Discovery shows oyster blood proteins improve antibiotic effectiveness

While slurping oysters is not likely to replace popping a pill, they could help in the fight against superbugs. A groundbreaking find by researchers has shown oysters might be able to help treat a growing worldwide public health problem: antibiotic-resistant bacteria.

In a study published in PLOS ONE, the researchers demonstrate a protein in the blood, or hemolymph, of a Sydney Rock Oyster not only kills bacteria but increases the effectiveness of some conventional antibiotics against a range of clinically important bacteria.

This new research supports the potential use of natural products from oysters to treat bacterial infections. Importantly, the oyster hemolymph proteins were not toxic to human lung cells, suggesting it should be possible to optimize a safe, effective dose. 

 Antimicrobial proteins from oyster hemolymph improve the efficacy of conventional antibiotics, PLOS ONE (2025). DOI: 10.1371/journal.pone.0312305. journals.plos.org/plosone/arti … journal.pone.0312305

**

Scientists finally know how cells build a structure that lets them migrate

Some of the body's cells stay put for life, while others are free to roam. To move, these migratory cells rely on filopodia—sensitive, finger-like protrusions that reach out from the cell membrane into the local environment. In a healthy cell, this can be a lifesaver: say, when an immune cell is speeding to the site of an infection. But filopodia can also wreak havoc: metastatic cancer cells use them to invade new regions of the body.

Filopodia are composed of hexagonal bundles of proteins that give them structure and strength. How these intricate bundles come together has been a puzzle for more than 40 years. A major piece of that puzzle has now been solved by Rockefeller University's Laboratory of Structural Biophysics and Mechanobiology, which developed advanced imaging technology to reveal how underlying proteins build these cohesive assemblies.

The findings, published in Nature Structural & Molecular Biology, may improve some cancer treatments already in development, as understanding the structure of filopodia and the changes they undergo may help to refine these therapies or inspire new ones.

The study marks the first time such a complex higher-order protein assembly has been imaged at the atomic level—a technological advance that other scientists can now use to study similarly complex configurations.

 Rui Gong et al, Fascin structural plasticity mediates flexible actin bundle construction, Nature Structural & Molecular Biology (2025). DOI: 10.1038/s41594-024-01477-2

New effective treatment for deadly pancreatic cancer may be on its way

Pancreatic cancer is one of the deadliest of all cancers. Only 12% of men diagnosed with pancreatic cancer are alive five years after diagnosis; for women it is 14%.

In pancreatic cancer, symptoms are unclear and often emerge late in its progression. It is difficult to treat once the cancer has spread, as it cannot be removed completely with surgery.

Now researchers  have made significant advances in developing a treatment for pancreatic cancer and a new study published in Science Advances depicts how it is done. The study is based on the ADC (antibody drug conjugates) technique, which is being used to treat other types of cancers.

This study shows promising results with a new type of drug that can fight the cancer on several fronts. The treatment directly kills the cancer cells and the support cells that the cancer uses to grow and shield itself.

By targeting the support cells, the treatment also releases toxins that can kill neighboring cancer cells. Additionally, destroying the support cells weakens the tumor structure, making it easier for the body's immune system to attack and eliminate it.

The ADC consists of three main components: an antibody, a chemical linker that ties the antibody to the drug, and a strong chemotherapeutic drug. Once the ADC has located and entered the cancer cell, the linker decomposes, activating the chemotherapy and killing the cancer cell from the inside. This Trojan horse strategy offers targeted treatment without affecting the healthy cells.

Because ADC treatment is extremely accurate and causes minimal damage to healthy cells, it is a likely candidate for treatment of the more difficult cancers.

As part of the process, the researchers have humanized the ADC antibody, which means that we have changed its structure to resemble antibodies naturally occurring in the human body. This adjustment ensures that the body's immune system does not recognize the antibody as foreign and attack it. Humanization is a critical step in making the treatment both safe and effective for patients and represents a key milestone on the path towards clinical trials.

The researchers are now working to further develop the drug and get it ready for clinical testing on humans with pancreatic cancer.

Virginia Metrangolo et al, Targeting uPAR with an antibody-drug conjugate suppresses tumor growth and reshapes the immune landscape in pancreatic cancer models, Science Advances (2025). DOI: 10.1126/sciadv.adq0513

An energy trap for tumor cells: Researchers find enzyme blockade halts liver cancer growth

Glycolysis is a central metabolic pathway by which cells obtain energy from sugar. Cancer cells in particular have long been thought to depend on the energy obtained through glycolysis, a phenomenon known as the Warburg effect. Today we know that cancer cells can use energy sources more flexibly than previously thought. Even when glycolysis is blocked, they survive by obtaining their energy through the respiratory chain.

This makes results published by Almut Schulze and colleagues from the German Cancer Research Center (DKFZ) all the more surprising: When the researchers blocked the enzyme aldolase A, which catalyzes an important step in glycolysis, liver cancer cells experienced "energy stress" and ceased their division activity. The team demonstrated this both in mouse liver cancer cells and in several human cancer cell lines.

The findings are published in the journal Nature Metabolism.

However, when the researchers blocked an earlier step in glycolysis, the enzyme glucose-6-phosphate isomerase, this had no effect on the growth of the cancer cells.

The glycolytic enzyme aldolase is essential for liver cancer cells, although the glycolytic pathway itself is apparently dispensable.

At first glance, the result seems surprising, since the enzyme blockade inhibits the sugar degradation pathway in both cases. However, a closer look at the biochemical steps of glycolysis provides clarity: The metabolic pathway, which involves many reactions, is divided into two parts. First, the cell has to invest energy to generate the highly energetic intermediate fructose-bisphosphate.

This is where aldolase A comes in. If it is switched off, fructose bisphosphate accumulates in the cell, and the energy bound in it remains unused, trapped as it is. The cell cannot reap the energy profit from the steps that would normally follow. Glycolysis has reversed from an energy-producing to an energy-consuming process. What's more, the lack of energy further stimulates the production of fructose bisphosphate, creating a vicious circle.

Sooner or later, this leads to energy consumption exceeding energy production. In liver cancer cells, this results in a massive energy deficiency, the cell cycle is stopped and tumor growth is inhibited. The team also demonstrated this in liver cancer-bearing mice: If the animals' aldolase A was genetically switched off, the cancer growth was reduced and the mice survived significantly longer.

By switching off Aldolase A, we can overcome the metabolic plasticity of cancer cells. We not only block energy production through glycolysis, but also prevent the cell from switching to other metabolic pathways, because the energy is trapped in the fructose bisphosphate. Targeted inhibition of aldolase A could therefore be a promising strategy for combating cancer cells.

Part 1

However, the only aldolase A inhibitor currently available has so far only been tested experimentally and is not approved as a drug. The Heidelberg team is now testing the substance for its potential in cancer therapy.

It is important to note that even a slight reduction in the activity of aldolase A could be enough to drive cancer cells into the energy trap.

Normal cells should tolerate this because they take up smaller amounts of glucose and produce less energy-rich fructose bisphosphate. The Warburg effect is therefore a weak point of cancer cells that makes them more sensitive to a blockade of aldolase A.

The results show how a deeper understanding of tumor metabolism can enable innovative approaches to cancer treatment. These findings could pave the way for new, highly specific therapies that target the weaknesses of cancer metabolism while sparing healthy cells.

Marteinn T. Snaebjornsson et al, Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation, Nature Metabolism (2025). DOI: 10.1038/s42255-024-01201-w

Part 2

Paralysed man flies virtual drone using brain implant

Paralysed man flies virtual drone
Researchers have developed a device that let a 69-year-old man with paralysis fly a virtual drone using only his thoughts. The brain–computer interface (BCI) decoded the man’s brain activity as he imagined moving three groups of digits in real time. By associating neural signals with the movements of multiple fingers, the work builds on previous BCI research, most of which has focused on moving a single computer cursor or whole virtual hand.

https://www.nature.com/articles/d41586-025-00167-3?utm_source=Live+...

Frequent social media use tied to higher levels of irritability

A survey led by researchers has analyzed the association between self-reported social media use and irritability among US adults. Frequent social media use, especially among active posters, was correlated with higher levels of irritability.

Existing studies on social media and mental health predominantly focus on depressive symptoms, with limited attention to other negative emotions such as irritability. Irritability, defined as a tendency toward anger and frustration, has been linked to functional impairments, poorer mental health outcomes, and suicidal behaviours.

While prior research has established connections between social media use and depressive symptoms, the extent to which social media engagement is associated with irritability or its influence on depression and anxiety has remained uncertain.

In the study, "Irritability and Social Media Use in US Adults," published in JAMA Network Open, the research team used data from two waves of the COVID States Project, a nationwide nonprobability web-based survey conducted between November 2, 2023, and January 8, 2024, which included questions about social media use and irritability.

Researchers evaluated the relationship between social media use and irritability by analyzing responses from 42,597 participants using multiple linear regression models.

Part 1

The survey collected sociodemographic data, self-reported social media usage, and measures of irritability. Participants completed the Brief Irritability Test (BITe), which consists of five statements evaluating irritability symptoms over the previous two weeks. Scores range from 5 to 30, with higher scores indicating higher levels of irritability. The analysis also included depression and anxiety metrics to account for overlapping psychological symptoms.

Social media use was categorized based on frequency: never, less than once per week, once per week, several times per week, once per day, several times per day, or most of the day. Platforms analyzed included Facebook, Instagram, TikTok, and Twitter/X. Frequency of active posting, political engagement, and political affiliation were also examined to identify potential confounding factors.

Participants had a mean age of 46 years, with 58.5% identifying as women, 40.4% as men, and 1.1% as nonbinary. Among respondents, 78.2% reported daily use of at least one social media platform. Frequent social media use correlated with higher irritability scores, even after adjusting for anxiety and depression.

For example, participants using social media most of the day scored 3.37 points higher on the BITe in unadjusted models. After adjusting for anxiety and depression, the increase remained significant at 1.55 points.

Platform-specific analyses revealed a dose-response relationship between posting frequency and irritability. Posting multiple times per day was associated with the highest irritability levels across all platforms, with TikTok users showing the largest increase (1.94 points; 95% CI, 1.57-2.32 points).

Political engagement variables, such as frequent political posting or consuming political news, were associated with increased irritability. Political engagement did not diminish the observed relationship between social media use and irritability, though following political news "not very closely" was associated with a slight decrease.

High social media engagement levels, particularly frequent posting, were associated with greater irritability in US adults. While the study could not establish direct causation, findings suggest a potential feedback loop relationship, where irritability may both influence a desire to engage and increase irritation from social media use.

 Roy H. Perlis et al, Irritability and Social Media Use in US Adults, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2024.52807

Part 2

**

Fighting experience plays key role in brain chemical's control of male aggression

Like humans, mice will compete over territory and mates, and show increased confidence in their fighting skills the more they win. At first, a brain chemical called dopamine is essential for young males to master this behavior. But as they gain experience, the chemical grows less important in promoting aggression, a new study shows.

Dopamine has been linked to male aggression for decades. How past experiences might influence this relationship, however, had until now been unclear.

In experiments in rodents, a team led by researchers at NYU Langone Health boosted activity in dopamine-releasing cells in a part of the brain called the ventral tegmental area. The findings revealed that in inexperienced male fighters, this led the animals to attack for twice as long as they would have fought naturally. When the cells were blocked, the novice mice would not fight at all.

By contrast, this pattern did not hold true in males that had extensive fighting experience. Whether or not dopamine-releasing cells were boosted or blocked, the duration of the attack did not change. Notably, though, the more clashes a mouse won, the more fights it would start in the future.

These findings show that while aggression is an innate behaviour, dopamine—and fighting experience—is essential for its maturation during adulthood.

A report on the findings was published online Jan. 22 in the journal Nature.

Dayu Lin, Experience-dependent dopamine modulation of male aggression, Nature (2025). DOI: 10.1038/s41586-024-08459-w. www.nature.com/articles/s41586-024-08459-w

Silver nanoparticles in packaging can contaminate dry foods, testing shows

A team of research scientists has found evidence of silver nanoparticles embedded in packaging used as an antimicrobial agent seeping into the dry food it is meant to protect. In their paper published in the journal ACS Food Science & Technology, the group describes how they created their own packaging with embedded silver nanoparticles and tested it with various foods, and what they learned by doing so.

Silver has been a known antimicrobial agent for centuries, but it has only recently been made into nanoparticle-sized grains for use in food packaging. Prior research has shown that when such packaging is used for liquid or gelatinous foods or beverages, the nanoparticles can easily seep into and permeate the food. It is still not known if such particles can cause harm to people who consume them—testing is still ongoing, which is why they are banned in many countries. In this new effort, the research team wanted to know if such particles also find their way into dry foods.

To find out, the team created samples of silver nanoparticles and embedded them in polyethylene film wraps, which could hold various types of food items. They tested wheat flour, slices of cheese, ground rice and spinach leaves. They then stored the packages in ways normal to consumers' homes.

The team then brought the packages into their lab for testing with mass spectrometry. In so doing, they found that the nanoparticles had made their way to all the foods, though to varying degrees. They found, for example, that there was far more contamination of the cheese than there was with the spinach leaves. They noted that the more surface contact between the food and the packaging, the more contamination. They also noted that most of the contamination was confined to the surface of the food, which meant that most of it could be easily rinsed away.

 Laxmi Adhikari et al, Silver Migrates to Solid Foods and Abiotic Surfaces from Model Plastic Packaging Containing Silver Nanoparticles, ACS Food Science & Technology (2025). DOI: 10.1021/acsfoodscitech.4c00813

Insulin-producing cells avoid immune attack

Gene-edited insulin-producing beta cells have survived for a month after being injected into a man with type 1 di.... These tweaked cells have a protein called CD47 on their surface, which tells the immune system not to destroy them. Only a small number of cells were injected into the man’s arm, but they have produced insulin and avoided his immune system’s crosshairs so far, suggesting that they could become an effective treatment for diabetes.

https://ir.sana.com/news-releases/news-release-details/sana-biotech...

https://www.newscientist.com/article/2463508-gene-edited-cells-that...

Uncovering the role of Y chromosome genes in male fertility in mice

Researchers at the Crick have uncovered which genes on the Y chromosome regulate the development of sperm and impact fertility in male mice. This research could help us understand why some men don't produce enough sperm and are infertile.

Males typically have one copy of the Y chromosome and one copy of the X chromosome, whereas females typically have two X chromosomes. Scientists know that the Y chromosome is essential for male fertility, but which genes are the most important and how they work is less clear till now.

In research published in Science, a research team at the Crick resolved this question by generating 13 different mouse models, each with different Y genes removed, and investigated their fertility.

The researchers studied the ability of these adult mice to reproduce, including looking at the number of offspring, number of sperm produced and the appearance and motility of the sperm.

They found that several Y genes were critical for reproduction. If these genes were removed, the mice couldn't produce young, due to absence or reduced number of sperm, failure to produce a reservoir of sperm stem cells or abnormal sperm shape or movement.

Interestingly, some other genes had no impact when removed individually, but did lead to the production of abnormal sperm when removed together.

This was the case for a group of three genes which model a region of the chromosome called AZFa in humans. AZFa deletions are a common cause of the most severe cases of male infertility, but it has been hard to tell which genes in the region are responsible.

Jeremie Subrini et al, Systematic identification of Y-chromosome gene functions in mouse spermatogenesis, Science (2025). DOI: 10.1126/science.ads6495. www.science.org/doi/10.1126/science.ads6495

Smart fabric can heat up by 30°C after 10 minutes of sun exposure

A new type of cloth developed by researchers at the University of Waterloo can heat up when exposed to the sun thanks to innovative nanoparticles embedded in the fabric's fibers. This advance represents an innovative and environmentally friendly option for staying warm in the winter.

Wearable heated clothing typically relies on metals or ceramic heating elements to heat up and an external power source, which could pose safety risks for users.

This new cloth incorporates conductive polymer nanoparticles that can heat up to 30°C when exposed to sunlight. The design requires no external power and can also change color to visually monitor temperature fluctuations. The study was recently published in Advanced Composites and Hybrid Materials.

The magic behind the temperature-sensitive color change lies in the combination of nanoparticles embedded in the polymer fibers. The nanoparticles are activated by sunlight, enabling the fabric to absorb heat and convert it into warmth.

The fiber is created using a scalable wet-spinning process, combining polyaniline and polydopamine nano particles to enhance light absorption and improve photothermal conversion. Thermoplastic polyurethane serves as the spinning matrix, while thermochromic dyes enable the reversible color-changing feature. The resultant fiber can be woven into fabric for wearable applications.

In addition to its temperature-changing capability, the Waterloo researchers' new fabric can stretch out by as much as five times its original shape and withstand as much as two-dozen washings while still maintaining its function and appearance. Its reversible color-changing ability provides a built-in temperature monitoring feature to ensure the wearer's safety and convenience.

The fabric's potential applications include aiding in cold rescue situations and solar-powered pet clothing to help keep them comfortable when outside during the winter.

 Fangqing Ge et al, Color tunable photo-thermochromic elastic fiber for flexible wearable heater, Advanced Composites and Hybrid Materials (2024). DOI: 10.1007/s42114-024-00994-4

An underestimated source of methane found in shallow coastal waters

Shallow coastal waters are hotspots for methane emissions, releasing significant amounts of this potent greenhouse gas into the atmosphere and contributing to global warming. New research highlights how tides, seasons, and ocean currents strongly influence methane emissions and how tiny microorganisms, called methanotrophs, help reduce their impact.

While human-made sources of methane are well-studied, natural sources like coastal waters remain less understood. These shallow, dynamic ecosystems are rich in methane, and because the water is not very deep, methane-eating microbes (methanotrophs) have little time to break it down before it escapes into the atmosphere.

The study investigated three regions: the Doggerbank seep area in the North Sea, the Dutch Wadden Sea, and coastal waters near Svalbard in the Arctic. Findings revealed that methane emissions are highly influenced by natural factors like tides and seasonal changes, which also affect the activity of methane-eating microbes.

In the Wadden Sea, methane levels and emissions were higher during warmer seasons when microbial activity was stronger. However, even in colder seasons, methane concentrations remained high, with windy conditions contributing to significant atmospheric releases. Tidal currents transported methane into neighboring waters, where it could still escape into the atmosphere, highlighting the broader impact of coastal methane dynamics.
At the Doggerbank seep area, falling tides triggered bursts of methane release while also stimulating microbial activity in deeper waters. However, during cooler autumn months, when water mixed, microbial activity decreased, leading to more methane escaping into the atmosphere compared to summer.

In the Arctic near Svalbard, methane concentrations were highest near the seafloor, where diverse and abundant microbial communities were present. Ocean currents played a key role in spreading methane and microbes, limiting their ability to fully break down the gas before it reached the atmosphere.
Part 1

In addition to fieldwork, laboratory experiments revealed that methanotrophic microbes are remarkably adaptable. They thrive in a range of environmental conditions, including shifts in temperature, salinity, and methane levels.
As ecosystems change, methane-eating microbes adapt. When one group struggles, another takes over, keeping nature's methane filter running even in a warming world.

Tim de Groot. Environmental controls on microbial methane oxidation in the coasta... ( PhD Dissertation)

Part 2

Mane attraction: Molecular 'switch' may control long scalp hair

Treating hair loss may be as simple as developing therapies to flip a molecular "switch," according to a new study by researchers .

The researchers reviewed the biological and social evolution of human scalp hair. Based on their analysis, they proposed a novel theory that points to a molecular basis underlying the ability to grow long scalp hair. In short, human ancestors may have always had the ability to grow long scalp hair, but the trait remained dormant until certain environmental and biological conditions—like walking upright on two legs—turned on the molecular program.

The team published their findings, which they said could serve as the basis for future experimental work, in the British Journal of Dermatology.

Humans grow extremely long scalp hair.

Likewise, attributes of scalp hair—its length, shape, color and loss of hair—play an essential role in social communication. They signify our ancestry, age, health, sexual maturity and social status, to name but a few. And yet, despite the importance of having long scalp hair, we know very little about how this feature of human skin came about and how it is regulated.

Previous research had shown that tightly curled hair, in particular, served as an effective shield against the sun, reducing the need for excessive sweating that can cause dangerous dehydration. 

Building on this work, the researchers proposed that long scalp hair initially evolved to protect early human ancestors in equatorial Africa from the intense heat and solar radiation of their environment, and then it came to have meaning in many other spheres of life, such as signaling age, health, maturity and social status.

Long, tightly curled hair was a crucial adaptation that allowed our ancestors to thrive in hot, open environments. Understanding when long scalp hair evolved will help to better appreciate when it acquired its essential non-biological purposes.

While long hair is rare among mammals, it is not entirely unique to humans. Animals like male lions, orangutans and even now-extinct wooly mammoths also grew remarkably long hair, albeit for different reasons, according to the researchers.

What these examples tell us is that the molecular blueprint for growing very long hair has always existed, albeit often in a 'silenced' state. When human ancestors evolved their ability to grow extremely long scalp hair, it was likely accomplished by just a few genetic tweaks that reactivated a dormant program rather than via the evolution of an entirely new molecular mechanism.

The findings have broader implications for medical research, particularly in addressing hair loss, a condition that impacts millions worldwide. Understanding how human scalp hair follicles normally grow very long hair will naturally result in novel molecular targets for more efficacious therapies for hair loss.

This knowledge could lead to treatments that help restore hair growth and alleviate the emotional distress that often accompanies hair loss.

Lo-Yu Chang et al, Evolution of long scalp hair in humans, British Journal of Dermatology (2025). DOI: 10.1093/bjd/ljae456

Mitochondria may be a promising therapeutic target for inflammatory diseases

Scientists have discovered how mitochondria influence the body's immune response through modulating specific cell signaling pathways, according to a study published in Science Advances.

The findings highlight the potential of targeting mitochondrial function specifically in immune cells to treat a range of inflammation-related diseases.

Therapies aimed at improving mitochondrial activity could benefit inflammatory diseases such as inflammatory bowel disease, sepsis, and chronic infections by enhancing the immune system's ability to regulate inflammation.

Mitochondria contain the mitochondrial electron transport chain (ETC), or a series of protein complexes in which electrons pass through and produce ATP, or energy, for the cell. Mitochondrial ETC function also controls macrophages, or specialized immune cells that are essential for fighting infections and regulating inflammation in the body.

Macrophages also release an anti-inflammatory protein called IL-10, which reduces inflammation and prevents excess immune responses that can harm the body. The underlying mechanisms that allow mitochondrial ETC to control macrophage immune responses, however, have remained poorly understood.

Using bulk-RNA sequencing to study mice with macrophages deficient in mitochondria ETC complex III, the scientists discovered that a type of reactive oxygen species (ROS), or unstable molecules that contain oxygen and easily react with other molecules in a cell, that is produced by mitochondrial complex III, called superoxide, is critical for macrophages to release IL-10.

The scientists also discovered those mice with the defective mitochondrial complex also struggled to recover from infection and inflammation because their cells released less IL-10. However, activating a specific ROS dependent signaling pathway in the cells restored IL-10 release, according to the study.

This finding highlights a previously unknown connection between mitochondrial activity, inflammation control and the signaling pathways that regulate it.

Overall, the findings underscore mitochondria's essential role beyond energy production and suggest that mitochondria may be a promising therapeutic target for treating a range of inflammatory diseases and enhancing current therapies, according to the researchers.

Boosting IL-10 levels through mitochondrial pathways offers promise for managing autoimmune disorders like rheumatoid arthritis and lupus, where the immune system mistakenly attacks the body. Enhancing the function of mitochondrial complex III, or mimicking its effects, may also improve recovery from severe infections. Additionally, inhibiting mitochondrial complex III would decrease IL-10 suppression of inflammation, and could cooperate with existing immunotherapies.

 Joshua S. Stoolman et al, Mitochondria complex III–generated superoxide is essential for IL-10 secretion in macrophages, Science Advances (2025). DOI: 10.1126/sciadv.adu4369

Eight psychiatric disorders share the same genetic causes, study says

Psychiatric disorders often overlap and can make diagnosis difficult. Depression and anxiety, for example, can coexist and share symptoms. Schizophrenia and anorexia nervosa. Autism and attention deficit/hyperactivity disorder, too. But, why?

Life experiences, environment, and genetics can all influence psychiatric disorders, but much of it comes down to variations in our genetics. Over the past few years, scientists in the field of psychiatric genetics have found that there are common genetic threads that may be linking and causing coexisting psychiatric disorders.

In 2019, researchers at the Psychiatric Genomics Consortium, Harvard University, and the UNC School of Medicine identified 136 "hot spots" within the genome that are associated with eight psychiatric disorders. Among them, 109 hot spots were shared among multiple disorders, or "pleiotropic."

A new genetic study has successfully delineated the functional consequences of genetic variants into two groups. Their findings, which were published in Cell, suggest that pleiotropic variants may be optimal targets for treatment, due to their extended roles in development and sensitivity to change.

Pleiotropy was traditionally viewed as a challenge because it complicates the classification of psychiatric disorders. However, if we can understand the genetic basis of pleiotropy, it might allow us to develop treatments targeting these shared genetic factors, which could then help treat multiple psychiatric disorders with a common therapy.

The human genome acts as the body's operating manual, containing the instructions that helped us develop from a single cell into a whole person. However, everyone's genetic foundation is unique. There are specific regions of the genome that are prone to genetic variations.

Specific genetic variants can impact biological processes, like protein overproduction or altered synapse formation, affecting brain development and contributing to psychiatric disorder. But researchers are armed with tools to track these variants and learn more about the origins of disease.

In 2019, an international team of researchers at the UNC School of Medicine and the Psychiatric Genomics Consortium conducted genome-wide association studies (GWAS) on eight disorders: autism spectrum disorder, attention deficit/hyperactivity disorder (ADD), schizophrenia, bipolar disorder, major depressive disorder, Tourette syndrome, obsessive-compulsive disorder (OCD), and anorexia nervosa, to better understand the shared genetic underpinnings between psychiatric disorders. The analysis previously revealed 136 "hot spots" on the genome that have a causal effect on one or more of the eight psychiatric disorders. Of those, 109 of these locations were identical across more than one disorder.

As part of their latest study, researchers wanted to pry more information from the genetic variants embedded within these 136 "hot spots." Using a powerful technology, called a massively parallel reporter assay, they sought to determine which causal variants could be interfering with gene regulation.

Gene regulation controls how and when proteins are produced in the body, allowing the tiny machines to carry out a wide array of functions in the body. If certain variants are interfering with this important process, researchers can use that information to home in on the variants of interest and use them as new targets for treatment.

Part 1

Researchers first took all 17,841 genetic variants from the 136 "hot spots" and inserted them into human neural cells to see how they acted in a living system. After putting the variants through the massively parallel reporter assay, researchers found that 683 of the 17,841 genetic variants had a measurable effect on gene regulation.
The researchers then categorized the 683 variants into two groups: those shared across multiple disorders (pleiotropic variants) and those specific to a single disorder (disorder-specific variants). After dividing them into categories, researchers performed a tried-and-true scientific method: compare and contrast.

Pleiotropic variants were found to be more active and more sensitive to change compared to disorder-specific variants. Researchers noted that pleotropic variants were active for much longer during brain development, compared to disease-specific ones. This extended activity suggests that pleiotropic variants may be influencing multiple stages of neurodevelopment and potentially contributing to various observable traits and disorders.

Additionally, the genes affected by these pleiotropic variants appear to be more sensitive to changes, meaning disruptions in these genes could have a bigger impact on human health.

The proteins produced by these genes are also highly connected to other proteins. Changes to these proteins in particular could ripple through the network, potentially causing widespread effects on the brain.
These findings mark an important step toward understanding how genetics contributes to shared symptoms across psychiatric disorders. Targeting these variants, their associated genes, and pathways could pave the way for treatments that address multiple conditions at once.

Sool Lee et al, Massively parallel reporter assay investigates shared genetic variants of eight psychiatric disorders, Cell (2025). DOI: 10.1016/j.cell.2024.12.022

Part 2

Microplastics block blood flow in the brain, mice study reveals

In mice, immune cells carry microplastics — specks of plastic less than 5 millimetres long — through the bloodstream, where they eventually become lodged in blood vessels in the brain. The plastic-packed cells appeared in the mice’s brains just hours after they were given polystyrene-laced water and piled up “like a car crash in the blood vessels”, says biomedical researcher and study author Haipeng Huang. The obstructions sometimes cleared eventually, but others stayed stuck for the entire month-long observation period and had effects including impairing the mice’s mobility. It’s not clear whether such blockages occur in people.

https://www.nature.com/articles/d41586-025-00178-0?utm_source=Live+...

https://www.science.org/doi/10.1126/sciadv.adr8243

Cancer cells ‘poison’ the immune system with tainted mitochondria

Cancer cells can sabotage immune cells that try to attack them by filling them with ..., the organelles that cells rely on to make energy. In samples from three people with cancer, researchers noticed that mitochondria in both the tumour cells and immune cells called tumour-infiltrating lymphocytes (TILs) shared the same mutations. When they grew cancer cells with fluorescent-tagged mitochondria alongside TILs, the TILs had taken on some faulty mitochondria after only 24 hours. By 15 days, their native mitochondria had been replaced almost entirely. Tainted TILs were less able to divide and more likely to commit cell ‘suicide’.

https://www.nature.com/articles/s41586-024-08439-0?utm_source=Live+...

https://www.nature.com/articles/d41586-025-00176-2?utm_source=Live+...

Record-Shattering 20,000 Mph Winds Detected on Wild Alien Planet
Winds circling a gas giant more than 500 light years from Earth have been detected flowing at supersonic speeds approaching 33,000 kilometers (20,000 miles) per hour, making them the fastest air currents on any known planet by a wide margin.
Researchers from Europe cleaned and analyzed the spectrum of light reflected from the planet WASP-127b, uncovering two contrasting peaks in water and carbon dioxide signals suggestive of supersonic flows disturbing the planet's cloud tops.

Part of the atmosphere of this planet is moving towards us at a high velocity while another part is moving away from us at the same speed.
This signal shows us that there is a very fast, supersonic, jet wind around the planet's equator.

Fast is an understatement. At an incredible 7.5 to 7.9 kilometers per second, they outstrip any hurricane or jetstream known to science.
Here on Earth, the fastest puff of wind on record was a blustery 407 kilometers (253 miles) per hour, measured on Australia's Barrow Island in 1996. Neptune has the highest wind speeds in our Solar System, but even its 1,770 kilometer-per-hour high-altitude currents feel more like a mild breeze by comparison.

It's also believed to be tidally locked, rotating in step with every 4.2-Earth-day lap around its star, so one side is perpetually baked to temperatures exceeding 1,000 degrees Celsius (1832 degrees Fahrenheit), and the other never turns from the cold night sky.

https://www.aanda.org/articles/aa/full_html/2025/01/aa50438-24/aa50...

Scientists uncover how cancer cells hijack T-cells, making it harder for the body to fight back

Researchers have discovered a surprising way cancer evades the immune system. It essentially hacks the immune cells, transferring its own faulty mitochondrial DNA (mtDNA) into the T-cells meant to attack it.

This sneaky move weakens the immune cells, making them less effective at stopping the tumor. The findings could help explain why some cancer treatments, like immunotherapy, are effective for some patients but not others.

In the study, "Immune evasion through mitochondrial transfer in the tumour microenvironment," published in Nature, the multi-group collaboration looked at how cancer cells interact with tumor-infiltrating lymphocytes, a type of T-cell that typically fights tumors. The research is also featured in a News and Views piece.

Clinical specimens from melanoma and non-small-cell lung cancer patients were analyzed for mtDNA mutations. Mitochondrial transfer was studied using mitochondrial-specific fluorescent reporters and multiple in vitro and in vivo models. Tumor-infiltrating lymphocyte functions, metabolic profiles, and responses to immune checkpoint inhibitors were evaluated.

Melanoma and lung sample analysis showed that mitochondria, the energy-making engines of cells, could jump from cancer cells into T-cells. These transferred mitochondria carried functional errors in their DNA that interfered with the T-cells' energy production and function processes.

Mitochondria are essential for powering cells, including T-cells, which depend heavily on energy production to fight cancer. But when cancer cells pass on their defective mitochondria, they lose their ability to function properly, throttling the energy of the T-cells and causing them to become exhausted.

Transfer was observed in two main ways: tunneling nanotubes and extracellular vesicles. The nanotubes extend out and tunnel into the T-cell, creating tiny passages between cells that deliver mitochondria directly. Extracellular vesicles form as bubbles released by the cancer cells, encapsulating mtDNA and other molecules.

Once inside the T-cells, the damaged mitochondria replace the healthy ones through a mechanism that would normally operate in reverse, where healthy mitochondria would migrate to replace damaged ones. The study found that cancer cells protect their transferred mitochondria by attaching molecules that prevent the T-cells from breaking them down.

Part 1

Immune checkpoint inhibitors have revolutionized cancer treatment. But not everyone responds well to these drugs. This study found that patients whose tumors had more mitochondrial mutations were less likely to benefit from checkpoint inhibitors, likely because the mitochondrial hack already compromised their T-cells.

Researchers blocked extracellular vesicle release from cancer cells using a compound called GW4869, which inhibits the production of small extracellular vesicle-like exosomes. Applying this inhibitor in their models showed a significant reduction in mitochondrial transfer from cancer cells to T-cells. This intervention helped prevent the T-cells from taking up damaged mitochondria, reducing their dysfunction.

As a result, T-cells showed improved energy production, reduced markers of exhaustion, and a better ability to perform their immune functions. The blocking strategy restored the effectiveness of immune checkpoint inhibitors, particularly in tumors with high levels of mitochondrial transfer. These findings suggest that targeting extracellular vesicles could be a promising strategy to counteract cancer's immune-evasion tactic.
Typically, science works in small, iterative steps toward discovery, with each new element of knowledge putting a piece of the larger puzzle into place. This discovery helps explain why some treatments are ineffective and discovers the mechanism behind their ineffectiveness. Remarkably, it also found a potential solution, representing a significant leap for future research to build from.

Hideki Ikeda et al, Immune evasion through mitochondrial transfer in the tumour microenvironment, Nature (2025). DOI: 10.1038/s41586-024-08439-0

Jonathan R. Brestoff, Mitochondrial swap from cancer to immune cells thwarts anti-tumour defences, Nature (2025). DOI: 10.1038/d41586-025-00077-4

Part 2

Research reveals how specific types of liver immune cells are required to deal with injury

Our livers contain many different types of immune cells. New research  now reveals that a specific activation state of one of these cell types is required for tissue repair following injury. This suggests these cells may be useful as new therapeutic targets for various liver conditions. The work appears in the journal Immunity.

Macrophages are specialized immune cells located in every tissue of the body, where they play crucial roles in maintaining tissue homeostasis, responding to injury, and facilitating tissue repair. In the healthy liver, most macrophages are classified as Kupffer cells (KCs). However, upon liver injury, as seen, for example, in obesity, another subset of macrophages called lipid-associated macrophages (LAMs) is recruited.

This work shows that the LAM phenotype is critical for liver repair. Moreover, this research revealed that the KCs are not static post-injury, as previously thought, and instead adapt to the new microenvironment also taking on a LAM-like phenotype, allowing them to also participate in the repair.

Federico F. De Ponti et al, Spatially restricted and ontogenically distinct hepatic macrophages are required for tissue repair, Immunity (2025). DOI: 10.1016/j.immuni.2025.01.002

**

Astronauts' eyes weaken during long space missions, raising concerns for Mars travel

The low levels of gravity (microgravity) in space cause significant changes in astronauts' eyes and vision after six to 12 months aboard the International Space Station (ISS), according to a study published in the IEEE Open Journal of Engineering in Medicine and Biology.

Researchers found that at least 70% of astronauts on the ISS have been affected by spaceflight-associated neuro-ocular syndrome, or SANS.

They analyzed data collected by the Canadian team at NASA on 13 astronauts who spent between 157 and 186 days on the ISS.

The subjects had an average age of 48 and came from the U.S., European, Japanese and Canadian space agencies; 31% were women; eight were on their first mission.

The researchers compared three ocular parameters before and after the astronauts' space missions: ocular rigidity, intraocular pressure, and ocular pulse amplitude.
They measured ocular rigidity using optical coherence tomography with a customized video module to improve the quality of images of the choroid. The other two parameters, intraocular pressure and ocular pulse amplitude, were measured using tonometry.

The study found significant changes in the biomechanical properties of the astronauts' eyes: a 33% decrease in ocular rigidity, an 11% decrease in intraocular pressure, and a 25% reduction in ocular pulse amplitude.

These changes were accompanied by symptoms including reduced eye size, altered focal field and, in some cases, optic nerve edema and retinal folds.

Part 1

The researchers also found that five astronauts had a choroidal thickness greater than 400 micrometers, which was not correlated with age, gender or previous space experience.

Weightlessness alters the distribution of blood in the body, increasing blood flow to the head and slowing venous circulation in the eye. This is probably what causes the expansion of the choroid, the vascular layer that nourishes the retina.
According to the researchers, the expansion of the choroid during weightlessness could stretch the collagen in the sclera, the white outer layer of the eye, causing long-lasting changes in the eye's mechanical properties.

They also think that blood pulsations under microgravity can create a water-hammer effect in which sudden changes in blood-flow-pressure cause a mechanical shock to the eye, leading to significant tissue remodeling.
According to the researchers, these ocular changes are generally not cause for concern when the space mission lasts six to 12 months. Although 80% of the astronauts they studied developed at least one symptom, their eyes returned to normal once back on Earth.

In most cases, wearing corrective eyeglasses was sufficient to correct the symptoms developed aboard the ISS.

However, the research community and international space agencies are cautious about the consequences of longer missions, such as a flight to Mars. The eye-health effects of prolonged exposure to microgravity remain unknown, and no preventive or palliative measures now exist.

Marissé Masís Solano et al, Ocular Biomechanical Responses to Long-Duration Spaceflight, IEEE Open Journal of Engineering in Medicine and Biology (2024). DOI: 10.1109/OJEMB.2024.3453049

Part 2

Scientists trace deadly cell-to-cell message chain that spreads in sepsis

Dying cells prick their neighbours with a lethal message. This may worsen sepsis, researchers  report in the Jan. 23 issue of Cell. Their findings could lead to a new understanding of this dangerous illness.

Sepsis is one of the most frequent causes of death worldwide, according to the World Health Organization (WHO), killing 11 million people each year. It's characterized by runaway inflammation, usually sparked by an infection. It can lead to shock, multiple organ failure, and death if treatment is not rapid enough or effective.

But recent research has shown that it isn't actually the infection that causes the spiraling inflammation: it's the cells caught up in it. Even if those cells aren't infected, they act as if they are, and die. As they die, they send out messages to other cells. Those messages somehow cause the recipient cells to die.

If scientists understood what caused this deadly message chain, they might be able to stop it. And that could help heal sepsis.

The deadly message mystery may now be solved. It appears that the "messages" are a byproduct of the cells trying to stay alive.

The process starts with cells that really are infected. To prevent the infection from spreading, those cells destroy themselves by sending a protein called gasdermin-D to their surface. Several gasdermin-D proteins will link together to create a round pore on the cell, like a hole punched in a balloon. The cell's contents leak out, the cell collapses, and dies.

But the collapse isn't inevitable. Sometimes cells can act quickly and eject the section of their surface membrane with the gasdermin-D pore. The cell then zips the membrane closed and survives. The ejected membrane forms a little bubble, called a vesicle , that just happens to carry the deadly gasdermin-D pore. The vesicle floats around, and when it encounters a cell nearby, that deadly gasdermin-D pore punches into the healthy nearby cell's membrane and causes that cell to spill and die.

When a dying cell releases these vesicles, they can transplant these pores to a neighboring cell's surface, which leads to the neighboring cell's death. 

 In other words, the deadly messages are a side effect of cells just trying to save themselves. A group of dying cells can release enough gasdermin-D vesicles to kill a considerable number of nearby cells. That spreading message of death fuels the spiraling inflammation of sepsis.

Researchers are now looking for a way to tamp down the deadly gasdermin-D vesicles. If successful, it could lead to a treatment for inflammatory diseases like sepsis. 

 Skylar S. Wright et al, Transplantation of gasdermin pores by extracellular vesicles propagates pyroptosis to bystander cells, Cell (2024). DOI: 10.1016/j.cell.2024.11.018

Why hibernating animals don't dream

Because hibernation isn’t the same as sleep. 

Sleep is a more physiologically ‘active’ state. Hibernation, in contrast, requires animals (like this hedgehog, above) to substantially reduce all activities to conserve energy.

Hibernating animals reduce their breathing rate, lower their body temperature and decrease their metabolic rate to around five per cent of their usual levels. There’s simply not enough brain activity while an animal is hibernating to enable dreaming.
There is one exception, however: the fat-tailed lemur. As the only primate to hibernate, scientists have observed them having periods of rapid eye movement (REM) sleep.

New water purification technology helps turn seawater into drinking water without using tons of chemicals

Water desalination plants could replace expensive chemicals with new carbon cloth electrodes that remove boron from seawater, an important step of turning seawater into safe drinking water.

A study describing the new technology has been published in Nature Water.

Boron is a natural component of seawater that becomes a toxic contaminant in drinking water when it sneaks through conventional filters for removing salts. Seawater's boron levels are around twice as high as the World Health Organization's most lenient limits for safe drinking water, and five to 12 times higher than the tolerance of many agricultural plants.

 Most reverse osmosis membranes don't remove very much boron, so desalination plants typically have to do some post treatment to get rid of the boron, which can be expensive. So researchers developed a new technology that's fairly scalable and can remove boron in an energy-efficient way compared to some of the conventional technologies.

In seawater, boron exists as electrically neutral boric acid, so it passes through reverse osmosis membranes that typically remove salt by repelling electrically charged atoms and molecules called ions. To get around this problem, desalination plants normally add a base to their treated water, which causes boric acid to become negatively charged. Another stage of reverse osmosis removes the newly charged boron, and the base is neutralized afterward by adding acid. Those extra treatment steps can be costly.

The new device now developed  reduces the chemical and energy demands of seawater desalination, significantly enhancing environmental sustainability and cutting costs by up to 15 percent, or around 20 cents per cubic meter of treated water.

The new electrodes remove boron by trapping it inside pores studded with oxygen-containing structures. These structures specifically bind with boron while letting other ions in seawater pass through, maximizing the amount of boron they can capture.

But the boron-catching structures still need the boron to have a negative charge. Instead of adding a base, the charge is created by splitting water between two electrodes, creating positive hydrogen ions and negative hydroxide ions. The hydroxide attaches to boron, giving it a negative charge that makes it stick to the capture sites inside the pores in the positive electrode. Capturing boron with the electrodes also enables treatment plants to avoid spending more energy on another stage of reverse osmosis. Afterward, the hydrogen and hydroxide ions recombine to yield neutral, boron-free water.

 Weiyi Pan et al, A highly selective and energy efficient approach to boron removal overcomes the Achilles heel of seawater desalination, Nature Water (2025). DOI: 10.1038/s44221-024-00362-y

AI-based pregnancy analysis discovers previously unknown warning signs for stillbirth and newborn complications

A new AI-based analysis of almost 10,000 pregnancies has discovered previously unidentified combinations of risk factors linked to serious negative pregnancy outcomes, including stillbirth.

The study also found that there may be up to a tenfold difference in risk for infants who are currently treated identically under clinical guidelines.

The researchers started with an existing dataset of 9,558 pregnancies, which included information on social and physical characteristics ranging from pregnant people's level of social support to their blood pressure, medical history, and fetal weight, as well as the outcome of each pregnancy. By using AI to look for patterns in the data, they identified new combinations of maternal and fetal characteristics that were linked to unhealthy pregnancy outcomes such as stillbirth.

Usually, female fetuses are at slightly lower risk for complications than male fetuses—a small but well-established effect. But the research team found that if a pregnant person has pre-existing diabetes, female fetuses are at higher risk than males.

This previously undetected pattern shows that the AI model can help researchers learn new things about pregnancy health.

The researchers were especially interested in developing better risk estimates for fetuses in the bottom 10% for weight, but not the bottom 3%. These babies are small enough to be concerning, but large enough that they are usually perfectly healthy. Figuring out the best course of action in these cases is challenging: Will a pregnancy need intensive monitoring and potentially early delivery, or can the pregnancy proceed largely as normal? Current clinical guidelines advise intensive medical monitoring for all such pregnancies, which can represent a significant emotional and financial burden.

But the researchers found that within this fetal weight class, the risk of an unhealthy pregnancy outcome varied widely, from no riskier than an average pregnancy to nearly ten times the average risk. The risk was based on a combination of factors such as fetal sex, presence or absence of pre-existing diabetes, and presence or absence of a fetal anomaly such as a heart defect.

For humans or AI models, estimating pregnancy risks involves taking a very large number of variables into account, from maternal health to ultrasound data. Experienced clinicians can weigh all these variables to make individualized care decisions, but even the best doctors probably wouldn't be able to quantify exactly how they arrived at their final decision. Human factors like bias, mood, or sleep deprivation almost inevitably creep into the mix and can subtly skew judgment calls away from ideal care.

To help address this problem, the researchers used a type of model called "explainable AI," which provides the user with the estimated risk for a given set of pregnancy factors and also includes information on which variables contributed to that risk estimation, and how much.

Part 1

Essentially, explainable AI approximates the flexibility of expert clinical judgment while avoiding its pitfalls. The researchers' model is also especially well-suited to judging risk for rare pregnancy scenarios, accurately estimating outcomes for people with unique combinations of risk factors. This kind of tool could ultimately help personalize care by guiding informed decisions for people whose situations are one-of-a-kind.
AI models can essentially estimate a risk that is specific to a given person's context and they can do it transparently and reproducibly, which is what human brains can't do.

 AI-based analysis of fetal growth restriction in a prospective obstetric cohort quantifies compound risks for perinatal morbidity and mortality and identifies previously unrecognized high risk clinical scenarios, BMC Pregnancy and Childbirth (2025). DOI: 10.1186/s12884-024-07095-6

Part 2

How tackling sepsis can save millions of lives—and prevent future pandemic deaths

Sepsis is an underestimated killer. Nearly a quarter of patients treated for sepsis in hospital will die, but because so many different illnesses can predispose patients to experiencing it, it's overlooked as a direct cause of death. Yet approximately 20% of deaths worldwide are caused by sepsis, and currently we have no treatments that tackle it directly.

Now researchers writing in Frontiers in Science explain how systems immunology can help us understand and treat sepsis—and how this could cut the death toll of future pandemics, no matter what disease causes them.

One of the reasons it's so hard to understand and treat sepsis is that it is multifaceted. Sepsis arises when the immune system fails to control an infection and malfunctions, causing multi-organ failure. Many different infections can cause sepsis, and its symptoms and progression vary between patients and over time in the same patient. Its early symptoms are similar to those of many other illnesses, which makes it difficult to diagnose quickly and initiate timely treatment, contributing to high mortality.

Systems immunology offers a potential solution to this diagnosis problem by using mathematical and computational modeling to study the immune system in the context of all the body's other systems. It does this by using different types of clustering analysis to identify patterns in large volumes of omics data, ranging from transcriptomic data (what genes show altered expression) to proteomic and metabolomic data—data that tell us about the body's reaction to its physical circumstances, in this case sepsis, in incredibly fine-grained detail.

These patterns help us work out the patterns and basis for the immune dysregulation that drives sepsis, come up with new hypotheses that we can research and use to develop new treatments, and identify diagnostic markers that we can use to catch sepsis early.

For instance, using these clustering analyses, scientists have identified changes to gene expression that act as early warnings for sepsis. They've also been able to identify five different subtypes of sepsis which are caused by different kinds of immune dysregulation and have different prognoses. In the future, we could build on these advances to diagnose different subtypes of sepsis earlier and treat them with the right drugs when we do.

However, systems immunology analysis is not yet in widespread use, because it is expensive and demands significant volumes of data—so we don't yet know how these diagnostics could translate into clinical results. The researchers call urgently for targeted funding and greater data availability.

"In sepsis we lack the depth of information required to enable more effective systems immunology and machine learning approaches.

Part 1

Successfully treating sepsis would be a multipurpose life-saver, preventing mortality regardless of the illness that triggered it. Viral sepsis is a major cause of deaths triggered by severe COVID-19, while many deaths in historical pandemics like the 1919 influenza pandemic and the bubonic plague are thought to have resulted from sepsis.

If we can tackle sepsis, we might be able to protect ourselves against the worst consequences and the highest death tolls in future pandemics, no matter what kind of infection causes them. Since immune dysregulation linked to sepsis can linger, causing symptoms similar to post-viral syndromes like long COVID-19, learning to treat this could also benefit some chronic illness patients.

But to make this happen, the researchers caution, more funding and larger studies will be needed.
The omics methods that underlie systems immunology are relatively expensive on a per patient basis. It will require a concerted drive from stakeholders to generate the data needed for further insights. We need to invest in larger omics studies of patients, develop new animal and organoid models that reflect sepsis heterogeneity, and invest in early diagnostics for sepsis and treatments that correct or supplement defective immunity in sepsis patients.

Deciphering sepsis: transforming diagnosis and treatment through systems immunology, Frontiers in Science (2025). DOI: 10.3389/fsci.2024.1469417

Part 2

Why you shouldn't scratch an itchy rash

New research published in the journal Science uncovers how scratching aggravates inflammation and swelling in a mouse model of a type of eczema called allergic contact dermatitis.

Scratching is often pleasurable, which suggests that, in order to have evolved, this behaviour must provide some kind of benefit. This new study helps resolve this paradox by providing evidence that scratching also provides defense against bacterial skin infections.

Allergic contact dermatitis is an allergic reaction to allergens or skin irritants—including poison ivy and certain metals such as nickel—leading to an itchy, swollen rash. Succumbing to the often-irresistible urge to scratch triggers further inflammation that worsens symptoms and slows healing.

To figure out what drives this vicious cycle,  researchers used itch-inducing allergens to induce eczema-like symptoms on the ears of normal mice and those that don't get itchy because they lack an itch-sensing neuron.

When normal mice were allowed to scratch, their ears became swollen and filled with inflammatory immune cells called neutrophils. In contrast, inflammation and swelling were much milder in normal mice that couldn't scratch because they wore tiny Elizabethan collars, similar to a cone that a dog might sport after a visit to the vet, and in animals that lacked the itch-sensing neuron. This experiment confirmed that scratching further aggravates the skin.

Next, the researchers showed that scratching causes pain-sensing neurons to release a compound called substance P. In turn, substance P activates mast cells, which are key coordinators of inflammation that drive itchiness and inflammation via recruitment of neutrophils.

In contact dermatitis, mast cells are directly activated by allergens, which drives minor inflammation and itchiness.

In response to scratching, the release of substance P activates mast cells through a second pathway, so the reason that scratching triggers more inflammation in the skin is because mast cells have been synergistically activated through two pathways.

Part 1

Mast cells are culprits in a range of inflammatory skin conditions and allergic reactions, but they're also important for protecting against bacteria and other pathogens. As such, the researchers wondered if scratching-induced activation of mast cells could affect the skin microbiome.
The researchers showed that scratching reduced the amount of Staphylococcus aureus, the most common bacteria involved in skin infections, on the skin.
The finding that scratching improves defense against Staphylococcus aureus suggests that it could be beneficial in some contexts. But the damage that scratching does to the skin probably outweighs this benefit when itching is chronic.

Andrew W. Liu et al, Scratching promotes allergic inflammation and host defense via neurogenic mast cell activation, Science (2025). DOI: 10.1126/science.adn9390. www.science.org/doi/10.1126/science.adn9390

Part 2

Your fridge still uses tech from the 50s, but scientists have an update

Researchers report on Jan. 30 in the journal Joule that a more efficient and environmentally friendly form of refrigeration might be on the horizon. The new technology is based on thermogalvanic cells that produce a cooling effect by way of a reversible electrochemical reaction.

Thermogalvanic refrigeration is cheaper and more environmentally friendly than other cooling methods because it requires a far lower energy input, and its scalability means that it could be used for various applications—from wearable cooling devices to industrial-grade scenarios.

Thermogalvanic cells use the heat produced by reversible electrochemical reactions to create electrical power. In theory, reversing this process—applying an external electrical current to drive electrochemical reactions—enables cooling power to be generated.

Previous studies have shown that thermogalvanic cells have a limited potential to produce cooling power, but  this new work was able to dramatically increase this potential by optimizing the chemicals used in the technology.

By tweaking the solutes and solvents used in the electrolyte solution, the researchers were able to improve the hydrogalvanic cell's cooling power. They used a hydrated iron salt containing perchlorate, which helped the iron ions dissolve and dissociate more freely compared to other previously tested iron-containing salts such as ferricyanide.
By dissolving the iron salts in a solvent containing nitriles rather than pure water, the researchers were able to improve the hydrogalvanic cell's cooling power by 70%.

The optimized system was able to cool the surrounding electrolyte by 1.42 K, which is a big improvement compared to the 0.1 K cooling capacity reported by previously published thermogalvanic systems.

Looking ahead, the team plans to continue optimizing their system's design and is also investigating potential commercial applications.

Solvation entropy engineering of thermogalvanic electrolytes for efficient electrochemical refrigeration, Joule (2025). DOI: 10.1016/j.joule.2025.101822. www.cell.com/joule/fulltext/S2542-4351(25)00003-0

The team then studied the impacts of the structural variation on the human cell lines. Using genomic sequencing, the team was able to take 'snapshots' of the human cells and their 'shuffled' genomes over the course of a few weeks, watching which cells survived and which died.

As expected, they found that when structural variation deleted essential genes, this was heavily selected against and the cells died. However, they found that groups of cells with large-scale deletions in the genomes that avoided essential genes survived.

The team also conducted RNA sequencing of the human cell lines, which measures gene activity, known as gene expression. This revealed that large-scale deletions of the genetic code, especially in non-coding regions, did not seem to impact the gene expression of the rest of the cell.

The researchers suggest that human genomes are extremely tolerant of structural variation, including variants that change the position of hundreds of genes, as long as essential genes are not deleted.

In another study related to this  another research  team used a different approach, adding recombinase sites to transposons—mobile genetic elements—that randomly integrated in the genomes of human cell lines and mouse embryonic stem cells.

Using their method, they demonstrated that the effects of the induced structural variants can be read out using single-cell RNA sequencing. This advance paves the way for large screens of structural variant impact, potentially improving the classification of structural variants found in human genomes as benign or clinically significant.

Both studies came to similar conclusions that human genomes are surprisingly tolerant to some substantial structural changes, although the full extent of this tolerance remains to be explored in future studies enabled by these technologies.

Jonas Koeppel et al, Randomizing the human genome by engineering recombination between repeat elements, Science (2025). DOI: 10.1126/science.ado3979. www.science.org/doi/10.1126/science.ado3979

Science (2025). DOI: 10.1126.science.ado5978

part2

Scientists replicate bone marrow

Hidden within our bones, marrow sustains life by producing billions of blood cells daily, from oxygen-carrying red cells to immune-boosting white cells. This vital function is often disrupted in cancer patients undergoing chemotherapy or radiation, which can damage the marrow and lead to dangerously low white cell counts, leaving patients vulnerable to infection.

Now researchers have developed a platform that emulates human marrow's native environment. This breakthrough addresses a critical need in medical science, as animal studies often fail to fully replicate the complexities of human marrow.

The team's new device is a small plastic chip whose specially designed chambers are filled with human blood stem cells and the surrounding support cells with which they interact in a hydrogel to mimic the intricate process of bone marrow development in the human embryo. This biologically inspired platform makes it possible to build living human marrow tissue that can generate functional human blood cells and release them into culture media flowing in engineered capillary blood vessels.

The bone marrow-on-a-chip allows researchers to simulate and study common side effects of medical treatments, such as radiotherapy and chemotherapy for cancer patients. When connected to another device, it can even model how the bone marrow communicates with other organs, like the lungs, to protect them from infections and other potentially life-threatening conditions.

Described in a new paper published in Cell Stem Cell, the bone marrow model and the demonstration of its large-scale production and automation could advance fields as diverse as drug development by enabling automated, high-throughput preclinical screening of marrow toxicity of anticancer drugs) and space travel (by allowing researchers to study the effects of prolonged radiation exposure and microgravity on the immune system of astronauts).  

Andrei Georgescu et al, Self-organization of the hematopoietic vascular niche and emergent innate immunity on a chip, Cell Stem Cell (2024). DOI: 10.1016/j.stem.2024.11.003

Future antibiotics face early bacterial resistance challenges, studies show

Researchers have made a concerning discovery about the future of antibiotics. Two recent studies, published just days apart in Nature Microbiology and Science Translational Medicine found that resistance can develop against new antibiotics even before they are widely used, compromising their effectiveness from the start. The studies focused on five critical bacterial species that cause major hospital infections and examined 18 new antibiotics, some already on the market and others still in development.

New antibiotics are often marketed as resistance-free, but this claim relies on limited data. 

This new work  highlights a major issue: antibiotic development tends to prioritize broad-spectrum activity - that is the number of bacterial species a drug targets- over long-term sustainability. While many new antibiotics indeed offer a broader spectrum, this doesn't guarantee they will remain effective in the long run in clinical use.

The studies found that resistance developed rapidly against nearly all the tested antibiotics, defying earlier expectations. For example, teixobactin, once hailed as a revolutionary drug, was believed to be less prone to resistance. However, the research revealed that bacteria can adapt to it with this adaptation resulting in cross-resistance to other critical antibiotics.

Alarmingly, the team also found that resistance mutations may already exist in bacterial populations, likely due to the overuse of older antibiotics and the shared resistance mechanisms between those and new drugs. These pre-existing mutations could render even the newest drugs ineffective shortly after they are introduced into clinical use.

Rethinking antibiotic development:  The studies call for a fundamental shift in how antibiotics are developed. Drug companies must incorporate resistance studies early in the development process to anticipate and mitigate risks before antibiotics are released. Integrating resistance prediction and genetic surveillance into drug design could reduce the chances of failure.

Some new antibiotics show more promise than others, as resistance develops more slowly or only in specific bacterial species. Understanding why these drugs perform better is the next crucial step.

The studies emphasize the importance of prioritizing antibiotics with novel modes of action to bypass existing resistance. In cases where only certain bacterial species are prone to resistance, narrow-spectrum therapy could provide an effective alternative. Finally, the studies stress the urgency of responsible antibiotic use to slow down the evolution of resistance and ensure the prolonged efficacy of new treatments in the future.

 Lejla Daruka et al, ESKAPE pathogens rapidly develop resistance against antibiotics in development in vitro, Nature Microbiology (2025). DOI: 10.1038/s41564-024-01891-8

Ana Martins et al, Antibiotic candidates for Gram-positive bacterial infections induce multidrug resistance, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adl2103

Bats' genetic adaptations: How they tolerate coronaviruses without becoming ill

New research has shown that bats can tolerate coronaviruses and other viruses without becoming ill, thanks to special adaptations of their immune system.

The study, published in Nature, shows that bats have more genetic adaptations in immune genes than other mammals. The ISG15 gene in particular plays a key role: in some bats, it can reduce the production of SARS-CoV-2 by up to 90%. 

The results could help to develop new medical approaches to combat viral diseases.

Bats have unique characteristics. As the only mammals that can actively fly, they play an important role in the ecosystem: They pollinate plants, spread seeds and contribute to the balance of the insect population through their feeding habits. Their exceptional orientation using ultrasonic echolocation shows how perfectly they are adapted to their nocturnal lifestyle.

Bats are of great interest to medical advancement, as their immune systems and unique viral tolerances can provide valuable insights for the development of new therapies. They are also known to carry numerous viruses, including those that are transmissible to humans—such as coronaviruses. However, bats do not show any symptoms of disease when infected with such viruses.

The new research team has sequenced high-quality genomes of 10 new bat species, as part of the international Bat1K project, including species known to carry coronaviruses and other viruses. Such adaptations can be detected as traces of positive selection and can indicate functional changes.

The result of the extensive analysis shows that bats exhibit such adaptations in immune genes much more frequently than other mammals.

The research also showed that the common ancestor of all bats had an unexpectedly high number of immune genes with selection signatures. This suggests that the evolution of the immune system could be closely linked to the evolution of the ability to fly.

Ariadna E. Morales et al, Bat genomes illuminate adaptations to viral tolerance and disease resistance, Nature (2025). DOI: 10.1038/s41586-024-08471-0

 India doubled its tiger population in a decade and credits conservation efforts

India doubled its tiger population in a little over a decade by protecting the big cats from poaching and habitat loss, ensuring they have enough prey, reducing human-wildlife conflict, and increasing communities' living standards near tiger areas, a study published this week found.

The number of tigers grew from an estimated 1,706 tigers in 2010 to around 3,682 in 2022, according to estimates by the National Tiger Conservation Authority, making India home to roughly 75% of the global tiger population. The study found that some local communities near tiger habitats have also benefited from the increase in tigers because of the foot traffic and revenues brought in by ecotourism.

The study in the journal Science says India's success "offers important lessons for tiger-range countries" that conservation efforts can benefit both biodiversity and nearby communities.

Wildlife conservationists and ecologists welcomed the study but said that tigers and other wildlife in India would benefit if source data were made available to a larger group of scientists. The study was based on data collected by Indian government-supported institutions.

Also there are several species, including the great Indian bustard and caracal which are all on the edge. "And there is really not enough focus on that."

 Yadvendradev V. Jhala et al, Tiger recovery amid people and poverty, Science (2025). DOI: 10.1126/science.adk4827

Amniotic fluid's protective properties: Study uncovers its role in blood clotting

Researchers have made new discoveries about amniotic fluid, a substance historically not well understood in medical research due to the difficulty in obtaining it during pregnancy, especially across gestation.

Amniotic fluid is the vital fluid that surrounds and protects a fetus during pregnancy. In addition to providing much-needed cushion and protection for the fetus, it also aids in development of vital organs—especially the lungs, digestive tract and skin—and stabilizes the temperature inside the womb.

The new study, published in the journal Research and Practice in Thrombosis and Haemostasis, found that the addition of amniotic fluid to plasma—the liquid portion of blood—improves the blood's ability to thicken and clot, which is a critical and likely a protective function throughout pregnancy and during delivery for both the birthing parent and the baby.

Researchers analyzed the properties of amniotic fluid obtained by amniocentesis, a prenatal test that involves sampling a small amount of amniotic fluid to examine the health of the pregnancy, from both human and non-human primates at gestational-age matched timepoints. The findings showed that amniotic fluid increases blood clotting through key fatty acids and proteins that change each trimester and help regulate coagulation.

 Chih Jen Yang et al, Characterization of the procoagulant phenotype of amniotic fluid across gestation in rhesus macaques and humans, Research and Practice in Thrombosis and Haemostasis (2025). DOI: 10.1016/j.rpth.2024.102676

Asteroid find upends story of life’s origin
Fragments collected from the asteroid Bennu contain the building blocks for life — all five nucleobases that form DNA and RNA and 14 of the 20 amino acids needed to make known proteins. But there’s a twist: on Earth, amino acids in living organisms tend to have a ‘left-handed’ structure. Those on Bennu, however, contain nearly equal amounts of these structures and their ‘right-handed’, mirror-image forms. This calls into question a hypothesis favoured by many scientists that asteroids similar to this one might have seeded life on Earth.

https://www.nature.com/articles/s41550-024-02472-9?utm_source=Live+...

https://www.nature.com/articles/d41586-025-00264-3?utm_source=Live+...

Ear muscle we thought humans didn't use—except for wiggling our ears—activates during focused listening

If you can wiggle your ears, you can use muscles that helped our distant ancestors listen closely. These auricular muscles helped change the shape of the pinna, or the shell of the ear, funneling sound to the eardrums.

There are three large muscles which connect the auricle to the skull and scalp and are important for ear wiggling. These muscles, particularly the superior auricular muscle, exhibit increased activity during effortful listening tasks. This suggests that these muscles are engaged not merely as a reflex but potentially as part of an attentional effort mechanism, especially in challenging auditory environments.

It's difficult to test how hard someone is listening without self-reported measures. But electromyography, which measures electrical activity in a muscle, can help identify activity in the auricular muscles linked to listening closely.

Similar research has already shown that the largest muscles, posterior and superior auricular muscles, react during attentive listening. Because they pull the ears up and back, they are considered likely to have been involved in moving the pinna to capture sounds.

The exact reason these became vestigial is difficult to tell, as our ancestors lost this ability about 25 million years ago. One possible explanation could be that the evolutionary pressure to move the ears ceased because we became much more proficient with our visual and vocal systems.

Scientists now found that the two auricular muscles reacted differently to the different conditions. The posterior auricular muscles reacted to changes in direction, while the superior auricular muscles reacted to the difficulty level of the task.

Electromyographic Correlates of Effortful Listening in the Vestigial Auriculomotor System, Frontiers in Neuroscience (2025). DOI: 10.3389/fnins.2024.1462507

Gut microbes may mediate the link between drinking sugary beverages and diabetes risk

It is well known that consuming sugary drinks increases the risk of diabetes, but the mechanism behind this relationship is unclear. Now, in a paper appearing in Cell Metabolism, researchers show that metabolites produced by gut microbes might play a role.

In a long-term cohort of US Hispanic/Latino adults, the researchers identified differences in the gut microbiota and blood metabolites of individuals with a high intake of sugar-sweetened beverages. The altered metabolite profile seen in sugary beverage drinkers was associated with a higher risk of developing diabetes in the subsequent 10 years. Since some of these metabolites are produced by gut microbes, this suggests that the microbiome might mediate the association between sugary beverages and diabetes.

This study suggests a potential mechanism to explain why sugar-sweetened beverages are bad for your metabolism. 

Previous studies in Europe and China have shown that sugar-sweetened beverages alter gut microbiome composition, but this is the first study to investigate whether this microbial change impacts host metabolism and diabetes risk.

The researchers found that high sugary beverage intake—defined as two or more sugary beverages per day—was associated with changes in the abundance of nine species of bacteria. Four of these species are known to produce short-chain fatty acids—molecules that are produced when bacteria digest fiber and that are known to positively impact glucose metabolism. In general, bacterial species that were positively associated with sugary beverage intake correlated with worse metabolic traits. Interestingly, these bacteria were not associated with sugar ingested from non-beverage sources. 

The researchers also found associations between sugary beverage consumption and 56 serum metabolites, including several metabolites that are produced by gut microbiota or are derivatives of gut-microbiota-produced metabolites.

These sugar-associated metabolites were associated with worse metabolic traits, including higher levels of fasting blood glucose and insulin, higher BMIs and waist-to-hip ratios, and lower levels of high-density lipoprotein cholesterol ("good" cholesterol). Notably, individuals with higher levels of these metabolites had a higher likelihood of developing diabetes in the 10 years following their initial visit.

They found that several microbiota-related metabolites are associated with the risk of diabetes. In other words, these metabolites may predict future diabetes.

These results have to be validated in other populations too for a final conclusion. 

 Sugar-sweetened beverage intake, gut microbiota, circulating metabolites, and diabetes risk in Hispanic Community Health Study/Study of Latinos, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2024.12.004. www.cell.com/cell-metabolism/f … 1550-4131(24)00486-8

BioSonics spectroscopy can 'listen' to the sounds made by individual viruses

A team of chemists and microbiologists has found that an all-optical method can be used to detect natural vibrational frequencies made by individual viruses as a way to identify them. In their study published in Proceedings of the National Academy of Sciences, the group found a way to bounce light off viruses and detect the resulting patterns of vibrations, which could be easily identified.

Light can be used to identify nanoparticle-scale objects. Prior research has shown that firing beams of light at such objects can cause them to vibrate slightly. The vibration patterns that emerge are unique for different targets. Thus, the technique can be used to identify nanoscale objects even among other similarly scaled objects.

The researchers wondered if the same technique could be used with biological agents like viruses and bacteria, so they conducted experiments that involved firing extremely tiny amounts of light at both kinds of microorganisms at such a small scale that they were able to watch the impact of single photons.

Eventually, they shifted their focus to viruses only and found that with the appropriate parameter settings, they could detect the vibrations emitted by the virus using a technique that they call BioSonics spectroscopy. The sound was not just too faint to hear with the human ear, but too high, at a frequency 1 million times higher than humans can hear.

After testing multiple viruses, the research team found that each of them vibrated in their own unique ways, distinct from one another and from all the other molecules they tested. That meant that BioSonics could be used as a sensor of sorts, enabling devices that could, for example, scan a room, detect viruses in the air and identify them.

They also note that the technology could reveal individual virus activity, opening the door to better understanding them. It could be used, for example, to watch as individual viruses assemble themselves, a phenomenon that is still not well understood.

Yaqing Zhang et al, Nanoscopic acoustic vibrational dynamics of a single virus captured by ultrafast spectroscopy, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2420428122

Myth busting: Purpose-bred dogs are not better at biting or scenting than those not bred for that purpose

Since their domestication millennia ago, dogs have been man's best friend, and aside from friendship, centuries of selective breeding have tailored them for tasks like herding, hunting and guarding—or so we thought.

Now, the results of a new study challenge the prevailing belief that some breeds are inherently superior at specific tasks, based on their skull morphology.

The study published in Science Advances on January 29, used advanced 3D reconstruction techniques to analyze 117 skulls from 40 domestic dog breeds and 18 wild canid species.

The researchers found substantial overlap in skull shapes across breeds and functional categories, but no clear evidence that breeds selected for bite work or scent work have developed distinct morphological traits that enhance these abilities. This suggests that humans have been breeding dogs primarily for preferred visible traits, and that other factors like individual personality affect dogs' performance of tasks.

In the past 200 years, humans have created hundreds of dog breeds that look really different and are pretty specialized at some tasks like herding, protecting, and detecting odors. We have assumed that these dogs look different because they are 'structurally' specialized at these tasks, but this new study shows that, at least for their skulls, they 'are not' specialized for tasks that involve the skull, such as biting tasks and scent work.

The study examined dog breeds commonly used for tasks like bite work and scent work, such as those in law enforcement and military programs, where dogs are trained for patrol and detection. Researchers used advanced methods, including 3D skull analysis, to compare breeds across various functional groups.

The results showed that domesticated dog breeds exhibit exceptional diversity in their skull shapes, but have high overlap among the parts of the skulls that correspond with functional tasks.

This indicates that specific breeds are not as morphologically specialized for such tasks as previously thought. For instance, bite-force measurements did not show any significant differences between breeds purpose-bred for bite work and those not.

Part 1

There are many news stories about dogs attacking people badly and often there are specific breeds that are targets of this reporting (such as pit bulls). Some people claim that these dogs will bite harder than other dogs of the same size, or they have special features like 'locking jaws' that make them especially dangerous to people. This study shows that this is simply not true; dogs bred to bite things aren't structurally different than dogs that have been bred to do other things.
Similarly, breeds selected for scent work did not demonstrate significantly enhanced olfactory morphology compared to other breeds. The lone group that showed distinct skull morphology was brachycephalic breeds (e.g., bulldogs), which are characterized by their shortened snouts, but this feature is not tied to functional specialization. Instead, human aesthetic preferences have played a larger role in shaping dog morphology.
Humans have done so much breeding work to alter the visual appearance of these animals that the researchers honestly expected to see really marked groupings of some kind but they really didn't see much of that.
However, researchers found that domesticated dog breeds' morphologies differed greatly from wild canids, such as wolves and foxes, which tend to have skull shapes that align more closely with their natural functional needs. Wolves and foxes tend to possess elongated snouts relative to their cranial length, which is a typical feature of species that rely on keen senses like smell.

Undomesticated animals, particularly wolves, show skull morphologies that reflect evolutionary adaptations for hunting and scent work, which contrasts with the lack of strong morphological specialization in domesticated breeds.

Interestingly, foxes' skull shapes overlap significantly with some domestic dogs, particularly terrier breeds, which were historically bred for pest control, suggesting functional similarities in skull structure for small prey pursuit.

While these results run counter to the popular notion that purpose-bred dogs are better at biting or scenting than those not bred for that purpose, they suggest that observable behavior traits are associated with performance, rather than morphological traits.
Recent research suggests that many breed-associated behaviors are partially heritable. This has important implications for how dogs are bred and selected for specific tasks in areas such as law enforcement and search and rescue—behavioral traits and individual trainability may be more important determinants of performance.

Nicholas Hebdon et al, Dog skull shape challenges assumptions of performance specialization from selective breeding, Science Advances (2025). DOI: 10.1126/sciadv.adq9590

Part 2