Too little salt may hurt memory just as badly as too much

Salt can make or break a dish. A little too much or too little can throw everything off, leaving even the most luxurious ingredients tasting off. But get the balance right, and salt can bring out the flavour in even the simplest ingredients. The brain relies on a similar balancing act for healthy function and memory. While we are aware of the ill effects of having too much salt, what happens when we consume too little?
A recent study compared how long-term low-salt and high-salt diets affected memory, gut health and brain health in mice whose guts were colonized with human gut bacteria. The researchers focused on the gut–metabolite–brain axis, examining how dietary salt alters gut bacteria and their chemical products, and how those changes signal back to the brain.

Mice on either a low-salt or a high-salt diet struggled with memory. Compared with mice eating a normal amount of salt, they did worse on tests of short-term working memory and long-term recognition memory.

Inside the hippocampus, the brain's memory center, both diets lowered critical synaptic proteins like SYN1, PSD95 and BDNF and suppressed CREB activation. All of these are essential tools neurons use to build memories and adapt, so weakening them reduced the brain's ability to form memories.
Tests by researchers indicated that both eating too little salt and eating too much salt impair memory and brain function, but through two different biological pathways. With a low-salt diet, a drop in essential hippocampal synaptic proteins impaired long-term and short-term memory.

A high-salt diet significantly increased pro-inflammatory signals circulating in the blood and shifted the gut microbiota toward a pro-inflammatory state by lowering faecal levels of propionate and butyrate. This led to increased oxidative stress markers in the intestine, which can often trigger higher anxiety-like behaviour.
The results demonstrate the importance of a balanced, normal salt intake for one's overall brain and gut health. Too little salt starves the brain of vital gut-derived chemical signals, while too much salt causes inflammatory damage.

Anji Chen et al, Long-term low-salt and high-salt diets differentially disrupt the gut–metabolite–brain axis and induce cognitive impairment, Food Research International (2026). DOI: 10.1016/j.foodres.2026.119719

First successful primate transplant of human pituitary tissue boosts cortisol levels

Researchers in Japan have transplanted pituitary tissue grown from human stem cells into a primate whose pituitary gland had been surgically removed, successfully restoring critical hormone signals. Led by researchers from Nagoya University in Japan, the team showed that the same method worked in mice over a longer period.
This is the first time lab-grown human pituitary cells have been shown to work and survive after transplantation into a primate. The study, published in the journal Stem Cell Research & Therapy, may offer a new pathway for treating lifelong hormone disorders.

The pituitary gland controls hormones for stress, growth and metabolism. When it is damaged or removed, patients rely on daily hormone pills that do not accurately mimic the body's natural fluctuations. This study tested whether lab-grown pituitary tissue can be transplanted to produce hormones naturally instead.

The pituitary gland sits at the base of the brain and releases hormones into the bloodstream. One of them is ACTH, adrenocorticotropic hormone, which signals the adrenal glands to release cortisol. Cortisol helps the body manage stress, blood pressure and blood sugar. When the pituitary fails, patients lose this signal, leading to a condition called hypopituitarism.

Without enough ACTH, the body struggles to respond to stress, which can become dangerous. Daily hormone pills for life are the standard treatment, but these pills cannot fully match the changing needs of the body because demand for cortisol shifts with stress and time of day. As a result, patients face a higher risk of sudden death.
To find a better option, the researchers turned to stem cells. They grew small lab-made masses of tissue that can act as miniature organs, called organoids, from human stem cells. The organoids contained cells that produce ACTH. The team first tested the tissue in mice whose pituitary glands were removed.

The organoids were transplanted just under the skin, in fat or muscle tissue. They produced ACTH for more than six months and clearly extended the lifespans of these mice compared to those that did not receive the transplant. No unwanted tumours or unusual cell growth were observed.
Part 1

The research team then moved a step closer to humans and transplanted the organoids into a macaque monkey whose pituitary gland had been removed. To prevent rejection of the tissue because it came from a different species, they used immune-suppressing drugs already used in transplants of human insulin-producing cells for diabetes.

The transplanted tissue worked for six weeks and successfully elevated ACTH and cortisol levels in the blood. Additionally, significant weight loss caused by the hormone deficiency slowed during this period. Three months later, tissue samples still showed surviving transplanted cells, despite strong immune rejection common in cross-species transplants, which limited how well the transplant worked.

Stem cell treatments have a known risk of cells moving from the transplant site and growing uncontrollably elsewhere in the body. The researchers checked the lungs and liver for signs of stray organoid tissue and found none.

Functional analysis of adrenocorticotropic-hormone-producing pituitary cells derived from human pluripotent stem cells in murine and primate models of hypopituitarism, Stem Cell Research & Therapy (2026). DOI: 10.1186/s13287-026-05098-y

Part 2

A food poisoning bacterium can cause severe wound infections

Bacteria belonging to the B. cereus group are found almost everywhere, including in soil, dust and food, and are best known for causing food poisoning. The same group of bacteria can also cause serious infections outside the gastrointestinal tract, including in open wounds.

The toxin NheABC, produced by Bacillus cereus, is particularly active in the pH conditions found in open wounds. Researchers found that the toxin damages both cell membranes and mitochondria and helps the bacterium establish infection in wounded tissue.

Bacillus cereus toxin NheABC forms pores in cell membranes and damages mitochondria, with cardiolipin enhancing toxicity. Its activity is greater at neutral or alkaline pH than under acidic conditions. In a mouse wound infection model, NheABC increased bacterial colonization and local inflammation.
The researchers showed that the NheABC toxin makes small holes in cell membranes and causes significant damage to mitochondria. Experiments using artificial membranes revealed that certain lipids in mitochondria, such as cardiolipin, enhance the damaging effects of the toxin.
The most surprising finding concerned acidity. The toxin's harmful activity was significantly lower under acidic conditions than at neutral or alkaline pH levels. Chronic wounds can develop a more alkaline environment due to the presence of blood, tissue fluids and metabolic byproducts such as ammonia. This may create conditions that favor bacterial growth and colonization. In a mouse model of wound infection, NheABC contributed to increased bacterial colonization and a stronger local inflammatory response.

These findings strengthen the view that disease-causing bacteria within the B. cereus group detected in deep or infected wounds should not always be dismissed as harmless contamination.

Naeem Ullah et al, NheABC is a pH-dependent cytotoxin that targets mitochondria and contributes to the virulence of Bacillus cereus in wound infections, Cell Communication and Signaling (2026). DOI: 10.1186/s12964-026-03235-x

Inflammation can reactivate 'sleeping' cancer cells hidden in the bone

The spread of cancer from a primary tumour to another place in the body, called metastasis, remains one of the greatest challenges in cancer treatment and is responsible for most cancer-related deaths.
Cancer cells that have moved to another part of the body can stay dormant for years after the original tumour has been treated.
It's a worrying period for people, as they don't know if these metastatic cells will reactivate, leading to a relapse.
Breast cancer cells often spread to the bone marrow, where they can lie dormant for years within the tissue that normally supports the production of new blood cells. These disseminated cancer cells enter a "sleeping" state, which helps them evade the immune system and resist chemotherapy. What causes them to "wake up" is not only a key issue in cancer biology but also a huge challenge to study.

Injuries to the bone like fractures can lead to the growth of metastatic cancer cells hosted in the bone marrow, but the team wanted to establish if more indirect insults throughout the body, such as those caused by injury or infections, could also kick-start tumour development.
So researchers induced intestinal colitis—inflammation in the gut—in the mice with the extramedullary bone hosting dormant metastatic cells. Because the replica bone responds to the immune system, gut inflammation triggered a rapid production of immune cells from the bone.
The bone marrow environment needs to remodel to boost production of new immune cells, and it turned out that this change had a profound effect on the dormant cancer cells. More cancer cells started replicating, which increased the risk of a tumour forming.
In mice with engineered bone tissue, gut inflammation increased immune cell production and HMGB2, promoting reactivation of dormant breast cancer cells. Increased HMGB2 alone stimulated reactivation; it was also present in regions containing dividing cancer cells in human breast and prostate cancer bone samples.
By analyzing which genes were being switched on in the bone cells and the cancer cells, the team showed that a molecule that stimulates cell growth, HMGB2, increased as immune cell production surged, but also promoted the awakening of dormant cancer cells.

Even without inflammation elsewhere in the body, just the increased HMGB2 in the artificial bone was enough to stimulate more cancer cells to activate.
All of these findings suggest that boosting immune cell production in the bone, as part of a normal response to inflammation, comes at the cost of disrupting tumour dormancy, tipping the balance toward reactivation and metastatic growth.
The research suggests that monitoring people in this critical period after remission for infections, inflammation or injury anywhere in the body may indicate whether dormant cells are more likely to reactivate.

Stefania Di Blasio et al, An extramedullary bone model of metastatic dormancy reveals an increased rate of metastatic reactivation upon distant insults, Cell Reports (2026). DOI: 10.1016/j.celrep.2026.118088

Lab‑grown 'mini‑bladder' helps explain why urinary tract infections keep coming back

UTIs affect more than 400 million people worldwide each year, according to a global analysis of UTI incidence. More than half of adult women will have at least one in their lifetime, and studies suggest around a quarter experience another within six months.

Antibiotics aren't simply failing. New research using a lab-grown human "mini-bladder" suggests part of the answer may lie inside the bladder wall itself.

Most UTIs are caused by a type of Escherichia coli that normally lives harmlessly in the gut. Problems start when bacteria travel up the urethra into the bladder.

A repeat infection can happen in two ways. New bacteria from the gut can make the same journey again, and many recurrences are reinfections. But sometimes bacteria from the original infection appear to survive treatment and later reemerge.
In 3D human bladder models, E. coli survived fosfomycin in deeper tissue in a cell-wall-deficient form and regrew after treatment ended. Concentrated urine weakened tissue barriers, while nitrofurantoin failed to eradicate tissue-associated bacteria in a separate model. These laboratory findings support a possible mechanism of UTI recurrence but do not establish its clinical frequency.
Why women are hit hardest
Anatomy is a major reason women tend to suffer more than men from UTIs. A woman's urethra is much shorter than a man's, so bacteria have a shorter distance to travel before reaching the bladder. The urethral opening is also close to the anus, where gut bacteria live.

Sexual activity and the use of spermicides are also established risk factors for recurrent infection in premenopausal women.

Risk rises again around and after menopause. Falling estrogen changes the tissues of the vagina and urinary tract and is associated with a reduction in protective Lactobacillus bacteria, creating conditions in which UTI-causing bacteria can become more established.
Part 1

No single approach works for everyone, but several options have evidence behind them.

During perimenopause and after menopause, the National Institute for Health and Care Excellence (NICE) recommends considering vaginal estrogen for recurrent UTIs. NICE produces health and care guidance for England and recommends this approach when behavioral and personal hygiene measures have not been effective or are unsuitable. It has some of the strongest evidence among nonantibiotic approaches.
Drinking more water can help people who do not normally drink much. In a trial of 140 premenopausal women who drank less than 1.5 liters (51 fluid ounces) of fluid a day, those asked to add another 1.5 liters (51 fluid ounces) of water averaged 1.7 bladder infections over a year, compared with 3.2 among those who continued their usual intake.

Cranberry products may reduce recurrence for some women, although the evidence varies between studies and formulations. Current guidance from the European Association of Urology advises patients that the evidence remains contradictory and generally low quality.

D-mannose, a type of sugar sold as a dietary supplement, is thought to help prevent UTIs by making it harder for some E. coli bacteria to stick to the bladder lining. It looked promising in smaller studies but failed to prevent infections in a much larger U.K. randomized trial involving 598 women.

For people with recurrent infections, NICE says doctors can consider preventive treatment after any current infection has been treated. Options can include methenamine hippurate, a nonantibiotic urinary antiseptic, or preventive antibiotics. The choice depends on factors including how frequent and severe the infections are, previous urine test results, previous antibiotic use and whether measures such as vaginal estrogen or a single antibiotic dose after an identifiable trigger have helped.

Long-term antibiotic use also needs to be weighed against side effects and antimicrobial resistance, which the World Health Organization describes as a growing threat to global health.

The mini-bladder findings recast a UTI as a disease shaped by interactions between bacteria, bladder tissue, the immune system and the chemical and physical conditions inside the bladder.

Bladder-model study also investigated whether bacteria-killing viruses called bacteriophages, or phages, could help target bacteria persisting in bladder tissue. Phages reduced clusters of bacteria inside bladder cells, but adding them to nitrofurantoin did not consistently clear more bacteria from the bladder tissue than the antibiotic alone.

For someone whose infection keeps coming back, one possible explanation is that a small population of bacteria survived the original treatment and was able to start growing again.

original article.

Part 2

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Virus nabbed gene from ancient people
The poxvirus molluscum contagiosum virus (MCV) contains two copies of an ancient human gene, which could be helping it to infect people. The gene, BC200, was originally a ‘jumping gene’ — a sequence that could move around in the genome — but has since lost its ability to relocate. Researchers found that the virus acquired BC200 around 150,000 years ago, which suggests that the gene was still mobile relatively recently in human evolutionary history. MCV might use BC200 to keep a host cell’s protein factories active so it can replicate, the team says.

https://www.science.org/doi/10.1126/science.aeh3441

Nine Patients Received a Personalized Kidney Cancer Vaccine. None Had a Recurrence.
How do you teach the immune system to recognize a cancer cell?

Researchers are taking clues from the tumor itself, selecting unusual protein fragments and putting them into a vaccine. The aim is to help the body recognize that particular patient's cancer.

In a small kidney cancer trial, this approach produced encouraging results. Nine people received an experimental vaccine tailored to their own tumors.

None experienced a recurrence during a median follow-up of roughly three years and four months after surgery.

All nine developed immune responses to the vaccine. In seven, vaccine-reactive T cells could also recognize the patient's own tumour. T cells are immune cells that help identify threats and coordinate or carry out an attack.
But these findings do not yet prove that vaccination prevented the cancer from returning.

With the limited number of patients, we must be cautious with further interpretation.

https://www.nature.com/articles/s41586-024-08507-5

The 2026 Nobel Prize in Physiology or Medicine was awarded to scientists Karl Deisseroth, Georg Nagel and Peter Hegemann for their discoveries underpinning the field of optogenetics, the ability to control genetically modified cells with light.
Optogenetics makes it possible to switch on, or off, the activity of individual nerve cells in a living brain. This method is now being used in laboratories around the world to reveal the brain’s mysteries.

This shows that extraordinary creativity and ability to bridge disciplines have given scientists powerful new tools to unravel the complexities of the human brain, bringing answers to questions once beyond reach and hope to patients and families worldwide.

The hope that the knowledge generated by using optogenetics will lead to new medical treatments has begun to come to fruition. The method has provided greater understanding of the distinguishing features of psychiatric and neurological disorders such as depression, anxiety, schizophrenia, Alzheimer’s disease and Parkinson’s disease.

Researchers have also taken the first steps towards using optogenetics as a medical treatment. In ongoing clinical trials they attempt to restore vision in people who have become blind due to retinitis pigmentosa, a disease that destroys the eye’s rods and cones. When they inserted a channelrhodopsin-like protein in the retina of a blind person, the person regained some vision. Using special glasses emitting light, the person was able to discern and grasp objects on a table.

There are also hopes that optogenetics could improve cochlea implants. Currently, these implants stimulate the auditory nerve using electricity. If it were instead possible to use optogenetics, the implant may be able to activate the auditory nerve with greater precision.

https://www.nobelprize.org/prizes/medicine/2026/popular-information/

Irrelevant visual details interfere with decisions under uncertainty, brain research shows

Cognitive flexibility, the ability to adjust one's way of thinking or behavior as a situation changes, is known to gradually decline with age or due to some conditions, including Alzheimer's disease, Parkinson's disease, schizophrenia and substance use disorders. One aspect of cognitive flexibility is being able to switch between different tasks without becoming distracted and losing focus.
Researchers recently carried out a study involving both people and monkeys to understand how suddenly changing the rules of a task influences how the brain processes available information. Their findings, presented in a paper published in Nature Neuroscience, suggest that uncertainty increases the likelihood that irrelevant visual features will interfere with decision-making.

Even healthy young people feel stretched when they juggle several tasks, and psychology research shows that we become slower and more error-prone right after a switch.
So researchers wanted to find a possible neuronal explanation for why switching between different tasks can reduce performance. Specifically, they wished to understand what brain changes are associated with mistakes during basic perceptual judgments when people and nonhuman primates are unsure about what task they should be performing.
To shed light on these neural changes, the researchers conducted experiments involving humans and monkeys. Both species were shown images as they performed one of two visual tasks.
The tasks required participants to focus on one feature of an image while ignoring another. The rule governing which visual feature mattered changed during the experiment, requiring participants to determine what task to perform at different times.

Their performance on the task they chose to do indeed became worse.
To find out why the brain makes such mistakes, they first taught a model to err in the same way. Instead of training an artificial neural network to perform the task well, they trained it to reproduce the animals' actual choices, mistakes included. The network then became a specimen they could take apart to generate precise hypotheses.
After training a machine learning model to reproduce the choices made by monkeys during the experiment, the researchers trained a second model to make correct choices on the same tasks. This allowed them to compare the performance of the two.

Analyzing the model showed that mistakes during task switching are likely driven by the interference of the task-irrelevant information with task-relevant information.
Then they tested the model's predictions with new behavioral experiments in humans, analyses of the neuronal recordings while the animals performed the task, and small artificial perturbations of the neuronal activities in the animals' visual cortex.

The team's findings suggest that the additional mistakes made by both humans and monkeys under uncertainty are not random. Instead, the mistakes appeared to follow a specific pattern, which the team dubbed "feature interference".
When we are unsure which rule applies, the brain holds on to information it should be ignoring.
The brain's representations of different features are not perfectly separate; they sit at an angle to one another. The lingering irrelevant information therefore leaks into the relevant information and biases decisions in a predictable direction.
The results gathered indicate that, under uncertainty, mistakes may not come from a shortage of mental resources. Instead, mistakes could arise, at least in part, when mental representations of different visual features interfere with one another.

Part 1

When unsure of the rule, people remembered the 'irrelevant' feature better. The value of the ignored feature pushed choices in a consistent direction.

Cheng Xue et al, Feature interference underlies a neuronal basis for the behavioral cost of task uncertainty, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02430-w.

Part 2

High blood pressure can accelerate osteoarthritis joint damage via a newly identified hormone pathway
For millions of people, osteoarthritis slowly breaks down the joints, bringing pain, swelling and stiffness that make free movement harder with time. It is largely a condition of age, with 73% of those living with it older than 55. For years, the wear and tear that comes with aging and physical trauma was considered a major driver of the disease. A recent study published in Science, however, points to a metabolic disease that is also highly common among this demographic as a contributing factor in osteoarthritis progression.
A look at national health data from 36,820 Korean adults ages 45 and older revealed that high blood pressure was linked to osteoarthritis, with stronger associations in more severely damaged knees.

In mouse models, the researchers saw that hypertension actively drives joint breakdown in aging or injured joints. The damaging mechanism was coordinated by a brain hormone and a hormone receptor found in joints. These two components created conditions that ramped up destructive enzymes that break down cartilage. At the same time, they suppressed the production of cartilage components, such as collagen and aggrecan, that joints need to repair themselves.
To test cause and effect in living organisms, the team performed surgery on male mice to simulate mechanical joint wear and tear. They cut microscopic knee sections and stained them with a dye to measure changes in knee and bone structures.
Gene profiling experiments showed that high blood pressure increases blood levels of a brain hormone called arginine vasopressin (AVP), which travels through the bloodstream and leaks into the joint fluid. Healthy joint cartilage has little to no place for this hormone to bind, but mechanical injury or aging changes that.

Damaged cartilage starts producing a receptor called AVPR1A, which binds the hormone AVP and switches on a gene regulator called NR4A3. This sets off a damaging chain reaction. Cells begin producing excessive amounts of enzymes that break down cartilage while simultaneously reducing the proteins needed to build and maintain it.

The researchers also compared damaged and healthy knee cartilage and joint fluid collected during human total knee replacement surgeries. The damaged human cartilage had higher levels of AVPR1A receptors and a biomarker of the hormone vasopressin, which is responsible for increased blood pressure.
They also found that removing the AVPR1A gene or injecting a vasopressin receptor antagonist called relcovaptan directly into the knee joint prevented high blood pressure from accelerating cartilage loss. However, treating mice with standard blood pressure medication did not improve the condition of the cartilage.

This study uncovers the biological mechanisms linking hypertension to accelerated osteoarthritis progression.

Su-Jin Kim et al, Hypertension fuels osteoarthritis through neuroendocrine signaling, Science (2026). DOI: 10.1126/science.aed8207

Chunyi Wen et al, Osteoarthritis as a vascular disease, Science (2026). DOI: 10.1126/science.ael3784

Heat-trapping gas once frozen in Arctic ground is slowly leaking and warming the planet
Arctic permafrost thaw releases methane and carbon dioxide from decomposing organic matter, amplifying global warming. These emissions are projected to add about 0.25°C of warming by 2100, beyond fossil-fuel-driven warming. Thaw also destabilizes ground, threatening buildings, roads and pipelines.

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How can the same El Niño cause drought in one part of the world and floods in another?

El Niño weakens trade winds, shifting warm water and rainfall eastward and favouring wetter conditions in the eastern Pacific and drought in the western Pacific. Changes in atmospheric heating, winds and other oceans extend these effects globally. El Niño shifts weather probabilities, but local systems can still produce opposing extremes.

original article.

A New Cause of High Blood Pressure?

A study has found evidence that a specific brain region could be contributing to some cases of high blood pressure.

And importantly, there may also be a way to reverse it.

According to the 2025 study, carried out by a team from the University of São Paulo in Brazil and the University of Auckland in New Zealand, the lateral parafacial (pFL) brain region can trigger biological changes that raise blood pressure.

The pFL is linked to breathing control – specifically those forceful and deliberate exhalations that happen during exercise or when we cough or laugh.

In tests carried out on rats, the researchers found it can also do something else: tighten up blood vessels.

That combination of breath control and blood vessel signaling could be driving hypertension in some cases, the researchers say.

It might explain why so many people (around 40 percent by some estimates) still have uncontrolled blood pressure despite taking anti-hypertensive medications.

The study suggests that pFL neurons may link changes in breathing rhythms – which wouldn't necessarily be noticeable – to increased activity in the sympathetic nervous system (our 'fight-or-flight' response) that helps control blood pressure, fitting with previous research that has linked hypertension to the brain and nervous system.
"Given that around 50 percent of patients with hypertension have a neurogenic component, the challenge is to understand mechanisms generating sympatho-excitation in hypertension," write the researchers in their published paper.

"Such a revelation would provide much-needed clinical orientation for new therapeutic strategies."

https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.125.326674

Rising heat linked to faster telomere loss in wild birds

Extreme heat can have a profound impact on wild animals, causing their death in the most extreme cases and leaving less visible marks in others. Understanding the effects of temperature changes on specific species could inform conservation efforts and other initiatives aimed at protecting natural ecosystems from climate change.
Researchers carried out a study investigating the effects of high heat on purple-crowned fairy-wrens, small birds living in the tropical savannas of northern Australia.

Their findings, presented in a paper published in Proceedings of the Royal Society B, link hotter conditions to faster shortening of the birds' telomeres, protective stretches of DNA at the ends of chromosomes.
To measure the hidden effects of heat, they examined damage to telomeres, protective regions of DNA that sit at the ends of chromosomes and shorten with stress and aging.
Shorter telomeres are associated with accelerated aging and reduced lifespan. so they used telomere shortening as an indicator of sublethal heat stress, then investigated whether environmental or social conditions could reduce that damage.
The researchers discovered that increased heat exposure pervasively increases telomere damage throughout a bird's life. Over time, this damage can reduce individual fitness and could quietly drive population declines.
The team found that none of the environmental or social conditions they examined appeared to lessen the heat-related telomere loss in young birds. In contrast, adults living in habitats with denser vegetation were found to be partly protected, exhibiting less telomere loss.

This highlights that preserving habitat with dense vegetation cover provides essential climate refugia, giving vulnerable species a fighting chance against increasingly hot conditions.

Justin R. Eastwood et al, Pervasive sublethal impacts of heat exposure revealed by telomere dynamics, Proceedings of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rspb.2025.2877.

Francis Halzen wins Nobel Prize in physics for work on mysterious ghost particles called neutrinos
Francis Halzen won the Nobel Prize in physics on Tuesday for his efforts to demystify a rare group of neutrinos, tiny cosmic particles that scientists believe offer clues to how the universe evolved.
Neutrinos are tiny cosmic particles with a mind-bogglingly small mass. Yet they are everywhere: they spew from stars like the sun and trillions zip through our bodies every second.

Scientists can't glimpse the mysterious ghost particles zooming around on their own. Instead, they measure what happens when the tiny particles collide with other bits of matter, producing flashes of light or charged particles.

Halzen helped pull the curtain back on a rare gang of neutrinos that scientists consider messengers from the cosmos, offering clues to how the universe evolved.

Do you really need to fast before every blood test says a new study

Even a routine blood test may come with an overnight fasting requirement. Many medical practices still ask patients to go without food for 8–12 hours before blood is drawn. While the protocol was originally recommended for glucose and lipid testing, over time, it became the default requirement for almost all routine blood panels. Why it is still followed for such a broad range of routine lab tests is a question that researchers asked in a recent study.
The team set out to determine whether fasting is really necessary before routine blood tests and whether the length of the fast actually matters. They analyzed millions of test results from routine blood work collected from 101,148 adults.

For most tests, it made little clinical difference whether patients had fasted for a few hours or much longer. Only a handful showed meaningful changes. Blood glucose, triglycerides, liver enzymes and lipase were noticeably higher when patients had fasted for less than 8 hours.
Lab tests act as the guiding light for many diagnoses. They also help monitor existing conditions while raising red flags regarding one's risk of developing a disease or condition in the future. Eating is one of many factors that can affect blood test results. Since it is also the most easily controllable, fasting for somewhere between 8 and 12 hours has become a norm for blood tests across the globe. However, people spend most of their day in a nonfasting state, so nonfasting tests better represent their habitual physiology.
Fasting also creates logistical and clinical challenges for both patients and laboratories. Patients may be unable to get blood tests done on the same day they are ordered, requiring a separate visit. Early-morning fasting blood draws can also create a rush at hospitals and laboratories. Unless fasting provides a clear clinical advantage for a particular test, these costs may outweigh the benefits of routinely requiring it.

Existing evidence on tests performed after fasting is heavily dominated by cholesterol and triglyceride testing, leaving very little data for other tests. To fill this gap, researchers designed this study as a large-scale retrospective analysis of real-world hospital data. They screened nearly 10 million test results collected from 670 hospitals.

Based on the time since the last meal documented by the phlebotomist, the team divided the patients into three main fasting-duration categories: less than 8 hours, 8–12 hours and more than 12 hours. Using statistical models, they compared average test results across the three fasting groups. To rule out differences in patients' health as the cause, they compared the same people across separate visits, each with a different fasting duration.

Part 1

Blood counts, kidney function markers, electrolytes and most liver enzymes gave the same results no matter how long patients had fasted. Across 121 routine laboratory tests, only a handful needed fasting to be accurate.

In the paired within-person comparisons, only 10 tests showed differences large enough to exceed clinical error thresholds. With fasting under 8 hours, blood glucose was 10.8% higher, triglycerides were 20.1% higher and lipase, a pancreatic digestive enzyme, was 36.4% higher. Glucose then dropped steadily, by about 4.3 mg/dL for each additional hour of fasting.

They also found that whether patients fasted for 8–12 hours or longer than 12 hours made no clinically meaningful difference to any of the test results. Extending the fast beyond 12 hours did nothing for the accuracy of test results and instead caused unnecessary discomfort for patients.

Based on these results, researchers proposed replacing a one-size-fits-all fasting rule with test-specific requirements, since fasting duration mattered for only a handful of tests. To ensure these findings hold water beyond the South Korean population, further research involving more diverse populations is required before clinical standards can be redefined.

Sunghwan Shin et al, Fasting Duration and Differences Across Routine Laboratory Tests, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2026.4718

Liv Tybjærg Nordestgaard et al, Time to Stop Fasting Before Blood Sampling, JAMA Internal Medicine (2026). DOI: 10.1001/jamainternmed.2026.4726

Part 2

Laughter, sighs and screams reveal unwritten social rules in everyday life

Alongside words, humans have a treasure trove of nonverbal tools to help express themselves. We chuckle, sigh and gasp to communicate our feelings without uttering a word. What has amazed researchers for ages is how we rarely stop to think about how we know which sound belongs in which situation. Could unwritten social rules guide these everyday nonverbal sounds?
Of the 10 nonverbal vocalizations studied, laughter topped the list at 7.55 on a nine-point scale, followed by sighs at 6.69 and gasps at 6.63. Moans, groans and grunts landed above 6 on the acceptability scale. The ones that drew the strongest disapproval were growls, cries, screams and retches.

These same sounds landed very differently depending on the setting. Laughter was rated highest in positive, lively social situations but was heavily restricted in formal settings or those marked by power differences. Screams weren't always frowned upon; instead, they were more acceptable in high-energy, positive settings. Sighs stood out as being considered appropriate only when alone.

Vocalizations were rated significantly more appropriate at home and in social settings like bars or parties than at work or in public places such as stores or libraries. These sounds were less welcome in formal settings, especially when there was a clear power difference between people, but became more acceptable in positive, relaxed social settings.

These findings reveal the situational principles behind everyday vocal display rules.

Roza G. Kamiloğlu, Vocal display rules in everyday life: when is it appropriate to laugh, sigh or scream?, Philosophical Transactions of the Royal Society B: Biological Sciences (2026). DOI: 10.1098/rstb.2025.0151

Stem cells survive rough space travel

In early 2024, laboratory-grown neurospheres (i.e. clusters of neural stem cells) were sent to the International Space Station (ISS) to be exposed to microgravity. The return trip was delayed several times due to bad weather in the landing zone. As a result, the cells were outside controlled culture conditions for longer than anticipated—beyond the limit of what they were expected to survive.
Despite being subjected to severe stress, some of the cells survived. After recovery, they were still able to develop into nerve cells and glial cells and functioned normally in the researchers' tests.

A key finding is that cells placed in 3D-printed support structures fared particularly well across all groups. They survived and continued to divide.

Some neural stem cells survived prolonged uncontrolled conditions during their return from the ISS. After recovery, they retained the ability to form neurons and glial cells and functioned normally in tests. Cells in 3D-printed support structures showed particularly good survival and continued to divide.

Robert Fredriksson et al, Boundary cap neural crest stem cells exhibit remarkable resilience to environmental stressors associated with International Space Station mission, npj Microgravity (2026). DOI: 10.1038/s41526-026-00646-5

Blue light could cut food poisoning from raw chicken

While cooking kills Campylobacter, cross-contamination from handling raw meat is thought to be the main route of infection. Symptoms typically last about a week and include stomach cramps, fever, nausea and, in many cases, bloody diarrhea.
A low-power blue light could be the key to significantly reducing food poisoning caused by raw chicken .

In a study published in the journal Microbiology, researchers working in collaboration with the Animal and Plant Health Agency, tested a new technique known as violet-blue photodynamic inactivation (VB-PDI) against 64 different strains of Campylobacter, which is found in around three-quarters of all raw chicken sold in the U.K. Every strain was killed by the treatment, regardless of species or antibiotic resistance profile.

The findings build on previous research that showed blue light treatments could work more effectively than treating chicken with chlorine to kill specific strains of bacteria.
Violet-blue light killed all 64 tested Campylobacter strains, including antibiotic-resistant strains, without added chemicals. One strain showed no increased tolerance after 15 exposure rounds. Trials on naturally contaminated poultry in processing settings are needed before commercial use.
VB-PDI works by shining a safe, visible violet-blue light onto bacteria, causing molecules naturally found inside their cells to produce lethal levels of destructive compounds called reactive oxygen species. Crucially, the method needs no physical contact with the food and no added chemicals, making it a promising option for use on poultry carcasses in processing plants after slaughter, before products reach consumers.

The researchers estimate that if the technique could reduce contamination of chicken carcasses by a factor of 100, the proportion of highly contaminated carcasses reaching retail could fall from around 1 in 10 to just 1 in 50.
The team also found no evidence that Campylobacter bacteria could develop resistance to the treatment. Strains that were already resistant to antibiotics were killed just as effectively as fully susceptible ones. When one strain was repeatedly exposed to the light over 15 rounds in the laboratory, in an attempt to force resistance to evolve, no increase in tolerance was seen.
Because VB-PDI uses simple, low-power LEDs with a long lifespan and minimal running costs, the team also thinks it could offer a low-cost option for poultry producers, including in low- and middle-income countries where food safety infrastructure is limited.

Finlay Bembridge et al, One light to rule them all: photodynamic inactivation of diverse Campylobacter, Microbiology (2026). DOI: 10.1099/mic.0.001769

Antifungal use during pregnancy shows link to altered hormone levels in babies

Many pregnant women develop fungal infections, which are often treated with widely used azole-based antifungal medicines. A new study suggests that the use of these medicines during pregnancy may be associated with changes in fetal hormone production, with effects persisting in children after birth.
In 589 mother–child pairs, azole antifungal use during pregnancy was associated with altered infant adrenal hormone levels at three months, still within normal ranges. Human fetal tissue and rat experiments supported the findings. Causality and long-term health effects remain unclear, warranting further safety research.

Gylli Mola et al, Prenatal antifungal exposure disrupts fetal steroidogenesis and is associated with persistent effects in children, Communications Medicine (2026). DOI: 10.1038/s43856-026-01815-z

Levitating glass sphere becomes entangled with light at room temperature

Today, many physicists are actively exploring how light could be used to link objects through quantum entanglement. By fully harnessing the effect, they hope to unlock a wide array of applications, from secure communication networks spanning vast distances to sensitive new tests of the fundamental laws of physics.
When two quantum particles become entangled, their properties are so deeply intertwined that neither can be fully described without the other. However, this delicate link is easily broken by tiny disturbances from the surrounding environment and becomes ever harder to protect as objects grow larger.

In previous experiments, researchers have created brief bursts of entanglement between photons and vibrating macroscopic particles, but only at temperatures close to absolute zero. More recently, physicists have recognized that tiny glass spheres levitated by light could offer a promising alternative, since they float almost completely isolated from their surroundings.
Researchers explored this idea using a glass sphere just 100 nanometers across. They held the sphere in a tightly focused laser beam called an "optical tweezer," positioned between two facing mirrors inside a near-vacuum chamber.

On its own, the light needed to create entanglement also tended to induce unwanted oscillations in the sphere, eventually knocking it out of its trap. To solve this, the researchers combined two lasers of slightly different colors. The first cooled and steadied the sphere's back-and-forth motion, while the second was free to entangle this movement with the light.

As the sphere oscillated, information about its motion became imprinted on the light leaving the mirrors. By measuring this light over many hours, the team reconstructed the full pattern of connections between the sphere's motion and the light.

Even when the surrounding lab was at room temperature, their measured correlations crossed a mathematical threshold confirming that the two had become genuinely entangled. Crucially, the entanglement persisted in light traveling away from the mirrors.
The team now hopes to strengthen the entanglement through refined experimental techniques and to control it actively rather than simply observe it.
It could also pave the way for quantum networks in which information passes seamlessly between moving objects that store it and light that carries it across extensive distances.

Q. Deplano et al, Stationary entanglement of a levitated oscillator with an optical field, Science (2026). DOI: 10.1126/science.aeh1375

IVF-conceived children show more 'jumping gene' DNA, study finds

Infertility affects more than 15% of couples worldwide. Thanks to medical science, infertility treatments have come a long way over the past few years. For millions of people, in vitro fertilization (IVF) has opened a medical pathway to having biological children. This procedure gives fertilization a helping hand outside the body. It involves retrieving eggs from the ovaries and fertilizing them with sperm in a laboratory to create embryos.

Despite its benefits, IVF has also raised questions about the long-term health of children conceived through the procedure. Large epidemiological studies have found that these children have a slightly higher risk of developing certain health conditions later in life.

A recent study published in the American Journal of Obstetrics and Gynecology examined whether the stress embryos experience during IVF laboratory procedures could alter how certain DNA elements move within the genome, potentially putting babies conceived through the process at higher risk of these long-term health conditions.

IVF-conceived babies had a higher overall amount of LINE-1 (short for Long Interspersed Nuclear Elements-1) DNA in their genomes compared with naturally conceived babies. Most of our DNA stays in one place, but LINE-1 (Long Interspersed Nuclear Element-1) is part of a family of transposable elements that can remodel the human genome. These jumping genes can copy themselves and insert those copies into new locations, and this movement showed up at specific points in the genome.

Researchers found 11 locations where the two groups differed in how often LINE-1, or L-1, was inserted and 14 where they differed in how often it was deleted. Genes located near these sites have been linked to metabolic conditions and cancer.
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IVF-conceived babies had a higher overall proportion of L-1 DNA in their genomes than naturally conceived babies, a statistically significant difference. This difference was also seen in all three sibling pairs studied. When the researchers examined the surrounding base pairs, they found a high concentration of genes linked to metabolic conditions, cardiovascular diseases, neuropsychiatric disorders and cancer development.

The levels of L-1 DNA did not differ significantly between children conceived through standard IVF and those conceived through ICSI.

This study sheds fresh light on a possible genomic mechanism that may connect the embryonic stress of in vitro fertilization (IVF) to a higher risk of disease. The findings make a strong case for further research on ways to optimize IVF protocols so that embryonic stress and its consequences for the genome can be kept as low as possible.

Jian Li et al, In vitro fertilization–conceived offspring exhibit altered Long Interspersed Nuclear Elements-1 retrotransposition dynamics associated with long-term disease risks, American Journal of Obstetrics and Gynecology (2026). DOI: 10.1016/j.ajog.2026.05.005

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Cricket's day-night pink ball not always so pretty

A new study has found that players with colour vision deficiency (CVD) struggle to see the pink ball around dusk or against the crowd and grass.

Color blindness affects about 8% of men (1 in 12) and 0.5% of women (1 in 200) globally
Spectral modelling indicates that pink cricket balls can be harder to see with colour vision deficiency, depending on lighting, background and ball condition. Red balls generally provide more consistent and equitable visibility, though no ball is optimal in every setting. Injuries and on-field performance were not measured.
Cricket balls are hard and travel very fast, so anything that makes them harder to see warrants attention. We also need to consider whether the choice of ball places some players at a greater disadvantage than others.

Peter M. Allen et al, Not So Pretty in Pink: Computational Modelling of Cricket Ball Visibility with Colour Vision Deficiency, Sports Medicine (2026). DOI: 10.1007/s40279-026-02518-0

194-year-old tortoise reveals stable gene switches that may help resist aging

Researchers studying a giant tortoise named Jonathan say it's not just good genes but a lack of genetic wear and tear that has kept him going for nearly two centuries.

An estimated 194-year-old giant tortoise carried 287 unique gene variants linked to DNA repair, inflammation, insulin regulation and cancer suppression. Epigenetic regulation of DNA repair and metabolism resembled that of younger tortoises, indicating limited age-associated changes in these pathways.
In a study published in the journal Science Advances, scientists have pinpointed 287 unique gene variants in this remarkably old giant tortoise that reduce the usual effects of aging. These control key processes in the body, including repairing DNA damage, reducing inflammation, regulating insulin and suppressing cancer.

Jonathan, an Aldabra giant tortoise (Aldabrachelys gigantea), is estimated to be 194 years old. This makes him the oldest living giant tortoise and the oldest land animal in the world today. He's thought to have hatched in 1832—making him a contemporary of Charles Darwin .

The team also compared the giant tortoise's epigenome—the "on/off" switches on his genes—with those of younger giant tortoises of the same species. Remarkably, they found the switches controlling Jonathan's DNA repair and metabolism genes were very similar to those in his younger relatives. Usually, the epigenome changes over time, contributing to the aging process—this is a key reason why things start to go wrong in older bodies.
Researchers found that the gene regulators involved in energy production and DNA repair have remained incredibly stable in Jonathan over almost two centuries.

Benjamin Vaisvil et al, Epigenetic insights into extreme longevity in the world's oldest terrestrial animal, Jonathan, Science Advances (2026). DOI: 10.1126/sciadv.adw8887. www.science.org/doi/10.1126/sciadv.adw8887

Scientists win chemistry Nobel for discoveries about mirrored molecules that led to many drugs
Developed chemical reactions demonstrate how homochirality can emerge spontaneously. Homochirality involves molecules sharing the same handedness rather than an equal mixture of mirror-image forms.
Scientists Henri B. Kagan and Kenso Soai won the Nobel Prize in chemistry this week for untangling mysterious mirror images in molecules, a discovery that has been used to develop countless drugs and transformed modern medicine.
Many molecules come in versions that look alike but are not exactly identical, like right and left hands. Kagan, who is from France, and Soai, from Japan, found ways to make chemistry pick a side, describing and designing reactions to produce the desired mirror image.

"The medicines we have today would not be possible without this chemistry".
The discovery enabled most modern medicines
Mirror images of the same molecule can have different properties. For example, one version of the chemical carvone smells like mint, while the other has a whiff of caraway, a spice often used in rye bread.
The alternate versions can also behave differently when interacting with other chemicals. When designing drugs to treat diseases, scientists are choosy about which mirror image they use. They want the version of a molecule to treat a cold, not one that will make the sniffles worse.

In the 1980s, Kagan's work showed there might be a way to design reactions to produce one form of a molecule over the other. Years later, Soai perfected the process. He created the first-ever chemical reaction to efficiently produce only one of a molecule's mirror images, in what's now known as the Soai reaction.

Allergic to gold jewelry? Lab tests reveal gold can dissolve from earrings under specific chemical conditions
Gold has a reputation for being chemically untouchable. But according to chemists that reputation is a little misleading—gold is not unreactive so much as selective about what it reacts with.

Every material has its own enemy. Its own kryptonite. For gold, one of those enemies is sulfur.
When researchers tested five pairs of 10K and 14K gold earrings purchased from a jeweller, all five pairs of 10K and 14K gold earrings released gold after one week in cysteine-containing artificial sweat, with a median release of 0.057 micrograms per square centimeter. Nickel release was undetectable. Gold can become soluble under these conditions, but the results do not establish exposure during wear or a dose that triggers allergy.

After a week in cysteine-modified artificial sweat, all five pairs released measurable amounts of gold. Cysteine is an amino acid, or protein building block, made naturally by the body that contains sulfur, which binds to gold.

The amounts were tiny, and the findings do not show that the released gold is enough to cause an allergic reaction. But the study, published in the journal Contact Dermatitis, demonstrates that gold in jewelry can become chemically available under the right conditions—a finding that helps explain how exposure to gold can occur at the skin.
Gold, silver and platinum are known as noble metals because they do not readily react with oxygen. That resistance to oxidation is a big part of gold's reputation for stability. But it does not mean the metal is universally unreactive.
Gold reacts to different things.
Gold doesn't react much with oxygen, but it can react with sulfur and some amino groups. And for some people, that reaction poses a problem.
Gold allergy is real, although it is less common than nickel allergy. But for a metal to trigger an allergic response, some of that metal has to become chemically available to the body.
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Sweat contains amino acids and other compounds that can interact with metals. The researchers added cysteine, an amino acid containing sulfur, to an artificial sweat solution and exposed the earrings to it for 168 hours at about 30 C (86°F). The team then measured the metals released into the solution using highly sensitive mass spectrometry, a scientific technique used to weigh molecules.

There is no standard artificial-sweat test specifically designed to capture how gold behaves in the presence of sulfur, so Hedberg added cysteine to the solution to create conditions that would reveal whether gold could become soluble.

The experiment was designed around a simple chemical principle. For a metal to cause an allergic response, it first has to become chemically available.
Gold was detected in the release solution from all five pairs of earrings.

Only tiny amounts of gold were released over the weeklong test, with a median of 0.057 micrograms per square centimeter. The amount varied among the earrings, ranging from 0.016 to 0.15 micrograms.

Copper was released in much greater amounts, exceeding gold in every sample. The median copper release was 0.53 micrograms per square centimeter per week. Copper is generally considered harmless for humans and has beneficial antibacterial properties. Its higher release was expected, since the earrings were alloys, meaning gold was combined with other metals. Surface analysis showed the materials consisted mainly of gold, copper, silver and zinc, with only small amounts of nickel detected at the surface.
None of the five pairs of jeweler-purchased earrings released detectable nickel under the conditions of the new experiment.

Gold-plated jewelry can have a thin gold coating over one or more underlying layers that may contain nickel. In the earlier study on inexpensive earrings, nickel was detected in the artificial sweat in which all 10 inexpensive gold-plated earrings were tested.
For the jewelry-store earrings, element-specific spectroscopy showed gold throughout the material, rather than just a thin surface coating, while the Temu earrings, if they contained any gold, had only a thin layer of plating.
The study measured how much gold became soluble (able to dissolve in a liquid) under specific laboratory conditions. It did not measure how much gold reaches or remains on a person's skin during actual wear, nor does it establish a dose at which gold jewelry triggers dermatitis.

Hedberg says the very small amounts of gold detected in the study would probably not be enough to trigger an allergic reaction in most circumstances. But that does not make the result irrelevant to someone who already knows they are allergic to gold.
For most people, however, nickel remains a more immediate concern with inexpensive jewelry, rather than gold.

Mikkel Bak Jensen et al, Gold and Nickel Release From Gold‐Plated Earrings Under Cysteine‐Modified Artificial Sweat Conditions, Contact Dermatitis (2026). DOI: 10.1111/cod.70187

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Bees struggle to smell flowers when air pollutants combine

Bees, moths and other pollinating insects have a harder time smelling flowers in polluted air, according to new research.
Scientists analyzed 22 experimental studies on how the air pollutants ozone and nitrogen oxides (NOx) affect pollinators. Both pollutants make it harder for pollinators to find flowers by breaking down or altering the scents that flowers give off.
The new research, published in the journal Frontiers in Ecology and the Environment, found that elevated ozone reduced pollinator performance by an average of 42%, while NOx cut performance by 46%. When the two pollutants occurred together, the average reduction was 68%.

Only a few studies tested both pollutants together, and in those the extra harm from combining them was smaller than the averages suggest. This is because the two gases react with each other in the air and partly cancel each other out.
The study also found specialist pollinators reliant on one plant's scent, such as some moths, are more at risk than generalists like many bees. Additionally, day-active pollinators such as bees and butterflies face higher ozone levels, while night-active pollinators (including many moths) encounter higher nitrogen oxides. Both need protection.

Pollinator risks and recovery from air pollutant interactions during the fossil fuel transition, Frontiers in Ecology and the Environment (2026). DOI: 10.1002/fee.70076

Strong magnetic fields could allow white dwarfs to grow beyond the Chandrasekhar limit

When a dying star runs out of fuel and sheds its outer layers, its remaining core can become an approximately Earth-sized, extremely dense stellar remnant called a white dwarf. For a white dwarf that is not strongly rotating or magnetized, there is a well-known upper mass limit of about 1.4 times the mass of the sun, known as the Chandrasekhar limit.
As a carbon-oxygen white dwarf approaches this limit, its core can become dense enough to ignite carbon, potentially triggering a thermonuclear explosion known as a Type Ia supernova.

If the Chandrasekhar limit is fixed, the supernova energy release rate and luminosity should be fixed. Scientists have used this constancy of luminosity to understand the evolution and size of the universe, which is presently thought to be expanding.
Now, simulations by researchers from the Department of Physics at the Indian Institute of Science (IISc) and collaborators show that strong internal magnetic fields could allow some white dwarfs to grow to substantially higher masses than the Chandrasekhar limit allows. In one of their simulations, the researchers found that a magnetized carbon-oxygen white dwarf can reach about 2.4 times the mass of the sun—well above the limit.
Stellar evolution simulations predict that magnetic pressure can support accreting carbon–oxygen white dwarfs up to about 2.4 solar masses, exceeding the usual 1.4-solar-mass Chandrasekhar limit. Accretion-driven contraction strengthens internal magnetic fields, providing additional support against gravity.

Zenia Zuraiq et al, Super-Chandrasekhar White Dwarfs by the Evolution of Magnetized Main-sequence Stars: New Mass Limits from STARS Simulation, The Astrophysical Journal Letters (2026). DOI: 10.3847/2041-8213/aea97e

Tiny marine microbe sheds new light on how little genetic machinery a cell needs to survive
The marine archaeon Candidatus Sukunaarchaeum mirabile has 189 protein-coding genes, retaining machinery for DNA replication and protein synthesis. It lacks nearly all genes for nutrient and energy production, suggesting strong dependence on other organisms. It has not been directly observed, and its host and possible parasitic lifestyle remain unknown.

A hidden archaeal lineage with an ultra-reduced genome retaining only its replicative core, Current Biology (2026). DOI: 10.1016/j.cub.2026.09.042. www.cell.com/current-biology/f … 0960-9822(26)01251-0

Embryonic origin of cancer in newborn twins

Cancer Passed Between Twins Before Birth
A facial mass detected before birth prompted the early delivery of identical twin sisters. A fetal MRI at 33 weeks showed the mass on one baby's face. When the sisters were born a week later, tumors were found in both.

Two children had the same cancer, raising a question that their shared beginnings alone could not answer.

Had the disease started separately in each sister, or had cancer cells crossed from one to the other before birth?

Researchers turned to a record hidden within their cells. DNA changes, accumulated as their bodies developed, allowed the team to reconstruct events that had happened months before anyone saw a tumor.

The study in Nature Communications shows that the cancer began in one sister and passed to the other in the womb, most likely through a single transfer late in the second trimester. The same investigation uncovered clues to how the sisters themselves had formed.

The two girls, Amelia and Amaya, died soon after birth. Their family consented to post-mortem examinations for research.
The baby with the facial mass is called twin A in the paper. At birth, she had tumor deposits in several organs. Her sister, twin B, initially had lesions in her skin; disease involving the membranes around the brain and spinal cord was detected later.
The tumors were reported as undifferentiated sarcomas. Soft tissue sarcomas arise in tissues such as muscle, fat and the body's supporting structures. All the twins' tumor samples carried the same fusion of two genes, MN1 and ZNF341.

Matching tumors were only the beginning: the team needed to identify whose cells had started the cancer.

Here, an apparent contradiction proved useful: identical twins are not necessarily genetically identical.

They begin with the same fertilized egg, but DNA changes can arise as their cells multiply. A change acquired by one cell can pass to its descendants, marking a particular branch of the developing body's cellular family tree.

Comparing those marks across tissues reveals shared ancestors and distinguishes one twin's cells from her sister's.

The team sequenced 10 tumor samples, 12 normal tissue samples from the twins and 11 placental samples. They also examined 12 placental samples enriched for cells involved in forming the placenta.

The researchers found that cancer began in twin A, then cancer cells passed to twin B before birth and formed tumors there too. The evidence was in the second baby's tumors: their cells carried genetic markers belonging to her sister.

The study points to spread across the placenta they shared. The genetic analysis establishes which sister the cancer came from, but does not directly show the cells crossing or the route they took.
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The most likely starting site was twin A's facial mass. The cancer diversified into different cell populations and spread within her body before reaching her sister. The pattern in twin B supported a relatively late, single transfer.

The researchers then used accumulated mutations to estimate when this happened. Assuming mutations built up at a constant rate, they placed the tumor's origin near the end of the first trimester and its transfer late in the second trimester.

Those dates are estimates that depend on the assumed mutation rate, rather than direct observations.

There was another surprise: normal cells had moved in the opposite direction. Genetic markers in a spleen sample from twin A suggested around 75 percent of the sampled cells originated in twin B, consistent with blood-cell mixing between the sisters.

The twins' earliest cell lineages also contributed unevenly to their bodies and placenta. One branch contributed almost exclusively to twin A, another to both sisters and the placenta, and a third to twin B and the placenta. The pattern favored an earlier embryonic split than the classical model for this type of identical twinning predicts.

However, this was one pair of twins, and the analysis could recover only lineages that survived in the tissues sampled.

Earlier research on twins with leukemia has also explored cancer's beginnings before birth. This case adds a detailed reconstruction of a soft tissue tumor's journey, without establishing how often such transfers occur.

https://www.nature.com/articles/s41467-026-78178-5

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Gut microbes from people with schizophrenia alter mouse behaviour

Schizophrenia is an often debilitating psychiatric disorder that can disrupt people's thinking, perception and behavior. While genetic and environmental factors can contribute to its emergence, researchers are still trying to understand its underlying biological processes.

Previous studies have identified differences in the gut microbiome, the community of microorganisms living in the intestine, of people with schizophrenia. Yet how these differences might influence brain function still needs further investigation.

Researchers  recently investigated whether gut microbes from people with schizophrenia could affect behaviour and immune activity in mice. Their findings, published in Translational Psychiatry, hint at a possible immune connection between the gut and brain.

In their new study, the team collected stool samples from three people with schizophrenia and three healthy donors. They then fed young mice gelatin portions containing material from individual donors repeatedly over a period of five weeks.
The mice already had their own gut microbial communities, so the transferred material entered an already established environment. The researchers then compared animals receiving samples from people with schizophrenia with healthy-donor recipients and untreated mice.

To assess their behavior, the team introduced the mice into a T-shaped maze. Each mouse explored one arm of the maze, took a brief break and then returned. Mice receiving schizophrenia-donor samples were less likely to choose the other arm than animals in either comparison group.

This test probes short-term working memory and the ability to switch between choices, although reduced alternation does not necessarily reflect forgetting alone.

In a separate test, the mice could approach a cage containing an unfamiliar mouse or an empty cage. Those receiving schizophrenia-donor samples showed less preference for investigating the unfamiliar animal.

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The researchers also examined microbes associated with the lining of the ileum, the final part of the small intestine. They observed changes in the relative abundance of several bacterial groups, alongside increases in intestinal inflammatory markers.

Compared with untreated mice, schizophrenia-donor recipients had lower levels of occludin, a protein that helps seal gaps between intestinal lining cells. This suggests a weakened intestinal barrier, although the researchers did not directly measure its permeability.

Blood tests revealed higher levels of two immune signaling proteins, interferon-gamma and interleukin-17, in animals that received gut microbes from people with schizophrenia compared with untreated animals. These increases were not statistically significant relative to healthy-donor recipients.

Immune cells called microglia in the prefrontal cortex, a brain region involved in cognition and social behavior, also exhibited some changes. These cells help maintain brain tissue and remodel connections between neurons.

The branching extensions of these cells were found to be less complex, while molecular measurements indicated a more reactive immune state. Together, the team's findings suggest a possible connection between intestinal microbes, circulating immune signals and brain inflammation, yet they do not establish whether any of these changes caused the others.
The team examined a separate collection of brain tissue obtained after death from four people with schizophrenia and three people without it. These samples showed some overlapping changes in microglial and inflammatory markers, although the patterns did not match completely.

Both the stool-donor sample and human brain comparison were small, which limits how broadly the study's findings can be applied. The experiment also does not establish that gut microbes cause or prompt the development of schizophrenia in humans.
Future experiments could change the microbes or block particular immune signals in mice, then assess whether this prevents the observed brain and behavioural changes. This would help determine whether the proposed gut-brain pathway could eventually be targeted therapeutically.

Ana Raquel Pereira-Santos et al., Unveiling the gut microbiome-immune-brain axis in schizophrenia, Translational Psychiatry (2026). DOI: 10.1038/s41398-026-04497-2

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Mushroom-derived peptides boost saltiness by up to 70%, offering a path to low-sodium foods

Cutting down on salt might be good for health but not so good for the taste buds. So, scientists have been looking for alternatives that keep the saltiness while reducing sodium content. The most common sodium chloride (NaCl) alternatives on the market contain potassium. With regular use, these alternatives can increase the risk of excess potassium retention, potentially posing health risks for older adults.

Scientists have found a way to make salt taste saltier without increasing its sodium content, a welcome development in the culinary world. Salt is a powerful flavour enhancer, drawing out the subtle flavours of a dish while balancing sweetness and bitterness. Its appeal comes hand in hand with some drawbacks. Salt activates the brain's reward system, making food more pleasurable, but eating too much salty food can negatively affect cardiovascular health.
In a recent study published in npj Science of Food, researchers turned to Hypsizygus marmoreus, a popular edible mushroom, to see whether its proteins contain natural peptides that can amplify how our taste buds perceive saltiness.

They successfully extracted three mushroom-derived peptides: ASHGEGF, GDDWT and LDDGF. To measure how much saltier the solution tasted, the researchers used an electronic tongue, a device that mimics our sense of taste by translating chemical signals in liquids into electrical readings.

ASHGEGF was the standout performer, delivering the strongest salty kick by increasing the saltiness intensity of a 3 mg/mL NaCl solution by 70.59%. The three peptides boosted saltiness on their own and in combination, reinforcing each other to deliver a saltier taste that lasted longer.
Peptides, short chains of amino acids often extracted from yeast, soy and bovine bone, offer a way to lower sodium in food without a major loss of flavor. They intensify the taste of salt solutions, so you can reduce sodium while the food still tastes salty. Interest in them is growing because they come from food sources, have nutritional value and are readily absorbed by the body.

In this study, researchers focused on the edible mushroom Hypsizygus marmoreus, which is rich in proteins and flavour compounds but whose specific saltiness-enhancing peptides remained poorly studied.
Taken together, these findings point to a promising route for creating new seasonings from Hypsizygus marmoreus mushrooms that enhance saltiness.

Wenping Kong et al., Discovery of saltiness-enhancing peptides from Hypsizygus marmoreus via virtual screening, multisensory evaluation, electronic tongue, and molecular simulation, npj Science of Food (2026). DOI: 10.1038/s41538-026-01088-9

Link between lithium in drinking water and a rare heart condition

Children living in areas with higher levels of lithium in drinking water were more likely to be diagnosed with Wolff-Parkinson-White syndrome, a rare heart condition that can cause a dangerously fast heartbeat, according to a new study.

The findings, which were published online in The Journal of Clinical Investigation, are based on health and water-quality data for more than 2.3 million children in California and were also observed among nearly 2 million children in New York. Children in California counties with lithium levels in the highest 25% had 71% greater odds of a Wolff-Parkinson-White (WPW) diagnosis than those living in counties with lower levels.

Lithium occurs naturally in groundwater, and concentrations vary widely by location. Although the research focused on California and New York, lithium is found in groundwater used for drinking water across the United States and elsewhere, raising questions about the potential broader public health significance of the findings.

WPW occurs when an extra strand of heart muscle, known as an accessory pathway, creates an abnormal electrical connection in the heart. These pathways form during fetal development, but why they develop has remained largely unknown. Most people with accessory pathways do not have a family history of the condition, suggesting that environmental exposures during fetal development could play a role.

Accessory pathways are among the most common causes of supraventricular tachycardia (SVT), a rapid heart rhythm that can cause palpitations and other symptoms. WPW, which involves a particular type of accessory pathway, is also associated with a small increased risk of sudden death.

The pathways can be treated with catheter ablation, a minimally invasive procedure that eliminates the small area of heart tissue responsible for the abnormal electrical connection.

Medicinal doses of lithium during pregnancy have been associated with an increased risk of congenital heart defects, including Ebstein's anomaly, a rare condition that is frequently accompanied by accessory pathways. That led the UCSF researchers to ask whether lithium in drinking water might also be associated with changes in the developing heart.

In addition to the association with WPW, higher lithium levels in California were associated with SVT, palpitations and fainting. Researchers then retested their main finding in New York, where children living in areas with lithium levels above 10 parts per billion also had greater odds of WPW.

The study does not prove that lithium causes WPW. Researchers did not know how much lithium individual children or their mothers consumed, and they used county of residence to estimate exposure. Other environmental or genetic factors could also help explain the association.

Elevated lithium levels in drinking water are associated with higher prevalence of Wolff-Parkinson-White diagnoses, Journal of Clinical Investigation (2026).

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Candida auris copies its entire genome to survive antifungal treatment, research reveals

New research has revealed an unexpected new mechanism through which the killer fungus Candida auris is resisting antifungal drug treatment.
Researchers discovered that the fungus creates multiple versions of its entire genome, including mutating a gene that plays a role in cell wall integrity, called "Crazy-one" (CRZ1).
In laboratory tests, Candida auris survived high antifungal concentrations by producing multiple copies of its entire genome. Surviving populations grew at different rates; faster-growing cells carried mutations in CRZ1, a regulator of cell wall synthesis, and their cell walls remained unaffected by treatment.
The researchers did not identify any of the DNA mutations that we might have expected. Antifungal drugs target the enzymes that make cell walls, so that fungi die by shriveling, exploding or not being able to grow. Somehow, these fungi had survived antifungal drugs.
Surviving cells had made multiple copies of their entire genome. This is a trick that other fungi have used in the past, but not one that is well known in C. auris. In fact, there were two populations, some growing slowly, others growing more rapidly. Researchers call it 'bet-hedging' when a bug uses multiple tactics to increase its chances of developing resistance and evading treatment."

Study authors say their findings unlock a new mechanism that allows Candida auris to adapt to antifungal treatment and survive, which could lead to new ways to tackle the fungus.
Researchers are now looking at options including the use of antifungal drugs in combination.

FKS1/2-variant independent mechanisms underlying the emergence of resistance in echinocandin-refractory Candida auris infections, Nature Communications (2026). DOI: 10.1038/s41467-026-76954-x. On bioRxiv: www.biorxiv.org/content/10.648 … /2026.01.17.700071v1

A gut microbe makes a fatty acid that cuts artery plaque in half in mice

A common gut bacterium produces a molecule that slows cholesterol production in the liver. When researchers gave the molecule to mice prone to artery disease, the animals developed roughly half as much fatty plaque as untreated controls.
The molecule acts on the same enzyme targeted by statins, the widely used cholesterol-lowering drugs. That connection offers a concrete explanation for something harder to untangle: how bacteria living in the intestine might influence the health of arteries elsewhere in the body.

Researchers identified the substance as pentadecanoic acid. Their study, published in Nature, followed its effects from bacterial production to cholesterol clearance.
Observational studies over the past two decades have shown that the gut microbiota plays an important role in metabolic health, and disruptions can lead to common disorders including diabetes, liver disease and cardiovascular disease. More recent cause-and-effect studies are trying to pinpoint the molecular mechanisms that drive the development of these conditions.

Investigating this connection, the researchers began with existing gut microbiome data from people with and without atherosclerotic cardiovascular disease, in which fatty deposits accumulate in artery walls. Several bacterial species were more abundant in healthy people, with Bacteroides uniformis standing out.

Was the bacterium helping protect arteries, or is it simply more common in healthier people?

To find out, the researchers gave it to male mice genetically prone to atherosclerosis that were fed a high-fat diet. After 12 weeks, treated mice had less plaque in their aortas and lower blood levels of LDL, often called "bad" cholesterol. Heat-killed bacteria did not produce the same benefits.

The key appeared to be something the living microbes produced. The team separated substances released into the bacterial culture fluid, testing which one helped the laboratory-grown liver cells take up LDL. Repeatedly narrowing the mixture led them to pentadecanoic acid.

Given directly to mice three times a week for eight weeks, the fatty acid lowered cholesterol and reduced plaque buildup by about half.
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The next puzzle was to untangle how a fatty acid could help clear cholesterol from blood.

Experiments showed that pentadecanoic acid binds to and inhibits HMG-CoA reductase, an enzyme needed to make cholesterol. As cholesterol production fell, liver cells increased their supply of LDL receptors: proteins that capture cholesterol-carrying particles from the bloodstream.

The two effects worked together. The liver made less cholesterol and took in more from circulating blood.

The researchers tested that explanation by disabling LDL receptor production specifically in the mouse liver. Without those receptors, neither the bacterium nor the fatty acid provided its usual protection against plaque buildup.

Changing the bacterium supplied another check. Engineered strains that made less pentadecanoic acid still colonized the gut but offered substantially weaker protection. That finding helped connect the bacterial product to the arterial benefit.
Pentadecanoic acid is a saturated fatty acid found in foods such as dairy fat. The study strengthens the evidence that gut microbes also supply it, but showing a protective mechanism in mice does not establish a treatment for people.

Human findings offer reasons to investigate further, alongside reasons for caution. A small 2024 trial in women with fatty liver disease found that adding pentadecanoic acid to a Mediterranean-style dietary intervention further reduced LDL cholesterol. However, a 2026 analysis of two long-running studies found no association between higher blood levels of the molecule and a lower incidence of cardiovascular disease.

The molecule is already marketed as a heart-health supplement. Yet the clinical evidence supporting a cardiovascular benefit remains limited.
It should be noted that the new experiments used only male mice, and human diets and gut communities could change the response seen in the animal experiments.

Chao Yin et al., A gut microbial odd-chain fatty acid alleviates atherosclerosis in mice, Nature (2026). DOI: 10.1038/s41586-026-11142-x

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Ovaries remain active decades after menopause, study reveals

Contrary to popular belief, the postmenopausal ovary is not defunct. In a new study of ovaries from 28 women, scientists found that in the decades well past menopause, the ovary remains biologically active and continues to remodel with age, showing increased inflammation and changes in tissue structure. The study also found a molecular link between ovarian aging and cancer.
In the ovary, we reach a point of no return with respect to fertility in which it's no longer producing eggs, and most people assume those ovaries are just sitting there doing nothing, similar to the appendix.
The findings challenge the notion that the ovary is an innocent bystander after reproduction ends, raising new questions about whether it could play a more active role in aging and chronic disease in women.

The ovary is not just a reproductive organ. It really influences how somebody ages because it speaks to all these other organs, such as the brain, and also to the bone, and women after menopause often experience a lot of bone problems. So, researchers think there is a connection between all these organs.
Women now routinely live for decades after menopause, making it increasingly important to understand what the ovary is doing during this long post-reproductive period.
The new data point to progressive aging features in which the ovary appears to lose its original identity and ends up doing something different.
To find out what was changing, the scientists went beyond ovarian hormones to analyze the composition of the tissue at high resolution.
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Those analyses painted a consistent picture: The ovary continues to change well after its reproductive life ends.

Ovaries of younger postmenopausal women had more proteins involved in maintaining cells and tissue structure, while older ovaries had more proteins associated with inflammation, immune activity and the ongoing breakdown and rebuilding of the tissue surrounding cells. The differences were most pronounced between ovaries of women in their 50s and those of women 70 and older.

When scientists analyzed the data in multiple different statistical ways, what became clear across all these methodologies is that the ovary was not stagnant.
In fact, over the decades, there were quite dramatic differences: Some proteins' levels would go up with age and some proteins' levels would go down, which tells us this organ is quite dynamic.
The aging ovaries also showed some of the same molecular patterns seen in cellular senescence, a state in which aging or damaged cells stop dividing but remain biologically active and can send signals that affect surrounding tissue.
As postmenopausal ovaries aged, proteins involved in maintaining tissue structure declined, while proteins involved in inflammation and reshaping the tissue environment became more prominent.

Although all the ovarian tissue in the study appeared normal and cancer-free, some proteins previously associated with ovarian cancer were more abundant in aging ovaries, with the strongest signal among women in their 60s. The finding does not mean the ovaries were cancerous or precancerous, but suggests healthy ovarian aging and ovarian cancer share some of the same biological processes.

It's not that all postmenopausal women get ovarian cancer, but we know that that fibrotic inflammatory environment is certainly an environment that cancer cells prefer to home in on.
This is all consistent with the idea that the aging ovary is a potential third hit for ovarian cancer, with the first hit being genetic and the second hit being environmental.

Mark A. Watson et al., The Human Ovary Exhibits Dynamic Molecular Remodeling in the Decades Post-Menopause, Aging Cell (2026). On bioRxiv DOI: 10.64898/2026.03.26.714635

onlinelibrary.wiley.com/doi/Mark A. Watson et al., The Human Ovary Exhibits Dynamic Molecular Remodeling in the Decades Post‐Menopause, Aging Cell (2026). DOI: 10.1111/acel.70714

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Abnormal antibodies that disrupt DNA repair could explain childhood cancer

Why do children get cancer?
Pediatric cancers, such as leukemia, myeloma, neuroblastoma and osteosarcoma, differ from adult cancers in their causes, location and type, and response to therapy.

Compared to adults, children have had less time to accumulate cancerous DNA damage through exposure to environmental stressors, lifestyle factors and aging. Paediatric cancers thus tend to carry fewer mutations than adult ones and arise from less mature cells, for example, stem or progenitor cells.

A team of scientists has now found evidence for a new mechanism for the development of cancer in children: They seem to produce an unusual amount of aberrant antibodies against the building blocks that make up the DNA repair machinery, a diverse set of hundreds of proteins that identify and correct damage or errors in the genome.
This discovery could open the door to the early screening of small children, in the hope of ultimately preventing them from developing such paediatric cancers in their teenage years.
The researchers showed that many children with various types of cancer have antibodies against some of their own DNA repair proteins. They also demonstrated that such 'autoantibodies' can enter live cells and bind to—and probably inhibit—the activity of these essential proteins.

The results showed that compared to young adults and older people, children between 2 and 19 years of age with pediatric cancer had much greater numbers of antibodies of the IgG class against DNA repair proteins circulating in their blood. These autoantibodies mainly targeted RAD52, NUMA1, ALKBH7, APBB1, UNG and MGMT, all key genes closely involved in DNA repair but not significantly mutated in these cancers.

Could these autoantibodies explain why these children had developed cancer? To find out, the scientists looked at selected samples from 59 school-age children who had taken part in the British "Avon Longitudinal Study of Parents and Children" and "Born in Bradford" long-term cohort studies. Half of these children had developed cancer years later (but before the age of 30 years), while the other half had not.
They were able to show that indeed, children who later got cancer (on average six years after blood sampling) were about eight times more likely than their healthy peers to have antibodies to at least one core antigen involved in DNA repair.
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The authors hypothesized that the targeting of DNA repair proteins by these autoantibodies could provide a phenotype resembling what we see for related proteins with defective hereditary variants that cause a predisposition to cancer.

When the autoantibodies enter a cell or its nucleus, they could bind to and immobilize or directly inhibit the targeted proteins and thus hinder normal DNA repair. Such weakened repair might in turn cause pediatric cancer.

In follow-up experiments, the scientists were able to show that these autoantibodies can enter cells, especially during the phase when cells end their growth and prepare to divide. Inside the cell, they seem to home in on the TIGER organelle, a site where transcription factors and other short-lived but essential proteins are produced and modified.

"[These results] together provide a plausible mechanism for increased cellular damage that could lead to cancer development," concluded the authors in their research paper.
But what might trigger the production of antibodies against normal DNA repair proteins?

They could be triggered by infections, by cross-reacting to some microbial proteins or overstimulation of the immune response, or by some imbalance in immune tolerance.
The results point to the possibility of screening children to detect any autoimmune predisposition to cancer early, with the hope of preventing their later progression to the disease or detecting it early.

Pathogenic autoantibodies targeting DNA repair proteins are shared by cancer patients and healthy children later diagnosed with cancer, Frontiers in Immunology (2026). DOI: 10.3389/fimmu.2026.1911932

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Microplastics are chemically active and could cause biological harm

Plastics are supposed to be chemically inert. It's the reason they're used so frequently to package food, bottle water and create children's toys: They're safe. But something important happens when a large piece of plastic fragments into micro- and nanoparticles. Its surface area increases dramatically relative to its volume. Vastly more of the material is now exposed to its surroundings.

A new study by researchers from Columbia University and the University of California, Berkeley, found that this newly created surface is not necessarily safe and identified the chemical reasons why.

As plastic fragments into smaller and smaller particles, its surface area increases enormously. Then microplastics change the water that surrounds them, generating high-energy, reactive radicals (reactive oxygen species, ROS) that very likely contribute to biological damage that we see in animals and potentially in humans as a result of microplastic exposure.

This is particularly noteworthy for human health because human blood is approximately 50% water, and individual human cells are generally 60% to 80% water. The new research suggests that microplastics that enter the bloodstream or cells could remain chemically active in this water-rich biological environment.

The research found that when microplastics interact with water, as they do when they're in bottled water, or when they're absorbed into our bloodstream, they spontaneously generate what we call reactive oxygen species (ROS).

ROS are textbook examples of the kinds of molecules that can damage animal and human tissue.

Water is a key active player here, rather than just a spectator. It's integral to making these microplastics reactive. Water molecules become chemically active when they come into contact with plastic, which is hydrophobic. Contact between the water and plastic creates an environment that facilitates electron transfer and the formation of reactive radicals. When plastics fragment into smaller particles, their increasing surface-to-volume ratio creates more of these chemically active areas.

The work challenges the common view of microplastics as largely passive fragments of inert material and contributes to a growing understanding of why the large-scale presence of microplastics is a cause for concern. The research was published recently in the journal Nature.

Wei Min, Intrinsic physicochemical activity at microplastic–water interfaces, Nature (2026). DOI: 10.1038/s41586-026-11141-y. www.nature.com/articles/s41586-026-11141-y

Sustained pressure halts cancer cell migration and triggers death in 3D lab models

In 3D models, sustained mechanical confinement halted migration and induced death in cancer cells undergoing the mesenchymal-to-amoeboid transition. Physical pressure activated MLKL-mediated necroptosis, linking mechanical stress to programmed cell death.

Long-term confinement triggers RIPK3-independent necroptosis in amoeboid cancer cells to shape tumor evolution, Developmental Cell (2026). DOI: 10.1016/j.devcel.2026.09.003

Introduced species aren't good or bad—they are labeled according to human interests
Animal classifications in Australia reflect human interests as well as ecological impacts. Introduced species can harm biodiversity, but valued livestock also cause damage, and native species can become invasive outside their bioregions. Context-specific management is proposed as an alternative to treating species as inherently good or bad.

original article.