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.

Part 1

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

Part 2

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.

Part 1

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

Part 2

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

Why some people are more resistant to developing blood cancer even when they carry cancer-risk mutations

Blood cancer is an umbrella term for a variety of diseases that affect the blood, bone marrow and lymphatic system. Like most cancers, the cause is usually mutations in the DNA, which are genetic errors that accumulate as we age. However, some people are more resistant to developing blood cancer even when they carry cancer-risk mutations.

In a new study published in the journal Science, researchers discovered why. They identified a rare genetic variant that reduces the risk of several blood cancers, including leukemia, by slowing down a process called clonal hematopoiesis (CH).

CH occurs when a hematopoietic stem cell, which can develop into any type of blood cell, mutates and grows into a large population of identical mutated cells.

In their study, the team performed a large-scale analysis (known as a GWAS meta-analysis) of more than 640,000 individuals. By comparing 43,000 people with CH mutations to 600,000 without them, they pinpointed the genetic variant that protects against CH.

The researchers identified a noncoding regulatory variant, rs17834140-T, on chromosome 17q22.

The experiments revealed that rs17834140-T reduces the amount of a protein called MSI2, which acts as a growth booster in stem cells. In cancer, MSI2 causes mutated cells to multiply rapidly and take over the bone marrow. However, the protective variant results in lower levels of the protein, forcing these mutated cells to grow much more slowly and reducing their chances of progressing to leukemia. According to the study authors, people with the variant have up to a 30% lower risk of developing CH.

The research could lead to new ways to prevent cancer even before it starts. Now that we know that lowering MSI2 is protective, scientists may be able to develop drugs or other therapeutic approaches that mimic or enhance this natural protection.

Gaurav Agarwal et al, Inherited resilience to clonal hematopoiesis by modifying stem cell RNA regulation, Science (2026). DOI: 10.1126/science.adx4174

Francisco Caiado et al, Genetic resistance to leukemia, Science (2026). DOI: 10.1126/science.aed5244

Tire rubber decays into a potentially dangerous chemical cocktail, research shows

Crumb rubber from recycled tires, commonly used in artificial turf, generates hundreds of transformation chemicals as it decays under sunlight and environmental conditions. Some of these chemicals, such as 6PPD-quinone, are highly toxic to aquatic life, while others are known human health hazards. The long-term effects of most transformation products remain unknown.

The small, spongy black beads used as fill material in most artificial turf fields are called crumb rubber, which has long been touted as a major win for recycling. However, conflicting studies have alternately identified crumb rubber as either safe for people to play atop or dangerous to human health.

New research out of Northeastern University investigated the decay cycle of crumb rubber, which is fashioned out of old tires. By simulating the conditions in which the rubber decays, like strong sunlight, they discovered that crumb rubber is highly reactive, generating hundreds of previously untracked chemicals as it decays, some of which are hazardous to humans.

The work is published in the journal Environmental Science & Technology.

Madison H. McMinn et al, From the Road to the Field: Decoding Chemical Transformation in Aging Tire and Artificial Turf Crumb Rubber, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c08260

AI shows bias against some Indian castes

Popular large language models (LLMs) often reproduce harmful stereotypes about Indian castes — hereditary groups traditionally associated with specific occupations and social status. Researchers used a custom-designed tool to detect ‘caste bias’ in LLMs and found that every model they tested exhibited some bias. GPT-4o and GPT-3.5, created by OpenAI, had some of the highest bias scores. Information on minority groups might be less likely to appear in prestigious journals or other outlets, and might be written in local languages, which could result in it being filtered out of AI training data who studies cultural biases in LLMs.

[2508.03712] How Deep Is Representational Bias in LLMs? The Cases o...

[2510.02742] IndiCASA: A Dataset and Bias Evaluation Framework in L...

[2505.14971] DECASTE: Unveiling Caste Stereotypes in Large Language...

AIs are biased toward some Indian castes — how can researchers fix ...

Immune stress during pregnancy changes how fetal brain cells communicate

Research has found that immune-related genes vary by location and cell type across the developing mouse brain before birth. Maternal immune activation and maternal microbiome depletion shifted parts of that immune signaling pattern, with differences observed between male and female embryos.

Immune molecules, including cytokines, chemokines, and cognate receptors, are critical regulators of synapse development, cellular communication, and neural precursor cell migration in the developing brain. During development, nerve cells are born in one area, move to their destinations, and settle into stacked layers, especially in the cortex. Those layers line up in an ordered way, with different types of neurons ending up in different layers.

Changes to the maternal immune system and microbiome have been linked to abnormal fetal neurodevelopment, influencing neurogenesis, cell fate, and precursor cell migration. Knowledge of immune signaling networks within the developing brain is needed to understand the mechanisms of how the mother's stressors impart influence.

In the study, "Spatial transcriptomics of the developing mouse brain immune landscape reveals effects of maternal immune activation and microbiome depletion," published in Nature Neuroscience, researchers used multiplexed error-robust fluorescence in situ hybridization (MERFISH) to measure immune activity in embryonic mouse brains during mid and late gestation to see how maternal immune activation and maternal microbiome depletion altered those patterns.

Embryonic mouse brain single-cell RNA sequencing data supported identification of spatially restricted cell populations, followed by cell clustering, differential gene expression analyses, and ligand–receptor analyses.

The research connects maternal immune activation and maternal microbiome depletion with sex-specific shifts in immune gene expression, ligand–receptor signaling, and cell spacing within the embryonic brain. Specifically, CXCL12 and CXCR7 signaling stood out as an important mediator of abnormal neural differentiation and migration after maternal immune activation and maternal microbiome depletion.

Bharti Kukreja et al, Spatial transcriptomics of the developing mouse brain immune landscape reveals effects of maternal immune activation and microbiome depletion, Nature Neuroscience (2026). DOI: 10.1038/s41593-025-02162-3

Spaceflight causes astronauts' brains to shift, stretch and compress in microgravity

Spaceflight takes a physical toll on astronauts, causing muscles to atrophy, bones to thin and bodily fluids to shift. According to a new study published in the journal PNAS, we can now add another major change to that list. Being in microgravity causes the brain to change shape.

Here on Earth, gravity helps to keep the brain anchored in place while the cerebrospinal fluid that surrounds it acts as a cushion. Scientists already knew that, without gravity's steady pull, the brain moves upward, but this new research showed that it is also stretched and compressed in several areas.

The study authors found significant differences between the brains of astronauts and those of the volunteers. While both groups experienced a shift, the astronauts' brains moved further upward. And the longer they stayed in space, the more pronounced these changes became. The supplementary motor cortex (which helps to control movement) moved upward by about 2.5 millimeters in astronauts on one-year missions.
The brain movement isn't uniform. The team discovered that as the brain moves, it becomes compressed at the top and the back while other areas stretch. This has a noticeable effect on balance and coordination. In tests, astronauts who experienced the largest brain shifts struggled the most to stay steady on their feet after returning to Earth.

While the brain mostly returns to its normal position after several months back on Earth, scientists still need to know more to ensure safer conditions for longer missions, such as those to Mars.

Tianyi Wang et al, Brain displacement and nonlinear deformation following human spaceflight, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2505682122

Tibetan Plateau-Himalayan uplift shaped Asian summer monsoons

The uplift of the Tibetan Plateau, particularly when it exceeded 3.5 km elevation around 27–38 million years ago, was crucial in intensifying and expanding the Asian summer monsoon. This topographic change shifted rainbelts northward and increased rainfall over South and Southeast Asia, with tectonic uplift playing a more dominant role than atmospheric CO2 in shaping monsoon evolution.

S. Abhik et al, A brief history of Asian summer monsoon evolution in the Cenozoic era, npj Climate and Atmospheric Science (2026). DOI: 10.1038/s41612-025-01259-7

The global water cycle and how is it amplifying climate disasters

The global water cycle, involving evaporation, precipitation, and runoff, is intensifying due to rising temperatures. This leads to faster evaporation, increased atmospheric moisture, and more frequent extreme events such as floods, droughts, and heatwaves. These amplified fluctuations, sometimes termed "climate whiplash," are destabilizing ecosystems and societies worldwide.

 original article.

The aggressive use of antibiotics could fuel mood disorders and anxiety

Antibiotics (ABs) are among the most used pharmaceutical drugs worldwide, as they are currently the most effective medicines for the treatment of bacterial infections. An excessive use of these drugs, however, can damage the gut microbiota, the population of microorganisms living in the intestines that help us to digest food.

Bacteria and other microorganisms in the gut are known to also communicate with the brain via a communication pathway that is referred to as the gut-brain axis. Recent research suggests that some gut bacteria help to reduce inflammation and support the healthy functioning of the brain.

Researchers have carried out a study exploring the possibility that the effects of ABs on gut bacteria could also facilitate the development of mental health disorders, particularly increasing anxiety. Their findings, published in Molecular Psychiatry, suggest that ABs do in fact damage gut bacteria that help regulate mood, linking their excessive use with higher levels of anxiety.

When they analyzed the data they collected, the researchers found that the use of ABs was linked to anxiety-like behaviors in mice and higher levels of anxiety in humans. Moreover, the drugs appeared to reduce the amounts of some helpful gut bacteria, particularly those in the Bacteroides group.

In addition, the team found an association between the intake of ABs and a reduction in the neurotransmitter acetylcholine, a chemical that supports communication between nerve cells. Mice and human patients who had received ABs were found to have lower levels of acetylcholine both in the gut and brain compared to those who had not taken ABs.

"In both AB-treated mice and patients, co-occurrence analysis indicated that the Bacteroides-acetylcholine pair may play an important role in AB-induced anxiety," wrote the researchers in their paper.

Ke Xu et al, Consistent decline of acetylcholine in microbiota-gut-brain axis mediates antibiotic-induced anxiety via regulating hippocampus microglial activation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03431-0.

Your voice gives away valuable personal information!

Human voices carry extensive personal information, including health, background, and emotional state, which can be extracted by advanced speech analysis technologies. This raises privacy risks such as misuse by insurers, employers, or malicious actors. New metrics now quantify how much information a speech recording contains, aiding the development of privacy-preserving tools and user interfaces.
You can probably quickly tell from a friend's tone of voice whether they're feeling happy or sad, energetic or exhausted. Computers can already do a similar analysis, and soon they'll be able to extract a lot more information. It's something we should all be concerned about, according to experts in the field.
Personal information encoded in your voice could lead to increased insurance premiums or to advertising that exploits your emotional state. Private information could also be used for harassment, stalking or even extortion.
When someone talks, a lot of information about their health, cultural background, education level and so on is embedded in the speech signal. That information gets transmitted with the speech, even though people don't realize it.
For example, even subtle patterns of intonation or word choice can be a giveaway as to your political preferences, while clues in breathing or voice quality may correlate with certain health conditions.
One important risk is that medical information inferred from voice recordings could affect insurance prices or be used to market medication.
The fear of monitoring or the loss of dignity if people feel like they're constantly monitored—that's already psychologically damaging.
And employers might extract personal information from voice recordings which could be used against employees or to screen candidates, or exes might use such tools for stalking or harassment.
So how can engineers tackle these problems?
Protecting against abuses means ensuring that only the information that's strictly necessary is transmitted and that this information is securely delivered to the intended recipient. One approach is to separate out the private information and only transmit the information needed to provide a service. Speech can also be processed locally on a phone or computer rather than sent to the cloud, and acoustic technologies can be used to make sure that sounds are only recorded from (or audible in) a specific place.

Tom Bäckström, Privacy in Speech Technology, Proceedings of the IEEE (2025). DOI: 10.1109/jproc.2025.3632102

How small mammals shrink their brains to survive the cold

An international team of researchers has conducted a study that explains the evolutionary origins of the Dehnel phenomenon, a unique seasonal adaptation in small mammals that involves the ability to reduce and recover brain volume and function. The study is published in Molecular Biology and Evolution.

The Dehnel phenomenon is a case of extreme plasticity through which some mammals reduce and regenerate their brains according to the season. This mechanism allows species such as the common shrew to reduce the size of their brain, skull and other organs by up to 30% during the winter to save energy in conditions of extreme cold and food scarcity.

In the spring, these tissues regenerate, making this phenomenon an exceptional example of physiological plasticity. Furthermore, comparative studies show that it is not exclusive to shrews: European moles and mustelids (such as weasels) also exhibit seasonal brain reductions, which extends the evolutionary framework of this strategy to mammals with high metabolisms.

Through comparative genomics and gene expression analysis in key tissues, such as the hypothalamus, the team identified genes associated with several fundamental processes, such as energy homeostasis and calcium signaling, essential for adjusting energy balance in demanding environments; the integrity of the blood-brain barrier, which ensures efficient control of molecules accessing the brain during the seasonal cycle; and water regulation, involved in reversible brain volume loss without cell death, a key finding for understanding how this adaptation is achieved.

The plasticity reflected by the Dehnel phenomenon influences survival, reproduction, and resilience to climate variability. According to the research team, even though these species are not human, understanding the mechanisms that allow reversible reductions in brain volume without permanent damage could inspire new lines of research in neurology and metabolism.

The role of genes related to energy homeostasis and the blood-brain barrier points to possible biomarkers and therapeutic targets for neurodegenerative diseases, always with the necessary caution when extrapolating to humans.

William R Thomas et al, Genomic comparisons shed light on the adaptive basis of brain size plasticity and chromosomal instability in the Eurasian common shrew, Molecular Biology and Evolution (2026). DOI: 10.1093/molbev/msag006

Gut bacteria cause rare alcohol syndrome
Researchers have found more evidence that ethanol-producing gut bacteria are the main drivers of auto-brewery syndrome (ABS) — a rare and poorly understood condition in which people become drunk when they haven’t consumed alcohol. A team found that strains of Klebsiella bacteria and Escherichia coli that produce ethanol were much more prevalent in the gut microbiomes of people with ABS than in those of people who didn’t have the condition. One person with ABS was successfully treated with a faecal microbiota transplant, but the authors say a targeted intervention, such as disrupting the metabolic pathways the bacteria use to produce ethanol, might be more effective.

Gut microbial ethanol metabolism contributes to auto-brewery syndro...

Vaccines create a halo of benefits
Growing evidence suggests that vaccines have benefits in older adults beyond protecting against infectious diseases. These ‘off-target effects’ include a reduced risk of dementia and cardiovascular events. Exactly why vaccines have these protective effects is unclear, but researchers suggest that in protecting against infection, vaccines also protect against the inflammation that comes with them. Many experts now worry that opposition to childhood vaccinations could dissuade some adults from getting vaccinated, which would leave them vulnerable to the diseases that vaccines can protect against, both infectious and not.

Vaccines Are Helping Older People More Than We Knew - The New York ...

How the gut microbiome affects transplants

Antibiotic and immunosuppressant treatment administered before, during and after a solid-organ or haematopoietic-stem-cell transplant can dysregulate the gut microbiome. On the flipside, the gut microbiome can also influence the long-term success of such procedures by, for example, metabolizing immunosuppressants into less active forms. A better understanding of these interactions could yield targeted interventions that improve outcomes in transplant recipients, write five internal-medicine specialists in their review.

The gut microbiome in solid-organ and haematopoietic-stem-cell tran...

Cancer cells use stolen goods to stay hidden

Hijacking the energy-producing organelles from immune cells seems to help tumours in mice to infiltrate lymph nodes.
Cancer cells use mitochondria stolen from immune cells to escape detection and spread. Researchers found that when cancer cells take on these mitochondria in mice, it both weakens the immune cells and triggers a molecular pathway in the cancer cells that help them fly under the immune system’s radar and invade lymph nodes. This beneficial molecular pathway was activated even when researchers disrupted the mitochondria’s ability to produce the energy-carrying molecule ATP. The findings could explain how cancer cells survive in lymph nodes, which are packed with immune cells that should be able to kill them.

Mitochondrial transfer from immune to tumor cells enables lymph nod...

Cancer might evade immune defences by stealing mitochondria