Can vitamin C cure a cold? How a Nobel Prize winner convinced us it could
Vitamin C does not prevent colds in the general population or help when started after symptoms begin. Regular supplementation may modestly reduce severe symptom duration and severity, with greater effects in athletes and military personnel. High doses can cause gastrointestinal effects, kidney-stone risk, increased iron absorption, and drug interactions.

original article.

Male Neanderthal pelvises resemble those of modern females, challenging decades-old assumptions
A new study published in Scientific Reports offers an explanation for one of the striking differences between men and women: the evolutionary development of the modern human pelvis.
By comparing Neanderthal pelvises with those of modern humans, the researchers reached a surprising conclusion: The unusual structure of the pelvis may not be that of the Neanderthal, as has been assumed for decades, but rather that of the modern human male.
According to the researchers, the male pelvis evolved into a unique biomechanical shock-absorbing mechanism that stores energy and makes long-distance walking more efficient.
The study is based on a comparison of two nearly complete male Neanderthal pelvises, one from Kebara Cave in Israel and the other from the Sima de los Huesos site in Spain, with dozens of modern human pelvises.

Surprisingly, despite their large size and robust construction, the Neanderthal pelvises were found to resemble those of modern human females in most measurements and proportions rather than those of modern human males.

During every step of bipedal walking, the body's center of mass drops downward. This drop strains the joints and requires energy to raise the body again in preparation for the next step.

According to the new model, the distinctive geometry of the male pelvis enables the thigh muscles to cushion the drop of the body's center of mass, store potential energy during the step and then release that energy immediately afterward—effectively "springing" the body upward into the next step.

In this way, the pelvis functions as a natural shock absorber and energy-return system. It may reduce energy expenditure, improve walking efficiency and thereby provide a significant advantage during long-distance travel on foot. The change in the position of the hip joints also required additional structural adaptations, including the thickening of the pubic bone and deepening of the anterior portion of the pelvis to withstand the new mechanical loads.
Modern human females, by contrast, could not adopt the full suite of these modifications. According to the researchers, the constraints imposed by childbirth require a relatively shallow pelvis and a sufficiently wide birth canal. As a result, the female pelvis remains closer to the ancestral configuration—the same general configuration found in male Neanderthals.
Part 1

The findings of the study change the way we understand the evolution of the human pelvis. It is not the Neanderthal pelvis that is the anomaly requiring explanation. Rather, it is the pelvis of the modern human male. The mechanism that evolved within the human male represents the evolutionary innovation.

The researchers note that the study presents a new biomechanical model that may explain a substantial part of the human pelvis's sexual dimorphism, the anatomical differences between females and males.

Yoel Rak et al, Neandertal pelvis reveals specialized walking apparatus in human males, Scientific Reports (2026). DOI: 10.1038/s41598-026-59915-8

Part 2

Restoring a missing slice of sunshine to indoor light may help prevent myopia

Myopia, or nearsightedness, develops when the eye grows too long from front to back. This prevents images from focusing directly on the retina in the back of the eye, causing distant objects to appear blurry.

Myopia usually begins in childhood and can progress through adolescence. Beyond the need for glasses or contact lenses, high myopia increases the risk of vision-threatening complications later in life, including retinal detachment, glaucoma and macular degeneration.

Research has already shown that the more time children spend playing with screens indoors instead of outdoors, the more likely they are to develop myopia. In fact, some experts predict that nearly 5 billion people (or 50% of the world's population) will be nearsighted by 2050.
Now, a new study led by vision researchers  suggests that myopia can be prevented with improved indoor lighting.

Details were published online Aug. 18, 2026, in Cell Reports Medicine.

The research focuses on indigo light—a short-wavelength light that is abundant in sunlight but poorly represented in standard white LED lighting. In experiments involving tree shrews—an animal model with a human-like visual system—the team demonstrated that exposure to indigo light completely prevented nearsightedness from developing.
The study used tree shrews because their eyes share anatomical and optical features with human eyes.
Part 1

The team used these animals in a series of tests that exposed them to different wavelengths of light while using a biometer to measure eye shape and axial length and an autorefractor to measure refractive changes over time.

Earlier work in mice suggested that violet light near 380 nanometers could suppress myopia and revealed that opsin 5 (OPN5), a light-sensing receptor, was required for this response. But that wavelength did not work in tree shrews because, as in humans, the ocular lens blocks most light below about 400 nanometers.

Human lenses, and now we know tree shrew lenses, don't transmit a lot of light in the ultraviolet spectrum.
The findings support a broader idea that modern indoor life has changed the lighting environment in ways that affect children's eye development. Standard white LEDs typically have a peak around 450 nanometers and emit substantial longer-wavelength light that supports vision. But they provide little of the indigo light that appears to stimulate nonvisual opsins—light-sensitive pathways involved in biological processes beyond image formation.
We evolved outside in the full-spectrum light provided by our sun. When we live inside, we don't get all the wavelengths the eye needs for normal refractive development, and so we get myopia. That's the basic message of this research paper.
One way to prevent myopia would be to encourage children to spend much more time outside, where their eyes can focus across a wider range of near and distant objects while their growing bodies are bathed in full-spectrum sunlight. But reversing the course of our increasingly technical culture appears unlikely.

Another way to prevent myopia would be to improve lighting systems.

Prevention of myopia in a near-primate by supplemental indigo light suggests a hypothesis for the myopia boom, Cell Reports Medicine (2026). DOI: 10.1016/j.xcrm.2026.102999. www.cell.com/cell-reports-medi … 2666-3791(26)00416-7

Part 2

A new mathematical tool to uncover 'who eats whom' in nature

Understanding "who eats whom" is the key to keeping our oceans alive—and our dinner plates full. However, this invisible network that makes up the food chain can unravel with the pull of just one thread. Overfish one species, and its predators starve. Cut off a tiny prey species, and the entire food chain collapses—including us.
The intricacies of this web have remained a mystery because traditional ecological research is almost forensic, incredibly slow and strictly limited to the number of species scientists can physically collect during fieldwork. To find a better way, marine scientists had to look outside the ocean entirely and delve into an unexpected specialty: mathematics.
New research published in Methods in Ecology and Evolution on Aug. 6, 2026, blends marine science and engineering mathematics to solve the "impossible" problem of this chaotic web. The resulting algorithm reconstructed invisible ocean networks with 80% accuracy, essentially turning the invisible visible.
The algorithm reconstructed invisible ocean networks with more than 80% accuracy. Even better, its calculations of the percentage of each prey that predators ate had an error rate of less than 5%. Even when fed "noisy" or imperfect field data, the system remained perfectly steady.

Ettore Barbieri et al, The superposition method for the reconstruction of food webs, Methods in Ecology and Evolution (2026). DOI: 10.1111/2041-210x.70376

**

Link between whale calls and special relativity

For a more precise and consistent way to detect the presence of whales, oceanographers rarely rely on sight.
Sound from a fin whale can be heard from 100 kilometers (62 miles) away underwater with a single hydrophone. Because those calls travel so far, we can use them to pinpoint where an animal is by comparing when its sound reaches receivers spread across the seafloor.
But there's a catch: If they were trying to track a nearby whale using just standard physics, they'd probably place the animal in the wrong spot—off by hundreds of meters.

In a paper recently published in the journal Physical Review E, researchers offer a potential explanation for why this occurs: The humble whale call is, improbably, tangled up with the same speed limits Einstein deduced from the universe. Their findings could improve whale tracking for conservationists.
When a whale calls, the sound doesn't take a single path to each receiver. Some of the sound travels directly to a receiver, while some of it ricochets off the ocean surface first, arriving fashionably late.
That delay can put the two signals out of phase, causing them to interfere with one another and shifting when sound appears to arrive at a receiver.
The researchers stumbled onto this while refining a computer program meant to calculate the correct speed of sound for his whale-tracking equations. The results were surprising.

The first time, they got a number that was around 1,000 meters per second, well below the roughly 1,500 meters per second that sound normally travels in seawater. And then, further on, they got values that were sometimes 3,000 meters per second.

After examining the software for a few hours, they discovered that the behaviour wasn't a coding error, but a physical effect caused when a receiver picked up both the direct signal and its reflected echo when a whale was near the ocean's surface.
Physicists call this "temporal interference," the same phenomenon that causes TV broadcasts at your home antenna to fade out because two paths arrive out of phase or out of sync. The interference can also shift the peak of the energy earlier and break the speed limit.

What appears to speed up is not the signal carrying information but the position of the signal's strongest peak. That crucial distinction is the reason their finding aligns with Einstein's theory.

For more than a century, physicists have known that waves can sometimes appear to travel faster than light when their shape changes. But the information encoded in those waves still cannot travel faster than light—the central principle of Einstein's theory of special relativity.

John L. Spiesberger et al, Supersonic and superluminal energy and speed of information via temporal interference in a dispersionless environment, Physical Review E (2026). DOI: 10.1103/1mth-rs2j. On arXiv: arxiv.org/abs/2510.20060

Why do we get sleepy? How neurons control sleep drive

Why does staying awake inevitably make us sleepy? Researchers have identified neuronal populations in the brains of mice that become activated during prolonged wakefulness and are crucial for sleep drive. Their findings provide new insights into how the brain generates the need for sleep.
After a long day or a sleepless night, the urge to sleep becomes almost impossible to resist. This increasing sleep pressure, also known as sleep drive, ensures that prolonged wakefulness is followed by deeper and longer recovery sleep. As sleep is essential for survival, scientists have long been investigating how the brain keeps track of time spent awake and translates it into the need for sleep.
They now have identified specific neurons that are crucial for this balanced relationship between sleep and wakefulness. This is an important missing piece of the puzzle in understanding why we become sleepy.
To identify the brain regions involved, the researchers compared brain activation patterns in mice during normal sleep-wake cycles, sleep deprivation and recovery sleep. This highlighted specific brain areas that reflected time spent awake. Within one of these regions, they further identified two distinct neuronal populations that influence sleep drive: GABAergic and serotonergic neurons in the brainstem. The activation of both neuronal populations increased the longer the animals stayed awake and declined again after sleep onset.

The researchers next asked whether these neuronal populations merely reflect wakefulness or actively generate a compensatory response to sleep. When both populations were artificially activated, mice slept longer and more deeply, displaying a form of recovery sleep that normally follows prolonged wakefulness. In contrast, inhibiting these neurons strongly reduced sleep and allowed animals to maintain alert wakefulness.
These neurons do not simply signal that an animal has been awake. The experiments show that they are crucial to promote sleep, and that they may be key components of the neural circuitry that generates sleep drive. The findings therefore provide one of the clearest demonstrations to date that specific wake-active neurons increase the drive to sleep rather than merely responding to wakefulness.
Further experiments showed that long-term inhibition of the two neuronal populations substantially reduced the need for sleep, with mice sleeping approximately 70% less than usual. Unexpectedly, most of these animals did not exhibit some of the severe behavioural impairments that typically accompany sleep deprivation. In other words, these neurons appear to determine not only how much the animals sleep but also how strongly their need for sleep builds over time.
Understanding how the brain generates sleep drive would provide entirely new opportunities for sleep research.

William Joo et al, Wake-activated neuronal populations that regulate sleep drive., Nature (2026). DOI: 10.1038/s41586-026-10928-3

Is the laundry still damp, or just cold? Why your skin can't tell the difference

Humans lack dedicated wetness receptors; perceived wetness arises from integrated cold, friction, pressure, and contextual sensory signals. Cold dry laundry can mimic dampness because both activate cold receptors. Rubbing, squeezing, visual inspection, or warming fabric can improve discrimination.

original article.

A new transmissible cancer in bullhead catfish
Genomic analysis showed melanoma tumours in brown bullhead catfish are clonally related to each other rather than to their hosts, indicating a transmissible cancer, brown bullhead transmissible melanoma. Historical reports suggest similar lesions may be longstanding and widespread, but their relationship to this disease is unconfirmed.

transmissible cancer.

original article.

Why does salmonella cause serious illness in some people but not others?
Salmonella usually remains in the gut, but some strains can survive within immune cells and spread to the bloodstream, potentially causing sepsis. Severe invasive disease depends on bacterial type and strain, infectious dose, age, immune status and underlying conditions. Hospitalization data may overrepresent severe cases and cannot alone establish unusual strain virulence.

original article.

A smarter antibody could skip the fetus
Researchers have engineered a possible way around the risk some antibody drugs pose in pregnancy. These drugs, used against cancer, autoimmune disease and migraines, are hard to use safely in pregnancy because they are actively carried to the fetus via a receptor called FcRn. But the process has a quirk: mouse models and human tissue showed that the receptor binds to both IgG antibodies — which are used in the majority of approved antibody therapies — and albumin, but only shuttles the antibody across the placenta. By fusing therapeutic antibodies to albumin, the team made drugs that reached the fetus far less and reduced adverse events in mice.

https://www.science.org/doi/10.1126/sciimmunol.aee5151?utm_source=L...

https://www.genengnews.com/topics/drug-discovery/albumin-fused-anti...

Dark energy and quantum gravity may be deeply intertwined

For close to a century, physicists have pursued a way to unite gravity with quantum mechanics. Known as quantum gravity, this goal has remained frustratingly out of reach so far. Similarly elusive is the force of dark energy, which is believed to be driving the universe's accelerating expansion.
But through new research published in Physical Review D, physicists have proposed a new explanation suggesting that these two phenomena might not be separate at all. Instead, dark energy could be a natural side effect of quantum gravity, acting on the geometry of space itself.
Gravity and quantum mechanics shape the universe on vastly different scales: While quantum mechanics concerns the realm of subatomic particles, gravity shapes structures as large as galactic clusters and cosmic filaments.

Individually, both of these theories have been tested to extraordinary precision through decades of painstaking experiments. However, the extreme conditions where both should apply at once, such as inside a black hole, have remained far beyond what any experiment can reach.
In his study, physicists took a different approach: suggesting that we can't pin down both the size and expansion rate of the universe at the same time with perfect accuracy. This limitation is built into the fundamental uncertainty that governs the quantum world: When applied to the universe as a whole, it subtly changes the equations that describe how cosmic expansion should behave over time. This built-in uncertainty could then produce exactly the kind of accelerating expansion that cosmologists currently attribute to dark energy.

Depending on the exact mathematical details, this macroscopic imprint of quantum gravity could also replace the singularity at the instant of the Big Bang, which cosmologists have long struggled to explain. Rather than relying on a point of infinite density, their proposal suggests that the Big Bang followed a gentler rebound from a previously contracting universe.
If this idea is correct, it could provide a far cleaner explanation for the origins of dark energy. In contrast to many existing theories, this would mean that the phenomenon doesn't need to be explained by some hidden particle or exotic field waiting to be discovered: Instead, it is a property of space itself, hiding in plain sight in our observations of the universe.

Savvas M. Koushiappas, Cosmological uncertainty relation and late-universe acceleration, Physical Review D (2026). DOI: 10.1103/zgnd-h2xv. On arXiv: arxiv.org/abs/2604.27771

Simple mouth rinse may help detect stomach and colorectal cancer signals
It's widely understood that the microbiome—especially microbes found in the mouth and the gut—can have a profound effect on health. In a study published in the journal Cell Host & Microbe on Aug. 20, researchers report that by analyzing the makeup of oral microbes, they may be able to detect signals associated with gastric (stomach) and colorectal cancer. These findings could lead to the development of new, less invasive screening tests for gastrointestinal cancers.
Many species of microbes associated with the mouth are also present in the gut and may flourish there. These observations made the researchers

wonder whether oral microbes reach and persist in the gastrointestinal tract differently in people with cancer.
To conduct the study, the researchers recruited 507 volunteers to donate both oral and fecal samples, using a highly standardized collection process. The cohort included 129 healthy individuals; 215 people with metabolic disorders such as metabolic syndrome, hypertension, hyperlipidemia and type 2 diabetes; 77 people with gastric cancer; and 86 people with colorectal cancer. For the volunteers with cancer, samples were collected before the start of any treatment.

The team used gene sequencing to create what they called a mouth-to-feces (MF) index, which measures the extent to which identical microbial sequence variants are found in oral and fecal samples from the same person. They then evaluated how well the MF index could distinguish cancer patients from healthy individuals. The analysis revealed distinct signatures in people with gastric or colorectal cancer.

The findings were more nuanced than a simple cancer-versus-healthy comparison. The MF index was significantly elevated in patients with gastric or colorectal cancer but not in people with metabolic disorders. After accounting for alcohol consumption, regular exercise and BMI, the association remained robust for both gastric and colorectal cancers.
The team also compared the signatures found in the cancer patients with results from fecal occult blood tests, a standard colorectal cancer screening tool that analyzes stool samples. They found higher sensitivity with the oral samples, which were collected by a simple mouth rinse.

"It was notable that cancer-related information could be recovered from oral samples alone," say the researchers. Although only a small fraction of oral bacterial variants were also detected in the gut, models built using only these oral features could distinguish patients with cancer from healthy individuals across several independent cohorts.
In the longer term, combining microbial patterns with genetics, lifestyle and clinical outcomes may help explain why oral microbes persist more readily in some people than in others and may improve individualized risk prediction.

Mouth-to-gut microbial transmission signatures enable robust, non-invasive diagnosis of gastrointestinal cancers, Cell Host & Microbe (2026). DOI: 10.1016/j.chom.2026.07.007. www.cell.com/cell-host-microbe … 1931-3128(26)00308-2

Why immune responses to vaccines vary from person to person

Vaccines protect most people from serious illness, but the strength of that protection can vary considerably from one person to another. A new study helps us understand why.
Before a vaccine ever enters the body, the immune system may already hold clues to how strongly it will respond. In blood samples from more than 4,000 people, researchers measured antibodies against 185 antigens—targets recognized by the immune system, including those from common viruses and bacteria as well as targets associated with autoimmune diseases.

They then used artificial intelligence to analyze patterns in samples collected before and after COVID-19 vaccination, identifying antibody signatures that helped distinguish strong vaccine responders from weak ones.

The research opens a possible path toward more personalized vaccination strategies.
What this study found is that certain biomarkers, when analyzed with AI, can predict who is likely to respond well to a vaccine, even before they receive it. This suggests that some people may be more immune-ready than others.
Usually, scientists evaluate vaccine response after the shot by measuring whether the immune system produces antibodies against the target. Here, the researchers asked a different question: Could patterns already present in the blood predict the response before vaccination?

Age, sex, genetics, prior illnesses and underlying health conditions have all been linked to how strongly people respond to vaccines. People with immune-compromising conditions are often at higher risk of weaker responses. But even within these groups, outcomes can differ sharply.

The new approach is one of the first to use a broad, pre-vaccine antibody "fingerprint" to assess immune readiness. Unlike some prediction methods that rely on genetic analyses, this strategy uses antibody patterns in blood, which may be easier to adapt for clinical use.
Part 1

To test whether that antibody fingerprint could reveal vaccine readiness, the researchers analyzed antibody responses to 185 antigens. These included SARS-CoV-2, the virus that causes COVID-19, other common viruses and bacteria, and targets associated with autoimmune diseases.

The study included 8,687 samples from 4,089 participants, spanning healthy volunteers and people with conditions or treatments linked to immune suppression, such as HIV, multiple myeloma, solid organ malignancy, autoimmune disease, inflammatory bowel disease and solid organ transplantation.

The researchers found that several immunosuppressed groups were more likely to have blunted responses to COVID-19 vaccination. But those categories were imperfect predictors. Some immunosuppressed participants mounted strong responses, while about 5% to 6% of healthy participants had weak responses.
The study found that higher levels of certain preexisting antibodies, including antibodies to common microbes such as Staphylococcus aureus, RSV and human respirovirus 3, were associated with stronger COVID-19 vaccine responses.

The researchers describe these as "sentinel" antibodies because they may indicate a person's baseline immune readiness. They are not necessarily fighting the vaccine target directly. Instead, they may reflect how responsive the antibody-producing arm of the immune system is likely to be.

The researchers then asked whether the full antibody fingerprint, not just a few individual markers, could help identify people likely to have weak vaccine responses. Their deep-learning model analyzed patterns across the antibody panel, combining many measurements into a broader immune profile.

The study highlights a key strength of AI in health research: its ability to find subtle, predictive patterns in millions of biological data points that might otherwise remain hidden. The approach suggests that vaccine readiness may be better understood by looking at the immune system as a whole, rather than focusing only on a single disease or a single antibody.

The work also highlights the value of newer technologies that can measure large numbers of antibody responses at once. Instead of asking whether someone has antibodies to one pathogen, the method can scan a wider immune landscape, capturing patterns formed by many previous encounters with viruses, bacteria and other immune targets.
Sentinel antibody profiling could help guide vaccine testing, vaccine development and clinical care for people at risk of weak immune responses.

The approach might eventually help doctors identify patients who need additional vaccine doses, closer follow-up or alternative protective measures. It could also help researchers better understand why some people respond well to vaccination while others do not.

Pre-vaccine sentinel antibodies predict blunted vaccine responses, Cell Press Blue (2026). DOI: 10.1016/j.cpblue.2026.100088. www.cell.com/cell-press-blue/f … 3051-3839(26)00086-1

Part 2

Too much RNA can starve cells of energy, study finds

Why do you feel very weak after viral infections?

A new study by researchers has uncovered a previously unknown consequence of viral infection: Too much RNA inside a cell can disrupt its ability to produce energy.
Published in the journal Proceedings of the National Academy of Sciences, the study found that when excess RNA builds up inside cells during poxvirus infection, it can impair mitochondria—the structures responsible for generating most of a cell's energy—reducing the cell's ability to function normally.

The discovery could have broad implications for understanding viral infections, age-related diseases and RNA-based therapeutics, including mRNA vaccines, because excess RNA can accumulate in each of these conditions.
Scientists have long known that RNA degradation helps control protein production and remove defective RNA. This new study reveals another important role: It helps cells maintain the energy they need to function properly.
The findings suggest that RNA degradation serves a broader purpose than scientists once realized. In addition to controlling protein production, supporting RNA quality control and helping cells regulate immune responses, it also helps protect the cell's ability to generate energy.

RNA exists in many forms. Messenger RNA (mRNA) carries the genetic instructions cells use to make proteins, which help cells perform their normal functions. Another form, double-stranded RNA (dsRNA), is commonly produced during viral infections and alerts the immune system that something is wrong.

During viral infection, viruses can produce large amounts of RNA. If cells cannot break down the excess RNA quickly enough, the buildup can damage mitochondria and reduce the cell's ability to generate energy.

While scientists already knew that excess dsRNA can trigger immune responses and that cells need to control dsRNA levels, the effects of mRNA came as a surprise.

mRNA is a normal component of our cells, but it seems like with many good things, if we get too much, that can become a problem for the cell. When too much RNA builds up, including mRNA, it can damage the mitochondria and interfere with the cell's ability to produce energy.
Viruses rely entirely on host cells for energy and protein production, but producing too much viral RNA can overwhelm the very cells viruses depend on to survive.
poxviruses—the family of viruses that includes smallpox and mpox—appear to use RNA cleanup systems to degrade RNAs and keep infected cells functioning long enough for the virus to continue replicating.

If the cell is not healthy, the virus would not replicate well. The virus needs to keep RNA levels balanced inside the cell.
The team also found that mitochondrial impairment occurred before major immune responses were activated and did not depend on the immune system's usual response to infection, further supporting the idea that RNA itself contributes to the damage.
Researchers think the negatively charged RNA may accumulate around mitochondria and disrupt the electrical balance needed for energy production, although how it happens is unknown.
Part 1

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

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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