Overall, first responders with elevated CH mutations were nearly six times likelier to develop leukemia than those without the mutations. Exposure of mice to WTC dust led to high levels of inflammatory markers and an increase in mutant cells, suggesting that toxin-induced inflammation plays a key role in propagating the blood cells.

In addition, researchers found that younger first responders (those under age 60) with elevated CH possessed a set of gene mutations quite distinct from the classic mutations associated with age-related CH—indicating that the gene-altering toxins in WTC dust may contribute to cancer risk by accelerating the aging process.
To learn how exposure to toxins is associated with CH mutations and increased leukemia risk, the researchers tested the dust collected from the WTC site in a mouse model.

The dust caused an inflammatory response traced to the protein IL1RAP; the high levels of IL1RAP were associated with increased numbers of defective blood-forming stem cells—mimicking the high CH levels observed in the first responders. Importantly, the researchers found they could prevent the rise in defective mutant cells by knocking out the gene that codes for IL1RAP.
IL1RAP has been implicated in many types of cancer as well as in inflammatory and autoimmune diseases and that several drugs aimed at inhibiting the protein are being evaluated in clinical trials.
By screening toxin-exposed populations for CH, we could identify people at risk for blood cancers and then potentially treat or even prevent those cancers by targeting IL1RAP, say the researchers.

Elevated clonal hematopoiesis in environmentally exposed 9/11 first responders has distinct age-related patterns and relies on IL1RAP for clonal expansion, Cancer Discovery (2025).

https://www.eurekalert.org/news-releases/1100191

Part 2

Mitosis, meiosis, or a new different option
Researchers have found a way to prompt a new cell division process to create a viable egg cell from a skin cell. First, they implanted the skin cell’s nucleus into an empty egg. Then, the team induced a process they called ‘mitomeiosis’. This forces the egg to discard one set of chromosomes, which are replaced by that of the sperm during fertilization. Only a few of the resulting embryos developed beyond eight cells, but the research demonstrates the potential of the process for in-vitro fertilization using skin cells, the researchers say.

https://www.reuters.com/business/healthcare-pharmaceuticals/scienti...

Reference: https://www.nature.com/articles/s41467-025-63454-7?utm_source=Live+...

Bird decorations

Bearded Vulture nests found to have hoards of cultural artifacts—some up to 650 years old

Many people have probably seen birds picking up small pieces of man-made materials, like strips of a plastic bag or paper litter, and taking them into their nest. This behavior appears to be fairly widespread among birds. What's unique about some larger bird species, like certain vultures, eagles, and falcons, is that the same nest is used for centuries if it continues to be in a safe space. Generations of birds will continue to occupy and add materials to these nests for hundreds of years.

These behaviors are well documented in the Bearded Vulture (Gypaetus barbatus), a threatened species that builds nests in cliff caves, rock shelters, or on cornices. The Bearded Vulture can most often be found in European mountain ranges, particularly the Pyrenees. The environment in many of these regions is dry, particularly in the cave-like structures where nests are found, creating an ideal environment for long-term preservation.

Over a decade ago, a group of researchers  had the opportunity to examine 12 of these nests in detail. Their study was recently published in the journal Ecology and discusses a number of surprising findings.

The team rifled through centuries worth of vulture eggshells, remains of prey, and nesting material and among these they also found 226 items that had been made or altered by humans—providing a window into both past ecosystems and human cultures from the region. The hoard included items like a slingshot made from esparto grass, shoes, a crossbow bolt, a decorated piece of sheep leather and a wooden lance.

Even more surprising was that several items were well over 600 years old, according to carbon-14 dating. Results from one shoe dated back to around 675 years ago, while the decorated leather dated to around 650 years ago. However, the dating revealed a range of time periods, with a piece of basket dating to about 150 years ago.

Thanks to the solidity of Bearded Vulture nest structures and their locations in the western Mediterranean, generally in protected places such as caves and rock shelters with relatively stable temperature and low humidity conditions, they have acted as natural museums, conserving historical material in good condition," the authors write.

In addition to the human-made items, the researchers found 2,117 bones, 86 hooves, 72 leather remains, 11 hair remains and 43 eggshells. The team notes that this study and its findings "can provide information about temporal
changes in the trophic spectrum, past environment, and the wild and domestic species present."

They also call these nests a powerful tool for investigating and understanding more about the ecology, biodiversity trends, and environmental changes that the vultures are subject to. The findings could potentially inform habitat restoration and species reintroduction efforts.

Antoni Margalida et al, The Bearded Vulture as an accumulator of historical remains: Insights for future ecological and biocultural studies, Ecology (2025). DOI: 10.1002/ecy.70191

Microbes trapped in permafrost awake after thousands of years

In a new study, a team of geologists and biologists  resurrected ancient microbes that had been trapped in ice—in some cases for around 40,000 years.

The study is a showcase of the planet's permafrost. That's the name for a frozen mix of soil, ice and rocks that underlies nearly a quarter of the land in the northern hemisphere. It's an icy graveyard where animal and plant remains, alongside plentiful bacteria and other microorganisms, have become stuck in time.

That is, until curious scientists try to wake them up.

The group discovered that if you thaw out permafrost, the microbes within will take a while to become active. But after a few months, like waking up after a long nap, they begin to form flourishing colonies.

The research has wide implications for the health of the Arctic, and the entire planet.

Today, the world's permafrost is thawing at an alarming rate because of human-caused climate change. Scientists worry this trend could kick off a vicious cycle. As permafrost thaws, microbes living in the soil will begin to break down organic matter, spewing it into the air as carbon dioxide and methane—both potent greenhouse gases.

It's one of the biggest unknowns in climate responses. How will the thawing of all this frozen ground, where we know there's tons of carbon stored, affect the ecology of these regions and the rate of climate change?

In the current study, the researchers collected samples of permafrost that was a few thousand to tens of thousands of years old from the walls of the tunnel. They then added water to the samples and incubated them at temperatures of 39 and 54 degrees Fahrenheit—chilly for humans, but downright boiling for the Arctic.

The researchers relied on water made up of unusually heavy hydrogen atoms, also known as deuterium. That allowed them to track how their microbes drank up the water, then used the hydrogen to build the membranes made of fatty material that surround all living cells.

What they saw was surprising.
In the first few months, these colonies grew at a creep, in some cases replacing only about one in every 100,000 cells per day. In the lab, most bacterial colonies can completely turn over in the span of a few hours.

But by the six-month mark, that had all changed. Some bacterial colonies even produced gooey structures called "biofilms" that you can see with the naked eye.
These microbes likely couldn't infect people, but the team kept them in sealed chambers regardless.

Part 1

The colonies didn't seem to wake up that much faster at hotter temperatures. The results could hold lessons for thawing permafrost in the real world: After a hot spell, it may take several months for microbes to become active enough that they begin to emit greenhouse gases into the air in large volumes.

In other words, the longer Arctic summers grow, the greater the risks for the planet.

T. A. Caro et al, Microbial Resuscitation and Growth Rates in Deep Permafrost: Lipid Stable Isotope Probing Results From the Permafrost Research Tunnel in Fox, Alaska, Journal of Geophysical Research: Biogeosciences (2025). DOI: 10.1029/2025jg008759

Part 2

Ancient viral DNA is essential for human embryo development, study shows

Our ancient past isn't always buried history. When it comes to our DNA, nearly 9% of the human genome is made up of leftover genetic material from ancient viruses (called endogenous retroviruses or ERVs) that infected our ancestors millions of years ago and became permanently integrated into our genetic code. In a new study published in the journal Nature, scientists have demonstrated that one piece of this viral junk is essential for the earliest stages of human life.

Knowledge of how ERVs affect human development is limited because scientists obviously cannot conduct ethical experiments on embryos. To overcome this, researchers in this study used human blastoids, 3D models grown from stem cells that mimic the structure and key cell types of a natural blastocyst. This is the ball of cells that form in early pregnancy, about five to seven days after fertilization.

The research team focused on a specific type of ERV known as HERVK LTR5Hs, which were introduced into our DNA after our lineage split from Old World monkeys. Although this event occurred millions of years ago, it is considered relatively recent in evolutionary genetic terms.
To determine the functional effect of these viral remnants on the early embryo, the research team used cutting-edge genetic tools that act like molecular scissors to switch off LTR5Hs elements or delete them completely. The results were dramatic. The blastoids either died or turned into disorganized clumps. This provided clear proof that this ancient DNA is essential for the pre-implantation stage of human development.

The researchers also dug deeper to find out what was going on at the subcellular level. They discovered that the LTR5Hs elements act as powerful enhancers, boosting the activity of neighboring genes. When their activity is suppressed, many nearby genes associated with the epiblast (the cell layer that eventually forms the embryo) are turned down. That is, their activity is reduced. This showed that the viral DNA is directly responsible for controlling these essential early developmental instructions.

One of the most important discoveries involved the ZNF729 gene. The team found that one specific LTR5Hs insertion (an extra piece of DNA added to a DNA sequence), unique to humans, acts as a master key for activating this gene. Since the gene regulates fundamental cellular processes, such as cell growth and metabolism, the viral DNA master key is crucial to our development.

Raquel Fueyo et al, A human-specific regulatory mechanism revealed in a pre-implantation model, Nature (2025). DOI: 10.1038/s41586-025-09571-1

Do stranded dolphins have Alzheimer's disease?

One of the most heartbreaking occurrences for nature lovers is to discover a beached marine mammal such as a dolphin or whale. If the animal is still alive, marine biologists assisted by citizen volunteers try to protect the beached marine mammal from sun exposure and skin desiccation by pouring buckets of sea water on them and sometimes covering them with wet blankets. Other volunteers try to find ways to help the animal return to their native ocean habitat when the tide rises.

Unfortunately, some beached marine mammals are discovered after they have died. Such unsettling events give rise to a broader question: why do dolphins and whales become stranded on shore in the first place?

A group of scientists  have come up with an unusual hypothesis: just as some adult humans with dementia are occasionally found wandering far from their homes, perhaps dolphins become similarly disoriented by suffering from a form of Alzheimer's disease. The research was published in Communication Biology.

In the case of marine mammals, it appears that Alzheimer's-type neuropathology and disorientation may result from chronic exposure to toxic molecules produced by cyanobacteria.

Studies of villagers on the island of Guam show that chronic dietary exposure to cyanobacterial toxins are associated with misfolded tau proteins and amyloid plaques characteristic of Alzheimer's disease.

The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA), as well as its isomers 2,4-diaminobutyric acid (2,4-DAB), and N-2-aminoethylglycine (AEG), have been found to be extremely toxic to neurons. BMAA triggers Alzheimer's-like neuropathology and cognitive loss in experimental animals. These toxins can be biomagnified up the food chain in the marine ecosystem.

A study of 20 common bottlenose dolphins stranded in the Indian River Lagoon in eastern Florida showed that their brains contained BMAA and its isomers, particularly 2,4-DAB.

Dolphins stranded during the summer cyanobacterial bloom season contained 2,900 times the concentration of 2,4-DAB than those from non-bloom seasons. Brain neuropathology similar to Alzheimer's patients, including β-amyloid plaques and hyperphosphorylated tau proteins were found in the dolphin brains.

In addition, TDP-43 protein inclusions characteristic of a particularly severe form of Alzheimer's were also found in the dolphin brains. During bloom seasons, the same dolphins showed 536 differentially expressed genes associated with Alzheimer's disease.

The duration of cyanobacterial blooms is increasing with climate warming and nutrient inputs associated with agricultural runoff and sewage discharges.

What is worse is scientists found that even among Guam villagers, exposure to cyanobacterial toxins appeared to trigger neurological diseases.

Wendy Noke Durden et al, Alzheimer's disease signatures in the brain transcriptome of Estuarine Dolphins, Communications Biology (2025). DOI: 10.1038/s42003-025-08796-0

Trauma in a puppy's first six months linked to adult aggression, says new study

As many dog owners can attest, their four-legged companions are delightful and loving. But for others, their animals have an aggressive side, such as biting and attacking strangers, which may ultimately lead to them having to be euthanized. But why do some dogs turn out this way?

According to a new study of 211 dog breeds published in the journal Scientific Reports, adverse experiences such as abuse or being given up during a dog's first six months of life mean they are more likely to be fearful and aggressive as adults.

To explore this link between early life experiences and adult behavior, scientists conducted a large-scale survey of 4,497 dog owners. Each owner filled out a detailed questionnaire about their canine companion, including its complete life history, breed and current living environment. They were also asked about any adversity their pet experienced during its first six months.

Additionally, owners completed a standard behavior test (C-BARQ) to rate their dog's current fear and aggression levels. The scientists then used powerful statistical tools to determine whether early trauma, breed, or a combination of the two was most responsible for a dog's behaviour.

Just like in humans, the first few months of life are crucial for emotional development. The research team found that dogs that experienced any kind of adversity in the first six months were more likely to be aggressive as adults, regardless of age or sex or whether the animal was neutered. Both genes and environment are involved, as indicated by the fact that the effect of adversity differed across different breeds.

For example, some breeds, such as Siberian Huskies, American Eskimo Dogs, and American Leopard Hounds, as well as pit-bull type dogs, were more likely to become aggressive or fearful after experiencing early trauma. Meanwhile, other breeds, such as the Labrador Retriever, were a lot more resilient. Even when they experienced trauma, the chances of them being aggressive adults were relatively low.

Overall, the study clearly demonstrates that a dog's early life is crucial and highlights the importance of responsible breeding and proper pet care.

Julia Espinosa et al, Influence of early life adversity and breed on aggression and fear in dogs, Scientific Reports (2025). DOI: 10.1038/s41598-025-18226-0

Making yogurt with ants revives a creative fermentation process

Researchers recreated a nearly forgotten yogurt recipe that once was common across the Balkans and Turkey—using ants. Reporting in iScience on October 3, the team shows that bacteria, acids, and enzymes in ants can kickstart the fermentation process that turns milk into yogurt. The work highlights how traditional practices can inspire new approaches to food science and even add creativity to the dinner table.

Today's yogurts are typically made with just two bacterial strains. 

But if you look at traditional yogurt, you have much bigger biodiversity, varying based on location, households, and season. That brings more flavours, textures, and personality.

Red wood ants (Formica species) can be found crawling through the forests of the Balkans and Turkey, where this yogurt-making technique was once popular.

In the present study researchers dropped four whole ants into a jar of warm milk .

The jar was then tucked into an ant mound to ferment overnight. By the next day, the milk had started to thicken and sour. That's an early stage of yogurt, and it tasted that way as well, they say.

The researchers, who tested the yogurt during their trip, described it as slightly tangy, herbaceous, and having flavors of grass-fed fat.

The team dissected the science behind the ant yogurt. They found that the ants carry lactic and acetic acid bacteria. Acids produced by these bacteria help coagulate the dairy. One type of these bacteria was similar to that found in commercial sourdough.

The insects themselves also help in the yogurt-making process. Formic acid, which is part of the ant's natural chemical defense system, acidifies the milk, affects its texture, and likely creates an environment for yogurt's acid-loving microbes to thrive, say the researchers. Enzymes from the ant and the microbes work in tandem to break down milk proteins and turn milk into yogurt.

The researchers compared yogurts made with live, frozen, and dehydrated ants. Only live ants seeded the right microbial community, meaning they are best suited for yogurt making. However, the team found that caution was necessary to make sure the ant products were safe to consume: live ants can harbor parasites, and freezing or dehydrating ants can sometimes allow harmful bacteria to flourish.

Giving scientific evidence that these traditions have a deep meaning and purpose, even though they might seem strange or more like a myth.

 Making yogurt with the ant holobiont uncovers bacteria, acids, and enzymes for food fermentation, iScience (2025). DOI: 10.1016/j.isci.2025.113595

Glioblastomas affect much more than just the brain, scientists discover

Scientists  have shown for the first time that glioblastoma—the deadliest form of brain cancer—affects not just the brain but also erodes the skull, alters the makeup of skull marrow, and interferes with the body's immune response. Drugs intended to inhibit skull-bone loss made the cancer more aggressive, according to results published in Nature Neuroscience. The paper is titled "Brain Tumors Induce Widespread Disruption of Calvarial Bone and Alteration of Skull Marrow Immune Landscape."

This discovery that this notoriously hard-to-treat brain cancer interacts with the body's immune system may help explain why current therapies—all of them dealing with glioblastoma as a local disease—have failed, and it will hopefully lead to better treatment strategies.

As is true for many other bones, the skull contains marrow in which immune cells and other blood cells form. 

Researchers used advanced imaging techniques on mice that developed two different types of glioblastomas. They found that the tumors caused skull bones to erode, especially along the sutures where skull bones fuse. Such erosions seem to be unique to glioblastoma and other malignant intracranial tumors, since they don't occur with strokes, other types of brain damage, or even other systemic cancers. Computerized-tomography (CT) images of patients with glioblastoma revealed that decreases in skull thickness were present in the same anatomic areas as in mice. 

The skull erosions in the mice were found to have increased the number and diameter of the skull-to-bone channels. The researchers hypothesized that these channels might allow the glioblastoma to transmit signals to the skull marrow that could profoundly change its immune landscape.

Using single-cell RNA sequencing, the researchers found that glioblastoma had dramatically shifted the skull marrow's immune-cell balance in favor of pro-inflammatory myeloid cells—nearly doubling the levels of inflammatory neutrophils, while nearly eliminating several types of antibody-producing B cells as well as other B cells.

The skull-to-brain channels allow an influx of these numerous pro-inflammatory cells from the skull marrow to the tumor, rendering the glioblastoma increasingly aggressive and, all too often, untreatable.

This indicates the need for treatments that restore the normal balance of immune cells in the skull marrow of people with glioblastoma. One strategy would be suppressing the production of pro-inflammatory neutrophils and monocytes while at the same time restoring the production of T and B cells.

'Brain tumors induce widespread disruption of calvarial bone and alteration of skull marrow immune landscape, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02064-4

Scientists create natural plastics for everyday packaging

Researchers have transformed food waste sugars into natural plastic films that could one day replace petroleum-based packaging, offering compostable alternatives to commonly used plastics for food and agricultural films like silage wrap.

With global plastic production exceeding 400 million metric tons annually, a Monash University study highlights the potential of a new type of biodegradable plastic by converting food waste sugars into polyhydroxyalkanoates (PHA) biopolymers.

The study is published in the journal Microbial Cell Factories.

By selecting different bacterial strains and blending their polymers, the researchers produced films that behave like conventional plastics and can be molded into other shapes or solids.

The study  provides a framework for designing bioplastics for temperature-sensitive packaging, medical films and other products, addressing the global challenge of single-use plastic waste.

The research teams fed two soil-dwelling bacteria—Cupriavidus necator and Pseudomonas putida—a carefully balanced "diet" of sugars with the right blend of salts, nutrients and trace elements.

Once the microbes fattened up, they began stockpiling natural plastic inside their cells. The scientists then "milked" these plastics out using solvents, cast them into ultrathin films about 20 microns thick and tested their stretchiness, strength and melting behavior.

This research demonstrates how food waste can be transformed into sustainable, compostable ultrathin films with tunable properties. The versatility of PHAs means we can reimagine materials we rely on every day without the environmental cost of conventional plastics.

By tailoring these natural plastics for different uses, scientists are opening the door to sustainable alternatives in packaging, especially where they can be composted along with food or agricultural waste.

The researchers  collaborating with industry partners, including Enzide and Great Wrap through the ARC RECARB and VAP hubs to develop biodegradable packaging and medical solutions with potential commercial applications.

Edward Attenborough et al, Bacterial species-structure-property relationships of polyhydroxyalkanoate biopolymers produced on simple sugars for thin film applications, Microbial Cell Factories (2025). DOI: 10.1186/s12934-025-02833-7

The Nobel Prize in medicine goes to 3 scientists for key immune system discoveries

Three scientists won the Nobel Prize in medicine this week for discoveries about how the immune system knows to attack germs and not our own bodies.

The work by Mary E. Brunkow, Fred Ramsdell and Dr. Shimon Sakaguchi uncovered a key pathway the body uses to keep the immune system in check, called peripheral immune tolerance. Experts called the findings critical to understanding autoimmune diseases such as Type 1 diabetes, rheumatoid arthritis and lupus.

In separate projects over several years, the trio of scientists identified the importance of what are now called regulatory T cells. Scientists are currently using those findings in a variety of ways: to discover better treatments for autoimmune diseases, to improve organ transplant success and to enhance the body's own fight against cancer, among others.

Their discoveries have been decisive for our understanding of how the immune system functions and why we do not all develop serious autoimmune diseases.

The immune system has overlapping ways to detect and fight bacteria, viruses and other intruders. But sometimes certain immune cells run amok, mistakenly attacking people's own cells and tissues to cause autoimmune diseases.

Scientists once thought the body regulated this system only in a centralized fashion. Key immune soldiers such as T cells get trained to spot bad actors and those that go awry in a way that might trigger autoimmunity get eliminated in the thymus.

The Nobel winners unraveled an additional way the body keeps the system in check if immune cells later get confused and mistake human cells for intruders, which is what happens when a person has an autoimmune disease.

These scientists were curious about the mechanism of immune response that is supposed to protect oneself but also reacts to and attacks itself.

Sakaguchi's experiments in mice showed that the thymus pathway couldn't be the only explanation. In 1995, he discovered a previously unknown T cell subtype, the regulatory T cells, that also could tamp down overreactive immune cells like a biological security guard.

Then in 2001, Brunkow and Ramsdell were working together at a biotech company investigating mice with an autoimmune disease. In painstaking work at a time when mapping genes was still an evolving field, they figured out that a particular mutation in a gene called Foxp3 was to blame—and quickly realized it could be a major player in human health, too.

From a DNA level, it was a really small alteration that caused this massive change to how the immune system works.

Sakaguchi linked the discoveries to show the Foxp3 gene controls the development of those regulatory T cells so they're able to curb other, overreactive cells.

The work is important because it opened a new field of immunology. Until the trio's research was published, immunologists didn't understand the complexity of how the body differentiates foreign cells from its own. 

One goal for scientists now is to figure out how to increase the number of regulatory T cells—also known as T-regs—to help fight autoimmune diseases. That would decrease the need for today's therapies, which instead suppress the immune system in ways that leave patients vulnerable to infection.

Nobel committee announcement:
The Nobel Assembly at Karolinska Institutet has decided to award the 2025 Nobel Prize in Physiology or Medicine to:

Mary E. Brunkow, Institute for Systems Biology, Seattle, U.S.

Fred Ramsdell, Sonoma Biotherapeutics,San Francisco, U.S.

Shimon Sakaguchi, Osaka University, Osaka, Japan

"for their discoveries concerning peripheral immune tolerance"
They discovered how the immune system is kept in check.

Source: www.nobelprize.org/prizes/medi … popular-information/

Part 2

Epigenetic shifts link maternal infection during pregnancy to higher risk of offspring developing schizophrenia

The health of mothers during pregnancy has long been known to play a role in the lifelong mental and physical health of offspring. Recent studies have found that contracting an infection during pregnancy can increase the risk that offspring will develop some neurodevelopmental disorders, conditions that are associated with the atypical maturation of some parts of the brain.

An infection is an invasion of pathogens, such as bacteria, viruses, fungi or parasites, which can then multiply and colonize host tissues. Findings suggest that when an expecting mother contracts an infection, her immune system can respond to it in ways that could impact the development of the fetus.

Researchers recently carried out a study aimed at further investigating the processes through which maternal infections during pregnancy could increase the risk that offspring will develop schizophrenia later in life. Schizophrenia is a typically debilitating mental health condition characterized by hallucinations, false beliefs about oneself or the world (e.g., delusions) and cognitive impairments.

The findings of the team's study, outlined in a paper published in Molecular Psychiatry, shed light on epigenetic shifts prompted by infection that could potentially be linked to a higher genetic risk of offspring developing schizophrenia. Epigenetic processes are changes in the expression of genes prompted by biological processes, which do not alter the DNA sequence of a living organism.

Maternal infection during pregnancy has been shown in epidemiological studies to increase the risk of neurodevelopmental disorders, like schizophrenia, in the developing fetus, wrote the researchers in their paper.

The results of the team's experiments and analyses revealed that the activation of a pregnant rat's immune system due to infection influenced the ratio between SAM and SAH molecules in the fetus. The ratio between these molecules is known to be an indication of the ability of cells to undergo methylation, a biological process that controls the expression of genes.

The findings revealed that MIA increased the SAM/SAH ratio and elevated both DNMT expression and activity in the fetal cortex," wrote the authors. Surprisingly, these changes were not present after birth but resurfaced in adulthood, coinciding with cognitive deficits. These methylation pathway changes in adulthood were accompanied by altered DNAm patterns, with differentially methylated genes linked to schizophrenia risk and enriched in pathways related to neurodevelopment and neuronal signaling.

The researchers were able to pinpoint epigenetic changes following infection in pregnant female rats that resulted in pups exhibiting cognitive deficits resembling those associated with schizophrenia. Their findings could soon pave the way for further investigations on this topic and could potentially contribute to the future development of more effective drugs to treat the cognitive symptoms of schizophrenia, such as attention, memory and language deficits.

Rebecca M. Woods et al, Developmental modulation of schizophrenia risk gene methylation in offspring exhibiting cognitive deficits following maternal immune activation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03147-1.

Bacteria survive space launch and re-entry unharmed

A world-first study has proven microbes essential for human health can survive the extreme forces of space launch. The study has been published in npj Microgravity.

Space agencies are planning to send crews to Mars within decades, but sustaining life on the red planet would be more difficult if important bacteria die during the flight.

Now a study has found the spores of Bacilus subtilis, a bacterium essential for human health, can survive rapid acceleration, short-duration microgravity and rapid deceleration.

The spores of bacteria were launched more than 260 kilometers into the sky, then studied once their rocket fell back to Earth, in what is believed to be the first study of its kind in real conditions outside the lab.

Effects of Extreme Acceleration, Microgravity, and Deceleration on Bacillus subtilis Onboard a Suborbital Space Flight, npj Microgravity (2025). DOI: 10.1038/s41526-025-00526-4

Strange 'rogue' planet spotted guzzling matter like a star

A mysterious "rogue" planet has been observed gobbling six billion tons of gas and dust a second—an unprecedented rate that blurs the line between planets and stars.

Unlike Earth and other planets in our solar system which orbit the sun, rogue planets float freely through the universe untethered to a star.

Scientists estimate there could be trillions of rogue planets in our galaxy alone—but they are difficult to spot because they mostly drift quietly along in perpetual night.

These strange objects intrigue astronomers because they are neither a star nor a proper planet. 

Their origin remains an open question: are they the lowest-mass objects formed like stars, or giant planets ejected from their birth systems?

The team of researchers behind the new study were stunned to observe an astonishing growth spurt in a rogue planet around 620 light years from Earth in the constellation Chamaeleon. The planet, officially called Cha 1107-7626, has a mass five to 10 times bigger than Jupiter. 

 The object is "still in its infancy," being roughly one or two million years old.

The object grows by sucking in matter from a disk that surrounds it—a process called accretion.

But what the astronomers saw happen to Cha 1107-7626 "blurs the line between stars and planets". 

In August this year, the planet suddenly started devouring matter from its disk at a record-breaking six-billion-tons per second—eight times faster than a few months earlier.

This is the strongest accretion episode ever recorded for a planetary-mass object.

By comparing light emitted before and during this binge-eating session, the scientists discovered that magnetic activity was playing a role in driving matter towards the object.

This phenomenon has previously only been observed in stars.

The chemistry in the disk also changed. Water vapor was detected in the disk during the accretion episode, but not beforehand.

This is also something that has previously been observed in stars—but never for a forming planet.

No matter how weird, Cha 1107-7626 is still expected to have similar characteristics to huge planets, because it is of similar size. Unlike stars, this object is "not massive enough to ever have fusion reactions in the core".

Discovery of an Accretion Burst in a Free-Floating Planetary-Mass Object The Astrophysical Journal Letters (2025). DOI: 10.3847/2041-8213/ae09a8

Scientists reverse Alzheimer's in mice using nanoparticles

A research team has demonstrated a nanotechnology strategy that reverses Alzheimer's disease in mice.

Unlike traditional nanomedicine, which relies on nanoparticles as carriers for therapeutic molecules, this approach employs nanoparticles that are bioactive in their own right: "supramolecular drugs." The work has been published in Signal Transduction and Targeted Therapy.

Instead of targeting neurons directly, the therapy restores the proper function of the blood-brain barrier (BBB), the vascular gatekeeper that regulates the brain's environment. By repairing this critical interface, the researchers achieved a reversal of Alzheimer's pathology in animal models.

The team demonstrated that targeting a specific mechanism enables undesirable "waste proteins" produced in the brain to pass through this barrier and be eliminated in the blood flow. In Alzheimer's disease, the main "waste" protein is amyloid-β (Aβ), whose accumulation impairs the normal functioning of the neurons.

Researchers used mouse models that are genetically programmed to produce larger amounts of Aβ protein and develop a significant cognitive decline mimicking Alzheimer's pathology. They administered only three doses of the supramolecular drugs and afterward regularly monitored the evolution of the disease.

Only one hour after the injection, they observed a reduction of 50–60% in Aβ amount inside the brain.

In one of the experiments, they treated a 12-month-old mouse (equivalent to a 60-year-old human) with the nanoparticles and analyzed its behavior after six months. The result was impressive: the animal, aged 18 months (comparable to a 90-year-old human), had recovered the behavior of a healthy mouse.

The long-term effect comes from restoring the brain's vasculature. 

What's remarkable is that these nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels.

 Multivalent modulation of endothelial LRP1 induces fast neurovascular amyloid-β clearance and cognitive function improvement in Alzheimer's disease models, Signal Transduction and Targeted Therapy (2025). DOI: 10.1038/s41392-025-02426-1

Nobel Prize in physics goes to 3 scientists whose work advanced quantum technology (Update)

Three scientists won the Nobel Prize in physics this week for research on the strange behavior of subatomic particles called quantum tunneling that enables the ultra-sensitive measurements achieved by MRI machines and lays the groundwork for better cellphones and faster computers.

The work by John Clarke, Michel H. Devoret and John M. Martinis, took the seeming contradictions of the subatomic world—where light can be both a wave and a particle and parts of atoms can tunnel through seemingly impenetrable barriers—and applied them in the more traditional physics of digital devices. The results of their findings are just starting to appear in advanced technology and could pave the way for the development of supercharged computing.

The prize-winning research in the mid-1980s took the subatomic "weirdness of quantum mechanics" and found how those tiny interactions can have real-world applications.

The experiments were a crucial building block in the fast-developing world of quantum mechanics.

Nobel committee announcement:

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Physics 2025 to

John Clarke, University of California, Berkeley, U.S.

Michel H. Devoret, Yale University, New Haven, CT and University of California, Santa Barbara, U.S.

John M. Martinis, University of California, Santa Barbara, U.S.

"for the discovery of macroscopic quantum mechanical tunnelling and energy quantisation in an electric circuit"

Their experiments on a chip revealed quantum physics in action

Instructions help you remember something better than emotions or a good night's sleep, scientists find

A good night's sleep has long been understood to help us consolidate new memories, but we don't understand how. Associations with negative feelings like fear or stress can improve recall, but intentionally trying to remember can also be effective. But these two mechanisms are very different—one involuntary, one deliberate. Which influences memory most?

To investigate, researchers asked participants to remember or forget words, some of which had negative emotional associations. They found that instructions improved recall more than emotion.

Researchers found that when it comes to memory, instructions do indeed work better than emotion. People were more likely to recall words they had been asked to remember. However, emotions did play a part: words participants had been asked to remember that had negative connotations were more likely to be remembered.

This suggests that although instructions were the primary influence on recall, emotional cues could amplify the effect of instructions. Emotions also increased the chances of false memories: negative foils were more likely to be misremembered as words participants had been asked to remember. 

During encoding, we will devote more attentional resources to words that we are told explicitly to remember. Along similar lines, cognitive control systems can 'tag' information as relevant, biasing the hippocampus to prioritize it. This increases the likelihood that the memory will be reactivated during sleep and transferred to long-term storage.

Lastly, instructions don't just enhance relevant items, they also suppress irrelevant ones. By inhibiting competing memories, remember-cued items face less interference, which improves recall.

Unexpectedly, whether participants had slept had no effect on how well they recalled words. However, the different types of brain wave activity measured by the EEG were linked to recall. For example, higher levels of REM theta power, a measure of REM sleep, were associated with the misremembering of negative foils.

Sleep spindles were associated with better recall of negative, remember-cued words.Sleep spindles are widely implicated in the transfer of information from temporary hippocampal storage to more stable representations in the neocortex.

This could indicate that sleeping only consolidates some memories—prioritizing things you're motivated to remember over things which are emotional—and that sleeping in general is less significant than your brain's activity during sleep. However, more research is needed to confirm this.

Top-Down Instruction Outweighs Emotional Salience: Nocturnal Sleep Physiology Indicates Selective Memory Consolidation, Frontiers in Behavioral Neuroscience (2025). DOI: 10.3389/fnbeh.2025.1643449

Microplastics found to change gut microbiome in first human-sample study

New research presented at UEG Week 2025 shows that microplastics—plastic particles smaller than 5 mm commonly found in the environment—can alter the human gut microbiome, with some changes resembling patterns linked to depression and colorectal cancer.

The study used stool samples from five healthy volunteers to grow ex vivo gut microbiome cultures. These cultures were then exposed to five common microplastic types—polystyrene, polypropylene, low-density polyethylene, poly(methyl methacrylate) and polyethylene terephthalate

—at concentrations reflecting estimated human exposure, as well as higher doses to investigate potential dose-dependent effects.

While total and viable bacterial cell counts remained largely unchanged, microplastic-treated cultures showed a consistent and significant increase in acidity (lower pH levels) compared to controls, indicating altered microbial metabolic activity.

Further analysis revealed microplastic-specific shifts in bacterial composition, with certain bacterial groups increasing or decreasing depending on the microplastic type. Changes were observed across several bacterial families, including Lachnospiraceae, Oscillospiraceae, Enterobacteriaceae and Ruminococcaceae, with the majority occurring within the phylum Bacillota—a key group of gut bacteria important for digestion and overall gut health.

These shifts in bacterial composition were accompanied by changes in the chemicals produced by the bacteria, some of which corresponded with the observed decreases in pH. Certain microplastic types altered levels of valeric acid and 5-aminopentanoic acid, while others affected lysine or lactic acid, highlighting the complexity of microplastic-microbiome interactions.

Importantly, some of these microplastic-induced changes in microbial composition reflected patterns previously linked to diseases such as depression and colorectal cancer, underscoring the potential implications of microplastic exposure for disease risk.

Pacher-Deutsch, C et al. Microplastic-induced alterations in gut microbiome and metabolism: Insights from an ex vivo bioreactor model. Presented at UEG Week 2025; 7 October 2025; Berlin, Germany.

Many newborn baby deaths linked to preventable or treatable factors

A new study has identified the most critical risk factors linked to neonatal deaths worldwide, providing comprehensive evidence to help guide global efforts to save newborn lives.

Researchers reviewed more than 60 studies published in the past 35 years, covering more than 50 risk factors for neonatal mortality—defined as a baby dying in the first 28 days of life.

The paper, "Risk factors for neonatal mortality: an umbrella review of systematic reviews and meta-analyses," is published in eClinicalMedicine.

It found strong evidence of conditions and factors that significantly increase the likelihood of neonatal mortality, covering maternal health and lifestyle factors (obesity, prenatal opioid exposure, anemia, bleeding disorders), socioeconomic and environmental factors (maternal age, low occupational status, arsenic exposure), neonatal factors (preterm birth, delayed breastfeeding, low birthweight) and protective factors (antenatal care, health facility delivery).

Babies born with low birthweight face more than 15 times the risk of dying compared to those born at a healthy weight, babies born preterm face up to seven times higher risk, delaying breastfeeding by more than 24 hours after birth increases the risk by 60% to 70%, while mothers who receive antenatal care can reduce the risk of losing their baby by up to 85%.

These are staggering numbers, but they are also clear, actionable areas where change could save countless lives, the researchers say.

These are preventable and treatable issues—if we get this right, the impact will be profound across the globe.

Bereket Kefale et al, Risk factors for neonatal mortality: an umbrella review of systematic reviews and meta-analyses, eClinicalMedicine (2025). DOI: 10.1016/j.eclinm.2025.103525

Three scientists win Nobel Prize in chemistry for the development of metal-organic frameworks

Three scientists won the Nobel Prize in chemistry this week for their development of new molecular structures that can trap vast quantities of gas inside, laying the groundwork to potentially suck greenhouse gases out of the atmosphere or harvest moisture from desert environments.

Heiner Linke, chairperson of the committee that made the award, compared the structures called metal-organic frameworks to the seemingly bottomless magical handbag carried by Hermione Granger in the "Harry Potter" series. Another example might be Mary Poppins' enchanted carpet bag. These containers look small from the outside but are able to hold surprisingly large quantities within.

The committee said Susumu Kitagawa, Richard Robson and Omar M. Yaghi were honored for "groundbreaking discoveries" that "may contribute to solving some of humankind's greatest challenges," from pollution to water scarcity.

The chemists worked separately but added to each other's breakthroughs over decades, beginning with Robson's work in the 1980s.

The scientists were able to devise stable atomic structures that preserved holes of specific sizes that allowed gas or liquid to flow in and out. The holes can be customized to match the size of specific molecules that scientists or engineers want to hold in place, such as water, carbon dioxide or methane.

That level of control is quite rare in chemistry.

A relatively small amount of the structure—which combines metal nodes and organic rods, somewhat like the interchangeable building pieces in Tinker Toys—creates many organized holes and a huge amount of surface area inside.

Why the work matters

Today researchers around the world are exploring possibilities that include using the frameworks to remove greenhouse gases from the atmosphere and pollution from industrial sites. Another possibility is to use them to harvest moisture from desert air, perhaps to one day provide clean drinking water in arid environments.

Scientists are also investigating using the structures for targeted drug delivery. The idea is to load them with medicine that may be slowly released inside the body. It could be a better way to deliver low doses continually.

The research "could be really, really valuable" in many industries.

Nobel committee announcement:

The Royal Swedish Academy of Sciences has decided to award the Nobel Prize in Chemistry 2025 to

Susumu Kitagawa, Kyoto University, Japan

Richard Robson, University of Melbourne, Australia

Omar M. Yaghi, University of California, Berkeley, U.S.

"for the development of metal-organic frameworks"

Their molecular architecture contains rooms for chemistry

The Nobel Prize laureates in chemistry 2025 have created molecular constructions with large spaces through which gases and other chemicals can flow. These constructions, metal-organic frameworks, can be used to harvest water from desert air, capture carbon dioxide, store toxic gases or catalyze chemical reactions.

https://www.nobelprize.org/prizes/chemistry/2025/press-release/

New type of diabetes discovered in babies

Advanced DNA sequencing technologies and a new model of stem cell research have enabled an international team to discover a new type of diabetes in babies.

The researchers established that mutations in the TMEM167A gene are responsible for a rare form of neonatal diabetes.

Some babies develop diabetes before the age of six months. In over 85% of cases, this is due to a genetic mutation in their DNA. Research  found that in six children with additional neurological disorders such as epilepsy and microcephaly identified alterations in a single gene: TMEM167A.

To understand its role, the researchers  used stem cells differentiated into pancreatic beta cells and gene-editing techniques (CRISPR). They found that when the TMEM167A gene is altered, insulin-producing cells can no longer fulfill their role. They then activate stress mechanisms that lead to their death.

This discovery shows that the TMEM167A gene is essential for the proper functioning of insulin-producing beta cells, but also for neurons, whereas it seems dispensable for other cell types. These results contribute to a better understanding of the crucial steps involved in insulin production and could shed light on research into other forms of diabetes, a disease which today affects almost 589 million people worldwide.

Enrico Virgilio et al, Recessive TMEM167A variants cause neonatal diabetes, microcephaly and epilepsy syndrome, Journal of Clinical Investigation (2025). DOI: 10.1172/jci195756

Novel blood test for chronic fatigue achieves 96% accuracy

Scientists  have developed a high accuracy blood test to diagnose chronic fatigue syndrome, also known as myalgic encephalomyelitis (ME/CFS).

The debilitating long-term illness affects millions worldwide but is poorly understood and has long lacked reliable diagnostic tools.

With 96% accuracy, the new test offers new hope for those living with the condition—which is often misunderstood and misdiagnosed. It is hoped that the breakthrough could pave the way for a similar blood test to diagnose long COVID.

Chronic fatigue syndrome is not a genetic disease you're born with. That's why using EpiSwitch 'epigenetic' markers—which can change during a person's life, unlike a fixed genetic code—was key to reaching this high level of accuracy.

The team discovered a unique pattern that appears consistently in people with ME/CFS that is not seen in healthy people.

The researchers also found signs of immune system and inflammation pathways involved in the disease, which may help guide future treatments and identify patients more likely to respond to specific therapies.

'Development and validation of blood-based diagnostic biomarkers for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) using EpiSwitch® 3-dimensional genomic regulatory immuno-genetic profiling, Journal of Translational Medicine (2025). translational-medicine.biomedc … 6/s12967-025-07203-w

Schizophrenia is linked to iron and myelin deficits in the brain, neuroimaging study finds

Schizophrenia is a severe and debilitating psychiatric disorder characterized by hallucinations, disorganized speech and thought patterns, false beliefs about the world or oneself, difficulties concentrating and other symptoms impacting people's daily functioning. While schizophrenia has been the topic of numerous research studies, its biological and neural underpinnings have not yet been fully elucidated.

While some past brain imaging studies suggest that schizophrenia is associated with abnormal levels of iron and myelin in the brain, the results collected so far are conflicting. Iron is a metal known to contribute to healthy brain function, while myelin is a fatty substance that forms a sheath around nerve fibers, protecting them and supporting their conduction of electrical signals.

Researchers  recently set out to further explore the possibility that schizophrenia is linked to abnormal levels of iron and myelin in the brain. Their findings, published in Molecular Psychiatry, uncovered potential new biomarkers of schizophrenia that could improve the understanding of its underlying brain mechanisms.

Iron is essential for many neuronal processes but excess causes oxidative damage, so brain levels are kept in a delicate balance. Iron-sensitive MRI studies focusing on schizophrenia have yielded conflicting results, with both increases and decreases reported. As myelin—which increases brain signal transmission—influences iron-sensitive MRI, myelin variation could complicate interpretation.

Researchers  examined the brains of 85 individuals diagnosed with schizophrenia and 86 matching control subjects. To study the brains of the study participants, they used iron-sensitive and myelin-sensitive magnetic resonance imaging (MRI), imaging techniques that allow researchers to detect iron and myelin levels in specific regions of the brain.

The researchers' results suggested iron and myelin anomalies that affected specific regions in the brains of individuals diagnosed with schizophrenia, including the caudate, putamen, and globus pallidus. Their findings are aligned with those of some earlier studies and could help to paint a clearer picture of disease pathophysiology.

They found that patients with schizophrenia had lower magnetic susceptibility, higher mean diffusivity, and lower magnetic susceptibility anisotropy, suggesting that both iron and myelin brain levels are lower in schizophrenia.

This was most significant in regions rich in oligodendrocytes. As oligodendrocytes utilize iron to synthesize myelin, this links oligodendrocyte dysfunction to schizophrenia, highlighting the mechanism underlying this as an important research area.

Luke J. Vano et al, The role of low subcortical iron, white matter myelin, and oligodendrocytes in schizophrenia: a quantitative susceptibility mapping and diffusion tensor imaging study, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03195-7.

Nanoparticle vaccine prevents multiple cancers and stops metastasis in mice

A new study by researchers demonstrates that their nanoparticle-based vaccine can effectively prevent melanoma, pancreatic and triple-negative breast cancer in mice. Not only did up to 88% of the vaccinated mice remain tumor-free (depending on the cancer), but the vaccine reduced—and in some cases completely prevented—the cancer's spread.

By engineering these nanoparticles to activate the immune system via multi-pathway activation that combines with cancer-specific antigens, they could prevent tumor growth with remarkable survival rates.

The first test paired their nanoparticle system with well-characterized melanoma peptides (called an antigen, similar to how a flu shot typically contains parts of the inactivated flu virus). The formulation activated immune cells called T cells, priming them to recognize and attack this type of cancer. Three weeks later, the mice were exposed to melanoma cells.

Eighty percent of these "super adjuvant" vaccinated mice remained tumor-free and survived until the completion of the study (250 days). In comparison, all of the mice vaccinated with traditional vaccine systems, non-nanoparticle formulations or unvaccinated mice developed tumors; none survived longer than 35 days.

The vaccine also protected against the spread of cancer to the lungs. When exposed to melanoma cells systemically, which mimics how cancer metastasizes, none of the nanoparticle-vaccinated mice developed lung tumors, while all of the other mice did.

The tumor-specific T-cell responses that the researchers are able to generate—that is really the key behind the survival benefit. 

There is really intense immune activation when you treat innate immune cells with this formulation, which triggers these cells to present antigens and prime tumor-killing T cells. This robust T-cell response is possible because of the particular nanoparticle design of the vaccine.

The researchers say that their design offers a platform approach that could be used across multiple cancer types.

"Super adjuvant" nanoparticles for platform cancer vaccination, Cell Reports Medicine (2025). DOI: 10.1016/j.xcrm.2025.102415. www.cell.com/cell-reports-medi … 2666-3791(25)00488-4

Certain dietary fatty acids can supercharge cancer-fighting immune cells

A research team has discovered that certain dietary fatty acids can supercharge the human immune system's ability to fight cancer. The team found that a healthy fatty acid found in olive oil and nuts, called oleic acid (OA), enhances the power of immune γδ-T cells, specialized cells known for their cancer-fighting properties.

Conversely, they found that another fatty acid, called palmitic acid (PA), commonly found in palm oil and fatty meats, diminishes the ability of these immune cells to attack tumors.

Their study, published in the journal Signal Transduction and Targeted Therapy, offers an innovative approach using dietary OA supplementation to strengthen the antitumor immunity of γδ-T cells.

Dietary fatty acids are essential for health, helping with growth and body functions. They may also play a role in cancer prevention and treatment, but understanding how they affect cancer is challenging because of the complexity of people's diets and the lack of detailed studies.
Recently, scientists have learned that fatty acids can influence the immune system, especially in how it fights cancer. Specialized immune cells, called γδ-T cells, are particularly good at attacking tumors. These cells, once activated, have helped some lung and liver cancer patients live longer.
However, this therapy is not effective for all patients, partly because the variation of metabolic status, such as fatty acid metabolism, can influence its efficacy in the patients.

The research team identified a correlation between PA and OA levels and the efficacy of cancer therapies. The research suggests that dietary fatty acid supplementation, particularly with foods rich in OA, such as olive oil and avocados, could enhance γδ-T cell immunosurveillance, leading to more effective cancer treatments.

The team also discovered that another fatty acid, called PA, can weaken these immune cells and how OA can counteract this.

The results indicate that cancer patients should avoid PA and consider OA supplementation in their diets to improve clinical outcomes of γδ-T cell-based cancer therapies.

By analyzing blood samples, the researchers confirmed that the levels of these fatty acids are linked to the outcome of cancer immunotherapy.

Part 1

For cancer patients, this discovery suggests simple changes, like eating more foods rich in OA (such as olive oil, avocados and nuts) and cutting back on PA (found in processed foods, palm oil and fatty meats), could improve the effectiveness of cancer treatments. The study also points to novel strategies, like combining dietary changes with specific drugs to further boost the immune system.

Yanmei Zhang et al, Oleic acid restores the impaired antitumor immunity of γδ-T cells induced by palmitic acid, Signal Transduction and Targeted Therapy (2025). DOI: 10.1038/s41392-025-02295-8

Part 2

Study suggests air pollution can contribute to obesity and diabetes

Long-term exposure to fine air pollution can impair metabolic health by disrupting the normal function of brown fat in mice. A study co-led by the University of Zurich shows that this occurs through complex changes in gene regulation driven by epigenetic mechanisms. The results demonstrate how environmental pollutants contribute to the development of insulin resistance and metabolic diseases.

There is growing evidence that air pollution is not just harmful to our lungs and heart, but also plays a significant role in the development of metabolic disorders like insulin resistance and type 2 diabetes.

For their investigation, the researchers exposed laboratory mice to either filtered air or concentrated PM2.5 for six hours a day, five days a week, over a period of 24 weeks. This setup was designed to closely mimic chronic urban exposure in humans.
Particular attention was paid to brown adipose tissue, a special type of fat that helps the body generate heat and burn calories, and therefore plays a key role in energy balance and glucose metabolism. After the exposure period of about five months, the mice that had inhaled PM2.5 showed signs of disrupted metabolism, including impaired insulin sensitivity.

Further examination revealed that the function of brown fat had been significantly altered. In particular, they found that the expression of important genes in brown adipose tissue which regulate its ability to produce heat, process lipids and handle oxidative stress were disturbed. These changes were accompanied by increased fat accumulation and signs of tissue damage and fibrosis within the tissue.

Part 1

The researchers then examined the underlying mechanisms driving these changes. They found that air pollution had triggered significant changes in the regulation of DNA in brown fat cells.

This included modifications in DNA methylation patterns and changes in how accessible certain genes were for being turned on or off—a process known as chromatin remodeling. These epigenetic changes affect how cells function by regulating gene activity without altering the genetic code itself.

Two enzymes were identified as main drivers of this process: HDAC9 and KDM2B. These enzymes are involved in modifying histones, the proteins around which DNA is wrapped. They were found to bind to specific regions of the DNA in brown fat cells of the mice exposed to PM2.5, leading to a reduction in key chemical tags, or methyl groups, that normally promote gene activity.

When these enzymes were experimentally suppressed, brown fat function improved, whereas increasing their activity led to further declines in metabolism.
The study shows that long-term exposure to fine air pollution can impair metabolic health by disrupting the normal function of brown fat. This occurs through complex changes in gene regulation controlled by epigenetic mechanisms.

Rengasamy Palanivel et al, Air pollution modulates brown adipose tissue function through epigenetic regulation by HDAC9 and KDM2B, JCI Insight (2025). DOI: 10.1172/jci.insight.187023

Part 2

Blood cancer: Scientists reprogram cancer cell death to trigger immune system

The aim of immunotherapy strategies is to leverage cells in the patient's own immune system to destroy tumor cells. Using a preclinical model, scientists successfully stimulated an effective anti-tumor immune response by reprogramming the death of malignant B cells. They demonstrated an effective triple-therapy approach for treating forms of blood cancer such as certain lymphomas and leukemias which affect B cells. The study was published on August 15 in the journal Science Advances. 

Immunotherapy strategies represent a major breakthrough in cancer treatment. They aim to harness the patient's immune system so that their own cells can recognize and specifically eliminate tumor cells. Immune cells can act like sentinels, scanning the body and identifying all residual tumor cells to reduce the risk of relapse. Various novel immunotherapy strategies are emerging, one of which makes use of a cell death mechanism known as necroptosis. Unlike apoptosis, which results in silent cell death, necroptosis releases warning signals that attract and stimulate immune cells so that they can kill any remaining tumor cells.

Scientists set out to explore the effectiveness of this necroptosis-based immunotherapy strategy on hematological malignancies. They began by observing that necroptosis cannot be easily induced in malignant B cells because of the absence of the MLKL protein.

To overcome this hurdle, the scientists combined administration of three drugs already used in clinical practice. They confirmed induction of necroptosis and observed a strong immune response leading to the complete elimination of leukemia in a preclinical model. 

The triple therapy they used forces cancer cells to die in a way that activates the immune system.

The results were observed in preclinical models using an innovative intravital imaging technique. The scientists were able to monitor the interactions between immune cells and cancer cells in real time for the different types of cell death induced.

"This novel immunotherapy strategy, successfully tested in preclinical models, turns tumor cells into triggers for the immune system, pointing to a potential therapeutic avenue for certain cancers, such as lymphomas or leukemias affecting B cell.

Ruby Alonso et al, Reprogramming RIPK3-induced cell death in malignant B cells promotes immune-mediated tumor control, Science Advances (2025). DOI: 10.1126/sciadv.adv0871

Menstrual cycle found to affect women's reaction time, but not as much as being active

Women performed best on cognitive tests during ovulation but physical activity level had a stronger influence on brain function, according to a new study .

The study, published in Sports Medicine–Open, explored how the different phases of the menstrual cycle and physical activity level affected performance on a range of cognitive tests designed to mimic mental processes used in team sports and everyday life, such as the accurate timing of movements, attention, and reaction time.

Researchers found that women had the fastest reaction times and made the fewest errors on the day of ovulation, when the ovaries release an egg ready to be fertilized (and when women's fertility is at its peak).

But while cognitive performance fluctuated across the menstrual cycle, much greater differences were observed between those who were active and those who weren't. Compared to active participants, inactive participants had reaction times on average around 70 milliseconds slower and made around three times as many impulsive errors, regardless of cycle phase.

The researchers say the findings are particularly relevant to women's sport, where slightly quicker reaction times of around 20 milliseconds may make the difference between sustaining or avoiding an injury like concussion. Previous research on elite athletes has suggested injuries are more common at certain points during the menstrual cycle, and the authors say that these changes in cognition might partially explain this occurrence.

However, while a difference of 20 milliseconds is likely to be inconsequential in everyday life, the much larger difference between active and inactive groups is more significant, where 70 milliseconds could determine whether we regain balance after tripping over an obstacle or not.

Menstrual cycle and athletic status interact to influence symptoms, mood, and cognition in females, Sports Medicine–Open (2025). DOI: 10.1186/s40798-025-00924-8

Easter Island's statues actually 'walked,' and physics backs it up

For years, researchers have puzzled over how the ancient people of Rapa Nui did the seemingly impossible and moved their iconic moai statues. Using a combination of physics, 3D modeling and on-the-ground experiments, a research team has confirmed that the statues actually walked—with a little rope and remarkably few people.

Studying nearly 1,000 moai statues, they found that the people of Rapa Nui likely used rope and "walked" the giant statues in a zig-zag motion along carefully designed roads. The paper is published in the Journal of Archaeological Science.

They 

 had previously demonstrated via experimental evidence that the large statues "walked" from their quarry to ceremonial platforms using an upright, rocking motion, challenging a theory that the statues were moved lying prone on wooden devices.

"Once you get it moving, it isn't hard at all—people are pulling with one arm. It conserves energy, and it moves really quickly," they say.

The hard part is getting it rocking in the first place. The question is, if it's really large, what would it take? Are the things that we saw experimentally consistent with what we would expect from a physics perspective?"

To explore how a larger statue might move, the team created high-resolution 3D models of the moai and identified distinctive design features—wide D-shaped bases and a forward lean—that would make them more likely to be moved in a rocking, zig-zagging motion.

Putting their theory to the test, the team built a 4.35-ton replica moai with the distinct "forward-lean" design. With just 18 people, the team was able to transport the moai 100 meters in just 40 minutes, a marked improvement over previous vertical transport attempts.

The physics makes sense, say the researchers, "What we saw experimentally actually works. And as it gets bigger, it still works. All the attributes that we see about moving gigantic ones only get more and more consistent the bigger and bigger they get, because it becomes the only way you could move it."

Adding to the support for this theory are the roads of Rapa Nui. Measuring 4.5 meters wide with a concave cross-section, the roads were ideal for stabilizing the statues as they moved forward.

 Carl P. Lipo et al, The walking moai hypothesis: Archaeological evidence, experimental validation, and response to critics, Journal of Archaeological Science (2025). DOI: 10.1016/j.jas.2025.106383

First device based on 'optical thermodynamics' can route light without switches

A team of researchers  has created a new breakthrough in photonics: the design of the first optical device that follows the emerging framework of optical thermodynamics.

The work, reported in Nature Photonics, introduces a fundamentally new way of routing light in nonlinear systems—meaning systems that do not require switches, external control, or digital addressing. Instead, light naturally finds its way through the device, guided by simple thermodynamic principles.

Universal routing is a familiar engineering concept. In mechanics, a manifold valve directs inputs to a chosen outlet. In digital electronics, a Wi-Fi router at home or an Ethernet switch in a data center directs information from many input channels to the correct output port, ensuring that each stream of data reaches its intended destination.

When it comes to light, the same problem is far more challenging, however. Conventional optical routers rely on complex arrays of switches and electronic control to toggle pathways. These approaches add technical difficulty, while limiting speed and performance.

The photonics team has now shown that there is another way. The idea can be likened to a marble maze that arranges itself.

Normally, you'd have to lift barriers and guide a marble step-by-step to make sure it reaches its destination—the right hole. In the team's device, however, the maze is built so that no matter where you drop the marble, it will roll on its own toward the right place—no guiding hands needed. And this is exactly how light behaves: it finds the correct path naturally, by following the principles of thermodynamics.

Party 1

Chaos tamed by thermodynamics : Nonlinear multimode optical systems are often dismissed as chaotic and unpredictable. Their intricate interplay of modes has made them among the hardest systems to simulate—let alone design for practical use. Yet, precisely because they are not constrained by the rules of linear optics, they harbor rich and unexplored physical phenomena.

Recognizing that light in these systems undergoes a process akin to reaching thermal equilibrium—similar to how gases reach equilibrium through molecular collisions—the researchers developed a comprehensive theory of "optical thermodynamics." This framework captures how light behaves in nonlinear lattices using analogs of familiar thermodynamic processes such as expansion, compression, and even phase transitions.
The team's demonstration in Nature Photonics marks the first device designed with this new theory. Rather than actively steering the signal, the system is engineered so that the light routes itself.

The principle is directly inspired by thermodynamics. Just as a gas undergoing what's known as a Joule-Thomson expansion redistributes its pressure and temperature before naturally reaching thermal equilibrium, light in the new device experiences a two-step process: first an optical analog of expansion, then thermal equilibrium. The result is a self-organized flow of photons into the designated output channel—without any need for external switches.

Hediyeh M. Dinani et al, Universal routing of light via optical thermodynamics, Nature Photonics (2025). DOI: 10.1038/s41566-025-01756-4

Part 2

Women Have Twice as Many Depression Genes as Men, Says  Study

Women are genetically at higher risk of clinical depression than men, Australian researchers found in a study published last week that could change how the disorder is treated.
Billed as one of the largest-ever studies of its kind, scientists pored through the DNA of almost 200,000 people with depression to pinpoint shared genetic "flags".

Women had almost twice as many of these genetic markers linked to depression as men, according to the study.
The genetic component to depression is larger in females compared to males. Around 13,000 genetic markers were linked with depression in women, the researchers found, compared with 7,000 markers in men.

Some of these genetic changes could alter biological pathways linked to metabolism or hormone production.

https://www.nature.com/articles/s41467-025-63236-1

Living in an unequal society impacts the structure of children's brains, study finds

The distribution of wealth between different people living in specific geographical regions has changed substantially over the past decades, with some segments of the population benefiting most from economic growth than others. In some parts of the United States, the United Kingdom and various European countries, the distribution of wealth has become increasingly uneven.

An uneven wealth distribution essentially means that there is significant disparity in the income and resources of the general population, with some people earning good salaries and others living in the same place struggling to meet their basic needs. This inequality is typically measured with a value ranging from 0 to 1, known as the Gini coefficient, where 0 represents perfect equality and 1 extreme inequality.

Researchers  recently carried out a study aimed at exploring the possible impact of living in a society where wealth is unevenly distributed on the brain's development in late childhood and pre-adolescence. Their findings, published in Nature Mental Health, suggest that living in places with a high income inequality is associated with differences in the structure of some brain regions, which could in turn predict the emergence of mental health disorders.

As part of their study, the researchers analyzed data from the ABCD dataset, which was collected from over 8,000 9–10-year-old children living across 17 U.S. states, along with Gini coefficients for these states. The data they analyzed included magnetic resonance imaging (MRI) scans showing the thickness, surface area and volume of specific regions of the children's brain, as well as functional magnetic resonance imaging (fMRI) scans showing the connections between 12 key regions in their brains.

In their analyses, the researchers controlled for other factors that might be influencing the development of the children's brains, such as their family's income, education, health care access and incarceration rates in their home state. In addition, they looked at the children's reported mental health 18 months after the brain scans were collected.

The results of the analyses  suggest that living in an unequal society is associated with a thinner cortex (i.e., the brain's outer layer), as well as significant differences in the surface area of various brain regions. In addition, the communication between some brain networks appeared to be altered in children living in places marked by higher income inequality.

The differences observed by the researchers could partly explain the relationship they found between state-wide inequality and children's mental health, particularly the emergence of disorders in children living in unequal environments.

 Divyangana Rakesh et al, Macroeconomic income inequality, brain structure and function, and mental health, Nature Mental Health (2025). DOI: 10.1038/s44220-025-00508-1.

DNA repair mechanisms help explain why naked mole-rats live a long life

Naked mole-rats are one of nature's most extraordinary creatures. These burrowing rodents can live for up to 37 years, around ten times longer than relatives of a similar size. But what is the secret to their extreme longevity? How are they able to delay the decay and decline that befalls other rodents? The answer, at least in part, is due to a switch in a common protein that boosts DNA repair, according to new research published in the journal Science.

One of the main causes of aging in all animals, including humans, is the accumulation of damaged DNA, our genetic instruction manual. When this damage is not fixed, it leads to defective cells, damaged proteins and eventually a breakdown in the body's functions.

To understand how the naked mole-rat is so resistant to DNA damage, a study focused on a common protein called cGAS (cyclic GMP-AMP synthase). In most mammals, cGAS interferes with DNA repair, but the researchers suspected it may have evolved a different function in the long-living rats.

Researchers compared the cGAS protein in naked mole-rats to that of humans and mice and identified four changes in amino acids (building blocks of cGAS) that flip the protein's function so that it enhances a cell's ability to repair damaged DNA.

To test this, the scientists inserted the mole-rat's unique cGAS into human and mouse cells in the lab. The result was a significant boost in the cells' ability to repair their DNA and a reduction in cellular aging. Then, they engineered fruit flies to produce naked mole-rat cGAS and found that they lived around ten days longer than a control group of fruit flies that couldn't produce cGAS. Finally, they used gene therapy to give the naked mole-rat cGAS to mice. These treated rodents were less frail, had less gray hair and there were fewer old, worn out cells in different organs than mice that didn't receive the gene.

"This alteration confers naked mole-rat cGAS with a greater capacity to stabilize the genome, counteract cellular senescence   and organ aging, and promote extended life span and health span," commented the researchers.

Yu Chen et al, A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging, Science (2025). DOI: 10.1126/science.adp5056

Atrial fibrillation after bypass found in nearly half of patients

Investigators  report a higher-than-expected one-year incidence of new-onset atrial fibrillation after coronary artery bypass grafting, paired with very low burden beyond 30 days.

Postoperative atrial fibrillation (AF) ranks among the most frequent early complications after cardiac surgery with reported incidence near 30%, tying into longer hospital stays, higher costs, discomfort, and observational links to thromboembolic stroke, heart failure, and recurrence.

North American guidelines state that 60 days of oral anticoagulation is reasonable with later reassessment, and European guidance advises that long-term anticoagulation should be considered in patients with new-onset AF after cardiac surgery.

Previous large cohort studies leaned on brief in-hospital telemetry and intermittent checks after discharge, leaving incidence, burden, and recurrence insufficiently characterized and prompting calls for long-term continuous monitoring.

In the study, "Long-Term Continuous Monitoring of New-Onset Atrial Fibrillation After Coronary Artery Bypass Grafting," published in JAMA, researchers conducted a prospective multicenter cohort study to test whether one-year AF incidence after coronary artery bypass grafting (CABG) exceeds prior literature and to assess AF burden.

Part 1

Enrollment involved 198 adults at two academic cardiac surgery centers in Germany, all undergoing first-time isolated CABG for three-vessel or left main disease, without prior arrhythmias, monitored for one year after implant of a device during surgery.

Patients were followed through continuous rhythm surveillance using an insertable cardiac monitor placed at skin closure. AF was defined as device-detected and adjudicated episodes lasting at least two minutes.

Within one year, 95 of 198 patients developed new-onset AF, yielding a cumulative incidence of 48% with a 95% CI of 41%–55%. Standard monitoring identified a 34% cumulative incidence with a 95% CI of 27%–41% and Gray's test P = .01 versus continuous monitoring. Sensitivity analyses using longer episode thresholds produced cumulative incidences of 46% at four minutes, 45% at six minutes, and 44% at 12 minutes.

Across the cohort with new-onset AF, median AF burden over the first year measured 0.07%, corresponding to 370 minutes. Early postoperative days carried the most arrhythmia time, with median burden of 3.65% on days 1–7, 0.04% on days 8–30, and 0% on days 31–365. A total of 2,053 episodes, accounting for 2,522 hours, were recorded, with a median episode length of six minutes and a median time-to-incident episode of 3.3 days. Asymptomatic presentations comprised 63% of episodes, and 67% were not captured by standard monitoring.

Among 95 patients with AF, 73 patients had incident episodes within seven days and 90 within 30 days, and 45% of accumulated AF time occurred within the first seven days and 77% within 30 days.

Recurrent AF later than 30 days appeared in 19 of 90 patients with incident episodes prior to 30 days, totaling 554 episodes with a median length of four minutes. Asymptomatic recurrences comprised 43% of these later episodes, and 3% were detected by standard monitoring.

The authors conclude that continuous monitoring uncovers substantially more AF than standard surveillance, while measured burden remains very low after 30 days.
Their findings question routine long-term oral anticoagulation after new-onset AF following CABG and support reassessment at 30 days when treatment is initiated.

Florian E. M. Herrmann et al, Long-Term Continuous Monitoring of New-Onset Atrial Fibrillation After Coronary Artery Bypass Grafting, JAMA (2025). DOI: 10.1001/jama.2025.14891

Gregory M. Marcus, Is There Really Something Different About Postoperative Atrial Fibrillation After Cardiac Surgery?, JAMA (2025). DOI: 10.1001/jama.2025.15275

Part 2

Rare Earth Elements: 17 Minerals More Valuable Than Gold in Today’s Tech World

Seafood unfairly singled out in microplastics debate, researchers say

Seafood has received disproportionate attention in media coverage about microplastics, despite evidence that fish and shellfish are not the main source of human exposure, according to a new scientific review.

Researchers found that more than 70% of scientific and media coverage on microplastics in food has focused on seafood, contributing to the public perception that eating fish is the biggest risk.

This misperception has real consequences, as some consumers report reducing consumption of seafood because of concerns over microplastics exposure, and thereby miss out on the health benefits of seafood consumption. The findings are reported in the journal Environmental Science & Technology Letters.

In reality, people are far more exposed to microplastics from indoor air and dust.

A previous study reported that the presence of microplastics in mussels collected from the environment was lower than the amount of microplastics that falls on a plate of mussels during dinner time in a typical household.

Seafood, including mussels and oysters and finfish like salmon and cod, may contribute 1–10 microplastic particles per day, which is consistent with other foods, like salt, honey and chicken.

Ingestion from bottled water is estimated at 10 to 100 particles per day, and exposure from indoor air accounts for considerably higher exposure—100 to 1,000 particles per day.

There is minimal evidence that they pose a health risk. The evidence we do have indicates that plastic particles readily pass through the digestive tract and exit the body.

While there are perceptions that toxic substances associated with plastic particles may pose health risks, evidence indicates concentrations are actually exceedingly low compared to other sources of exposure.

Theodore B. Henry et al, Examining Misconceptions about Plastic-Particle Exposure from Ingestion of Seafood and Risk to Human Health, Environmental Science & Technology Letters (2025). DOI: 10.1021/acs.estlett.5c00551

The migration period has started. Millions of birds are migrating now.

But birds face a variety of threats during migration—collisions with windows, communications towers and wind turbines; light pollution that disorients them; habitat loss or degradation in their migration stopover areas; human disturbance while feeding at stopover areas; predators; and storms.

Artificial light is one of the biggest dangers for birds traveling at night. It can confuse or attract them toward buildings, where they may crash into windows.

Birds collide with windows when they can't see them or, even worse, are attracted to them because of reflections of plants or the sky.This happens during the day, as well as at night during migration when lights disorient birds or if fog is causing them to fly low.

That's why people have an important role to play, say experts. The three most important things you can do for birds this time of year are to keep cats indoors, turn your lights off and use window mitigation.

Turn off unnecessary outdoor lighting at night or use motion sensors and timers so lights are only on when needed. If you must leave a light on, use warm-colored lights with shields that face downward.

Homeowners can also help reduce window collisions by: Placing bird feeders within three feet of windows or more than 30 feet away

Using window screens, UV tape or hanging cords to make glass visible

Closing blinds to limit reflections

Leaving fallen logs or stick piles in yards to give birds shelter as they stop to rest.

Enjoy these visitors as they pass through. But feed responsibly! Clean your feeders regularly, follow window guidance, and keep your cats indoors.

Nanoplastics detected in farm animal cells: Study warns of possible human consequences

Scientists at the Research Institute for Farm Animal Biology (FBN) in Dummerstorf and the University of Udine have detected the uptake of nanoplastics in farm animal cell cultures. The results provide evidence of potential risks to animal health, meat production and also human food safety.

Plastic bags, packaging, yogurt lids—items that are carelessly thrown away decompose over years into tiny plastic particles. They end up in soil, waterways and ultimately in our food chain. Although numerous studies have already shown that microplastics can harm marine animals, birds and insects, the effects of nanoplastics on livestock have hardly been researched to date.

Unlike microplastics (1 µm–5 mm), there are currently few adequate methods for detecting nanoplastics (< 1 µm) in humans and animals. However, researchers assume that these small particles can also accumulate in tissue.

In a new study, researchers have demonstrated the uptake of nanoplastic particles made of polystyrene into cultured cells from cattle and pigs. This absorption led to changes that could impair the cell function and health of the animals in the long term.

The study examined granulosa cells from cattle, which play an important role in reproduction, and myoblasts from pigs, which are used to form muscle tissue. Even low concentrations led to microscopically visible accumulations. These could impair the fertility of the animals and their products.
Farm animals are part of the human food chain. Direct health risks to consumers cannot be inferred at present. Nevertheless, the researchers urge for more detailed investigations into the long-term consequences of microplastics and nanoplastics.

Francesca Corte Pause et al, Exploring the influence of polystyrene-nanoplastics on two distinct in vitro systems in farm animals: A pilot study, Science of The Total Environment (2025). DOI: 10.1016/j.scitotenv.2025.179378

Do plastics have toxic effects on the heart? Higher exposure linked to changes in heart rhythms

We've all heard warnings about BPA—a chemical found in plastics and personal care products. Studies show that nearly millions of people around the world have detectable levels of BPA in their bodies. Now, new research has revealed this everyday exposure is tied to changes in the heart's electrical system.

Phenols are a wide variety of chemicals. The best-known example is BPA.

BPA can be found in water bottles, food can linings, cash register receipts, eyeglass lenses, even baby bottles and makeup. These are environmental phenols—chemicals in products we touch every day.

 So researchers studied 600 people. Urine tests and EKGs found higher exposure was linked to changes in heart rhythms.

The electrical conduction literally keeps us alive. If it gets altered in any way, you could die immediately, say cardiologists.

Healthy individuals should not be affected by this. But if you find a person that's genetically predisposed, that is older, these can lead to potential changes.

https://www.uc.edu/news/articles/2025/10/do-plastics-have-toxic-eff...

Rewriting the rules of genetics: Study reveals gene boundaries are dynamic, not fixed

Molecular biologists have long thought that the beginning of a gene launched the process of transcription—the process by which a segment of DNA is copied into RNA and then RNA helps make the proteins that cells need to function.

But a new study published in Science by researchers challenges that understanding, revealing that the beginning and end of genes are not fixed points, but move together—reshaping how cells build proteins and adapt through evolution.

This work rewrites a textbook idea: the beginning of a gene doesn't just launch transcription—it helps decide where it stops and what protein you ultimately make. 

For years, we taught that a gene's 'start' only decides where transcription begins. We now show the start also helps set the finish line—gene beginnings control gene endings, say the researchers  of this new work.

The discovery offers a promising new strategy for targeting cancer and neurological disorders, as well as developmental delays and aging. When gene transcription is disrupted or misregulated, protein production can become abnormal, potentially causing tumor growth.

The understanding that the beginning and ends of genes are connected could allow physicians to redirect gene expression—restoring healthy protein variants and suppressing harmful ones, without altering the underlying DNA sequence.

Misplacing a start or an end isn't a small mistake—it can flip a protein's domain structure and change its function, too. In cancer, that flip can mean turning a tumor suppressor into an oncogene. An oncogene is a mutated gene that has the potential to cause cancer by promoting uncontrolled cell growth and division.

These new findings show that controlling where a gene begins is a powerful way to control where it ends—and, ultimately, what a cell can do. 

Ezequiel Calvo-Roitberg et al, mRNA initiation and termination are spatially coordinated, Science (2025). DOI: 10.1126/science.ado8279

Flipping the switch on sperm motility offers new hope for male infertility

Infertility affects about one in six couples, and male factors account for roughly half of all cases—often because sperm don't swim well. Researchers have uncovered a key component of the "switch" that keeps the movement signal strong, offering a promising new avenue for both diagnosis and treatment. When this switch is absent, sperm slow down, and fertilization fails. By restoring that signal in the lab, the team rescued swimming and achieved healthy births in mice.

The study has been published in Proceedings of the National Academy of Sciences.

For sperm to successfully fertilize an egg, they must be able to swim, a process driven by their tail. This movement is activated by an essential signaling molecule called cyclic AMP (cAMP). While it was known that an enzyme named soluble adenylyl cyclase (sAC) produces cAMP inside sperm, the precise mechanism controlling this enzyme's stability and function remained largely a mystery.

The study focused on a protein with a previously unknown function, TMEM217, which is produced specifically in the testes. They engineered mice that could not produce TMEM217 and found that the males were completely infertile, with sperm that were almost entirely immotile. Further investigation revealed that TMEM217 partners with another protein, SLC9C1, to form a stable complex.

This complex is crucial for maintaining the presence of the sAC in mature sperm. Without TMEM217, SLC9C1 is lost and sAC is markedly reduced, causing cAMP levels to plummet and sperm motility to fail.  

In a significant breakthrough, the team took the immotile sperm from these mice and treated them with a cAMP analog—a molecule that mimics cAMP. This treatment successfully restored the sperm's movement and enabled them to fertilize eggs in vitro, leading to the birth of healthy pups.

The study has revealed a fundamental "switch" in sperm, providing a deeper understanding of sperm motility regulation. The discovery of the TMEM217-SLC9C1-sAC axis offers a new target for diagnosing unexplained cases of male infertility.

Formation of a complex between TMEM217 and the sodium-proton exchanger SLC9C1 is crucial for mouse sperm motility and male fertility, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2516573122

New lab-grown human embryo model produces blood cells

Scientists have used human stem cells to create three-dimensional embryo-like structures that replicate certain aspects of very early human development—including the production of blood stem cells. The findings are published in the journal Cell Reports.

Human blood stem cells, also known as hematopoietic stem cells, are immature cells that can develop into any type of blood cell, including red blood cells that carry oxygen and various types of white blood cells crucial to the immune system.

The embryo-like structures, which the scientists have named "hematoids," are self-organizing and start producing blood after around two weeks of development in the lab—mimicking the development process in human embryos.

The structures differ from real human embryos in many ways, and cannot develop into them because they lack several embryonic tissues, as well as the supporting yolk sac and placenta needed for further development.

Hematoids hold exciting potential for a better understanding of blood formation during early human development, simulating blood disorders like leukemia, and for producing long-lasting blood stem cells for transplants.

The human stem cells used to derive hematoids can be created from any cell in the body. This means the approach also holds great potential for personalized medicine in the future, by allowing the production of blood that is fully compatible with a patient's own body.

A post-implantation model of human embryo development includes a definitive hematopoietic niche, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116373. www.cell.com/cell-reports/full … 2211-1247(25)01144-1

A neural basis for flocking

When animals move together in flocks, herds, or schools, neural dynamics in their brain become synchronized through shared ways of representing space, a new study by researchers  suggests. The findings challenge the conventional view of how collective motion arises in nature.

Flocking animals, such as hundreds of birds sweeping across the sky in unison, are a mesmerizing sight. But how does their collective motion—seen in many species, from swarming locusts to schooling fish and flocking birds—arise?

Researchers have developed a novel theoretical framework that integrates neurobiological principles to upend long-held assumptions about how flocking behavior emerges in nature.

In a recent article published in Nature Communications they demonstrate that flocking does not require individuals to rely on rigid behavioral rules, as is typically assumed. Instead, it can arise naturally from a simple and widespread neural architecture found across the animal kingdom: the ring attractor network.

In the new model, flocking arises because neural activity in each animal becomes linked through perception: Every individual processes its surroundings using a ring attractor—a circular network of neurons that tracks the direction toward perceived objects in space. This way, the animal can maintain bearings toward others relative to stable features in the environment. The researchers found that when many such individuals interact, their neural dynamics synchronize, giving rise to spontaneous alignment and collective movement.

This means that coordinated motion can emerge directly from navigational processes in the brain, challenging decades of theory.

The new framework shows that collective motion emerges when individuals represent the directions of others relative to stable features in their surroundings—a world-centered, or allocentric, perspective. This mechanism underlies what the authors describe as "allocentric flocking."

Mohammad Salahshour et al, Allocentric flocking, Nature Communications (2025). DOI: 10.1038/s41467-025-64676-5