The findings may also have implications beyond viral infections.

Researchers have observed RNA accumulation in a variety of conditions—including some cancers, neurodegenerative diseases and age-related disorders—suggesting that mitochondrial damage may be one way excess RNA contributes to those conditions.

Perturbation of RNA homeostasis impairs mitochondrial respiration during poxvirus infection through excess RNA accumulation, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.26051941

Part 2

Gray and white matter jointly shape cognitive aging, new evidence shows

Researchers have found that two distinct types of brain tissue work together to support cognition in older adults and that the health of the brain's short-range wiring may help soften the cognitive effects of gray matter loss.
The study, published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association, analyzed brain scans and cognitive assessments from 459 community-dwelling adults 60 and older across India.

It is among the first studies to examine the brain's superficial white matter in a community-based population from a low- and middle-income country.

Superficial white matter is a thin layer of nerve fibers immediately beneath the brain's outer gray matter. These short, curved fibers act like local roads, carrying signals between nearby areas of the cerebral cortex. Gray matter, by comparison, contains many of the brain cells that process information.

Gray matter and superficial white matter are physically close and may play different roles: gray matter processes information, while superficial white matter helps nearby brain regions communicate.
These new findings suggest that cognitive health depends not only on how much gray matter is preserved, but also on the condition of the wiring that connects it.
The researchers used an advanced form of diffusion MRI, which measures how water moves through brain tissue, to assess microscopic features of superficial white matter. They focused on measures that reflect neurite density, the small projections that allow nerve cells to send and receive signals, and the amount of freely moving water around them. Lower neurite density or more free water can indicate tissue disruption associated with processes such as loss of myelin, inflammation or swelling.
Participants also completed tests of language, memory, executive function and visuospatial ability. The team found that healthier superficial white matter was most consistently associated with stronger language skills. The clearest links appeared in frontotemporal areas involved in recognizing words, speaking fluently and holding language information in mind.

Gray matter atrophy measures remained the strongest overall predictors of cognition. However, the relationship between gray matter and cognitive performance depended in part on superficial white matter: When this local wiring showed poorer integrity, gray matter loss was more strongly tied to worse language performance and cognitive impairment. When superficial white matter was healthier, those associations were weaker.

The findings point to superficial white matter as a possible source of resilience.
Two people with a similar degree of gray matter loss may not experience the same cognitive effects if the local connections surrounding that gray matter differ in health. Following participants over time will be essential to test whether preserving these connections can help maintain cognition.

Yingxu Liu et al, Superficial white matter and gray matter jointly support cognition among older adults in India, Alzheimer's & Dementia (2026). DOI: 10.1002/alz.71697

Dehydration can cause more than thirst: Expert explains how it can affect the heart
Dehydration reduces circulating blood volume, increasing cardiac workload and triggering faster heart rate and blood-vessel constriction. Severe dehydration can impair organ blood flow, causing dizziness, palpitations, chest discomfort, fainting, or heatstroke. Older adults, children, people with heart disease, and those using fluid-altering medications are at increased risk.
Think of the heart as a pump. For it to work properly, enough blood needs to return to it with every heartbeat.
When you become dehydrated, the amount of fluid circulating in your bloodstream decreases. That means less blood returns to the heart, so it has to work harder to keep blood moving throughout your body."

Your body has several built-in ways to respond to dehydration. Blood vessels narrow to help maintain blood pressure, and your heart beats faster to keep blood moving. If dehydration becomes more severe, those usual responses can begin to fail. As a result, organs such as the brain, kidneys, liver and digestive system may not receive enough blood to function properly.
As dehydration worsens, symptoms can include:

Racing heartbeat or palpitations
Fatigue
Lightheadedness
Dizziness
Vision changes
Shortness of breath
Chest discomfort
If dehydration becomes severe, it can lead to heatstroke or fainting. These are medical emergencies and should be evaluated by a health care professional immediately.
Anyone can become dehydrated, but some people are at greater risk, including:

Older adults
Children
Athletes
Outdoor workers
People with heart disease
People taking certain medications, such as diuretics or GLP-1 receptor agonists
"People with heart failure or other forms of heart disease should be especially careful.
Part 1

Staying hydrated and preventing complications
There isn't a one-size-fits-all recommendation for how much water you need. For most healthy people, thirst is a reliable guide. If you feel thirsty, drink something. If you know you'll be spending time outdoors in the heat or exercising for an extended period, increase your fluid intake beforehand.

Dehydration isn't always easy to recognize, so it helps to look for other signs. Dry mouth, dry skin, dark urine, foamy urine or a burning sensation when you urinate may all indicate you need more fluids. One of the simplest ways to monitor your hydration is to pay attention to the color of your urine. Pale or clear urine generally suggests you're well hydrated, while darker urine may be a sign that you need more fluids.

Water is an excellent first choice for staying hydrated, but if you're truly dehydrated, water alone may not always be enough. Your blood contains electrolytes such as sodium, potassium and magnesium. Drinking water along with consuming something salty may help replace both fluids and electrolytes. People participating in prolonged exercise or endurance activities also may benefit from electrolyte-containing sports drinks.
Alcohol is a major contributor to dehydration because it changes how the brain and kidneys regulate fluids and can increase fluid loss. Highly caffeinated drinks also can contribute to dehydration. If you're trying to rehydrate, choose water or electrolyte-containing drinks instead of sugary drinks or soda.

The best way to prevent dehydration is to stay ahead of it. Make drinking fluids a regular part of your day. Drinking smaller amounts throughout the day is often more effective than consuming a large amount all at once.
If you'll be gardening, exercising or working outdoors in hot, humid weather, plan ahead, stay aware of how you're feeling and adjust your activities if needed."

Most importantly, know your personal risk. If you're older, have heart disease or take medications that affect your body's fluid balance, you may need to pay especially close attention to staying hydrated. Planning ahead, listening to your body and recognizing the signs of dehydration can help protect your heart and your overall health.

Part 2

Cabin crew at greater risk of radiation‑based cancer than nuclear technologists, new study suggests
Analysis of 12.7 million death records linked pilots and cabin crew with the highest proportions of deaths from selected radiation-associated cancers (6.7% and 6.9%). Repeated cosmic-radiation exposure at flight altitude may contribute, but individual flight histories and doses were unavailable, so causation cannot be established.

original article.

How the brain distinguishes the consequences of our own choices from events beyond our control

A new study has identified the brain mechanisms that help us work out whether the consequences we experience are caused by our own actions or by circumstances beyond our control.
The study, published in Neuron, found that both confidence in our own decisions and estimates of external circumstances provide important clues. When people were confident in a decision but received an unexpected negative outcome, they were more likely to attribute it to external circumstances. On the other hand, when they were less certain about their decision, they were more likely to consider their own performance as the cause.
At the same time, they used these experiences to continually update their estimate of how much control they generally had over the external circumstances.
Participants made these conclusions partly because they tracked how certain they were about their own performance throughout the assessment, even before they obtained any feedback.
Using ultra-high-field brain imaging and targeted noninvasive brain stimulation, the researchers identified two prefrontal-subcortical brain circuits involved in this process. The findings provide new insight into how our sense of control is formed and how it subsequently shapes learning from success and failure.
Using an ultra-high-resolution functional MRI scanner in 22 participants, the researchers traced this process to a circuit connecting the dorsomedial prefrontal cortex (dmPFC) with the dorsal raphe nucleus, a small structure deep in the brain. Activity in the dmPFC tracked participants' confidence, their estimate of how much control they had, and whether they attributed an outcome to their own performance or to randomness.

A second circuit, connecting another region of the prefrontal cortex with dopamine-associated regions of the midbrain, was linked to how these judgments influenced the brain's response to feedback.
The findings could ultimately help researchers better understand why people's perceptions of control can sometimes become distorted. Altered perceptions of control and causal attribution have been associated with conditions including depression, anxiety and schizophrenia, although the researchers stress that the present study investigated healthy adults and was not designed to test clinical interventions.

Two prefrontal-subcortical circuits estimate controllability and reflect its impact on learning, Neuron (2026). DOI: 10.1016/j.neuron.2026.07.029. www.cell.com/neuron/fulltext/S0896-6273(26)00584-2

Why memories get fuzzier with age

New Research shows how our memories change with age and why specific details associated with past events can fade over time. The new study reveals that as people age, they not only remember fewer details from their past—but also struggle more when switching between different types of memories.
The work is published in the journal Psychology and Aging. It points to a shift in how we remember things as we age—where vivid, moment-specific recollections gradually give way to broader, more generalized knowledge.

Rather than portraying memory decline as a simple loss, the study offers a nuanced picture of aging cognition and sheds light on how memory evolves over a lifetime. The team hopes its findings could help guide new approaches to support healthy cognitive aging.

As we get older, our memories tend to become less detailed and more general, focusing on the overall story rather than specific moments.
This shift is linked to changes in how the brain recalls information, meaning older people often remember the big picture but with fewer vivid details.
Researchers found that across all age groups, memory performance declined when participants had to switch between memory types.

However, older adults were particularly affected in one area—they were less accurate at recalling more mundane repetitive memories like commuting to work under switching conditions.

Interestingly, their ability to recall specific memories like a birthday party was less affected by the task-switching challenge.

This suggests that certain types of memory retrieval may be more vulnerable to the effects of aging when multitasking or adapting to changing demands.
The most striking findings came from analyzing the content of the memories themselves.

When recalling specific events, older adults' narratives contained fewer details such as sights, sounds and emotions tied to a moment.

However, they remembered more semantic details—general knowledge or interpretations of the event. A similar pattern was observed when participants in the study were asked to recall categoric memories.
The findings highlight that changes in memory are not simply about forgetting, but about how memories are accessed and expressed.

When older adults recall events, the richness of those memories may be reduced.

This shift may reflect changes in underlying brain systems involved in memory, particularly those responsible for retrieving detailed contextual information and managing complex cognitive tasks.
This has practical implications for everyday life. Tasks that require people to quickly adapt their thinking or switch between different kinds of recall—such as storytelling, decision-making or problem-solving—may become more challenging with age.
At the same time, the increased reliance on semantic knowledge may have benefits. Generalized memories can support wisdom, pattern recognition and efficient communication, even if the finer details are lost.

Greta Melega et al, Age-related differences in autobiographical memory recall: Impact of retrieval mode switching., Psychology and Aging (2026). DOI: 10.1037/pag0001009

Some city trees have an ozone downside
Some of the species of trees planted in urban areas — species that are often chosen for their quick growth and climate resilience — have an unfortunate downside: they emit high levels of volatile organic compounds (VOCs) that contribute to ozone pollution. VOCs react with nitrogen oxides (NOx) to create ozone, which can cause breathing difficulties. A study in Beijing found that vegetation accounted for about 10% of the total VOC emissions during a period in 2021. Reducing NOx emissions, which mostly come from vehicles and industry, would help keep ozone in check.

https://www.science.org/doi/10.1126/sciadv.aee5583

These trees are making air quality in cities worse

The people who research their own disease
Molecular biologist Francesca Granata studies a rare condition called porphyria that can cause burning or itching skin — a path she chose after her own diagnosis in 2008. She and other researchers who study their own rare diseases told Nature that their personal experience with an illness enables them to empathize with other patients, driving them to find better therapies for themselves and others. There is potential bias in studying their own disease, but contributing to an increased understanding of their condition can be deeply fulfilling, they say.

https://www.nature.com/articles/d41586-026-02455-y?utm_source=Live+...

When you eat may matter as much as what you eat for longevity and heart health

What we eat plays a vital role in maintaining a healthy lifestyle. A well-balanced meal rich in essential micronutrients not only fuels the body but may also help protect against metabolic and cardiovascular diseases. There is another question worth asking: Does when we eat matter just as much as what we eat?
We have a decent understanding of the circadian rhythm—the body's internal clock, synced to the 24-hour cycle, that regulates not just sleep but essential biological functions, from hormone release to cellular repair. Scientists are now digging deeper into its links with food in a field of research called chrononutrition—the study of how meal timing interacts with our body's circadian rhythms to influence health, metabolism and weight regulation.
researchers have found that skipping breakfast or eating late could disrupt our internal body clocks and harm metabolic health.

A recent study explored this question in greater depth by examining whether meal timing and the length of our daily eating window are associated with mortality risk and life expectancy among U.S. adults.

Data tracking more than 30,000 adults age 40 and older revealed that when we eat our first and last meals may be linked to our risk of death and overall life expectancy. Starting the day with a later first meal was associated with a progressively higher risk of death from any cause and cardiovascular disease. People whose first meal was after noon had a 29% higher risk of death from any cause compared with those who ate their first meal between 7 and 8 a.m.

For the last meal, the lowest risk was observed around 7–8 p.m., and the highest risk was observed among those who ate past midnight.
Using a first meal between 7 and 8 a.m. as the ideal baseline, the researchers found that having that first meal between 8 and 10 a.m. was linked to a 10% higher risk of death from any cause. Waiting until 10 a.m. to noon, that risk climbed to 19%, while stroke-related deaths nearly doubled, rising 59%. Skipping breakfast altogether and waiting until after noon, overall death risk rose to 29%, with heart disease deaths jumping to 43%.

When it came to dinner, eating too early or too late came with a cost. Eating before 7 p.m. was tied to a 13% higher risk of death, while eating too late, past midnight, proved far more dangerous, driving overall mortality up by 27% and heart disease deaths up by 51%. The sweet spot was between 7 and 8 p.m.
The researchers say that while the results point to potential links among meal timing, mortality and life expectancy, this was an observational study, so it cannot prove that meal timing causes earlier death.

Wen Hu et al, Meal timing and eating window with all-cause and cardiovascular mortality and life expectancy: population-based cohort study, European Journal of Clinical Nutrition (2026). DOI: 10.1038/s41430-026-01796-1

Getting pregnant while already pregnant is an extremely rare phenomenon known as superfetation. It happens when a second egg is released, fertilized, and implants in the uterus weeks after an initial pregnancy has already begun, resulting in two fetuses with different gestational ages.
How It Normally Blocked
Your body has strong natural barriers to prevent this:
No Ovulation: Pregnancy hormones like progesterone stop your ovaries from releasing more eggs.
Cervical Plug: Thick mucus blocks sperm from entering the uterus.
Uterine Lining Changes: The lining changes so a new embryo cannot implant.
Why It Is So Rare
For superfetation to happen, all natural body blocks must fail at the same time.
Only a tiny number of natural cases are documented worldwide.
Most reported cases involve fertility treatments or assisted reproductive technology.
However, some people of science that different fetal sizes on early scans are usually just fraternal twins or normal growth variations rather than true superfetation.

Hidden Pulses Within Your Brain May Hold Your Thoughts Together
When you recognize a familiar face, your brain must connect that face with a name, a place, and perhaps a memory.

Those pieces of information are not necessarily handled in the same part of the brain. Yet they come together so smoothly that you experience them as a single thought.

Scientists may now have found one way the brain pulls off this trick.

A new study suggests that distant parts of the brain briefly fall into the same rhythm when we hold and retrieve information. During these fleeting moments, their cells become more likely to send signals together, potentially allowing separate pieces of a thought to be joined.

Researchers were especially interested in extremely brief bursts of electrical activity called ripples. A ripple is a very brief burst of rhythmic oscillations in neuron excitability – roughly 90 cycles per second, lasting only about a tenth of a second.
Part 1

A 4-star system caught eclipsing itself in a way never seen before
Astronomers have found a four-star system doing something that has never been confirmed before. The system, TIC 433545934, has two close pairs of stars orbiting each other. While each pair eclipses its own two stars, as usual, only one pair eclipses the other. A paper outlining the properties of this unique system was submitted to the arXiv preprint server on Aug. 13. It has been accepted for publication in the journal Astronomy & Astrophysics.

Tamás Borkovits et al, TIC 433545934: The first 2+2 type doubly eclipsing binary with extra, mutual eclipses, arXiv (2026). DOI: 10.48550/arxiv.2608.13034

How space rocks become meteorites

What happens to a space rock as it falls through Earth's atmosphere and becomes a meteorite? By studying 75 meteorite falls captured on video and in photographs, researchers identified seven distinct phases in the journey from space rock to meteorite. Their findings show that melting and fragmentation, rather than simply evaporation and "burning up," control how a rock loses mass, slows down and ultimately reaches the ground.
Phase 1 starts high in the atmosphere, when the air is dense enough to create a shock wave in front of the falling rock. Collisions with air molecules heat the rock and the gas around it until they glow. This is what we see as a meteor or "shooting star."

As the rock falls into thicker air, Phase 2 begins and the meteor gets brighter. Some meteors show that the rock is spinning rapidly by changing brightness in a regular pattern. The fastest-spinning rocks in the study made a full turn every 0.5 to 5 seconds.

In Phase 3, the meteor gets much brighter and turns into a fireball. The researchers found that melting now causes most of the rock's mass loss. The fast-moving air pulls melted material off the surface, leaving droplets behind that keep evaporating.
At around 60 kilometers (around 40 miles) above Earth, the fireball reaches Phase 4 by settling into a melting equilibrium. Its brightness stays the same or grows at a steady pace. The rock ultimately can lose up to 40% of its mass just from melting.
Deeper in the atmosphere, higher pressure makes the rock break apart, starting Phase 5. The fireball may flare up several times as pieces break off.

The researchers discovered that rocks start to break apart when the air pressure in front of the rock is only about one-fifth of the strength measured in meteorites found on Earth. They think that heat and cracks from earlier collisions in space can explain why the rocks break earlier than expected.

Only at this time does the remaining rock quickly become smaller and slow down significantly, more rapidly if the rock breaks aggressively.
If the back of the main rock stays whole, it creates a low-pressure area behind it that pulls smaller pieces along.
When the back of the rock finally breaks apart in Phase 6, the fireball gives off a last bright flare and sends pieces flying out faster. Since the rock has already slowed down, these late flares are usually red instead of the bright green seen earlier.

That final disruption sends fragments flying at higher relative speeds.
In Phase 7, melting and fragmentation keep happening until the last pieces slow down enough to stop glowing. Melting ends, leaving a thin fusion crust on their surfaces. Winds can then blow the darkened fragments off course as they finish falling to the ground as meteorites.
The 75 investigated meteorite falls included several different meteorite types. The study identified the altitudes at which these different materials went through the seven phases.

By studying the atmospheric slowdown of small, solid space rocks of different types, researchers also gained insight into what happens to more dangerous airbursting asteroids the size of cars to city blocks.

Asteroids up to tens of meters in size are also solid rocks because they tend to spin faster than do the larger rubble-pile asteroids.

Peter Jenniskens et al, Bolide Light Curve Systematics from 75 Recovered Meteorites, Meteoritics & Planetary Science (2026). DOI: 10.1111/maps.70203

How chromosomes find their partners

For a long time, so-called satellite DNA was considered largely worthless. Now, researchers have shown in fruit flies that these repetitive sections of genetic material act as a kind of barcode, enabling the correct chromosomes to recognize one another.
The body cells of humans and animals contain a double set of chromosomes. One-half of the genetic material comes from the mother; the other stems from the father.

During the formation of sperm or egg cells, this double set of chromosomes must be halved to form a single set. This takes place during what is known as meiosis. In this process, a cell with a double set of chromosomes gives rise to daughter cells with a single set of chromosomes. This halving is necessary because, during fertilization, two germ cells—and thus their genetic material—fuse together.

Afterwards, there is once again a double set of chromosomes. If this did not happen, the number of chromosomes would double from one generation to the next as the germ cells fuse.

To ensure that chromosomes can be distributed evenly during meiosis, the maternal and paternal versions of the same chromosome must locate one another within a cell and temporarily pair up. This is no easy task amid the vast jumble of the cell nucleus. Mismatches must be avoided at all costs during the pairing phase to prevent chromosomes from being distributed incorrectly.
But how do the matching chromosome pairs actually find each other?
Researchers have now investigated—using the example of egg cell formation in female fruit flies (Drosophila)—how this "matchmaking" process takes place in the cell nucleus and have made a surprising discovery.
For a long time, scientists have known that large swaths of animal genomes consist of repetitive DNA sequences. Known as satellite DNA, experts regarded these repeats as useless "junk DNA" because they do not contain blueprints for proteins. Nor were other researchers able to attribute any role to satellite DNA during meiosis. Indeed, when they removed these satellite DNA repeats from just one chromosome, chromosome pairing still proceeded without error.

In Nature Communications, researchers demonstrate that unique satellite DNA patterns on each pair of chromosomes, comparable to a barcode on a product in a supermarket, help matching chromosomes find each other.
Part 1

The researchers argue that it is not enough to simply remove satellite DNA from just one chromosome. With only one "barcode" disrupted, all the other chromosome pairs with intact satellite DNA "barcodes" can find each other. Ultimately, only the pair of chromosomes from which the researchers removed the barcode remains. They find each other like the last two face-down cards in a game of Memory.

Therefore, the ETH researchers removed the satellite DNA barcode from two different chromosomes, leaving the two pairs without any guidance.

And indeed, without their barcode, partner selection went awry and failed, meaning that the chromosomes frequently docked with the wrong partners. "This showed us that satellite DNA functions as a recognition aid and ensures that the chromosomes that belong together can reliably find one another.
Simply recognizing each other, however, is not enough. The researchers went on to discover that chromosome pairing also requires a molecular "glue" to properly "marry" the two partners together. A protein called D1 plays this role. It recognizes the matching barcodes on the chromosomes that belong together, binds them and holds the two together.

However, if the recognition pattern on one of the two chromosomes is altered—for example, if part of the barcode is deleted or changes occur due to natural mutations—the D1 protein can bond two chromosomes together that do not belong together. The pairing then goes wrong.
The new findings also explain how new species arise. Satellite DNA changes a great deal more rapidly than the rest of the genome. As long as individuals of a species produce offspring with one another, the satellite DNA barcodes remain similar across the population. because of the constant mixing of genetic material. Individuals with recognition patterns that differ too greatly suffer from meiosis defects and are unable to reproduce.

However, if a population of an animal species becomes geographically isolated—for example, because of the formation of a mountain range over millions of years—the satellite DNA in both groups evolves independently. When the two groups meet again after a long period, the recognition patterns of the chromosomes no longer match. The result: The animals can no longer reproduce, and one species has become two.

Studies on crosses between Drosophila melanogaster and its relative Drosophila simulans are consistent with this idea. The two species diverged two to three million years ago. The barcodes of their chromosomes now differ so greatly that massive chromosome-pairing defects occur during meiosis in hybrids.

Lena Skrutl et al, Meiotic pairing through barcode-like satellite DNA repeats, Nature Communications (2026). DOI: 10.1038/s41467-026-74398-x

Part 2

Antarctic bacteria share 'life‑support' genes to survive extreme conditions

Antarctic soil microbes extensively exchange genes via horizontal transfer; evidence occurred in ~98% of 676 analyzed species. Frequently transferred genes support aerotrophy, enabling energy generation from atmospheric hydrogen and carbon monoxide. Selection retains beneficial genes, supporting survival in cold, dry, nutrient-poor soils.

original article.

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

**

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

**

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.