Vampire bats’ mutual grooming helps spread innovative rabies vaccine

A gel that bats lick off one another’s fur could help prevent rabies outbreaks in cattle, a growing problem in Latin America

Bat vaccine can be spread lickety-split

An oral vaccine could curb rabies infections among vampire bats (Desmodus rotundus) in Central and South America. The vaccine is applied to the bats’ fur in a thick gel. The bats can then spread the vaccine among themselves through mutual grooming — licking one another’s fur to keep clean. In a small test, researchers applied the gel to 24 bats in a colony of 117. After seven days, they found that the vaccine had been spread among 88% of the colony. Vaccinating the bats against rabies could stop them from spreading the virus to farm animals without resorting to harmful measures such as poisons.

https://www.biorxiv.org/content/10.1101/2025.06.03.657068v2

https://www.science.org/content/article/vampire-bats-mutual-groomin...

Scientists identify 4,200 plastic chemicals of concern and highlight safer approaches

Countries are currently negotiating a global treaty to end plastic pollution and make plastics safer and more sustainable. Plastic chemicals are a core issue because all plastics, from food packaging to car tires, contain hundreds of chemicals that can leach into foodstuffs, homes, and the environment.

Many of these are known to harm the health of humans and the environment. However, a comprehensive overview of these chemicals is currently missing, which limits society's ability to protect people and the planet from hazardous plastic chemicals.

A new study published in Nature provides a comprehensive and systematically compiled overview of all chemicals that can be present in plastics, their properties, uses, and hazards.

It encompasses both chemicals intentionally added during production and contaminants detected in plastics. Importantly, the study provides a scientific approach for identifying chemicals of concern. This allows scientists and manufacturers to develop safer plastics and policymakers to promote a non-toxic circular economy.

The new study shows that there are more plastic chemicals than previously known, with 16,325 chemicals included in the PlastChem database that accompanies the work. Importantly, the scientists discovered at least 4,200 plastic chemicals are of concern because of the hazards they pose to health and the environment. These chemicals of concern can be present in each major plastic type, including in food packaging, and all tested plastics can release hazardous chemicals.

Plastics should not contain harmful chemicals to begin with. Yet, the scientific evidence shows that they are intentionally used or unintentionally present in all types of plastics. This underpins the urgent need to make plastics safer, say the authors of this paper.

The new study outlines three major pathways towards safer and more sustainable plastics: safer chemicals, transparency, and chemically simpler plastics.

Laura Monclús, Mapping the chemical complexity of plastics, Nature (2025). DOI: 10.1038/s41586-025-09184-8. www.nature.com/articles/s41586-025-09184-8

Scientists use AI to create protein that kills E. coli

In the last year, there has been a surge in proteins developed by AI that will eventually be used in the treatment of everything from snakebites to cancer. What would normally take decades for a scientist to create—a custom-made protein for a particular disease—can now be done in seconds.

For the first time,  scientists have used Artificial Intelligence (AI) to generate a ready-to-use biological protein, in this case, one that can kill antibiotic-resistant bacteria like E. coli.

This study, published in Nature Communications, provides a new way to combat the growing crisis caused by antibiotic-resistant superbugs.

These proteins are now being developed as pharmaceuticals, vaccines, nanomaterials and tiny sensors, with many other applications yet to be tested.

Inhibiting heme piracy by pathogenic Escherichia coli using de novo-1 designed proteins, Nature Communications (2025). DOI: 10.1038/s41467-025-60612-9 On BioRxiv. DOI: 10.1101/2024.12.05.626953

From injury to agony: Scientists discover brain pathway that turns pain into suffering

Pain isn't just a physical sensation—it also carries emotional weight. That distress, anguish, and anxiety can turn a fleeting injury into long-term suffering.

Researchers  have now identified a brain circuit that gives physical pain its emotional tone, revealing a new potential target for treating chronic and affective pain conditions such as fibromyalgia, migraine, and post-traumatic stress disorder (PTSD).

Published in Proceedings of the National Academy of Sciences, the study identifies a group of neurons in a central brain area called the thalamus that appears to mediate the emotional (affective) side of pain in mice. This new pathway challenges the textbook understanding of how pain is processed in the brain and body.

For decades, the prevailing view was that the brain processes sensory and emotional aspects of pain through separate pathways. This study provides strong evidence that a branch of the sensory pain pathway directly mediates the affective experience of pain.

The physical sensation of pain is what allows you to immediately detect it, assess its intensity, and identify its source. The affective part of pain is what makes it so unpleasant. This emotional discomfort motivates you to take action and helps you learn to associate negative feelings with the situation so you can avoid it in the future.

This is a critical distinction. Most people start to perceive pain at the same stimulus intensities, meaning we all process the sensory side of pain fairly similarly. In comparison, our ability to tolerate pain varies greatly. How much we suffer or feel threatened by pain is determined by our affective processing, and if it becomes too sensitive or lasts too long, it can result in a pain disorder. This makes it important to understand which parts of the brain control these different dimensions of pain.
Sensory pain was thought to be mediated by the spinothalamic tract, a pathway that sends pain signals from the spinal cord to the thalamus, which then relays them to sensory processing areas across the brain.

Affective pain had generally been thought to be mediated by a second pathway called the spinoparabrachial tract, which sends pain information from the spinal cord into the brainstem.
Part 1

Using advanced techniques to manipulate the activity of specific brain cells, the researchers discovered a new spinothalamic pathway in mice. In this circuit, pain signals are sent from the spinal cord into a different part of the thalamus, which has connections to the amygdala, the brain's emotional processing center. This particular group of neurons in the thalamus can be identified by their expression of CGRP (calcitonin gene-related peptide), a neuropeptide.
When the researchers "turned off" (genetically silenced) these CGRP neurons, the mice still reacted to mild pain stimuli, such as heat or pressure, indicating their sensory processing was intact. However, they didn't seem to associate lasting negative feelings with these situations, failing to show any learned fear or avoidance behaviors in future trials. On the other hand, when these same neurons were "turned on" (optogenetically activated), the mice showed clear signs of distress and learned to avoid that area, even when no pain stimuli had been used.

Pain processing is not just about nerves detecting pain; it's about the brain deciding how much that pain matters.
Understanding the biology behind these two distinct processes will help us find treatments for the kinds of pain that don't respond to traditional drugs.
Many chronic pain conditions—such as fibromyalgia and migraine—involve long, intense, unpleasant experiences of pain, often without a clear physical source or injury. Some patients also report extreme sensitivity to ordinary stimuli like light, sound, or touch, which others would not perceive as painful.
Overactivation of the CGRP spinothalamic pathway may contribute to these conditions by making the brain misinterpret or overreact to sensory inputs. In fact, transcriptomic analysis of the CGRP neurons showed that they express many of the genes associated with migraine and other pain disorders.
Notably, several CGRP blockers are already being used to treat migraines. This study may help explain why these medications work and could inspire new nonaddictive treatments for affective pain disorders.

 Sukjae J. Kang et al, Thalamic CGRP neurons define a spinothalamic pathway for affective pain, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2505889122

Part 2

Genomic study reveals deep roots of human survival and adaptation in Himalayas

A new genomic study reveals how human populations adapted, survived, and diversified in the Himalayas, one of the most extreme and challenging environments on Earth.

Researchers analyzed whole-genome sequences from diverse Himalayan ethnic groups, many of which had never been genetically studied before at this level.

Published in Current Biology, the study shows that population structure in the Himalayas began over 10,000 years ago, thousands of years before archaeological evidence of permanent settlement at high altitudes. This early divergence challenges long-standing assumptions about when and how diverse groups first began accessing the extreme elevations of the Himalayas.

 This study offers an unprecedented window into the genetic legacy of Himalayan populations and their extraordinary adaptations to high-altitude life. It reveals how migration, isolation, and natural selection came together to shape human survival in one of the world's most challenging environments.

The study identifies novel genetic variants linked to adaptation in hypoxia, metabolism, immunity, and physical activity. It also confirms that the Denisovan EPAS1-derived gene, known to be crucial for surviving low-oxygen conditions, is widespread across all high-altitude Himalayan groups.

The gene variants originate from the extinct archaic human species known as Denisovan. Strikingly, other variants were also found in some lowland populations, including those previously reported in Southeast Asian groups known for their exceptional breath-hold diving abilities, pointing to unexpected evolutionary links.

Whole-genome sequences provide insights into the formation and adaptation of human populations in the Himalayas, Current Biology (2025). DOI: 10.1016/j.cub.2025.06.048. www.cell.com/current-biology/f … 0960-9822(25)00808-5

Vaccines work: Data show real-world evidence of stable protection against HPV-related cervical cancer

Among the more than 100 types of human papillomavirus (HPV), at least 14 are considered as "high-risk" types which can cause (cervical) cancer. After breast cancer, cervical cancer is the most common cancer  among women aged 15–44 years.

Before HPV vaccination among teenage girls started in Denmark, high-risk HPV was found in all cervical cancers. HPV types 16/18 accounted for around three quarters (74%) of cervical cancers. These two types are covered in the 4-valent HPV vaccine offered to girls since 2008 as well as the 9-valent vaccine, which has been in use in Denmark since November 2017.
One third (26%) of cervical cancers prior to the HPV immunization campaign were caused by high-risk types that are not covered by the 2- and 4-valent vaccine.

In their research article published in Eurosurveillance, a team led by Mette Hartmann Nonboe examined the HPV status of cervical samples over time among women (22–30 years) at the screening age for cervical cancer who were vaccinated as girls.

They tested up to three consecutive cervical cell samples per participant provided by the contributing pathology departments in Denmark for HPV.

In total, 17,252 women with at least one cervical cell sample were registered between 1 February 2017 and 29 February 2024. During the seven years of the randomized "Trial23" study (cervical cancer screening starts at age 23 in Denmark), 84% of women in the study had at least one cell sample taken. The authors compared HPV prevalence, persistence and incidence among vaccinated and unvaccinated women.
Part 1

Based on the data gathered during the study period, HPV16/18 has been almost eliminated among vaccinated women in Denmark. The prevalence of these two types in the samples decreased to < 1% in 2021 from 15–17% before the vaccination of girls. In addition, the prevalence of types 16/18 in women who had not been vaccinated against HPV remained at 5%, which, according to the authors, "strongly indicates population immunity."

Despite the evidence of protection through vaccination, about one-third of women screened during the study period still had HPV infection with high-risk HPV types not covered by the offered vaccines—and new infections with these types were more frequent in vaccinated women than in unvaccinated women.
There was a low prevalence of HPV16/18 during the seven-year study period and women who have been vaccinated against HPV as girls are expected to have a considerably lower risk of cervical cancer compared with previous generations.

Human papillomavirus prevalence in first, second and third cervical cell samples from women HPV-vaccinated as girls, Denmark, 2017 to 2024: data from the Trial23 cohort study, Eurosurveillance (2025). DOI: 10.2807/1560-7917.ES.2025.30.27.2400820

Part 2

Global vaccine stockpiles prevented more than 5.8 million cases

The life-saving impact of global vaccine stockpiles to address outbreaks of vaccine-preventable diseases has been demonstrated in new Burnet Institute research.

Published in the journal BMJ Global Health, the study considered 210 outbreaks that occurred between 2000 and 2023 for five diseases—cholera, Ebola, measles, meningitis and yellow fever.

Outbreak response immunization was estimated to have prevented more than 5.8 million cases and 327,000 deaths across these outbreaks, providing economic benefits of almost US$32 billion.

For diseases with routine vaccination programs, maintaining high levels of population immunity is vital for preventing large outbreaks.

But when outbreaks do occur, a rapid vaccine response typically provides the greatest protective impact for the population at risk—and the faster the response, the greater the impact. While vaccines are amazing preventively, they are also excellent when used reactively to control outbreaks and save lives.

Vaccine stockpiles have not only prevented many cases and deaths, but they have also prevented outbreaks from reaching the point where they cause substantive issues, and that's really important, say the researchers.

 Dominic Delport et al, Estimating the historical impact of outbreak response immunisation programmes across 210 outbreaks in low and middle-income countries, BMJ Global Health (2025). DOI: 10.1136/bmjgh-2024-016887. gh.bmj.com/content/10/7/e016887

Newly discovered molecule may explain reduced muscle mass in type 2 diabetes

Researchers  have discovered a previously unknown molecule that may explain why people with type 2 diabetes often suffer from muscle weakness and muscle loss—a condition that has a major impact on quality of life and overall health.

In the new study, published in Science Advances, researchers have identified a previously unknown molecule, TMEM9B-AS1, which may explain why people with type 2 diabetes often suffer from muscle weakness and loss of muscle mass. The molecule is a long non-coding RNA that plays an important role in regulating cellular functions.

The researchers discovered that TMEM9B-AS1 is significantly reduced in skeletal muscles in individuals with type 2 diabetes, and its absence disrupts the machinery needed to build new muscle proteins.

The study shows that TMEM9B-AS1 supports the stability of MYC, a key gene that drives the production of ribosomes—the factories that manufacture proteins. Without this RNA molecule, MYC becomes unstable, and muscle cells lose their ability to maintain normal protein production. This may help explain the muscle deterioration we often see in people with metabolic diseases.  

Ilke Sen et al, Down-regulation of human-specific lncRNA TMEM9B-AS1 in skeletal muscle of people with type 2 diabetes affects ribosomal biogenesis, Science Advances (2025). DOI: 10.1126/sciadv.ads4371

Bacteria takes the poison out of mercury
An engineered strain of the gut microbe Bacteroides thetaiotaomicron can break down methylmercury (MeHg), a potent neurotoxin that’s increasingly found in seafood as a result of pollution. Researchers inserted two genes into the bacteria that snip MeHg into a carbon molecule and plain mercury, which isn’t as easily absorbed by the body. Pregnant mice that were given the engineered B. thetaiotaomicron and fed a diet high in MeHg-laced tuna excreted more mercury in their faeces and had lower levels of mercury in both maternal and foetal tissues than those with a normal microbiome.

https://www.cell.com/cell-host-microbe/abstract/S1931-3128(25)00142-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1931312825001428%3Fshowall%3Dtrue

3I/ATLAS: Interstellar object 'may be oldest comet ever seen'

A mystery interstellar object discovered last week is likely to be the oldest comet ever seen—possibly predating our solar system by more than 3 billion years, researchers say.

The "water ice-rich" visitor, named 3I/ATLAS, is only the third known object from beyond our solar system ever spotted in our cosmic neighborhood and the first to reach us from a completely different region of our Milky Way galaxy.

It could be more than 7 billion years old.

Unlike the previous two objects to enter our solar system from elsewhere in the cosmos, 3I/ATLAS appears to be traveling on a steep path through the galaxy, with a trajectory that suggests it originated from the Milky Way's "thick disk"—a population of ancient stars orbiting above and below the thin plane where the sun and most stars reside.

All non-interstellar comets such as Halley's comet formed with our solar system, so are up to 4.5 billion years old.

But interstellar visitors have the potential to be far older, and of those known about so far our statistical method suggests that 3I/ATLAS is very likely to be the oldest comet we have ever seen.

The object was first spotted on 1 July 2025 by the ATLAS survey telescope in Chile, when it was about 670 million km from the sun.

Research predicts that, because 3I/ATLAS likely formed around an old, thick-disk star, it should be rich in water ice.

This is an object from a part of the galaxy we've never seen up close before. Researchers think there's a two-thirds chance this comet is older than the solar system, and that it's been drifting through interstellar space ever since.

As it approaches the sun, sunlight will heat 3I/ATLAS's surface and trigger cometary activity, or the outgassing of vapor and dust that creates a glowing coma and tail.

Early observations already suggest the comet is active, and possibly larger than either of its interstellar predecessors, 1I/'Oumuamua (spotted in 2017) and 2I/Borisov (2019).

The Galactic Interstellar Object Population in the LSST. conference.astro.dur.ac.uk/eve … 7/contributions/751/

Matthew J. Hopkins et al, From a Different Star: 3I/ATLAS in the context of the Ōtautahi-Oxford interstellar object population model, arXiv (2025). DOI: 10.48550/arxiv.2507.05318 ,
doi.org/10.48550/arXiv.2507.05318

Premenstrual symptoms linked to increased risk of cardiovascular disease

Women diagnosed with premenstrual symptoms have a slightly increased risk of developing cardiovascular disease later in life. This is shown by a new study  published in Nature Cardiovascular Research.

Premenstrual symptoms include premenstrual syndrome (PMS) and the more severe form, premenstrual dysphoric disorder (PMDD). The symptoms, which appear a few days before menstruation and then subside, can be both psychological and physical.

The study included more than 99,000 women with premenstrual symptoms who were followed for up to 22 years. The researchers compared their health with women without these symptoms—both in the general population and by comparing them with their own sisters to take into account hereditary factors and upbringing.

The results show that women with premenstrual symptoms had about a 10% higher risk of developing cardiovascular disease. When the researchers also looked at different types of cardiovascular disease, they found that the link was particularly strong for heart rhythm disorders (arrhythmias), where the risk was 31% higher, and for stroke caused by a blood clot, where the risk was 27% higher.

Even after the researchers took into account other factors such as smoking, BMI and mental health, the link between premenstrual symptoms and increased disease risk remained.

The increased risk was particularly clear in women who were diagnosed before the age of 25 and in those who had also experienced postnatal depression, a condition that can also be caused by hormonal fluctuations.

Research has not yet identified the cause of this link, but the researchers behind the study suggest three possible explanations. One is that women with premenstrual symptoms may have a disrupted regulation of the renin-angiotensin-aldosterone system (RAAS), which controls blood  pressure and fluid balance in the body, among other things.

The second is that these women have increased levels of inflammation in the body, which is a known risk factor for atherosclerosis and other heart problems. Finally, it may be because women with premenstrual symptoms may have metabolic abnormalities, which are linked to an increased risk of both stroke and heart attack.

Yihui Yang, et al. Premenstrual disorders and risk of cardiovascular diseases, Nature Cardiovascular Research (2025). DOI: 10.1038/s44161-025-00684-4

Quantum objects' dual nature mapped with new formula for 'wave-ness' and 'particle-ness'

Quantum mechanics has revolutionized our understanding of nature, revealing a bizarre world in which an object can act like both waves and particles, and behave differently depending on whether it is being 'watched'.

In recent decades, researchers exploring this wave-particle duality have learned to measure the relative "wave-ness" and "particle-ness" of quantum objects, helping to explain how and when they veer between wave-like or particle-like behaviors.

Now, in a paper for Physical Review Research, researchers at the Stevens Institute of Technology report an important new breakthrough: a simple but powerful formula that describes the precise closed mathematical relationship between a quantum object's "wave-ness" and "particle-ness."

Previous research showed that wave-ness and particle-ness could be expressed as an inequality, with the sum of an object's wave-like behaviors (such as visible interference patterns) and particle-like behaviors (such as the predictability of its path or location) being equal to or less than one.

That's important, because it means that if an object is fully wave-like, then it shows no particle-like behaviors, and vice versa. 

Such models were incomplete, however, because they can describe situations in which an object's wave-like and particle-like behaviors increase simultaneously—the opposite of the actual exclusive relationship between the two behaviors.

To remedy that, the authors introduced a new variable: the coherence of the quantum object.

That enables the calculation of both wave-ness and particle-ness with far more precision. By measuring the coherence in a system, in fact, it becomes possible to calculate a quantum object's level of wave-ness and particle-ness—not simply as "less than one," but as an exact value.

The relationship between wave-ness and particle-ness can then be plotted as an elegant curve on a graph—a perfect quarter-circle for a perfectly coherent system, and a flatter ellipse as the level of coherence declines.

 Pawan Khatiwada et al, Wave-particle duality ellipse and application in quantum imaging with undetected photons, Physical Review Research (2025). DOI: 10.1103/dyg6-l19j

How do rivers choose their path?

Rivers choose their path based on erosion, a discovery that could transform flood planning and restoration

Rivers are Earth's arteries. Water, sediment and nutrients self-organize into diverse, dynamic channels as they journey from the mountains to the sea. Some rivers carve out a single pathway, while others divide into multiple interwoven threads. These channel patterns shape flood risks, erosion hazards and ecosystem services for more than three billion people who live along river corridors worldwide.

Understanding why some waterways form single channels, while others divide into many threads, has perplexed researchers for over a century. Geographers recently mapped the thread dynamics along 84 rivers with 36 years of global satellite imagery to determine what dictates this aspect of river behavior.

The researchers found that rivers will develop multiple channels if they erode their banks faster than they deposit sediment on their opposing banks. This causes a channel to widen and divide over time.

The results, published in the journal Science, solve a longstanding quandary in the science of rivers. They also provide insight into  natural hazards and river restoration efforts.

Austin J. Chadwick et al, Single- and multithread rivers originate from (im)balance between lateral erosion and accretion, Science (2025). DOI: 10.1126/science.ads6567

Artificial sweeteners leave bitter aftertaste for the environment

New research has found increasing levels of artificial sweeteners in wastewater treatment plants, with downstream impacts on the environment.

Artificial sweeteners, widely used in soft drinks, processed foods and sugar-free products such as toothpaste, are increasingly turning up far from supermarket shelves—in our rivers, waterways and natural ecosystems.

Some sugar substitutes have faced controversy for potential negative health effects, including links to type-2 diabetes, heart disease and cancer. Some also pose toxicity risks to aquatic animals. In zebrafish, sucralose causes birth defects and high levels of saccharin are neurotoxic.

In a systematic review, researchers examined the type and prevalence of artificial sweeteners in wastewater treatment plants across 24 countries, changes in concentration, and how effectively they are removed.

The researchers found that globally, sucralose, acesulfame, saccharin, and cyclamate are the most prevalent artificial sweeteners. The highest concentrations of these chemicals were found in the U.S., Spain, India and Germany.

Concentrations were 10%–30% higher in summer for most countries, however, in China they were highest in winter. Other artificial sweeteners found in wastewater include neotame, stevia, acesulfame-K and neo hesperidin dihydrochalcone (NHDC).

Unlike natural sugars, artificial sweeteners are designed to resist digestion, meaning they often pass through the human body largely unchanged. As a result, they enter wastewater systems where standard treatment processes aren't always equipped to deal with them.

The researchers found that while saccharin and cyclamate were easily removed from wastewater, other artificial sweeteners such as sucrose and acesulfame were harder to remove, and were released into the wider environment.

Sweeteners such as sucralose are incredibly persistent. Its chemical stability means it can survive both conventional and advanced treatment processes, so it eventually makes its way into rivers, lakes and coastal waters where it can affect aquatic ecosystems.

The study calls for ongoing monitoring, tighter regulations, and improved treatment technologies to reduce the environmental risks posed by artificial sweeteners.

 Jibin Li et al, Artificial sweeteners in wastewater treatment plants: A systematic review of global occurrence, distribution, removal, and degradation pathways, Journal of Hazardous Materials (2025). DOI: 10.1016/j.jhazmat.2025.138644

How the genome defends itself against internal enemies

An international research team has deciphered a mechanism of the evolutionary arms race in human cells. The findings provide insights into how mobile elements in DNA hijack cellular functions—and how cells can defend themselves against this in order to prevent conditions such as tumor formation or chronic inflammation.

An international research team has discovered how the LINE1 retrotransposon exploits a cell protein to become active itself, as occurs in tumors. At the same time, the researchers have also deciphered the cell's appropriate countermeasures to prevent conditions such as tumor formation or chronic inflammation. The results have been published in the journal Nature Communications.

"Sleepers" are the name the Secret Service gives agents who live inconspicuously in a society for years before being activated by their employers. The human genome contains thousands of such sleepers, known as retrotransposons. These—probably left over from virus attacks millions of years ago—are equipped with only minimal information to jump out of the genome and multiply when the opportunity arises. To do this, they misuse the enzyme machinery of human cells.

LINE1 is the name of the most common of these elements, accounting for almost 20% of the entire genome. When LINE1 becomes active, it copies itself and reintegrates itself into the genetic material  at a different location, thereby disrupting the cell's blueprint. This may sometimes be beneficial in terms of introducing diversity into the genome, but it can easily become uncontrollable, especially in progressive tumors.

In addition, active LINE1 can alert the cell's immune system, which can lead to chronic inflammation. Over the course of evolution, human cells have therefore developed many mechanisms to prevent precisely this activation. How LINE1 itself is mobilized has been largely misunderstood until now.

Part 1

The research team has unlocked the mechanisms for how this works: LINE1 recruits a non-working protein in the cells called NRBP1. This former kinase had lost its enzymatic functions through mutations in its gene over time. Since the uncontrolled reproduction of LINE1 is a major problem for the host cell, it has also developed a counter-mechanism over time. A slightly modified copy of this protein, the paralog NRBP2, marks NRBP1 so that it is recognized as waste and thereby disposed of.

The competition between the two proteins must be won by NRBP2 in order to prevent damage. Until now, both factors had only been noticed in cancer biology due to their different involvement in tumors, without their functions being known. An analysis of the evolutionary history of this competition shows that the blocking function of NRBP2 was probably acquired later in evolution in order to escape the destructive influence of NRBP1 and LINE1.

Wei Yang et al, Opposing roles of pseudokinases NRBP1 and NRBP2 in regulating L1 retrotransposition, Nature Communications (2025). DOI: 10.1038/s41467-025-61626-z

Part 2

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Late eating is associated with impaired glucose metabolism

Our metabolic processes differ depending on the time of day and many of them are more active in the morning than in the evening. Although studies show that eating late in the day is associated with an increased risk of obesity and cardiovascular diseases, little is known about how the time we eat affects glucose metabolism and to what extent this is genetically defined.

Researchers  recently investigated this using data from a twin cohort from 2009–10. Their article was published in the journal eBioMedicine.

The circadian system is a hierarchically structured 24-hour time control system in the body that regulates behavior and metabolism via a central clock in the brain and peripheral clocks in organs such as the liver or pancreas. As a result, our metabolic processes differ depending on the time when we eat, which leads to diurnal fluctuations in glucose metabolism and the release of hormones after a meal.

Food intake itself acts as an important timer that synchronizes our internal clocks. Decoupling meal times from the natural light-dark rhythm, e.g., when working at night, can lead to an internal clock disorder and negative metabolic changes.

Previous studies have shown that eating late at night is associated with an increased risk of obesity and cardiovascular diseases.

However, little is known about how exactly the timing of food intake interacts with the individual circadian rhythm and thus influences glucose metabolism and the risk of diabetes. It is also unclear which mechanisms determine one's individual eating behavior, as it depends on the interaction of cultural, personal, physiological and genetic factors.

When someone eats during the course of a day in relation to the individual biological daily rhythm is measured as the interval between mealtime and the midpoint of sleep. The midpoint of sleep describes the time that lies exactly in the middle between falling asleep and waking up. It is a measure of the chronotype—in other words, whether someone is an early riser or a night owl.

This work was done on identical and fraternal twin pairs. 

Janna Vahlhaus et al, Later eating timing in relation to an individual internal clock is associated with lower insulin sensitivity and affected by genetic factors, eBioMedicine (2025). DOI: 10.1016/j.ebiom.2025.105737

Sand and dust storms affect about 330 million people in over 150 countries

Sand and dust storms affect about 330 million people in over 150 countries and are taking an increasing toll on health, economies and the environment, the U.N. World Meteorological Organization says.

About 2 billion tons of dust are emitted yearly.

More than 80% of the world's dust comes from the deserts in North Africa and the Middle East, but it has a global impact because the particles can travel hundreds and even thousands of kilometers (miles) across continents and oceans.

Dust and dust storms are driven by climate change, land degradation and unsustainable practices.

Airborne particles from sand and dust storms contribute to 7 million premature deaths every year. They trigger respiratory and cardiovascular disease, and reduce crop yields by up to 25%, causing hunger and migration, according to experts. The storms' economic costs are "staggering."

Over 20 U.N. and international agencies are working to unite efforts on early warning systems for storms and to deal with other issues, including health and financing.

From land restoration and sustainable agriculture to integrated early warning systems, we have the tools to act, the exerts say.

Source: News Agencies

**

A few bright buildings light up the entire night sky

When millions of people turn off their lights for Earth Hour each year, something remarkable happens in the night sky above cities. New research from Hong Kong published in Scientific Reports shows that just a small number of decorative buildings and advertising boards can dramatically brighten the entire urban night sky and when they go dark, the sky becomes up to 50% darker.

The scientists studied 14 years of Earth Hour data from 2011 to 2024 in Hong Kong, using specialized light sensors to measure exactly how much the night sky changed when the city participated in the global lights-out event.
The research team discovered that the most significant improvements in night sky darkness came from turning off lights in central business districts, particularly the decorative lighting on building facades and large LED advertising screens. Using crowdsourced photographs from social media, they could pinpoint exactly which buildings went dark during Earth Hour and correlate this with measurements of sky brightness.

Interestingly, the weekend lighting patterns during Earth Hour remained largely unchanged, suggesting that the dramatic darkening came specifically from commercial and decorative lighting rather than everyday residential use. This finding challenges common assumptions about what contributes most to light pollution in cities.

The researchers didn't just measure overall brightness, they analyzed the specific colors of light pollution using spectroscopic sensors. They found that the biggest reductions occurred in blue-green wavelengths (445–500 nanometers), green (500–540 nanometers), and orange-red (615–650 nanometers) ranges. These correspond precisely to the peak emissions from LED advertising boards that dominate many urban landscapes.
They also detected significant reductions in the yellow-orange spectrum (585–595 nanometers), which matches the signature of metal halide floodlights commonly used to illuminate buildings and large outdoor advertisements. This spectral analysis provides a detailed fingerprint of exactly which types of artificial lighting contribute most to urban light pollution.

This research finally offers hope for tackling light pollution without requiring massive citywide changes. Instead of asking every building to dim their lights, cities could achieve substantial improvements by focusing on a relatively small number of high-impact sources.

Chu Wing So et al, Natural experiments from Earth Hour reveal urban night sky being drastically lit up by few decorative buildings, Scientific Reports (2025). DOI: 10.1038/s41598-025-05279-4

Chronological age determined within 1.36 years using DNA methylation patterns

Researchers  have developed an exceptionally accurate method for predicting chronological age from DNA, based on two short genomic regions. Using deep learning networks analyzing DNA methylation patterns at a single-molecule resolution, they achieve age predictions with a median error as low as 1.36 years in individuals under 50. The method is unaffected by smoking, BMI, and sex, and has potential applications in forensics, aging research, and personalized medicine.

Using cutting-edge artificial intelligence, the scientists created a tool called MAgeNet that can determine a person's chronological age—the number of years since birth—with a margin of error as small as 1.36 years for individuals under 50. And all it takes is a simple blood draw.

It turns out that the passage of time leaves measurable marks on our DNA and this new model decodes those marks with astonishing precision.

The secret lies in how our DNA changes over time through a process called methylation—the chemical "tagging" of DNA by methyl group (CH₃) . By zooming in on just two key regions of the human genome, the team was able to read these changes at the level of individual molecules, then use deep learning to translate them into accurate age predictions.

The study, published in Cell Reports, analyzed blood samples from over 300 healthy people, as well as data from a decade-long longitudinal analysis of the Jerusalem Perinatal Study (JPS). As they show, the model worked consistently across a range of variables—like smoking, body weight, sex, and even different signs of biological aging.

Beyond potential medical uses, the method could also revolutionize forensic science by allowing experts to estimate a suspect's age from just a trace of DNA—something existing tools struggle to do.

 Time is encoded by methylation changes at clustered CpG sites, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115958. www.cell.com/cell-reports/full … 2211-1247(25)00729-6

Comparing first-trimester UTI antibiotics and congenital malformations

Researchers produced a population-based cohort study suggesting first-trimester treatment of urinary tract infection (UTI) with trimethoprim-sulfamethoxazole (TMP-SMX) is associated with a higher risk of congenital malformations compared with β-lactam antibiotics, whereas nitrofurantoin and fluoroquinolones show no clear elevated risk.

Untreated UTIs are associated with adverse perinatal outcomes, including preterm birth, low birth weight, pyelonephritis, and maternal sepsis. Routine screening for asymptomatic UTI is recommended at the initial prenatal visit and frequently leads to antibiotic treatment during the first trimester.

Many antibiotics can cross the placenta, including TMP and SMX, which can inhibit folic acid metabolism and interfere with rapidly growing fetal tissues.

The American College of Obstetricians and Gynecologists (ACOG) suggests that nitrofurantoin and TMP-SMX be avoided during the first trimester when possible. Despite this suggestion, many clinicians have been slow to adopt the guidance and nitrofurantoin and TMP-SMX combined still account for more than half of first-trimester UTI prescriptions.

In the study, "First-Trimester Antibiotic Use for Urinary Tract Infection and Risk of Congenital Malformations," published in JAMA Network Open, researchers designed a population-based cohort analysis to compare malformation risk following first-trimester exposure to antibiotics nitrofurantoin, TMP-SMX, fluoroquinolones, and β-lactams.

Among 71,604 pregnancies considered during the research work, 42,402 individuals (59.2%) were exposed to nitrofurantoin, 3,494 (4.9%) to TMP-SMX, 3,663 (5.1%) to fluoroquinolones, and 22,045 (30.8%) to β-lactams.

Unadjusted absolute risk of any congenital malformation per 1,000 infants was 19.8 for β-lactams, 21.2 for nitrofurantoin, 23.5 for fluoroquinolones, and 26.9 for TMP-SMX.

After adjusting for confounding, TMP-SMX was associated with a higher risk of any malformation compared to β-lactams (risk ratio, 1.35; 95% CI, 1.04–1.75). For nitrofurantoin and fluoroquinolones, adjusted risk was similar to β-lactams.

TMP-SMX exposure was associated with increased risk of severe cardiac malformations (risk ratio, 2.09; 95% CI, 1.09–3.99), other cardiac malformations (risk ratio, 1.52; 95% CI, 1.02-2.25), and cleft lip and palate (risk ratio, 3.23; 95% CI, 1.44–7.22).

Analyses of other malformation types did not show consistent differences by antibiotic group, and some estimates were imprecise. Sensitivity analyses yielded results consistent with the primary findings.

 Sarah S. Osmundson et al, First-Trimester Antibiotic Use for Urinary Tract Infection and Risk of Congenital Malformations, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.19544

Built-in extinguishers can prevent battery fires and explosions

Researchers have designed a working prototype of a lithium metal battery equipped with a built-in fire extinguisher, which is activated if the battery overheats.

Lithium metal batteries are currently in limited use but have huge potential because they can store ten times as much energy as lithium-ion batteries. They deliver high energy density, which means they can store large amounts of energy relative to their size. This makes them ideal for electric vehicles, portable electronics and plenty of other energy-hungry devices.

However, there is a problem. These types of batteries use lightweight lithium metal anodes and high-voltage nickel-rich oxide cathodes, a setup that can produce flammable gases. If these gases build up in a battery, they can cause fires or explosions.

To tackle this,  researchers incorporated a flame-retardant polymer into the cathode of their prototype lithium metal battery.

Published in Proceedings of the National Academy of Sciences, the researchers exposed the prototype battery and a standard lithium metal battery to gradually increasing temperatures, starting at 50 °C. When temperatures exceeded 100°C, both batteries began to overheat.

However, in the prototype, the special polymer started to break down and release chemicals (flame-inhibiting radicals) that acted like mini fire extinguishers. Specifically, they suppressed reductive reactions at the anode that are responsible for generating flammable gases.

When temperatures rose beyond 120 °C, the standard battery overheated to 1,000 °C within 13 minutes and burst into flames. Meanwhile, under the same experimental conditions, the prototype with the flame-retardant polymer reached a peak temperature of 220 °C and did not catch fire or explode.

"This smart gas management strategy enhances both thermal safety and electrochemical stability, offering a transformative pathway to fire-safe Li metal batteries for advanced energy storage applications," explained the researchers in their paper.

Jun-Chen Guo et al, A fire-safe Li metal battery via smart gas management, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2501549122

Obesity more likely caused by high calorie diet than lack of exercise

It's common knowledge that obesity is a global epidemic, particularly in industrialized countries, and that it is a major cause of disease and poor overall health. However, there has been a tug-of-war in the debate of whether the main cause of obesity is diet or a lack of exercise.

Calories consumed must be expended as energy, whether through physical activity or basal activity—the inherent processes within the body that use up energy, such as breathing or digesting food. When it comes to obesity, it has been unclear if too many calories are being consumed on average to be used by normal activity or if there is not enough activity to expend a reasonable amount of calories.

A new study, published in the journal Proceedings of the National Academy of Sciences, focuses on the problem of diet vs. exercise. Researchers analyzed data from 4,213 adults, aged 18 to 60, across 34 populations in six continents. The sample is impressively diverse and covers people from hunter-gatherer groups, pastoralists, farmers, and industrialized societies. This includes people with a wide range of diets and activity levels.

The results initially found TEE, AEE and BEE to be higher in more developed populations, along with body mass, BMI and body fat, meaning obesity was more prevalent in more economically developed countries, but it appeared that they were also expending more energy overall. However, this is not the total picture.

The researchers acknowledged that body size in general, like height, was overall larger in industrialized places. There are also fluctuations in weight and energy expenditure due to age and sex. The researchers further refined their data by adjusting for these factors.

The results then showed that TEE and BEE decreased slightly, by around 6–11%, with economic development. After adjusting for age, sex and body size, AEE was still higher overall in more economically developed populations, indicating that it is not likely to be a lack of exercise that is causing higher BMI or body fat.

The researchers found that total energy expenditure is only weakly associated with obesity, accounting for about 10% of the increased incidence of obesity in more economically developed countries. Instead, they indicate that a higher consumption of ultra processed foods (UPF), like processed meats, ready-made meals and snack cakes, is to blame, noting that "the percent of UPFs in the diet was positively correlated with body fat percentage."

Despite exercise not being the main driver of obesity, the study authors encourage regular exercise, as it is still known to be key in preventing disease and maintaining better mental health.

Amanda McGrosky et al, Energy expenditure and obesity across the economic spectrum, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2420902122

Scientists discover a simple set of rules that may explain how the body's tissues stay organized

Every day, your body replaces billions of cells—and yet, your tissues stay perfectly organized. How is that possible?

A team of researchers think they've found an answer. In a study published in Biology of the Cell, they show that just five basic rules may explain how the body maintains the complex structure of tissues like those in the colon, for example, even as its cells are constantly dying and being replaced.

This research is the product of more than 15 years of collaboration between mathematicians and cancer biologists to unlock the rules that govern tissue structure and cellular behavior.

Just like we have a genetic code that explains how our genes work, we may also have a 'tissue code' that explains how our bodies stay so precisely organized over time.

The researchers used mathematical modeling—essentially, creating a computer simulation of how cells behave—to see if a small number of rules could account for the highly organized structure of the lining of the colon. That's an ideal place to study: cells in the colon renew every few days, but the overall shape and structure stays remarkably stable.

After running many simulations and refining their models, the team identified five core biological rules that appear to govern the structure and behavior of cells:

1. Timing of cell division.
2. The order in which cells divide.
3. The direction cells divide and move.
4. How many times cells divide.
5. How long a cell lives before it dies.

These rules work together like choreography. They control where cells go, when they divide and how long they stick around—and that's what keeps tissues looking and working the way they should.

The researchers think these rules may apply not just to the colon, but to many different tissues throughout the body—skin, liver, brain and beyond. If true, this "tissue code" could help scientists better understand how tissues heal after injury, how birth defects happen and how diseases like cancer develop when that code gets disrupted.

Your tissues don't just grow and shrink randomly. They know what they're supposed to look like, and they know how to get back to that state, even after damage. That level of precision needs a set of instructions. What  has been found now is a strong candidate for those instructions.

Bruce M. Boman et al, Dynamic Organization of Cells in Colonic Epithelium is Encoded by Five Biological Rules, Biology of the Cell (2025). DOI: 10.1111/boc.70017

Tool use declines with age in wild chimpanzees

Wild chimpanzees use tools during some of the most cognitively and physically demanding foraging behaviors observed in non-human animals. While the behavioral changes that occur with aging have been widely studied in humans and some captive primates, exceptionally little is known about how growing older affects the lives of elderly wild apes. This includes how the capacity to address technical, real-world tasks changes as chimpanzees become progressively older.

Researchers have found that old age likely impacts the habitual tool-use behaviours of some wild chimpanzees—although the extent to which different individuals are affected appears to be highly variable. The findings have been published this week in the journal eLife.

The wild chimpanzees showed reduced participation and performance in their tool-use behaviors as they grew older, according to the long-term video observations used in the new study. This provides solid evidence that old age leads to gradual withdrawal from tool use, and is a contributing factor to lower efficiency in chimps' stone tool selection and use.

The findings also indicate that chimpanzees mirror human beings in how the aging process affects their ability to carry out dexterous and cognitively-challenging daily tasks. Similar to humans, the effects of old-age varied considerably between individuals, with some chimpanzees struggling to use tools, while others maintained excellent performance into later life.

Tool use is uncommon among animals, possibly because it requires a suite of physical and cognitive abilities, such as planning, fine motor coordination, understanding causal relationships, and identifying physical properties of objects in the environment. Given many of these faculties can be impacted by aging, animals' tool-use behaviors could be vulnerable to decline with old age.

Elderly chimpanzees also showed changes in their efficiency when selecting tools (with some taking noticeably longer in later years), and when using tools to crack open nuts. Nut-cracking efficiency declined across several metrics, including increases in the time taken and the number of actions required to process each nut.

 Elliot Howard-Spink et al, Old age variably impacts chimpanzee engagement and efficiency in stone tool use, eLife (2025). DOI: 10.7554/eLife.105411.3

Research finds chromosomes are covered in liquid-like coating to prevent stickiness and DNA damage

New research into mitotic chromosomes has found that they are covered in a liquid-like coating that could allow them to bounce off one another, like bumper cars, protecting them from being damaged during cell division.

Researchers  looked into the coatings of mitotic chromosomes, the highly condensed and organized structures that DNA morphs into during cell division. Their findings are published in the journal Nature Communications.

The mitotic chromosome periphery (MCP) is a poorly understood "coat" that covers all chromosomes. This latest work  showed an unexpected finding—that the coat is actually liquid-like.

This work is an important step towards understanding how chromosomes and cells divide normally during mitosis and how a liquid-like coat helps this.

The research also highlights the significant role of the chromosome coating in maintaining chromosome stability and function during cell division. Understanding these mechanisms could provide insights into diseases, including cancer, where cell division processes are often disrupted.

Tania Mendonca et al, The mitotic chromosome periphery modulates chromosome mechanics, Nature Communications (2025). DOI: 10.1038/s41467-025-61755-5

Eight babies born after mitochondrial donation treatment to reduce transmission of mitochondrial DNA disease

Every year, around one in 5,000 children is born with mitochondrial DNA mutations that can cause devastating disease. Mitochondria produce the energy required for life and contain a small piece of DNA that only encodes some of the instructions required for energy production.

Harmful mutations in mitochondrial DNA can result in reduced availability of energy, particularly affecting tissues that have high energy demands—for example, heart, muscle and brain.

Mitochondrial DNA is maternally inherited, and these diseases are therefore passed from mother to child. Although males can be affected, they do not pass on the disease.

In the absence of a cure for mitochondrial DNA diseases, attention has focused on IVF-based technologies to reduce the risk of disease by limiting transmission of disease-causing mitochondrial DNA mutations from mother to child.

The new IVF-based mitochondrial donation technology, pronuclear transfer, which was legalized in the UK in 2015, is designed to reduce the risk of mitochondrial DNA disease in children born to women who carry high levels of disease-causing mitochondrial DNA mutations.

The pioneering licensed IVF technique to reduce the risk of mitochondrial diseases carried out in Newcastle has seen eight babies born, research shows.

All eight babies show no signs of having mitochondrial DNA disease. The babies, four girls and four boys, including one set of identical twins, were born to seven women at high risk of transmitting serious disease caused by mutations in mitochondrial DNA.

The findings, reported by the Newcastle team who pioneered mitochondrial donation using fertilized human eggs, indicate that the new treatment, known as pronuclear transfer, is effective in reducing the risk of otherwise incurable mitochondrial DNA diseases.

Published in two papers in The New England Journal of Medicine (NEJM), the findings describe the reproductive and clinical outcomes of pronuclear transfer treatments performed to date. All babies were healthy at birth, meeting their developmental milestones, and the mother's disease-causing mitochondrial DNA mutations were either undetectable or present at levels that are very unlikely to cause disease.

The technique, known as pronuclear transfer, is performed after the egg is fertilized. It involves transplanting the nuclear genome (which contains all the genes essential for our individual characteristics, for example, hair color and height) from an egg carrying a mitochondrial DNA mutation to an egg donated by an unaffected woman that has had its nuclear genome removed. The resulting embryo inherits its parents' nuclear DNA, but the mitochondrial DNA is inherited predominantly from the donated egg.

Mitochondrial Donation and PGT to Reduce Risk of Mitochondrial DNA Disease. New England Journal of Medicine www.nejm.org/doi/full/10.1056/NEJMoa2415539

Mitochondrial Donation in a Reproductive Care Pathway for mtDNA Disease, New England Journal of Medicine (2025). DOI: 10.1056/NEJMoa2503658

Extremely severe obesity is on the rise in kids—along with a barrage of health problems

Obesity rates in children have been on the rise for decades, having quadrupled from 1990 to 2022, and along with the rise in obesity, comes a rise in health risks. However, obesity can be broken down further into categories based on severity.

In children, obesity is defined as having a body mass index (BMI) above 95% of kids of a similar age and sex. This differs from the way adult obesity is defined, which uses a simple BMI number of 30 or higher. Currently, childhood obesity is separated into three categories defined by BMI, with class 1 at or above the 95th percentile, class 2 at 120% to 140% and class 3 (severe obesity) at 140% or higher of the 95th percentile.

A new study by researcher published in the JAMA Network Open, suggests breaking up these categories even further by adding a class 4 and 5, defined as a BMI from 160% to 180% of 95th percentile and a BMI over 180% of 95th percentile, respectively. This further refinement seeks to differentiate the health risks involved with these "extremely severe" categories of obesity.

The study highlights how the health risks of children at these levels of obesity become increasingly dangerous when compared to children in lower obesity classes or to children with healthy weights.

The researchers found a startling increase of 253% in the prevalence of extremely severe obesity in children from 2008 to 2023. In addition, all other categories of obesity increased over this time period, although at lower rates. They found the increase was particularly dramatic in adolescents from the ages of 16 to 18 and in non-Hispanic black children.

The analysis of health complications in these children revealed an increased risk of multiple diseases with increasing classes of obesity. In particular, diabetes, prediabetes, metabolic disease—which is associated with increased risk of heart disease and stroke—and liver diseases were common.

Insulin resistance, a precursor to many of these health problems, was found in 100% of the class 4 and 5 participants, compared to 81% in classes 1–3 and 27% in those without obesity. Across the board, all diseases were more prevalent in higher classes of obesity than in lower classes and the lower classes of obesity were associated with increased risk compared to healthy BMI risks.

The study authors point to the need for action on this increasingly severe problem.

Eliane Münte et al, Prevalence of Extremely Severe Obesity and Metabolic Dysfunction Among US Children and Adolescents, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.21170

Scientists discover genetic condition that causes paralysis following mild infections

Doctors and genetic researchers  have discovered that changes in a gene leads to severe nerve damage in children leading to paralysis following a mild bout of infection.

The paper, "Acute-onset axonal neuropathy following infection in children with biallelic RCC1 variants: a case series," is published in The Lancet Neurology.

Researchers have now discovered that changes in a gene called RCC1 led to this severe nerve damage. In over half of the children, doctors suspected the diagnosis of a different severe nerve condition that can develop after infection called Guillain Barré syndrome.

The researchers performed laboratory studies on skin cells taken from patients and in specially genetically engineered fruit flies to show that the damage to nerves can be caused by certain chemicals.

Skin cells from patients when looked at under special microscopes have changes very similar to those seen in the cells of patients with motor neuron disease where muscles, including those controlling breathing and swallowing, become weak.

As children are well before they develop nerve damage following an infection, this gives us an opportunity to treat at risk children before problems occur.

J Robert Harkness et al, Acute-onset axonal neuropathy following infection in children with biallelic RCC1 variants: a case series, The Lancet Neurology (2025). DOI: 10.1016/S1474-4422(25)00198-X

New research says it is okay to eat eggs 

Researchers clear eggs of heart disease blame

From poached to panfried, when it comes to eggs, it's all sunny side up, as new research  confirms that this breakfast favorite won't crack your cholesterol.

Long blamed for high cholesterol, eggs have been beaten up for their assumed role in cardiovascular disease (CVD). Now,  researchers have shown definitively that it's not dietary cholesterol in eggs but the saturated fat in our diets that's the real heart health concern.

In a world-first study published in The American Journal of Clinical Nutrition, researchers examined the independent effects of dietary cholesterol and saturated fat on LDL cholesterol (the "bad" kind), finding that eating two eggs a day—as part of a high cholesterol but low saturated fat diet—can actually reduce LDL levels and lower the risk of heart disease.

CVD is the leading cause of death worldwide, responsible for nearly 18 million deaths each year.

Eggs have long been unfairly cracked by outdated dietary advice, the researchers  say, 

They're unique—high in cholesterol, yes, but low in saturated fat. Yet it's their cholesterol level that has often caused people to question their place in a healthy diet.

In this study, the researchers separated the effects of cholesterol and saturated fat, finding that high dietary cholesterol from eggs, when eaten as part of a low saturated fat diet, does not raise bad cholesterol levels.

Instead, it was the saturated fat that was the real driver of cholesterol elevation.

Sharayah Carter et al, Impact of dietary cholesterol from eggs and saturated fat on LDL cholesterol levels: a randomized cross-over study, The American Journal of Clinical Nutrition (2025). DOI: 10.1016/j.ajcnut.2025.05.001

Don't feed the animals: Researchers warn of risks tied to wildlife interactions

A study by  scientists  offers new warnings on the dangers of human interactions with wildlife.

The researchers study endangered Asian elephants and has previously reported on their shrinking habitats, a downturn that has resulted in territorial conflicts between people and elephants.

The new study now provides fresh evidence in the journal Ecological Solutions and Evidence on the serious consequences of humans supplying food to wild animals. The report indicates that such provisioning can lead wildlife to become habituated to people, causing the animals to become bolder and more prone to causing problems. Even for those who live in areas without native elephant populations, the new study provides cautionary information about interactions with any wildlife species living among us.

In Sri Lanka, they studied 18 years of elephant-tourist interactions at Udawalawe National Park. They found that the elephants congregating near tourists at the park's southern boundary have developed "begging" behaviour and have become habituated to sugary foods, sometimes breaking through fences to continue being fed.

As a result of elephants being drawn to the fence, several people have been killed or injured, and at least three elephants have been killed, while others have ingested plastic food bags and other contaminants. Such close human-wildlife encounters, including tourists feeding animals from sightseeing vehicles, also increases the risk of disease transmission to animals.

In India's Sigur region, study co-authors observed feeding interactions with 11 male Asian elephants, four of whom died from suspected human causes. One elephant was successfully rehabilitated and returned to natural foraging behaviour.

Many people, especially foreign tourists, think Asian elephants are tame and docile, like domestic pets, the researchers say, that they don't realize these are formidable wild animals and try to get too close in order to take photographs or selfies, which can end badly for both parties.

Of the 800 to 1,200 elephants estimated to live in Udawalawe National Park, the study found that 66 male elephants, or 9–15% of the local male population of Asian elephants, were observed begging for food. Some elephants, including a popular male named Rambo, became local celebrities as they solicited food from tourists over several years.

"Food-conditioned animals can become dangerous, resulting in the injury and death of wildlife, people or both," the researchers note in their paper. "These negative impacts counteract potential benefits."

Since wild elephant feeding cannot be adequately regulated as an ongoing activity, the authors of the study recommend that feeding bans should be strictly enforced.

Such interactions  can change animals' movement patterns and possibly force them to lose knowledge of natural food sources if they become too dependent on handouts.

With rare exceptions, people should avoid feeding wild animals, the researchers urge, and encourages people to engage in responsible tourism.

Don't Feed The Elephant: A Critical Examination of Food-Provisioning Wild Elephants, Ecological Solutions and Evidence (2025). DOI: 10.1002/2688-8319.70060

Vision problems emerge as astronauts spend months in orbit

When astronauts began spending six months and more aboard the International Space Station, they started to notice changes in their vision. For example, many found that, as their mission progressed, they needed stronger reading glasses. Researchers studying this phenomenon identified swelling in the optic disk, which is where the optic nerve enters the retina, and flattening of the eye shape. These symptoms became known as Space-Associated Neuro-Ocular Syndrome (SANS).

Microgravity causes a person's blood and cerebrospinal fluid to shift toward the head and studies have suggested that these fluid shifts may be an underlying cause of SANS.

A current investigation, Thigh Cuff, examines whether tight leg cuffs change the way fluid moves around inside the body, especially around the eyes and in the heart and blood vessels.

If so, the cuffs could serve as a countermeasure against the problems associated with fluid shifts, including SANS. A simple and easy-to-use tool to counter the headward shift of body fluids could help protect astronauts on future missions to the moon and Mars. The cuffs also could treat conditions on Earth that cause fluid to build up in the head or upper body, such as long-term bed rest and certain diseases.

These and other studies ultimately could help researchers prevent, diagnose, and treat vision impairment in crew members and people on Earth.

Source: NASA

Why do we need sleep? Researchers find the answer may lie in mitochondria

Sleep may not just be rest for the mind—it may be essential maintenance for the body's power supply. A new study by University of Oxford researchers, published in Nature, reveals that the pressure to sleep arises from a build-up of electrical stress in the tiny energy generators inside brain cells.

The discovery offers a physical explanation for the biological drive to sleep and could reshape how scientists think about sleep, aging, and neurological disease.

The team found that sleep is triggered by the brain's response to a subtle form of energy imbalance. The key lies in mitochondria—microscopic structures inside cells that use oxygen to convert food into energy.

When the mitochondria of certain sleep-regulating brain cells (studied in fruit flies) become overcharged, they start to leak electrons, producing potentially damaging byproducts known as reactive oxygen species. This leak appears to act as a warning signal that pushes the brain into sleep, restoring equilibrium before damage spreads more widely.

The researchers found that specialized neurons act like circuit breakers—measuring this mitochondrial electron leak and triggering sleep when a threshold is crossed. By manipulating the energy handling in these cells—either increasing or decreasing electron flow—the scientists could directly control how much the flies slept.

Even replacing electrons with energy from light (using proteins borrowed from microorganisms) had the same effect: more energy, more leak, more sleep.

In certain sleep-regulating neurons, they discovered that mitochondria—the cell's energy producers—leak electrons when there is an oversupply. When the leak becomes too large, these cells act like circuit breakers, tripping the system into sleep to prevent overload.

The findings help explain well-known links between metabolism, sleep, and lifespan. Smaller animals, which consume more oxygen per gram of body weight, tend to sleep more and live shorter lives. Humans with mitochondrial diseases often experience debilitating fatigue even without exertion, now potentially explained by the same mechanism.

This research answers one of biology's big mysteries. "Why do we need sleep? The answer appears to be written into the very way our cells convert oxygen into energy."

Raffaele Sarnataro et al, Mitochondrial origins of the pressure to sleep, Nature (2025). DOI: 10.1038/s41586-025-09261-y

Study reveals hidden regulatory roles of 'junk' DNA

A new international study suggests that ancient viral DNA embedded in our genome, which were long dismissed as genetic "junk," may actually play powerful roles in regulating gene expression. Focusing on a family of sequences called MER11, researchers have shown that these elements have evolved to influence how genes turn on and off, particularly in early human development.

The findings are published in the journal Science Advances.

Transposable elements (TEs) are repetitive DNA sequences in the genome that originated from ancient viruses. Over millions of years, they spread throughout the genome via copy-and-paste mechanisms.

Today, TEs make up nearly half of the human genome. While they were once thought to serve no useful function, recent research has found that some of them act like "genetic switches," controlling the activity of nearby genes in specific cell types.

However, because TEs are highly repetitive and often nearly identical in sequence, they can be difficult to study. In particular, younger TE families like MER11 have been poorly categorized in existing genomic databases, limiting our ability to understand their role.

To overcome this, the researchers developed a new method for classifying TEs. Instead of using standard annotation tools, they grouped MER11 sequences based on their evolutionary relationships and how well they were conserved in the primate genomes.

This new approach allowed them to divide MER11A/B/C into four distinct subfamilies, namely, MER11_G1 through G4, ranging from oldest to youngest.

This new classification revealed previously hidden patterns of gene regulatory potential. The researchers compared the new MER11 subfamilies to various epigenetic markers, which are chemical tags on DNA and associated proteins that influence gene activity. This showed that this new classification aligned more closely with actual regulatory function compared with previous methods.

Part 1

To directly test whether MER11 sequences can control gene expression, the team used a technique called lentiMPRA (lentiviral massively parallel reporter assay). This method allows thousands of DNA sequences to be tested at once by inserting them into cells and measuring how much each one boosts gene activity.

The researchers applied this method to nearly 7,000 MER11 sequences from humans and other primates, and measured their effects in human stem cells and early-stage neural cells.

The results showed that MER11_G4 (the youngest subfamily) exhibited a strong ability to activate gene expression. It also had a distinct set of regulatory "motifs," which are short stretches of DNA that serve as docking sites for transcription factors, the proteins that control when genes are turned on. These motifs can dramatically influence how genes respond to developmental signals or environmental cues.

Further analysis revealed that the MER11_G4 sequences in humans, chimpanzees, and macaques had each accumulated slightly different changes over time. In humans and chimpanzees, some sequences gained mutations that could increase their regulatory potential in human stem cells.

Young MER11_G4 binds to a distinct set of transcription factors, indicating that this group gained different regulatory functions through sequence changes and contributes to speciation
The study offers a model for understanding how "junk" DNA can evolve into regulatory elements with important biological roles. By tracing the evolution of these sequences and directly testing their function, the researchers have demonstrated how ancient viral DNA has been co-opted into shaping gene activity in primates.

Xun Chen et al, A phylogenetic approach uncovers cryptic endogenous retrovirus subfamilies in the primate lineage, Science Advances (2025). DOI: 10.1126/sciadv.ads9164. www.science.org/doi/10.1126/sciadv.ads9164

Part 2

Scientists discover a signature 'wave' of activity as the brain awakens from sleep

Each morning, your brain embarks on a remarkable series of events: it transitions from being asleep, potentially in an alternate reality, to waking up. Within a short time, you regain waking consciousness, reorient yourself and reconnect with your surroundings, becoming ready to interact with the world again. But how does your brain accomplish this transition so safely and efficiently?

To better understand the awakening brain, researchers  analyzed over 1,000 awakenings using high-density EEG recordings on a second-by-second basis.

The study, published in Current Biology, reveals that the brain doesn't wake up all at once. Instead, it orchestrates a precise sequence of activation.

The researchers worked with high-density EEG data, which offers information about the time and location of brain activity. When looking at the activity progression throughout the awakening brain, they observed a clear sequence: it starts in central and frontal brain regions and gradually spreads toward the back of the brain.

This progression likely reflects how signals from subcortical arousal centers (deeper in the brain) reach the cortex, with shorter paths to frontal areas and longer ones toward regions further back.

To better understand how the brain navigates waking up at any moment, the researchers specifically studied awakening patterns in two stages: REM sleep, commonly associated with vivid dreams, and non-REM sleep, also known as deep sleep.

When participants awoke from non-REM sleep, their brain activity first showed a brief surge in slower sleep-like waves immediately followed by faster activity related to wakefulness. When participants awoke from REM sleep, the slower waves were skipped, leading to a more direct boost in faster brain activity.

"The brain responds differently to arousing signals depending on the stage it's in", the researchers say. "In non-REM sleep, neurons that connect arousal centers to the cortex alternate between states of activity and silence—a dynamic known as 'bistability.'

"As a result of this bistability, any arousing stimulus first triggers a slow wave, before transitioning to faster activity. In contrast, REM sleep does not have this bistable pattern, so the cortex immediately responds with the fast, wake-like, activity."

Part 1

The researchers also investigated how sleepy a participant felt when they woke up. While participants felt the sleepiest when awoken from REM sleep, the impact of the slow waves in non-REM sleep stages is quite intriguing.

They found a new aspect in which slow waves can present very distinct and opposite behaviors. Some slow waves are actually acting like arousal elements—they are part of the 'wake up!' signal. The more these waves occur just before awakening, the more alert you tend to feel upon awakening. While the other slow waves—whether they are present before waking up or persisting after—are the reason we sometimes feel so sleepy in the first moments of the day.
These findings can be used for future research into sleep disorders, such as insomnia or conditions involving incomplete awakenings.

Aurélie M. Stephan et al, Cortical activity upon awakening from sleep reveals consistent spatio-temporal gradients across sleep stages in human EEG, Current Biology (2025). DOI: 10.1016/j.cub.2025.06.064

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Quantum internet moves closer as researchers teleport light-based information

Quantum teleportation is a fascinating process that involves transferring a particle's quantum state to another distant location, without moving or detecting the particle itself. This process could be central to the realization of a so-called "quantum internet," a version of the internet that enables the safe and instant transmission of quantum information between devices within the same network.

Quantum teleportation is far from a recent idea, as it was experimentally realized several times in the past. Nonetheless, most previous demonstrations utilized frequency conversion rather than natively operating in the telecom band.

Researchers recently demonstrated the teleportation of a telecom-wavelength photonic qubit (i.e., a quantum bit encoded in light at the same wavelengths supporting current communications) to a telecom quantum memory. Their paper, published in Physical Review Letters, could open new possibilities for the realization of scalable quantum networks and thus potentially a quantum internet.

 Yu-Yang An et al, Quantum Teleportation from Telecom Photons to Erbium-Ion Ensembles, Physical Review Letters (2025). DOI: 10.1103/3wh8-2gh1.

Engineered bacteria pave the way for vegan cheese and yogurt

Bacteria are set to transform the future of dairy-free milk products. Scientists have successfully engineered E. coli to produce key milk proteins essential for cheese and yogurt production, without using any animal-derived ingredients. This paves the way for plant-based dairy alternatives that mimic traditional dairy at a molecular level but are sustainable and cruelty-free.

A recent study published in Trends in Biotechnology reported two methods for producing casein (a milk protein) that are nutritionally and functionally similar to bovine casein.

Casein is a highly sought-after component in both infant and adult diets, as it is digestible, of high quality, and provides several essential amino acids our body needs.

The food and pharmaceutical industries have utilized microorganisms as cell factories for the large-scale production of biomolecules, dietary supplements, and enzymes for quite some time. Scientists were curious to see if the same approach could be used for recombinant casein proteins, produced through genetic engineering in microbial cell factories. However, these techniques often fail to replicate a key factor that imparts casein its unique properties—phosphorylation, a biological process where a phosphate group is added to a protein.

Phosphorylation of serine residues (amino acid components) is critical for casein's ability to bind calcium, which makes milk stable and provides it with nutritional properties. Calcium binding also ensures the formation of nanoscale protein structures called casein micelles, which act as delivery agents for bioavailable calcium and phosphate.

To overcome this issue, the researchers adopted two main strategies. First, they engineered bacteria to co-express three Bacillus subtilis protein kinases, which are enzymes that catalyze the addition of phosphate groups to proteins. Second, they designed a phosphomimetic version of αs1-casein, in which serine residues normally phosphorylated in the naturally occurring protein were replaced with aspartic acid to mimic the negative charge and functional effects of phosphorylation.

The team carried out structural analysis, calcium-binding tests, and simulated gastrointestinal digestion of the derived αs1-casein. The results indicated that both the phosphorylated and phosphomimetic caseins of bacterial origin had a high calcium-binding capacity, and their digestibility and structure were comparable to that of cattle-derived casein.

The researchers highlighted that while kinase-mediated phosphorylation provides a route for closely mimicking native casein, phosphomimetic casein provides a simpler path for producing functionally similar proteins. 

 Suvasini Balasubramanian et al, Production of phosphorylated and functional αs1-casein in Escherichia coli, Trends in Biotechnology (2025). DOI: 10.1016/j.tibtech.2025.05.015

Scientists use dental floss to deliver vaccines without needles

Flossing your teeth at least once a day is an essential part of any oral health routine. But it might also one day protect other parts of the body as scientists have created a novel, needle-free vaccine approach using a specialized type of floss.

In a study published in Nature Biomedical Engineering, researchers demonstrated that when floss laced with vaccine  components, such as proteins and inactive viruses, was applied along the gum lines of mice, it triggered an immune response.

This method of vaccine delivery is effective because the areas of gum between the teeth are highly permeable, allowing them to absorb vaccine molecules easily.

In the experiment, researchers flossed 50 mice every two weeks for 28 days, which wasn't an easy task. To floss each mouse, one person had to gently pull their jaw down with the metal ring from a keychain while another did the flossing.

Four weeks after the final vaccine dose, the mice were exposed to a lethal strain of flu.

All rodents that received the floss-based vaccine survived while the unvaccinated animals died. Additionally, the mice that had been flossed had a more widespread immune response throughout their bodies. Flu antibodies were detected in their feces, saliva and even in their bone marrow.

Finding antibodies in the bone marrow suggests the mice's bodies had established a long-term immune response. The researchers also saw an increase in T Cells (a type of immune cell that fights off infections) in the mice's lungs and spleen.

Next, the researchers wanted to see whether flossing would be a viable approach for humans. So they asked 27 healthy volunteers to floss with dental picks coated with food dye. On average, the dye reached the gums about 60% of the time.

The mouth and nose are the primary entry points for many viruses, making the oral cavity an ideal site for vaccine delivery. However, scientists have faced significant hurdles in developing needle-free vaccine alternatives for these areas due to the body's tough defenses against foreign invaders. A floss-based approach could bypass these challenges, offering a promising new method.

 Rohan S. J. Ingrole et al, Floss-based vaccination targets the gingival sulcus for mucosal and systemic immunization, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01451-3

A Fungus, Not Its Insect Host, Paints the World Red

Lac insects carry a yeast-like symbiont that produces a commercially important bright red pigment, revealing insights about insect-microbe symbiosis.

For thousands of years, artisans have been dyeing textiles, jewelry, and handicrafts with a rich, vibrant red pigment that they obtain from lac insects. The most widely-cultivated lac insect, Kerria lacca, is bright crimson because of its natural pigments called laccaic acids.

Researchers now  found that K. lacca carry a yeast-like symbiont, which produces the colorful lac pigment and provides essential nutrients that the insects’ plant diet lacks.

Their findings, published in Proceedings of the National Academy of Sciences, highlight the role of fungal symbionts in insects for providing nutrition and other metabolites.

To characterize the lac insect, the research  team sequenced its genome, as well as that of its known symbionts: bacteria belonging to the genus Wolbachia, and an unidentified yeast-like fungus. They discovered that neither the lac insect nor Wolbachia carried the genes required to produce the molecules that make up laccaic acids. However, genes in the yeast-like symbiont encoded various enzymes that did, indicating the fungus as the only plausible source of the pigment. 

The researchers validated that the pigment originated in the yeast-like symbiont by spraying lac insects with fungicides. Depleting the fungal symbiont reduced the expression of genes required for pigment synthesis. Mass spectrometry revealed lower concentrations of laccaic acids in fungicide-treated insects, which also appeared paler in comparison to untreated insects. However, the fungicide treatment did not eliminate the yeast completely. “Therefore, the insects weren't completely colorless”.

Vaishally, et al. An endosymbiotic origin of the crimson pigment from the lac insect. Proc Natl Acad Sci USA. 2025;122(25):e2501623122.

Vashishtha A, et al. Co-existence, phylogeny and putative role of Wolbachia and yeast-like symbiont (YLS) in Kerria lacca (Kerr). Curr Microbiol. 2011;63(2):206-212.

https://www.the-scientist.com/a-fungus-not-its-insect-host-paints-t...

Humanity Has Dammed So Much Water It's Shifted Earth's Magnetic Poles

Recent shifts in Earth's magnetic field have human fingerprints all over them. While it is normal for our planet's magnetic poles to sporadically wander, new research shows we've now amassed enough water behind dam walls to account for at least some of the current movements. Harvard University geophysicist Natasha Valencic and colleagues calculated that the masses concentrated in just under 7,000 of Earth's biggest dams have knocked the crust's axis of rotation off kilter by around one meter (three feet) relative to the dynamo that drives the magnetic fields beneath the crust. What's more, all this water hoarding has also caused a 21-millimeter-drop in sea levels. As we trap water behind dams, not only does it remove water from the oceans, thus leading to a global sea level fall, it also distributes mass in a different way around the world This mass redistribution can impact Earth's magnetic pole positions relative to the surface. Extra weight added to a spinning sphere pulls the weighted part towards the equator, shifting the axis around which the sphere spins. So, redistributing Earth's surface weight re-orientates its spin axis, whether that be through damming water, melting glaciers, or groundwater removal. But it's only Earth's outer crust floating over its gooey inner parts – not the inner goo generating the magnetic field – that shift, leading to a different part of Earth's surface sitting over our planet's inner magnetic north. So, while north itself hasn't really moved in space, Earth's surface has shifted around, over the top of it. This phenomenon is called true polar wander.

https://agupubs.onlinelibrary.wiley.com/doi/10.1029/2025GL115468

Study links caffeine intake to decreased antibiotic potency in common bacteria

Ingredients of our daily diet—including caffeine—can influence the resistance of bacteria to antibiotics. This has been shown in a new study by a team of researchers.

They discovered that bacteria such as Escherichia coli (E. coli) orchestrate complex regulatory cascades to react to chemical stimuli from their direct environment, which can influence the effectiveness of antimicrobial drugs.

In a systematic screening, the researchers investigated how 94 different substances—including antibiotics, prescription drugs, and food ingredients—influence the expression of key gene regulators and transport proteins of the bacterium E. coli, a potential pathogen. Transport proteins function as pores and pumps in the bacterial envelope and control which substances enter or leave the cell. A finely tuned balance of these mechanisms is crucial for the survival of bacteria.

Their data shows that several substances can subtly but systematically influence gene regulation in bacteria. The findings suggest even everyday substances without a direct antimicrobial effect—e.g., caffeinated drinks—can impact certain gene regulators that control transport proteins, thereby changing what enters and leaves the bacterium.

Caffeine triggers a cascade of events starting with the gene regulator Rob and culminating in the change of several transport proteins in E. coli—which in turn leads to a reduced uptake of antibiotics such as ciprofloxacin. This results in caffeine weakening the effect of this antibiotic. The researchers describe this phenomenon as an "antagonistic interaction."

This weakening effect of certain antibiotics was not detectable in Salmonella enterica, a pathogen closely related to E. coli. This shows that even in similar bacterial species, the same environmental stimuli can lead to different reactions—possibly due to differences in transport pathways or their contribution to antibiotic uptake.

 Christoph Binsfeld et al, Systematic screen uncovers regulator contributions to chemical cues in Escherichia coli, PLOS Biology (2025). DOI: 10.1371/journal.pbio.3003260

Scientists discover blood protein albumin transforms harmless fungus into dangerous pathogens

A research team has uncovered a new way in which the yeast Candida albicans can damage human tissue. In a study published in Nature Communications, the scientists describe an alternative pathogenicity strategy involving the human serum protein albumin. This mechanism has not previously been described and may help explain why certain clinical isolates of Candida albicans appear harmless in laboratory tests, yet cause infections in patients.

Candida albicans is part of the normal human microbiome, colonizing mucosal surfaces without causing harm. Under specific conditions, however, the fungus can become pathogenic—particularly in people with weakened immune systems. Scientists have long known that Candida albicans causes infections using well-described mechanisms, such as toxin production and hyphae formation to invade host tissues.

Now, an international research team has uncovered another tool with which the yeast can cause damage. They found that even strains or mutants previously considered non-virulent in the lab became cytotoxic when albumin was present.

Albumin is the most abundant protein in human blood serum. It plays various roles in transport, nutrient binding, and immune regulation. In carefully controlled infection models, the researchers found that albumin triggered a shift in fungal behavior: even previously non-harmful Candida strains began to grow more strongly, form biofilms, and release a cytotoxic lipid molecule called 13-HODE, which directly damages human cells.

The fungus doesn't necessarily need to grow long hyphae or produce great amounts of toxin in order to cause infection. Depending on the condition it's facing, it will adapt—and it can take advantage of the host.

To uncover the mechanism leading to infection, the team used a combination of methods including microscopy, cell-based damage assays, transcriptomics, and metabolomics. They showed that albumin triggered a reprogramming of fungal metabolism, including lipid oxidation pathways that lead to the production of the toxic compound 13-HODE—which previously had not been associated with Candida albicans virulence.

Sophia U. J. Hitzler et al, Host albumin redirects Candida albicans metabolism to engage an alternative pathogenicity pathway, Nature Communications (2025). DOI: 10.1038/s41467-025-61701-5

Meta's wristband breakthrough lets you use digital devices without touching them

Could Meta be on the verge of transforming how we interact with our digital devices? If the company's latest innovation takes off, we might soon be controlling our computers, cell phones and tablets with a simple flick of the wrist.

Researchers at Meta's Reality Labs division have unveiled an experimental wristband that translates hand gestures and subtle finger movements into commands that interact with a computer. This allows a user to push a cursor around a screen or open an app without needing a mouse, touchscreen or keyboard. The technology can even transcribe handwriting in the air into text (currently at a speed of 20.9 words per minute).

In a paper published in Nature, the team describes how its sEMG-RD (surface electromyography research) works. The wristband uses a technique called electromyography to pick up electrical signals when the brain tells the hand to perform an action. It then converts those signals into commands that control a connected device, such as your phone.

 Patrick Kaifosh et al, A generic non-invasive neuromotor interface for human-computer interaction, Nature (2025). DOI: 10.1038/s41586-025-09255-w

Scientists create an artificial cell capable of navigating its environment using chemistry alone

Researchers  have created the world's simplest artificial cell capable of chemical navigation, migrating toward specific substances like living cells do.

This breakthrough, published in Science Advances, demonstrates how microscopic bubbles can be programmed to follow chemical trails. The study describes the development of a "minimal cell" in the form of a lipid vesicle encapsulating enzymes that can propel itself through chemotaxis.

Cellular transport is a vital aspect of many biological processes and a key milestone in evolution. Among all types of movement, chemotaxis is an essential strategy used by many living systems to move towards beneficial signals, such as nutrients, or away from harmful ones.

Bacteria rely on it to find food, white blood cells use it to reach sites of infection, and even sperm cells navigate toward the egg through chemotaxis. 

 This type of directed movement can occur even without the complex machinery typically involved, such as flagella or intricate signaling pathways. By recreating it in a minimal synthetic system, researchers aim to uncover the core principles that make such movement possible.

Being able to engineer an artificial cell could help scientists better understand how cell units drive further evolution into more complex structures.

Part 1

To achieve this, the research team studied how cell-like vesicles move in gradients of two substrates: glucose and urea. They enclosed glucose oxidase or urease enzymes within lipid-based vesicles, called liposomes, to convert glucose and urea into their respective end products.

The liposomes were then modified by adding an essential membrane pore protein. This protein acts as a channel for substrates to enter the synthetic cell and for the products of the reactions to exit.

It is known that active motion depends on breaking symmetry. By trapping the enzymes inside the particle and utilizing the pores as the primary exchange points, a difference in chemical concentration is generated around the particle. This causes fluid flow along the vesicle's surface and directs the particle's movement. It is as if the liposome were a boat, and the pore and the enzyme were its engine and navigation system.
The research team analyzed the transport of over 10,000 vesicles inside microfluidic channels with glucose or urease gradients to understand general population behavior. They studied the trajectories of vesicles with varying numbers of pores and compared them with those of control vesicles lacking pores.
They observed that the control vesicles move towards lower substrate concentrations due to passive effects other than chemotaxis. As the number of pores in the vesicles increases, so does the chemotactic component. Eventually, this reverses the direction of movement, causing the vesicles to move towards areas with higher substrate concentrations.
These results are promising from a biochemical perspective because the elements studied are ubiquitously present in the structure of a large majority of cells.

Barbara Borges Fernandes et al, The minimal chemotactic cell, Science Advances (2025). DOI: 10.1126/sciadv.adx9364. www.science.org/doi/10.1126/sciadv.adx9364

Part 2

Do We Have To Die? With Nobel prize winning Venki Ramakrishnan