With the world moving towards more sustainable options, researchers have been on the lookout for high-performance, non-toxic adhesives derived from renewable resources.

Several studies have ventured into the extraction of bio-based adhesives from natural sources like soybean protein, starch, chitin, cellulose, and lignin. However, they suffered from limitations such as low bonding strength and lack of reusability.
To synthesize the high-performance bio-based adhesive, the researchers sourced xylan from viscose fiber mills, which were then freeze-dried and oxidized in the sodium periodate (NaIO4) solution. This step selectively oxidized the 2,3-hydroxyl groups of xylan into aldehyde groups while cleaving the carbon bonds (C2–C3) in the anhydroxylose units, resulting in dialdehyde xylan (DAX).

After purification, the DAX powder was treated with a monobasic sodium phosphate solution, followed by sodium borohydride (NaBH4), which reduced the hydroxyl groups and yielded the final product, dialcohol xylan (RDAX).
The researchers used the xylan adhesive to bond together some woodchips and found that it exhibited a lap-shear strength—the ability to maintain adhesion when force is applied parallel to the bonded joint—of up to around 30 MPa, a value that surpasses many commercially available HMAs. High-performance hot-melt adhesive (XA) also works well in extreme cold, too, maintaining strong adhesion even at –25°C.

This enhanced adhesion strength traces back to the formation of a continuous layer that mechanically interlocks with the wood by penetrating its vessel pores. At the molecular level, strong adhesion arises primarily from hydrogen bonding and van der Waals forces between the adhesive and the substrate surface.

A biocompatible and reusable adhesive obtained from a waste byproduct strengthens the shift towards a greener and more circular economy.

Ziwen Lv et al, Bio-based hot-melt adhesive from xylan, Nature Sustainability (2025). DOI: 10.1038/s41893-025-01579-9

Part 2

Statins may reduce risk of death by 39% for patients with life-threatening sepsis, large study finds

Sepsis is when the immune system overshoots its inflammatory reaction to an infection, so strongly that the vital organs begin to shut down. It is life-threatening.

In about 15% of cases, sepsis worsens into septic shock, characterized by dangerously low blood pressure and reduced blood flow to tissues. The risk of death from septic shock is even higher, between 30% and 40%.

The earlier patients with sepsis are treated, the better their prospects. Typically, they receive antibiotics, intravenous fluids, and vasopressors to raise blood pressure. But now, a large cohort study published in Frontiers in Immunology has shown for the first time that supplementary treatment with statins could boost their chances of survival.

This cohort study found that treatment with statins was associated with a 39% lower death rate for critically ill patients with sepsis, when measured over 28 days after hospital admission.

Statins are best known as a protective treatment against cardiovascular disease, which function by lowering 'bad' LDL cholesterol and triglycerides, and raising 'good' HDL cholesterol. But they have been shown to bring a plethora of further benefits, which explains the burgeoning interest in their use as a supplementary therapy for inflammatory disorders, including sepsis.

Not just lowering cholesterol,  Statins have anti-inflammatory, immunomodulatory, antioxidative, and antithrombotic properties too. They may help mitigate excessive inflammatory response, restore endothelial function, and show potential antimicrobial activities.

The authors sourced their data from the public Medical Information Mart for Intensive Care-IV (MIMIC-IV) database, which holds the anonymized e-health records of 265,000 patients admitted to the emergency department and the intensive care unit of the Beth Israel Deaconess Medical Center of Boston between 2008 and 2019. Only adults with a diagnosis of sepsis hospitalized for longer than 24 hours were included.

The authors compared outcomes between patients who received or didn't receive any statins during their stay besides standard of care, regardless of the type of statin.

The results showed that the 28-day all-cause mortality rate was 14.3% in the statin group and 23.4% in the no statin group, indicating a relative reduction of 39% [9.1 percentage points].

"These results strongly suggest that statins may provide a protective effect and improve clinical outcomes for patients with sepsis," concluded the researchers.

Statin use during Intensive Care Unit Stay Is Associated with Improved Clinical Outcomes in Critically Ill Patients with Sepsis: A Cohort Study, Frontiers in Immunology (2025). DOI: 10.3389/fimmu.2025.1537172

Airborne toxin detected in Western Hemisphere for the first time

Once in a while, scientific research resembles detective work. Researchers head into the field with a hypothesis and high hopes of finding specific results, but sometimes, there's a twist in the story that requires a deeper dive into the data.

That was the case for some researchers who led a field campaign in an agricultural region of Oklahoma. Using a high-tech instrument to measure how aerosol particles form and grow in the atmosphere, they stumbled upon something unexpected: the first-ever airborne measurements of medium chain chlorinated paraffins (MCCPs), a kind of toxic organic pollutant, in the Western Hemisphere. Their results published today in ACS Environmental Au.

MCCPs are currently under consideration for regulation by the Stockholm Convention, a global treaty to protect human health from long-standing and widespread chemicals. While the toxic pollutants have been measured in Antarctica and Asia, researchers haven't been sure how to document them in the Western Hemisphere's atmosphere until now.

MCCPs are used in fluids for metalworking and in the construction of PVC and textiles. They are often found in wastewater and as a result, can end up in biosolid fertilizer, also called sewage sludge, which is created when liquid is removed from wastewater in a treatment plant. Researchers suspect the MCCPs they identified came from biosolid fertilizer in the fields near where they set up their instrument. When sewage sludges are spread across the fields, those toxic compounds could be released into the air, the researchers said. They can't show directly that that's happening, but they think it's a reasonable way that they could be winding up in the air. Sewage sludge fertilizers have been shown to release similar compounds.

Daniel John Katz et al, Real-Time Measurements of Gas-Phase Medium-Chain Chlorinated Paraffins Reveal Daily Changes in Gas-Particle Partitioning Controlled by Ambient Temperature, ACS Environmental Au (2025). DOI: 10.1021/acsenvironau.5c00038

**

Aged dust particles act as 'chemical reactors in sky' to drive air pollution, study finds

Dust particles thrown up from deserts such as the Sahara and Gobi are playing a previously unknown role in air pollution, a new study has found.

The international study published in National Science Review has revealed that, contrary to long-held scientific assumptions, aged desert dust particles, which were once considered too big and dry to host significant chemical reactions, actually act as "chemical reactors in the sky"—facilitating the formation of secondary organic aerosols (SOA), a major component of airborne particles.

Published in a collaborative effort led by scientists from China, Japan, the UK, and other nations, the study shows that during dust events such as those stemming from the Sahara and Gobi deserts, around 50% of water-soluble secondary organic aerosols, primarily considered as SOA, are found in coarse (supermicron) dust particles.

This finding challenges the conventional wisdom on its head as, until now, scientists thought that such SOA is primarily formed in fine (submicron) particles or cloud droplets.

This discovery marks a major advance in understanding the chemistry of secondary organic aerosols.

The team found that the formation of secondary organic aerosols (SOA) occurs in water-containing coatings of aged dust, specifically those that have reacted with atmospheric nitric acid to form calcium nitrate. This compound absorbs water even in dry conditions (relative humidity as low as 8%), creating a micro-environment where gas-phase pollutants like glyoxal can dissolve, react, and form aqueous-phase secondary organic aerosol (aqSOA).

To validate their findings, the team combined cutting-edge microscopic analysis with global-scale computer modeling. They showed that these dust-driven reactions could account for up to two thirds of total secondary organic aerosol in some of the world's dustiest regions, from North Africa to East Asia—orders of magnitude more than previous estimates.

Air pollution from fine particles is linked to millions of premature deaths annually and contributes to climate change. Understanding how and where these particles form helps improve forecasts, guide pollution controls, and ultimately protect human health.

Weijun Li et al, Aqueous-phase secondary organic aerosol formation on mineral dust, National Science Review (2025). DOI: 10.1093/nsr/nwaf221

Solar Analemma

Why the Sun Makes a Figure Eight in the Sky

The figure-8 pattern is due to a combination of the tilt of Earth's axis and the ellipticity of Earth's orbit which cause the Sun's position to change over the course of a year.

Excessive oleic acid, found in olive oil, shown to drive fat cell growth

We have been told that olive fat is good for health. Olive oil this and olive oil that. 

Now listen to this ....

Eating a high-fat diet containing a large amount of oleic acid—a type of fatty acid commonly found in olive oil—could drive obesity more than other types of dietary fats, according to a study published in the journal Cell Reports.

The study found that oleic acid, a monounsaturated fat associated with obesity, causes the body to make more fat cells. By boosting a signaling protein called AKT2 and reducing the activity of a regulating protein called LXR, high levels of oleic acid resulted in faster growth of the precursor cells that form new fat cells.

Researchers  fed mice a variety of specialized diets enriched in specific individual fatty acids, including those found in coconut oil, peanut oil, milk, lard and soybean oil. Oleic acid was the only one that caused the precursor cells that give rise to fat cells to proliferate more than other fatty acids.

You can think of the fat cells as an army. When you give oleic acid, it initially increases the number of 'fat cell soldiers' in the army, which creates a larger capacity to store excess dietary nutrients. Over time, if the excess nutrients overtake the number of fat cells, obesity can occur, which can then lead to cardiovascular diseases or diabetes if not controlled.

If someone is at risk for heart disease, high levels of oleic acid may not be a good idea, researchers conclude.

 Allison Wing et al, Dietary oleic acid drives obesogenic adipogenesis via modulation of LXRα signaling, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115527

There's an Invisible Line That Animals Usually Don't Cross 

The animal kingdoms of Asia and Australia are worlds apart, thanks to an invisible line that runs right between the two neighboring continents.

Most wildlife never cross this imaginary boundary, not even birds.

And so it has been for tens of millions of years, shaping animal evolution in different ways on each side.

It all started about 30 million years ago, when the Australian tectonic plate bashed up against the Eurasian tectonic plate and created an archipelago, rerouting ocean currents and creating new regional climates.

On one side of the map, in Indonesia and Malaysia, monkeys, apes, elephants, tigers, and rhinos evolved; while on the other side, in New Guinea and Australia, marsupials, monotremes, rodents, and cockatoos flourish.  Very few species are abundant on both sides.

The curious faunal divide is named Wallace's Line – after the naturalist Alfred Russel Wallace, who first noticed the stark difference in animal life (mostly mammals) while exploring the region in the mid-19th century.

An Invisible Barrier Keeping Two Worlds Apart

Generally speaking, Wallace's line separates a shelf of the Asian continent from a shelf of the Australian tectonic plate. It is a geological line, but it is also a climatic and biological one.

While Wallace's invisible line is most obvious when comparing mammals in Asia and Australia, it also exists for birds, reptiles, and other animals.

Even creatures with wings don't typically make the trip across Wallace's line, and in the ocean, some types of  fish and microbes show genetic differences on one side of the border compared to the other, indicating very little mixing between populations.

Scientists have yet to figure out what invisible barriers are holding these species back. Habitat and climate, however, are probably factors accentuating the evolutionary divide.

Wallace's divide isn't an absolute border, but more of a gradient, scientists say. Even still, the blurry line helps us make sense of animal evolution for thousands of species.

https://www.sciencealert.com/theres-an-invisible-line-that-animals-...

Image source:

https://rgssa.org.au/lectures/the-wallace-line

Sources:

The Wallace Line - The Royal Geographical Society of South Australia

Wallace Line - Wikipedia

Part 2

Why Do Some Runners Get Sick After a Marathon?

An intense training load, such as running long distances, can temporarily suppress the immune system, which may render athletes susceptible to falling ill.

It has been observed that marathon runners  tended to get sick during the week or two after running a marathon. 

Research results revealed a link between exercise load and illness: Runners were more likely to fall sick the week after the race than non-participants.¹ The risk was higher among athletes who trained more than 60 miles a week, indicating that greater exercise intensity raised the chance of illness.

These findings led to broader investigations in the lab. Thorough research in the field  has shown that while people draw a multitude of benefits from moderate exercise, heavy exertion during endurance sports, such as marathons and ultra marathons, triggers transient immune dysfunction and increased risk of upper respiratory illness.

They observed that people who took daily 45-minute brisk walks had increased circulation of some immune cells and enhanced activity of the body’s natural killer (NK) cells. Those who regularly walked also experienced less severe symptoms of respiratory infections compared to sedentary people. Other researchers have consistently reported similar observations: Bouts of moderate exercise send immune cells out of the tissues they reside in and into the bloodstream, where they patrol to spot and strike any invading pathogens.

In contrast, when researchers monitored athletes who ran for three hours, mimicking heavy exertion, they observed reduced numbers and activity of NK cells. This high-intensity exercise also increased the levels of the stress hormone cortisol, which can weaken the immune response. The levels returned to baseline in about a day. But it's still enough of an interruption in normal immunity such that the omnipresent viruses then can multiply, gain a foothold, and then increase infection rates.

However, some researchers have questioned whether this “open window” is sufficient to cause infections, debating whether athletes suffer from illness symptoms due to infections or simply as a result of exercise-associated inflammation. Nevertheless, researchers largely agree that heavy exercise temporarily suppresses some immune functions, which may compromise athletes’ resistance to minor illnesses if they do not rest and recover sufficiently between exercise sessions.

https://www.the-scientist.com/why-do-some-runners-get-sick-after-a-...

**

When antibiotics backfire: How a bacterial energy crisis fuels rapid resistance

Antibiotics are supposed to wipe out bacteria, yet the drugs can sometimes hand microbes an unexpected advantage. A new study  shows that ciprofloxacin, a staple treatment for urinary tract infections, throws Escherichia coli (E. coli) into an energy crisis that saves many cells from death and speeds the evolution of full-blown resistance.

Antibiotics can actually change bacterial metabolism. Researchers wanted to see what those changes do to the bugs' chances of survival. They focused on adenosine triphosphate (ATP), the molecular fuel that powers cells. When ATP levels crash, cells experience "bioenergetic stress".

To mimic that stress, the team engineered E. coli with genetic drains that constantly burned ATP or its cousin nicotinamide adenine dinucleotide (NADH). Then, they pitted both the engineered strains and normal bacteria against ciprofloxacin.

The results surprised the researchers. The drug and the genetic drains each slashed ATP, but rather than slowing down, the bacteria revved up. Respiration soared, and the cells spewed extra-reactive oxygen molecules that can damage DNA. That frenzy produced two troubling outcomes.

First, more of the bacteria cells survived.  In time-kill tests, 10 times as many stressed cells weathered a lethal ciprofloxacin dose compared with unstressed controls. These hardy stragglers, called persister cells, lie low until the drug is gone and then rebound to launch a new infection.

People have long blamed sluggish metabolism for persister cell formation. People expected a slower metabolism to cause less killing.  Researchers saw the opposite. The cells ramp up metabolism to refill their energy tanks and that turns on stress responses that slow the killing.

Follow-up experiments traced the protection to the stringent response, a bacterial alarm system that reprograms the cell under stress.

Part 1

Second, stressed cells mutated faster to evolve antibiotic resistance.
While persisters keep infections smoldering, genetic resistance can render a drug useless outright. The researchers cycled E. coli through escalating ciprofloxacin doses and found that stressed cells reached the resistance threshold four rounds sooner than normal cells. DNA sequencing and classic mutation tests pointed to oxidative damage and error-prone repair as the culprits.

The changes in metabolism are making antibiotics work less well and helping bacteria evolve resistance.
Preliminary measurements show that gentamicin and ampicillin also drain ATP in addition to ciprofloxacin. The stress effect may span very different pathogens, including the pathogen Mycobacterium tuberculosis, which is highly sensitive to ATP shocks.

If so, the discovery casts new light on a global threat. The findings suggest several changes to antibiotic development and use.
First, screen candidate antibiotics for unintended energy-draining side effects. Second, pair existing drugs with anti-evolution boosters that block the stress pathways or mop up the extra oxygen radicals. Third, reconsider the instinct to blast infections with the highest possible dose. Earlier studies and the new data both hint that extreme concentrations can trigger the very stress that protects bacteria.

Bacteria turn our attack into a training camp. We have to think and take measures to stop that.

 B Li, et al. Bioenergetic stress potentiates antimicrobial resistance and persistence, Nature Communications (2025). DOI: 10.1038/s41467-025-60302-6.

Part 2

Sexual selection: Human odor-based mating preferences do not guarantee gamete-level compatibility

A recent study  explored sexual selection in humans by investigating whether female odor-based mating preferences could predict how compatible male and female gametes are.

Major histocompatibility complex (MHC) genes are known to mediate sexual selection both at the individual and gamete level. Previous studies have shown that perceived body odor attractiveness is strongly affected by these genes. However, it has remained unclear whether MHC-based mating preferences are consistent prior and after copulation.

To study this, the researchers performed a full-factorial experiment where 10 women first ranked the attractiveness and intensity of body odor samples collected from 11 men, followed by an analysis of whether female body odor preferences in these same 110 male–female combinations predicted sperm performance in the presence of follicular fluid. The results are published in the journal Heredity.

An analysis of the total MHC similarity—including both classical and non-classical MHC genes—of the male-female combinations showed that women preferred the body odors of MHC-similar men, but that sperm motility was positively affected by the MHC dissimilarity of the male–female combinations.

Women showed a preference for the body odors of MHC-similar men. However, sperm from MHC-dissimilar men exhibited higher motility when exposed to female follicular fluid, suggesting that the most attractive males may not necessarily always be the most optimal partners in terms of fertilization success.

The results indicate that individual and gamete-level mate choice processes may in fact act in opposing directions, and that gamete-mediated mate choice may have a definitive role in disfavoring genetically incompatible partners from fertilizing oocytes.

 Annalaura Jokiniemi et al, Female-mediated selective sperm activation may remodel major histocompatibility complex-based mate choice decisions in humans, Heredity (2025). DOI: 10.1038/s41437-025-00759-9

Why don't bats get cancer? Researchers discover protection from genes and strong immune systems

A study to look at why long-lived bats do not get cancer has broken new ground about the biological defenses that resist the disease.

Reporting in the journal Nature Communications, a  research team has found that four common species of bats have superpowers allowing them to live up to 35 years, which is equal to about 180 human years, without cancer.

Their key discoveries about how bats prevent cancer include:
Bats and humans have a gene called p53, a tumor-suppressor that can shut down cancer. (Mutations in p53, limiting its ability to act properly, occur in about half of all human cancers.) A species known as the "little brown" bat—found in Rochester and upstate New York—contains two copies of p53 and has elevated p53 activity compared to humans. High levels of p53 in the body can kill cancer cells before they become harmful in a process known as apoptosis. If levels of p53 are too high, however, this is bad because it eliminates too many cells. But bats have an enhanced system that balances apoptosis effectively.
An enzyme, telomerase, is inherently active in bats, which allows their cells to proliferate indefinitely. This is an advantage in aging because it supports tissue regeneration during aging and injury. If cells divide uncontrollably, though, the higher p53 activity in bats compensates and can remove cancerous cells that may arise.
Bats have an extremely efficient immune system, knocking out multiple deadly pathogens. This also contributes to bats' anti-cancer abilities by recognizing and wiping out cancer cells. As humans age, the immune system slows, and people tend to get more inflammation (in joints and other organs), but bats are good at controlling inflammation, too. This intricate system allows them to stave off viruses and age-related diseases.

Part 1

How can we use this knowledge with regard to humans?
One surprising thing about the bat study, the researchers said, is that bats do not have a natural barrier to cancer. Their cells can transform into cancer with only two "hits"—and yet because bats possess the other robust tumor-suppressor mechanisms described above, they survive.

Importantly, the authors said, they confirmed that increased activity of the p53 gene is a good defense against cancer by eliminating cancer or slowing its growth. Several anti-cancer drugs already target p53 activity and more are being studied.
Safely increasing the telomerase enzyme might also be a way to apply their findings to humans with cancer.

Fathima Athar et al, Limited cell-autonomous anticancer mechanisms in long-lived bats, Nature Communications (2025). DOI: 10.1038/s41467-025-59403-z

Part 2

The Moon's shiny Glass Beads

The Apollo astronauts didn't know what they'd find when they explored the surface of the moon, but they certainly didn't expect to see drifts of tiny, bright orange and black glass beads glistening among the otherwise monochrome piles of rocks and dust.

The beads, each less than 1 mm across, formed some 3.3 to 3.6 billion years ago during volcanic eruptions on the surface of the then-young satellite. They're some of the most amazing extraterrestrial samples the astronauts brought home.

 "The beads are tiny, pristine capsules of the lunar interior."

Using a variety of microscopic analysis techniques not available when the Apollo astronauts first returned samples from the moon,  a team of researchers have been able to take a close look at the microscopic mineral deposits on the outside of lunar beads. The unprecedented view of the ancient lunar artifacts was published in Icarus. 

The study relied, in part, on the NanoSIMS 50, an instrument at WashU that uses a high-energy ion beam to break apart small samples of material for analysis. WashU researchers have used the device for decades to study interplanetary dust particles, presolar grains in meteorites, and other small bits of debris from our solar system.

The study combined a variety of techniques—atom probe tomography, scanning electron microscopy, transmission electron microscopy and energy dispersive X-ray spectroscopy—at other institutions to get a closer look at the surface of the beads.

Each glass bead tells its own story of the moon's past. The beads—some shiny orange, some glossy black—formed when lunar volcanoes shot material from the interior to the surface, where each drop of lava solidified instantly in the cold vacuum that surrounds the moon.

The very existence of these beads tells us the moon had explosive eruptions.

The minerals (including zinc sulfides) and isotopic composition of the bead surfaces serve as probes into the different pressure, temperature and chemical environment of lunar eruptions 3.5 billion years ago. Analyses of orange and black lunar beads have shown that the style of volcanic eruptions changed over time.

T.A. Williams et al, Lunar volcanic gas cloud chemistry: Constraints from glass bead surface sublimates, Icarus (2025). DOI: 10.1016/j.icarus.2025.116607

Green light activates modified penicillin only where it's needed

To treat bacterial infections, medical professionals prescribe antibiotics. But not all active medicine gets used up by the body. Some of it ends up in wastewater, where antimicrobial-resistant bacteria can develop.

Now, to make a more efficient antibiotic treatment, researchers have modified penicillin, so that it's activated only by green light. In early tests, the approach precisely controlled bacterial growth and improved survival outcomes for infected insects.

Controlling drug activity with light will allow precise and safe treatment of localized infections. Moreover, the fact that light comes in different colors gives us the ability to take the spatial control of drug activity to the next level.

Scientists can add a light-sensitive molecule to drug compounds to keep them inactive in the body until they're needed. When light shines on a modified compound, the extra molecule breaks away and then releases the active drug. This process gives scientists precise control over when and where drugs are activated.

Green-Light-Activatable Penicillin for Light-Dependent Spatial Control of Bacterial Growth, Biofilm Formation, and In Vivo Infection Treatment, ACS Central Science (2025). DOI: 10.1021/acscentsci.5c00437

Your gut microbiome could be a calorie 'super harvester'!

In the jungle of microbes living in your gut, there's one oddball that makes methane. This little-known methane-maker might play a role in how many calories you absorb from your food, according to a new study.

The entire ecosystem of microbes is called the microbiome. Some people's gut microbiomes produce a lot of methane, while others produce hardly any.

The study found that people whose gut microbiomes produce a lot of methane are especially good at unlocking extra energy from a high-fiber diet. This may help explain why different individuals get different amounts of calories from food that makes it to the colon.

The researchers note that high-fiber diets are not the villain here. People absorb more calories overall from a Western diet of processed foods, regardless of methane production. On a high-fiber diet, people absorb fewer calories overall—but the amount varies according to methane production.

That difference has important implications for diet interventions. It shows people on the same diet can respond differently. Part of that is due to the composition of their gut microbiome.

The study, published in The ISME Journal, found that methane-producing microbes called methanogens are associated with a more efficient microbiome and higher energy absorption from food.

One of the microbiome's main jobs is helping to digest food. Microbes ferment fiber into short-chain fatty acids, which the body can use for energy. In the process, they produce hydrogen. Too much hydrogen pauses their activity, but other microbes can help keep this process going by using up the hydrogen.

Methanogens are hydrogen-eaters. As they consume hydrogen, they create methane. They are the only microbes to make this chemical compound.

The human body itself doesn't make methane, only the microbes do. So researchers suggested it can be a biomarker that signals efficient microbial production of short-chain fatty acids.

The research suggests that these microbe interactions affect the body's metabolism. The team found that higher methane production was associated with more short-chain fatty acids being made and absorbed in the gut.

Insights from this study could be a foundation for personalized nutrition.

Blake Dirks et al, Methanogenesis associated with altered microbial production of short-chain fatty acids and human-host metabolizable energy, The ISME Journal (2025). DOI: 10.1093/ismejo/wraf103

In utero exposure to climate disasters linked to changes in child brain development

Climate disasters may be leaving invisible imprints on developing brains before birth, according to new research.

 Scientists discovered that children whose mothers experienced Superstorm Sandy during pregnancy showed distinct brain differences that could affect their emotional development for years to come.

The study, published in PLOS One, reveals that prenatal exposure to extreme climate events, particularly when combined with extreme heat, appears to rewrite critical emotion regulation centers in the developing brain. We're seeing how climate change may be reshaping the next generation's brains before they even take their first breath. These children's brains bear invisible scars from climate disasters they never personally experienced.

The research team analyzed brain imaging data from a group of 8-year-old children whose mothers were pregnant during Superstorm Sandy, which devastated parts of New York and other coastal regions in 2012. The scans revealed that children exposed to the storm in utero had significantly larger volumes in the basal ganglia, deep brain structures involved in emotion regulation.

The combination of storm stress and extreme heat created a perfect neurological storm in developing brains.

The researchers found that while extreme heat alone didn't significantly alter brain volume, when combined with the stress of living through a major storm during pregnancy, it amplified the effects dramatically.

As extreme weather events become more frequent and severe, we need to consider the invisible toll on future generations, the researchers say.

Donato DeIngeniis et al, Prenatal exposure to extreme ambient heat may amplify the adverse impact of Superstorm Sandy on basal ganglia volume among school-aged children, PLOS One (2025). DOI: 10.1371/journal.pone.0324150

New therapeutic strategy designed to help lower cholesterol levels

When the amount of cholesterol in the blood is too high, hypercholesterolemia can develop, causing serious damage to the arteries and cardiovascular health. Now, a study presents a new therapeutic tool capable of regulating blood cholesterol levels and thus opening up new perspectives in the fight against atherosclerosis caused by the accumulation of lipid plaques in the artery walls.

Specifically, the team has designed a strategy to inhibit the expression of PCSK9, a protein that plays a decisive role in modulating plasma levels of low-density lipoprotein cholesterol (LDL-C). The new method, based on the use of molecules known as polypurine hairpins (PPRH), facilitates the uptake of cholesterol by cells and prevents it from accumulating in the arteries without causing the side effects of the most common statin-based medication.

Major sugar substitute found to impair brain blood vessel cell function, posing potential stroke risk

Erythritol may impair cellular functions essential to maintaining brain blood vessel health, according to researchers. Findings suggest that erythritol increases oxidative stress, disrupts nitric oxide signaling, raises vasoconstrictive peptide production, and diminishes clot-dissolving capacity in human brain microvascular endothelial cells.

Erythritol has become a fixture in the ingredient lists of protein bars, low-calorie beverages, and diabetic-friendly baked goods. Its appeal lies in its sweetness-to-calorie ratio, roughly 60–80% as sweet as sucrose with a tiny fraction of the energy yield, and its negligible effect on blood glucose. Erythritol is also synthesized endogenously from glucose and fructose via the pentose phosphate pathway, leaving baseline levels subject to both dietary and metabolic influences.

Concerns about erythritol's safety have escalated following epidemiological studies linking higher plasma concentrations with increased cardiovascular and cerebrovascular events. Positive associations between circulating erythritol and incidence of heart attack and stroke have been observed in U.S. and European cohorts, independent of known cardiometabolic risk factors. 

In the study, "The Non-Nutritive Sweetener Erythritol Adversely Affects Brain Microvascular Endothelial Cell Function," published in the Journal of Applied Physiology, researchers designed in vitro experiments to test the cellular consequences of erythritol exposure on cerebral endothelial function.

Human cerebral microvascular endothelial cells were cultured and exposed to an amount of erythritol equivalent to consuming a typical beverage. Experimental conditions included five biological replicates per group.

Part 1

Cellular assays measured oxidative stress, antioxidant protein expression, nitric oxide bioavailability, endothelin production, and fibrinolytic capacity. Capillary electrophoresis immunoassay and ELISA were used to quantify expression of superoxide dismutase-1 (SOD-1), catalase, endothelial nitric oxide synthase (eNOS), phosphorylated eNOS, endothelin-1 (ET-1), and tissue-type plasminogen activator (t-PA).

Cells exposed to erythritol exhibited a substantial increase in oxidative stress. Reactive oxygen species levels rose by approximately 75% relative to untreated controls. Antioxidant defense markers were also elevated, with SOD-1 expression increasing by approximately 45% and catalase by approximately 25%.

Nitric oxide production declined by nearly 20% in response to erythritol. Although total eNOS expression remained unchanged, phosphorylation at the Ser1177 site, which is associated with enzymatic activation, fell by approximately 33%. In contrast, phosphorylation at the inhibitory Thr495 site increased by approximately 39%.

In another test, t-PA release in response to thrombin stimulation was blunted in erythritol-treated cells, indicating reduced fibrinolytic responsiveness.

The researchers conclude that erythritol exposure disrupts multiple mechanisms vital to maintaining cerebral endothelial health. Although results are limited to acute in vitro conditions, the findings align with prior epidemiological associations between erythritol and elevated stroke risk.

Auburn R. Berry et al, The Non-Nutritive Sweetner Erythritol Adversely Affects Brain Microvascular Endothelial Cell Function, Journal of Applied Physiology (2025). DOI: 10.1152/japplphysiol.00276.2025

Part 2

Humans have unique breathing 'fingerprints' that may signal health status

A study published in Current Biology demonstrates that scientists can identify individuals based solely on their breathing patterns with 96.8% accuracy. These nasal respiratory "fingerprints" also offer insights into physical and mental health.

The study found that the respiratory fingerprints correlated with a person's body mass index,sleep-wake cycle, levels of depression and anxiety, and even behavioral traits. For example, participants who scored relatively higher on anxiety questionnaires had shorter inhales and more variability in the pauses between breaths during sleep.

 The results suggest that long-term nasal airflow monitoring may serve as a window into physical and emotional well-being.

Humans Have Nasal Respiratory Fingerprints, Current Biology (2025). DOI: 10.1016/j.cub.2025.05.008. www.cell.com/current-biology/f … 0960-9822(25)00583-4

When bacteria get hungry, they kill—and eat—their neighbours!

Scientists have discovered a gruesome microbial survival strategy: when food is scarce, some bacteria kill and consume their neighbours.

The study, published in Science, was conducted by an international team. 

The researchers show that under nutrient-limited conditions, bacteria use a specialized weapon—the Type VI Secretion System (T6SS)—to attack, kill, and slowly absorb nutrients from other bacterial cells.

The T6SS is like a microscopic harpoon gun. A bacterium fires a needle-like weapon into nearby cells, injecting toxins that fatally rupture them.

Historically, scientists thought this system was mainly for competition, clearing out rivals to make space, but the multi-institutional research team discovered that bacteria aren't just killing for territory, they're strategically killing for dinner, and to help themselves grow.

Using time-lapse imaging, genetic tools, and chemical labeling, the scientists watched in slow-motion the microscopic assassins at work.

In both ocean bacteria and human gut microbes, bacteria equipped with T6SS attacked neighbors when starved of nutrients, and then grew by feeding off the deceased's leaking remains.

To prove this wasn't just coincidence, the researchers then genetically "turned off" the T6SS in some strains. When these genetically edited bacteria were placed in a nutrient-poor environment with potential prey, they couldn't grow. But the unedited bacteria, the ones still able to kill, thrived.

Their survival depended on murder.

The team also analyzed bacterial genomes across marine environments and found that these killing systems are widespread.

This isn't just happening in the lab. It's present in many different environments and it's operational and happening in nature from the oceans to the human gut.

This insight has wide-ranging implications.

If scientists can better understand how and why these bacterial weapons work, they can begin to design smarter probiotics, ones that don't just coexist in your gut, but actively protect it by taking out harmful microbes.

It could also lead to new antibiotics, at a time when drug resistance is on the rise. The same harpoon that bacteria use to extract nutrients from competitors could be harnessed to deliver drugs directly into problem pathogens—offering a new frontier in targeted, resistance-proof therapies.

And beyond our bodies, in the ocean, bacteria help regulate the planet's carbon cycle. When killer bacteria take out the ones breaking down algae and recycling carbon, it can shift how we understand how much carbon stays in the ocean or gets released back into the atmosphere.

By decoding how microscopic bacteria kill and consume each other, the research could reshape how we think about ecosystems—from the human gut to the vast oceans that regulate Earth's climate.

Astrid K. M. Stubbusch, Antagonism as a foraging strategy in microbial communities, Science (2025). DOI: 10.1126/science.adr8286. www.science.org/doi/10.1126/science.adr8286

Cancer cells use cholesterol armor to survive heat shock treatment, study discovers

Cancer has been recognized long back as being sensitive to heat. Today, this principle forms the basis of hyperthermia treatment—a promising cancer therapy that uses controlled heat to kill tumor cells while sparing healthy ones.

Unlike chemotherapy or radiation, hyperthermia works by heating cancerous tissue to temperatures around 50°C, causing cancer cell death while simultaneously activating the body's immune system against the tumor. This approach holds particular promise when combined with immunotherapy, as heat-killed cancer cells can trigger a stronger anti-tumor immune response.

Researchers have discovered that some cancer cells—even those from the same organ—react differently to heat shock, with some surprisingly more heat-resistant than others. This resistance involves two distinct cell death types: necrosis, which occurs rapidly through direct physical damage to cell membranes, and apoptosis, a slower, programmed cell death that happens hours later. In particular, how heat-resistant cancer cells regulate necrosis has received little scientific attention, limiting hyperthermia's potential as a standard cancer treatment.

Through a series of experiments in mice and cell cultures, the researchers compared the characteristics and behaviors of heat-sensitive cancer cells with heat-resistant ones. They discovered that cholesterol could act as a protective shield for cancer cells during heat treatment. Heat-resistant cancer cells contained significantly higher levels of cholesterol than heat-sensitive ones. This, in turn, helped maintain the stability of cell membranes when exposed to heat, preventing the rapid membrane breakdown that leads to necrosis.

Notably, when researchers artificially removed cholesterol from cancer cells using a cholesterol-depleting drug, even the most heat-resistant cells became vulnerable to hyperthermia treatment.

Using advanced imaging techniques, the researchers observed that heat treatment causes cell membranes to become more fluid (increased membrane fluidity). In cells with high cholesterol levels, this increase in membrane fluidity was suppressed, thereby protecting the cells from heat damage. However, when cholesterol was removed, membrane fluidity increased, making the cells much more susceptible to heat-induced damage, leading to rapid cell death through necrosis.

Part 1

Testing their findings across multiple human and mouse cancer cell lines confirmed that cholesterol levels were consistently related to heat resistance. The researchers further validated their discovery in living mice with implanted tumors, using gold nanoparticles and near-infrared light to create localized heating. Tumors treated with both cholesterol depletion and hyperthermia showed dramatic shrinkage, with most tumors completely disappearing—a far superior result compared to heat treatment alone.

This research suggests that measuring cholesterol levels in tumors could help doctors identify which patients are most likely to benefit from hyperthermia treatment. More importantly, the combination of cholesterol-depleting drugs with localized heat therapy could transform hyperthermia from an inconsistent treatment into a powerful weapon against cancer. Since cholesterol depletion primarily triggers necrosis, this approach may also enhance the immune system's ability to recognize and attack the remaining cancer cells.

 Taisei Kanamori et al, Cholesterol depletion suppresses thermal necrosis resistance by alleviating an increase in membrane fluidity, Scientific Reports (2025). DOI: 10.1038/s41598-025-92232-0

Part 2

Low sodium in blood triggers anxiety in mice by disrupting their brain chemistry

Hyponatremia, or low blood sodium concentration, is typically viewed as a symptomless condition—until recently. A research team has demonstrated that chronic hyponatremia (CHN) can directly cause anxiety-like behaviors in mice by disrupting key neurotransmitters in the brain.

Their findings, published online in the journal Molecular Neurobiology, reveal that CHN alters monoaminergic signaling in the amygdala, a brain region critical for processing fear and emotion. 

Hyponatremia is usually caused by conditions like liver cirrhosis, heart failure, or syndrome of inappropriate antidiuresis (SIAD). In chronic cases, the brain adapts to the low-sodium environment by adjusting its cellular content through a compensatory mechanism known as volume regulatory decrease (VRD). But this adaptation, while protective, comes at a physiological cost.

This compensation process involves the loss of organic osmolytes and neurotransmitter precursors that help stabilize brain cell volume under low-sodium conditions. Over time, this may lead to disruption in the production, release, or recycling of key mood-regulating chemicals.

The researchers  found that the mice in their experiments exhibited significantly lower serum sodium levels, which were maintained over a prolonged period, consistent with chronic hyponatremia (CHN) and exhibited increased anxiety-like behaviors in both the light/dark transition and open field tests—standard behavioral assays in neuroscience.

Further biochemical analyses revealed that levels of serotonin and dopamine, two key neurotransmitters that regulate mood, were significantly reduced in the amygdala of mice with CHN. These changes were accompanied by a drop in extracellular signal-regulated kinase (ERK) phosphorylation—a molecular signal for emotional regulation.

The data  suggest that CHN disrupts the balance of monoamines in the amygdala, especially serotonin and dopamine, which in turn modulates innate anxiety.

This shows not only that CHN causes anxiety-like symptoms but also that these symptoms can be alleviated with proper correction of sodium imbalance.

While the study focused on mice, the findings could apply to humans. CHN is fairly common among elderly patients and those with chronic illnesses. Identifying and treating its neurological manifestations can improve their quality of life.

Haruki Fujisawa et al, Chronic Hyponatremia Potentiates Innate Anxiety-Like Behaviors Through the Dysfunction of Monoaminergic Neurons in Mice, Molecular Neurobiology (2025). DOI: 10.1007/s12035-025-05024-y

Some plants make their own pesticide—but at what cost to the atmosphere?

A natural alternative to pesticides may be hiding in a misunderstood plant compound—but it could come at an environmental cost.

For years, scientists knew little about isoprene, a natural chemical produced by plants. New  research 40 years in the making now sheds light on how this natural chemical can repel insects—and how some plants that don't normally make isoprene could activate production in times of stress.

A  research paper in Science Advances uncovers a hormonal response triggered by isoprene that makes insects steer clear of those plants. Insects that munched on isoprene-treated leaves got a stomachache, thanks to indigestible proteins that kick in when the compound is present. Those proteins also stunt the growth of worms that dare to keep eating them.

Another paper, published in the Proceedings of the National Academy of Sciences, reveals that soybeans produce isoprene when their leaves are wounded. This discovery was particularly surprising since researchers previously thought modern crops didn't produce isoprene. This ability could make crops more resilient to heat and pests.

But that benefit could come at a cost. Isoprene is a hydrocarbon that worsens air pollution, especially in areas that already have poor air quality. If more crop plants were engineered to release isoprene, that could further damage Earth's atmosphere. The research also has implications for how soybeans may impact air pollution.

Isoprene is one of the highest emitted hydrocarbons on Earth, second only to methane emissions from human activity. These organic compounds interact with sunlight and nitrogen oxide from coal-burning facilities and vehicle emissions, creating a toxic brew of ozone, aerosols and other harmful byproducts.

Not all plants produce isoprene, however, and the ones that do tend to make more in hot weather. It's mostly found in oak and poplar trees, but unlike similar molecules in pine and eucalyptus trees, isoprene doesn't have a scent.

But as plants make more isoprene, they sacrifice some of their growth potential. When plants make isoprene, they divert carbon away from growth and storage and invest instead in their defense. Some think this is why many plants folded under evolutionary pressure to get rid of the isoprene synthase.

 Abira Sahu et al, Isoprene deters insect herbivory by priming plant hormone responses, Science Advances (2025). DOI: 10.1126/sciadv.adu4637

Mohammad Golam Mostofa et al, Cryptic isoprene emission of soybeans, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2502360122

Scientists detect light passing through entire human head, opening new doors for brain imaging

For decades, scientists have used near-infrared light to study the brain in a noninvasive way. This optical technique, known as fNIRS (functional near-infrared spectroscopy), measures how light is absorbed by blood in the brain, to infer activity.

Valued for portability and low cost, fNIRS has a major drawback: it can't see very deep into the brain. Light typically only reaches the outermost layers of the brain, about 4 centimeters deep—enough to study the surface of the brain, but not deeper regions involved in critical functions like memory, emotion, and movement.

This drawback has restricted the ability to study deeper brain regions without expensive and bulky equipment like MRI machines.

Now, researchers  have demonstrated something previously thought impossible: detecting light that has traveled all the way through an adult human head.

Their study, "Photon transport through the entire adult human head," published in Neurophotonics, shows that, with the right setup, it is possible to measure photons that pass from one side of the head to the other, even across its widest point.

To achieve this, the team used powerful lasers and highly sensitive detectors in a carefully controlled experiment. They directed a pulsed laser beam at one side of a volunteer's head and placed a detector on the opposite side. The setup was designed to block out all other light and maximize the chances of catching the few photons that made the full journey through the skull and brain.

The researchers also ran detailed computer simulations to predict how light would move through the complex layers of the head. These simulations matched the experimental results closely, confirming that the detected photons had indeed traveled through the entire head.

Interestingly, the simulations revealed that light tends to follow specific paths, guided by regions of the brain with lower scattering, such as the cerebrospinal fluid.

This breakthrough suggests that it may be possible to design new optical devices that can reach deeper brain areas than current technologies allow.

While the current method is not yet practical for everyday use—it requires 30 minutes of data collection and worked only on a subject with fair skin and no hair—this extreme case of detecting light diametrically across the head may inspire the community to rethink what is possible for the next generation of fNIRS systems.

With further development, this approach might help bring deep brain imaging into clinics and homes in a more affordable and portable form and better diagnosing platforms. This could eventually lead to better tools for diagnosing and monitoring conditions like strokes, brain injuries, or tumors, especially in settings where access to MRI or CT scans is limited.

Jack Radford et al, Photon transport through the entire adult human head, Neurophotonics (2025). DOI: 10.1117/1.NPh.12.2.025014

Study ties midlife vascular health to later dementia risk

Dementia before age 80 is potentially preventable through early intervention on common vascular risk factors, according to new research. Findings suggest that up to 44% of dementia cases could be attributed to vascular risk factors, specifically hypertension, diabetes, or smoking.

Hypertension, diabetes, and smoking are commonly implicated risk factors, likely acting through arteriosclerotic cerebral small vessel disease (CSVD).

CSVD is a catch-all term for a variety of conditions resulting from damage to small blood vessels in the brain. Narrowing, hardening, or obstruction of small blood vessels in the brain can starve brain cells of oxygen, which can damage nearby brain cells.

Early symptoms are often easily confused with, or overlap with, the normal effects of aging. Mental fog, forgotten names, misplaced objects, can occur naturally throughout a lifetime of remembering things, such that when vascular-related damage reaches the point of a dementia diagnosis, it may appear as a rapid onset, usually presenting later in life.

Attribution is further complicated by the frequent co-occurrence of vascular injury and Alzheimer's pathology, leaving unresolved how much dementia could be prevented by controlling vascular conditions earlier in life.

In the study, "Contribution of Modifiable Midlife and Late-Life Vascular Risk Factors to Incident Dementia," published in JAMA Neurology, researchers designed a prospective cohort analysis to estimate the proportion of dementia attributable to midlife and late-life  vascular risk factors.

Part 1

Analyses drew on 33 years of follow-up from over 12,000 adults across four US communities, with participant age at vascular risk measurement ranging from 45 to 74 years. Dementia incidence was tracked through standardized clinical assessments, proxy interviews, and linked medical records. Analyses were limited to self-identified Black and white participants.

Among participants with vascular risk factors measured at ages 45–54, 21.8% of dementia cases by age 80 were attributable to those risks. This proportion increased to 26.4% when measured at ages 55–64, and to 44.0% at ages 65–74. For dementia occurring after age 80, attributable fractions dropped sharply to between 2% and 8%.

Subgroup analyses revealed higher attributable risk in APOE ε4 noncarriers (up to 61.4% for those aged 65–74), Black participants (up to 52.9%), and females (up to 51.3%). APOE ε4 noncarriers are individuals who lack the gene variant with the strongest known risk factor for Alzheimer's disease. In this lower genetic-risk group, modifiable vascular conditions such as hypertension, diabetes, and smoking accounted for a greater share of dementia risk.

The authors conclude, "Results suggest that maintaining ideal vascular health into late life could substantially reduce dementia risk before age 80 years."

Jason R. Smith et al, Contribution of Modifiable Midlife and Late-Life Vascular Risk Factors to Incident Dementia, JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.1495

Roch A. Nianogo et al, Targeting Vascular Risk Factors to Reduce Dementia Risk, JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.1493

Part 2

Nanoplastics can disrupt gut microbes in mice by interfering with extracellular vesicle-delivered microRNA

Nanoplastics can compromise intestinal integrity in mice by altering the interactions between the gut microbiome and the host, according to a paper in Nature Communications. The study explores the complex interactions of nanoplastics with the gut microenvironment in mice.

Nanoplastics are pieces of plastic less than 1,000 nanometers in diameter, which are created as plastics degrade. Previous research has suggested that nanoplastic uptake can disrupt the gut microbiota; however, the underlying mechanism behind this effect is poorly understood.

Researchers  used RNA sequencing, transcriptomic analysis and microbial profiling to analyze the effects of polystyrene nanoplastics on the intestinal microenvironment when ingested in mice. They found that nanoplastic accumulation in the mouse intestine was linked to altered expression of two proteins involved in intestinal barrier integrity (ZO-1 and MUC-13), which could disrupt intestinal permeability.

The nanoplastics were also shown to induce an intestinal microbiota imbalance, specifically an increased abundance of Ruminococcaceae, which has been implicated in gastrointestinal dysfunction in previous research.

These findings suggest a mechanism by which nanoplastics may affect the microbiota and the intestinal environment in mice. However, research would be needed to explore the ways in which nanoplastic accumulation could affect humans.

 Wei-Hsuan Hsu et al, Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs, Nature Communications (2025). DOI: 10.1038/s41467-025-59884-y

Novel coating shields iron from rust with 99.6% efficiency

Researchers have developed a highly effective dual-layer coating that provides 99.6% protection against iron corrosion. The breakthrough combines a thin molecular primer with a durable polymer layer, creating a strong, long-lasting barrier against rust. This innovation could significantly reduce maintenance costs and extend the lifespan of iron-based materials used in construction, transportation, and manufacturing.

The new research presents a solution by combining two protective layers that work together to create a strong and long-lasting barrier. The first layer is an ultra-thin coating made of N-Heterocyclic Carbene (NHC) molecules, which form a tight bond with the iron surface.

This primer layer ensures that the second layer—a polymer-based coating—sticks firmly, creating a highly stable and durable protective shield. Thanks to this improved adhesion, the coating remains intact even in harsh conditions, such as prolonged exposure to saltwater.

Experiments showed that this dual-layer system dramatically reduced the amount of corrosion, with tests conducted in a highly corrosive saltwater environment confirming its exceptional efficiency. By forming a strong chemical connection between the iron and the protective layers, this method offers far greater durability than conventional coatings, which often wear down or peel off over time.

Linoy Amar et al, Self‐Assembled Monolayer of N‐Heterocyclic Carbene as a Primer in a Dual‐Layer Coating for Corrosion Protection on Iron, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202422879

Why the salmon on your plate contains less omega-3 than it used to

It has long been known that eating oily fish such as salmon is the best way to consume long-chain omega-3 fatty acids. These are essential for brain development, mental health and cognition. In salmon, omega-3 fatty acids must come from the fish's diet. For farmed fish, this means fishmeal and fish oil—so–called "marine ingredients" made from ground-up wild fish such as anchovy and fish by-products.

But the global supply of omega-3s is severely limited, whether from farmed or wild seafood. Many of the key fisheries supplying marine ingredients reached full exploitation in the mid-1990s. Since the growth of salmon aquaculture, increasing volumes of the limited marine ingredients supply have been taken up by fish farming.

This has raised concerns over sustainability and inflated the cost of these ingredients. The result has been a steady decline in the proportion of fish oil in farmed salmon diets, which has been replaced by plant oils. But these oils do not contain long-chain omega-3s.
In turn, the amount of omega-3s in a portion of salmon halved between 2006 and 2015. However, the salmon industry increasingly uses omega-3 as a key selling point for its product—two portions of farmed Scottish salmon per week would meet the recommended intake for an adult at current levels.
Moreover by trimming and removing skins and heads, the amount of omega-3 is reduced more.

Source: https://theconversation.com/why-the-salmon-on-your-plate-contains-l...

Study Finds a Potential Downside to Vigorous Exercise

Tumour microbes contribute to resistance
A signalling molecule produced by bacteria in breast tumours can help the cancer resist certain treatments. The cancer drug trastuzumab blocks the action of a protein called HER2, which cancer cells use to grow. Pseudomonas aeruginosa — a bacterial species commonly found in breast tumours — produces a molecule called 3oc, mainly to kill immune cells. But researchers found that 3oc has an off-target effect: it activates a chemical pathway in breast cancer cells that triggers HER2 production, dampening the effect of trastuzumab.

A Bacterial Signaling Molecule Lends Tumors Drug Resistance

Aggressive breast cancer can become unresponsive to monoclonal antibody treatment, but targeting tumor-resident bacteria may extend its effectiveness.

https://www.the-scientist.com/a-bacterial-signaling-molecule-lends-...

https://www.pnas.org/doi/10.1073/pnas.2421710122

Astronomers have located the universe's 'missing' matter

A new landmark study has pinpointed the location of the universe's "missing" matter, and detected the most distant fast radio burst (FRB) on record. Using FRBs as a guide, astronomers at the Center for Astrophysics | Harvard & Smithsonian (CfA) and Caltech have shown that more than three-quarters of the universe's ordinary matter has been hiding in the thin gas between galaxies, marking a major step forward in understanding how matter interacts and behaves in the universe.

They've used the new data to make the first detailed measurement of ordinary matter distribution across the cosmic web. The research is published in the journal Nature Astronomy.

For decades, scientists have known that at least half of the universe's ordinary, or baryonic matter—composed primarily of protons—was unaccounted for. Previously, astronomers have used techniques including X-ray emission and ultraviolet observations of distant quasars to find hints of vast amounts of this missing mass in the form of very thin, warm gas in between galaxies. Because that matter exists as hot, low-density gas, it was largely invisible to most telescopes, leaving scientists to estimate but not confirm its amount or location.

Enter FRBs—brief, bright radio signals from distant galaxies that scientists only recently showed could measure baryonic matter in the universe, but until now could not find its location. In the new study, researchers analyzed 60 FRBs, ranging from ~11.74 million light years away—FRB20200120E in galaxy M81—to ~9.1 billion light years away—FRB 20230521B, the most distant FRB on record. This allowed them to pin down the missing matter to the space between galaxies, or the intergalactic medium (IGM).

 Thanks to FRBs, we now know that three-quarters of it is floating between galaxies in the cosmic web. In other words, scientists now know the home address of the "missing" matter.

By measuring how much each FRB signal was slowed down as it passed through space, researchers tracked the gas along its journey. They shine through the fog of the intergalactic medium, and by precisely measuring how the light slows down, we can weigh that fog, even when it's too faint to see.

The results were clear: Approximately 76% of the universe's baryonic matter lies in the IGM. About 15% resides in galaxy halos, and a small fraction is burrowed in stars or amid cold galactic gas.

This distribution lines up with predictions from advanced cosmological simulations, but has never been directly confirmed until now.

This is a triumph of modern astronomy.

Liam Connor et al, A gas-rich cosmic web revealed by the partitioning of the missing baryons, Nature Astronomy (2025). DOI: 10.1038/s41550-025-02566-y

First artificial solar eclipses created by two European satellites

A pair of European satellites have created the first artificial solar eclipses by flying in precise and fancy formation, providing hours of on-demand totality for scientists.

The European Space Agency released the eclipse pictures at the Paris Air Show this week. Launched late last year, the orbiting duo have churned out simulated solar eclipses since March while zooming tens of thousands of miles (kilometers) above Earth.

Flying 492 feet (150 meters) apart, one satellite blocks the sun like the moon does during a natural total solar eclipse as the other aims its telescope at the corona, the sun's outer atmosphere that forms a crown or halo of light.

It's an intricate, prolonged dance requiring extreme precision by the cube-shaped spacecraft, less than 5 feet (1.5 meters) in size. Their flying accuracy needs to be within a mere millimeter, the thickness of a fingernail. This meticulous positioning is achieved autonomously through GPS navigation, star trackers, lasers and radio links.

Dubbed Proba-3, the $210 million mission has generated 10 successful solar eclipses so far during the ongoing checkout phase. The longest eclipse lasted five hours.

Scientists already are thrilled by the preliminary results that show the corona without the need for any special image processing.

Source: ESA

Seeing clearly through thick fog: Researchers develop ultra-low noise, high sensitivity photodetector

Technologies enabling safe visual recognition in low-visibility environments are gaining increasing attention across sectors such as autonomous driving, aviation, and smart transportation. Thick fog remains a major challenge on highways, mountainous roads, and airport runways, where vision-based recognition systems frequently fail.

Traditional visible light cameras, LiDAR, and thermal infrared (IR) sensors experience a sharp drop in signal-to-noise ratio(SNR) under scattering conditions, making object and pedestrian detection unreliable. To overcome these challenges, researchers are seeking near-infrared (NIR) sensors that can operate stably and with low noise in real-world conditions.

A research team  has developed a high-sensitivity organic photodetector (OPD) that maintains ultra-low noise performance even in light-scattering environments.

The study is published in the journal Advanced Materials.

The team successfully reconstructed transmission images in simulated fog and smoke conditions and quantitatively verified the sensor's performance.

The study is notable as it presents the first experimental demonstration of a hardware-based visibility enhancement system in realistic fog-like environments—following the team's earlier development of an AI-based software fog removal technology that received a CES 2025 Innovation Award.

Based on this achievement, the team is advancing a software-hardware integrated solution for visibility enhancement, targeting applications in autonomous driving, smart transportation infrastructure, and drone-based surveillance.

A core innovation of the OPD lies in a self-assembled monolayer electronic blocking layer developed by the team, called 3PAFCN.

This layer, characterized by a deep HOMO energy level and high surface energy, effectively suppresses dark current and reduces interfacial charge traps, thereby enhancing device stability and responsiveness.

Through this structural innovation, the OPD achieved a low noise current of 2.18 fA, along with the highest detectivity reported among NIR OPDs of its kind—surpassing the performance of commercial silicon-based photodetectors and indicating strong commercialization potential.

The team also constructed a laboratory environment simulating real fog, where they conducted single-pixel imaging experiments using the new OPD. Even under low-light conditions where visible-spectrum sensors failed to detect targets, the OPD successfully captured optical signals and reconstructed object shapes.

Seunghyun Oh et al, Robust Imaging through Light‐Scattering Barriers via Energetically Modulated Multispectral Organic Photodetectors, Advanced Materials (2025). DOI: 10.1002/adma.202503868

Artificial light in big cities is extending the growing season of urban plants

Artificial light may be lengthening the growing season in urban environments by as much as 3 weeks compared to rural areas, according to an analysis of satellite data from 428 urban centers in the Northern Hemisphere over 7 years, published in Nature Cities.

Rapid urbanization is leading to hotter and brighter cities. More specifically, buildings and concrete absorb and radiate heat, causing urban heat islands, in which urban areas have higher atmospheric temperatures throughout the day and night compared to their surroundings. Likewise, the amount of artificial light at night has increased by 10% in cities within the past decade.

Light and temperature also largely regulate plant growing seasons. For example, increased lighting and temperature cause trees in cities to bud and flower earlier in the spring and change color later in the autumn than trees in rural surroundings.

Researchers analyzed satellite observations, taken between 2014 and 2020, of 428 cities in the Northern Hemisphere—including New York City, Paris, Toronto, and Beijing—and data on artificial light at night, near-surface air temperature and plant growing seasons.

They  found that the wattage of artificial light at night increases exponentially from rural areas towards urban centers. Meng and colleagues suggest that this increased amount of light appears to influence the start and end of urban growing seasons more than the increase of temperature from rural to urban areas.

They also found that the effect of artificial light is especially pronounced at the end of the growing season compared to its influence on the start. More specifically, the start of the growing season is an average of 12.6 days earlier than in rural surroundings and the end is 11.2 days later in the cities analyzed.

The authors suggest that the effect of artificial light on the growing season may be further complicated by the relatively recent general switch from high-pressure sodium lamps to LED lighting, which plants may be more responsive to.

Lvlv Wang et al, Artificial light at night outweighs temperature in lengthening urban growing seasons, Nature Cities (2025). DOI: 10.1038/s44284-025-00258-2

RNA has newly identified role: Repairing serious DNA damage to maintain the genome

Your DNA is continually damaged by sources both inside and outside your body. One especially severe form of damage called a double-strand break involves the severing of both strands of the DNA double helix.

Double-strand breaks are among the most difficult forms of DNA damage for cells to repair because they disrupt the continuity of DNA and leave no intact template to base new strands on. If mis-repaired, these breaks can lead to other mutations that make the genome unstable and increase the risk of many diseases, including cancer, neurodegeneration and immunodeficiency.

Cells primarily repair double-strand breaks by either rejoining the broken DNA ends or by using another DNA molecule as a template for repair. However, researchers discovered that RNA, a type of genetic material best known for its role in making proteins, surprisingly plays a key role in facilitating the repair of these harmful breaks.

These insights could not only pave the way for new treatment strategies for genetic disorders, cancer and neurodegenerative diseases, but also enhance gene-editing technologies.

https://www.nature.com/articles/s41467-024-51457-9

Light Squeezed Out of Darkness in  Quantum Simulation

A careful alignment of three powerful lasers could generate a mysterious fourth beam of light that is throttled out of the very darkness itself.

What sounds like occult forces at work has been confirmed by a simulation of the kinds of quantum effects we might expect to emerge from a vacuum when ultra-high electromagnetic fields meet.

What we think of as empty space is – on a quantum level – an ocean of possibility. Fields representing all kinds of physical interactions hum with the promise of particles we'd recognize as the foundations of light and the building blocks of matter itself. These virtual particles essentially pop into and out of existence in fractions of a second.

All it takes for them to manifest longer-term is the right kind of physical persuasion that discourages them from canceling one another out; the kind of persuasion a series of strong electromagnetic fields might provide when arranged in a suitable fashion.

Using nothing but photons to generate the necessary electromagnetic fields, it's hoped the light being scattered out of the darkness won't be hidden in a fog of other particles, finally proving once and for all that it is possible in physics to squeeze something out of nothing.

A team of researchers from the University of Oxford in the UK and the University of Lisbon in Portugal used a semi-classical equation solver to simulate quantum phenomena in real time and in three dimensions, testing predictions on what ought to occur when incredibly intense laser pulses combine in empty space.

Waste can turn to rock within decades
Industrial waste is turning into solid rock in as little as 35 years. Researchers analysed a cliff made up of millions of cubic metres of slag produced by now-defunct iron and steel foundries along a stretch of the English coast. A coin from 1934 and an aluminium can tab manufactured after 1989 were embedded in the material, showing that it had lithified — essentially turning into rock — within that period. “All the activity we’re undertaking at the Earth’s surface will eventually end up in the geological record as rock, but this process is happening with remarkable, unprecedented speed,” said study co-author John MacDonald.

Industrial waste can turn into rock in as little as 35 years, new research reveals, instead of the thousands or millions of years previously assumed. The finding challenges what scientists know about rock formation, revealing an entirely new "anthropoclastic rock cycle."

The scientists found that waste from seaside industrial plants turns into rock especially rapidly due to the ocean water and air, which activate minerals such as calcium and magnesium in the waste, or slag, cementing it together faster than natural sediments.

Researchers dubbed this newly discovered process the "rapid anthropoclastic rock cycle." The findings challenge long-standing theories about how rocks form and suggest industries have far less time to dispose of their waste properly than previously thought

https://pubs.geoscienceworld.org/gsa/geology/article-abstract/doi/1...

Industrial waste is turning into a new type of rock at 'unprecedented' speed, new study finds

https://www.livescience.com/planet-earth/geology/industrial-waste-i...

How chemical bonds are formed: Physicists observe energy flow in real time

For the first time, a research team  has tracked in real time how individual atoms combine to form a cluster and which processes are involved.

To achieve this, the researchers first isolated magnesium atoms using superfluid helium and then used a laser pulse to trigger the formation process. The researchers were able to observe this cluster formation and the involved energy transfer between individual atoms with a temporal resolution in the femtosecond range.

Normally, magnesium atoms instantaneously form tight bonds, which means that there is no defined starting configuration for observation of the bond-formation processes

The researchers have solved this problem, which often arises when observing chemical processes in real time, by conducting experiments with superfluid helium droplets. These droplets act like ultra-cold "nano-fridges" that isolate the individual magnesium atoms from each other at extremely low temperatures of 0.4 Kelvin (= -272.75 degrees Celsius or 0.4 degrees Celsius above absolute zero) at a distance of a millionth of a millimeter.

This configuration allowed them to initiate cluster formation with a laser pulse and track it precisely in real time.

The researchers observed the processes triggered by the laser pulse using photoelectron and photoion spectroscopy. While the magnesium atoms combined to form a cluster, they were ionized with a second laser pulse.

Researchers were able to reconstruct the processes involved in detail on the basis of the ions formed and electrons released.

A key discovery here is energy pooling. As they bind to each other, several magnesium atoms transfer the excitation energy received from the first laser pulse to a single atom in the cluster, so that it reaches a much higher energy state. This is the first time that energy pooling has been demonstrated with time resolution.

Michael Stadlhofer et al, Real-time tracking of energy flow in cluster formation, Communications Chemistry (2025). DOI: 10.1038/s42004-025-01563-6

Wildfires could be harming the oceans and disrupting their carbon storage

Wildfires pollute waterways and could affect their ability to sequester carbon, recent research shows.

When forests burn, they release ash, soil particles and chemicals into the environment. In a Science of The Total Environment study which analyzed water quality and wildfire data, researchers were able to link increases in the concentrations of compounds like arsenic and lead, as well as nutrients such as nitrogen and phosphorus, to fires which had burned within the river's basin months prior.

Using monitoring data collected by Environment Canada over the last 20 years, they calculated that up to 16.3% of the variation in water quality could be attributed to wildfires. 

Black carbon is formed when fires burn the carbon in trees. Black carbon cycles very slowly in the environment, especially the particulate form, and may sequester carbon from the atmosphere when it is buried in the ocean.

In a study earlier in 2025, researchers found that there is an important seasonal aspect to this. Most of the water in the northern rivers currently comes from snowmelt, but with climate change, this could shift to being more rain-driven in the future.

This change could lead to more rapidly degradable dissolved black carbon being exported to the ocean, which means that this carbon sequestration may lessen in the future and black carbon could become an additional source of carbon dioxide to the atmosphere.

Emily Brown et al, Cumulative effects of fire in the Fraser River basin on freshwater quality and implications for the Salish Sea, Science of The Total Environment (2025). DOI: 10.1016/j.scitotenv.2025.179416

**

Websites are tracking you via browser fingerprinting, researchers show

Clearing your cookies is not enough to protect your privacy online. New research  has found that websites are covertly using browser fingerprinting—a method to uniquely identify a web browser—to track people across browser sessions and sites.

The findings are published as part of the Proceedings of the ACM on Web Conference 2025.

Fingerprinting has always been a concern in the privacy community, but until now, we had no hard proof that it was actually being used to track users.

When you visit a website, your browser shares a surprising amount of information, like your screen resolution, time zone, device model and more. When combined, these details create a "fingerprint" that's often unique to your browser. Unlike cookies—which users can delete or block—fingerprinting is much harder to detect or prevent. Most users have no idea it's happening, and even privacy-focused browsers struggle to fully block it.

It is like a digital signature you didn't know you were leaving behind. You may look anonymous, but your device or browser gives you away.

This research marks a turning point in how computer scientists understand the real-world use of browser fingerprinting by connecting it with the use of ads.

To investigate whether websites are using fingerprinting data to track people, the researchers had to go beyond simply scanning websites for the presence of fingerprinting code. They developed a measurement framework called FPTrace, which assesses fingerprinting-based user tracking by analyzing how ad systems respond to changes in browser fingerprints.

This approach is based on the insight that if browser fingerprinting influences tracking, altering fingerprints should affect advertiser bidding—where ad space is sold in real time based on the profile of the person viewing the website—and HTTP records—records of communication between a server and a browser.

This kind of analysis lets the researchers go beyond the surface. They were  able to detect not just the presence of fingerprinting, but whether it was being used to identify and target users—which is much harder to prove.

Part 1

The researchers found that tracking occurred even when users cleared or deleted cookies. The results showed notable differences in bid values and a decrease in HTTP records and syncing events when fingerprints were changed, suggesting an impact on targeting and tracking.

Additionally, some of these sites linked fingerprinting behavior to backend bidding processes—meaning fingerprint-based profiles were being used in real time, likely to tailor responses to users or pass along identifiers to third parties.

Perhaps more concerning, the researchers found that even users who explicitly opt out of tracking under privacy laws like Europe's General Data Protection Regulation (GDPR) and California's California Consumer Privacy Act (CCPA) may still be silently tracked across the web through browser fingerprinting.

Based on the results of this study, the researchers argue that current privacy tools and policies are not doing enough. They call for stronger defenses in browsers and new regulatory attention to fingerprinting practices. They hope that their FPTrace framework can help regulators audit websites and providers who participate in such activities, especially without user consent.

Zengrui Liu et al, The First Early Evidence of the Use of Browser Fingerprinting for Online Tracking, Proceedings of the ACM on Web Conference 2025 (2025). DOI: 10.1145/3696410.3714548

Part 2

Before dispersing out of Africa, humans likely had to learn to thrive in diverse habitats

All non-Africans are known to have descended from a small group of people that ventured into Eurasia around 50,000 years ago. However, fossil evidence shows that there were numerous failed dispersals before this time that left no detectable traces in living people.

In a paper published in Nature, new evidence explains for the first time why those earlier migrations didn't succeed.

It was found that before expanding into Eurasia 50,000 years ago, humans began to exploit different habitat types in Africa in ways not seen before.

The results showed that the human niche began to expand significantly from 70,000 years ago, and that this expansion was driven by humans increasing their use of diverse habitat types, from forests to arid deserts.

Previous dispersals seem to have happened during particularly favorable windows of increased rainfall in the Saharo-Arabian desert belt, thus creating 'green corridors' for people to move into Eurasia. However, around 70,000–50,000 years ago, the easiest route out of Africa would have been more challenging than during previous periods, and yet this expansion was sizable and ultimately successful.

Part 1

The researchers showed that humans greatly increased the breadth of habitats they were able to exploit within Africa before the expansion out of the continent. This increase in the human niche may have been a result of positive feedback of greater contact and cultural exchange, allowing larger ranges and the breakdown of geographic barriers.

Unlike previous humans dispersing out of Africa, those human groups moving into Eurasia after approximately 60–50,000 years ago were equipped with a distinctive ecological flexibility as a result of coping with climatically challenging habitats. This likely provided a key mechanism for the adaptive success of our species beyond their African homeland.

 Emily Hallett, Major expansion in the human niche preceded out of Africa dispersal, Nature (2025). DOI: 10.1038/s41586-025-09154-0. www.nature.com/articles/s41586-025-09154-0

Part 2

Chemical profile of fecal samples can help predict mortality in critically ill patients

The gut microbiome and the metabolites it produces offer promising insight into disease severity in critically ill patients. In a collaborative effort, researchers developed the metabolic dysbiosis score (MDS), a novel biomarker index based on the levels of 13 key fecal metabolites—the chemical byproducts of digestion. The designed index can identify high-risk patients early and guide timely interventions that could save the lives of critically ill hospitalized patients.

According to the research article published in Science Advances, the team collected fecal specimens from 196 critically ill patients admitted to the medical intensive care unit (MICU) for non-COVID-19 respiratory shock or failure. They analyzed the samples by mapping the microbiome's composition using shotgun metagenomic sequencing and measuring the gut-derived metabolites with high-precision mass spectrometry. The MDS assigned based on the results helped identify MICU patients who are at a higher risk of 30-day mortality.

Experts have long observed that the complex ecosystem of microorganisms residing in our digestive tract plays a crucial role in maintaining overall health, and its dysbiosis or imbalance in this microbiota has been linked to a range of metabolic and chronic illnesses.

Several studies have investigated possible links between fecal microbiome diversity profiles and mortality in critically ill patients in search of a potentially treatable trait. They found that ICU stays can reduce microbiome diversity, allowing harmful species such as Enterococcus and Enterobacterales to dominate over beneficial bacteria that support healthy gut function. These imbalances are often associated with serious outcomes, including an increased risk of infection and death.

Short-chain fatty acids (SCFAs), bile acids, and tryptophan metabolites are key groups of metabolites produced by the gut microbiota. Admission to the ICU, particularly following antibiotic treatment, can cause significant disruptions in these metabolites, leading to fecal metabolic dysbiosis—a condition that may contribute to increased susceptibility to various diseases.

Upon scoring the fecal samples based on the MDS, researchers found that a high MDS (>7.5) increased the risk of 30-day mortality by a factor of 8.66 in critically ill patients. The researchers, however, found no independent association between traditional microbiome diversity profile (or Enterococcus abundance) and 30-day mortality.

The researchers noted that fecal metabolic dysbiosis may represent a treatable trait in critically ill patients, with the MDS serving as a potential biomarker to identify those who could benefit from targeted interventions to correct this imbalance and improve outcomes.

 Alexander P. de Porto et al, Fecal metabolite profiling identifies critically ill patients with increased 30-day mortality, Science Advances (2025). DOI: 10.1126/sciadv.adt1466

Acute and chronic pain are different

A new study reveals that when we experience short-term (acute) pain, the brain has a built‑in way to dial down pain signals—like pressing the brakes—to keep them from going into overdrive. But in long‑term (chronic) pain, this braking system fails, and the pain signals just keep firing. This discovery helps explain why some pain goes away while other pain lingers, and it opens the door to new treatments that could stop pain from becoming chronic in the first place.

In a study published in Science Advances, researchers reveal that our bodies respond to acute (short‑term) and chronic (long‑lasting) pain in surprisingly different ways at the cellular level. Their discovery sheds new light on how pain becomes chronic—and opens the door to better‑targeted treatments.

The team studied a small but crucial region in the brainstem called the medullary dorsal horn, home to neurons that act as a relay station for pain signals. These projection neurons help send pain messages from the body to the brain.

The scientists found that during acute inflammatory pain, these neurons actually dial down their own activity. This built‑in "braking system" helps limit the amount of pain‑related signals sent to the brain. Once the inflammation and pain subside, the neurons return to their normal state.

However, in chronic pain, this braking system fails. The neurons don't reduce their activity—in fact, they become more excitable and fire more signals, potentially contributing to the persistence of pain.

Using a combination of electrophysiology and computer modeling, the researchers identified a key mechanism: a specific potassium current known as the A‑type potassium current (IA). This current helps regulate the excitability of neurons.

In acute pain, IA increases—acting like a natural sedative for the pain pathways. But in chronic pain, this current doesn't ramp up, and the neurons become hyperactive. The absence of this regulation may be one of the biological switches that turns temporary pain into a long‑lasting condition.

This is the first time  the researchers have seen how the same neurons behave so differently in acute versus chronic pain. The fact that this natural 'calming' mechanism is missing in chronic pain suggests a new target for therapy. If we can find a way to restore or mimic that braking system, we might be able to prevent pain from becoming chronic.

Ben Title et al, Opposite regulation of medullary pain-related projection neuron excitability in acute and chronic pain, Science Advances (2025). DOI: 10.1126/sciadv.adr3467. www.science.org/doi/10.1126/sciadv.adr3467