Cells have a mailing system of sorts. They can release tiny molecular balls, called extracellular vesicles (EVs), that contain biological matter or messages and attach to other cells to share whatever they contain.
In cancer, EVs often depart from tumour cellsto seed the cancer elsewhere in the body, leading to metastasis. However, how the EVs connected to recipient cells to deliver their payload has remained a mystery—until now. A team of researchers has now revealed the molecular mechanisms underpinning the process for small EVs (sEVs), which they said could have implications for developing better cancer treatments.
The teampublishedtheir findings in theJournal of Cell Biology.
EVs can serve as biomarkers, since they carry specific proteins and genetic material that can indicate disease progression. Researchers have also started to explore their potential to treat cancers, either by inhibiting their binding to host cells or by encouraging the binding of EVs with therapeutic payloads.
The researchers now focused on understanding the role of integrin heterodimers, which are molecules that help sEVs adhere to the host cell. The same team previously found that sEVs could be sorted into subtypes with different properties, depending on which tetraspanin protein it has. This type of protein is small but critical to EV formation and regulation.
Using this understanding, the researchers sorted and tracked the sEVs with single-molecule resolution.
They examined the sorted subtypes with super-resolution microscopy to find that all subtypes primarily used integrin heterodimers associated with a specific tetraspanin protein known as CD151 and a molecule containing carbohydrates and fats called GM1 to bind to laminin, a protein critical to cellular membranes and heavily involved in cell membrane structure and cell adhesion, among other responsibilities.
Laminin is specifically a glycoprotein, meaning it is a protein with a carbohydrate, or sugar, molecule attached to it. It exists in the extracellular matrix, or the molecular network surrounding cells and supports their signaling and structure.
Quantitative analysis using single-molecule imaging and super-resolution microscopy demonstrated that all EV subtypes derived from four distinct tumor cell lines, irrespective of size, predominantly bind to laminin via CD151-associated integrin heterodimers and GM1, thereby eliciting responses in recipient cells.
EVs bound to laminin significantly more than they bound to fibronectin, which is another protein responsible for cell adhesion in the extracellular matrix.
Two other proteins associated with adhesion in the EVs, talin and kindlin, did not activate the integrin heterodimers. Taken all together, the researchers concluded that GM1 and integrin heterodimers associated with CD151 are key for EV binding. This understanding could help researchers better inhibit or encourage binding as needed in the name of disease treatment.
Tatsuki Isogai et al, Extracellular vesicles adhere to cells primarily by interactions of integrins and GM1 with laminin, Journal of Cell Biology (2025). DOI: 10.1083/jcb.202404064
Tetracycline antibiotics impair T cell function by targeting mitochondria
A team of international researchers has revealed in unprecedented detail how tetracycline antibiotics impair T cell function by binding mitochondrial ribosomes and inhibiting oxidative metabolism (OXPHOS). The study, reported in Nature Communications, raises mechanistic considerations for antibiotic therapy and the design of new molecules that can better discriminate between pathogen and host.
Antibiotics historically developed to inhibit bacterial protein synthesis cross-react with mitochondrial ribosomes due to shared evolutionary features, impairing translation of key phosphorylation complex subunits in host cells. Indeed, certain antibiotics, such as tetracyclines, have a long history in the treatment of inflammatory conditions, such as rheumatoid arthritis, although large controlled cohort studies are lacking, in part due to the lack of a molecular mechanism.
When you take antibiotics, the effects are not solely restricted to commensal and pathogenic bacteria. Some of your cells take a hit, and there is good evidence in the literature to support reversible inhibition of that mitochondrial translation can be used to treat inflammatory diseases.
The researchers identified specific structural features of mitochondrial ribosomes that could potentially be targeted to develop more selective therapeutics.
"The discrimination between bacterial and human mitochondrial ribosomes represents an important frontier for antibiotic development. By understanding the specific binding domains within the mitoribosome that interact with tigecycline, it will be possible to design next-generation entities with different specificities, whether those affect the host or pathogen.
Qiuya Shao et al, T cell toxicity induced by tigecycline binding to the mitochondrial ribosome, Nature Communications (2025). DOI: 10.1038/s41467-025-59388-9
Experimental peptide treatment could triple survival rates in severe blood loss cases
Researchers have discovered a promising new therapeutic approach to treating hemorrhagic shock, a life-threatening condition caused by severe blood loss that remains the leading cause of preventable death in trauma cases globally.
The study demonstrated that activating Protein Kinase C epsilon (PKC-ε) significantly improves early survival rates and physiological stability following severe hemorrhage.
The work is published in the journal Scientific Reports.
In a carefully controlled experiment using a porcine model, researchers induced hemorrhagic shock by withdrawing 35% of the animals' total blood volume. Animals treated with a PKC-ε activator peptide just five minutes after the onset of bleeding showed dramatically improved survival—73% of treated subjects survived compared to only 25% of those left untreated.
Additionally, treated animals maintained significantly better cardiovascular stability, including blood pressure, heart rate, and cardiac output, all critical indicators of effective response during severe trauma.
Moreover, detailed analysis of mitochondrial activity revealed enhanced function within the heart tissues of animals receiving the PKC-ε activator. As mitochondria are vital cellular energy producers, these findings suggest that activating PKC-ε helps maintain organ energy levels under stress, potentially protecting tissues against further damage associated with severe blood loss.
The implications of this study are far-reaching. Current therapeutic strategies for severe hemorrhagic shock often involve fluid resuscitation, which can unintentionally exacerbate tissue damage by triggering ischemic-reperfusion injury.
This new approach—administering a PKC-ε activator peptide—has the potential to significantly minimize these detrimental effects, thereby improving survival chances and reducing complications associated with severe trauma.
Maya Simchoni et al, Protein kinase C epsilon activation improves early survival in an acute porcine model of controlled hemorrhage, Scientific Reports (2025). DOI: 10.1038/s41598-025-92310-3
Tire additives found deposited on fruits and vegetables
A new study has found that tire additives enter into and pass through the food chain. Further research is needed to establish the implications for human health.
Traces of the additives typically used in tire manufacturing have been detected in all of the most common types of fruits and vegetables. The scientists don't yet know the long-term implications of exposure to these substances for human health. Further research is needed to clarify this point.
The study follows on from two Austrian studies demonstrating that these additives were present in leafy vegetables.
Researchers sampled around 100 of the most commonly eaten fruits and vegetables from major supermarket chains to organic markets and small, grocery stores.
After rinsing the fruits and vegetables and turning them into workable samples, the scientists tested them for 11 compounds typically found in tire additives. Using consumption data held by the FSVO, they were then able to calculate theoretical daily intake values for these substances.
They found that 31% of the samples contained traces of the compounds, including 6-PPD and 6-PPD-quinone, with no difference according to where the fruits and vegetables came from or whether they were organic.
Previous studies have established that tire additives, especially DPG, 6-PPD and 6-PPD-quinone, are toxic to mammals. This research, which has so far been carried out only on rodents, found that these additives lead to decreased fertility in males and have neurotoxic and neuroinflammatory effects.
Scientists in China are also conducting in-depth research into the subject, analyzing human blood and urine for the presence of these substances.
When tires wear against road surfaces, they release additives such as antioxidants and vulcanizing agents (which give rubber more strength, elasticity and durability). These particles, the toxicity of which is yet to be determined, disperse through the air, settle on the ground, and are transported in runoff water. Humans are exposed to them in two ways: by inhaling them and, as the EPFL-FSVO study shows, by ingesting them in contaminated food.
According to apaperpublished in 2017, six million metric tons of these additives are released into the environment every year. Our exposure to these additives is similar to that for other micropollutants.
They're around us constantly, in every part of our environment. What we don't know is whether we need to introduce tighter controls, such as by phasing them out in tire manufacturing in favor of less toxic alternatives.
Scientists are currently exploring ways in which roads can be decontaminated to prevent tire additives from entering the environment. Several studies have shown that aggressive driving—with hard acceleration and braking—increases tire wear, making it more likely that these particles will transfer into the air, soil and surface water.
Florian Breider et al, Assessment of tire-derived additives and their metabolites into fruit, root and leafy vegetables and evaluation of dietary intake in Swiss adults, Journal of Hazardous Materials (2025). DOI: 10.1016/j.jhazmat.2025.138432
Scientists have been trying to discover exactly why some animals glow under ultraviolet light as photoluminescence in mammal fur is common.
Rats, along with bandicoots, possums, bats, tree-kangaroos and many other creatures around the world are photoluminescent; they glow under ultraviolet, violet or blue light.
Scientists' aim 's to identify luminophores (molecules or groups of molecules) contributing to photoluminescence.
The researchers shaved fur from roadkill and subjected it to high-performance liquid chromatography.
The fur of the northern long-nosed and northern brown bandicoots photoluminesces strongly, displaying pink, yellow, blue and/or white colors. The researchers wanted to find out whether the luminophores present in bandicootfur might be common across multiple species.
So they compared the results from the two bandicoots to the northern quoll, the coppery brushtail possum, the Lumholtz's tree-kangaroo, the pale field rat and the platypus—all of which photoluminesce in different ways.
The scientists confirmed metabolites of the amino acid tryptophan and identified derivatives of the chemical compound porphyrin that cause bandicoots, quolls and possums to glow bright pink in UV light.
They also found a contributing cause of the colour of coppery brushtail possum fur—not photoluminescent, but a strong purple colouration in white light—a match for the molecule Indigo—which is also extracted as a dye from plants.
A recently-discovered termite terminator is better, more targeted and won't harm humans
Drywood termites, the ones that hide in wooden structures, molt about seven times in their lives. Researchers have found that a chemical preventing them from growing new exoskeletons will also end their infestation of your home.
The chemical, bistrifluron, and its ability to kill about 95% of a termite colony without off-target effects on mammals, are documented in a paper published in the Journal of Economic Entomology.
This chemical is more environmentally friendly than ones traditionally used for drywood termite infestation. It's specific to insects and can't harm humans.
Unlike humans with skeletons located inside their flesh, termites have exoskeletons on the outside that protect them from the elements. The main component of these external skeletons is chitin, which is also found in fungal cell walls, fish scales, and the beaks of squids and octopuses. Chitin also provides mechanical strength for insect exoskeletons, making them suitable as armor as well as sites for muscle attachment.
As termites are getting ready to molt, something they must do in order to grow, they also produce chitin to create the new exoskeleton. Bistrifluron prevents them from doing so.
Once the termites reach a certain stage, they have to molt. They cannot avoid that. With a lethal dose of this chemical, they'll try to shed their old exoskeleton but won't have a new one ready to protect them.
The researchers observed that bistrifluron initially slows the termites down, reducing their feeding activity. Eventually it prevents them from molting, and they die. This is one of the first studies that looks at the impact of chitin-inhibiting chemicals on drywood termites.
As the termites eat the treated wood, they also spread the chemical to other members of the colony. Full collapse happens in about two months, which is slower than other methods but carries certain advantages in addition to lower toxicity.
Nicholas A Poulos et al, Toxicity and horizontal transfer of chitin synthesis inhibitors in the western drywood termite (Blattodea: Kalotermitidae), Journal of Economic Entomology (2025). DOI: 10.1093/jee/toaf064
Several prominent figures in science and invention were known to get by on significantly less sleep than the typical 7-8 hours recommended for adults. Notable examples include Thomas Edison, Nikola Tesla, and Leonardo da Vinci, Benjamin Franklin who reportedly slept as little as two to four hours per night.
I too sleep for just four and half to six hours, never more than that. Rest of the time I work like mad. I am used to it.
When your mind is in the grip of something, you can't sleep and feel very restless if you don't complete your work in art, literature, science, or any other field.
And there are some natural short sleepers. Science says ....
Not everyone needs 8 hours of sleep to function properly. Some people can feel well-rested and show no negative effects of sleep deprivation, even after just 4 hours of sleep, which is likely the result of a genetic mutation.
A recent study has reported that a mutation in salt-induced kinase 3 (hSIK3-N783Y)—a gene critical for regulating sleep durationand depth—may be the reason why some people are natural short sleepers (NSS).
The findings of this study arepublishedinProceedings of the National Academy of Sciences.
We might be physically inactive when sleeping, but our body is far from being idle. It goes into servicing mode, repairing cells, replenishing essential hormones and facilitating neural reorganization.
As a result, sleep deprivation can significantly impair both physical and cognitive functioning. Over time, chronic sleep loss may even raise the risk of serious health issues such as heart disease, diabetes, stroke, obesity, and depression. Hence, it is medically advised to sleep for at least 7–8 hours to maintain good physical and mental health.
Natural short sleepers seem to bypass all these negative outcomes of sleep deprivation with only 4–6 hours of sleep per night, and sleeping beyond that can sometimes make them feel worse. Previous studies have identified five mutations in four genes—DEC2, ADRB1, NPSR1, and GRM1—that have been linked to the natural short sleep (NSS) trait in humans.
It has also been found that intracellular signaling pathways of protein kinases—enzymes catalyzing the transfer of phosphate groups from ATP to other proteins—such as salt-inducible kinase 3 (Sik3), play a key role in regulating sleep and wakefulness. However, there was a lack of direct evidence of their role in regulating NSS traits.
Computational analysis showed that the point mutation caused significant structural changes in the SIK3 protein, impairing its ability to transfer phosphate molecules to other proteins and resulting in reduced sleep duration.
Hongmin Chen et al, The SIK3-N783Y mutation is associated with the human natural short sleep trait, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2500356122
Formaldehyde releasers found in common personal care products
Formaldehyde is known to cause cancer in humans but several women use personal health care products that release this chemical.
In recent years, growing concerns about exposure to formaldehyde in personal care products have focused on hair relaxers. For instance, recent studies show a link between the use of hair relaxers and increased risk of uterine and breast cancer.
A new study, published in the journal Environmental Science & Technology Letters, is among the first to demonstrate that formaldehyde-releasing preservatives are present in a wide range of personal care products, including shampoo, lotions, body soap, and even eyelash glue.
These chemicals are in products we use all the time, all over our bodies. Repeated exposures like these can add up and cause serious harm.
Companies add formaldehyde to personal care products to extend their shelf-life. Formaldehyde-releasing preservatives are often used as an alternative—these are chemicals that slowly release formaldehyde over time and serve the same purpose.
But lotions can vary widely: some might have a few natural ingredients, like beeswax and shea butter, while others might have many toxic chemicals like formaldehyde releasers, phthalates, and parabens.
In the study, fifty-three percent of participants reported using at least one personal care product that listed formaldehyde releasers on its label. Many of the products with formaldehyde releasers that participants reported using were applied daily or multiple times per week.
DMDM hydantoin was the most common formaldehyde-releasing preservative. Roughly 47% of skincare products and 58% of hair products with formaldehyde-releasing preservatives contained DMDM hydantoin.
One way to reduce exposures would be to require that companies add warning labels to formaldehyde-releasing products, say the researchers.
But it can be hard for the average consumer—and even chemists—to identify a formaldehyde-releasing preservative on a label. They have long, weird, funny names, and they typically don't have the word formaldehyde in them.
While warning labels might be a good first step banning the use of formaldehyde releasers altogether would be the best-case scenario. Companies shouldn't be putting these chemicals in products in the first place.
Formaldehyde and formaldehyde releasing preservatives in personal care products used by Black women and Latinas, Environmental Science & Technology Letters (2025). DOI: 10.1021/acs.estlett.5c00242
A new tool unlocks the body's 'messages in a bottle' to detect and treat diseases
Have you ever dreamed of writing a heartfelt letter, sealing it in a bottle, and letting the ocean carry it to someone special? It's a romantic image we've seen in movies like "Message in a Bottle." But did you know this beautiful act of connection is happening inside your body every minute of every day?
Our cells, much like us, are constantly trying to communicate. But instead of ink and paper, they send out tiny biological packages called extracellular vesicles (EVs). These are the body's real-life messages in a bottle, carrying precious cargo—like proteins and genetic material—from one cell to another. Each EV holds a snapshot of its sender's identity and condition, making them incredibly promising for diagnosing diseases and tailoring treatments.
It's like thousands of bottles with messages washing up on shore, and we still don't know which ones carry lifesaving information.
Now researchers offer a solution.
They've developed a technology called SHINER, short for Subpopulation Homogeneous Isolation and Nondestructive EV Release, designed to gently capture and release specific EV subpopulations without damaging them.
SHINER is like a molecular claw machine. Using specially designed "claws" made from antibodies and DNA, it reaches into the crowded sea of EVs, grabs the ones with just the right surface markers, and gently lifts them out, intact and ready to be read.
At the core of this technology is a clever tool called SWITCHER, which ensures that only EVs with a specific molecular "barcode" are captured. Then, a matching DNA "key" activates the claw to gently release the captured EVs unharmed. No harsh chemicals. No broken "bottles." Just pure, readable messages, delivered safely to scientists for analysis.
What makes this work even more exciting is that SHINER doesn't just work in theory.
The research team showed it can purify EVs from real-world biological samples, like blood, while preserving their full structure and function. When paired with the earlier invention by the team, the ultrasensitive EV single-molecule array, SHINER opens the door to next-generation diagnostics and therapeutics. Doctors could one day use it to detect cancer earlier, monitor treatment response, or even deliver precision drugs using EVs as natural carriers.
Chen‐Wei Hsu et al, Decoding Complex Biological Milieus: SHINER's Approach to Profiling and Functioning of Extracellular Vesicle Subpopulations, Small (2025). DOI: 10.1002/smll.202503638
Superbug can digest medical plastic, making it even more dangerous
A dangerous hospital superbug has been found to digest plastic—specifically the kind used in some sutures, stents and implants inside the human body. Microbiologists show the bacteria can feed on plastic to survive, potentially enabling these pathogens to survive longer in hospital wards and within patients.
The discovery, published in Cell Reports , challenges the widely held belief that pathogens cannot degrade medical plastics. A patient isolate of the common hospital-acquired bacterial infection Pseudomonas aeruginosa was shown to degrade polycaprolactone (PCL)—a plastic often used in sutures, wound dressings, stents, drug-delivery patches and surgical mesh.
Plastics, including plastic surfaces, could potentially be food for these bacteria. Pathogens with this ability could survive for longer in the hospital environment. It also means that any medical device or treatment that contains plastic could be susceptible to degradation by bacteria.
Researchers isolated the enzyme, named Pap1, from a strain of Pseudomonas aeruginosa that was originally sampled from a patient's wound. Tested in the lab, the enzyme degraded 78% of a plastic sample in just seven days. Crucially, the bacteria could also use the plastic as its only carbon source—effectively eating it.
This plastic-digesting power also makes the bug more dangerous. The team showed that the broken-down plastic fragments helped it form tougher biofilms—the protective clingy bacterial coatings that help bacteria overcome antibiotics and make infections harder to treat.
The implications stretch beyond one material. While the team confirmed degradation only for PCL, they identified signs of similar enzymes in other pathogens. This means that other plastics could also be vulnerable to microbial attack—and some of the most widely used medical materials made from polyethylene terephthalate or polyurethane may be at risk.
These include:
Bone scaffolds and dental implants Bandages and wound dressings Catheters Breast implants "The bug's plastic-eating ability is likely helping it survive on surfaces in hospitals, potentially driving hospital outbreaks. We should start to consider focusing on plastics that are harder for microbes to digest and potentially screening pathogens for these enzymes, especially in unexplained prolonged outbreaks
ALICE detects the conversion of lead into gold at the Large Hadron Collider
In a paper published in Physical Review C, the ALICE collaboration reports measurements that quantify the transmutation of lead into gold in CERN's Large Hadron Collider (LHC).
Transforming the base metal lead into the precious metal gold was a dream of medieval alchemists. This long-standing quest, known as chrysopoeia, may have been motivated by the observation that dull gray, relatively abundant lead is of a similar density to gold, which has long been coveted for its beautiful color and rarity. It was only much later that it became clear that lead and gold are distinct chemical elements and that chemical methods are powerless to transmute one into the other.
With the dawn of nuclear physics in the 20th century, it was discovered that heavy elements could transform into others—either naturally, by radioactive decay—or in the laboratory, under a bombardment of neutrons or protons. Though gold has been artificially produced in this way before, the ALICE collaboration has now measured the transmutation of lead into gold by a new mechanism involving near-miss collisions between lead nuclei at the LHC.
Extremely high-energy collisions between lead nuclei at the LHC can create quark–gluon plasma, a hot and dense state of matter that is thought to have filled the universe around a millionth of a second after the Big Bang, giving rise to the matter we now know. However, in the far more frequent interactions where the nuclei just miss each other without "touching," the intense electromagnetic fields surrounding them can induce photon–photon and photon–nucleus interactions that open further avenues of exploration.
The electromagnetic field emanating from a lead nucleus is particularly strong because the nucleus contains 82 protons, each carrying one elementary charge. Moreover, the very high speed at which lead nuclei travel in the LHC (corresponding to 99.999993% of the speed of light) causes the electromagnetic field lines to be squashed into a thin pancake, transverse to the direction of motion, producing a short-lived pulse of photons.
Often, this triggers a process called electromagnetic dissociation, whereby a photon interacting with a nucleus can excite oscillations of its internal structure, resulting in the ejection of small numbers of neutrons and protons. To create gold (a nucleus containing 79 protons), three protons must be removed from a lead nucleus in the LHC beams.
The ALICE team used the detector's zero degree calorimeters (ZDC) to count the number of photon–nucleus interactions that resulted in the emission of zero, one, two and three protons accompanied by at least one neutron, which are associated with the production of lead, thallium, mercury and gold, respectively.
While less frequent than the creation of thallium or mercury, the results show that the LHC currently produces gold at a maximum rate of about 89,000 nuclei per second from lead–lead collisions at the ALICE collision point. Gold nuclei emerge from the collision with very high energy and hit the LHC beam pipe or collimators at various points downstream, where they immediately fragment into single protons, neutrons and other particles. The gold exists for just a tiny fraction of a second. The ALICE analysis shows that, during Run 2 of the LHC (2015–2018), about 86 billion gold nuclei were created during the four major experiments. In terms of mass, this corresponds to just 29 picograms (2.9 × 10-11 g). Since the luminosity in the LHC is continually increasing thanks to regular upgrades to the machines, Run 3 has produced almost double the amount of gold that Run 2 did, but the total still amounts to trillions of times less than would be required to make a piece of jewelry.
While the dream of medieval alchemists has technically come true, their hopes of riches have once again been dashed.
S. Acharya et al, Proton emission in ultraperipheral Pb-Pb collisions at √sNN=5.02 TeV, Physical Review C (2025). DOI: 10.1103/PhysRevC.111.054906
Eggs less likely to crack when dropped side-on, research reveals
Eggs are less likely to crack when dropped on their side than when dropped vertically, finds research published in Communications Physics. Controlled trials simulating the "egg drop challenge," a common classroom science experiment, found that the shell of an egg can better withstand an impact when dropped side-on.
Researchers conducted a series of 180 drop tests to compare how chicken eggs break when oriented vertically or side-on. After dropping 60 eggs from each of three different heights—8, 9, and 10 millimeters—on to a hard surface, the authors observed that, on average, eggs dropped vertically broke at lower drop heights.
More than half of the eggs dropped vertically from 8 millimeters cracked, with which end of the egg pointed downwards making no difference.
However, less than 10% of horizontally-dropped eggs cracked from the same height. A further 60 eggs were subjected to compression tests, which measured the force required to crack the eggs vertically and horizontally.
While 45 newtons of force was required to break the eggs in both orientations, the horizontally-loaded eggs could compress further before cracking. The authors suggest that this means that eggs are more flexible around their equator, and therefore able to absorb more energy in this orientation before breaking.
The authors conclude that the reason behind the common misassumption that an egg dropped vertically is less likely to crack is a confusion between the physical properties of stiffness, strength, and toughness.
Eggs are stiffer when compressed vertically, but the authors say that this does not necessarily mean that eggs are also tougher in that direction.
Challenging common notions on how eggs break and the role of strength versus toughness, Communications Physics (2025). DOI: 10.1038/s42005-025-02087-0
DNA-like molecule may survive Venus-like cloud conditions
Punishing conditions in the clouds of Venus could be home to a DNA-like molecule capable of forming genes in life very different to that on Earth, according to a new study.
Long thought to be hostile to complex organic chemistry because of the absence of water, the clouds of Earth's sister planet are made of droplets of sulphuric acid, chlorine, iron, and other substances.
But new research shows how peptide nucleic acid (PNA)—a structural cousin of DNA—can survive under lab conditions made to mimic conditions that can occur in Venus' perpetual clouds.
Their findings add to the evidence that shows that concentrated sulfuric acid can sustain a diverse range of organic chemistry that might be the basis of a form of life different from Earth.
People think concentrated sulfuric acid destroys all organic molecules and therefore kills all life, but this is not true. While many biochemicals, like sugars, are unstable in such an environment, but research to date shows that other chemicals found in living organisms, such as nitrogenous bases, amino acids, and some dipeptides, don't break down.
Janusz J. Petkowski et al, Astrobiological implications of the stability and reactivity of peptide nucleic acid (PNA) in concentrated sulfuric acid, Science Advances (2025). DOI: 10.1126/sciadv.adr0006
The first genetic editing in spiders with CRISPR‐Cas yields colourful silk
A research group for the first time, successfully applied the CRISPR-Cas9 gene-editing tool to spiders. Following the genetic modification, the spiders produced red fluorescent silk.
The findings of the study have beenpublishedin the journalAngewandte Chemie.
Spider silk is one of the most fascinating fibers in the field of materials science. In particular, its dragline thread is extremely tear-resistant, while also being elastic, lightweight and biodegradable. If scientists succeed in influencing spider silkproduction in vivo—in a living animal—and thereby gain insights into the structure of the dragline thread, it could pave the way for the development of new silk functionalities for a wide range of applications.
Researchers developed an injection solution that included the components of the gene-editing system as well as a gene sequence for a red fluorescent protein. This solution was injected into the eggs of unfertilized female spiders, which were then mated with males of the same species. As a result, the offspring of the gene-edited spiders showed red fluorescence in their dragline silk—clear evidence of the successful knock-in of the gene sequence into a silk protein.
The spider silk protein manipulated in this study thus serves as the first model for developing silk fibers with new properties, supporting their functionalization for future applications.
Edgardo Santiago‐Rivera et al, Spider Eye Development Editing and Silk Fiber Engineering Using CRISPR‐Cas, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202502068
Your fingers wrinkle in the same pattern every time you're in the water for too long, study shows
Do your wrinkles always form in the same pattern every time you're in the water for too long? According to new research the answer is yes.
Research found that blood vessels beneath the skin actually contract after prolonged immersion, and that's where the wrinkles come from.
And in a paper recently published in the Journal of the Mechanical Behavior of Biomedical Materials, researchers show that the topography patterns remain constant after multiple immersions.
Blood vessels don't change their position much—they move around a bit, but in relation to other blood vessels, they're pretty static. That means the wrinkles should form in the same manner, and this work proved that they do.
They also made an interesting side discovery: that wrinkles don't form in people who have median nerve damage in their fingers! got median nerve damage in my fingers.' They tested a person with median nerve damage and no wrinkles were formed on his fingers!
Rachel Laytin et al, On the repeatability of wrinkling topography patterns in the fingers of water immersed human skin, Journal of the Mechanical Behavior of Biomedical Materials (2025). DOI: 10.1016/j.jmbbm.2025.106935
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 cellsin 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.
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 cellsin 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.
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 bacteriumPorphyromonas 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.
Part 1
Twelve weeks after infection, mice exposed to P. gingivalis already 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.
Shunsuke Miyauchi et al, Atrial Translocation of Porphyromonas gingivalis Exacerbates Atrial Fibrosis and Atrial Fibrillation, Circulation (2025). DOI: 10.1161/CIRCULATIONAHA.124.071310
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 namedCa. Electrothrix yaqonensis and it conducts electricity just like a wire does. This is not unique, butCa. Electrothrix yaqonensishas 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.
These bacteria can transfer electrons to clean up pollutants, so they could be used to remove harmful substances from sediments. Also, their design of a highly conductive nickel protein can possibly inspire new bioelectronics.
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 theJournal 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).
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 1078years 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 101100years. 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."
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
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.
Astudyby 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 inScience.
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.
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
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 workpublishedin theProceedings 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.
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.
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
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.
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.
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
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
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.
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.
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).
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 Tregs.
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 Tregs.
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 onionsis 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 microscopeto accurately measure the knives before use.
The videos revealed that the differences in the amount of sprayreleased, 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 layersto 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.
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.
Dr. Krishna Kumari Challa
Probing the molecular mechanisms of metastasis
Cells have a mailing system of sorts. They can release tiny molecular balls, called extracellular vesicles (EVs), that contain biological matter or messages and attach to other cells to share whatever they contain.
In cancer, EVs often depart from tumour cells to seed the cancer elsewhere in the body, leading to metastasis. However, how the EVs connected to recipient cells to deliver their payload has remained a mystery—until now. A team of researchers has now revealed the molecular mechanisms underpinning the process for small EVs (sEVs), which they said could have implications for developing better cancer treatments.
The team published their findings in the Journal of Cell Biology.
EVs can serve as biomarkers, since they carry specific proteins and genetic material that can indicate disease progression. Researchers have also started to explore their potential to treat cancers, either by inhibiting their binding to host cells or by encouraging the binding of EVs with therapeutic payloads.
The researchers now focused on understanding the role of integrin heterodimers, which are molecules that help sEVs adhere to the host cell. The same team previously found that sEVs could be sorted into subtypes with different properties, depending on which tetraspanin protein it has. This type of protein is small but critical to EV formation and regulation.
Using this understanding, the researchers sorted and tracked the sEVs with single-molecule resolution.
They examined the sorted subtypes with super-resolution microscopy to find that all subtypes primarily used integrin heterodimers associated with a specific tetraspanin protein known as CD151 and a molecule containing carbohydrates and fats called GM1 to bind to laminin, a protein critical to cellular membranes and heavily involved in cell membrane structure and cell adhesion, among other responsibilities.
Laminin is specifically a glycoprotein, meaning it is a protein with a carbohydrate, or sugar, molecule attached to it. It exists in the extracellular matrix, or the molecular network surrounding cells and supports their signaling and structure.
Quantitative analysis using single-molecule imaging and super-resolution microscopy demonstrated that all EV subtypes derived from four distinct tumor cell lines, irrespective of size, predominantly bind to laminin via CD151-associated integrin heterodimers and GM1, thereby eliciting responses in recipient cells.
EVs bound to laminin significantly more than they bound to fibronectin, which is another protein responsible for cell adhesion in the extracellular matrix.
Two other proteins associated with adhesion in the EVs, talin and kindlin, did not activate the integrin heterodimers. Taken all together, the researchers concluded that GM1 and integrin heterodimers associated with CD151 are key for EV binding. This understanding could help researchers better inhibit or encourage binding as needed in the name of disease treatment.
Tatsuki Isogai et al, Extracellular vesicles adhere to cells primarily by interactions of integrins and GM1 with laminin, Journal of Cell Biology (2025). DOI: 10.1083/jcb.202404064
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May 6
Dr. Krishna Kumari Challa
Tetracycline antibiotics impair T cell function by targeting mitochondria
A team of international researchers has revealed in unprecedented detail how tetracycline antibiotics impair T cell function by binding mitochondrial ribosomes and inhibiting oxidative metabolism (OXPHOS). The study, reported in Nature Communications, raises mechanistic considerations for antibiotic therapy and the design of new molecules that can better discriminate between pathogen and host.
Antibiotics historically developed to inhibit bacterial protein synthesis cross-react with mitochondrial ribosomes due to shared evolutionary features, impairing translation of key phosphorylation complex subunits in host cells. Indeed, certain antibiotics, such as tetracyclines, have a long history in the treatment of inflammatory conditions, such as rheumatoid arthritis, although large controlled cohort studies are lacking, in part due to the lack of a molecular mechanism.
When you take antibiotics, the effects are not solely restricted to commensal and pathogenic bacteria. Some of your cells take a hit, and there is good evidence in the literature to support reversible inhibition of that mitochondrial translation can be used to treat inflammatory diseases.
The researchers identified specific structural features of mitochondrial ribosomes that could potentially be targeted to develop more selective therapeutics.
"The discrimination between bacterial and human mitochondrial ribosomes represents an important frontier for antibiotic development. By understanding the specific binding domains within the mitoribosome that interact with tigecycline, it will be possible to design next-generation entities with different specificities, whether those affect the host or pathogen.
Qiuya Shao et al, T cell toxicity induced by tigecycline binding to the mitochondrial ribosome, Nature Communications (2025). DOI: 10.1038/s41467-025-59388-9
May 6
Dr. Krishna Kumari Challa
Experimental peptide treatment could triple survival rates in severe blood loss cases
Researchers have discovered a promising new therapeutic approach to treating hemorrhagic shock, a life-threatening condition caused by severe blood loss that remains the leading cause of preventable death in trauma cases globally.
The study demonstrated that activating Protein Kinase C epsilon (PKC-ε) significantly improves early survival rates and physiological stability following severe hemorrhage.
The work is published in the journal Scientific Reports.
In a carefully controlled experiment using a porcine model, researchers induced hemorrhagic shock by withdrawing 35% of the animals' total blood volume. Animals treated with a PKC-ε activator peptide just five minutes after the onset of bleeding showed dramatically improved survival—73% of treated subjects survived compared to only 25% of those left untreated.
Additionally, treated animals maintained significantly better cardiovascular stability, including blood pressure, heart rate, and cardiac output, all critical indicators of effective response during severe trauma.
Moreover, detailed analysis of mitochondrial activity revealed enhanced function within the heart tissues of animals receiving the PKC-ε activator. As mitochondria are vital cellular energy producers, these findings suggest that activating PKC-ε helps maintain organ energy levels under stress, potentially protecting tissues against further damage associated with severe blood loss.
The implications of this study are far-reaching. Current therapeutic strategies for severe hemorrhagic shock often involve fluid resuscitation, which can unintentionally exacerbate tissue damage by triggering ischemic-reperfusion injury.
This new approach—administering a PKC-ε activator peptide—has the potential to significantly minimize these detrimental effects, thereby improving survival chances and reducing complications associated with severe trauma.
Maya Simchoni et al, Protein kinase C epsilon activation improves early survival in an acute porcine model of controlled hemorrhage, Scientific Reports (2025). DOI: 10.1038/s41598-025-92310-3
May 6
Dr. Krishna Kumari Challa
Tire additives found deposited on fruits and vegetables
A new study has found that tire additives enter into and pass through the food chain. Further research is needed to establish the implications for human health.
Traces of the additives typically used in tire manufacturing have been detected in all of the most common types of fruits and vegetables. The scientists don't yet know the long-term implications of exposure to these substances for human health. Further research is needed to clarify this point.
The study follows on from two Austrian studies demonstrating that these additives were present in leafy vegetables.
Researchers sampled around 100 of the most commonly eaten fruits and vegetables from major supermarket chains to organic markets and small, grocery stores.
After rinsing the fruits and vegetables and turning them into workable samples, the scientists tested them for 11 compounds typically found in tire additives. Using consumption data held by the FSVO, they were then able to calculate theoretical daily intake values for these substances.
They found that 31% of the samples contained traces of the compounds, including 6-PPD and 6-PPD-quinone, with no difference according to where the fruits and vegetables came from or whether they were organic.
Previous studies have established that tire additives, especially DPG, 6-PPD and 6-PPD-quinone, are toxic to mammals. This research, which has so far been carried out only on rodents, found that these additives lead to decreased fertility in males and have neurotoxic and neuroinflammatory effects.
Scientists in China are also conducting in-depth research into the subject, analyzing human blood and urine for the presence of these substances.
When tires wear against road surfaces, they release additives such as antioxidants and vulcanizing agents (which give rubber more strength, elasticity and durability). These particles, the toxicity of which is yet to be determined, disperse through the air, settle on the ground, and are transported in runoff water. Humans are exposed to them in two ways: by inhaling them and, as the EPFL-FSVO study shows, by ingesting them in contaminated food.
According to a paper published in 2017, six million metric tons of these additives are released into the environment every year. Our exposure to these additives is similar to that for other micropollutants.
They're around us constantly, in every part of our environment. What we don't know is whether we need to introduce tighter controls, such as by phasing them out in tire manufacturing in favor of less toxic alternatives.
Scientists are currently exploring ways in which roads can be decontaminated to prevent tire additives from entering the environment. Several studies have shown that aggressive driving—with hard acceleration and braking—increases tire wear, making it more likely that these particles will transfer into the air, soil and surface water.
Florian Breider et al, Assessment of tire-derived additives and their metabolites into fruit, root and leafy vegetables and evaluation of dietary intake in Swiss adults, Journal of Hazardous Materials (2025). DOI: 10.1016/j.jhazmat.2025.138432
May 7
Dr. Krishna Kumari Challa
Why some mammals glow under ultraviolet light
Scientists have been trying to discover exactly why some animals glow under ultraviolet light as photoluminescence in mammal fur is common.
Rats, along with bandicoots, possums, bats, tree-kangaroos and many other creatures around the world are photoluminescent; they glow under ultraviolet, violet or blue light.
Scientists' aim 's to identify luminophores (molecules or groups of molecules) contributing to photoluminescence.
The researchers shaved fur from roadkill and subjected it to high-performance liquid chromatography.
The fur of the northern long-nosed and northern brown bandicoots photoluminesces strongly, displaying pink, yellow, blue and/or white colors. The researchers wanted to find out whether the luminophores present in bandicoot fur might be common across multiple species.
So they compared the results from the two bandicoots to the northern quoll, the coppery brushtail possum, the Lumholtz's tree-kangaroo, the pale field rat and the platypus—all of which photoluminesce in different ways.
The scientists confirmed metabolites of the amino acid tryptophan and identified derivatives of the chemical compound porphyrin that cause bandicoots, quolls and possums to glow bright pink in UV light.
They also found a contributing cause of the colour of coppery brushtail possum fur—not photoluminescent, but a strong purple colouration in white light—a match for the molecule Indigo—which is also extracted as a dye from plants.
Linda M. Reinhold et al, Luminophores in the fur of seven Australian Wet Tropics mammals, PLOS One (2025). DOI: 10.1371/journal.pone.0320432. journals.plos.org/plosone/arti … journal.pone.0320432
May 7
Dr. Krishna Kumari Challa
A recently-discovered termite terminator is better, more targeted and won't harm humans
Drywood termites, the ones that hide in wooden structures, molt about seven times in their lives. Researchers have found that a chemical preventing them from growing new exoskeletons will also end their infestation of your home.
The chemical, bistrifluron, and its ability to kill about 95% of a termite colony without off-target effects on mammals, are documented in a paper published in the Journal of Economic Entomology.
This chemical is more environmentally friendly than ones traditionally used for drywood termite infestation. It's specific to insects and can't harm humans.
Unlike humans with skeletons located inside their flesh, termites have exoskeletons on the outside that protect them from the elements. The main component of these external skeletons is chitin, which is also found in fungal cell walls, fish scales, and the beaks of squids and octopuses. Chitin also provides mechanical strength for insect exoskeletons, making them suitable as armor as well as sites for muscle attachment.
As termites are getting ready to molt, something they must do in order to grow, they also produce chitin to create the new exoskeleton. Bistrifluron prevents them from doing so.
Once the termites reach a certain stage, they have to molt. They cannot avoid that. With a lethal dose of this chemical, they'll try to shed their old exoskeleton but won't have a new one ready to protect them.
The researchers observed that bistrifluron initially slows the termites down, reducing their feeding activity. Eventually it prevents them from molting, and they die. This is one of the first studies that looks at the impact of chitin-inhibiting chemicals on drywood termites.
As the termites eat the treated wood, they also spread the chemical to other members of the colony. Full collapse happens in about two months, which is slower than other methods but carries certain advantages in addition to lower toxicity.
Nicholas A Poulos et al, Toxicity and horizontal transfer of chitin synthesis inhibitors in the western drywood termite (Blattodea: Kalotermitidae), Journal of Economic Entomology (2025). DOI: 10.1093/jee/toaf064
May 7
Dr. Krishna Kumari Challa
Natural short sleepers have a genetic mutation
Does everybody need 8-hours sleep? NO!
Several prominent figures in science and invention were known to get by on significantly less sleep than the typical 7-8 hours recommended for adults. Notable examples include Thomas Edison, Nikola Tesla, and Leonardo da Vinci, Benjamin Franklin who reportedly slept as little as two to four hours per night.
I too sleep for just four and half to six hours, never more than that. Rest of the time I work like mad. I am used to it.
When your mind is in the grip of something, you can't sleep and feel very restless if you don't complete your work in art, literature, science, or any other field.
And there are some natural short sleepers. Science says ....
Not everyone needs 8 hours of sleep to function properly. Some people can feel well-rested and show no negative effects of sleep deprivation, even after just 4 hours of sleep, which is likely the result of a genetic mutation.
A recent study has reported that a mutation in salt-induced kinase 3 (hSIK3-N783Y)—a gene critical for regulating sleep duration and depth—may be the reason why some people are natural short sleepers (NSS).
The findings of this study are published in Proceedings of the National Academy of Sciences.
We might be physically inactive when sleeping, but our body is far from being idle. It goes into servicing mode, repairing cells, replenishing essential hormones and facilitating neural reorganization.
As a result, sleep deprivation can significantly impair both physical and cognitive functioning. Over time, chronic sleep loss may even raise the risk of serious health issues such as heart disease, diabetes, stroke, obesity, and depression. Hence, it is medically advised to sleep for at least 7–8 hours to maintain good physical and mental health.
Natural short sleepers seem to bypass all these negative outcomes of sleep deprivation with only 4–6 hours of sleep per night, and sleeping beyond that can sometimes make them feel worse. Previous studies have identified five mutations in four genes—DEC2, ADRB1, NPSR1, and GRM1—that have been linked to the natural short sleep (NSS) trait in humans.
It has also been found that intracellular signaling pathways of protein kinases—enzymes catalyzing the transfer of phosphate groups from ATP to other proteins—such as salt-inducible kinase 3 (Sik3), play a key role in regulating sleep and wakefulness. However, there was a lack of direct evidence of their role in regulating NSS traits.
Computational analysis showed that the point mutation caused significant structural changes in the SIK3 protein, impairing its ability to transfer phosphate molecules to other proteins and resulting in reduced sleep duration.
Hongmin Chen et al, The SIK3-N783Y mutation is associated with the human natural short sleep trait, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2500356122
May 8
Dr. Krishna Kumari Challa
Formaldehyde releasers found in common personal care products
Formaldehyde is known to cause cancer in humans but several women use personal health care products that release this chemical.
In recent years, growing concerns about exposure to formaldehyde in personal care products have focused on hair relaxers. For instance, recent studies show a link between the use of hair relaxers and increased risk of uterine and breast cancer.
A new study, published in the journal Environmental Science & Technology Letters, is among the first to demonstrate that formaldehyde-releasing preservatives are present in a wide range of personal care products, including shampoo, lotions, body soap, and even eyelash glue.
These chemicals are in products we use all the time, all over our bodies. Repeated exposures like these can add up and cause serious harm.
Companies add formaldehyde to personal care products to extend their shelf-life. Formaldehyde-releasing preservatives are often used as an alternative—these are chemicals that slowly release formaldehyde over time and serve the same purpose.
But lotions can vary widely: some might have a few natural ingredients, like beeswax and shea butter, while others might have many toxic chemicals like formaldehyde releasers, phthalates, and parabens.
In the study, fifty-three percent of participants reported using at least one personal care product that listed formaldehyde releasers on its label. Many of the products with formaldehyde releasers that participants reported using were applied daily or multiple times per week.
DMDM hydantoin was the most common formaldehyde-releasing preservative. Roughly 47% of skincare products and 58% of hair products with formaldehyde-releasing preservatives contained DMDM hydantoin.
One way to reduce exposures would be to require that companies add warning labels to formaldehyde-releasing products, say the researchers.
But it can be hard for the average consumer—and even chemists—to identify a formaldehyde-releasing preservative on a label. They have long, weird, funny names, and they typically don't have the word formaldehyde in them.
While warning labels might be a good first step banning the use of formaldehyde releasers altogether would be the best-case scenario. Companies shouldn't be putting these chemicals in products in the first place.
Formaldehyde and formaldehyde releasing preservatives in personal care products used by Black women and Latinas, Environmental Science & Technology Letters (2025). DOI: 10.1021/acs.estlett.5c00242
May 8
Dr. Krishna Kumari Challa
A new tool unlocks the body's 'messages in a bottle' to detect and treat diseases
Have you ever dreamed of writing a heartfelt letter, sealing it in a bottle, and letting the ocean carry it to someone special? It's a romantic image we've seen in movies like "Message in a Bottle." But did you know this beautiful act of connection is happening inside your body every minute of every day?
Our cells, much like us, are constantly trying to communicate. But instead of ink and paper, they send out tiny biological packages called extracellular vesicles (EVs). These are the body's real-life messages in a bottle, carrying precious cargo—like proteins and genetic material—from one cell to another. Each EV holds a snapshot of its sender's identity and condition, making them incredibly promising for diagnosing diseases and tailoring treatments.
It's like thousands of bottles with messages washing up on shore, and we still don't know which ones carry lifesaving information.
Now researchers offer a solution.
They've developed a technology called SHINER, short for Subpopulation Homogeneous Isolation and Nondestructive EV Release, designed to gently capture and release specific EV subpopulations without damaging them.
SHINER is like a molecular claw machine. Using specially designed "claws" made from antibodies and DNA, it reaches into the crowded sea of EVs, grabs the ones with just the right surface markers, and gently lifts them out, intact and ready to be read.
At the core of this technology is a clever tool called SWITCHER, which ensures that only EVs with a specific molecular "barcode" are captured. Then, a matching DNA "key" activates the claw to gently release the captured EVs unharmed. No harsh chemicals. No broken "bottles." Just pure, readable messages, delivered safely to scientists for analysis.
What makes this work even more exciting is that SHINER doesn't just work in theory.
The research team showed it can purify EVs from real-world biological samples, like blood, while preserving their full structure and function. When paired with the earlier invention by the team, the ultrasensitive EV single-molecule array, SHINER opens the door to next-generation diagnostics and therapeutics. Doctors could one day use it to detect cancer earlier, monitor treatment response, or even deliver precision drugs using EVs as natural carriers.
Chen‐Wei Hsu et al, Decoding Complex Biological Milieus: SHINER's Approach to Profiling and Functioning of Extracellular Vesicle Subpopulations, Small (2025). DOI: 10.1002/smll.202503638
May 8
Dr. Krishna Kumari Challa
Superbug can digest medical plastic, making it even more dangerous
A dangerous hospital superbug has been found to digest plastic—specifically the kind used in some sutures, stents and implants inside the human body. Microbiologists show the bacteria can feed on plastic to survive, potentially enabling these pathogens to survive longer in hospital wards and within patients.
The discovery, published in Cell Reports , challenges the widely held belief that pathogens cannot degrade medical plastics. A patient isolate of the common hospital-acquired bacterial infection Pseudomonas aeruginosa was shown to degrade polycaprolactone (PCL)—a plastic often used in sutures, wound dressings, stents, drug-delivery patches and surgical mesh.
Plastics, including plastic surfaces, could potentially be food for these bacteria. Pathogens with this ability could survive for longer in the hospital environment. It also means that any medical device or treatment that contains plastic could be susceptible to degradation by bacteria.
Researchers isolated the enzyme, named Pap1, from a strain of Pseudomonas aeruginosa that was originally sampled from a patient's wound. Tested in the lab, the enzyme degraded 78% of a plastic sample in just seven days. Crucially, the bacteria could also use the plastic as its only carbon source—effectively eating it.
This plastic-digesting power also makes the bug more dangerous. The team showed that the broken-down plastic fragments helped it form tougher biofilms—the protective clingy bacterial coatings that help bacteria overcome antibiotics and make infections harder to treat.
Part 1
May 8
Dr. Krishna Kumari Challa
The implications stretch beyond one material. While the team confirmed degradation only for PCL, they identified signs of similar enzymes in other pathogens. This means that other plastics could also be vulnerable to microbial attack—and some of the most widely used medical materials made from polyethylene terephthalate or polyurethane may be at risk.
These include:
Bone scaffolds and dental implants
Bandages and wound dressings
Catheters
Breast implants
"The bug's plastic-eating ability is likely helping it survive on surfaces in hospitals, potentially driving hospital outbreaks. We should start to consider focusing on plastics that are harder for microbes to digest and potentially screening pathogens for these enzymes, especially in unexplained prolonged outbreaks
Pseudomonas aeruginosa clinical isolates can encode functional plastic-degrading enzymes that allow survival on plastic and augment biofilm formation., Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115650. www.cell.com/cell-reports/full … 2211-1247(25)00421-8
Part 2
May 8
Dr. Krishna Kumari Challa
Cuttlefish use their arms to wave at each other
May 8
Dr. Krishna Kumari Challa
ALICE detects the conversion of lead into gold at the Large Hadron Collider
In a paper published in Physical Review C, the ALICE collaboration reports measurements that quantify the transmutation of lead into gold in CERN's Large Hadron Collider (LHC).
Transforming the base metal lead into the precious metal gold was a dream of medieval alchemists. This long-standing quest, known as chrysopoeia, may have been motivated by the observation that dull gray, relatively abundant lead is of a similar density to gold, which has long been coveted for its beautiful color and rarity. It was only much later that it became clear that lead and gold are distinct chemical elements and that chemical methods are powerless to transmute one into the other.
With the dawn of nuclear physics in the 20th century, it was discovered that heavy elements could transform into others—either naturally, by radioactive decay—or in the laboratory, under a bombardment of neutrons or protons. Though gold has been artificially produced in this way before, the ALICE collaboration has now measured the transmutation of lead into gold by a new mechanism involving near-miss collisions between lead nuclei at the LHC.
Extremely high-energy collisions between lead nuclei at the LHC can create quark–gluon plasma, a hot and dense state of matter that is thought to have filled the universe around a millionth of a second after the Big Bang, giving rise to the matter we now know. However, in the far more frequent interactions where the nuclei just miss each other without "touching," the intense electromagnetic fields surrounding them can induce photon–photon and photon–nucleus interactions that open further avenues of exploration.
The electromagnetic field emanating from a lead nucleus is particularly strong because the nucleus contains 82 protons, each carrying one elementary charge. Moreover, the very high speed at which lead nuclei travel in the LHC (corresponding to 99.999993% of the speed of light) causes the electromagnetic field lines to be squashed into a thin pancake, transverse to the direction of motion, producing a short-lived pulse of photons.
Often, this triggers a process called electromagnetic dissociation, whereby a photon interacting with a nucleus can excite oscillations of its internal structure, resulting in the ejection of small numbers of neutrons and protons. To create gold (a nucleus containing 79 protons), three protons must be removed from a lead nucleus in the LHC beams.
The ALICE team used the detector's zero degree calorimeters (ZDC) to count the number of photon–nucleus interactions that resulted in the emission of zero, one, two and three protons accompanied by at least one neutron, which are associated with the production of lead, thallium, mercury and gold, respectively.
Part 1
May 9
Dr. Krishna Kumari Challa
While less frequent than the creation of thallium or mercury, the results show that the LHC currently produces gold at a maximum rate of about 89,000 nuclei per second from lead–lead collisions at the ALICE collision point. Gold nuclei emerge from the collision with very high energy and hit the LHC beam pipe or collimators at various points downstream, where they immediately fragment into single protons, neutrons and other particles. The gold exists for just a tiny fraction of a second.
The ALICE analysis shows that, during Run 2 of the LHC (2015–2018), about 86 billion gold nuclei were created during the four major experiments. In terms of mass, this corresponds to just 29 picograms (2.9 × 10-11 g). Since the luminosity in the LHC is continually increasing thanks to regular upgrades to the machines, Run 3 has produced almost double the amount of gold that Run 2 did, but the total still amounts to trillions of times less than would be required to make a piece of jewelry.
While the dream of medieval alchemists has technically come true, their hopes of riches have once again been dashed.
S. Acharya et al, Proton emission in ultraperipheral Pb-Pb collisions at √sNN=5.02 TeV, Physical Review C (2025). DOI: 10.1103/PhysRevC.111.054906
Part 2
May 9
Dr. Krishna Kumari Challa
Eggs less likely to crack when dropped side-on, research reveals
Eggs are less likely to crack when dropped on their side than when dropped vertically, finds research published in Communications Physics. Controlled trials simulating the "egg drop challenge," a common classroom science experiment, found that the shell of an egg can better withstand an impact when dropped side-on.
Researchers conducted a series of 180 drop tests to compare how chicken eggs break when oriented vertically or side-on. After dropping 60 eggs from each of three different heights—8, 9, and 10 millimeters—on to a hard surface, the authors observed that, on average, eggs dropped vertically broke at lower drop heights.
More than half of the eggs dropped vertically from 8 millimeters cracked, with which end of the egg pointed downwards making no difference.
However, less than 10% of horizontally-dropped eggs cracked from the same height. A further 60 eggs were subjected to compression tests, which measured the force required to crack the eggs vertically and horizontally.
While 45 newtons of force was required to break the eggs in both orientations, the horizontally-loaded eggs could compress further before cracking. The authors suggest that this means that eggs are more flexible around their equator, and therefore able to absorb more energy in this orientation before breaking.
The authors conclude that the reason behind the common misassumption that an egg dropped vertically is less likely to crack is a confusion between the physical properties of stiffness, strength, and toughness.
Eggs are stiffer when compressed vertically, but the authors say that this does not necessarily mean that eggs are also tougher in that direction.
Challenging common notions on how eggs break and the role of strength versus toughness, Communications Physics (2025). DOI: 10.1038/s42005-025-02087-0
May 9
Dr. Krishna Kumari Challa
DNA-like molecule may survive Venus-like cloud conditions
Punishing conditions in the clouds of Venus could be home to a DNA-like molecule capable of forming genes in life very different to that on Earth, according to a new study.
Long thought to be hostile to complex organic chemistry because of the absence of water, the clouds of Earth's sister planet are made of droplets of sulphuric acid, chlorine, iron, and other substances.
But new research shows how peptide nucleic acid (PNA)—a structural cousin of DNA—can survive under lab conditions made to mimic conditions that can occur in Venus' perpetual clouds.
Their findings add to the evidence that shows that concentrated sulfuric acid can sustain a diverse range of organic chemistry that might be the basis of a form of life different from Earth.
People think concentrated sulfuric acid destroys all organic molecules and therefore kills all life, but this is not true. While many biochemicals, like sugars, are unstable in such an environment, but research to date shows that other chemicals found in living organisms, such as nitrogenous bases, amino acids, and some dipeptides, don't break down.
Janusz J. Petkowski et al, Astrobiological implications of the stability and reactivity of peptide nucleic acid (PNA) in concentrated sulfuric acid, Science Advances (2025). DOI: 10.1126/sciadv.adr0006
May 9
Dr. Krishna Kumari Challa
The first genetic editing in spiders with CRISPR‐Cas yields colourful silk
A research group for the first time, successfully applied the CRISPR-Cas9 gene-editing tool to spiders. Following the genetic modification, the spiders produced red fluorescent silk.
The findings of the study have been published in the journal Angewandte Chemie.
Spider silk is one of the most fascinating fibers in the field of materials science. In particular, its dragline thread is extremely tear-resistant, while also being elastic, lightweight and biodegradable. If scientists succeed in influencing spider silk production in vivo—in a living animal—and thereby gain insights into the structure of the dragline thread, it could pave the way for the development of new silk functionalities for a wide range of applications.
Researchers developed an injection solution that included the components of the gene-editing system as well as a gene sequence for a red fluorescent protein. This solution was injected into the eggs of unfertilized female spiders, which were then mated with males of the same species. As a result, the offspring of the gene-edited spiders showed red fluorescence in their dragline silk—clear evidence of the successful knock-in of the gene sequence into a silk protein.
The spider silk protein manipulated in this study thus serves as the first model for developing silk fibers with new properties, supporting their functionalization for future applications.
Edgardo Santiago‐Rivera et al, Spider Eye Development Editing and Silk Fiber Engineering Using CRISPR‐Cas, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202502068
May 9
Dr. Krishna Kumari Challa
The Medical Gaslighting of Endometriosis: Why doctors ignore women's pain
May 9
Dr. Krishna Kumari Challa
Your fingers wrinkle in the same pattern every time you're in the water for too long, study shows
Do your wrinkles always form in the same pattern every time you're in the water for too long? According to new research the answer is yes.
Research found that blood vessels beneath the skin actually contract after prolonged immersion, and that's where the wrinkles come from.
And in a paper recently published in the Journal of the Mechanical Behavior of Biomedical Materials, researchers show that the topography patterns remain constant after multiple immersions.
Blood vessels don't change their position much—they move around a bit, but in relation to other blood vessels, they're pretty static. That means the wrinkles should form in the same manner, and this work proved that they do.
They also made an interesting side discovery: that wrinkles don't form in people who have median nerve damage in their fingers! got median nerve damage in my fingers.' They tested a person with median nerve damage and no wrinkles were formed on his fingers!
Rachel Laytin et al, On the repeatability of wrinkling topography patterns in the fingers of water immersed human skin, Journal of the Mechanical Behavior of Biomedical Materials (2025). DOI: 10.1016/j.jmbbm.2025.106935
May 10
Dr. Krishna Kumari Challa
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.
Part 1
May 10
Dr. Krishna Kumari Challa
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.
Part 1
May 10
Dr. Krishna Kumari Challa
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.
Part 1
Twelve weeks after infection, mice exposed to P. gingivalis already 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.
May 10
Dr. Krishna Kumari Challa
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.
May 10
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 13
Dr. Krishna Kumari Challa
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
May 14
Dr. Krishna Kumari Challa
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
May 14
Dr. Krishna Kumari Challa
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
May 14
Dr. Krishna Kumari Challa
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
May 14
Dr. Krishna Kumari Challa
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
May 15
Dr. Krishna Kumari Challa
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
May 15
Dr. Krishna Kumari Challa
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
May 15
Dr. Krishna Kumari Challa
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
May 15
Dr. Krishna Kumari Challa
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
May 17
Dr. Krishna Kumari Challa
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
May 17
Dr. Krishna Kumari Challa
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
May 17
Dr. Krishna Kumari Challa
May 17
Dr. Krishna Kumari Challa
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
May 20
Dr. Krishna Kumari Challa
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 Tregs.
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 Tregs.
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
May 20
Dr. Krishna Kumari Challa
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
May 20
Dr. Krishna Kumari Challa
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....
May 20