How bacteria help plants survive drought
A Flavobacterium strain increased plant drought tolerance by stimulating root-hair formation. The enhanced root hairs increase root surface area for water and nutrient uptake through a plant signaling and gene-regulation pathway, identifying a microbial contribution to drought adaptation.

Arezoo Rahimi et al, Endophytic Flavobacterium promotes root hair development and enhances drought tolerance via an ERF–CEP5 hormonal regulatory module, Nature Plants (2026). DOI: 10.1038/s41477-026-02350-4

Stress gene 'stuck on' in the brains of people with schizophrenia, study finds

Experts  have found that a gene involved in regulating the body's response to stress switches on more easily in the brains of people who live with schizophrenia.
The study, published in the American Journal of Psychiatry, looked at the FKBP5 gene and the corresponding FKBP51 protein, which help regulate how strongly the body responds to stress hormones such as cortisol.

Using donated brain tissue, the researchers found that for people with schizophrenia, the chemical tags that normally keep the FKBP5 gene in check had been stripped away. This change was linked to higher activity of the FKBP5 gene, opening up the possibility of developing new treatments that target it.
For people who have lost the chemical tags that keep their stress gene in check, it is like having the volume on their speaker stuck on high.

Responding to stress so strongly can affect the brain over time, making it more vulnerable to serious psychiatric conditions. Understanding what controls this response gives us fresh insights that will help us to develop more effective treatments.
The researchers also found that changes in the stress-response system become more pronounced with age, potentially affecting the brain's internal circuitry over time. This means that the system may be switched on more easily and stay on for longer. These changes, in turn, increase vulnerability to developing psychiatric disorders such as schizophrenia later in life.
Having a persistently heightened stress response may mean that, as the brain ages, the circuits in the frontal cortex become more vulnerable to damage, increasing susceptibility to serious psychiatric illness.

Age-dependent DNA methylation changes at FKBP5 enhancer sites drive increased gene expression in schizophrenia, American Journal of Psychiatry (2026).

Experimental Zika vaccine reveals T cells can drive protection without antibodies

Zika virus is carried by different species of Aedes mosquitoes. These mosquitoes had spread into new regions and found new victims. More people were getting sick, including pregnant women.

Doctors around the world realized that increased cases of microcephaly (significantly reduced head and brain development) in newborns were caused by Zika virus infection. Women who contracted Zika virus during pregnancy were also much more likely to miscarry. Babies who survived could be born with eye and ear problems and joint issues, a pattern of birth defects doctors now group together as congenital Zika syndrome.

Today, at least 97 countries and territories have reported evidence of Zika virus transmission, according to the WHO. Reported cases have fallen sharply since 2017, but researchers expect the pool of susceptible people to rebuild over the coming decade, and a warming climate and the spread of insecticide-resistant Aedes mosquitoes keep widening the map of who is at risk. We still do not have specific Zika virus treatments or vaccines.
Researchers published a study in Nature Microbiology showing that an experimental Zika virus vaccine can protect mice through T cells alone, without help from virus-fighting antibodies. The catch: On their own, those T cells do not keep the protection going.

This discovery is a critical step in the fight against Zika virus and its close viral relatives, including the life-threatening dengue virus.
Part 1

Most vaccines work by prompting the body to make antibodies, which bind to part of a pathogen—the outside of a virus, say—and neutralize it before it can cause infection. Antibodies and the B cells that produce them can then linger in the blood for years, lying in wait for their targets.

But in the case of Zika virus vaccines, antibodies pose a big problem. Zika belongs to a family of mosquito-borne viruses—the orthoflaviviruses—that also includes dengue and Japanese encephalitis virus, and these viruses overlap across much of the world. Zika and dengue are especially close cousins: The envelope proteins that coat them are so similar that antibodies raised against one routinely latch onto the other.
The researchers studied a phenomenon called antibody-dependent enhancement (ADE). When antibodies bind a virus without disabling it—because they were raised against a relative or because their levels have waned—they can end up ferrying the virus into immune cells instead of blocking it, driving a more severe infection. Because of ADE, a person who receives a vaccine that prompts the body to make antibodies against Zika virus could be vulnerable to a severe case of Zika or dengue infection later on.

The risk of ADE means vaccine researchers need to find innovative ways of protecting the body from orthoflaviviruses.
In past studies, the rsearchers uncovered the potential power of T cells in fighting orthoflaviviruses. T cells patrol the body for signs of disease and adapt over time to recognize specific threats, and vaccines can train them just as they train antibodies. They have shown that T cells offer a chance to fight these viruses when you can't depend on antibodies.
In their tests, the unmodified vaccine got the immune system to fight Zika virus infection with a double whammy of antibodies and T cells. Transferring CD8+ T cells from those mice into unvaccinated animals cut Zika levels on its own—so T cells were pulling real weight even in the vaccine whose antibodies worked as intended.

The fusion-loop mutant vaccine came with an even bigger surprise. Its antibodies shared many features with those from the unmodified vaccine in cell cultures and test tubes, but they did not protect unvaccinated animals at all. Stripping out the CD8+ T cells, by contrast, wiped the protection away. "This vaccine wasn't protecting via antibodies," says Shresta. "It was protecting via T cells."

"The protection came from CD8+ T cells, a type of immune cell that finds and destroys virus-infected cells.
This protection was effective, but it didn't last. Twelve weeks after the final dose, mice given the fusion-loop mutant vaccine were no better off than unvaccinated animals, while those given the unmodified vaccine were still protected. The lesson is a cautionary one: A change made to reduce ADE risk quietly cost the vaccine its staying power.

A Zika virus vaccine with E protein fusion loop mutations protects via CD8+ T cells, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02465-6

Part 2

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New approach cuts sepsis diagnosis from days to hours

Sepsis, a life-threatening condition that stems from the body trying to fight off an infection, plagues millions of people worldwide, with one in three deaths recorded in hospitals attributed in part to sepsis. Despite the severity of the condition, which can kill in as little as 12 hours, it takes between two and seven days for most traditional approaches to definitively identify sepsis-causing bacteria in blood infections.
A research team has developed a way to condense the days long diagnosis timeline to just hours. The new approach rapidly grows the bacteria present in collected blood samples, intermittently analyzing the samples with advanced techniques that help scientists identify the specific pathogens causing infection.
With a bloodstream infection, it is critical to find and neutralize the cause as quickly as possible before it triggers a septic response from the body.
Physicians must not only detect the presence of bacteria—they must also identify the specific pathogens, as well as the best antibiotic for treatment. The dire stakes of a false positive or negative complicate this further, as every hour counts when treating a bloodstream infection.
Many different bacteria can cause sepsis, and they may respond differently to treatment. Therefore, analysis must be thorough to ensure the best treatment is prescribed.
To identify the bacteria causing a bloodstream infection, current best practices require bacterial culturing: blood samples are enriched over a few days so that bacteria present grow to measurable levels. Then, technicians further analyze the samples to identify the specific bacteria, a process that adds another day or two to diagnosis.

Researchers now report in a paper published in Science Advances that their approach facilitated faster diagnosis and could help clinical decision-making that avoids worsening antibiotic resistance in the bacterial strains causing infections.
To accelerate diagnosis without sacrificing accuracy, the team had to rethink culturing. Traditionally, bacterial growth in a cultured blood sample is measured through the carbon dioxide released by the bacteria. When this change in carbon dioxide levels confirms the presence of pathogens, bacteria are separated from the blood sample and analyzed.

The team's new approach, called STREAM, fast-tracks this culturing by facilitating rapid bacterial growth while isolating and analyzing the pathogens simultaneously—blood samples are mixed in a specialized "broth" that separates whole blood cells from the individual bacteria found in the sample during culturing.

Molecular analysis, a process known formally as barcoding, allows the team to detect tiny fragments of genetic information from isolated bacteria. From these smaller samples collected intermittently during culturing, the researchers can identify the specific bacterial species present.

These smaller samples are then subjected to a series of new, single-cell-based techniques that allow researchers to analyze a bacterium with microscopic imaging. These images are then analyzed by computer algorithms the team developed to eliminate visual clutter, helping physicians determine the specific bacteria causing infection. These analyses also suggest which antibiotics the strain is susceptible to and any existing antibiotic resistance the strain may have.

Part 1

The team tested their approach with about 100 positive bloodstream infection samples donated by patients and stored at Penn State Hershey Medical Center's clinical microbiology laboratory. The researchers found that combining these techniques offered comprehensive diagnosis in as little as seven hours, enabling confident identification of the infection-causing pathogen from whole blood.
They also integrated antibiotic susceptibility testing into the same process, providing physicians with the information needed to select the most appropriate treatment.

Siew Chin et al, Rapid and robust diagnosis of bloodstream infections by single-cell analysis, Science Advances (2026). DOI: 10.1126/sciadv.aeh3580. www.science.org/doi/10.1126/sciadv.aeh3580

Part 2

El Niños have been more intense over the last 40 years than in the previous 1,000 years, coral records reveal

El Niño is a natural phenomenon that, every few years, causes the tropical Pacific to become warmer than usual. Under normal conditions, trade winds blow along the equator from east to west. This pushes warm water from South America toward Australia. But when the trade winds weaken, warm water spreads eastward, back toward South America, kicking off an El Niño event.
The atmospheric circulation responds as heavy rainfall shifts from Indonesia into the central Pacific, leaving the western Pacific in drought. This weakens the trade winds further, locking in El Niño conditions that can persist for one to two years. These temperature and precipitation fluctuations originate in the tropical Pacific, but they affect weather all over the world.
For instance, storm tracks over the U.S. shift southward, bringing more rain to the desert Southwest and less to the Northwest. Similar shifts around the world lead to droughts and flooding that bring disease, crop failure, wildfires and other crises that affect people's health and well-being.
The question is not whether the current El Niño will happen, but how bad it is going to be, and how bad the impacts will be? This event now is superimposed on global warming, and it's likely to supercharge the temperature increase that we would normally see from greenhouse gases. There are forecasts that we might get as hot as 1.7 or 1.8 degrees Celsius above preindustrial temperatures, which is quite a bit higher than the current record.

As an El Niño of historic proportions is taking shape in the tropical Pacific now, a new study has found that El Niño events have become nearly 40% stronger in the last 40 years than they were in the preindustrial era.
In fact, the study, which examined modern and ancient corals in the Galápagos Islands, found that El Niño events in the last four decades were stronger than any in the 1,000 years before about 1850, when humans began affecting the climate with greenhouse gases.
We don't see a time in the past where El Niños have been as strong as today, and researchers show that the strength of El Niño changes in parallel with warming global temperatures.
These findings tell us that the big El Niño events of the last 40 years are not normal in the context of the last thousand years.

J.E. Cole, Recent strengthening of eastern Pacific ENSO is unprecedented in the last millennium paleorecord, Science (2026). DOI: 10.1126/science.ady2660. www.science.org/doi/10.1126/science.ady2660

Cell therapy substantially reduces severe rheumatoid arthritis in first clinical trial

Rheumatoid arthritis is a chronic disease in which the immune system mistakenly attacks the body's own joints. This causes recurrent inflammation and joint swelling and, as the disease progresses, can lead to joint damage. Currently available treatments can usually keep the inflammation under control but do not cure the disease. Patients therefore require lifelong medication, including anti-inflammatory drugs and medications that suppress the immune system, with all the associated side effects.

In some patients, even several of the newer treatments fail to produce an adequate response. Doctors then call the disease treatment-refractory. For those affected, this means persistent pain, restricted mobility and a substantial impact on quality of life.
One reason could be disease-driving B cells—memory cells of the adaptive immune system that may survive in the lymph nodes, bone marrow or joint tissue after an infection, where they produce harmful antibodies directed against the body's own tissues and repeatedly reignite the inflammation

Immunotherapies such as CAR T-cell therapy are used primarily to treat cancer. In the future, these patient-specific therapies, manufactured from patients' own immune cells, could also help cure autoimmune diseases. Six patients with particularly severe rheumatoid arthritis have now received this treatment at Charité—Universitätsmedizin Berlin. In the journal Nature Medicine, the researchers report the results from the world's first clinical trial of its kind: Disease activity decreased substantially in all participants. By the end of the observation period, three of the patients no longer required any medication for rheumatoid arthritis.
The researchers hope that CAR T cells, patients' own immune cells genetically modified in the laboratory, could selectively track down the disease-driving B cells, even deep within tissues, reset the pathological B-cell memory as fully as possible and thereby effectively give the B-cell system a fresh start.
Originally developed for cancer treatment, CAR T cells are now being used more widely. In cancer treatment, patients' immune cells are given a kind of "training" to specifically recognize and eliminate tumour cells; in autoimmune diseases, the aim is instead to direct immune cells toward disease-driving memory cells.

Fredrik N. Albach et al, CD19 CAR T cell therapy for treatment-refractory seropositive rheumatoid arthritis: a phase 1 trial, Nature Medicine (2026). DOI: 10.1038/s41591-026-04603-3

Scented cleaners can create nanoparticles that reach deep into the lungs within minutes, tiny-home experiment finds

What does a clean room smell like? Many people say citrus, pine, or flowers because these fragrances are common in cleaning products. A research team found that scent compounds in cleaning products—conventional and botanical essential oil-based—quickly react in the air, forming nanoparticles that can travel deep into the lungs if inhaled.
Researchers showed that indoor ozone reactions with fragrances from cleaning produce nanoparticles that carry a respiratory dose comparable to or greater than what you would experience from standing outside along a busy road.
The particles are different in terms of their composition, but the total dose can be higher. You're not seeing smoke, dust or haze in the air. Instead, you think the air smells great, so it must be clean.

To reduce exposure to this invisible pollution, the team suggests using unscented products, running exhaust fans, and avoiding ozone-generating devices while cleaning.
Steps to cut exposure
The researchers want these findings to inform consumers' choices, not alarm them, and provides several steps people can take to reduce their exposure while cleaning:

Choose low-fragrance or fragrance-free products.
Avoid applying several scented products in the same cleaning session.
Run exhaust fans or open windows to ventilate the space.
Do not simultaneously clean surfaces with scented products while using ozone-generating devices, such as far UV-C lamps.
Importantly, cleaning removes viruses and bacteria from surfaces, but it can also generate invisible air pollution. There's no visible dust or smoke in the air, but these particles are forming.

acs.digitellinc.com/live/37/session/591663

Electrically charged raindrops could be corroding metal with protective coatings

Water droplets acquire 0.2–2 nC charges after sliding on common natural and synthetic surfaces. After 3,000 charged droplets contacted Teflon-coated copper, the coating degraded and underlying copper corroded; uncharged droplets caused no detectable damage. This mechanism may affect protective coatings on outdoor metal structures.

Zhongyuan Ni et al, Spontaneously charged water drops induce corrosion, Nature (2026). DOI: 10.1038/s41586-026-10941-6

Overuse of inhalers found to increase heart attack risk in asthma and COPD patients

Overuse of reliever inhalers is associated with higher risks of developing and dying from cardiovascular disease, including heart failure, heart attack and ischemic stroke, in patients with asthma and COPD, according to a study published this week in ERJ Open Research.
In asthma and COPD, greater short-acting bronchodilator use was associated with higher cardiovascular disease and mortality risk. Use of ≥3 inhalers annually increased mortality versus ≤2; risks were greater in those without prior cardiovascular disease. Overuse may indicate poorly controlled disease requiring treatment review.
These "reliever" inhalers can help people breathe more easily when their symptoms are particularly bad. However, it is possible to overuse them if a patient's asthma or COPD is not being managed well by "preventer" treatments.
The study assessed real-world data from primary and secondary care for more than 280,000 COPD and asthma patients who used either SABA (short-acting beta-agonist), SAMA (short-acting muscarinic antagonist), both or no short-acting bronchodilators to manage their condition. Researchers took into account differences in age, sex, socioeconomic status, smoking history, nursing home residency, disease severity and other conditions or medications.

Both SABA and SAMA bronchodilators are often used as reliever therapies by asthma and COPD patients. SABA bronchodilators increased the risk of death by 12% and 14% in asthma and COPD patients, respectively, compared with no use. The risk of death from SAMA bronchodilators increased by 73% and 36%, respectively.

The researchers also assessed how the number of inhalers used per year affected cardiovascular health. They found that using three or more inhalers per year for either bronchodilator was associated with an increased risk of death compared with two or fewer inhalers per year. Patients who did not have any prior history of cardiovascular disease were found to be more vulnerable to cardiovascular problems resulting from inhaler overuse.
Overuse of short-acting bronchodilators is an alarm signal that indicates uncontrolled airway inflammation and requires a medical review of treatment. It should prompt patients to have their lungs checked and health care providers to check adherence and inhaler technique against treatment guidelines.
Patients should be informed that short-acting bronchodilators only relax airway muscles briefly. Uncontrolled asthma and COPD are already linked to an increased risk of cardiovascular disease and death. When this is combined with overuse of SABA and SAMA bronchodilators—which both cause faster, irregular heart rates as a side effect—these risks become even more pronounced. Overreliance on this short relief may allow the underlying disease activity to progress unchecked. This research should draw clinicians' attention to the fact that overuse is common and may be associated with adverse effects, even in patients without cardiac history.

Overuse of inhalers found to increase heart attack risk in asthma and COPD patients, ERJ Open Research (2026). DOI: 10.1183/23120541.00462-2026

Why do some people react so badly to mosquito bites? The answer lies in mosquito saliva
Mosquito saliva contains anticoagulant and immune-modulating proteins that trigger histamine release and a Th2-type inflammatory response, causing itching, redness, and swelling. Reaction severity varies with immune genetics, age, prior exposure, and mosquito species; hypersensitivity can cause large local reactions. Saliva may also enhance establishment of mosquito-borne infections.

Bumblebees may self-medicate when exposed to fungal infections

It's already known that some animals try to heal themselves when ill. For example, wild chimpanzees have been shown to reach for plants with pain-relieving and antibacterial properties, and some birds line their nests with cigarette butts because the chemicals ward off mites. Previous studies have also shown that honey bees with some types of infections collect more protective plant resin.
Now a new study published in the journal Royal Society Open Science suggests that buff-tailed bumblebees (Bombus terrestris) may self-medicate when exposed to a fungal brood disease.

In the experiments conducted, after five days of free foraging, colonies exposed to the fungus Ascosphaera apis became increasingly likely to visit the quercetin-laced flowers and spent more time drinking from them.

However, those exposed to the bacterium Serratia marcescens showed no significant change in their preference for quercetin nectar as the experiment progressed. Colonies from the healthy control group also showed no significant change in their preference for quercetin nectar.

So while the researchers observed a clear behavioral shift toward quercetin nectar, it did not occur for both types of pathogens, suggesting that disease type matters. "Overall, these results indicate that pathogen identity shapes behavioral plasticity in nectar foraging," wrote the study authors in their paper.

However, because the study did not measure whether drinking quercetin actually reduced infection levels or helped more larvae survive, the findings should be treated with caution. The results do not provide a definitive demonstration of formal self- or social medication.

Kamiel Debeuckelaere et al, Hints of self-medication? Pathogen exposure-dependent foraging decisions of bumblebees, Royal Society Open Science (2026). DOI: 10.1098/rsos.260777

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Engineered bacteria offer a new way to accelerate rock weathering for carbon removal

Rock weathering, the breakdown and dissolving of rocks and minerals caused by their exposure to water, air and biological life, is a major regulator of Earth's atmospheric CO2 levels and climate. Throughout Earth's history, rock weathering has been faster during warm periods with increased atmospheric CO2 levels.
Dissolved minerals ultimately wash into the ocean, where they draw CO2 from the atmosphere and cool the planet again. While this thermostat is responsible for the temperate climate we enjoy on Earth, the weathering cycle occurs over hundreds of thousands of years.

In search of climate solutions, scientists have asked whether the rock weathering cycle could be sped up, resulting in a number of new companies pursuing enhanced rock weathering (ERW).

By scattering crushed silicate rocks on agricultural surfaces or into water, they aim to pull excess CO2 out of the atmosphere. Although this strategy is generally safe and environmentally friendly, it is still too slow to affect the global carbon balance or to be economically viable on an industrial scale.
Now a research team has engineered a potential solution to this problem.
The research team genetically engineered Alteromonas macleodii, a widespread marine bacterium, to produce much higher amounts of so-called siderophores, molecules that extract iron from silicate minerals.
In customized bioreactors with a continuous flow of seawater, the engineered bacterium sped up the weathering of the silicate mineral olivine by 2.6-fold, boosting the amount of CO2 removed from the air.
Part 1

During natural rock weathering, silicate minerals like olivine dissolve to release primarily magnesium (Mg), iron (Fe) and silicate (SiO4), trapping atmospheric CO2 in the water as bicarbonate (HCO3-).

MgFeSiO4 + 4CO2 + 4H2O → Mg2+ + Fe2+ + H4SiO4 + 4HCO3−

Specifically, the released iron is not soluble when exposed to the atmosphere. Instead, it covers the mineral surface as rust, slowing down the entire process.

4Fe2+ + 3O2 → Fe2O3 (rust)

By producing siderophores, bacteria can capture, solubilize and take up oxidized (rusted) iron to sustain their own growth. Conveniently, this effectively derusts the mineral surface, speeding up rock weathering.

Researchers used custom bioreactors to tease apart when natural bacteria produce siderophores. They found that even a small amount of iron-containing mineral completely inhibited siderophore production, posing a major problem for siderophore production at an industrial scale.
Once wild bacteria have enough iron to grow, they stop making siderophores completely. To enable enhanced weathering at scale, the researchers engineered A. macleodii to always produce siderophores. They essentially decoupled siderophore production from environmental iron levels.
This way they succeeded in achieving their goal.

Neil C. Dalvie et al, Engineered bacterial siderophore production accelerates rock weathering for carbon removal, Nature Biotechnology (2026). DOI: 10.1038/s41587-026-03288-w. On bioRxiv: www.biorxiv.org/content/10.110 … .04.08.647837v2.full

Part 2

Hitting bacteria hard and early with diverse phage cocktails may curb resistance

As multidrug antibiotic resistance emerges as a potent public health challenge, medical science has renewed attention on the potential for bacteriophage therapy. Bacteriophages, or phages, are viruses that target, infect and replicate inside bacteria, destroying them in the process. To help maximize the success rate of this approach, researchers recently modeled the dynamics of bacteriophage therapy to explain particular therapies and optimize the composition of bacteriophage cocktails.

Phage are the most prevalent organisms on the planet. They exist everywhere bacteria exist. However, each phage has evolved to narrowly target specific bacteria, and bacteria have evolved various mechanisms of resistance.
Phage cocktails—combinations of particular phages for a patient facing a specific bacterial infection—represent a complicated form of personalized medicine. Given the fast and complex dynamics of bacterial responses to phages, it is not typically known why a particular phage therapy succeeded or failed. As described in the journal PLOS Computational Biology, the research team developed a mathematical model that could describe effective phage cocktails and optimize their diversity and timing.
The researchers developed their mathematical model by building on an existing model calibrated with data from phage therapy in a live mouse. The mathematical model was extended to humans and included multiple phages infecting multiple bacterial strains with varying phage resistance.
The model was able to predict success based on several key factors. The bacteria's pretreatment resistance level was critical, as were the diversity of the phage cocktail and the timing of its delivery. Phage therapy is a complicated dynamic in which more infective phages can wipe out more sensitive (i.e., less resistant) bacteria faster. That leaves resistant bacteria to expand, and they can quickly evolve better resistance, mutating to avoid infection by the phage.

The team found that therapy is best served by a diversity of phages, which overwhelm the bacteria's ability to evolve resistance quickly enough. The team also focused on the timing of phage delivery, determining that immediate treatment with the full phage cocktail offered the most success. That creates a high genetic barrier to bacterial resistance, meaning that the bacteria would need to accumulate several genetic changes or mutations to survive the therapy.
The rapid evolution of resistance is the main challenge to therapy.
That capacity is why antibiotics may not work in the first place. For phage therapy to be effective, the cocktails should be diverse, sufficient and immediate. The approach amounts to 'hit the bacteria hard and early.

Rob J. de Boer et al, Towards modeling phage therapy, PLOS Computational Biology (2026). DOI: 10.1371/journal.pcbi.1014408

Can total joint replacement particles reach the brain?
Total joint replacement is a proven treatment to relieve chronic knee pain, but concerns have been raised that particles from the device may migrate to the brain and cause memory problems. New research from Rush University shows this may not be a concern.
In 701 deceased older adults, implant-derived wear particles were detected in brains of some people with joint replacements but were not associated with cognitive decline. Cobalt exposure was associated with greater Alzheimer disease pathology, particularly raising concern for hip implants with accelerated wear.

In a study published in Acta Biomaterialia, researchers found that particles in some people with total joint replacements traveled to the brain but did not cause cognitive decline.

Researchers did find an association between cobalt, a key element in most implants, and greater Alzheimer's disease pathology in the brain.

The particles, called wear debris, are caused by friction and movement in the joint or, in some cases, corrosion. The newer materials used in joint replacements today make this less likely to occur.

Implants have a very specific combination of metals such as cobalt, and when they show up together in one particle in the brain in the exact same composition that the implant is, we know it can't come from any other source.
For years, we've known that particles can deposit in tissues surrounding the joint, but this is the first study to look at the particles deposited in the brain.
Total joint arthroplasty remains one of the most successful and life-changing interventions in modern medicine. But it does suggest that wear particles from the implant, particularly in certain hip replacements involving accelerated wear, may travel beyond the joint and warrant further study, say the researchers.

Robin Pourzal et al, Cobalt and titanium levels in the brain are associated with Alzheimer's disease pathology but not cognition: A study of older adults with and without total joint replacement, Acta Biomaterialia (2026). DOI: 10.1016/j.actbio.2026.05.006

Three shifting immune states in sepsis could explain why treatments miss their window
Researchers have mapped how the immune response in people with sepsis changes over time. The work could help pave the way for treatments that target the specific parts of the immune system that are altered over the time course (trajectory) of sepsis illness in adults.

Sepsis is a life-threatening condition that occurs when the immune response to infection misfires. In sepsis, vital organs fail, and the condition can be fatal even when treated quickly. It's estimated that there are over 160 million cases and about 21 million deaths from sepsis worldwide each year.

Current treatments for sepsis focus on treating the underlying infection with antimicrobials and providing supportive care for failing vital organs. Despite efforts to treat the misfiring immune system, none have successfully improved outcomes for patients.

In the new study, published this week in Immunity, researchers sought a more detailed understanding of the immune response mechanisms that change over time in patients with sepsis.

They analyzed blood samples collected at four different time points (between admission to and discharge from critical care) from critically ill patients with sepsis . To build a detailed picture of the immune response, called an "immune profile," the researchers examined multiple layers of immune response information in the blood samples, including data on immune cells, gene expression and changing protein expression.

Using machine learning approaches, they then combined these layers of information to generate a more comprehensive immune profile for the first time in patients with sepsis.
The analyses revealed an immune trajectory with three distinct temporal immune states (referred to as STImS) between admission and recovery, with each state involving different immune cell activity and immune response programs.

Importantly, these sepsis immune states didn't match the clinical stage of sepsis. For example, the "early" immune state (STImS1) was not the same as the early clinical stage of sepsis, which is often the day a clinician diagnoses sepsis.

The researchers say these findings could have important implications for determining how best to treat patients with sepsis—specifically, which treatments to use and when.

The main aim of this work was to build a profile of sepsis immune responses over time. When people are admitted to a hospital with sepsis, they are usually classed as having 'early' sepsis—but the new findings show that this isn't necessarily the case—their immune system may already be at later stages of the immune response. Knowing exactly what is happening to a patient's immune system during sepsis could identify which treatments are likely to work best.
This research shows the importance of looking at the changing architecture of the immune system in sepsis over time, rather than just taking a snapshot view. We need to find better ways to treat the misfiring immune system. Only by understanding the intricacies of the immune system in all its component parts—by integrating and dynamically mapping cell and molecular immunobiology to determine why the very system designed to protect us from infections is misfiring in sepsis—can we begin to improve outcomes for patients by treating the misfiring immune system, say the researchers.
part 1

The researchers say the next step for this work is to understand what causes changes in the immune system between the onset of infection and the development of sepsis. Understanding these changes could help identify new treatment targets and approaches to reduce either progression to sepsis or the severity of sepsis, with the potential to improve outcomes and make a difference in the lives of millions affected by serious infections worldwide.

Temporal Analyses of Immune Responses in Sepsis Reveal Asynchrony Between Clinical stage of illness and Immune State, Immunity (2026). DOI: 10.1016/j.immuni.2026.08.003. www.cell.com/immunity/fulltext … 1074-7613(26)00325-0

Part 2

Physics behind the shape of rose thorns

Roses are known, not only for their flowers, but also for their thorns, the sharp structures that can sting and prickle the skin. Thorns, botanically known as prickles, are thought to discourage animals from feeding on plants and may also help climbing roses grip other vegetation.
Compared with the prickles found on many other plants and those artificially created by humans, rose thorns have a somewhat unusual shape. When sliced across their width, various other stingers are approximately round, yet rose prickles tend to have an oval cross section.
Researchers recently tried to better understand why roses may have evolved this unusually flat thorn geometry by running laboratory experiments with artificial prickles and skin-like materials.
Their findings, published in Journal of the Royal Society Interface, suggest that the oval shape of rose prickles could be a compromise between more stable round stingers and flattened, less stable prickles that look more like tiny blades.
When studying various stingers (i.e., sharp and pointed structures) found in nature, they realized that rose prickles differed from those of many other plants. Specifically, they found that they had an unusually flattened oval cross section, particularly when compared with the cylindrical spines of other plants such as cacti or hawthorn trees.
To understand why rose prickles are flatter than those of many other plants, the researchers created artificial stingers using a flexible silicone-based material called polydimethylsiloxane (PDMS). They ensured that these stingers differed in their cross-sectional shapes, ranging from approximately circular to increasingly narrow and flatter shapes.

They then moved the artificial stingers through gelatin using a small robot. This allowed them to determine how each prickle dragged across soft materials, including human skin.

It turned out that oval stingers are relatively better at cutting (or maybe helping the plant climb). They outperform circular prickles, which tend to bend or buckle when you shear them.
The researchers observed that circular stingers tended to bend in the direction in which they were moving, producing only superficial scratches on the gelatin. In contrast, moderately flattened stingers had a blade-like edge and enough structural stability to cut through the gelatin.

The team's results suggest that the unusual shape of rose prickles could allow them to cut better through soft surfaces.

Sabrina Gennis et al, Mechanical limits shape the eccentric form of rose prickles, Journal of the Royal Society Interface (2026). DOI: 10.1098/rsif.2025.1300.

Heart capillaries may build natural bypasses for blood flow after heart attacks

Heart disease caused by blocked arteries is a leading cause of death and illness worldwide. Doctors can restore blood flow with stents or bypass surgery, but these invasive procedures carry risks, including damage caused when blood flow is suddenly restored. But what if a less invasive approach could harness the body's own repair system?

Research shows that some hearts can grow collateral arteries, natural detours that route blood around a blockage. But many heart attack patients lack enough of these backup vessels to survive the injury. Learning how to trigger their growth could save lives, but first doctors need a clear understanding of how the body builds them.

The heart powers a busy highway of arteries and vessels, providing a constant to-and-fro passage for blood. During a heart attack, this passage becomes blocked, usually when a blood clot forms on plaque in a coronary artery and cuts off blood flow to the heart muscle. A study published in Science found that the heart tries to save itself by growing new natural bypass channels to bring blood and oxygen back to damaged tissue.
For a long time, the prevailing theory was that new backup vessels, also known as coronary collateral arteries, grew when cells from existing arteries broke away and assembled into new arteries. The researchers designed genetic tools with fluorescent markers that glow in different colors depending on whether they contact the smooth muscle cells (SMCs) of mature arteries or the bare surface of capillaries, the tiniest blood vessels.

When injected into mice, the tools revealed that capillaries, rather than existing arteries, did most of the heavy lifting in forming new coronary collateral arteries after a heart attack. Capillaries changed their identity and grew into larger, fully mature arteries through a process called capillary arterialization.
The team mapped out the chain reaction inside the cells that drove the transformation of capillary cells into backup vessels. The growth signal VEGF-A activated a protein switch, YY1, which then recruited a methyltransferase protein, SETD1A, to modify the cell's DNA packaging chemically. This activated the gene HES1, which instructed simple capillary cells to reprogram themselves into mature, robust arteries.
The findings challenged a long-standing view and offered a clearer picture of how the heart builds its own backup blood vessels after a heart attack. The researchers identified capillary arterialization as central to the heart's natural effort to restore blood flow, which could be a promising new strategy for helping the heart rebuild its blood supply after injury.

Mingjun Zhang et al, Tracing the origins of de novo coronary collateral formation in cardiac repair, Science (2026). DOI: 10.1126/science.ady3027

Chemistry behind glow-in-the-dark art

Some of the world's brightest colours don't just reflect light; they create it. Scientists and museum conservators are now uncovering why these luminous pigments fade and how to preserve them for future generations. The findings could help protect artwork while informing the development of longer-lasting phosphorescent materials for a variety of applications, from fashion runways to airport runways.
Most paints and dyes are seen because they bounce visible light back to our eyes. Fluorescent and glow-in-the-dark pigments are different: They absorb light and give it back as a vivid glow. This produces the attention-grabbing visual effects found in pop art, fashion, traffic signage and the glowing stars that many people stick to their bedroom ceilings as children.
Over time, however, these bright materials break down. As the colours become duller, the artwork loses some of the oomph initially intended. For artists, the effect isn't simply cosmetic, because they intentionally use these colours for their visual impact.
Because fluorescent and phosphorescent materials attract attention and improve visibility, they're also important parts of safety signs and markings. By understanding how these materials break down over time, researchers want to help manufacturers develop products that stay brighter longer, such as luminescent paint for airplane runways.
They first identified what the materials are made of. Then, the researchers examined the pigments' photophysics—how they absorb, store and emit light—and how the processes change as the materials age.

The team found that many phosphorescent materials contain inorganic compounds and mineral-based pigments and differ significantly from the organic dyes commonly used in fluorescent colourants.
One of the most surprising initial findings is that prolonged exposure to high levels of humidity can play an equally important—and sometimes greater—role than prolonged exposure to ambient light in breaking down phosphorescent pigments. This information will inform improved storage and exhibition conditions for artworks containing this pigment.
Earlier studies of fluorescent pigments revealed that the compounds responsible for enhancing brightness, called optical brighteners, degrade faster than the pigmentary dyes themselves. As a result, colours appear to darken even when the pigment molecules remain intact.
These results also highlight why conserving modern artworks can be challenging. Conservators restoring fluorescent artworks must match colours under both visible and UV light, while the pigments themselves continue to change over time, making long-term restoration difficult.

Glow in the light & dark: Investigations of the photochemistry of emissive pigments used in art, acs.digitellinc.com/live/37/session/595033

Additional transfusion risk emerges for patients with tick-borne alpha-gal syndrome, beyond meat allergy

A new multi-institutional study suggests that alpha-gal syndrome, a tick-borne disease that can result in a chronic allergy to meat and animal byproducts, also may complicate certain patients' ability to safely receive a blood plasma or platelet transfusion.

Alpha-gal syndrome (AGS) is a serious allergy transmitted by a sugar molecule called alpha-gal in the saliva of lone star ticks. First documented in 2025, the allergy is triggered by ingesting meat from mammals, such as beef, pork and lamb, as well as other products from these animals, like dairy and gelatin. An AGS reaction can trigger delayed, severe reactions like hives, stomach pain and anaphylaxis.
At the same time, Dartmouth Health's Dartmouth Hitchcock Medical Center (DHMC) has seen an uptick in recent years in patients with type O blood experiencing severe and even life-threatening allergic reactions after receiving platelets or plasma from type B or AB donors.
Alpha-gal syndrome may increase allergic transfusion reactions in blood group O recipients of B or AB plasma or platelets, particularly in regions with high prevalence. Analysis of >550,000 transfusions supports avoiding B or AB platelet and plasma units for O recipients at risk.
Pathologists hypothesized that these patients may have pre-existing antibodies to alpha-gal from tick bites and that hospitals in regions with higher concentrations of AGS patients, like DHMC, might also see an increase in allergic reactions among O patients receiving B or AB units.
The international team of researchers now reports that transfusion-related alpha-gal syndrome, or TRAGS, is a legitimate manifestation of AGS and should be taken into account in the safety practices of hospital transfusion services.

Richard M. Kaufman et al, Epidemiologic Study of Transfusion-Related Alpha-Gal Syndrome, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2026.3983

Women with type 2 diabetes are more likely than men to develop mental health conditions, study finds
After type 2 diabetes diagnosis, women had higher rates of mental health conditions than men (8.1% vs 5.3%), whereas men had more cardiovascular disease (8.4% vs 5.3%), end-stage renal disease, and hypertension. Mental health comorbidity was associated with premature mortality in both sexes; hypertension was the most frequent subsequent event.

Eto F, et al. Sex differences in trajectories to cardio-renal and mental health outcomes following the onset of type 2 diabetes: An observational cohort study using multi-state analysis in the UK Clinical Practice Research Datalink.PLOS Medicine (2026). DOI: 10.1371/journal.pmed.1005196

High folic acid in pregnancy linked to early bleeding risk
Among 2,400 first-time mothers, folic acid supplementation ≥800 µg/day was associated with increased spotting or mild vaginal bleeding before 16 weeks, particularly in male-bearing pregnancies. Early bleeding was associated with shorter gestation, spontaneous preterm birth, and placental abruption. Folic acid remains essential for neural tube defect prevention.

Hongyan Wang et al, High folic acid supplementation is associated with vaginal bleeding in early pregnancy in a fetal sex-specific manner: findings from two prospective cohort studies, Reproductive Health (2026). DOI: 10.1186/s12978-026-02344-7

Immune cells may have a biological memory that makes weight loss harder after obesity

According to the World Health Organization, one in eight people lives with obesity. Yet despite numerous health education programs, books, articles and treatments, many individuals still struggle to lose weight once they have developed obesity. Why this is so difficult remains a complex puzzle.
However, a new study published in the journal Science Translational Medicine may provide some insights. Researchers discovered that changes in a particular type of immune cell known as adipose tissue macrophages (ATMs) may make weight loss difficult in mice. That's because they carry a biological "memory" of obesity.

Researchers from various institutions studied ATMs in mice. These immune cells regulate fat tissue health by, among other things, safely removing dying cells. The team fed the lab animals a high-fat diet for 12 weeks until they became obese and then switched them to a low-fat diet for a further six weeks.

The scientists noticed that mice that lost the least weight after the dietary switch had less of a protein called CWC22 in the nucleus of their ATM cells. This suggested it may play a role in helping the body shed weight.

To investigate this, the scientists genetically modified a group of mice to lack the Cwc22 gene in a group of immune cells that includes macrophages. CWC22 normally helps cells splice messenger RNA, a process in which RNA is edited before it is used to make proteins.
When these mice were put on a weight-loss diet, they struggled to shed fat. The ATMs could not effectively clear away dead cells, causing more dead cells to build up in fat tissue.

Analysis of these immune cells revealed that a lack of the Cwc22 gene caused a splicing error involving a gene called Scarb1. As a result, the macrophages destroyed their own cleanup receptors before they could reach the cell surface.

Because the macrophages were less able to clear dead cells, they released less inosine. This chemical normally acts as a signal that tells fat cells to break down stored fat. With less inosine available, fat breakdown was impaired.

The research team also discovered that 51.9% of the genes with obesity-induced RNA splicing changes in these immune cells remained altered even after weight loss. This revealed that the immune cells retained a biological memory of obesity, including changes that impaired their normal cleanup duties.

"These findings reveal that aberrant alternative splicing in macrophages underlies resistance to post obesity weight loss," commented the study authors in their paper.
However, it appears one part of this memory can be overridden. When the scientists fixed the Scarb1 splicing error with a synthetic genetic patch, the cleanup receptors were restored, increasing the amount of inosine available and helping the mice lose fat again.

This study suggests that specific alternative splicing events can shape macrophage phenotypes under defined environmental conditions.
This work could help design treatments for people struggling with obesity.

Takuro Miyazaki et al, Aberrant alternative splicing memorized in adipose tissue macrophages impedes efferocytosis during postobesity weight loss, Science Translational Medicine (2026). DOI: 10.1126/scitranslmed.adv0221

SwRI-led study models new scenarios for Moon formation

Dozens of genes tied to OCD and tic disorders discovered

An international collaboration has identified 36 genes that substantially raise the risk of obsessive-compulsive disorder (OCD) and chronic tic disorders—providing the most detailed biological understanding of how these conditions develop and might eventually be treated.

Before this study, published in Nature Neuroscience, scientists had found a few genetic clues, each linked separately to OCD or chronic tic disorders.

OCD is characterized by persistent intrusive thoughts and repetitive behaviours, while chronic tic disorders, including Tourette syndrome, involve sudden, repeated movements or vocalizations that are difficult to control. Together, the conditions affect millions worldwide, often beginning in childhood and frequently co-occurring within the same individuals and families.
In the past we knew about a couple of strong genes, so there were few opportunities for the pharmaceutical industry to develop drugs.

Now you've got over 30 targets, and that opens up new possibilities for treatment development.

The study analyzed DNA from nearly 4,000 people diagnosed with OCD, chronic tic disorders such as Tourette syndrome or both conditions. Researchers focused on rare mutations that disrupt genes that help build and operate the brain.

Many of the newly identified genes are shared between OCD and chronic tic disorders. The findings help explain why the conditions often occur together in the same people and families. At the biological level, the disorders appear to involve many of the same brain pathways.

These genes don't act individually. They act in networks. And now you can target whole networks, which will make it easier to design new therapies.
The researchers also found that several of the newly identified genes were previously linked to autism and schizophrenia, reinforcing increasing evidence that multiple psychiatric conditions may stem from related disruptions in brain development and communication.

Brain cells communicate using chemical signals called neurotransmitters that carry messages from one nerve cell to another. The genes identified in the study appear to influence how those signals move through the brain's circuitry.

By revealing the biological systems behind the disorders, the findings could help scientists design drugs that target the underlying mechanisms rather than simply managing symptoms.

Whole-exome sequencing in individuals with obsessive–compulsive disorder and chronic tic disorders identifies 36 large-effect risk genes, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02419-5

Nature's colour palette explains why everything we see is a mix of red, yellow, green and blue

Biologists and linguists alike have long puzzled over the universal human tendency to see and name colours as a combination of four "pure" hues—red, yellow, green and blue.
Most people and most cultures do not perceive red as a combination of orange or purple, for example, whereas they naturally perceive orange as a combination of yellow and red. We also perceive some colors as opposites of one another: red is the opposite of green; blue, the opposite of yellow. We would never describe a color as reddish-green or bluish-yellow.

Biologists have tried and failed to reconcile these four primary opposing colors with the three kinds of cone cells in our eyes that detect different wavelengths of light. Similarly, our subjective experience of colour can't be explained by the network of neurons that process vision in the brain. Yet, as painstakingly documented by linguist Paul Kay and the late anthropologist Brent Berlin at UC Berkeley, dozens of human languages, including many unwritten ones, categorize colour based on these four hues, hinting at a unique aspect of human perception.
We tend to think of red as just red, not as a mixture. This same unique property holds for green, blue and yellow: Each appears perceptually pure rather than as a mixture of neighbouring hues.
Neuroscientists have now come up with a theory that explains this conundrum. They demonstrate that the natural world—as distinct from the more colourful human-created world—displays a restricted palette of colours that the human brain, for the sake of simplicity, represents as combinations of only four pure colours. Basically, a combination of just four opposing hues—red versus green and blue versus yellow—provides the simplest way to encode the range of colours found in nature.
The new theory offers "a possible resolution of two historically competing accounts of colour vision that emerged around the same time and were vigorously debated in the late 19th century: Hermann von Helmholtz's theory that colour vision begins with three receptor types versus Ewald Hering's theory of the four unique hues and their opponent nature
We now know that both are valid accounts for how we see colour. The resolution is that while the former speaks to physiological sensory mechanisms in the retina, the latter describes a psychological basis for describing our subjective experience of colour … that is grounded in the structure of the natural visual environment.

Alexander Belsten et al, Emergence of unique hues from sparse coding of color in natural scenes, Journal of the Optical Society of America A (2026). DOI: 10.1364/josaa.598897

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Research identifies lasting brain changes associated with adolescent binge alcohol exposure
In male rats, intermittent ethanol exposure during adolescence caused persistent disruption of astrocyte–synapse coupling in the dorsal hippocampus and heightened fear-related behaviour in adulthood after abstinence. Enhancing astrocyte calcium signalling partially restored gliotransmitter availability and reduced behavioural effects, indicating astrocyte dysfunction as a potential therapeutic target.

O. Coulter et al, Adolescent alcohol exposure disrupts astrocyte-synaptic structural and functional coupling in the male dorsal hippocampus, Molecular Psychiatry (2026). DOI: 10.1038/s41380-026-03817-8

More than 120 molecular species found in giant cloud near Milky Way's center

Astronomers have discovered a second interstellar cloud near the center of the Milky Way that is extraordinarily rich in complex molecules, including several molecules associated with prebiotic chemistry. The newly studied cloud, G+0.633-0.0604, or G+0.633, contains more than 120 identified molecular species and is the first confirmed chemical twin of another famous molecule-rich cloud. Their paper, posted to the arXiv preprint server on Aug. 14, outlines the chemistry of the newfound cloud.
Finding molecules in space isn't new. So far, astronomers have found almost 350 different molecules in interstellar space. Most recent progress has been concentrated around a small handful of unusually chemically rich locations—the most famous being a molecular cloud called G+0.693-0.027, or G+0.693 for short, near the crowded, extreme region surrounding the Milky Way's central black hole.

This cloud contains roughly 40% of all molecules ever detected in interstellar space, including many linked to the chemical building blocks of life. Interestingly, it is not actively forming stars. Instead, its chemical richness comes from a combination of physical and chemical properties. The cloud is warm enough to sustain plenty of chemical activity, but the molecules emit significantly cleaner, easier-to-read "cool" signals.

The cloud is also thought to have been stirred up by low-velocity shock waves, likely from colliding gas clouds. The shock waves might violently blast icy coatings off dust grains, releasing a wide variety of molecules that had been frozen inside the ice. This leaves more of these molecules in the gas phase, boosting detectability. 

D. San Andrés et al, The Galactic Centre G+0.633-0.0604 Molecular Cloud: A New Gold Mine for Astrochemistry, arXiv (2026). DOI: 10.48550/arxiv.2608.14381

Adding AI agents to a system sometimes reduces its performance

Computer scientists worldwide have been developing a wide range of artificial intelligence (AI) systems. Some of these systems rely on an individual AI agent, while others consist of multiple interacting agents that exchange information, cooperate and revise each other's responses or predictions.
Researchers recently carried out a controlled experiment exploring the potential advantages and limitations of multi-agent AI systems.

Their findings, published in Nature Machine Intelligence, suggest that adding more AI agents to a system is not always beneficial, as a single capable agent can perform better on some tasks than multi-agent systems.
Overall, the results of this study suggest that adding more agents to an AI system is not always beneficial. Instead, performance appears to depend on how well a system's architecture suits the specific task.

Yubin Kim et al, Capable language models can outgrow the benefits of collaboration, Nature Machine Intelligence (2026). DOI: 10.1038/s42256-026-01268-y.

Scientists observe Einstein's gravity in the quantum world

An international team has observed a long-predicted effect of gravity on a falling quantum object for the first time. The result shows that a fundamental principle at the heart of Einstein's theory of gravity remains consistent with the behaviour of matter in the quantum world.
For more than a century, physicists have relied on two extraordinarily successful descriptions of nature. Quantum mechanics explains the strange behavior of atoms and other tiny objects. Einstein's theory of gravity explains how objects fall and how gravity shapes the universe. Yet physicists still do not fully understand how the two fit together.

Now, an international team has performed an experiment that probes the point where they meet. In the study, the researchers observed a distinctive change in the quantum properties of atoms as they fell under gravity. Crucially, the effect they measured is the same one predicted when Einstein's equivalence principle, a cornerstone of his theory of gravity, is applied to a quantum object.

The equivalence principle states that for an observer in free fall, gravity should locally disappear. Someone falling freely in an elevator, for example, would experience weightlessness. While this theory has survived extraordinarily precise tests involving ordinary matter, it was unclear how it could be experimentally tested with quantum objects, which can behave as waves and effectively travel along more than one path.
Although previous experiments have used quantum particles to measure gravity, the researchers say this is the first direct measurement of the predicted quantum phase of a freely falling object.

Observation of the quantum phase of free fall and the consistency with the equivalence principle, Science Advances (2026). DOI: 10.1126/sciadv.aec8045

When biology inspires mathematics: Hidden symmetries explain why widely used evolutionary methods can give false answers
Why do some groups of organisms contain thousands of species while others have only a handful? Evolutionary biologists have spent decades trying to answer this question using mathematical models that estimate how biological traits and environmental factors influence the formation and extinction of species.
These models have become a cornerstone of modern biology and have been used in more than 1,000 scientific studies. Yet the models carry a known weakness: They can sometimes lead scientists to the wrong conclusions. For years, no one fully found out why.
Several years ago, researchers found that many evolutionary models can generate exactly the same observations even when they rest on entirely different assumptions about evolutionary history. This meant that scientists could unknowingly reach different conclusions that were all equally consistent with the same data. Whether the same ambiguity also affected the more sophisticated models used to study how traits shape biodiversity remained unclear because their mathematics was too complex to analyze directly.
Sergei Tarasov at the Finnish Museum of Natural History and Josef Uyeda at Virginia Tech approached the problem from a different angle. Their path to the solution started with a simple but unusual question: Imagine three apples—one red, one light green and one dark green. Should the two green apples be grouped together or treated as different colors? The researchers ran into the same classification puzzle while studying beetle anatomy.

Searching for an answer led them to lumpability, a mathematical concept introduced in the 1960s that defines when different states of a Markov model can be safely grouped together without changing how a system behaves. Building on it, they unexpectedly discovered a new way of representing Markov models, one of the most fundamental classes of stochastic models used across science.

They showed that every discrete-state Markov model can be rewritten as an equivalent hidden-state model, a decomposition they call Hidden Expansion. Although the rewritten model looks larger, it is built from simple, identical mathematical components. This representation exposed previously hidden mathematical symmetries and turned an intractable problem into a solvable one.
This mathematical property had gone unnoticed despite decades of research on Markov models.
Part 1

The new decomposition allowed the researchers to answer the question that had resisted mathematical analysis for years. They showed that the same hidden symmetries also affect the sophisticated models used to study biodiversity and that the misleading conclusions these models sometimes produce are not isolated statistical mistakes. Instead, they stem from a deeper mathematical ambiguity built into the models themselves.
Scientific discoveries often begin with advances in mathematics that later transform biology. This study followed the opposite path. A biological question about how to represent anatomical traits of beetles led to a new mathematical discovery, which in turn solved a long-standing problem in evolutionary biology.

It's a wonderful example of biology and mathematics driving each other forward.

Sergei Tarasov et al, Unidentifiability and false-positive inference in state-dependent diversification models, Nature Communications (2026). DOI: 10.1038/s41467-026-75829-5

Part 2

Scientists discover how fructose may help drive obesity
High-fructose corn syrup is just one of many food additives linked to obesity. It is typically found in sweetened beverages and processed foods and is added to enhance flavour and sweetness.
But exactly how it it contributes to weight gain and obesity ?
New research
suggests the calories the sweetener contains are not the only drivers of these body changes. It could also be due to how fructose is processed, which may alter the intestine's physical structure and affect fat absorption. Details of the work are published in a paper in Science Advances.

The scientists wanted to study the gut specifically because the small intestine is the first place in the body that processes dietary fructose. They designed a series of controlled experiments in mice to examine a highly active form of a fructose-processing enzyme called Ketohexokinase-C.

For up to 12 weeks, the mice were given drinking water containing a high concentration of high-fructose corn syrup. Meanwhile, a control group of normal mice was given the exact same high-fructose diet, while another set of mice received normal drinking water without added sugar.

Throughout the study, the research team tracked the animals' body weight, fat mass and blood sugar levels. They also measured fat absorption. To do this, they gave the mice a dose of soybean oil and monitored how much fat entered their bloodstream versus how much passed into their waste.

According to the paper, mice lacking intestinal Ketohexokinase-C consumed the same total number of calories as normal mice but put on significantly less weight, stayed leaner and showed better glucose tolerance and lower fasting insulin levels.

Because the modified mice lacked Ketohexokinase-C in their intestinal cells, fructose was not broken down normally in the small intestine. Consequently, it traveled further down the digestive tract, where it altered the gut microbiome.

This, in turn, lowered the number of immune cells in the gut wall, which caused fat-absorbing tubes in the intestine (lacteals) to shrink. Because shorter fat tubes couldn't absorb as much dietary fat into the body, more of it passed straight out in their feces.

To confirm this, the researchers transplanted the altered gut bacteria into normal mice. They too developed shorter fat tubes and stopped absorbing as much fat.
"We found an unexpected role of small intestinal fructose catabolism [the biological breakdown of fructose for energy] in modulating gut microbiome, ileum-specific lacteal growth, dietary fat absorption, and eventually whole-body metabolic fitness," wrote the team in their paper.

Part 1

If this intestinal process is the same in humans, it could help explain why diets high in both sugar and fat may be particularly harmful and point to new ways to tackle obesity by targeting fructose metabolism, for example, with drugs that inhibit Ketohexokinase.

"This previously unappreciated link between intestinal fructose catabolism and dietary lipid absorption may explain the synergistically stronger effects of a diet enriched with both fat and fructose."

Miranda L. Lopez et al, Intestinal fructose catabolism promotes obesity and insulin resistance via ileal lacteal remodeling, Science Advances (2026). DOI: 10.1126/sciadv.aec0481

Part 2

To promote climate action, emotion may matter more than information

Every year, public authorities and nongovernmental organizations spend millions on communication campaigns designed to encourage people to take action on climate change. But which strategies work best? Should campaigns rely on fear or positive messages, prioritize facts or appeal to emotions, and focus on words or visuals?
Across 71 studies involving 216,000 participants, most climate communication strategies increased pro-climate intentions, behaviours, or policy support. Emotionally engaging storytelling, awe, moral framing, and images outperformed factual information alone. Individual or collective responsibility messages showed little benefit and may provoke reactance.

The strategies reviewed encompassed 15 different approaches, ranging from providing factual information to fill knowledge gaps to appealing to emotions—for example, by evoking a sense of wonder or awe at the beauty of nature. They also included approaches based on the principle of bounded rationality, which are designed to facilitate decision-making by highlighting specific aspects of climate change, such as its health or financial consequences.

Research shows that almost all of these strategies are likely to have a positive effect on people's intentions and behaviours, as well as on their support for climate policies. Only strategies based on individual and collective responsibility—with messages such as 'success depends largely on you'—appear to have little or no effect. They may even foster reactance.
But not all effective strategies are equally effective. "Campaigns that evoke a strong emotional response—particularly through storytelling or by inspiring a sense of wonder at the beauty of nature—are significantly more effective than simply presenting facts and scientific evidence. Messages that draw on moral, ethical or even religious considerations, highlighting our connection to something greater than ourselves that we have a responsibility to preserve, also achieve better results.
The researchers also found that messages are more effective when they include images.

Despite these differences, the fact that almost all of these strategies can have a positive effect is encouraging.
This is particularly encouraging given that the studies reviewed mainly measured the effects of messages to which people were exposed only once. Yet we know that repeated exposure can strengthen their impact. At a time when the scientific evidence is well established and the challenge is to turn knowledge into action, there is considerable scope to improve climate communication.

Mario Herberz et al, A systematic review and meta-analysis of communication strategies to promote climate action, Journal of Environmental Psychology (2026). DOI: 10.1016/j.jenvp.2026.103176

UN report finds 1.5°C warming limit likely to be exceeded by 2030

For more than a decade, the world has been trying to limit global warming to 1.5°C.

That's no longer possible, according to a new United Nations report. We will likely pass 1.5°C in 2030. That's not good news for anyone

Global warming is likely to exceed 1.5°C around 2030, increasing risks of extreme events, sea-level rise, ecosystem loss and potentially irreversible climate tipping points. Rapid emission cuts could limit peak warming and enable a later decline through carbon removal, but current policies remain insufficient.

original article.

How cells teach themselves to move together

Scientists have long wondered how cells organized into sheets begin to move together to form organs, especially when the sheets form closed, sphere-like surfaces and tissues with no edges to direct motion. Researchers used a combination of live imaging, genetic experiments and mathematical modelling to understand how cells in the fruit fly egg chamber synchronize their movement.
In fruit fly egg chambers, epithelial cells initiate collective rotation through feedback between cell motion and protein polarization. Movement polarizes a protein rearward, promoting aligned motion in neighbouring cells via mechanical coupling. Support-tissue forces initiate long-axis rotation, while chamber elongation stabilizes its direction.
Researchers found that cells can spontaneously organize and rotate together through a self-reinforcing mechanism in which a specific protein helps individual cells align their movement.

Once the cells start moving, that motion polarizes the protein to the back of the cell, which promotes further movement by the cells behind it in the same direction. Mechanical connections between adjacent support cells and the global egg chamber geometry mediate the coordination of cell movements.

Epithelial cells that form surfaces in the body undergo collective migrations while tissues are developing, during the closing of wounds, the spread of cancers or the constant turnover of things like your intestinal lining. But when there are closed surfaces, there are no external cues that tell the cells which way to go. So, this is a self-organized process.
The study, published in PNAS, also explains why the egg chamber always rotates around its long axis. Initially, this is caused by the physical forces through which the egg chamber interacts with nearby support tissues. As the egg chamber grows and becomes more oval-shaped, its own geometry helps stabilize the rotation axis.

This work holds potential implications for understanding both normal development and diseases in which collective cell movement goes awry.

Sierra Schwabach et al, Initiation of rotational collective migration in Drosophila through tissue geometry and mechanochemical feedback, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2528342123

Is this the first glimpse of dark matter?
A single data point from a dark-matter detector in the United States could be the first discovery of the elusive particle we call dark matter. The LUX-ZEPLIN experiment at the Sanford Underground Research Facility in South Dakota contains 10 tonnes of liquid xenon. It seeks evidence of a candidate particle called a WIMP (weakly interacting massive particle) by looking for flashes created when such a particle collides with the nucleus of just one xenon atom. If the finding can be backed up with more data, it could mean that the material that seems to make up most of the mass of the Universe has finally been discovered.

https://lz.lbl.gov/wp-content/uploads/sites/6/2026/08/LZ_Preprint_2...

https://www.nature.com/articles/d41586-026-01985-9?utm_source=Live+...

Diabetes drug metformin could be repurposed to help slow aging mechanisms

Over the past few years, a new field of science has been gaining momentum: geroscience. Instead of treating age-related diseases one by one, geroscience asks a bigger question: What if we could target the biological drivers of aging itself? Researchers are uncovering the common mechanisms that fuel aging and multiple chronic diseases, hoping to slow these processes and help people stay healthier for longer.

Metformin, a widely prescribed, safe and inexpensive drug for type 2 diabetes, is a first-line treatment that lowers blood sugar and improves the body's response to insulin. The drug appears to trick cells into sensing an energy shortage, similar to what happens during fasting or dieting. This activates a key cellular energy sensor called AMPK, which helps trigger cellular waste cleanup and supports cellular repair. Now, a recent review suggests metformin might also help counter some effects of aging.

Researchers compiled decades of global research, from cellular and molecular studies to animal and human studies, to provide a comprehensive, unified picture of how metformin might affect aging and longevity. The collective data indicated that metformin acts as a geroprotective agent that can target the biological root causes of aging and potentially improve health span.

Metformin's anti-aging effects are evident across species. Male monkeys treated for 40 months saw their tissues become biologically younger, with their brains alone reversing by nearly 6 years—a leap equivalent to 18 years in human terms. A similar pattern was seen in humans, where observational data indicate that people taking metformin had biological ages up to 3.43 years younger, with people with diabetes taking the drug living as much as 15% longer than their peers without diabetes.
A large body of evidence indicates that people prescribed metformin to manage blood sugar levels also had fewer cardiovascular events and showed lower rates of cognitive decline. Because developing new drugs takes years, researchers shifted their focus toward investigating whether metformin could be repurposed to slow the effects of aging.
Part 1

Instead of treating just one disease, metformin acts on multiple biological root causes of aging at the same time. It can trigger autophagy, the cell's cleanup system, helping clear cellular waste while supporting DNA stability. As we age, the chemical tags on our DNA called methylation begin to shift, affecting how genes are regulated. Metformin slows abnormal changes in DNA by stabilizing an enzyme called TET2, helping preserve a more youthful genetic profile. Its effects also reach the gut and its microbiome, where it can boost beneficial, mucus-protecting bacteria and the production of short-chain fatty acids. This is promising news, as previous studies have found that a healthy gut microbiome can lower age-related inflammation throughout the body.

In microscopic worms called C. elegans, metformin extended lifespan by 36% to 40% by putting the animals into a state similar to calorie restriction. In mice, across different models, metformin increased average lifespan by 5.8% to 20.1% and delayed the onset of certain tumours.

Jarra Manneh et al, Metformin at the convergence of aging and longevity, Aging (2026). DOI: 10.18632/aging.206407

Part 2

Healthy aging shaped by more varied biology than previously thought

Molecular changes in aging are far more unique than previously thought, meaning two healthy individuals of identical age can experience significantly different aging journeys.
A new study is the most comprehensive molecular study of aging to date. It demonstrates for the first time that genetic factors and environmental influences continuously interact across a person's lifespan.

The study, published in Science, observed how multiple genetic variants shape how an individual ages.

Notably, researchers found different courses of change among participants with a gene linked to cardiac aging (CXCL9). They also found that levels of the tumour suppressor gene tumour protein p53 (TP53) declined in certain individuals as they grew older, potentially altering their risk of cancer.

Such biological shifts can indicate distinct environmental exposures or reveal an underlying genetic predisposition to disease. Pinpointing individuals at higher risk offers future opportunities for earlier targeted health care interventions.

Importantly, the research also highlights correlations between environmental exposures, such as shifting blood levels of PFAS, commonly referred to as "forever chemicals," and evolving molecular profiles over time. This highlights how public health measures targeting environmental risks can affect the molecular level.

Molecular aging involves the steady accumulation of cellular damage alongside chemical changes in key molecules like DNA, proteins and lipids. Over time, this progression drives a gradual deterioration of tissue function, heightened physical vulnerability and a higher risk of age-related conditions, including cancer as well as cardiometabolic and neurodegenerative disorders.

Understanding how aging happens at the molecular level is vital to preventing or even reversing a range of age-related diseases—as well as increasing longevity.
Rather than there being a single molecular roadmap of aging, this study shows that people follow distinct biological journeys. Two healthy people of the same age can be aging in surprisingly different ways at the molecular level. That raises the possibility of much more personalized approaches to predicting disease risk and maintaining health as we grow older.
Over eight years, the team repeatedly measured blood RNA levels, the activity levels of around 16,000 genes and hundreds of metabolites in the same 335 individuals from TwinsUK during the study, creating one of the most detailed long-term multi-omic studies of healthy aging to date. They found that some study participants had markedly different, and sometimes opposite, molecular changes.

Aging patterns were not uniform across the immune system, which is key to the aging process—molecular changes over time differed between innate and adaptive immune cells. Innate immune cells are the fast, first line of defense you are born with, while adaptive immunity is a slower immune response that builds memory over time.
These findings suggest that human aging at the molecular level is not a uniform process, but one that is dynamic and environment-dependent.

Longitudinal dynamics of gene expression and metabolomics in an ageing population cohort, Science (2026). DOI: 10.1126/science.aed6452

Brain scans reveal new link between progesterone and women's mood

The influence of the hormone progesterone on mood is well known. Now, researchers have shown how higher levels of progesterone during the menstrual cycle are linked to less distinct patterns of activity in areas of the brain involved in controlling emotions.
The study, published in Psychological Medicine, explored how natural levels of the ovarian hormones estradiol and progesterone influence parts of the brain involved in emotion control and whether this could help explain differences in mood.

Emotion control is the ability to regulate behaviour in response to emotional information, particularly when automatic emotional responses need to be overridden. For example, if someone needed to ask an unfriendly person for help, their instinct might be to avoid them—emotion control would help overcome that impulse and approach them anyway.
Analysis of MRI scan data from study participants revealed that when progesterone levels were higher, there was a less clear distinction between "easy" and "difficult" emotional situations in the brain scans. This suggests that the brain would be less able to distinguish between different emotional situations in real life.

In contrast, participants whose brain scans had a clearer distinction between "easy" and "difficult" emotional situations tended to report better mood in the preceding week.

This brain mechanism accounted for roughly 7% of the variation in mood scores.
The researchers found that higher progesterone levels were linked to brain activity patterns that made it harder to tell different emotion control situations apart, which also corresponded with lower mood in participants.

This suggests that if the brain can tell different emotional situations apart more clearly, it may be better at regulating emotion in daily life.

Endogenous progesterone blurs frontostriatal representations of emotion control in healthy young women, Psychological Medicine (2026). DOI: 10.1017/S0033291726105315

Cancer cells release antioxidants to prevent immune cells from destroying them

Molecules called reactive oxygen species, which include so-called "free radicals," have long been viewed as damaging by-products of our body's metabolism—a reason antioxidant supplements have been considered a potential way to reduce cancer risk.
Now, scientists have discovered that certain immune cells depend on these molecules to activate and destroy cancer cells and that tumours exploit this dependency by releasing natural antioxidants to shut down the immune attack.
Our immune system keeps us healthy by hunting down and destroying harmful material, including invading bacteria and viruses, as well as cancer cells. It does so by deploying a number of different types of immune cells, including specialized cells known as T cells. These T cells hunt down and destroy tumor cells, but they need small amounts of reactive oxygen species to activate and switch on their killing ability.
Researchers analyzed the fluid surrounding cells within tumours grown in mice and found that cancers chemically 'smother' T cells, stopping their activation and preventing them from destroying cancer cells. Tumours do this by releasing large amounts of a protein that is a natural antioxidant, Peroxiredoxin 1 (PRDX1), which mops up reactive oxygen species and deprives T cells of the activating signals they need to kill cancer cells.

Next, the team used CRISPR gene-editing technology to create mouse cancer cells that could no longer make the antioxidant protein. They found that removing the cancer cells' capacity to produce the antioxidant promoted immune-cell activity and limited tumor growth.

Finally, the team looked for the same mechanism in people. They analyzed published data on the proteins released by human cancer cell lines, examined gene activity across thousands of human tumours, and isolated the fluid surrounding tumours removed from patients. All three approaches pointed the same way: Human cancers also release PRDX1 into their surroundings, where it can strip away the reactive oxygen species that T cells depend on.
Now that the researchers found a new way by which cancers shut down the immune system, we can block this process and make tumours that don't respond to some immunotherapies start responding to treatment. That tells us this is a pathway worth targeting therapeutically, and there are several ways we might be able to achieve this.
The findings also carry broader implications. Several large randomized clinical trials have found that antioxidant supplements fail to reduce cancer risk and, in some cases, worsen outcomes.

The discovery that T cells depend on reactive oxygen species to fight tumours may help explain why: Antioxidants could inadvertently blunt the immune system's ability to attack cancer.

Tumor-derived antioxidants suppress immunity by depriving T cells of reactive oxygen species, Science (2026). DOI: 10.1126/science.adz8203

Patients diagnosed with lung cancer found to have more microplastic in their lungs

People with lung cancer are more likely to have microplastics in their lungs and to have larger quantities of microplastics in their lungs, according to research that has been presented at the European Respiratory Society (ERS) Congress in Barcelona, Spain.
Among 100 patients undergoing bronchoscopy, microplastics were detected in 70%, with higher detection frequency and burden in those later diagnosed with lung cancer. Polypropylene and polyethylene predominated. The observational results show an association but cannot determine whether microplastics contribute to cancer or are retained differently by diseased lungs.
Researchers say their study adds to evidence that microplastics are entering our bodies via the air we breathe and suggests that there may be a link between microplastics and lung disease.
Across all samples, the researchers identified a total of 232 microplastic particles. Overall, 70% of patients had detectable microplastics in at least one sample (either the lung wash, tissue or both). When the lung wash and tissue samples from each patient were analyzed together, patients with lung cancer were more likely to have detectable microplastics and had a higher overall microplastic burden than those without cancer.

Patients with lung cancer were also more likely to have detectable microplastics in their lung wash samples (66% versus 46%) and had a higher microplastic burden than patients without lung cancer.

When the researchers compared the lung wash and tissue samples from the same individual, they found that patients with more microplastic in their lung wash tended to have less in the corresponding tissue sample, and vice versa. Because lung wash samples collect particles from the airspaces whereas tissue samples capture particles embedded within the lung itself, this finding suggests that microplastics may not be distributed evenly throughout the lung and that different regions may retain particles differently.

Analysis of the microplastics showed that polypropylene and polyethylene were the most common types of plastic. These are widely used in everyday products such as packaging, textiles, household materials and consumer goods.
This adds to the growing evidence that reducing environmental plastic pollution may have benefits that extend beyond ecosystems and into human health.

‘High respiratory microplastic burden across paired airway and tissue samples in patients with lung cancer’ by Ilias E. Dimeas et al. was presented in session at European Respiratory Society Congress 2026 on Thursday 3rd September.

Scientists studying cockroach milk and nose-blowing win Ig Nobel prizes for quirky science

Ten research teams were honoured this week at a satirical science awards ceremony that was hosted outside the U.S. for the first time due to travel concerns.
Ig Nobel prizes recognized unconventional work on cockroach milk, nose blowing, kissing evolution, and soil decomposition measured using buried underwear. The ceremony moved to Zurich because of travel and visa concerns, with future events planned across Europe.
Researchers who studied milk from cockroaches and analyzed soil health using underwear received Ig Nobel prizes celebrating unusual and imaginative contributions to science.
Another research team buried 1,000 pairs of underwear in more than 25 countries to study how critters in the soil helped them decompose.

Could damaged sperm be causing miscarriages?

Local neural wiring may set the brain's range of activity patterns

The human brain contains billions of neurons, specialized nerve cells that receive, transmit and process information through electrical and chemical signals. Human thoughts, sensory perceptions and behaviors are known to emerge not from the activity of individual neurons but from collective patterns of activity distributed across different neuron populations.

One way to characterize the collective activity of neurons is to measure its dimensionality, or, in other words, the number of independent activity patterns (i.e., degrees of freedom) exhibited by a specific neuronal population. High-dimensional activity can encompass various distinct activity patterns, while low-dimensional activity is restricted to a smaller range of possible patterns.

A new study  published in Nature Neuroscience, suggest that the collective activity of cortical networks is strongly influenced by the structure of neural circuits. As a result, local neural wiring could shape the breadth of activity states available to the brain.

The brain contains an astronomical number of neurons, but it is their collective activity that underlies brain function. The number of degrees of freedom that this activity explores (its dimensionality) is therefore a fundamental signature of neural dynamics. However, it is not known what controls dimensionality in the biological brain.

Researchers analyzed neural activity recordings collected in the mouse visual cortex using Neuropixels. These are tiny probes that can be used to monitor the electrical  activity of hundreds of neurons at once.

"Through analysis of high-density Neuropixels recordings, here, we argue that areas across the mouse cortex predominantly operate in a sensitive regime that gives recurrent synaptic networks a strong role in regulating dimensionality," the authors wrote. "This control is expressed across time, as cortical activity transitions among states with different dimensionalities. Moreover, this control is mediated through highly tractable features of synaptic networks (network motifs)."

The researchers tried to determine how many independent activity patterns were required to describe the collective activity of neurons in the mouse visual cortex. They also tracked this dimensionality over time to shed light on whether cortical activity remained in a single state or shifted between states with different dimensionalities.

The researchers also analyzed a dataset that contained physiological measurements of synaptic connections among more than 32,000 pairs of neurons in mouse and human cortical tissue. This allowed them to investigate whether network motifs predicted to affect dimensionality were prevalent in both species.

"Analyzing a massive synaptic physiology dataset, we find that motifs impacting dimensionality are prevalent in both mouse and human brains," the authors wrote. "Thus, local circuitry scales up systematically to help control the degrees of freedom that brain networks may explore and exploit."

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