Heart rhythm disorder traced to bacterium lurking in gums

Tempted to skip the floss? Your heart might thank you if you don't. A new study  finds that the gum disease bacterium Porphyromonas gingivalis  can slip into the bloodstream and infiltrate the heart. There, it quietly drives scar tissue buildup—known as fibrosis—distorting the heart's architecture, interfering with electrical signals, and raising the risk of atrial fibrillation (AFib). 

Clinicians have long noticed that people with periodontitis, a common form of gum disease, seem more prone to cardiovascular problems. One recent meta-analysis has linked it to a 30% higher risk of developing AFib, a potentially serious heart rhythm disorder that can lead to stroke, heart failure, and other life-threatening complications.

Globally, AFib cases have nearly doubled in under a decade, rising from 33.5 million in 2010 to roughly 60 million by 2019. Now, scientific curiosity is mounting about how gum disease might be contributing to that surge.

Past research has pointed to inflammation as the likely culprit. When immune cells in the gums rally to fight infection, chemical signals they release can inadvertently seep into the bloodstream, fueling systemic inflammation that may damage organs far from the mouth.

But inflammation isn't the only threat escaping inflamed gums. Researchers have discovered DNA from harmful oral bacteria in heart muscle, valves, and even fatty arterial plaques. Among them, P. gingivalis has drawn particular scrutiny for its suspected role in a growing list of systemic diseases, including Alzheimer's, diabetes, and certain cancers. It has previously been detected in the brain, liver, and placenta. 

This study, published in Circulation, provides the first clear evidence that P. gingivalis in the gums can worm its way into the left atrium in both animal models and humans, pointing to a potential microbial pathway linking periodontitis to AFib.

In the experiments conducted, twelve weeks after infection, mice exposed to P. gingivalis  showed more heart scarring than their uninfected counterparts. At 18 weeks, scarring in the infected mice had climbed to 21.9% compared to the likely aging-related 16.3% in the control group, suggesting that P. gingivalis may not just trigger early heart damage, but also speed it up over time.

And this troubling connection was not only seen in mice. In a separate human study, researchers analyzed left atrial tissue from 68 AFib patients who underwent heart surgery. P. gingivalis was found there, too, and in greater amounts in people with severe gum disease.

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Scientists Discover New Bacteria That Conduct Electricity Like a Wire

A newly discovered bacterium wiggling about in the mudflats of the Oregon coast could advance a new era of bioelectric devices.

It's been named Ca. Electrothrix yaqonensis and it conducts electricity just like a wire does. This is not unique, but Ca. Electrothrix yaqonensis has some fascinating traits of its own that set it apart from other conducting microbes.

Collectively, these organisms are known as cable bacteria, and only a handful are known, split between two candidate (Ca.) genera that are yet to be cultured and formally described – Ca. Electrothrix and Ca. Electronema. They live in sedimentary environments, and arrange themselves, end-to-end, in long threads that transport electrons.

It stands out from all other described cable bacteria species in terms of its metabolic potential, and it has distinctive structural features, including pronounced surface ridges, up to three times wider than those seen in other species, that house highly conductive fibers made of unique, nickel-based molecules

These strands are how the bacteria perform reduction-oxidation reactions over long distances (up to several centimeters). The cells buried deeper in the sediment, where they can't access oxygen, create energy by metabolizing sulfide. This produces electrons, which they transport up to the oxygen rich layer, where the upper cells use oxygen or nitrate to receive the electrons.

This behavior, the researchers say, is something humans could tap into for purposes such as food safety and environmental cleanup.

Universe expected to decay in 10⁷⁸ years, much sooner than previously thought

The universe is decaying much faster than thought. This is shown by calculations of three Dutch scientists on the so-called Hawking radiation. They calculate that the last stellar remnants take about 10⁷⁸ years to perish. That is much shorter than the previously postulated 10¹¹⁰⁰ years.

The researchers have published their findings in the Journal of Cosmology and Astroparticle Physics.

The research by black hole expert Heino Falcke, quantum physicist Michael Wondrak, and mathematician Walter van Suijlekom (all from Radboud University, Nijmegen, the Netherlands) is a follow-up to a 2023 paper by the trio (1).

Footnotes: 

1.  Michael F. Wondrak et al, Gravitational Pair Production and Black Hole Evaporation, Physical Review Letters (2023). DOI: 10.1103/PhysRevLett.130.221502 , journals.aps.org/prl/abstract/ … ysRevLett.130.221502

In that paper, they showed that not only black holes, but also other objects such as neutron stars, can "evaporate" via a process akin to Hawking radiation. After that publication, the researchers received many questions from inside and outside the scientific community about how long the process would take. They have now answered this question in the new article.

The researchers calculated that the end of the universe is about 10⁷⁸ years away, if only Hawking-like radiation is taken into account. This is the time it takes for white dwarf stars, the most persistent celestial bodies, to decay via Hawking-like radiation.

Previous studies, which did not take this effect into account, put the lifetime of white dwarfs at 10¹¹⁰⁰ years. Lead author Heino Falcke said, "So the ultimate end of the universe comes much sooner than expected, but fortunately it still takes a very long time."

Part1

The researchers did the calculations dead-seriously and the basis is a reinterpretation of Hawking radiation.
In 1975, physicist Stephen Hawking postulated that contrary to the theory of relativity, particles and radiation could escape from a black hole. At the edge of a black hole, two temporary particles can form, and before they merge, one particle is sucked into the black hole and the other particle escapes.

One of the consequences of this so-called Hawking radiation is that a black hole very slowly decays into particles and radiation. This contradicts Albert Einstein's theory of relativity, which says that black holes can only grow.
The researchers calculated that the process of Hawking radiation theoretically also applies to other objects with a gravitational field. The calculations further showed that the evaporation time of an object depends only on its density.

To the researchers' surprise, neutron stars and stellar black holes take the same amount of time to decay: 1067 years. This was unexpected because black holes have a stronger gravitational field, which should cause them to evaporate faster.

But black holes have no surface. They reabsorb some of their own radiation which inhibits the process.

 H. Falcke et al, An upper limit to the lifetime of stellar remnants from gravitational pair production, Journal of Cosmology and Astroparticle Physics. On arXiv (2024). DOI: 10.48550/arxiv.2410.14734

Part 2

Antibiotics from human use are contaminating rivers worldwide, study shows

Millions of kilometers of rivers around the world are carrying antibiotic pollution at levels high enough to promote drug resistance and harm aquatic life, a new study warns.

Published in PNAS Nexus, the study is the first to estimate the scale of global river contamination from human antibiotics use. Researchers calculated that about 8,500 tons of antibiotics—nearly one-third of what people consume annually—end up in river systems around the world each year even after, in many cases, passing through wastewater systems.

While the amounts of residues from individual antibiotics translate into only very small concentrations in most rivers, which makes them very difficult to detect, the chronic and cumulative environmental exposure to these substances can still pose a risk to human health and aquatic ecosystems.

The research team used a global model validated by field data from nearly 900 river locations. They found that amoxicillin, the world's most-used antibiotic, is the most likely to be present at risky levels. 

The study, however,  did not consider antibiotics from livestock or pharmaceutical factories, both of which are major contributors to environmental contamination.

Heloisa Ehalt Macedo et al, Antibiotics in the global river system arising from human consumption, PNAS Nexus (2025). DOI: 10.1093/pnasnexus/pgaf096

Gene mutations help flowers mimic foul odor to attract carcass-loving pollinators

A wild ginger has a clever trick up its sleeve to lure in pollinators. No, it's not a sweet fragrance that fills the air, but the foul stench of rotting flesh and dung. To attract carrion-loving flies and beetles, the flowers of the plant genus Asarum brew a malodorous chemical called dimethyl disulfide (DMDS) with the help of a disulfide synthase (DSS)—an enzyme derived from another enzyme, methanethiol oxidase (MTOX), found in both animals and plants.

A study by researchers  discovered that a few tweaks in a gene primarily responsible for detoxifying smelly compounds have independently evolved in three different plant lineages to produce unpleasant odors.

The same three amino acid changes, found in all the independently evolved DSS enzymes, enabled the transition from MTOX to DSS activity, according to the research published in Science.

Yudai Okuyama, Convergent acquisition of disulfide-forming enzymes in malodorous flowers, Science (2025). DOI: 10.1126/science.adu8988. www.science.org/doi/10.1126/science.adu8988

Lorenzo Caputi, Flowers with bad breath, Science (2025). DOI: 10.1126/science.adx4375. www.science.org/doi/10.1126/science.adx4375

Lethal bacteria use sugar-sensing mechanism to recognize and infect cells

Scientists have discovered previously unknown molecular mechanisms that help a type of food-borne bacteria recognize host cells and initiate infection on the cell surface, according to a recent study published in Science Advances.

Multifunctional autoprocessing repeats-in-toxin (MARTX) toxins are secreted by bacteria and support the spread of many Gram-negative bacteria, including Vibrio vulnificus, a lethal food-borne bacterium commonly found in raw or undercooked shellfish.

MARTX toxins use precise intracellular mechanisms to infiltrate host cells and cause life-threatening infections.

In the current study, the investigators used a combination of cellular techniques to map the small portion of the large MARTX toxin from Vibrio vulnificus that directly interacts with the surface of cells.

The scientists found this domain binds N-acetylglucosamine (GlcNAc) (an amino sugar and key building block of complex glycans on the exposed surfaces of epithelial cells) to N-glycans (sugar molecules that decorate proteins on the surface of the host cell) with select preference for the L1CAM protein and clusters of N-glycans on host cell surfaces.

Different cell types have different kinds of sugars on them, and this is one way that toxins can discriminate one cell versus a different kind of cell.

The scientists also found that this domain is essential for Vibrio vulnificus infection during intestinal infection.

Jiexi Chen et al, Vibrio MARTX toxin binding of biantennary N-glycans at host cell surfaces, Science Advances (2025). DOI: 10.1126/sciadv.adt0063

Parasitic amoeba kills human cells and wears their remains as disguise!

The single-celled parasite Entamoeba histolytica infects 50 million people each year, killing nearly 70,000. Usually, this wily, shape-shifting amoeba causes nothing worse than diarrhea. But sometimes it triggers severe, even fatal disease by chewing ulcers in the colon, liquefying parts of the liver and invading the brain and lungs.

It can kill anything you throw at it, any kind of human cell.

E. histolytica can even evade the immune system—and it can kill the white blood cells that are supposed to fight it.

E. histolytica enters the colon after a person ingests contaminated food or water.

Its species name, histolytica, means "tissue-dissolving"—because it creates festering pockets of liquefied tissue, called abscesses, in the organs it infects. As it rampages through a person's organs, it doesn't neatly eat the cells that it kills; instead, it leaves the wounded cells to spill out their contents while it hurries on to kill other cells.

As scientists watched it under a microscope 

But as she watched it through a microscope, they saw something very different.

E. histolytica was actually taking bites out of human cells. Peering through the microscope, you could see little parts of the human cell being broken off. Those ingested cell fragments, shining fluorescent green under their microscope, accumulated inside the amoeba.

 The report that the parasite kills cells through this process, called "trogocytosis," was published in the journal Nature in 2014

Part 1

After the amoeba ingests parts of human cells, it becomes resistant to a major component of the human immune system—a class of molecules called "complement proteins" that finds and kills invading cells.

In a new paper, posted to bioRxiv in October 2024, researchers found that the amoeba gains this resistance by ingesting proteins from the outer membranes of human cells and placing them on its own outer surface. Two of these human proteins, called CD46 and CD55, prevent complement proteins from latching onto the amoeba's surface.
In essence, the amoebae are killing human cells and then donning their protein uniforms as a disguise, allowing them to evade the human immune system.

This discovery can now be targeted to control this organism.

 Wesley Huang et al, Work with me here: variations in genome content and emerging genetic tools in Entamoeba histolytica, Trends in Parasitology (2025). DOI: 10.1016/j.pt.2025.03.010

Why so many microbes fail to grow in the lab

Microbial ecosystems—for example, in seawater, the soil or in the human gut—are astonishingly diverse, but researchers often struggle to reproduce this diversity in the lab: Many microorganisms die when attempts are made to cultivate them.

A new study by researchers offers fresh insights into this longstanding puzzle, suggesting that the survival of microbes does not depend solely on the needs of individual microbes but on a hidden web of relationships that can be caused to collapse by even small structural changes.

In work published in the Proceedings of the National Academy of Sciences, biodiversity experts  take a simplified view of microbial communities as a network based on cross-feeding, the exchange of metabolic by-products between populations. Each species needs nutrients and at the same time releases substances that are needed as food by others.

Scientists modeled this complex network by taking a novel approach. They used tools from network theory—a mathematical method developed by physicists—to understand the behavior of complex systems.

The result of the analysis: in the model, the loss of individual populations can cause the entire network to collapse, with the microbial community transitioning abruptly to a state of lower diversity. These collapses act as tipping points, resembling blackouts in power grids or supply chain breakdowns seen during the COVID-19 pandemic.

Trying to grow a microbial community in the laboratory is an example of such a perturbation according to the researchers. For example, if not all members of a natural microbial community are included in a sample, they will be missing as producers of metabolic products that are vital for other species. 

Although researchers have long suspected that the dependencies between microbes play a key role in our ability to grow them, this study is the first to show how this works across whole communities. The findings offer a new perspective on microbial resilience, highlighting how even in resource-rich environments like lab cultures, communities can fail if the networks of relationships are disrupted.

Tom Clegg et al, Cross-feeding creates tipping points in microbiome diversity, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2425603122

Flamingos create water tornados to trap their prey

Flamingos standing serenely in a shallow alkaline lake with heads submerged may seem to be placidly feeding, but there's a lot going on under the surface.

Through studies of Chilean flamingos in the Nashville Zoo and analysis of 3D printed models of their feet and L-shaped bills, researchers have documented how the birds use their feet, heads and beaks to create a storm of swirling tornados, or vortices, in the water to efficiently concentrate and slurp up their prey.

Part 1

Flamingos are super-specialized animals for filter feeding. It's not just the head, but the neck, their legs, their feet and all the behaviors they use just to effectively capture these tiny and agile organisms.

 Victor M. Ortega-Jimenez et al, Flamingos use their L-shaped beak and morphing feet to induce vortical traps for prey capture, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503495122

How typhoid fever triggers severe neurological symptoms

Typhoid fever, caused by Salmonella Typhi, is one of the oldest documented human diseases. Most commonly spread by contaminated food or water, it is characterized by high fever, headaches, nausea, and, in some cases, potentially deadly neurological complications.

About 15% of patients with typhoid fever develop serious neurological complications, including delirium and seizures, that are collectively described as acute encephalopathy.

A new  study  published in the journal Nature Microbiology provides critical insights into how typhoid fever leads to encephalopathy. Researchers found that typhoid toxin, a key virulence factor only produced by the bacterium Salmonella Typhi, does not directly damage brain cells, as previously thought. Instead, it targets the endothelial cells lining the blood-brain barrier (BBB), causing significant barrier disruption and subsequent brain pathology.

The findings will inform treatment of this life-threatening infection, which annually afflicts about 12 million people and causes about 200,000 deaths, mostly in the world's poorest countries.

Researchers discovered that typhoid toxin severely damages the endothelial cells lining the BBB, a crucial protective barrier separating the bloodstream from the brain. This damage triggered inflammation, edema, and neurological dysfunction in mice models. Crucially, mice engineered to protect endothelial cells from toxin binding showed no neurological symptoms.

The team demonstrated that treatment with the corticosteroid dexamethasone effectively mitigated toxin-induced damage of the BBB and reduced brain inflammation and edema.

 Heng Zhao et al, Typhoid toxin causes neuropathology by disrupting the blood–brain barrier, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02000-z

Golf course proximity linked to higher Parkinson's disease risk

Researchers report an association between living near golf courses and increased Parkinson's disease (PD) risk in a study published in JAMA Network Open.

Reasons?

Residents within 1 to 2 miles of a golf course demonstrated nearly triple the odds of having PD, with the greatest risk identified among those in water service areas with a golf course situated in regions susceptible to groundwater contamination.

Environmental risk factors, including pesticide exposure, have been identified as contributors to PD risk. Golf courses in some countries are treated with high levels of pesticides  raising concerns about potential environmental contamination. Earlier reports have proposed that proximity to golf courses may increase PD risk through groundwater and drinking water contamination.

In the study, "Proximity to Golf Courses and Risk of Parkinson Disease," researchers conducted a population-based case-control study to assess the relationship between proximity to golf courses and PD risk.

Addressing pesticide application practices on golf courses and monitoring groundwater quality in susceptible areas may serve as preventive strategies to reduce PD risk in nearby populations.

Brittany Krzyzanowski et al, Proximity to Golf Courses and Risk of Parkinson Disease, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.9198

MRI scans can identify cardiovascular disease ten years in advance, study reveals

People at risk of cardiovascular disease could be identified a decade before they have a heart attack or stroke, a breakthrough study has discovered.

Experts  have identified that an increased, but still normal, mass of the heart's left ventricle could be used to indicate an increased risk of future cardiovascular events, even when the organ was functioning correctly at the time of assessment. The findings, which also indicated different risk factors in men and women, have been published in Radiology.

The researchers  looked at thousands of health records and it became apparent that the mass of the left ventricle was a clear indicator of future risk of cardiovascular disease.

What made these findings particularly interesting was the difference the researchers noted between men and women.

In men, they found that a larger left ventricle, associated with heart attack and stroke, was linked to the diastolic—the bottom measure,—blood pressure. This level was what we would consider to be normal, albeit in the upper level. In women, they found a link between an increase in left ventricle mass and cholesterol.

Again, this level was in the upper end of what we would consider normal. Both the level of blood pressure and cholesterol level were such that, normally, no preventive treatment would be offered.

The researchers  have clearly identified a very early marker of future cardiovascular disease which can be detected via a simple MRI scan. This is a widely available, easy-to-perform procedure that this study has proven to be able to identify people at risk of cardiovascular disease who may have no other identifiable risk factors, 10 years before the event.

The ability to provide pre-emptive treatment for patients at a stage where their heart is working perfectly well could save vast numbers of lives that are cruelly taken from us as a consequence of cardiovascular disease.

The findings of this study make it clear that we need to encourage men to monitor and reduce their diastolic blood pressure, while for women we should be looking at increasing the use of statins at an earlier stage to control cholesterol levels.

 Jonathan R. Weir-McCall et al, Sex-specific Associations between Left Ventricular Remodeling at MRI and Long-term Cardiovascular Risk, Radiology (2024). DOI: 10.1148/radiol.232997

5G safety confirmed: Study finds no genetic changes in exposed skin cells

The adoption of 5G wireless technology has raised concerns about the health effects of the associated electromagnetic exposure, but a new study published in PNAS Nexus claims 5G wireless is safe.

The frequencies involved can only penetrate a few millimeters into human skin, so  researchers studied the gene expression and methylation profiles of human skin cells exposed to 5G electromagnetic fields at different frequencies (27 GHz and 40.5 GHz), power flux densities (1 mW/cm2 and 10 mW/cm2) and exposure times (2h and 48h).

Gene expression and DNA methylation remained statistically unchanged after 5G exposure, even at 10 times the recommended exposure limits. According to the authors, the quantum energies are far too low to have photochemical or even ionizing effects on cells.

The authors controlled for temperature in their experiments; some previous studies that found effects of 5G failed to do so, and effects are likely to have been caused by heat alone.

 Jyoti Jyoti et al, 5G-exposed human skin cells do not respond with altered gene expression and methylation profiles, PNAS Nexus (2025). DOI: 10.1093/pnasnexus/pgaf127

We Emit a Visible Light That Vanishes When We Die

A new study hints that plants and animals — including people — emit a tiny glow when alive, which disappears after death. This ‘ultraweak photon emission’ — equivalent to a few photons a second per square centimetre of skin tissue — might be a byproduct of energy-producing processes within cells.

An extraordinary experiment on mice and leaves from two different plant species has uncovered direct physical evidence of an eerie 'biophoton' phenomenon ceasing on death, suggesting all living things – including humans – could literally glow with health, until we don't.

To determine whether the process could be scaled from isolated tissues to entire living subjects, the researchers used electron-multiplying charge-coupled device and charge-coupled device cameras to compare the faintest of emissions from whole mice – first alive, then dead.

Four immobilized mice were individually placed in a dark box and imaged for an hour, before being euthanized and imaged for another hour. They were warmed to body temperature even after death, to keep heat from being a variable.

The researchers found they could capture individual photons in the visible band of light popping out of the mouse cells before and after death. The difference in the numbers of these photons was clear, with a significant drop in UPE in the measurement period after they were euthanized.

A process carried out on thale cress (Arabidopsis thaliana) and dwarf umbrella tree (Heptapleurum arboricola) leaves revealed similarly bold results. Stressing the plants with physical injuries and chemical agents provided strong evidence that reactive oxygen species could in fact be behind the soft glow.

The results show that the injury parts in all leaves were significantly brighter than the uninjured parts of the leaves during all 16 hours of imaging.

https://pubs.acs.org/doi/10.1021/acs.jpclett.4c03546

Chimpanzees use medicinal leaves to perform first aid, scientists discover

Scientists studying chimpanzees in Budongo Forest, Uganda, have observed that these primates don't just treat their own injuries, but care for others, too—information which could shed light on how our ancestors first began treating wounds and using medicines.

Although chimpanzees elsewhere have been observed helping other community members with medical problems, the persistent presence of this behaviour in Budongo could suggest that medical care among chimpanzees is much more widespread than we realized, and not confined to care for close relatives.

This  research helps illuminate the evolutionary roots of human medicine and health care systems. By documenting how chimpanzees identify and utilize medicinal plants and provide care to others, we gain insight into the cognitive and social foundations of human health care behaviours. 

Part 1

The researchers spent four months observing each community, as well as drawing on video evidence from the Great Ape Dictionary database, logbooks containing decades of observational data, and a survey of other scientists who had witnessed chimpanzees treating illness or injury.

Any plants chimpanzees were seen using for external care were identified; several turned out to have chemical properties which could improve wound healing and relevant traditional medicine uses.

During their direct observational periods, the scientists recorded 12 injuries in Sonso, all of which were likely caused by within-group conflicts. In Waibira, five chimpanzees were injured—one female by a snare, and four males in fights. The researchers also identified more cases of care in Sonso than in Waibira.

This likely stems from several factors, including possible differences in social hierarchy stability or greater observation opportunities in the more thoroughly habituated Sonso community.
The researchers documented 41 cases of care overall: seven cases of care for others—prosocial care—and 34 cases of self-care. These cases often included several different care behaviors, which might be treating different aspects of a wound, or might reflect a chimpanzee's personal preferences.

Chimpanzee wound care encompasses several techniques: direct wound licking, which removes debris and potentially applies antimicrobial compounds in saliva; finger licking followed by wound pressing; leaf-dabbing; and chewing plant materials and applying them directly to wounds.
All chimpanzees mentioned in our tables showed recovery from wounds, though, of course, we don't know what the outcome would have been had they not done anything about their injuries.

They also documented hygiene behaviours, including the cleaning of genitals with leaves after mating and wiping the anus with leaves after defecation—practices that may help prevent infections.
Of the seven instances of prosocial care, the researchers found four cases of wound treatment, two cases of snare removal assistance, and one case where a chimpanzee helped another with hygiene. Care wasn't preferentially given by, or provided to, one sex or age group. On four occasions, care was given to genetically unrelated individuals.

These behaviors add to the evidence from other sites that chimpanzees appear to recognize need or suffering in others and take deliberate action to alleviate it, even when there's no direct genetic advantage.

Elodie Freymann et al, Self-Directed and Prosocial Wound Care, Snare Removal, and Hygiene Behaviors Amongst the Budongo Chimpanzees, Frontiers in Ecology and Evolution (2025). DOI: 10.3389/fevo.2025.1540922

Part 2

Uncovering compounds that tame the heat of chili peppers: Study challenges reliability of Scoville scale

When biting into a chili pepper, you expect a fiery sensation on your tongue. This spiciness is detected because of capsaicinoid compounds. But for some peppers, despite high levels of capsaicinoids, the heat is mysteriously dull.

Now, researchers reporting in the Journal of Agricultural and Food Chemistry have identified three compounds that lessen peppers' pungency. These results challenge the reliability of the century-old Scoville scale, which traditionally bases its rating on two capsaicinoids.

Capsaicinoids are a group of compounds that produce the strong spicy sensation or pungency that comes with consuming chili peppers. The combined amount of capsaicin and dihydrocapsaicin in a pepper is used to calculate its heat intensity rating on the Scoville scale, ranging from zero Scoville Heat Units (SHU) for bell peppers to millions of SHU for the hottest peppers.

However, some of these fruits have less heat than would be expected from their Scoville rating, which suggests that something else in the pepper influences that spicy sensation. So, researchers wanted to investigate multiple chili pepper varieties for potential spiciness suppressors.

In their experiments, the researchers identified five compounds that could be modulating pepper spiciness.

Another set of panelists assessed whether these compounds, alone or in combination, changed the pungency of capsaicin and dihydrocapsaicin. Three of the five compounds (capsianoside I, roseoside and gingerglycolipid A) reduced the heat intensity, though they didn't have an additive effect when combined. In addition, none of the spiciness suppressors had a noticeable flavor in water.

These advancements could enable the customization of desirable spicy flavor profiles or lead to the creation of a household ingredient designed to tone down excessive heat in dishes—the anti-spice. Also, they hold significant medical potential in the design of (non-opioid) analgesic agents for pain management.

Identification of Chili Pepper Compounds That Suppress Pungency Perception, Journal of Agricultural and Food Chemistry (2025). DOI: 10.1021/acs.jafc.5c01448

Patchy geographical coverage of dog vaccinations is a key barrier for rabies elimination

Dog vaccination programs are a highly effective way to control and, ultimately, eliminate rabies; however, new research has shown just how detrimental geographical gaps in vaccine coverage can be for virus control.

The new research examined two decades of dog vaccination data from the Serengeti district, from 2002 to 2022. The study is published in PLOS Biology.

Through analysis of detailed local data, researchers were able to show where vaccination programs had been effective, and, importantly, why some dog-mediated rabies outbreaks had occurred.

Researchers found that when district-wide dog vaccination was both routine and comprehensive in its geographical coverage, rabies outbreaks in humans were few or none. However, rabies cases in humans did begin to occur when some areas, such as clusters of villages, remained unvaccinated for more than two years.

The study findings show that sustained control of rabies  will require scaled-up dog vaccination efforts, focused on uniform coverage across a wide area, as frequent dog movements mean that neighboring unvaccinated areas are a persistent source of rabies cases in vaccinated areas.

Rabies circulates so widely that even if you protect some villages for a period, it's likely that disease will return, spreading from domestic dogs in nearby villages that are unvaccinated. That means dog vaccination needs to be a concerted and coordinated effort, say the researchers.

Despite effective post-exposure human vaccines being available, dog-mediated rabies is still responsible for tens of thousands of human deaths every year. These are predominantly in Africa and Asia, where rural communities are most at-risk of both bites from infected dogs and being unable to secure post-bite vaccination on time. Of those who die of the disease, the WHO estimate four in ten are children.

Elaine A. Ferguson et al, Improved effectiveness of vaccination campaigns against rabies by reducing spatial heterogeneity in coverage, PLOS Biology (2025). DOI: 10.1371/journal.pbio.3002872

How do middle-aged folks get dementia?

Dementia usually affects older people, so when it occurs in middle age, it can be hard to recognize. The most common form is frontotemporal dementia (FTD), which is often mistaken for depression, schizophrenia, or Parkinson's disease before the correct diagnosis is reached.

Now, researchers  have found some clues about how FTD develops that could lead to new diagnostics and get more patients into clinical trials. The findings appear in Nature Aging.

The team measured more than 4,000 proteins found in spinal tap fluid from 116 FTD patients and compared them to those from 39 of their healthy relatives. All 116 patients had inherited forms of FTD, enabling researchers to study the disease in living people with a confirmed diagnosis, something that isn't possible in non-inherited FTD cases, which can only be confirmed after death.

The composition of the proteins that changed in FTD suggests that these patients have problems with RNA regulation—required for the proper expression of genes in the brain—along with defects that affect connections in their brains. These proteins, researchers think, could be the first specific markers for FTD that emerge as the disease develops in middle age.

Using some of the proteins the researchers have identified, we can now direct patients to the right resources, get them into the right therapeutic trials, and, ultimately, we can now provide them with precision treatments.

Nature Aging (2025). DOI: 10.1038/s43587-025-00878-2

Researchers have coaxed stem cells to grow into amniotic sacs filled with fluid

The model sacs, which grew to roughly the same size as a four-week-old sac surrounding a developing embryo, could be used to study the protective structure.

The amnion is a thin, transparent film that forms a fluid-filled sac that shields and cushions an embryo, potentially supporting its development. But researchers can’t easily access and study the tissue at early stages of pregnancy. Stem-cell models are a way to investigate early embryo development, but researchers first need to recreate in the laboratory what grows in the womb. The latest study, published in Cell today, is the most advanced model of the amniotic sac so far.

https://www.cell.com/cell/fulltext/S0092-8674(25)00458-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867425004581%3Fshowall%3Dtrue

Heart break can kill people

We're all aware of the psychological pain of a broken heart – countless books, songs, and movies have been written and made on the topic – but there's also scientific evidence that a broken heart can be fatal too.

The technical term is takotsubo cardiomyopathy (TC), a weakening of the heart brought on by physical or emotional stress. A new study from researchers looked at data on 199,890 patients in the US between 2016 and 2020.

Incidence of TC rose slightly over the study period for both males and females, but overall incidence was generally higher for females. Fatalities and complications caused by the condition were relatively high. This fits in with previous research suggesting this 'broken heart syndrome' is becoming more common

Although the condition was more common in women, deaths were more than twice as likely in men, with 11.2 percent of males dying compared with 5.5 percent of females. The overall death rate was 6.5 percent.

The researchers have put forward a hypothesis for the gap between men and women. TC is believed to be brought on by a surge of stress hormones, triggered by either physical or emotional stress – so a physical stress might be surgery or an infection, whereas emotional stress could be a divorce or the death of a loved one.

Physical stress TC is more common in men, which may explain the higher numbers of deaths brought on by the condition. The researchers also think differences in hormone balances between the sexes could play a role. Complications resulting from TC included congestive heart failure (35.9 percent of patients), atrial fibrillation (20.7 percent), cardiogenic shock (6.6 percent), stroke (5.3 percent) and cardiac arrest (3.4 percent).

https://www.ahajournals.org/doi/10.1161/JAHA.124.037219

Better than stitches: Researchers develop biocompatible patch for soft organ injuries

Researchers developed an injectable sealant for rapid hemostasis and tissue adhesion in soft, elastic organs.

Formulated with methacryloyl-modified human recombinant tropoelastin (MeTro) and Laponite silicate nanoplatelets (SNs), the engineered hydrogel demonstrated substantial improvements in tissue adhesion strength and hemostatic efficacy in preclinical models involving lung and arterial injuries.

Injuries to soft tissues such as lungs, heart, and blood vessels complicate surgical closure due to their constant motion and elasticity. Sutures, wires, and staples are mechanically fixed, risking blood loss when applied to tissues that expand and contract with each breath or heartbeat. Existing hemostatic agents, including fibrin-based sealants, aim to stem blood flow but may trigger intense coagulation responses in patients with clotting disorders.
In the study, "Rapid closure and hemostasis of ruptured soft tissues using a modified human tropoelastin-based sealant in preclinical models," published in Science Translational Medicine, researchers conducted preclinical testing of an engineered hydrogel combining MeTro and Laponite SNs to assess tissue adhesion and hemostatic efficacy in soft tissues.

Preclinical testing involved arterial injury models in rat and lung injury in pig subjects to assess the sealant's performance in soft, elastic organs. Researchers measured adhesion strength, clotting time, and tissue response to evaluate the effectiveness of the MeTro/SN formulation under dynamic physiological conditions.

Prepolymer solutions of MeTro and varying concentrations of SNs were prepared and cross-linked using visible light. Rat and pig subjects underwent injury procedures to assess the sealant's efficacy.

Testing involved ex vivo adhesion strength measurements on pig skin, lung, and heart tissues, with burst pressure evaluated on punctured collagen sheets. Hemostatic performance was assessed through clotting time analysis using fresh human blood treated with MeTro/SN hydrogels and commercial hemostatic agents.

Integration of SNs reduced clotting time without inducing inflammatory responses, supporting the hydrogel's potential for rapid intervention in hemorrhagic wounds. Biocompatibility analysis demonstrated minimal immune response and tissue damage after implantation, suggesting a low-risk profile for clinical translation.

Mahsa Ghovvati et al, Rapid closure and hemostasis of ruptured soft tissues using a modified human tropoelastin-based sealant in preclinical models, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adr6458

Positive proof-of-concept experiments may lead to the world's first treatment for celiac disease

An investigational treatment for celiac disease effectively controls the condition—at least in an animal model—in a first-of-its-kind therapeutic for a condition that affects approximately 70 million people worldwide.

Currently, there is no treatment for celiac disease, which is caused by dietary exposure to gluten, a protein in wheat, barley and rye. The grains can produce severe intestinal symptoms, leading to inflammation and bloating.

A series of innovative experiments has produced "a cell soothing" technique that targets regulatory T cells, the immune system components commonly known as T_regs.

The cell-based technique borrows from a form of cancer therapy and underlies a unique discovery that may eventually lead to a new treatment strategy, data in the study suggests.

In an animal model, Porret and his global team of researchers have tested the equivalent of CAR T cell therapy against celiac disease. The team acknowledged that the "Treg contribution to the natural history of celiac disease is still controversial," but the researchers also demonstrated that at least in their animal model of human celiac disease, the treatment worked.

CAR T cell therapy is a type of cancer immunotherapy in which a patient's T cells are genetically modified in the laboratory to recognize and kill cancer cells. The cells are then infused back into the patient to provide a round-the-clock form of cancer treatment. In the case of celiac disease, the T cells are modified to affect the activity of T cells that become hyperactive in the presence of gluten.

To make this work, the researchers had to know every aspect of the immune response against gluten. "Celiac disease, a gluten-sensitive enteropathy, demonstrates a strong human leukocyte antigen association, with more than 90% of patients carrying the HLA-DQ2.5 allotype, the researchers wrote, describing the human leukocyte antigen profile of most patients with celiac disease.

As a novel treatment against the condition, the team engineered effector T cells and regulatory T cells and successfully tested them in their animal model. Scientists infused these cells together into mice and evaluated the regulatory T cells' ability to quiet the effector T cells response to gluten. They observed that oral exposure to gluten caused the effector cells to flock to the intestines when they were infused without the engineered T_regs.

However, the engineered regulatory T cells prevented this gut migration and suppressed the effector T cells' proliferation in response to gluten. Although this is a first step, the promising early results indicate that cell therapy approaches could one day lead to a long-sought treatment for this debilitating intestinal disorder.

 Raphaël Porret et al, T cell receptor precision editing of regulatory T cells for celiac disease, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adr8941

Physicists determine how to cut onions with fewer tears

A team of physicists, biologists and engineers  has discovered some of the factors that lead to more or less spray when cutting onions and found a couple of ways to reduce the amount of eye irritation. The group has published a paper describing their study on the arXiv preprint server.

Prior research has shown that eye irritation when cutting onions is caused by the release of syn-propanethial-S-oxide into the air along with other juices in the onion. For this new study, the team in New York wanted to know what factors led to more or less of the juices being spewed into the air during slicing.

To find out, the research team outfitted a special guillotine that could be fitted with different types of blades. They also coated onion chunks with paint to allow for better viewing of the cutting process. They used the guillotine to cut samples, each of which was recorded. Trials varied knife size, sharpness and cutting speed. They even used an electron microscope to accurately measure the knives before use.

The videos revealed that the differences in the amount of spray released, and thus the amount of eye irritation, were due to the sharpness of the knife and the speed at which it cut the onion. The sharper the knife, and slower the cut, the less spray. This was because duller knives tended to push down on the onion, forcing its layers to bend inward—as the cut ensued, the layers sprang back, forcing juice out into the air.

They also noted that as the juice droplets were flung into the air, they tended to fragment into smaller drops, which allowed them to persist longer. Faster cutting also resulted in more juice generation, and thus more mist to irritate the eyes.

They conclude that onion cutters use the sharpest knife they can find and cut their onions slowly.

Zixuan Wu et al, Droplet Outbursts from Onion Cutting, arXiv (2025). DOI: 10.48550/arxiv.2505.06016

World’s first bladder transplant
A 41-year-old man has become the first person to receive a bladder transplant. Surgeons in the United States transplanted the bladder, together with a kidney, earlier this month, in an operation that lasted eight hours.

https://www.nytimes.com/2025/05/18/health/bladder-transplant-human....

Climate change emerges as third major threat to global wildlife, scientists warn

New research published in BioScience reveals that climate change is rapidly emerging as a third major threat to Earth's wild animals, joining habitat alteration and overexploitation in what scientists call a shift from "twin to triple threats."

The research team analyzed data for 70,814 animal species from 35 classes, using two publicly available biodiversity datasets to assess climate change vulnerability among the world's wild animal populations.

Their findings indicate that 5.1% of all assessed animal species are threatened by climate change, with six animal classes having at least 25% of assessed species at risk. The researchers note that these figures likely underestimate the true scale of the crisis.

"We are entering an existential crisis for the world's wild animals," say the authors. Although some species might benefit, increases in global temperature can lead to a variety of impacts on wild animals, including changes in their physiology, behavior, life cycle, distribution, and interactions among species.

"Rapid and effective climate mitigation is crucial now more than ever for saving the world's biodiversity," the researchers conclude.

 William Ripple et al, Climate change threats to Earth's wild animals, BioScience (2025). DOI: 10.1093/biosci/biaf059

Color-correcting algorithm removes the effect of water in underwater scenes

The ocean is teeming with life. But unless you get up close, much of the marine world can easily remain unseen. That's because water itself can act as an effective cloak: Light that shines through the ocean can bend, scatter, and quickly fade as it travels through the dense medium of water and reflects off the persistent haze of ocean particles. This makes it extremely challenging to capture the true color of objects in the ocean without imaging them at close range.

Now, a team has developed an image-analysis tool that cuts through the ocean's optical effects and generates images of underwater environments that look as if the water had been drained away, revealing an ocean scene's true colors. The team paired the color-correcting tool with a computational model that converts images of a scene into a three-dimensional underwater "world," that can then be explored virtually.

The researchers have dubbed the new tool SeaSplat, in reference to both its underwater application and a method known as 3D Gaussian splatting (3DGS), which takes images of a scene and stitches them together to generate a complete, three-dimensional representation that can be viewed in detail, from any perspective.

Daniel Yang et al, SeaSplat: Representing Underwater Scenes with 3D Gaussian Splatting and a Physically Grounded Image Formation Model, arXiv (2024). DOI: 10.48550/arxiv.2409.17345

Stopping infections before they can start: Promising approach blocks bacteria from binding to cells

As concerns about waning antibiotic effectiveness grow, researchers are using unique tools to search for new ways to keep bacteria from causing infections in both humans and animals.

Researchers used the Canadian Light Source (CLS) at the University of Saskatchewan to visualize the structure of long, thin proteins called adhesins, which most bacteria have, and which bind to a sugar molecule on the surface of a cell. Once attached, the bacteria start to form a colony and then eventually a biofilm. This is how they get started in an infection.

The goal of the research, recently published in the journal mBio, is to find a way to interrupt that attachment process—to "put something in there that would fool them (bacteria) and not allow them to bind to the host cells."

Researchers  learned how to recognize those parts of the protein that stick to the surface of cells and begin causing infections. The researchers noted one spot on the protein that attaches to a simple sugar called fucose found on human blood cells and other organisms.

Special imaging at the CLS—called crystallography—confirmed the model and revealed a possible way to inhibit bacteria from binding to cells. 

Adding more fucose in with the bacterium disrupts the binding process "because they're confused by all of this free fucose floating around" . The protein sensorsrs "that are looking out for the sugar on our cells" are unable to bind "because we're flooding the market with fucose."

The next steps in the research will be to produce compounds that mimic fucose "but that cannot be metabolized by either the bacteria or by the human cells that scientists are trying to protect" .  We won't have to put so much sugar in the system.

Qilu Ye et al, Aeromonas hydrophila RTX adhesin has three ligand-binding domains that give the bacterium the potential to adhere to and aggregate a wide variety of cell types, mBio (2025). DOI: 10.1128/mbio.03158-24

Markers in blood and urine may reveal how much ultra-processed food we are eating

Molecules in blood and urine may reveal how much energy a person consumes from ultra-processed foods, a key step to understanding the impact of the products, a new study finds.

It's the first time that scientists have identified biological markers that can indicate higher or lower intake of the foods, which are linked to a host of health problems. The study is published   this week in the journal PLOS Medicine.

It can potentially give us some clues as to what the underlying biology might be between an ultraprocessed food association and a health outcome.

Ultraprocessed foods—sugary cereals, sodas, chips, frozen pizzas and more—are products created through industrial processes with ingredients such as additives, colours and preservatives not found in home kitchens. 

The scientists found that hundreds of metabolites—products of digestion and other processes—corresponded to the percentage of energy a person consumes from ultra-processed foods. From those, they devised a score of 28 blood markers and up to 33 urine markers that reliably predicted ultra-processed food intake in people consuming typical diets.

The researchers  found this signature that was sort of predictive of this dietary pattern that's high in ultra-processed food and not just a specific food item here and there.

A few of the markers, notably two amino acids and a carbohydrate, showed up at least 60 times out of 100 testing iterations. One marker showed a potential link between a diet high in ultraprocessed foods and type 2 diabetes, the study found.

The research team found that they could use the metabolite scores to tell when the individual participants were eating a lot of ultra-processed foods and when they weren't eating those foods.

The results suggested the markers were "valid at the individual level".

With more research, these metabolic signatures can begin to untangle the biologic pathways and harms of UPF and also differences in health effects of specific UPF food groups, processing methods and additives.

Abar L, et al. Identification and validation of poly-metabolite scores for diets high in ultra-processed food: An observational study and post-hoc randomized controlled crossover-feeding trial.PLOS Medicine (2025). DOI: 10.1371/journal.pmed.1004560

Could Mitochondria Be Rewriting the Rules of Biology?

Why are men usually taller than women?

A recent study, analyzing genetic data from nearly a million individuals, sheds light on why men are typically taller than women. Researchers focused on the SHOX gene, located on both X and Y chromosomes, and its role in height determination.

While scientists have long suspected that genetics contribute to these differences, the biological mechanisms behind this sexual dimorphism independent of hormones remained unclear, until a team of researchers from the U.S. shed some light onto it with their study published in PNAS.

The team analyzed a large-scale dataset with 928,605 adult participants, including 1,225 adults with sex chromosome aneuploidies (SCAs)—genetic conditions where individuals have an abnormal number of X or Y chromosomes, either extra or missing.

They found that having an extra Y chromosome led to a greater increase in height compared to an additional X chromosome, regardless of the influence of male hormones.

The sex chromosomes X and Y are non-homologous, meaning they do not share many gene sequences or structures, but both contain a gene called SHOX located in pseudoautosomal region 1 (PAR1), a small section where X and Y chromosomes share sequence identity and work like a regular chromosome. The SHOX gene is a key player in influencing height.

In human females, most of the X chromosome is inactivated, except for PAR1, which escapes X-inactivation, and both human males and females typically have two active copies of PAR1 genes.

Research indicated that the SHOX and other genes in the PAR1 region have lower levels of expression in the inactive X chromosome (Xi), suggesting they are only partially protected from silencing.

This partial silencing means that males (46,XY) may have higher levels of SHOX since it is expressed in both the X and Y chromosomes, compared to females (46,XX) with two X chromosomes. This difference in gene expression is especially noticeable in musculoskeletal tissues, thus explaining sex differences in growth and height.

The findings indicated that the height contribution of the Y chromosome was larger than that of a second X chromosome, irrespective of hormonal differences.

The researchers highlight that understanding genetic underpinnings of sex dimorphisms is crucial not just for traits like height, but also for uncovering the biological mechanisms behind sex-based disparities in the occurrence of autoimmune, neuropsychiatric, and other medical conditions.

Alexander S. F. Berry et al, X and Y gene dosage effects are primary contributors to human sexual dimorphism: The case of height, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503039122

Engineered bacteria can deliver antiviral therapies and vaccines

New research  demonstrates how specially engineered bacteria taken orally can operate as a delivery system for antiviral therapies and vaccines. The research is published in the journal Gut Microbes.

The work focuses on engineering probiotic bacteria to accomplish a wide variety of functions, from breaking down cancer's defenses to imaging and diagnosing lung infections.

A few years ago, researchers asked whether the same chassis, using the bacterium E.coli Nissle 1917, could ferry antiviral therapeutic agents or vaccine antigens directly to the gut, a major portal of viral entry. They focused on the COVID-19 virus, SARS-CoV-2, for the proof-of-concept research.

Oral delivery lets us target the mucosal surfaces where pathogens first gain a foothold while avoiding needles and cold-chain logistics.

Most engineered bacteria keep their therapeutic cargo inside the cell, but vaccines work best when antigens are presented to the immune system. The researchers therefore displayed viral proteins on the bacterial surface and harnessed outer-membrane vesicles (OMVs)—nano-sized spheres that bacteria naturally shed—to act as self-propelled delivery vehicles. Once released, OMVs traffic through the gut epithelium, enter blood circulation and distribute their payload to distant tissues.

The researchers systematically screened anchor motifs and expression cassettes to optimize antigen density on the probiotic surface. For the vaccine version, the bacteria was designed to express the spike protein found on the surface of the virus that causes COVID-19. This same spike protein is currently delivered through mRNA COVID-19 vaccines.

Current vaccines are safe and effective at providing what is called systemic immunity, as antibodies move throughout the whole body in the bloodstream. But there are gateways in the body where viruses typically enter—through mucosal lining in the gastrointestinal system, lungs and other organs—that can be targeted to provide what is called mucosal immunity.

Part 1

In preclinical animal studies, a two-dose oral regimen generated blood-borne (systemic) antibody levels comparable to intramuscular mRNA vaccination. Notably, it produced markedly higher levels of secretory immunoglobulin A (IgA) in the gut and airways—the antibodies that underlie mucosal immunity, considered critical for blocking infection at the point of entry.
While vaccines are delivered before a person is infected with a virus, antiviral therapies such as monoclonal antibodies are given as a treatment after infection.

The team developed another version of engineered E.coli Nissle 1917 to display therapeutic proteins on the surface. To create a post-exposure therapy, the team encoded anti-spike nanobodies: antibodies that are one-tenth the size of conventional monoclonal antibodies.

Although full viral-challenge studies are pending, nanobodies released from the engineered bacteria reached the bloodstream, likely facilitated by OMVs, and accumulated in lung tissue, where they neutralized SARS-CoV-2 in ex-vivo assays.
Clinical trials will validate the safety and efficacy of this delivery system for new engineered bacteria targeting other viruses.
So far the engineered bacteria have been found to be safe to use and do not generate any adverse immune response or side effects in animal models. Moreover, the parent strain of bacteria has decades of safe use as a probiotic.

Nitin S. Kamble et al, Engineered bacteria as an orally administered anti-viral treatment and immunization system, Gut Microbes (2025). DOI: 10.1080/19490976.2025.2500056

Part 2

Newfound mechanism rewires cellular energy processing for drastic weight loss

Mice genetically engineered to lack the ability to make the amino acid cysteine, and fed a cysteine-free diet, lost 30% of their body weight in just one week, a new study shows.

Published online in Nature, the work found that cysteine depletion disrupts the normal metabolic pathways used by mammalian to convert food into energy, forcing the animals to rapidly burn fat stores in a futile attempt to meet energy demands.

 The study reveals key details about how cells process fuels like carbohydrates and fats (metabolism), and how cysteine depletion affects tissues. Experiments showed that lowering cysteine levels caused a drop in levels of the small molecule called coenzyme A (CoA), which rendered inefficient mechanisms that convert carbohydrates and fats into energy.

Despite CoA being involved in more than 100 intermediate metabolic reactions and serving as a partner (cofactor) for 4% of all enzymes in the body, scientists had previously been unable to study its function directly. This is because mice with defective CoA synthesis typically do not survive beyond three weeks of age. The current findings detail, for the first time, how CoA shapes metabolism in adult mice.

The current finding does not immediately suggest a new approach to weight loss, the authors caution, as cysteine is found in nearly all foods.

Achieving a truly cysteine-free diet would require patients to consume a specially formulated solution that would be challenging for most. Moreover, because cysteine is involved in numerous cellular pathways, eliminating it—such as through a drug that inhibits cysteine production—could make organs more vulnerable to everyday toxins, including medications.

That said, the study authors say it is worth considering that fruits, vegetables, and legumes contain much lower levels of cysteine and its precursor, the sulfur-containing amino acid methionine, than red meat. While earlier studies have linked low sulfur amino acid intake to health benefits, this study clarifies that these benefits are due to cysteine depletion specifically, and not methionine restriction.

Part 1

The study is the first to examine the effects of removing cysteine, or any of the nine of the essential amino acids, which must be obtained through diet and are required for building proteins that make up most of the body's enzymes, tissues, and signaling molecules. The findings revealed that eliminating cysteine from the mammalian body led to far greater weight loss than the removal of any other essential amino acid.

Specifically, cysteine deprivation disrupted oxidative phosphorylation, the main process for producing adenosine triphosphate (ATP), the molecule that serves as cells' energy currency. Oxidative phosphorylation is known to be tightly dependent on CoA.

As a result, sugar-derived intermediate molecules (carbon skeletons) such as pyruvate, orotate, citrate, and α-ketoglutarate were no longer used efficiently, and were instead lost in the urine. In response, the body turned to stored lipids (fats) to make energy.

Further, the team found that cysteine restriction activates both the integrated stress response (ISR), a signaling network that restores cellular balance after stress, and the oxidative stress response (OSR), which is triggered by higher levels of reactive oxygen species (ROS) following depletion of glutathione, the body's primary antioxidant. ROS can oxidize (take away electrons from) and damage sensitive cell parts like DNA.

Remarkably, this simultaneous activation of ISR and OSR—previously observed only in cancer cells—was shown to occur in normal tissues in mice in the cysteine-restriction group, with the two stress responses reinforcing each other.

The study also shows that ISR and OSR, acting independently of CoA depletion, increase production of the stress hormone GDF15, which contributes to food aversion and degradation of acetyl-CoA-carboxylase, a key enzyme in lipid synthesis. This increased weight loss further in the study mice by preventing the replenishment of their fat stores.

Evgeny Nudler, Unravelling cysteine-deficiency-associated rapid weight loss, Nature (2025). DOI: 10.1038/s41586-025-08996-y. www.nature.com/articles/s41586-025-08996-y

Part 2

**

How the placebo effect tricks the mind into relieving pain

The detailed mechanism of how the placebo effect reduces the perception of pain in rats has been uncovered by  neuroscientists. These findings, published in Science Advances, could potentially lead to ways to harness the placebo effect in therapy.

If you're convinced you are taking a powerful painkiller, it could well reduce your perception of pain, even if the painkiller turns out to be a sham.

That's the power of the placebo effect. The brain, tricked into anticipating a benefit, produces the benefit itself.

Harnessing the placebo effect for pain relief could help to reduce dosages of painkillers, lowering the risk of both side effects and becoming dependent on medication.

Because it's a psychological effect, the placebo effect is much easier to induce and monitor in humans than in animals. But since only relatively noninvasive techniques can be used on people, it's hard to determine what's happening on a neural-circuit level.

The researchers conditioned rats by injecting them with a painkiller over four days. The animal came to associate injections with pain relief, so that when they were injected with a saline solution, the placebo effect kicked in. Many researchers didn't think that animals could experience the placebo effect. But the researchers succeeded in inducing it in rodents by using Pavlovian conditioning.

About a third of the rats exhibited the full placebo effect, another third had a partial placebo effect, and the remaining third hardly experienced any pain relief.

The research team was then able to study what was going on in the animal brains using neuroimaging methods that are too invasive to use on people.

Several brain regions were found to activate in response to placebo in neuropathic animals. That's very similar to results in humans. 

The team found that the placebo effect occurred as a result of brain signals related to the endogenous opioid system in the medial prefrontal cortex, a region at the front of the brain, which in the presence of the placebo injections set off the descending pain inhibitory system.

They strongly suspect that the same mechanism operates in people. The mechanism is similar to how pain relief occurs in humans.

Hiroyuki Neyama et al, Opioidergic activation of the descending pain inhibitory system underlies placebo analgesia, Science Advances (2025). DOI: 10.1126/sciadv.adp8494

How a mold can unbalance the lungs

An invisible intruder puts the delicate balance in our lungs to the test: the mold Aspergillus fumigatus, harmless in nature, can become a serious danger if the immune system is weakened—and change the entire bacterial world in the lungs. But that's not all: The intestines and metabolism also appear to be affected by a lung infection.

Aspergillus fumigatus can be found almost everywhere—in soil, compost or in the air. It is usually harmless for healthy people. However, in patients with a weakened immune system, it can cause severe lung infection, known as invasive aspergillosis.

The fungus may potentially alter the oxygen levels in the lungs to a degree that it creates a more suitable environment for certain bacteria—such as Ligilactobacillus murinus, typically found in the intestines, oral cavity and lungs of mice—to better survive and potentially thrive. This interaction could possibly influence disease progression and enable new treatment strategies.

It has long been known that the gut and lungs are closely connected. New data from a research team in Jena has now deepened this understanding.

Researchers found evidence that not only the lung microbiome, but also the gut microbiome and certain metabolic products in the blood change during infection of the lungs with Aspergillus fumigatus. This so-called "gut-lung axis" could play an important role in future therapy.

A key finding of the study was that the fungal infection unbalances both the lung and gut microbiome. In the lungs, this leads to an accumulation of anaerobic bacteria. Particularly striking was the increased growth of Ligilactobacillus murinus, suggesting that the fungus creates a microaerophilic niche (low oxygen concentrations) that favors this bacterium.

Fungal infections are a serious problem, especially for immunocompromised people or those who are already seriously ill—for example in intensive care units or with cancer. The new findings provide important information on how such infections can be better understood and possibly prevented.

In the future, it may be possible to specifically influence the microbiome in order to support the body in its fight against the fungus—or to develop new drugs that target precisely this area.

Liubov Nikitashina et al, The murine lung microbiome is disbalanced by the human-pathogenic fungus Aspergillus fumigatus resulting in enrichment of anaerobic bacteria, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115442

Lethal mutations cause 1 in 136 in pregnancy losses, study estimates

In a study published in Nature recently "Sequence diversity lost in early pregnancy," scientists from deCODE genetics, estimate that around one in 136 pregnancies are lost due to new mutations in the fetus. In other words, millions of pregnancies worldwide are lost because of mutations every year.

The human genome varies between individuals, but there are some locations in the genome where there seems to be little or no sequence variation between individuals. This raises the question of whether the sequences at these locations are essential for human development.

It is known that mutations in essential genomic sequences are major contributors to neurodevelopmental disorders. The question remains, do they also contribute to pregnancy loss? As part of a Nordic collaboration, scientists from deCODE genetics sought to answer these questions by sequencing 467 samples from pregnancy losses from a prospective study. Interestingly, by comparing the genomes of the fetuses from pregnancy losses to their parents, the scientists found that the fetuses harbored a similar number of new mutations as adults. Despite the similar numbers, they discovered that the main difference between the lost fetuses and adults was that the mutations in the fetuses occurred in essential genomic sequences. Moreover, they managed to pinpoint when, in the development of the fetus, some of the mutations occurred.

In addition to mapping new mutations in the lost fetuses, they also showed that some couples are at a higher risk of pregnancy loss due to genetic compatibility issues. You inherit one copy of a gene from each parent, and most of the time, you are fine with one defective copy, but problems can arise if you inherit a defective copy from both parents.

Along with recombination, the continuous generation of mutations enables us to evolve as a species. However, this continuous influx of new mutations comes at the expense of rare diseases. This study demonstrates the contribution of mutations to pregnancy loss and sheds new light on conserved sequences in the human genome.

Gudny A. Arnadottir et al, Sequence diversity lost in early pregnancy, Nature (2025). DOI: 10.1038/s41586-025-09031-w

Small molecules in plant-based foods may reduce efficacy of anti-cancer drugs

A Cancer Research study has uncovered a surprising link between diet, intestinal microbes and the efficacy of cancer therapy.

The study could help explain why drugs known as PI3 kinase (PI3K) inhibitors—which disrupt an abnormally activated biochemical signaling pathway that spurs cancer cell proliferation—haven't led to consistent, durable cancer control in patients with solid tumors.

Many cancer x drugs don't work equally well for all patients, and one emerging possibility is that diet plays a role in this variability.

This study showed that diet can indeed alter cancer treatment outcomes in preclinical models and can do so in an unexpected way, unrelated to its immediate nutritional effects. It turns out that certain small molecules in plant-based foods are transformed in mice by commensal gut bacteria into compounds that activate the liver to clear PI3K inhibitors more quickly, lowering the efficacy of the drug.

The liver enzymes involved in clearing these drugs break down many others as well. This suggests these findings could be of relevance to multiple classes of drugs used to treat cancer and other diseases.

Asael Roichman et al, Microbiome metabolism of dietary phytochemicals controls the anticancer activity of PI3K inhibitors, Cell (2025). DOI: 10.1016/j.cell.2025.04.041

Rather, experiments revealed that the key determinant was the molecular complexity of the diet—whether it was made of "whole foods" versus highly processed ones.

The ketogenic food consumed by mice in preclinical studies is a highly processed formulation lacking the complex mix of plant-derived chemicals (phytochemicals), especially from legumes and soy, that are present in standard chow. It turned out that gut microbes break down phytochemicals, namely soyasaponins derived from soybeans, into molecules that induce the expression of a detoxifying liver enzyme, cytochrome P450.

Experiments revealed that elevated production of these hepatic enzymes in the chow-fed mice led to rapid clearance of PI3K inhibitors, reducing the anti-cancer efficacy of the regimen. In line with these findings, the researchers demonstrated that a high-carbohydrate but low-phytochemical diet—as well as antibiotics that suppressed the gut microbiome—enhanced PI3K inhibitor activity in the mice.

Part 2

Infrared contact lenses allow people to see in the dark, even with their eyes closed

Neuroscientists and materials scientists have created contact lenses that enable infrared vision in both humans and mice by converting infrared light into visible light. Unlike infrared night vision goggles, the contact lenses, described in the journal Cell, do not require a power source—and they enable the wearer to perceive multiple infrared wavelengths. Because they're transparent, users can see both infrared and visible light simultaneously, though infrared vision was enhanced when participants had their eyes closed.

The contact lens technology uses nanoparticles that absorb infrared light and convert it into wavelengths that are visible to mammalian eyes (e.g., electromagnetic radiation in the 400–700 nm range). The nanoparticles specifically enable the detection of "near-infrared light," which is infrared light in the 800–1600 nm range, just beyond what humans can already see.

To create the contact lenses, the team combined the nanoparticles with flexible, nontoxic polymers that are used in standard soft contact lenses. After showing that the contact lenses were nontoxic, they tested their function in both humans and mice.

They found that contact lens-wearing mice displayed behaviors suggesting that they could see infrared wavelengths. For example, when the mice were given the choice of a dark box and an infrared-illuminated box, contact-wearing mice chose the dark box whereas contact-less mice showed no preference.

The mice also showed physiological signals of infrared vision: the pupils of contact-wearing mice constricted in the presence of infrared light, and brain imaging revealed that infrared light caused their visual processing centers to light up.

In humans, the infrared contact lenses enabled participants to accurately detect flashing Morse code-like signals and to perceive the direction of incoming infrared light.

It's totally clear-cut: without the contact lenses, the subject cannot see anything, but when they put them on, they can clearly see the flickering of the infrared light.

The researchers also found that when the subject closes their eyes, they're even better able to receive this flickering information, because near-infrared light penetrates the eyelid more effectively than visible light, so there is less interference from visible light.

Near-Infrared Spatiotemporal Color Vision in Humans Enabled by Upconversion Contact Lenses, Cell (2025). DOI: 10.1016/j.cell.2025.04.019. www.cell.com/cell/fulltext/S0092-8674(25)00454-4

Ancient DNA used to map evolution of fever-causing bacteria

Researchers  have analyzed ancient DNA from Borrelia recurrentis, a type of bacteria that causes relapsing fever, pinpointing when it evolved to spread through lice rather than ticks, and how it gained and lost genes in the process.

This transition may have coincided with changes in human lifestyles, like living closer together and the beginning of the wool trade.

B. recurrentis bacteria cause relapsing fever, an illness with many recurring episodes of fever, which is typically found today in areas with poor sanitation or overcrowding, such as refugee camps. It is a distant cousin of the bacteria that today cause Lyme disease.

Only three known species of bacteria, including B. recurrentis, have transitioned from being carried primarily by ticks to lice, changing the potential severity of the disease. Until now, it was unknown when B. recurrentis made the jump from ticks to lice and what impact this had on disease transmission and severity in humans.

In research published in Science, the scientists sequenced the whole genome from four samples of B. recurrentis. Ranging from 2,300 to 600 years ago, their samples include the oldest B. recurrentis genome to date. These ancient samples were obtained from the skeletons of people who were infected hundreds of years ago. The DNA is a shadow of the bacteria that once circulated in their blood and has been captured in bones and teeth.

The individuals' teeth contained traces of B. recurrentis DNA. Two samples had relatively high amounts of the pathogen, suggesting these individuals may have died from a severe, acute infection, or that the DNA was particularly well preserved.

The researchers looked at differences in the ancient genomes and modern-day B. recurrentis to map how the bacteria have changed over time, finding that the species likely diverged from its nearest tick-borne cousin, B. duttonii, about 6,000 to 4,000 years ago.

They compared the B. recurrentis genomes with B. duttonii, finding that much of the genome was lost during the tick-to-louse transition but that new genes were also gained over time. These genetic changes affected the bacteria's ability to hide from the immune system and also share DNA with neighboring bacteria, suggesting B. recurrentis had specialized to survive within the human louse.
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Based on these ancient and modern genomes, the divergence from the bacteria's tick-borne ancestor happened during the transition from the Neolithic period to the Early Bronze Age. This was a time of change in human lifestyles, as people began to domesticate animals and live in more dense settlements. This may have helped B. recurrentis spread from person to person more easily.
The researchers also raise the possibility that the development of sheep farming for wool at this time may have given an advantage to louse-borne pathogens, as wool has better conditions for lice to lay eggs.
They conclude that the evolution of B. recurrentis highlights that a combination of genetic and environmental changes can help pathogens spread and infect populations more easily.

Ancient Borrelia genomes document the evolutionary history of louse-borne relapsing fever., Science (2025). DOI: 10.1126/science.adr2147

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Climate change may make it harder to reduce smog in some regions

Global warming will likely hinder our future ability to control ground-level ozone, a harmful air pollutant that is a primary component of smog, according to a new  study.

The results could help scientists and policymakers develop more effective strategies for improving both air quality and human health. Ground-level ozone causes a host of detrimental health impacts, from asthma to heart disease, and contributes to thousands of premature deaths each year.

The researchers' modeling approach reveals that, as the Earth warms due to climate change, ground-level ozone will become less sensitive to reductions in nitrogen oxide emissions in eastern North America and Western Europe. In other words, it will take greater nitrogen oxide emission reductions to get the same air quality benefits.

The researchers found that eastern North America and Western Europe are especially sensitive to increases in nitrogen oxide emissions from the soil, which are natural emissions driven by increases in temperature.

Due to that sensitivity, as the Earth warms and more nitrogen oxide from soil enters the atmosphere, reducing nitrogen oxide emissions from human activities will have less of an impact on ground-level ozone.

However, the study also shows that the opposite would be true in northeast Asia, where cutting emissions would have a greater impact on reducing ground-level ozone in the future.

The researchers combined a climate model that simulates meteorological factors, such as temperature and wind speeds, with a chemical transport model that estimates the movement and composition of chemicals in the atmosphere.

By generating a range of possible future outcomes, the researchers' ensemble approach better captures inherent climate variability, allowing them to paint a fuller picture than many previous studies.

Future air quality planning should consider how climate change affects the chemistry of air pollution. We may need steeper cuts in nitrogen oxide emissions to achieve the same air quality goals, say the researchers.

Emmie J. Le Roy et al, Impact of Climate Variability and Change on the Surface Ozone Response to NO_x Emissions Reductions, Environmental Science & Technology (2025). DOI: 10.1021/acs.est.5c01347

Hawaiian volcanic rocks reveal Earth's core contains vast hidden gold reserves

Earth's largest gold reserves are not kept inside Fort Knox, the United States Bullion Depository. In fact, they are hidden much deeper in the ground than one would expect. More than 99.999% of Earth's stores of gold and other precious metals lie buried under 3,000 km of solid rock, locked away within Earth's metallic core and far beyond the reaches of humankind.

Now, researchers  have found traces of the precious metal ruthenium (Ru) in volcanic rocks on the islands of Hawaii that must ultimately have come from Earth's core. The findings were published in Nature.

Compared to Earth's rocky mantle, the metallic core contains a slightly higher abundance of a particular Ru isotope: 100Ru. This is because part of the Ru, which was locked in Earth's core together with gold and other precious metals when it formed 4.5 billion years ago, came from a different source than the scarce amount of Ru that is contained in the mantle today. These differences in 100Ru are so tiny that it was impossible to detect them in the past.

Now, new procedures developed by researchers  make it possible to resolve them. The unusually high 100Ru signal they found in lavas on Earth's surface can only mean that these rocks ultimately originated from the core-mantle boundary.

New  data confirmed that material from the core, including gold and other precious metals, is leaking into Earth's mantle above. 

This means that at least some of the precarious supplies of gold and other precious metals that we rely on for their value and importance in so many sectors such as renewable energy, may have come from Earth's core.

Nils Messling et al, Ru and W isotope systematics in ocean island basalts reveals core leakage, Nature (2025). DOI: 10.1038/s41586-025-09003-0