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Over 50% of Heart Attacks in Younger Women Aren't From Clogged Arteries

Traditionally, most heart attacks have been blamed on clogged arteries causing atherothrombosis – where blood clots block flow to the heart.
But research suggests we may be underestimating the role of other causes, particularly in younger adults.

Scientists from the Mayo Clinic in the US analyzed 1,474 heart attack events in people aged 65 or younger, recorded between 2003 and 2018 in Olmsted County, Minnesota. By carefully reviewing medical records and imaging, they identified a primary cause behind each case.

Strikingly, more than half of heart attacks in women were found to have non-atherothrombotic causes.

Atherothrombosis accounted for 75 percent of heart attacks in men, which wasn't surprising. But in women, it was behind 47 percent – less than half. That has major implications for the prevention and treatment of heart attacks.

This research shines a spotlight on heart attack causes that have historically been under-recognized, particularly in women. In women, 34 percent of all heart attack events were attributed to supply/demand mismatch secondary myocardial infarctions (SSDMs) – defined as an imbalance of oxygen supply and demand caused by other stressors on the body, such as anemia or an infection.

Among the other factors significantly contributing to heart attacks were spontaneous coronary artery dissections (SCADs), where tears in artery walls collect blood, and embolisms (blood clots traveling from other areas of the body).

Causes of Myocardial Infarction in Younger Patients: Troponin-Eleva...

Why the human brain matures slower than its primate relatives

The human brain is a fascinating and complex organ that supports numerous sophisticated behaviors and abilities that are observed in no other animal species. For centuries, scientists have been trying to understand what is so unique about the human brain and how it develops over the human lifespan.

Researchers have recently set out to study both the human and macaque brain, comparing their development over time using various genetic and molecular analysis tools. Their paper, published in Nature Neuroscience, highlights some key differences between the two species, with the human pre-frontal cortex (PFC) developing slower than the macaque PFC.

The researchers collected several samples of brain tissue that was surgically removed from the PFC of macaques and humans at different stages after birth. The human subjects were children with epilepsy who were undergoing surgical procedures as part of their treatment plan.

The researchers analyzed the expression of genes in single cells taken from the tissues they collected, as well as chromatin accessibility (i.e., how open DNA is within individual cells). They also mapped the expression of genes across the entire brain tissues, using a technique known as spatial transcriptomics, and looked at the types of cells that were present.

"Integrative analyses outlined species-specific dynamic trajectories of different cell types, highlighting key windows and gene regulatory networks for processes such as synaptogenesis, synaptic pruning and gliogenesis," wrote the authors in their paper.

The researchers' analyses revealed that the human PFC takes longer to develop than that of macaques. They also observed that glial progenitors (i.e., stem-like cells that later divide and develop into specific types of glial cells) proliferate more in humans.
"We identified regulatory correlates of the prolonged development of human PFC relative to macaques," wrote the researchers. "Glial progenitors showed higher proliferation capability in humans compared to macaques, associated with distinct gene expression profiles. Furthermore, we uncovered cell types and lineages most susceptible to neurodevelopmental and neuropsychiatric disorders, focusing on transcription factors with human-specific expression features."

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they gathered new valuable observations that could explain in greater detail known differences between the brain functions of humans and other primates. Notably, the researchers also identified transcription factors that modulate the development of the human brain but not of macaques, while also pinpointing types of cells in human tissues that are known to be affected in the brains of patients with specific disorders.

Jiyao Zhang et al, Single-cell spatiotemporal transcriptomic and chromatin accessibility profiling in developing postnatal human and macaque prefrontal cortex, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02150-7

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"Our discoveries shed light on human-specific regulatory programs extending postnatal cortical maturation through coordinated neuronal and glial development, with implications for cognition and neurodevelopmental disorders," wrote the team.

How do I make clear ice at home? A food scientist shares easy tips

Clear ice forms when water freezes in a single direction, pushing air and impurities to one end, unlike typical home freezing that traps them throughout the cube and causes cloudiness. Using an insulated container to promote directional freezing produces clear ice, while water quality or boiling alone does not prevent cloudiness. Clear ice is denser, melts slower, and resists imparting flavors.

Clear ice is actually made from regular water—what's different is the freezing process.

With a little help from science, you can make clear ice at home, and it's not even that tricky. However, there are quite a few hacks on the internet that won't work. Let's dive into the physics and chemistry involved.

Why ice goes cloudy

Homemade ice is often cloudy because it has a myriad of tiny bubbles and other impurities. In a typical ice cube tray, as freezing begins and ice starts to form inward from all directions, it traps whatever is floating in the water: mostly air bubbles, dissolved minerals and gases.

These get pushed toward the center of the ice as freezing progresses and end up caught in the middle of the cube with nowhere else to go.

That's why when making ice the usual way—just pouring water into a vessel and putting in the freezer—it will always end up looking somewhat cloudy. Light scatters as it hits the finished ice cube, colliding with the concentrated core of trapped gases and minerals. This creates the cloudy appearance.

The point of clear ice

As well as looking nice, clear ice is denser and melts slower because it doesn't have those bubbles and impurities. This also means that it dilutes drinks more slowly than regular, cloudy ice.

Because it doesn't have impurities, the clear ice should also be free from any inadvertent flavors that could contaminate your drink.

Additionally, because it's less likely to crumble, clear ice can be easily cut and formed into different shapes to further dress up your cocktail.

If you've tried looking up how to make clear ice before, you've likely seen several suggestions. These include using distilled, boiled or filtered water, and a process called directional freezing. Here's the science on what works and what doesn't.

Myths about clear ice that don't work

You might think that to get clear ice, you simply need to start out with really clean water. However, a recent study found this isn't the case.

Using boiling water: Starting out with boiling water does mean the water will have less dissolved gases in it, but boiling doesn't remove all impurities. It also doesn't control the freezing process, so the ice will still become cloudy.

Using distilled water: While distilling water removes more impurities than boiling, distilled water still freezes from the outside in, concentrating any remaining impurities or air bubbles in the center, again resulting in cloudy ice.

Using filtered or tap water: Filtering the water or using tap water also doesn't stop the impurities from concentrating during the conventional freezing process.

What actually works

As it turns out, it's not the water quality that guarantees clear ice. It's all about how you freeze it. The main technique for successfully making clear ice is called "directional freezing."

Directional freezing is simply the process of forcing water to freeze in a single direction instead of from all sides at once, like it does in a regular ice cube tray.

This way, the impurities and air will be forced to the opposite side from where the freezing starts, leaving the ice clear except for a small cloudy section.

In practice, this means insulating the sides of the ice container so that the water freezes in one direction, typically from the top down. This is because heat transfer and phase transition from liquid to solid happens faster through the exposed top than the insulated sides.

Part 2

How to make clear ice at home

The simplest way to have a go at directional freezing at home is to use an insulated container—you can use a really small cooler (that is, an "esky"), an insulated mug or even a commercially available insulated ice cube tray designed for making clear ice at home.

Fill the insulated container with water and place it in the freezer, then check on it periodically.

Once all the impurities and air bubbles are concentrated in a single cloudy area at the bottom, you can either pour away this water before it's fully frozen through, or let the block freeze solid and then cut off the cloudy portion with a large serrated knife, then cut the ice into cubes for your drinks.

If using a commercial clear ice tray, it will likely come with instructions on how to get rid of the cloudy portion so you can enjoy the sparkling clear ice.

How do I make clear ice at home? A food scientist shares easy tips

Author: Paulomi (Polly) Burey

The gut bacteria that put the brakes on weight gain in mice

The gut bacterium Turicibacter reduces weight gain and improves metabolic health in mice on a high-fat diet by producing fatty molecules that lower ceramide levels. Obese individuals tend to have less Turicibacter, suggesting a potential role in human weight regulation. Turicibacter’s effects depend on dietary fat, indicating a feedback loop between diet and gut microbiota.

The gut microbiome is intimately linked to human health and weight. Differences in the gut microbiome—the bacteria and fungi in the gut—are associated with obesity and weight gain, raising the possibility that changing the microbiome could improve health. But any given person's gut contains hundreds of different microbial species, making it difficult to tell which species could help.

Now, new research has identified a specific type of gut bacteria, called Turicibacter, that improves metabolic health and reduces weight gain in mice on a high-fat diet.

People with obesity tend to have less Turicibacter, suggesting that the microbe may promote healthy weight in humans as well. The results could lead to new ways to control weight by adjusting gut bacteria.

The results are published in Cell Metabolism.

The researchers found that a rod-shaped bacterium called Turicibacter could single-handedly reduce blood sugar, levels of fat in the blood, and weight gain for mice on a high-fat diet.

Turicibacter appears to promote metabolic health by producing fatty molecules that are absorbed by the small intestine. When the researchers added purified Turibactor fats to a high-fat diet, they had the same weight-controlling effects as Turicibacter itself.

They don't yet know which fatty molecules are the important part—the bacterium produces thousands of different fats, in what Klag describes as a "lipid soup"—but they hope to narrow down on the most important molecules in future work for potential therapeutic use.

Turicibacter appears to improve metabolic health by affecting how the host produces a fatty molecule called ceramides, the researchers found.

 The fats produced by Turicibacter are able to keep ceramide levels low, even for mice on a high-fat diet.

Turicibacter levels are themselves affected by how much fat the host eats, the researchers discovered. The bacterium won't grow if there's too much fat in its environment, so mice fed a high-fat diet will lose Turicibacter from their gut microbiome unless their diet is regularly supplemented with the microbe.

The results point to a complex feedback loop, in which a fatty diet inhibits Turicibacter and fats produced by Turicibacter improve how the host responds to dietary fats.

Kendra Klag et al, Dietary fat disrupts a commensal-host lipid network that promotes metabolic health, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2025.10.007

With every extinction, we lose not just a species but a treasure trove of knowledge

Extinction results in the irreversible loss of unique scientific knowledge, cultural traditions, and spiritual connections associated with each species. Current extinction rates, driven mainly by human activities, far exceed natural background levels, threatening up to 1 million species this century. These losses diminish biodiversity, erode cultural and spiritual heritage, and reduce opportunities for future discoveries.

Study shows tooth loss, not low-protein intake, drives memory decline in aging mice
Tooth loss in aging mice leads to significant memory decline and increased markers of brain cell death, independent of dietary protein intake. Reduced chewing, rather than low-protein diet, promotes inflammation and neuronal loss in hippocampal regions critical for memory, highlighting a direct link between oral health and cognitive function.

Tooth loss doesn't just make eating harder, it may also make thinking more challenging. A new study shows that aging mice missing their molars experience measurable cognitive decline, even when their nutrition remains perfectly intact.

The study examined whether tooth loss itself, independent of nutritional deficiency such as a low-protein diet, can cause cognitive decline in male mice.

To explore how chewing ability and nutrition jointly influence the brain, the research team used aging-prone male mice and assigned them to one of four conditions: a normal-protein diet with no tooth extraction, a low-protein diet with no extraction, molar extraction with a normal-protein diet, and molar extraction with a low-protein diet.

After six months, the mice underwent behavioral tests and detailed analyses of their brain tissue for markers of inflammation, neuronal loss, and cell death–related gene expression.

The results were striking: mice that lost their molars showed significant memory decline even though they received the same diet as the control groups.

This suggests that reduced masticatory stimulation, not dietary protein intake, contributes to cognitive deterioration. It is surprising that a peripheral event in the mouth can so profoundly affect the central nervous system.

Brain tissue analysis supported these behavioral findings. The results showed no interaction effect between tooth loss and low-protein diet on the levels of the Bax/Bcl-2 mRNA ratio, a marker representing cell death versus survival.

Instead, tooth loss alone significantly increased this ratio, indicating a shift toward pro-apoptotic, or cell death–promoting, activity in the brain. Losing teeth caused inflammation and cell loss in the CA1 and dentate gyrus regions of the hippocampus—areas essential for memory formation and storage.

Meanwhile, the effects of a low-protein diet were limited to the CA3 region, which plays a role in pattern completion. These findings suggest that a reduction in chewing induces pro–cell death pathways in the brain.

This study adds to growing evidence that oral health is deeply connected to brain health, and that protecting one's chewing ability may be a simple but powerful strategy for preserving cognitive function later in life.

Rie Hatakeyama et al, Tooth loss induces cognitive decline independent of low-protein diet intake in male mice, Archives of Oral Biology (2025). DOI: 10.1016/j.archoralbio.2025.106421

New sprayable powder forms instant gel barrier to stop severe bleeding in seconds

A sprayable powder hemostatic agent rapidly forms a hydrogel barrier within one second upon contact with blood, effectively stopping severe bleeding, including from deep or irregular wounds. Composed of biocompatible natural materials, it demonstrates high absorption (725%), strong adhesion (>40 kPa), low hemolysis (<3%), high cell viability (>99%), and antibacterial properties (99.9%).

Youngju Son et al, An Ionic Gelation Powder for Ultrafast Hemostasis and Accelerated Wound Healing, Advanced Functional Materials (2025). DOI: 10.1002/adfm.202523910

'Don't use them': Tanning beds triple skin cancer risk, study finds

Tanning bed use is associated with nearly a threefold increase in melanoma risk, with users developing more DNA mutations in skin cells, particularly melanocytes. Melanomas in tanning bed users often appear on body areas usually shielded from sunlight. Over 80% of common melanomas are linked to ultraviolet radiation, including that from tanning beds.

Pedram Gerami et al, Molecular effects of indoor tanning, Science Advances (2025). DOI: 10.1126/sciadv.ady4878. www.science.org/doi/10.1126/sciadv.ady4878

Clouds are vital to life—but many are becoming wispy ghosts. Here's how to see the changes above us
Cloud cover, especially highly reflective clouds near the equator, is steadily declining by 1.5–3% per decade, reducing Earth's ability to reflect solar radiation and increasing heat retention. This shift alters rainfall patterns and climate stability, with the loss often unnoticed. Clouds play a crucial role in moderating temperature and sustaining life, making their decline a significant concern.

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skies that feel hollowed out, clouds that look like they have lost their conviction. I think of them as ghost clouds. Not quite absent, but not fully there. These wispy formations drift unmoored from the systems that once gave them coherence. Too thin to reflect sunlight, too fragmented to produce rain, too sluggish to stir up wind, they give the illusion of a cloud without its function.

Clouds are vital to life – but many are becoming wispy ghosts. Here...

Traffic Has a Curious Effect on The Atmosphere's Electric Field, Study Shows

Detailed measurements collected in metropolitan Tel Aviv, Israel, have revealed how the ebb and flow of traffic throughout the week affects the electric field generated by Earth's atmosphere.

A number of specific pollutants were tracked, including gases and particles from car exhaust and tire wear, and additional compounds formed in chemical reactions with gases in the atmosphere.

The atmospheric electric field is the result of natural differences in charge between the surface and upper atmosphere, powered largely by the swirl of currents that form in thunderstorms.

A number of factors influence this planetary circuit, including fluctuations in local weather and air pollution. 

The data showed that traffic pollution in Tel Aviv has an immediate impact on the atmospheric electric field in the region, with both NOx gases and vehicle congestion peaking at the same times (the rush hours at the start and end of the working day).

There was also an association between PM2.5 particles and the electric field, though this was delayed by around two-and-a-half hours. The researchers put this down to different particle size, chemical composition, and lifetime in the atmosphere.

The team reports a noticeable weekend effect as well, with significant drops in traffic pollution corresponding with a weakening of the electrical field. That's further confirmation that the two are indeed linked.

What they observed is a direct physical link between emission peaks and electrical variability.

Nitrogen oxides reduce atmospheric conductivity very quickly, so the electric field responds almost instantaneously during traffic rush hours.

The reason behind the effect is ions: the charged particles in the air. Pollutants can capture these ions, reducing the conductivity of the atmospheric electric field, which then triggers a compensatory effect where the electric field gets stronger.

These changes aren't dangerous, and nor is the electric field itself .

Effects of urban air pollution on the fair-weather electric field i...

Ancient African bedrock reveals the violent beginnings of life on our blue planet

Ancient bedrock from the Makhonjwa Mountains reveals that early Earth featured extensive oceans, intense volcanic activity, and a hostile atmosphere rich in methane and CO2 but lacking oxygen. Life began as anaerobic microbes near undersea vents, thriving despite frequent volcanic eruptions, earthquakes, and asteroid impacts. Plate tectonics and a stable climate enabled Earth to remain habitable and blue.

The Oldest Rocks on Earth | Columbia University Press

Ancient African bedrock reveals the violent beginnings of life on o...

Evidence of upright walking found in 7-million-year-old Sahelanthropus fossils

Analysis of Sahelanthropus tchadensis fossils using 3D methods identified features unique to bipedal hominins, including a femoral tubercle, femoral antetorsion, and gluteal muscle attachments. These findings indicate that this seven-million-year-old species was adapted for upright walking, making it the earliest known bipedal hominin.

The analysis revealed three features that point to bipedalism in Sahelanthropus:

The presence of a femoral tubercle, which provides attachment for the iliofemoral ligament linking the pelvis to the femur and has so far been identified only in hominins

A natural twist, specifically within the range of hominins, in the femur—or femoral antetorsion—that helps legs to point forward, thereby aiding walking.

The presence, drawn from the 3D analysis, of gluteal, or butt, muscles similar to those in early hominins that keep hips stable and aid in standing, walking, and running.

Scott Williams, Earliest evidence of hominin bipedalism in Sahelanthropus tchadensis, Science Advances (2026). DOI: 10.1126/sciadv.adv0130. www.science.org/doi/10.1126/sciadv.adv0130

Two white-blooded fish, two paths: Icefish and noodlefish independently lose red blood cell function

Both Antarctic icefish and Asian noodlefish independently evolved to lack hemoglobin and red blood cells, resulting in white blood. Icefish survive in cold, oxygen-rich waters by dissolving oxygen directly in their blood, while noodlefish, living in warmer waters, lost myoglobin and have nonfunctional hemoglobin genes, likely aided by their short, juvenile-like life span. These findings highlight distinct evolutionary paths to similar physiological outcomes.

 Yu-Long Li et al, Independent evolutionary deterioration of the oxygen-transport system in Asian noodlefishes and Antarctic icefishes, Current Biology (2025). DOI: 10.1016/j.cub.2025.05.050

Bacteria reveal second 'shutdown mode' for surviving antibiotic treatment
Bacteria can survive antibiotic treatment through two distinct growth-arrest states: a regulated, protective dormancy and a disrupted, dysregulated arrest marked by impaired membrane stability. This duality explains conflicting observations of antibiotic persistence and suggests that targeting each state differently could improve treatment effectiveness and reduce infection relapse.

A new study reveals that bacteria can survive antibiotic treatment through two fundamentally different "shutdown modes," not just the classic idea of dormancy. The paper is published in the journal Science Advances.

The researchers show that some cells enter a regulated, protective growth arrest, a controlled dormant state that shields them from antibiotics, while others survive in a disrupted, dysregulated growth arrest, a malfunctioning state marked by vulnerabilities, especially impaired cell membrane stability. This distinction is important because antibiotic persistence is a major cause of treatment failure and relapsing infections even when bacteria are not genetically resistant, and it has remained scientifically confusing for years, with studies reporting conflicting results.

By demonstrating that persistence can come from two distinct biological states, the work helps explain those contradictions and provides a practical path forward: different persister types may require different treatment strategies, making it possible to design more effective therapies that prevent infections from coming back.

For years, persistence has largely been blamed on bacteria that shut down and lie dormant, essentially going into a kind of sleep that protects them from antibiotics designed to target active growth. But new research reveals that this explanation tells only part of the story.

The study shows that high survival under antibiotics can originate from two fundamentally different growth-arrest states, and they are not just variations of the same "sleeping" behavior. One is a controlled, regulated shutdown, the classic dormancy model. The other is something entirely different: a disrupted, dysregulated arrest, where bacteria survive not by protective calm but by entering a malfunctioning state with distinct vulnerabilities.

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Two 'survival modes' and why they matter
The researchers identified two archetypes of growth arrest that can both lead to persistence, but for very different reasons:

Regulated growth arrest: a protected dormant state. In this mode, bacteria intentionally slow down and enter a stable, defended condition. These cells are harder to kill because many antibiotics rely on bacterial growth to be effective.

Disrupted growth arrest: survival through breakdown. In the second mode, bacteria enter a dysregulated and disrupted state. This is not a planned shutdown, but a loss of normal cellular control. These bacteria show a broad impairment in membrane homeostasis, a core function needed to maintain the integrity of the cell. That weakness could become a key treatment target.
Antibiotic persistence plays a role in recurring infections across a wide range of settings, from chronic urinary tract infections to infections tied to medical implants. Yet despite intense research, scientists have struggled to agree on a single mechanism explaining why persister cells survive. Different experiments have produced conflicting results about what persisters look like and how they behave.

This study offers an explanation: researchers may have been observing different types of growth-arrested bacteria without recognizing they were distinct.

By separating persistence into two different physiological states, the findings suggest a future where treatments could be tailored, targeting dormant persisters one way, and disrupted persisters another.
How the researchers saw what others missed
The team combined mathematical modeling with several high-resolution experimental tools, including:

Transcriptomics, to measure how bacterial gene expression shifts under stress
Microcalorimetry, to track metabolic changes through tiny heat signals
Microfluidics, allowing scientists to observe single bacterial cells under controlled conditions
Together, these approaches revealed clear biological signatures distinguishing regulated growth arrest from disrupted growth arrest, along with the specific vulnerabilities of the disrupted state.

Adi Rotem et al, Differentiation between regulated and disrupted growth-arrests allows tailoring of effective treatments for antibiotic persistence, Science Advances (2026). DOI: 10.1126/sciadv.adt6577. www.science.org/doi/10.1126/sciadv.adt6577

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Tumor bacteria linked to immunotherapy resistance in head and neck cancer

Researchers have discovered that bacteria inside cancerous tumors may be key to understanding why immunotherapy works for some patients but not others.
Elevated bacterial levels within head and neck squamous cell carcinoma tumors suppress immune responses and contribute to resistance against immunotherapy. These bacteria attract neutrophils, which can inhibit the immune activity required for effective treatment. Reducing tumor bacteria with antibiotics may enhance immunotherapy efficacy, suggesting new avenues for patient selection and targeted interventions.

These studies shift the focus of immunotherapy resistance research beyond tumor genetics to unexpected factors like the tumor microbiome.

By identifying bacteria as a key barrier to treatment, we're opening the door to new strategies for patient selection and targeted antibiotic therapies, potentially improving outcomes for those who don't benefit from immunotherapy, the researchers say.

The research confirmed that patients with high tumor bacteria levels had poorer outcomes with immunotherapy compared to standard chemoradiotherapy.

Together, the two studies showed that elevated bacteria levels in tumors attract neutrophils, white blood cells that fight infection. While neutrophils are essential for combating bacterial infections, in cancer they can suppress the immune system needed for immunotherapy to work effectively.

These findings lay the foundation for future research on why bacteria are attracted to tumors and how to modify them to improve treatment.

1. Tumor ecosystem and microbiome features associated with efficacy and resistance to avelumab plus chemoradiotherapy in head and neck cancer, Nature Cancer (2025). DOI: 10.1038/s43018-025-01068-0

2. Nature Cancer (2025). www.nature.com/articles/s43018-025-01067-1

Assisted reproductive technology associated with higher risk of childhood atopic diseases

Researchers  report higher risks of atopic disease among children conceived via assisted reproductive technology compared to those conceived naturally.

Assisted reproductive technology use has increased, with estimates placing assisted reproductive technology at 1% to 4% of births, especially in high-income societies, alongside wider use of embryo transfer.

Atopic disease covers three conditions; asthma, allergic rhinitis, and atopic dermatitis. Atopic diseases are believed to be influenced by genetic factors and environmental triggers, with developmental origins of health and disease theory proposing that fetal-stage factors can program changes in organ and tissue structure and function.

In the study, "Atopic Disease Development in Offspring Conceived via Assisted Reproductive Technology," published in JAMA Network Open, researchers conducted a retrospective, population-based cohort analysis to investigate whether conception via assisted reproductive technology was associated with atopic disease development in offspring.

Data came from a pool of 23.5 million people in Taiwan through Taiwan's National Health Insurance Research Database, Assisted Reproduction Database, and the Maternal and Child Health Database.

Assisted reproductive technology included procedures such as in vitro fertilization and embryo transfer, intracytoplasmic sperm injection, gamete intrafallopian transfer, zygote intrafallopian transfer, and tubal embryo transfer.

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Cohort groups included 13,957 children conceived via assisted reproductive technology and 55,828 children conceived naturally after 1:4 matching by maternal age, neonatal sex, and birth month.

Asthma, allergic rhinitis, and atopic dermatitis were analyzed and reported individually, allowing a child to receive one, two, or all three diagnoses during follow-up. Mean follow-up for asthma measured 7.99 years in the assisted reproductive technology group and 8.41 years in the control group, with allergic rhinitis at 5.79 and 6.34 years, and atopic dermatitis at 7.34 and 7.62 years.
Intracytoplasmic sperm injection use showed no statistically significant differences in risk estimates across the three outcomes. Adjusted hazard ratios measured 1.04 for asthma, 0.99 for allergic rhinitis, and 1.04 for atopic dermatitis.

Fresh embryo transfer carried a higher allergic rhinitis risk than frozen embryo transfer, with an adjusted hazard ratio of 1.12. Asthma showed no statistically significant difference between fresh and frozen embryo transfer, with an adjusted hazard ratio of 0.96, and atopic dermatitis showed no statistically significant difference, with an adjusted hazard ratio of 1.01.

Interaction testing showed no statistically significant interaction between intracytoplasmic sperm injection and embryo type for asthma, allergic rhinitis, or atopic dermatitis.
Researchers conclude that children conceived via assisted reproductive technology had a higher risk of developing asthma, allergic rhinitis, or atopic dermatitis than children conceived naturally. Findings supported an association between assisted reproductive technology conception and later atopic disease development across the outcomes evaluated.

Yao-Chi Hsieh et al, Atopic Disease Development in Offspring Conceived via Assisted Reproductive Technology, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.51690

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The (metabolic) 'cost of life': New method quantifies hidden energy costs of maintaining metabolic pathways
A new thermodynamic framework quantifies the hidden energetic costs required to maintain specific metabolic pathways and suppress alternatives, beyond direct metabolic energy use. This method ranks pathways by their maintenance and restriction costs, revealing that nature often selects the least dissipative routes, providing insights into the evolution and selection of metabolic processes.

There are "costs of life" that mechanical physics cannot calculate. A clear example is the energy required to keep specific biochemical processes active—such as those that make up photosynthesis, although the examples are countless—while preventing alternative processes from occurring.

In mechanics, no displacement implies zero work, and, put simply, there is no energetic cost for keeping things from happening. Yet careful stochastic thermodynamic calculations show that these costs do exist—and they are often quite significant.

A paper published in the Journal of Statistical Mechanics: Theory and Experiment (JSTAT) proposes a way to calculate these costs from a thermodynamic perspective and thus to offer a new tool for understanding the selection and evolution of metabolic pathways at the root of life.

When, in an ancient ocean, a handful of organic molecules formed an external boundary—the first cell membrane—a sharp distinction between an inside and an outside appeared for the first time.

From that moment on, that primordial system had to invest energy to maintain this compartmentalization and to select, among the many chemical reactions that could occur, only a few metabolic pathways capable of exploiting valuable substances taken from the "outside" and transforming them into new products. Life was born together with this effort of compartmentalization and choice.

Metabolic processes have a direct energetic cost, but they also require an "extra cost" to keep steering chemical flows into a preferred pathway rather than letting them disperse into all physically possible alternatives.

Part 1

Yet from the viewpoint of classical mechanics, compartmentalization and reaction selection—the "constraints" imposed at a system's boundaries—should have no cost at all, as they are treated as fixed external conditions that do not contribute to entropy production.
Researchers now developed a method to calculate these overlooked costs to rank the pathways. This allows researchers to assess their biological efficiency—valuable information for evolutionary studies exploring how life emerged on our planet.
devised a general method to estimate the thermodynamic costs of metabolic processes systematically. In their framework, the cell is imagined as a system crossed by a constant flow, where, for instance, one molecule (a nutrient) enters and another (a product or waste) exits.

Given the underlying chemistry, one can generate all chemically possible pathways that convert the input into the output. Each pathway has its own "thermodynamic cost." Instead of calculating energy in the classical sense, the method estimates how improbable it would be—in a world driven solely by spontaneous chemistry—to see the network (the set of molecules and reactions that convert input to output) behave in exactly that way.

This improbability has two components. The first is the maintenance cost, meaning how unlikely it is to sustain a constant flow through a certain pathway. The second is the restriction cost, which measures how unlikely it is to block all the alternative reactions in the network while keeping only the pathway of interest active.

The calculated improbability represents the cost of that process, which can then be used to classify metabolic pathways according to how "expensive" it is for the cell to keep one pathway active and silence the others.
Part 2

In nature we usually see that one process is favoured over many. Why is this?

It's true, but in biological systems, catalysis often intervenes—the action of facilitating molecules, enzymes—which accelerate reactions and make them less costly, achieving the same effect as having multiple pathways in parallel. This evolutionary choice happens because maintaining many pathways can have other drawbacks, such as producing many potentially toxic molecules.

 Thermodynamic ranking of pathways in reaction networks, Journal of Statistical Mechanics Theory and Experiment (2025). DOI: 10.1088/1742-5468/ae22eb.

Part 3

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Orange pigments in birds and human redheads prevent cellular damage, study shows

A pigment that makes feathers and hair orange helps prevent cellular damage by removing excess cysteine from cells. Pheomelanin is an orange-to-red pigment that is built with the amino acid cysteine and found in human red hair and fair skin, as well as in bird feathers. Previous research has shown that pheomelanin is associated with increased melanoma risk, raising questions about why evolution has maintained genetic variants that promote pheomelanin production.

Published in PNAS Nexus, researchers studied 65 adult zebra finches divided into treatment and control groups. In the treatment group, male zebra finches received dietary cysteine and ML349, a drug that blocks pheomelanin synthesis.

Male birds treated with both cysteine and ML349 showed increased oxidative damage in blood plasma compared to males receiving only cysteine, when the authors controlled for overall expression of the regulator of antioxidants by melanocytes. Female birds, which do not produce pheomelanin, tended to show increased oxidative damage when treated with cysteine alone as compared to female controls.

According to the authors, pheomelanin synthesis helps maintain cysteine homeostasis by converting excess cysteine into inert pigment, which may explain why pheomelanin-promoting genetic variants persist despite being associated with increased melanoma risk.

 Ismael Galván et al, MC1R depalmitoylation inhibition reveals a physiological role for pheomelanin, PNAS Nexus (2026). DOI: 10.1093/pnasnexus/pgaf391

Vitamin C may help protect fertility from a harmful environmental chemical

Exposure to potassium perchlorate impairs sperm production and damages testes in a fish model, indicating potential reproductive risks. Co-administration of vitamin C reduces this damage and improves fertility, likely by counteracting oxidative stress. These results suggest vitamin C may help protect reproductive health from certain environmental contaminants.

Sourav Chakraborty et al, Vitamin C Mitigates Potassium Perchlorate Exposure-Induced Disruption of Spermatogenesis in Medaka, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c09514

Diet may influence tinnitus risk in women

Diet may influence the risk of women developing tinnitus, according to a study published online Dec. 17 in the American Journal of Epidemiology.
Higher fruit intake is associated with reduced risk of developing persistent tinnitus in women, while greater consumption of whole grains, legumes, and sugar-sweetened beverages is linked to increased risk. Overall healthy diet patterns did not consistently affect tinnitus risk. These associations remained after accounting for lifetime noise exposure.

This study provides compelling evidence that dietary intake can influence the development of persistent tinnitus.

Sharon G Curhan et al, Longitudinal Study of Dietary Intake and Risk of Persistent Tinnitus in Two Large Independent Cohorts of Women, American Journal of Epidemiology (2025). DOI: 10.1093/aje/kwaf277

Jellyfish don’t need brains to sleep!

Jellyfish sleep like humans — even though they don’t have brains

Jellyfish and sea anemones have neurons, but no brains — and yet they still seem to sleep in ways strikingly similar to humans. The findings bolster a theory that sleep evolved — before centralized nervous systems — to repair DNA damage that builds up in individual nerve cells while animals are awake. Neurons are very precious. They don’t divide, so you need to keep them intact.

The findings bolster a theory that sleep evolved, at least in part, to protect the DNA in individual nerve cells, helping to repair damage that builds up while animals are awake.

Sleep is a risky state for animals. It leaves them vulnerable to predators and environmental hazards, and it cuts into time that could otherwise be spent foraging, mating or caring for offspring. Scientists broadly agree that sleep must serve a fundamental biological function, because evolution has preserved it across all animals with nervous systems studied so far.

These results suggest that DNA damage and cellular stress in simple nerve nets may have driven the evolution of sleep.

https://www.nature.com/articles/s41467-025-67400-5

https://www.nature.com/articles/d41586-026-00044-7?utm_source=Live+...

Restoring mitochondria shows promise for treating chronic nerve pain

For millions living with nerve pain, even a light touch can feel unbearable. Scientists have long suspected that damaged nerve cells falter because their energy factories known as mitochondria don't function properly.

Now, research published in Nature suggests a way forward: supplying healthy mitochondria to struggling nerve cells.

Using human tissue and mouse models, researchers found that replenishing mitochondria significantly reduced pain tied to diabetic neuropathy and chemotherapy-induced nerve damage. In some cases, the relief lasted up to 48 hours. By giving damaged nerves fresh mitochondria—or helping them make more of their own—we can reduce inflammation and support healing, say the scientists. Their findings build on growing evidence that cells can swap mitochondria, a process that scientists are beginning to recognize as a built-in support system that may affect many conditions including obesity, cancer, stroke, and chronic pain.

When this mitochondrial handoff is disrupted, nerve fibers begin to degenerate—triggering pain, tingling and numbness, often in the hands and feet, the distal ends of the nerve fibers.

By sharing energy reserves, satellite glial cells may help keep neurons out of pain.

When this energy transfer was boosted, pain behaviors in mice dropped by as much as 50%, the study showed.

Researchers also tried a more direct approach. Injecting isolated mitochondria—whether from humans or mice—directly into the dorsal root ganglia, a cluster of nerve cells that send messages to the brain, produced similar results, but only when the donor mitochondria were healthy; samples from people with diabetes had no effect.

The team also identified a protein, MYO10, as essential for forming the nanotubes that enable the mitochondrial transfer.

Instead of masking symptoms, the approach could fix what the team sees as the root problem—restoring the energy flow that keeps nerve cells healthy and resilient.

Ru-Rong Ji, Mitochondrial transfer from glia to neurons protects against peripheral neuropathy, Nature (2026). DOI: 10.1038/s41586-025-09896-x. www.nature.com/articles/s41586-025-09896-x

The work highlights a previously undocumented role for satellite glial cells, which appear to deliver mitochondria to sensory neurons through tiny channels called tunneling nanotubes.

Oil residues can travel over 5,000 miles on ocean debris, study finds

Oil residues can adhere to ocean debris such as plastic, glass, and rubber, enabling them to travel over 5,200 miles across the Atlantic. Chemical analyses and ocean current modeling linked oily debris found in Florida to a 2019 oil spill off Brazil, demonstrating that plastics can act as long-distance carriers for oil pollution, extending the environmental impact of oil spills.

"Long-Range Transport of Oil by Marine Plastic Debris: Evidence from an 8500 km Journey," Environmental Science & Technology (2026). DOI: 10.1021/acs.est.5c14571

Dark matter and neutrinos may interact, challenging standard model of the universe

Scientists are a step closer to solving one of the universe's biggest mysteries as new research finds evidence that two of its least understood components may be interacting, offering a rare window into the darkest recesses of the cosmos.

The  findings relate to the relationship between dark matter, the mysterious, invisible substance that makes up about 85% of the matter in the universe, and neutrinos, one of the most fundamental and elusive subatomic particles. Scientists have overwhelming indirect evidence for the existence of dark matter, while neutrinos, though invisible and with an extremely small mass, have been observed using huge underground detectors.

The standard model of cosmology (Lambda-CDM), with its origins in Einstein's general theory of relativity, posits that dark matter and neutrinos exist independently and do not interact with one another.

New new research published in Nature Astronomy casts doubt on this theory, challenging the long-standing cosmological model. The research detects signs that these elusive cosmic components may interact, offering a rare glimpse into parts of the universe we can't see or easily detect.

By combining data from different eras, scientists have found evidence of interactions between dark matter and neutrinos that could have affected the way cosmic structures, such as galaxies, formed over time.

Data regarding the early universe comes from two main sources: the highly sensitive ground-based Atacama Cosmology Telescope (ACT), and the Planck Telescope, a space observatory operated by the European Space Agency (ESA) from 2009 to 2013. Both instruments were specifically designed to study the faint afterglow of the Big Bang.

Lei Zu et al, A solution to the S₈ tension through neutrino–dark matter interactions, Nature Astronomy (2026). DOI: 10.1038/s41550-025-02733-1

Eating more food preservatives linked to higher risk of type 2 diabetes

Higher intake of food preservatives, including both non-antioxidant and antioxidant additives, is associated with an increased risk of type 2 diabetes, with incidence rates rising by 47%, 49%, and 40% respectively for higher consumption groups. Twelve commonly used preservatives, such as potassium sorbate (E202) and citric acid (E330), showed significant associations with elevated diabetes risk.

Higher consumption of food preservatives, widely used in industrially processed foods and beverages to extend their shelf life, has been linked to an increased risk of type 2 diabetes.

Preservatives belong to the family of food additives and are widely used by the food industry worldwide. Of the three and a half million foods and beverages listed in the Open Food Facts World database in 2024, more than 700,000 contain at least one of these substances.

Additives with preservative properties have been grouped into two categories in the work carried out by Inserm researchers: non-antioxidants (which inhibit microbial growth or slow down the chemical changes that lead to food spoilage) and antioxidants (which delay or prevent food spoilage by eliminating or limiting oxygen levels in packaging).

On packaging, they generally correspond to European codes between E200 and E299 (for preservatives in the strict sense) and between E300 and E399 (for antioxidant additives).

Experimental studies have suggested that certain preservatives may damage cells and DNA and have adverse effects on metabolism.

A research team set out to examine the links between exposure to these preservatives and type 2 diabetes. The team drew on data provided by more than 100,000 French adults.

Analyses of data showed higher consumption of preservative additives overall, non-antioxidant preservatives and antioxidant additives was associated with an increased incidence of type 2 diabetes, by 47%, 49% and 40% respectively, compared to the lowest levels of consumption.

Of the 17 preservatives studied individually, higher consumption of 12 of them was associated with an increased risk of type 2 diabetes: widely used non-antioxidant food preservatives (potassium sorbate (E202), potassium metabisulfite (E224), sodium nitrite (E250), acetic acid (E260), sodium acetates (E262) and calcium propionate (E282)) and antioxidant additives (sodium ascorbate (E301), alpha-tocopherol (E307), sodium erythorbate (E316), citric acid (E330), phosphoric acid (E338) and rosemary extracts (E392)).

This is the first study in the world on the links between preservative additives and the incidence of type 2 diabetes. Although the results need to be confirmed, they are consistent with experimental data suggesting the harmful effects of several of these compounds.

Associations between preservative food additives and type 2 diabetes incidence in the NutriNet-Santé prospective cohort, Nature Communications (2026). DOI: 10.1038/s41467-025-67360-w

Your genes determine how fast your DNA mutates with age, study shows

Analysis of genetic data from over 900,000 individuals shows that common DNA repeats in blood cells expand with age, with inherited variants at 29 genetic locations modifying expansion rates by up to four-fold. Some DNA repair genes have opposite effects on different repeats. Expansion in the GLS gene is linked to increased risk of kidney and liver disease, highlighting new potential biomarkers and therapeutic targets.

An analysis of genetic data from over 900,000 people shows that certain stretches of DNA, made up of short sequences repeated over and over, become longer and more unstable as we age. The study found that common genetic variants can speed up or slow down this process by up to four-fold, and that certain expanded sequences are linked to serious diseases including kidney failure and liver disease.

More than 60 inherited disorders are caused by expanded DNA repeats: repetitive genetic sequences that grow longer over time. These include devastating conditions like Huntington's disease, myotonic dystrophy, and certain forms of ALS.

Most people carry DNA repeats that gradually expand throughout their lives.

This study demonstrates that DNA repeat expansion is far more widespread than previously recognized and identifies dozens of genes that regulate this process, opening new avenues for developing treatments that could slow disease progression.

Margaux Hujoel, Insights into DNA repeat expansions among 900,000 biobank participants, Nature (2026). DOI: 10.1038/s41586-025-09886-z. www.nature.com/articles/s41586-025-09886-z

Young cancer survivors may face faster aging and possible early-onset dementia

Adolescent and young adult cancer survivors exhibit accelerated aging at both cellular and brain function levels, regardless of treatment type, with chemotherapy contributing most to this effect. Increased biological age correlates with cognitive deficits such as impaired memory and attention. Lifestyle changes like exercise and improved nutrition may help reverse some aging effects.

AnnaLynn M. Williams et al, Epigenetic age acceleration, telomere length, and neurocognitive function in long-term survivors of childhood cancer, Nature Communications (2025). DOI: 10.1038/s41467-025-65664-5

Millions of Your Mother's Cells Persist Inside You

Every human born on this planet is not entirely themselves.

A tiny fraction of our cells – around one in a million – is actually not our own, but comes from our mothers. That means each of us has millions of cells that our immune systems would normally recognize as foreign; yet somehow, in most of us, they hang around peacefully without causing any immune problems.

Now, immunologists have figured out why. A small number of maternal immune cells that cross the placenta during pregnancy actively train the fetus's immune system to tolerate the mother's cells for their entire life.

Micro chimerism is increasingly linked with so many health disorders. This study provides an adaptable platform for scientists to investigate whether these rare cells are the cause of disease, or alternatively, found in diseased tissue at increased levels as part of the natural healing process.

Tolerance to non-inherited maternal antigen is sustained by LysM+ C...

The oldest animal keeps its eyes sharp
Greenland sharks (Somniosus microcephalus) can live to be up to 400 years old, making them the longest-lived vertebrate. They dwell in the almost-sunless waters of the Arctic deep sea, and are often infested with parasites that attach to their eyes, leading scientists to suppose that the animals might be functionally blind. But researchers who studied the sharks’ eyeball in the lab say that it’s quite the contrary: the sharks appear to maintain their vision over centuries with no signs of retinal degeneration — perhaps thanks to a DNA repair mechanism in the retina — and could offer clues to treating age-related vision loss in people.

The visual system of the longest-living vertebrate, the Greenland s...

Omega-3 supplements fail to improve depressive symptoms in young people

Is fish oil the new snake oil?

Fish oil pills rich in omega-3 fatty acids gained attention as a possible add-on treatment for depression, as a few studies on adults found noticeable improvements in symptoms when combined with antidepressants.

When a similar study was conducted with children and adolescents, omega-3 fatty acids did not do any better than a placebo.

A team of researchers from Switzerland carried out a large clinical trial at five different centers, spanning nine months, to test whether adding omega-3 supplements to standard treatment could help teenagers and young adults with moderate-to-severe depression. The study involved 257 participants aged 8 to 18 who were randomly assigned to receive either 1.5 grams of omega-3 supplements or placebo pills daily.

The results are published in JAMA Network Open.

This study revealed that supplementing depression treatment with fish oil pills didn't prove more effective than placebo at improving quality of life, reducing suicidal ideation, or the need for antidepressants. Both groups showed similar improvements during the study and showed depression scores of 36.5 with omega-3 vs. 36.8 with placebo.

The results indicate that omega-3 supplements provide no additional benefit for depression.

Please note that the trial was conducted during the COVID-19 pandemic, which may have influenced the outcomes. 

Gregor Berger et al, ω-3 Fatty Acids in Pediatric Major Depressive Disorder, JAMA Network Open (2026). DOI: 10.1001/jamanetworkopen.2025.48703

Tree bark microbes also clean the air by removing greenhouse and toxic gases

Microbes living on tree bark consume significant amounts of climate-active gases such as methane, hydrogen, and carbon monoxide, in addition to CO2 absorbed by trees. This microbial activity occurs on a global scale, enhancing air purification and contributing to both climate regulation and improved air quality. Different tree species host distinct microbial communities with varying gas-removal capacities.

 Pok Man Leung et al, Bark microbiota modulate climate-active gas fluxes in Australian forests, Science (2026). DOI: 10.1126/science.adu2182. www.science.org/doi/10.1126/science.adu2182

Twin study ties childbearing timing to biological aging

Analysis of Finnish twins indicates that both the number and timing of pregnancies are linked to women's biological aging and lifespan. Women with two to three children and pregnancies between ages 24 and 38 show slower aging and longer life expectancy, while childlessness, early childbearing, or having more than four children are associated with accelerated aging. Epigenetic data support these associations.

A study based on Finnish twins shows that reproductive history is associated, at the population level, with women's lifespan and biological aging. In the study, mothers of large families, women who had no children, or women who had their first child at a very young age appeared to age somewhat faster than other women.

The results suggest that both the number of children and the timing of pregnancies are reflected in women's adult health and life expectancy. The paper is published in the journal Nature Communications.

From an evolutionary biology perspective, organisms have limited resources such as time and energy. When a large amount of energy is invested in reproduction, it is taken away from bodily maintenance and repair mechanisms, which could reduce lifespan.

Somewhat unexpectedly, the study also found that childless women showed faster aging than women with a few children. This result may be explained by other lifestyle or health-related factors whose effects could not be fully controlled for in the analyses.

The research group emphasizes that the findings apply only at the population level. They do not demonstrate cause–effect relationships, nor do they provide a basis for individual recommendations for women of reproductive age. For example, family size has decreased and the age at first birth has increased compared with the period covered by the study.

Part 1

A novel aspect of this study was that aging was also measured biologically. Epigenetic clocks were determined from blood samples from more than one thousand participants. Epigenetic clocks aim to measure biological aging—that is, the gradual deterioration of cells and tissues. With such methods, aging-related changes can be detected years or even decades before death.

The results supported earlier conclusions based on mortality data. According to the epigenetic clocks, women who had either many children or no children at all were biologically somewhat older than their chronological age.
A person who is biologically older than their calendar age is at a higher risk of death.
Having a child at a young age was also associated with biological aging. This too may relate to evolutionary theory, as natural selection may favor earlier reproduction that entails shorter overall generation times, even if it entails health-related costs associated with aging.

Mikaela Hukkanen et al, Epigenetic aging and lifespan reflect reproductive history in the Finnish Twin Cohort, Nature Communications (2026). DOI: 10.1038/s41467-025-67798-y

Part 2

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Suppressing postoperative inflammation may prolong pain

Suppressing inflammation after surgery by inhibiting TNF-α can delay recovery and prolong pain, rather than relieve it. Allowing natural inflammation leads to quicker pain resolution and recovery. These findings suggest that inflammation plays a beneficial role in healing, and indiscriminate use of anti-inflammatory drugs post-surgery may increase the risk of chronic pain.

Taking anti-inflammatory drugs after surgery is fairly standard protocol. But a new study by researchers suggests this approach may be backfiring and that blocking inflammation during this critical time may, in fact, delay recovery and prolong pain rather than relieve it.

If you look across all types of surgeries—anything from an extracted tooth to a hip replacement—the pain resolves normally for 90% of patients. But the other 10% develop chronic pain. That persistent pain is very hard to treat; it's very resistant to medication and it can last for years.

In the new study, published recently in the Journal of Pain Research, the researchers report that letting inflammation run its course led to a quicker cessation of pain and an overall quicker recovery after a surgery or injury.

Although this study suggests that blocking TNF-α after surgery is likely unwise, there are other scenarios where it may still make sense, such as improving mobility by reducing arthritic inflammation in the joints for autoimmune diseases like rheumatoid arthritis.

Inflammation is not necessarily a bad thing, the researchers say.

Yes, it hurts, but it's also working on the inside to promote the resolution of that pain. The idea in the medical field that when you have an injury, you should absolutely block the inflammation right away might not always be the best strategy, they conclude.

They think that one day we'll be able to block the pain but allow the healing inflammation.

Sophie Laumet et al, Unexpected Role of TNFα Signaling in the Resolution of Postoperative Pain in Mice, Journal of Pain Research (2025). DOI: 10.2147/jpr.s543971

Cancer Immunotherapy May Work Better Before 3PM

People with cancer receiving immunotherapy earlier in the day survived longer, suggesting that adjusting treatment timing may improve outcomes.

Mounting evidence suggests that the time of day at which cancer patients receive treatment could impact their outcomes. This effect is likely due to the circadian rhythm-dependent fluctuations in the function of immune cells as well as proteins that regulate their function, also called checkpoints.

In line with this, in a recent meta-analysis, researchers found that patients with various types of advanced cancer who underwent immune checkpoint inhibitor (ICI) infusions earlier in the day survived longer than their counterparts treated in the late afternoons or evenings.

In a new study, researchers discovered that patients with a highly aggressive lung cancer who received treatment before 3PM survived significantly longer than their counterparts who were treated later in the day.

Landré T, et al. Effect of immunotherapy-infusion time of day on survival of patient.... ESMO Open. 2024;9(2):102220.

Huang Z, et al. Overall survival according to time-of-day of immunochemotherapy for.... Cancer. 2025.

Genetic study uncovers unknown causes of blindness

Researchers have discovered new genetic causes of inherited blindness. Their study, published in Nature Genetics, shows that changes in specific pieces of DNA, which play a role in processing genetic information, can lead to retinitis pigmentosa.

This eye condition affects about one in 5,000 people worldwide, causing "tunnel vision" and often leads to legal blindness. The discovery provides clarity for dozens of families globally and opens new possibilities for diagnostics and counseling in hereditary conditions.

Retinitis pigmentosa (RP) is a disorder in which the rod and cone cells in the retina gradually die. Affected individuals first experience night blindness, followed by tunnel vision. Some eventually lose their sight completely.

Although more than a hundred genes are known to cause RP, in 30 to 50% of patients the genetic cause remains unresolved, even after extensive DNA testing. Researchers have now solved part of this puzzle.

Researchers found a variation in the gene RNU4-2. The change occurs in a special gene, RNU4-2, which does not produce a protein but only RNA. RNA from such genes associate with proteins and other RNAs and the whole resulting complex assists in editing genetic information (splicing), a step required before a cell can make proteins.

Other changes in RNU4-2 were recently linked to developmental disorders.

This breakthrough goes beyond these specific genetic variants causing RP. It shows that we should also look beyond protein-coding genes.

De novo and inherited dominant variants in U4 and U6 snRNA genes cause retinitis pigmentosa, Nature Genetics (2026). DOI: 10.1038/s41588-025-02451-4

Roads can become more dangerous on hot days—especially for pedestrians, cyclists and motorcyclists

Road injury risk increases significantly on very hot days, with pedestrians, cyclists, and motorcyclists facing the greatest danger due to direct heat exposure. The risk rises sharply above 30°C, with pedestrian injuries more than doubling and cyclist and motorcyclist injuries increasing by 80% and 50%, respectively. Heat also elevates crash severity and fatality risk, especially on rural roads and among older drivers. Effects can persist for days due to fatigue and sleep disruption.

During heat waves, everyday life tends to feel more difficult than on an average day. Travel and daily movement are no exception.

But while most of us know rain, fog and storms can make driving conditions challenging, not many people realize heat also changes transport risk. At very high temperatures, overall crash risk is about 15% higher than on cool days.

In particular, research evidence consistently suggests roads, trips and daily commutes can become more dangerous on very hot days compared with an average day. Road injury risk rises much more steeply once temperatures move into the 30°C–40°C range.

Importantly, the increase is even larger for crashes linked to driver fatigue, distraction or illness.

Ambient temperature and risk of motor vehicle crashes: A countrywid...

Heat waves and fatal traffic crashes in the continental United Stat...

The hidden carbon footprint of wearable health care

 Researchers analyzed wearable health care electronics and reported carbon impacts of 1.1–6.1 kg CO₂-equivalent per device. With global device consumption projected to rise 42-fold by 2050, approaching 2 billion units annually, their moderate projection adds 3.4 million metric tons of CO₂-equivalent emissions alongside ecotoxicity and e-waste.

Wearable electronics—glucose, heart and blood pressure monitors, integrated into patches, chest straps, clothes and smartwatches—are transforming health care through real-time monitoring, device interaction, and therapeutic interventions.

Compared with rigid consumer electronics, wearable health care systems—ranging from biophysical and biochemical sensors to e-textiles and biointegrated therapeutics—offer high compliance and continuous tracking and intervention capabilities.

With wireless integration, wearable health care electronics are evolving into digital infrastructure networks adopted globally by patients, older people, athletes, and health-conscious people.

Reliance on energy-intensive manufacturing, hazardous chemicals, fossil-based plastics, and critical metals can lead to substantial carbon emissions, ecological risks, and e-waste issues. Rising energy demands from artificial-intelligence-driven data processing and advanced digital infrastructures further enlarge the eco-footprint of even the smallest devices.

In the study, "Quantifying the global eco-footprint of wearable health care electronics," published in Nature, researchers integrated life-cycle assessment with forecasting adoption growth over time to quantify global eco-footprint hotspots and evaluate mitigation strategies.

Four devices anchored the assessment—a non-invasive continuous glucose monitor, a continuous electrocardiogram monitor, a blood pressure monitor, and a point-of-care ultrasound patch. Selection criteria included clinical relevance, diversity of sensing modalities, and coverage across an expanding technology spectrum.

Cradle-to-grave attributional life-cycle assessment covered raw-material acquisition, manufacturing, transportation, use, and end-of-life disposal. Monte Carlo simulation quantified uncertainty for environmental impacts, and diffusion modeling projected future scale of use.

Part 1

A single continuous glucose monitor from production to use carried a carbon footprint equivalent to about 2 kg CO2-equivalent, or driving a gas-powered car for around 5 miles. More than 95% of that impact was attributed to printed circuit boards and semiconductors inside the device, tied to energy required to purify raw materials and power manufacturing processes.

Single glucose monitor use lasted 14 days before being discarded and replaced. Repetition of that short cycle has stacked impacts across the scale of users. Wearable glucose monitor sales are estimated to exceed 1.4 billion devices a year by 2050.

Expected greenhouse-gas emissions from these units alone were around 2.7 million metric tons CO2-equivalent annually.

Per-device warming impacts ranged from 1.06 kg CO2-equivalent for a blood pressure monitor to 6.11 kg CO2-equivalent for a point-of-care ultrasound patch. Values of 1.30 kg CO2-equivalent for a continuous electrocardiogram monitor.

Annualized warming impacts, accounting for typical replacement frequencies, were 0.5 kg CO2-equivalent for the blood pressure monitor, 33.8 kg CO2-equivalent for the continuous electrocardiogram monitor, 50.6 kg CO2-equivalent for the non-invasive continuous glucose monitor, and 6.1 kg CO2-equivalent for the point-of-care ultrasound patch.

Greenhouse-gas emissions from all wearables in the model were 3.4 million metric tons CO2-equivalent annually, or about the carbon footprint of the transport sector of Chicago. Component-level analysis placed flexible printed circuit board assemblies at the center of warming impacts across all four devices, with hotspots tied to gold in integrated circuits, silicon wafers, polyimide, and batteries.
part 2

Researchers modeled four mitigation approaches that included plastic substitution or recycling, critical-metal substitution, modular designs for reuse and replacement, and a transition to green energy.

Chuanwang Yang et al, Quantifying the global eco-footprint of wearable healthcare electronics, Nature (2025). DOI: 10.1038/s41586-025-09819-w

Part3

Fatigue before cancer treatment linked to adverse events

Investigators found that higher patient-reported fatigue before cancer treatment aligned with higher odds of severe, life-threatening, and fatal treatment-related toxic effects.

Cancer-related fatigue harms quality of life and is a persistent tiredness or exhaustion tied to cancer or cancer treatment. It interferes with usual physical and mental functioning and does not match the patient's normal recent activity. Patients report that fatigue is among the most distressing symptoms of cancer and its treatment, yet physicians routinely underreport fatigue.

Some studies have suggested prevalence ranging from 25% to 50%. Separate estimates place moderate fatigue at 25% and severe fatigue at 15% to 20%, levels often associated with poor performance status.

In the study, "Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy," published in JAMA Oncology, researchers pooled baseline fatigue data to evaluate associations between pretreatment fatigue and subsequent adverse events in cancer treatment trials.

Across 17 trials, 103,738 adverse events were recorded. Higher baseline fatigue aligned with higher odds of severe toxic effects. Some or greater baseline fatigue, compared with less than some fatigue, yielded an odds ratio of 2.11 for grade 3 or higher toxic effects and 1.98 for life-threatening toxic effects.
Comparison between quite a lot or very much fatigue and no baseline fatigue produced an odds ratio of 4.99 for grade 5 toxic effects.
Fatal toxic effects were uncommon, though risk rose with higher fatigue to an odds ratio of 2.35.
Severe or worse toxic effects occurred in 34.2% of patients reporting no fatigue, 39.4% reporting a little fatigue, 52.8% reporting some fatigue, and 58.3% reporting quite a lot or very much fatigue.
Subset analyses did not show statistically significant differences in the fatigue to adverse event association by age, sex, race, ethnicity, or obesity status.
Cancer stage mattered in subgroup patterns. Advanced-disease trials showed clearer monotonic relationships between baseline fatigue and adverse events, while adjuvant or early-stage trials did not show statistically significant associations for grade 3 or higher or grade 4 or higher adverse events.

Part 1

Patient-reported fatigue before cancer treatment was associated with increased risk of severe, life-threatening, and fatal adverse events during treatment.
Pre-treatment fatigue assessments could be seen as an early marker of vulnerability that could inform treatment strategies and symptom monitoring.

Joseph M. Unger et al, Baseline Fatigue and Severe Toxic Effects in Patients With Cancer Receiving Systemic Therapy, JAMA Oncology (2025). DOI: 10.1001/jamaoncol.2025.5549

Part 2