AI-generated voices now indistinguishable from real human voices

Many people still think of AI-generated speech as sounding "fake" or unconvincing and easily told apart from human voices. But new research shows that AI voice technology has now reached a stage where it can create "voice clones" or deepfakes which sound just as realistic as human recordings.

The study compared real human voices with two different types of synthetic voices, generated using state-of-the-art AI voice synthesis tools. Some were "cloned" from voice recordings of real humans, intended to mimic them, and others were generated from a large voice model and did not have a specific human counterpart.

Participants were asked to evaluate which voices sounded most realistic, and which sounded most dominant or trustworthy. Researchers also looked at whether AI-generated voices had become "hyperreal," given that some studies have shown that AI-generated images of faces are now judged to be human more often than images of real human faces.

While the study did not find a "hyperrealism effect" from the AI voices, it did find that voice clones can sound as real as human voices, making it difficult for listeners to distinguish between them. Both types of AI-generated voices were evaluated as more dominant than human voices, and some were also perceived as more trustworthy.

Voice clones sound realistic but not (yet) hyperrealistic, PLOS One (2025). DOI: 10.1371/journal.pone/0332692

A new look at how the brain works reveals that wiring isn't everything

How a brain's anatomical structure relates to its function is one of the most important questions in neuroscience. It explores how physical components, such as neurons and their connections, give rise to complex behaviors and thoughts. A recent study of the brain of the tiny worm C. elegans provides a surprising answer: Structure alone doesn't explain how the brain works.

C. elegans is often used in neuroscience research because, unlike the incredibly complex human brain, which has billions of connections, the worm has a very simple nervous system with only 302 neurons. A complete, detailed map of every single one of its connections, or brain wiring diagram (connectome), was mapped several years ago, making it ideal for study.

In this research, scientists compared the worm's physical wiring in the brain to its signaling network, how the signals travel from one neuron to another. First, they used an electron microscope to get a detailed map of the physical connections between its nerve cells. Then, they activated individual neurons with light to create a signaling network and used a technique called calcium imaging to observe which other neurons responded to this stimulation.

Finally, they used computer programs to compare the physical wiring map and the signal flow map, identifying any differences and areas of overlap.

The team discovered that the brain's functional organization differs from its anatomical structure. An analogy is that the brain's structure is like a city map showing every street. However, the function is more akin to traffic flow, with jams, detours and shortcuts that are not visible on the map. In other words, brain activity does not always follow the predictable pathways of its physical wiring.

Sophie Dvali et al, Diverging Network Architecture of the C. elegans Connectome and Signaling Network, PRX Life (2025). DOI: 10.1103/6wgv-b9m6

Lab-grown kidneys yield urine
Researchers have created the most sophisticated kidney organoid to date, offering a real shot at growing transplantable kidneys from stem cells. These mini kidneys were capable of making urine when transplanted into mice. “You wouldn’t mistake it for a real kidney,” says experimental anatomist Jamie Davies. “But it is trying to do the right things.” Plumbing — encouraging the organoid to develop blood vessels and the duct that carries urine to the bladder — is the major hold-up. The researchers estimate a transplantable kidney will be ready for animal testing in less than five years.

https://www.sciencedirect.com/science/article/abs/pii/S193459092500...

https://www.science.org/content/article/scientists-make-most-authen...

Scientists discover that cell nucleus is actually less dense than surrounding cytoplasm

Just as life pulsates in big vibrant cities, it also prospers in crowded environments inside cells. The interior of cells is densely packed with biomolecules like proteins and nucleic acids. How is all this material distributed within a cell and what regulates its distribution?

In a study published in Nature Communications, researchers measure subcellular densities across a wide range of organisms. Their aim is to better understand biomolecular processes ranging from yeast cells  to human cells.

Conventional scientific textbooks describe the cell nucleus as a compartment packed with an impressive amount of DNA wrapped around histone proteins.

Now, an international team of researchers has discovered that—contrary to expectations—the nucleus is less dense than the surrounding cytoplasm.

Despite their rich biomolecular composition, nuclei contain less dry mass than the same volume of the surrounding cytoplasm.

How can density be measured in microscopic objects such as individual cell compartments? Scientists use light for this purpose. Not only does light allow cells to be examined, it also enables them to be manipulated. Light can exert forces, enabling laser beams to "pull" on cells and measure their mechanical properties using an "optical stretcher."

The researchers developed an optical setup which allowed them to obtain three-dimensional density distributions inside cells at high resolution by combining optical diffraction tomography and confocal fluorescence microscopy.

While NC density ratios are maintained from yeast to human cells, we do start seeing deviations in disease. During stressed cellular states such as aging, the so-called senescence, cell nuclei become denser than the cytoplasm. Thus, the study points to the fundamental importance of density as a variable that determines healthy cellular processes, the researchers note in their paper.

 Abin Biswas et al, Conserved nucleocytoplasmic density homeostasis drives cellular organization across eukaryotes, Nature Communications (2025). DOI: 10.1038/s41467-025-62605-0

Camouflage or caution? How anti-predator strategies have evolved

Predators and the environment determine why some animals use camouflage to avoid being eaten, while others use bright colors to warn them off, new research reveals. Published recently  in the journal Science, the findings help explain the evolution and global distribution of the most common color strategies used by insects to avoid predators.

The global study took place across six continents and involved over 50 scientific collaborators.

Using the same experiment, researchers deployed more than 15,000 artificial prey with three different colors to investigate which strategy works best to deter predators: a classic warning pattern of orange and black, a dull brown that blends in, and an unusual bright blue and black.

The researchers found the answer to why some animals use camouflage over warning colors to deter predators turned out to be more complex than expected.

The findings showed there is no single best color strategy to deter predators, but that context is critical. The different characteristics of the predator and prey communities, as well as habitat in that part of the globe, heavily decide which strategy performs better in each place. This makes sense when we see animals employing so many varying camouflage and warning color strategies as defense systems all over the world.

Predators had the biggest influence on which color strategy was most successful for prey, the study revealed.

In environments where predators are competing intensely for food, they are more likely to risk attacking prey that might be dangerous or distasteful. Hence, the researchers saw that camouflage worked best in areas with lots of predation.

Whereas, in places where cryptic prey (insects who use camouflage) are abundant, hiding becomes less effective, as predators are better at looking for those types of animals.

The findings help scientists understand why some species, such as the cryptic bogong moth or the brightly colored harlequin bug, have evolved their strategies against predators.

 Iliana Medina et al, Global selection on insect antipredator coloration, Science (2025). DOI: 10.1126/science.adr7368. www.science.org/doi/10.1126/science.adr7368

Trees are dying at an alarming rate

The rise in tree mortality is troubling for local forest ecosystems. As a global phenomenon, however, it has a significant social impact that remains poorly understood.

We don't currently know whether climate change will lead to the death of 10% or 50% of all trees worldwide.

An international group of more than 100 forest researchers are reviewing almost 500,000 forest monitoring studies from 89 countries and five continents. The researchers found that the main cause of tree mortality is anthropogenic (human-induced) climate change and its consequences: heat, dry air and soil, forest fires, storms, and increased insect damage and plant diseases.  

In the article published in New Phytologist, the researchers aimed to identify methods, requirements and data gaps in monitoring tree mortality trends. 

Towards a global understanding of tree mortality, New Phytologist (2025). DOI: 10.1111/nph.20407

Squirrels bite when they feel threatened, cornered, or are aggressively seeking food. They can also bite inadvertently by mistaking a finger for a treat or startling when a hand is presented to them. While usually a defensive action or a form of play, squirrels lack the bite inhibition of domesticated animals, and their bites, though not typically malicious, can be deep and pose a risk of infection. 

Reasons for biting:

Self-defense: Like any wild animal, squirrels will bite to protect themselves if they feel endangered.
Aggression for food: Squirrels may become aggressive if they are accustomed to being fed by humans and approach to get a meal, according to Critter Control.
Accidental bites: Squirrels don't have the same depth perception as humans and can mistakenly bite a finger when trying to take a treat.
Nesting: A mother squirrel in a nesting area, such as an attic, may bite if she feels cornered or threatened.
Play behaviour: Squirrels also "play bite" to practice skills they will use as adults, similar to how siblings interact.
Risks of a squirrel bite:
Infection: Because squirrels are wild rodents, a bite can lead to an infection.
Diseases: Though rabies is rare in squirrels, they can carry other diseases, such as the plague, which is transmitted by fleas.
What to do if a squirrel bites:
Wash the wound: Immediately wash the wound thoroughly with soap and water to reduce the risk of infection.
Seek medical attention: Consult a healthcare professional to determine if a tetanus shot is needed and to monitor for any signs of infection.

Mucus contains molecules that block Salmonella infection, study reveals

Mucus is more than just a sticky substance: It contains a wealth of powerful molecules called mucins that help to tame microbes and prevent infection. In a new study,  researchers have identified mucins that defend against Salmonella and other bacteria that cause diarrhea.

The researchers now hope to mimic this defense system to create synthetic mucins that could help prevent or treat illness in soldiers or other people at risk of exposure to Salmonella. It could also help prevent "traveler's diarrhea," a gastrointestinal infection caused by consuming contaminated food or water.

Mucins are bottlebrush-shaped polymers made of complex sugar molecules known as glycans, which are tethered to a peptide backbone. In this study, the researchers discovered that a mucin called MUC2 turns off genes that Salmonella uses to enter and infect host cells.

Mucus lines much of the body, providing a physical barrier to infection, but that's not all it does.

Researchers identified mucins that can help to disarm Vibrio cholerae, as well as Pseudomonas aeruginosa, which can infect the lungs and other organs, and the yeast Candida albicans.

The researchers found in the new study that when they exposed Salmonella to a mucin called MUC2, which is found in the intestines, the bacteria stopped producing the proteins encoded by SPI-1, and they were no longer able to infect cells.

Further studies revealed that MUC2 achieves this by turning off a regulatory bacterial protein known as HilD. When this protein is blocked by mucins, it can no longer activate the T3SS genes.

Using computational simulations, the researchers showed that certain monosaccharides found in glycans, including GlcNAc and GalNAc, can attach to a specific binding site of the HilD protein. However, their studies showed that these monosaccharides can't turn off HilD on their own—the shutoff only occurs when the glycans are tethered to the peptide backbone of the mucin.

The researchers also discovered that a similar mucin called MUC5AC, which is found in the stomach, can block HilD. And, both MUC2 and MUC5AC can turn off virulence genes in other foodborne pathogens that also use HilD as a gene regulator.

The researchers now plan to explore ways to use synthetic versions of these mucins to help boost the body's natural defenses and protect the GI tract from Salmonella and other infections.

Kelsey M. Wheeler et al, Mucus-derived glycans are inhibitory signals for Salmonella Typhimurium SPI-1-mediated invasion, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116304

Million-year-old skull could change human evolution timeline

A digital reconstruction of a million-year-old skull suggests humans may have diverged from our ancient ancestors 400,000 years earlier than thought and in Asia not Africa, a study said this week.

The findings are based on a reconstruction of a crushed skull discovered in China in 1990, and have the potential to resolve the longstanding "Muddle in the Middle" of human evolution, researchers said.

But experts not involved in the work cautioned that the findings were likely to be disputed, and pointed to ongoing uncertainties in the timeline of human evolution.

The skull, labeled Yunxian 2, was previously thought to belong to a human forerunner called Homo erectus.

But modern reconstruction technologies revealed features closer to species previously thought to have existed only later in human evolution, including the recently discovered Homo longi and our own Homo sapiens.

It suggests that by one million years ago, our ancestors had already split into distinct groups, pointing to a much earlier and more complex human evolutionary split than previously thought.

If the findings are correct, it suggests there could have been much earlier members of other early hominins, including Neanderthals and Homo sapiens, the study says.

It also "muddies the waters" on longstanding assumptions that early humans dispersed from Africa.

There's a big change potentially happening here, where east Asia is now playing a very key role in hominin evolution.

The research, published in the journal Science, used advanced CT scanning, structure light imaging and virtual reconstruction techniques to model a complete Yunxian 2.

The scientists relied in part on another similar skull to shape their model, and then compared it to over 100 other specimens.

The resulting model "shows a distinctive combination of traits," the study said, some of them similar to Homo erectus, including a projecting lower face.

But other aspects, including its apparently larger brain capacity, are closer to Homo longi and Homo sapiens, the researchers said.

"Yunxian 2 may help us resolve what's been called the 'Muddle in the Middle,' the confusing array of human fossils from between 1 million and 300,000 years ago.

The findings are only the latest in a string of recent research that has complicated what we thought we know about our origins.

Xiaobo Feng et al, The phylogenetic position of the Yunxian cranium elucidates the origin of Homo longiand the Denisovans, Science (2025). DOI: 10.1126/science.ado9202

Origins of the 'Ostrich Effect': Researchers pinpoint the age we start avoiding information—even when it's helpful

In a world of information overload, it can feel soothing to stick your head in the sand.

According to psychologists, avoiding information when it's uncomfortable is a common adult behavior, often referred to as the "Ostrich Effect."

But how do we become an ostrich? Children are notorious for seeking out information, often in the form of endless questions. So when do we sprout feathers and decide that, actually, the number of calories in a slice of cake is none of our business?

This behavioral origin point was exactly what researchers wanted to pin down.

In a study published in Psychological Science, a research team discovered that as children aged, the tendency to avoid information grew stronger.

Though 5- and 6-year-olds still actively sought information, 7- to 10-year-olds were much more likely to strategically avoid learning something if it elicited a negative emotion.

Why is it that children are these super curious people, but then we somehow end up as these information avoiders as adults?

In their initial experiment, the researchers looked at five reasons why we might willfully choose to remain ignorant:
To avoid negative emotions like anxiety or disappointment
To avoid negative information about our own likability or competence
To avoid challenges to our beliefs
To protect our preferences
To act in our own self-interest (perhaps while trying to appear not self-interested)
Part 1

Researchers then adapted these into five scenarios for children to see if they could elicit information avoidance. For example, each child was asked to imagine their favorite and least favorite candy. They were then asked if they wanted to watch a video about why eating that candy was bad for their teeth.

They found that, whereas younger children really wanted to seek information, older children started to exhibit these avoidance tendencies. For example, they didn't want to know why their favorite candy was bad for them, but they were totally fine learning why their least favorite candy is bad for them.
This finding held for all motivations except for competency. Children of all ages were not afraid to learn if they'd done badly on a test, for example.

To avoid avoidance, she suggests thinking through why you might be avoiding something—possibly prioritizing short-term comfort over long-term benefits. Researchers posit that it could help to reframe uncomfortable information as useful and valuable.

Research suggests that intervening while children are still young could keep them from falling into avoidance traps and have compounding benefits.
Humans have this propensity to want to resolve uncertainty, but when the resolution is threatening, people might flip to avoidance instead.
If all else fails, she advises, mimic what children do best: Follow your curiosity.

Radhika Santhanagopalan et al, Becoming an Ostrich: The Development of Information Avoidance, Psychological Science (2025). DOI: 10.1177/09567976251344551

Part 2

Bacterial endotoxins are high-potency, low-mass drivers of PM₂.₅ toxicity, sampling study reveals

Endotoxin, a toxic chemical found in bacteria, makes up only 0.0001% of PM_2.5 fine particles but packs a serious punch when it comes to its bioactivity.

According to a study by researchers endotoxin drives 0.1–17% of the inflammatory responses triggered by these airborne particles, with its toxicity contribution being three to five orders of magnitude higher than its mass contribution.

Air pollution is now the world's leading environmental health threat, linked to more than three million premature deaths every year. One of the key culprits is PM2.5, which refers to airborne particles smaller than 2.5 micrometers, small enough to slip deep into the lungs and even seep into the bloodstream.

Scientists have long been focusing on PM2.5 because evidence consistently links it to respiratory illnesses, such as asthma, chronic obstructive pulmonary disease, and airway inflammation. Studies suggest that the damage caused by PM2.5 could be due to oxidative stress and the triggering of immune responses in the lungs following exposure.

PM2.5 is a complex atmospheric cocktail of natural and anthropogenic particles containing biological, inorganic, and organic constituents. For decades, researchers have extensively studied the impact of chemicals—including transition metals, polycyclic aromatic hydrocarbons, and industrial smoke—produced by human activities. These components, however, contribute to less than half of the respiratory damage inflicted by PM2.5, leaving roughly 60% of its impact still unexplained.

Researchers of this study conducted daily 24-hour PM_2.5 sampling for a year across an urban and coastal area of Hong Kong. To assess inflammatory responses, the researchers exposed human bronchial epithelial cells to PM_2.5 and measured the release of interleukin-8 (IL-8)—a small protein, called a cytokine, that is released by the immune system— as a marker of inflammation.

Part 1

Endotoxin concentrations were measured using the Limulus Amebocyte Lysate (LAL) assay, then researchers used DNA sequencing and source tracking to identify the Gram-negative bacteria they came from. Finally, they applied mixture-toxicity modeling to estimate how much these endotoxins contributed to the overall harmful effects of PM2.5 exposure.

They found that despite making up only a minuscule fraction of the total PM2.5 mixture, it drove about 0.1 to 17% of the IL-8 release triggered by PM2.5.

Among all reported PM2.5 components, endotoxin demonstrated the highest toxicity-to-mass contribution ratio, 10,000:1 to 100,000:1, establishing its extreme biological potency. These findings show that less is indeed more.

The researchers note that this study brings to light the importance of identifying highly toxic components present in low concentrations and tracing their sources. Pinpointing these toxicity drivers can help us design cost-effective strategies in which even modest reductions in PM2.5 mass could yield substantial decreases in overall toxicity.

 Jinyan Yu et al, Disproportionately Higher Contribution of Endotoxin to PM_2.5 Bioactivity than Its Mass Share Highlights the Need to Identify Low-Concentration, High-Potency Components, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c07255

Part 2

Mamba snake bites worsen after antivenom

Mamba (Dendroaspis species) snake bites are a significant threat in sub-Saharan Africa, accounting for 30,000 deaths annually.

A breakthrough study has discovered a hidden dangerous feature of the black mamba, one of the most venomous snakes in the world.

The study revealed the venoms of three species of mamba were far more neurologically complex than previously thought, explaining why antivenoms were sometimes ineffective. This research was published in Toxins.

The black mamba, western green mamba and Jamesons mamba snakes aren't just using one form of chemical weapon, they're launching a coordinated attack at two different points in the nervous system.

If you're bitten by 3 out of 4 mamba species, you will experience flaccid or limp paralysis caused by postsynaptic neurotoxicity.

Current antivenoms can treat the flaccid paralysis but this study found the venoms of these three species are then able to attack another part of the nervous system causing spastic paralysis by presynaptic toxicity.

Researchers previously thought the fourth species of mamba, the eastern green mamba, was the only one capable of causing spastic paralysis.

This finding resolves a long-standing clinical mystery of why some patients bitten by mambas seem to initially improve with antivenom and regain muscle tone and movement only to start having painful, uncontrolled spasms.

The venom first blocks nerve signals from reaching the muscles, but after the antivenom is administered, it then overstimulates the muscles.

It's like treating one disease and suddenly revealing another.

Researchers  also found the venom function of the mambas was different depending on their geographic location, particularly within populations of the black mamba from Kenya and South Africa.

This further complicates treatment strategies across regions because the antivenoms are not developed to counteract the intricacies of the different venoms.

By identifying the limitations of current antivenoms and understanding the full range of venom activity, we can now directly inform evidence-based snakebite care.

 Lee Jones et al, Neurotoxic Sleight of Fang: Differential Antivenom Efficacy Against Mamba (Dendroaspis spp.) Venom Spastic-Paralysis Presynaptic/Synaptic vs. Flaccid-Paralysis Postsynaptic Effects, Toxins (2025). DOI: 10.3390/toxins17100481

Scientists read mice's 'thoughts' from their faces

It's easy to read emotions on people's faces—each one has its clear, unmistakable signature. But what about thoughts? A study published in Nature Neuroscience shows that mice's problem-solving strategies can be deciphered from subtle facial movements.

According to the authors, this is a proof of concept that the contents of the mind can be read out from video recordings, potentially offering powerful new research and diagnostic tools.

Scientists found that they can get as much information about what the mouse was 'thinking' as they could from recording the activity of dozens of neurons.

Having such easy access to the hidden contents of the mind could provide an important boost to brain research. However, it also highlights a need to start thinking about regulations to protect our mental privacy.

 Facial expressions in mice reveal latent cognitive variables and their neural correlates, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02071-5.

Stem cells from fat tissue may help prevent kidney dialysis access failure

To undergo kidney dialysis, doctors must first surgically create an access route—an arteriovenous fistula—usually in an arm, a conduit that will accommodate hemodialysis treatments. It is a routine outpatient procedure performed for years worldwide.

But it is a procedure beset by problems.

An arteriovenous fistula must first "mature," a process in which the newly established connection between an artery and a vein becomes large enough to support the turbulent flow of blood in hemodialysis. For many patients, this artificially created channel tends to narrow, leaving it useless as a conduit.

Researchers investigating a possible way to prevent problematic narrowing—a condition called stenosis—with a procedure that relies on the use of stem cells.

The study, researchers asserted, is a crucial step toward improving a necessary treatment for patients with kidney failure by tapping into a population of cells that are essentially blank slates. 

 The investigation is reported in the journal Science Translational Medicine.

The phase 1 randomized trial involved patients undergoing an arteriovenous fistula (AVF) placement in an arm. Some of the patients in the small trial also received autologous adipose-derived mesenchymal stem cells. The cells were delivered at the time of the AVF procedure.

The stem cells were placed along the AVF starting at the distal artery, one centimeter upstream to the anastomosis [the surgical connection between adjacent blood vessels] and extending to the first four centimeters of the vein just distal to the anastomosis by dripping them onto the adventitia of the vessels slowly over five minutes.

The adventitia is the outermost layer of a blood vessel.

Mesenchymal stem cells are a form of somatic, or adult stem cells, which can be found in a variety of tissues throughout the body, including adipose (fat) tissue, which is an abundant source.

The stem cells are aimed at improving AVF function by preventing vascular narrowing. The cells were also a site-specific treatment for another problem tied to arteriovenous fistulas: inflammation, a hallmark of AVFs. Fortunately, anti-inflammatory activity is a function of mesenchymal stem cells.

Side-by-side images in the study show the vascular opening to be wide and capable of handling the turbulence of hemodialysis among patients who received mesenchymal stem cells. Patients who did not receive the stem cell treatment suffered vascular narrowing.

The research  team sees promise in their unique approach, which is producing positive results at a critical time.

The team's phase 1 clinical trial involved 21 patients who received arteriovenous fistulas in the arm; 11 of the 21 patients also received mesenchymal stem cells derived from their own fat tissue. After 42 months, fistulas had matured faster in patients who received stem cells. Additional study and approval by the U.S. Food and Drug Administration are required before the treatment can become available.

Sreenivasulu Kilari, et al Periadventitial delivery of mesenchymal stem cells improves vascular remodeling and maturation in arteriovenous fistulas, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adp7723

Scientists finally prove that a quantum computer can unconditionally outperform classical computers

A quantum computer has demonstrated that it can solve a problem more efficiently than a conventional computer. This achievement comes from being able to unlock a vast memory resource that classical computing cannot match.

Instead of using classical bits that can only be 0 or 1, quantum machines use qubits, which can exist in multiple states and store exponentially more information than their traditional counterparts. However, proving that a quantum computer can access this memory advantage in the real world has been a challenge for two main reasons.

First, any successful demonstration has to be feasible on realistic quantum hardware, and second, there must be unconditional mathematical proof that no future classical algorithm could achieve the same performance.

In a study published on the arXiv preprint server, a  research team  reports how they achieved this feat of quantum supremacy.
They constructed a complicated mathematical task designed to test this memory advantage. Their experiment was like a game between two parts of the quantum system referred to as Alice and Bob. Alice's task was to create a quantum state and send it in a message to Bob, who had to measure it to figure out what it was. The goal was to build a process so accurate that Bob could predict the state before Alice finished preparing the message.

The researchers optimized this process over 10,000 independent trials, and their analysis revealed that a classical computer would need at least 62 bits of memory to complete the task with the same success rate. The quantum device performed it using only 12 qubits.

The result provides the most direct evidence yet that currently existing quantum processors can generate and manipulate entangled states of sufficient complexity to access the exponentiality of Hilbert space (the vast memory resource of a quantum computer)," wrote the researchers in their paper.

This form of quantum advantage—which we call quantum information supremacy—represents a new benchmark in quantum computing, one that does not rely on unproven conjectures.

 William Kretschmer et al, Demonstrating an unconditional separation between quantum and classical information resources, arXiv (2025). DOI: 10.48550/arxiv.2509.07255

The Red Sea went completely dry before being flooded by the Indian Ocean over 6 million years ago

Scientists have provided conclusive evidence that the Red Sea completely dried out about 6.2 million years ago, before being suddenly refilled by a catastrophic flood from the Indian Ocean. The findings put a definitive time on a dramatic event that changed the Red Sea.

Using seismic imaging, microfossil evidence, and geochemical dating techniques, the  researchers showed that a massive change happened in about 100,000 years—a blink of an eye for a major geological event. The Red Sea went from connecting with the Mediterranean Sea to an empty, salt-filled basin. Then, a massive flood burst through volcanic barriers to open the Bab el-Mandab strait and reconnect the Red Sea with the world's oceans.

The findings show that the Red Sea basin records one of the most extreme environmental events on Earth, when it dried out completely and was then suddenly reflooded about 6.2 million years ago.

The Red Sea was initially connected from the north to the Mediterranean through a shallow sill. This connection was severed, drying the Red Sea into a barren salt desert. In the south of the Red Sea, near the Hanish Islands, a volcanic ridge separated the sea from the Indian Ocean.

But around 6.2 million years ago, seawater from the Indian Ocean surged across this barrier in a catastrophic flood. The torrent carved a 320-kilometer-long submarine canyon that is still visible today on the seafloor. The flood rapidly refilled the basin, drowning the salt flats and restoring normal marine conditions in less than 100,000 years. This event happened nearly a million years before the Mediterranean was refilled by the famous Zanclean flood, giving the Red Sea a unique story of rebirth.

Tihana Pensa et al, Desiccation of the Red Sea basin at the start of the Messinian salinity crisis was followed by major erosion and reflooding from the Indian Ocean, Communications Earth & Environment (2025). DOI: 10.1038/s43247-025-02642-1

Forensic test recovers fingerprints from fired ammunition casings despite intense heat

A pioneering new test that can recover fingerprints from ammunition casing, once thought nearly impossible, has been developed by  scientists.

The researchers have developed a unique electrochemical method which can visualize fingerprints on brass casings, even after they have been exposed to the high temperature conditions experienced during gunfire. The study is published in the journal Forensic Chemistry.

For decades, investigators have struggled to recover fingerprints from weapons because any biological trace is usually destroyed by the high temperatures, friction and gas released after a gun is fired. As a result, criminals often abandon their weapons or casings at crime scenes, confident that they leave no fingerprint evidence behind.

Traditionally, the intense heat of firing destroys any biological residue. However,  the technique has been able to reveal fingerprint ridges that would otherwise remain imperceptible.

The team found they could coat brass casings with a thin layer of specialized materials to make hidden fingerprint ridges visible. Unlike existing methods that need dangerous chemicals or high-powered equipment, the new process uses readily available non-toxic polymers and minimal amounts of energy to quickly reveal prints from seemingly blank surfaces.

It works by placing the brass casing of interest in an electrochemical cell containing specific chemical substances. When a small voltage is applied, chemicals in the solution are attracted to the surface, coating the spaces between fingerprint ridges and creating a clear, high contrast image of the print. The fingerprint appears within seconds as if by magic!

Tests showed that this technique also worked on samples aged up to 16 months, demonstrating remarkable durability.

The research has significant implications for criminal investigations, where the current assumption is that firing a gun eliminates fingerprint residues on casings.

Colm McKeever et al, Electrodeposition of redox materials with potential for enhanced visualisation of latent finger-marks on brass substrates and ammunition casings., Forensic Chemistry (2025). DOI: 10.1016/j.forc.2025.100663

Population bottlenecks cause decline of mammals' immunity, researchers find

Population bottlenecks caused by stark population loss due to illness or habitat destruction caused mammals' disease immunity to decline, according to a new study led by computational biologists .

 The finding comes from the first comparative study of genomic sequences—roadmaps of DNA instructions responsible for encoding how the body works—encoding immunity in 46 mammals.

The study, published in Molecular Biology and Evolution, is the first step for scientists analyzing regions of mammalian DNA that were previously inaccessible without modern biotechnology computational tools.

Genes influence how our body works: Humans and animals have genetics predisposed to certain diseases based on DNA. Although the same basic building blocks make up DNA across the 46 mammals assessed, the genomic sequences diverged wildly. So, even though we might have a similar set of genes, they are different based on variations in the DNA architecture.

In the immune system,  things are complicated further by something known as adaptive immunity. As opposed to the non-discriminatory defense the immune system deploys at the first hint of an infection, adaptive immunity refers to the parts of the immune system that study the specifics of a pathogen and design antibodies precisely targeted for it, should it invade again.

Antibodies are produced from highly variable "template" genes encoded in the genome, and this variability enables versatile immune responses through the generation of antibodies against diverse targets.

The question is, how did this adaptive immunity evolve?

To answer this Q, researchers  analyzed five types of gene clusters that control various aspects of immune system production—specifically the building of antibodies and the receptors on another immune cell type known as the T-cell—across 46 mammals to better understand how genetic variation could affect immune function.

Researchers scanned, aligned and compared publicly available DNA sequences of 46 mammals of 13 taxonomic orders, such as primates, rodents, bats, carnivores and marsupials, to draw conclusions about how their immune systems evolved.

Researchers found that a decline in adaptive immunity, and possible vulnerability to certain diseases among mammals as a result, was likely caused by genetic bottlenecks: a stark decrease in population over certain periods in history due to factors such as habitat loss or disease.

 Bottlenecks happened during medieval times when humanity was devastated by various diseases like the Black Plague, or when animals suffered widespread habitat loss due to forest fire.

Species with these past population bottlenecks include felines, aquatic mammals, seals, some primates and ruminants, which are mammals that adapted a special stomach for digesting tough plants.

 Genetic bottlenecks result in limited gene pool diversity for these animals,  the researchers  explained, which led to possible declining of adaptive immunity.

Mariia Pospelova et al, Comparative Analysis of Mammalian Adaptive Immune Loci Revealed Spectacular Divergence and Common Genetic Patterns, Molecular Biology and Evolution (2025). DOI: 10.1093/molbev/msaf152

 

 

Dads influence embryo growth via molecular signatures, research reveals

Over the past few decades, growing evidence has challenged the belief that inheritance is governed solely by DNA sequences. Scientists now recognize the crucial role of epigenetic inheritance—the transmission of biological traits via chemical modifications to DNA and its associated proteins. These modifications do not alter the genetic code itself but influence how genes are switched on or off, often in response to environmental factors such as stress, diet, or drug exposure.

While the concept of maternal epigenetic inheritance is relatively intuitive—given the direct biological connection between mother and embryo during gestation—recent research shows that fathers, too, can transmit environmentally induced epigenetic changes to their offspring. However, the prevalence of epigenetic inheritance—and the mechanisms behind it—remains unclear.

In a recent study, researchers demonstrated that disrupting the gut microbiome of male mice increases disease risk in their future offspring. On the other hand, some have focused on mechanisms that regulate embryonic development in response to changes in paternal diet.
A collaborative study between the  groups, now published in The EMBO Journal, examined how specific paternal environments affect early embryonic development in a systematic manner and under tightly controlled genetic and environmental conditions in mice.

To induce environmental perturbations, prospective fathers were exposed to either non-absorbable antibiotics (disrupting the gut microbiota) or to a low-protein, high-sugar diet. To minimize experimental variability, the analyses were performed on embryos resulting from in vitro fertilization (IVF). Embryos were collected approximately four days after fertilization (blastocyst stage) and individually analyzed to measure differences in gene expression compared to controls (blastocysts that resulted from fathers without any treatment).
The results were striking. Both environmental perturbations led to significant changes in embryonic gene expression. Disruption of the paternal gut microbiota reduced the expression of key genes involved in extra-embryonic tissue development, while changes in the diet were linked with a modest developmental delay.

To further investigate the influence of the genetic background, scientists repeated the experiments using a different mouse strain. The outcome differed, suggesting the importance of the genetic component in shaping how environmental exposures affect offspring.

Additionally, embryos derived from older fathers showed a stronger effect on gene expression, especially on genes involved in immune-related processes, indicating that paternal age is another important factor involved in epigenetic inheritance.

Mathilde Dura et al, Embryonic signatures of intergenerational epigenetic inheritance across paternal environments and genetic backgrounds, The EMBO Journal (2025). DOI: 10.1038/s44318-025-00556-4

Microlightning causes eerie lights of lore
Spontaneous flashes of ‘microlightning’ between bubbles of gas could explain will-o’-the-wisps — flickering lights that can appear on marshlands. Researchers blew tiny bubbles of methane and air into water, where smaller bubbles took on a negative charge and larger ones, a positive charge. As the charges equalized, they produced a small zap of electricity and a flash of light. This could explain why the ghostly-looking lights appear over methane-rich bogs.

https://www.pnas.org/doi/10.1073/pnas.2521255122

Microplastics reduce soil fertility and boost production of a potent greenhouse gas, study shows

More than 90% of plastic waste ends up in the soil, where it breaks down into microplastics that are invisible to the naked eye. Microplastic pollution of the soil poses a severe threat to soil health as it can harm essential microbial communities and reduce crop yields. The presence of these tiny plastics may also worsen climate change by boosting the production of greenhouse gases, according to a new study published in Environmental Science & Technology.

Most previous research focused on one plastic at a time and their effect on soil function and nutrient cycling, but microplastics do not tend to occur in isolation.

in the present study, the researchers went for the combined effect of various types of plastics on soil and key functions, such as the nitrogen cycle.

To quantify the problem, the team ran a microcosm experiment in the lab, using soil samples mixed with six different types of plastic, including polyethylene terephthalate (PET) and polyvinyl chloride (PVC). They created four distinct groups with varying levels of plastic, from zero plastics (the control group) to five different types of plastic. After 40 days of incubation, they collected the soil and ran several tests. These included measuring soil properties, such as acidity and key enzyme activities, as well as DNA sequencing to identify bacteria and their associated functional genes.

The team's analysis revealed that increasing microplastic diversity leads to significant shifts in soil health. For example, the plastic mixture considerably raised soil pH (making the soil more alkaline) and increased soil carbon content.

However, one of the most important findings was that microplastic diversity boosted the activity of bacterial genes responsible for denitrification. This is the process by which bacteria convert plant nutrient material into nitrogen gas, which is then released into the atmosphere. It not only makes the soil less fertile, but also releases nitrous oxide, a greenhouse gas that is around 300 times more potent in warming the planet than carbon dioxide. The primary cause of this accelerated nitrogen loss was a family of bacteria known as Rhodocyclaceae.

Tian-Gui Cai et al, Microplastic Diversity as a Potential Driver of Soil Denitrification Shifts, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c04981

Parkinson's 'trigger' directly observed in human brain tissue for the first time

Scientists have, for the first time, directly visualized and quantified the protein clusters believed to trigger Parkinson's, marking a major advance in the study of the world's fastest-growing neurological disease.

These tiny clusters, called alpha-synuclein oligomers, have long been considered the likely culprits for Parkinson's disease to start developing in the brain, but until now, they have evaded direct detection in human brain tissue.

Now, researchers  have developed an imaging technique that allows them to see, count and compare oligomers in human brain tissue, a development one of the team says is "like being able to see stars in broad daylight."

Their results, reported in the journal Nature Biomedical Engineering, could help unravel the mechanics of how Parkinson's spreads through the brain and support the development of diagnostics and potential treatments.

The team examined post-mortem brain tissue samples from people with Parkinson's and compared them to healthy individuals of similar age. They found that oligomers exist in both healthy and Parkinson's brains. The main difference between disease and healthy brains was the size of the oligomers, which were larger, brighter and more numerous in disease samples, suggesting a direct link to the progression of Parkinson's.

The team also discovered a sub-class of oligomers that appeared only in Parkinson's patients, which could be the earliest visible markers of the disease—potentially years before symptoms appear.

Rebecca Andrews et al, Large-scale visualisation of α-synuclein oligomers in Parkinson's disease brain tissue, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01496-4

Why women live longer than men

Tracing the evolutionary roots of why women live longer than men

Around the world, women on average live longer than men. This striking pattern holds true across nearly all countries and historical time periods. Although the gap between the sexes has narrowed in some countries due to medical advances and improved living conditions, new research now provides clues as to why this difference is unlikely to disappear anytime soon. The causes are deeply rooted in evolutionary history and can be observed in many animal species.

An international team of scientists  conducted the most comprehensive analysis of sex differences in lifespan across mammals and birds to date. Their findings, published in Science Advances, provide novel insight into one of biology's long-standing puzzles: why males and females age differently.

Among mammals, females usually live longer—for instance, in baboons and gorillas, females often outlive males. Yet this pattern is not universal: In many birds, insects, and reptiles, males are the longer-lived sex. One genetic explanation, the heterogametic sex hypothesis, points to differences in sex chromosomes.

In mammals, females have two X chromosomes, while males have only one X and one Y (making them the heterogametic sex). Some research suggests that having two X chromosomes may protect females from harmful mutations, offering a survival advantage. In birds, however, the system is reversed: females are the heterogametic sex.

Using records from over 1,176 bird and mammal species in zoos worldwide, the researchers found a striking contrast in lifespan, supporting the heterogametic sex hypothesis: in most mammals (72 percent), females lived longer, by on average twelve percent, while in most bird species (68 percent), males lived longer, overall by an average of five percent.

Still, there was remarkable variation with many exceptions. Some species showed the opposite of the expected pattern. For example, in many birds of prey, females are both larger and longer-lived than males. So sex chromosomes can only be part of the story.

Sexual selection and parental care shape lifespan differences

In addition to genetics, reproductive strategies also play a role. Through sexual selection, males in particular develop conspicuous characteristics such as colorful plumage, weapons, or large body size, which increase reproductive success but can shorten lifespan. The new study supports this assumption: In polygamous mammals with strong competition, males generally die earlier than females.

Many birds, on the other hand, are monogamous, which means that competitive pressure is lower and males often live longer. Overall, the differences were smallest in monogamous species, while polygamy and pronounced size differences were associated with a more pronounced advantage for females.

Parental care also plays a role. The researchers found evidence that the sex that invests more in raising offspring—in mammals, this is often the females—tends to live longer. In long-lived species such as primates, this is likely to be a selective advantage: females survive until their offspring are independent or sexually mature.

Part 1

Zoo life reduces—but does not erase—lifespan gaps
A long-standing idea is that environmental pressures—such as predation, pathogens, or harsh climates—drive the observed gaps between males and females. To test this, the researchers turned to zoo populations, where such pressures are largely absent.
They found that lifespan gaps persisted even under these protected conditions. Comparing zoo and wild populations showed that the gaps were often smaller in zoos but rarely disappeared—mirroring the human case, where advances in medicine and living conditions have narrowed but not eliminated the lifespan gap.

The findings suggest that sex differences in lifespan are deeply rooted in evolutionary processes—shaped by sexual selection and parental investment and that genetic differences in the sex determination system may also play a role. Environmental factors influence the extent of the differences, but cannot eliminate them. The differences between the sexes are therefore not only a product of the environment, but part of our evolutionary history, and will most likely continue to exist in the future.

Sexual selection drives sex difference in adult life expectancy across mammals and birds, Science Advances (2025). DOI: 10.1126/sciadv.ady8433

Part 2

Rare fossil reveals ancient leeches weren't bloodsuckers

A newly described fossil reveals that leeches are at least 200 million years older than scientists previously thought, and that their earliest ancestors may have feasted not on blood, but on smaller marine creatures.

Roughly 430 million years old, the fossil includes a large tail sucker—a feature still found in modern leeches—along with a segmented, teardrop-shaped body. But one important feature isn't found in this fossil: the forward sucker that many of today's leeches use to pierce skin and draw blood.

This absence, along with the fossil's marine origin, suggests a very different early lifestyle for the group known as Hirudinida. Rather than sucking blood from mammals, reptiles, and other vertebrates, the earliest leeches may have roamed the oceans, consuming soft-bodied invertebrates whole or feeding on their internal fluids.

Blood feeding takes a lot of specialized machinery. Anticoagulants, mouthparts, and digestive enzymes are complex adaptations. It makes more sense that early leeches were swallowing prey whole or maybe drinking the internal fluids of small, soft-bodied marine animals.

Previously, scientists thought leeches emerged about 150–200 million years ago. That timeline has now been pushed back by at least 200 million years, thanks to the fossil found in the Waukesha biota, a geological formation in Wisconsin known for preserving the bodies of soft tissue animals that usually decay before fossilization.

Preserving a leech fossil is no small feat. Leeches lack bones, shells, or exoskeletons that are most easily preserved over millions of years. Fossils like this require exceptional circumstances to preserve, often involving near-immediate burial, a low-oxygen environment, and unusual geochemical conditions.

A rare animal and just the right environment to fossilize it—it's like hitting the lottery twice.

de Carle D, et al. The first leech body fossil predates estimated hirudinidan origins by 200 million years, PeerJ (2025). doi.org/10.7717/peerj.19962

9/11 study shows how toxic exposures may lead to blood cancers

A study by researchers has found that mutations in blood-forming cells may explain the increased risk for leukemia and other blood disorders among first responders exposed to the 9/11 World Trade Center (WTC) disaster site and its toxic dust.

The study also points to a novel strategy for use against inflammation and blood disorders associated with environmental toxins. The research is published in Cancer Discovery in a study titled "Elevated clonal hematopoiesis in environmentally exposed 9/11 first responders has distinct age-related patterns and relies on IL1RAP for clonal expansion."

The findings provide new insights into the long-term health impacts of environmental catastrophes, such as wildfires, and suggest targeted interventions for those affected by 9/11 or similar disasters.

The collapse of the WTC produced tremendous quantities of airborne particulate matter—a potent mixture of carcinogens and genetically toxic substances to which an estimated 400,000 responders, area workers, and residents were exposed.

In previous studies, researchers noted a higher incidence of cancers, cardiovascular disease, and other health problems among 9/11 first responders compared with the general population. However, few studies have examined how such environmental exposures can lead to blood cancers.

For this study,  scientists sequenced blood samples from nearly 1,000 first responders who were exposed to the WTC site, along with blood from two control groups: 255 firefighters who were not at the WTC and 198 unexposed people in the general population.
All samples were collected between December 2013 and October 2015. The toxic 9/11 dust cloud was found to be associated with mutations in the blood cells of many responders.

Compared with control-group individuals, WTC-exposed first responders had a significantly higher prevalence of clonal hematopoiesis (CH)—a condition in which a group, or clone, of a person's blood-forming (hematopoietic) stem cells contain the same gene mutations. Typically associated with aging, CH is a precancerous condition known to increase the risk of blood cancer and inflammation.

Part 1

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