already absorbs around a quarter of human-generated carbon dioxide emissions, making it one of Earth's most important natural carbon sinks. Ocean alkalinity enhancement seeks to increase this capacity by raising the alkalinity of seawater, allowing it to take up additional carbon dioxide from the atmosphere.

Scientists investigating a proposed way to remove carbon dioxide from the atmosphere using seawater have found that adding too much alkalinity to neutralize acids can trigger chemical reactions that undermine the process.
The study, published in Frontiers in Marine Science, examined a form of marine carbon dioxide removal known as ocean alkalinity enhancement. The approach aims to increase the ocean's capacity to absorb carbon dioxide by adding alkaline substances that shift seawater chemistry and encourage more carbon dioxide to move from the atmosphere into the ocean.

Using dissolved calcium carbonate (the main mineral found in limestone and seashells), the researchers found that there are clear limits to how much alkalinity can be added before the chemistry becomes unstable. At high doses, calcium carbonate rapidly forms solid mineral particles, effectively undoing some of the intended carbon storage benefits. The findings help define practical boundaries for the technique and highlight the importance of tailoring it to local conditions.
However, there is a catch. If conditions become too favorable for minerals to form, dissolved calcium carbonate can begin to crystallize and precipitate back out of the water. This removes some of the added alkalinity before it has had time to draw down atmospheric carbon dioxide and, in extreme cases, could even release carbon dioxide back into the atmosphere.

To investigate where these limits lie, the researchers tested three different alkalinity additions under a range of temperatures and carbon dioxide conditions. They also explored how mixing treated seawater with natural river water affected stability.

The lowest dose remained stable for more than a month, while the highest dose consistently caused calcium carbonate precipitation within a day. An intermediate level showed mixed behavior, with the timing of precipitation strongly influenced by temperature and the precise chemical conditions of the water.

The results revealed a threshold effect: Below certain levels, the enhanced seawater remained chemically stable, but above them the risk of precipitation increased sharply. Although the highest additions led to rapid mineral formation, the researchers did not observe a worst-case "runaway" scenario in which more alkalinity was lost than had originally been added.

The team also found that mixing treated seawater with natural estuarine water improved stability

Amanda B. Melendez-Perez et al, Stability assessment of calcium carbonate dissolution as a marine carbon dioxide removal mechanism, Frontiers in Marine Science (2026). DOI: 10.3389/fmars.2026.1796693

Decline in plankton across Northeast Atlantic sends stark warning for ocean health
Long-term analyses of 23 data sets across the Northeast Atlantic show widespread declines and community changes in phytoplankton and zooplankton, with no pelagic region achieving Good Environmental Status. Shelf habitats exhibit the poorest condition. Changes correlate with warming, nutrient shifts, acidification, and altered mixing, indicating impaired food webs and carbon cycling and underscoring the need for emission cuts, nutrient control, and sustained plankton monitoring.

Abigail McQuatters-Gollop et al, Integrating plankton indicators to assess the state of pelagic habitats in the Northeast Atlantic, Ecological Indicators (2026). DOI: 10.1016/j.ecolind.2026.115005

Childbirth is not uniquely difficult to humans

The tight fit of a baby's head through a mother's birth canal, which causes great difficulty in childbirth, is not unique to humans, as previously understood. Instead, some small-bodied primate babies have heads almost twice as large as their mothers' pelvic space, a new study led by UCL researchers has found.

Birth canal–neonate head mismatch occurs widely among small-bodied primates, not only humans, challenging the notion of a uniquely human obstetrical dilemma. Expanded 3D comparative analysis across 29 species shows especially tight fits in American monkeys, with some neonate heads nearly twice maternal pelvic space. Several taxa exhibit pelvic adaptations, such as delayed or absent pelvic bone fusion, that facilitate parturition.

The findings, published in Nature Ecology & Evolution, challenge the theory of an exclusively human "obstetrical dilemma"—the idea that our large heads and narrow pelvises, adapted for upright walking, have made childbirth uniquely difficult for our species.
Researchers have revisited the evidence and found that although constricted birth is not experienced by other apes, it is common among many small-bodied primates, particularly American monkeys like bushbabies and squirrel monkeys. For example, the heads of newborn squirrel monkeys can be almost twice the size of the mother's pelvic space.
Much of the data that informed earlier studies was flawed. It had been collected in a human-centric way that failed to consider the anatomy of other species.
In the past, the measurement for the newborns' heads was from the forehead to the back of the skull. This assumed that all babies are born crown-first, as most humans are. But species like the gelada monkey, with their pronounced snouts, are often birthed face-first.
Using advanced 3D modeling techniques and greatly expanding the number of species studied—from eight to 29—the research team found that tight fits at birth were especially common among proportionally smaller species.
The researchers found that some of the small-bodied primates that experience a constrained fit during childbirth have developed clever adaptations to make the process less difficult. The pelvic bones of female rhesus macaques fuse together later than in males, during their reproductive years, and in bushbabies they never fuse, allowing the pelvis to expand during birth to accommodate the neonatal head.

Nicole Torres-Tamayo, Comparative primate analysis shows that humans are not unique in having a tight cephalopelvic fit at birth, Nature Ecology & Evolution (2026). DOI: 10.1038/s41559-026-03102-5. www.nature.com/articles/s41559-026-03102-5

Scientists uncover how ovarian cancer resists chemotherapy—and how to reverse it
Ovarian cancer cells acquire cisplatin and carboplatin resistance by stabilizing microtubules via elevated TPPP3, altering the tubulin “code” beyond DNA repair mechanisms. High TPPP3 correlates with poorer survival, while TPPP3 loss restores cisplatin sensitivity in models, suggesting TPPP3 as a therapeutic target and potential biomarker for platinum resistance and treatment optimization.

Sachi Horibata et al, Cisplatin resistance in an ovarian cancer model is mediated by microtubule dynamics regulator TPPP3 in synergy with tubulin code rewiring, Cell Reports (2026). DOI: 10.1016/j.celrep.2026.117414

Scratching that bug bite might feel good at first but science explains why it's a bad idea
Scratching itch-inducing skin lesions amplifies inflammation by mechanically triggering pain fibers that release substance P, which activates mast cells via a non-allergen pathway, increasing swelling and itch. Mouse “cone” experiments show preventing scratching markedly reduces inflammatory cells and edema. Although scratching can modestly reduce skin bacteria, the net effect is detrimental, and topical anti-itch therapies are recommended to break the itch-scratch cycle.

A lot of things can cause itchiness, sometimes serious diseases. Whatever the cause, doctors have long warned that scratching too much can damage the skin. Now researchers better understand why even a mildly annoying itch could put you on an itch-and-scratch cycle if you give in.
They also gained insight into why a good scratch at least at first brings a sigh of relief. After all, not just people and other mammals scratch, even fish do. The commonality suggests there must be some evolutionary reason and the mouse experiment hints at a little germ protection—but still not a reason to scratch.

Evidence matches people's everyday experiences that scratching really can make things worse.

Ignore a mosquito bite and the itch is "gone in five or 10 minutes for most people. But if you start scratching it, it's your friend for a week, getting itchier and more inflamed.
To understand what was happening in the skin, researchers took a deeper look at mast cells, among the immune system's first responders. When called into action, they release compounds that can help fight germs or toxins—or, through a compound called histamine, trigger itchy allergic reactions.

Scientists have long known that allergens can activate mast cells. But other signals can summon mast cells, too, including pain. And when we scratch, we tend to scratch until it starts to hurt.
Pain-sensing nerve cells release a chemical messenger called substance P. In findings published last year, the same team reported that substance P can activate mast cells through a different molecular pathway than allergens do—a double whammy that explains why scratching further inflames itchy rashes or bites.
If we experience pain like touching a hot stove, we'll learn not to do that again. Yet relief from a good scratch, in evolutionary terms, is positive feedback. Why?

One long-held theory is that it may help creatures slough off parasites like fleas or mites.

"Ultimately, scratching is deleterious," the researchers stressed. "You should avoid scratching, although it's "easier said than done."
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What fights an itch depends on its cause and there's a need for better treatments. For now, antihistamines and certain other drugs for hives can tamp down some itchiness triggered by mast cells. Drug companies are experimenting with other approaches called MRGPRX2 blockers that target the pathway the team linked to scratching.
For the summer itchiness of bug bites, poison ivy and other types of contact dermatitis, dermatologists recommend anti-itch balms such as hydrocortisone cream, calamine lotion or oatmeal baths.

Another trick : Menthol-containing creams can temporarily fool the skin into sensing cold instead of itch, just long enough that "if you don't scratch, then you break that itch-scratch cycle" . "It's like a cheat code."
- Dematologists!

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The brain's physical shape guides its internal wiring
A new study by researchers has shed light on the factors shaping the intricate wiring of our brains. The research, published in the journal Cell, reveals that the brain's complex wiring diagram, known as the cortical connectome, does not form at random. Instead, a new mathematical model shows that connections preferentially form between locations that support natural, shape-driven "resonant patterns."
Just as the physical shape of a bell or a drum determines its vibrations and the music that it produces, the physical geometry of the brain constrains the patterns of neural activity it can support.
By testing their mathematical formula against publicly available datasets, the research team showed that this geometric rule holds true across various species, from mice to humans.

This demonstrates that the physical shape of the brain has served as a blueprint in guiding its internal wiring for at least 90 million years of mammalian evolution.
The researchers also showed that the formula successfully predicts both how the brain is wired—its "topology"—and where the wires physically go—its "topography"—important properties that previous theories have failed to predict.
Their new model suggests the brain wires itself in an energy-efficient way to support these resonant patterns, strongly favouring low-frequency patterns, resembling a deep, low hum rather than a high-pitched chirp. These broad, brain-wide patterns require far less energy to sustain.
The fact that a single mathematical formula can accurately predict brain networks in both a tiny mouse and a human reveals just how powerful physical geometry is in shaping brain connectivity.

Francis Normand et al, Geometric constraints on the architecture of mammalian cortical connectomes, Cell (2026). DOI: 10.1016/j.cell.2026.05.048

Rising summer heat linked to higher youth suicide rates, especially ages 15 to 24

From India to the U.S. and across Europe, millions are enduring an intense heat wave as temperatures soar to an unbearable range. Summers over the past few years have been extremely hot in these regions because of the combined effects of climate change and persistent weather patterns that amplify these sweltering conditions.
As temperatures climb, so do the risks of a range of mental health disorders, including suicide.

Heat exposure doesn't affect everyone equally. It hits harder on people who work outdoors, people facing housing instability in neighborhoods with fewer resources, and those without air conditioning. Young people are also particularly vulnerable.

Children and adolescents have a higher surface-area-to-mass ratio and sweat less efficiently than adults, causing their bodies to absorb heat more quickly and making it harder to cool down. Studies also suggest that young adults adapt to prolonged summer heat less effectively than older adults.
A recent study found that higher summer temperatures were strongly associated with increased suicide rates among youth, with the connection appearing specifically in summer. During those months, every 1°C (1.8°F) rise in average monthly temperature was associated with a 2.68% increase in the suicide rate. The summer heat effect was strongest among older teens and young adults ages 15 to 24.
Across the full year, for every 1°C rise in average monthly temperature, youth suicide rates increased by 0.75%, about the same as what was seen in the general population. That pattern changed considerably when the team looked at each season individually.

The link between heat and suicide turned out to be statistically significant only in summer (July–September), when rates jumped 2.68% for every 1°C increase, more than 3.5 times higher than the average for the rest of the year.

They also found that heat had a stronger effect on females, raising their rate by 5.20% per 1°C compared with 2.37% for males. They observed the summer effect across most regions of the country, though it weakened, moving from east to west.
As temperatures rise because of global warming and climate patterns such as El Niño, protecting the mental health of young people will require not only better science but also structural interventions.

Pranav Jayaraman et al, Deadly Heat: The Association Between Ambient Temperature and Suicide in Young People in the United States, American Journal of Psychiatry (2026). DOI: 10.1176/appi.ajp.20250096

PFAS in most medicines can be replaced with alternatives
Analysis of 139 PFAS-containing active ingredients shows that 87% of human and 65% of veterinary medicines have PFAS-free alternatives, and alternatives are in development for most remaining human drugs. PFAS structures are not required for pharmacological action but drive environmental persistence and TFA formation. Findings support preferential prescription and development of PFAS-free medicines.
Certain medicines contain per- and polyfluorinated alkyl compounds, known as PFAS, which are causing increasing environmental harm because of their long-lasting effects. A study published in Sustainable Chemistry and Pharmacy shows that many PFAS-based active ingredients used in medicines can be replaced by alternative active ingredients. Based on the report's findings, doctors will in the future be able to give preference to prescribing PFAS-free medicines, where this is appropriate from a therapeutic point of view.
Researchers have shown that, for 87% of the identified human medicines and 65% of the veterinary medicines containing PFAS structures, active ingredients without PFAS properties already exist for the same applications.

The study examined 111 active pharmaceutical ingredients for human medicines and 28 for veterinary medicines that are classified as PFAS according to the definition of the Organization for Economic Co-operation and Development (OECD). Furthermore, the researchers were able to demonstrate that PFAS-free alternatives are already in development for almost all the remaining human medicines.

"The fact that PFAS-free alternatives already exist for almost all indications is a clear indication that, from a pharmacological point of view, per- or polyfluorination is not strictly necessary.
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The report also provides fundamental insights for pharmaceutical research: In the case of the active pharmaceutical ingredients examined, which have a known mechanism of action, the PFAS content is not responsible for the intended medical effect. Per- and polyfluorination are used in pharmacology to improve the stability and distribution of active ingredients within the body.

However, it is precisely these properties that mean these substances are difficult or impossible to break down in nature and, once excreted by humans, place a burden on ecosystems. There, they may accumulate in living organisms and break down into problematic, persistent transformation products such as trifluoroacetic acid (TFA). TFA does not degrade in the environment, is carried by the water cycle and is considered toxic to reproduction. According to the expert report, more than 80% of the PFAS active ingredients examined have the potential to break down into TFA.
There is no immediate risk to patients from medicines containing PFAS, as these are thoroughly tested for potential risks to human health before they are authorized.
Doctors can use these new findings to prioritize prescribing PFAS-free medicines—particularly when starting new patients on treatment—provided this is appropriate from a therapeutic point of view.

Johanna Greinke et al, Per- and polyfluorinated active pharmaceutical ingredients: Overview and alternatives, Sustainable Chemistry and Pharmacy (2026). DOI: 10.1016/j.scp.2026.102416

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Improving growth outcomes for children living with dwarfism

Achondroplasia occurs in 1 out of every 26,000 to 40,000 children and is caused by genetic changes that affect bone growth, proportionality, and differences in the shape of the spine and limbs. Children with the condition often have disproportionately short stature and may experience health challenges involving the spine, legs, ears, nose and throat.

New findings from a trial conducted at Children's Hospital Coloradodemonstrate significantly increased growth rates in children with achondroplasia, the most common form of dwarfism.
The children who received oral therapy experienced a statistically significant increase in height—an observed improvement of 2.10 centimeters per year compared with those who received the placebo. Furthermore, proportionality improved among children ages 3 to less than 8 years, an age range in which changes in body proportions are most evident.
A phase 3 randomized, placebo-controlled trial of the oral FGFR1–3 inhibitor infigratinib in 114 children with achondroplasia showed a statistically significant additional annual height gain of 2.10 cm versus placebo over 52 weeks, with improved body proportionality in children aged 3 to <8 years. Adverse events were mainly mild to moderate, with no treatment-related serious events or deaths; long-term effects remain under investigation.

Ravi Savarirayan et al, Phase 3 Trial of Oral Infigratinib in Children with Achondroplasia, New England Journal of Medicine (2026). DOI: 10.1056/nejmoa2604565

Chain reaction in cells may be driving low energy in ME/CFS patients

Researchers have identified a key immune cell dysfunction in people with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), offering new clues about the condition.
The study addressed a critical question: Are the mitochondrial deficits reported by other researchers a downstream consequence of the ion-channel and calcium abnormalities previously identified?
Researchers used advanced live-cell imaging to observe TRPM3-dependent calcium movement into mitochondria in real time.

The paper "Deficient TRPM3-linked mitochondrial Ca2+ influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome" has been published in BMC Immunology.

Symptoms included profound, persistent exhaustion; post-exertional malaise; pain; cognitive difficulties; dizziness; temperature instability; and sensory sensitivity, which could severely restrict day-to-day functioning, education, employment and social participation.
The researchers found a significant TRPM3-calcium pathway dysfunction in ME/CFS, resulting in impaired calcium entry into mitochondria, a region of the cell responsible for energy production.
It explains how reduced calcium entry into mitochondria may impair immune cell function and energy production, effectively triggering a chain reaction in the body.

Chandi Tabeth Magawa et al, Deficient TRPM3-linked mitochondrial Ca²⁺ influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome, BMC Immunology (2026). DOI: 10.1186/s12865-026-00849-1

Growing evidence shows sugar substitutes disrupt gut health and metabolism

Since the first introduction of saccharin, an array of artificial and other non-nutritive (i.e., low-calorie or calorie-free) sweeteners have become ubiquitous in the food supply. However, a growing body of research suggests that these compounds are not inert in the body and may be disrupting metabolism.
A new review and meta-analysis by researchers, published in Current Atherosclerosis Reports, pulls together the best available evidence on how non-nutritive sweeteners affect health. Across 21 randomized clinical trials in adults, researchers observed that artificial and other low-calorie sweeteners, compared with noncaloric controls such as water or placebo, raised fasting insulin and HbA1c, a marker of long-term blood sugar control, and showed a trend toward worsening insulin sensitivity.

Non-nutritive sweeteners, compared with noncaloric controls, increase fasting insulin and HbA1c and tend to worsen insulin sensitivity, indicating adverse metabolic effects. Evidence suggests they alter gut microbiome composition and function and are associated with higher cardiometabolic disease risk in observational data. Heterogeneity among sweeteners and labelling gaps limit precise risk assessment.

One explanation based on the current evidence, the researchers say, involves the gut microbiome. Non-nutritive sweeteners generally pass through the gut and come into direct contact with these microbes. In one trial they reviewed that used detailed microbiome profiling along with experiments transferring microbes from humans to mice, certain low-calorie sweeteners were shown to alter both the composition and the function of the gut microbiota.
In addition to randomized trials, the researchers reviewed large observational studies, which generally found that consuming non-nutritive sweeteners is linked to a higher risk of developing cardiometabolic diseases. The team notes that these studies have limitations, as people already at risk for these conditions may be more likely to choose these products. Different sweeteners may also have different health effects, so grouping them together may obscure the full picture. Taken together with the clinical trial findings, however, the researchers say the overall body of evidence raises concern.

Meng Wang et al, Artificial and Other Non-Nutritive Sweeteners, the Microbiome, and Cardiometabolic Health, Current Atherosclerosis Reports (2026). DOI: 10.1007/s11883-026-01429-9

Food noise: Why thoughts about eating aren't always something to be feared
Food noise denotes persistent, intrusive food-related thoughts arising from diverse mechanisms, including hunger signals, cravings, cue reactivity, emotion-driven eating, and perceived loss of control. It becomes problematic when it impairs functioning or promotes overeating or binge eating. GLP‑1 agonists can dampen multiple appetite processes and reduce food noise, but complete silencing of appetite is neither realistic nor desirable. Management focuses on distinguishing hunger from cravings, minimizing external cues, addressing emotional drivers, engaging in physical activity, and seeking professional support when distress or dysfunction occurs.

original article.

Chaos-courting pigeons break all the rules
Pigeons live at “the edge of chaos” to maintain their legendary flexibility and adaptability, suggests new research. Scientists presented common pigeons (Columba livia) with five colourful buttons, and pecking any sequence of five resulted in a tasty reward. Despite cutting down the number of sequences they used, the birds never fully gave up on trying new versions, and their favourites fell in and out of favour. The findings run counter to ‘Thorndike’s Law of Effect’ — proposed by psychologist Edward Thorndike in 1905 — that rewarded behaviours become more frequent and less variable.

https://psycnet.apa.org/record/2027-47688-001

How a giant planet survived its star's death, then migrated inward

When astronomers discovered a giant planet orbiting a dead star in 2020, they wondered how it survived its star's violent demise. Now, observations from NASA's James Webb Space Telescope (JWST) may finally explain the planet's unlikely escape from destruction.
In a new study, an international team of scientists analyzed the planet's atmosphere for the first time. Using measurements of the planet's atmosphere, mass and temperature, the researchers reconstructed the planet's journey. They found the planet (called WD1856b) originally orbited its star from a safe distance. But billions of years after the star died, the planet migrated toward its dead companion.

The findings give an unprecedented glimpse into the distant future of planetary systems—including our own.
The findings have bearing on the long-term fate of our solar system.
In roughly 5 billion years, our sun will die, and we don't know precisely what will happen to the planets at that time. The fact that planets can survive into that final stage of the stellar life cycle really widens the range of possibilities for where and when habitable planets might exist in the universe.

Ryan MacDonald, Aerosols and hydrocarbons in the atmosphere of a white dwarf planet, Nature (2026). DOI: 10.1038/s41586-026-10514-7. www.nature.com/articles/s41586-026-10514-7

Algae may have launched coral reefs by hijacking coral cells, genetic experiments suggest

The reefs scattered throughout the tropics arose only after algae took up full-time residence in coral cells, supplying corals with abundant food and enabling them to build extensive shallow-water communities. But with warming oceans, algae are often abandoning coral—causing what's known as bleaching—and turning reefs that were once teeming with life into ghost towns.
Based on genetic manipulations of the lab-grown corals and related anemones, which also incorporate algae into their cells, the researchers are challenging the assumption that coral long ago absorbed algae into specialized compartments inside their cells called symbiosomes.
Symbiosomes resemble mitochondria, the powerhouses of the cell, and chloroplasts, which harbor the photosynthetic machinery in plants. Both are thought to have been independent organisms that were long ago incorporated into cells and are now essential cellular components in all animals, plants and fungi.
Part 1

The researchers theorised that instead that algae parasitized coral, having found a way to live unscathed inside a type of lysosome, the cellular organelles that normally digest food and invading organisms. In doing so, the algae learned how to absorb carbon from the host cell and release the products of photosynthesis—primarily glucose—to feed the coral. That's a win-win for both algae and coral, and for other animals that harbour symbiotic algae.

In a paper published in the journal Cell, the researchers report experiments that support this idea that symbiosomes form by fusing with lysosomes, and that algae have somehow evolved to resist the active digestive enzymes in the lysosome.

Parasites basically trick cells to do what they want. That's what they think is happening here. The algae are hijacking the nutrient centers of the cells and acting like food that just never gets digested because they can fix carbon and make glucose from photosynthesis. They think about it as an everlasting gobstopper.

They noted that the difference is not always clear between a parasite, which exploits its host without the host benefiting, and a symbiont, which lives mutualistically with its host. The coral-algae relationship could be a new type of symbiosis that involves parasitizing a cellular organelle.

It's good for the coral, it's good for the algae, so it's symbiosis. But they think it's basically repurposing the entire cell and taking over that nutrient center.

In genetic experiments they identified at least 200 proteins located on the symbiosome in which algae live.
One of the proteins transports bicarbonate, which is converted to carbon dioxide in the symbiosome, potentially explaining how the alga gets the carbon dioxide it needs to convert sunlight into sugars, despite being isolated inside a cell inside the stomach of the coral.

Co-option of lysosomal machinery shapes the evolution of the intracellular photosymbiosis supporting coral reefs, Cell (2026). DOI: 10.1016/j.cell.2026.06.015. www.cell.com/cell/fulltext/S0092-8674(26)00701-4

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Orbit overload could devastate astronomy if 1.7 million proposed satellites brighten night sky
Mass deployment of satellite constellations could severely impair ground-based optical astronomy through bright trails and a several-fold increase in night-sky background. Simulations indicate up to 1.7 million proposed satellites would cause drastic data loss, whereas limiting the total to ≤100,000 objects fainter than magnitude 7 keeps impacts comparable to other technical losses.

Olivier R. Hainaut, Large or bright satellite constellations: Effects on observations, including on the background sky brightness, arXiv (2026). DOI: 10.48550/arxiv.2604.09427

Martian dust storms may generate atmospheric electrical conditions that could impact future missions
Global dust storms on Mars can structure the lower atmosphere into regions where charge separation persists and electric fields approach breakdown thresholds. These conditions create localized, altitude-dependent environments favorable for electrostatic discharges. Such electrified dust may affect spacecraft systems, dust–surface interactions, and near-surface chemistry relevant to habitability.

Chali Idosa Uga et al, Turbulence-coupled Electrodynamics of the Martian Year 34 Global Dust Storm on Mars, The Planetary Science Journal (2026). DOI: 10.3847/psj/ae69db

A holoparasitic plant replaces its own genes with host DNA to survive

All living organisms are known to inherit genes, DNA sequences that contain instructions for producing specific proteins and performing biological functions, from their parents. In some cases, however, genes can also shift between different species via a process known as horizontal gene transfer (HGT).

HGT essentially entails the movement of genetic material between different living organisms that are unrelated and of different species. So far, this phenomenon has primarily been observed in microbes and bacteria.

Researchers  recently observed HGT in Lophophytum, a holoparasitic plant that is incapable of photosynthesis and obtains water, nutrients and energy from host plants.

Their paper, published in Proceedings of the Royal Society B, shows not only that this plant can acquire genes from a host plant, but also that acquired genes are sometimes expressed, replacing the plant's original genes.

The researchers particularly focused on the mitochondrial genome, which is particularly prone to HGT. Most of the foreign DNA remains nonfunctional in the recipient plant and is eventually lost. This is expected because being expressed and becoming functional in the recipient plant is highly unlikely, given the barriers to foreign gene expression and evolutionarily unlikely, given the requirement for cytonuclear compatibility between mitochondrial and nuclear genes.

While studying the transfer of genes from a host plant to the holoparasite the researchers made an unexpected discovery. Specifically, they found that this plant carried massive amounts of mitochondrial DNA (i.e., DNA stored in the mitochondria (i.e., membrane-bound organelles found in almost all cells with a nucleus)) that was acquired from a host plant.

This host-acquired material included several genes that became functional and had replaced native genes.

The team's analyses revealed that the holoparasites they studied had successfully replaced many of their own mitochondrial genes with functional copies acquired from host plants. These genes appeared to become functional without the need for the host plant's nuclear regulatory processes, relying solely on the holoparasitic plants' own cellular mechanisms.

This study offers one of the most striking examples of HGT in plants, while also providing a possible explanation for why genes acquired by a holoparasite can sometimes become functional.

Maria Emilia Roulet et al, A structural solution to functional HGT: gene chimaerism bypasses mitochondrial expression barriers in parasitic plants, Proceedings of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rspb.2025.2955.