Super agers tend to have at least two key genetic advantages
The gene variant posing the greatest genetic risk of late-onset Alzheimer's disease (AD) is called APOE-ε4. A different variant of the same gene, APOE-ε2, is thought to confer protection against AD.
A comparatively large study reported in Alzheimer's & Dementia by researchers measures the frequency of APOE-ε4 and APOE-ε2 in so-called super agers—people ages 80 or older whose cognitive function is comparable to people 20 or 30 years younger.
Super agers were 68% less likely to harbor the gene nobody wants, APOE-ε4, compared to individuals with AD dementia in the same 80+ age group.
Most notably, super agers were 19% less likely to harbor APOE-ε4 than were cognitively normal participants in the same age group.
Super agers were also found for the first time to have higher frequency of the variant you'd want, APOE-ε2: They were 28% more likely to carry APOE-ε2 than were cognitively normal controls ages 80+, and 103% more likely to carry the variant than were participants with AD dementia aged 80 or older.
Focusing on variety and balance is the best way to reduce exposure to heavy metals in food while keeping your plate full of nutritious choices.
Mix it up. Eat a variety of grains, proteins, fruits, and vegetables—and even vary the brands you buy. Relying too heavily on one food type, source, or growing location can risk repeated exposure to an element that happens to be particularly high in that food or region. Low levels of heavy metals make their way into foods. A varied, healthy diet can limit exposure and absorption.
Choose safer seafood. Fish is one of the healthiest foods you can eat. Opt for smaller fish, which are lower on the food chain, such as salmon, canned light and skipjack tuna, sardines, pollock, or tilapia. Shellfish like scallops, clams, crab, and shrimp are good choices as well. Limit large predatory fish, like swordfish, orange roughy, and king mackerel.
Cook rice smartly. Cook rice with extra water (like pasta) that you drain off. This simple step can reduce arsenic levels (but it also lowers nutritional value). Try other grains like oats, quinoa, bulgur, or barley for variety.
Check your home. If you have older pipes, test your tap water for lead and consider a certified filter if needed. Paint in houses built before 1978 should be tested for lead. (Test kits can be purchased at home improvement stores and may be available for free through local health departments and/or water utilities.)
Refer to trusted sources. The U.S. Food and Drug Administration and Environmental Protection Agency are tasked with helping to ensure your food and water meet safety standards. If unusually high levels of any heavy metals are discovered in a particular food, the media will be alerted, and recalls will be put in place. Heavy metals are part of our environment, and small amounts do make their way into foods. But research shows that the benefits of a varied, nutrient-rich diet far outweigh the minimal risks from trace exposure.
As they roll across shadowed regions of the moon's surface, future lunar rovers could develop hazardous buildups of electric charge on their wheels.
With an interest in lunar exploration now reigniting worldwide, several space agencies are considering how the moon's surface could be explored in unprecedented detail using wheeled rovers. One challenge these vehicles will face is the buildup of 'triboelectric charge' as their wheels move across the regolith: a dry, granular, and highly insulating layer of dust and rock that blankets the moon. If allowed to accumulate, this charge could trigger discharges that threaten a rover's sensitive electronics and instruments.
Under many circumstances, charge buildup is naturally limited by the solar wind—a continuous stream of charged particles that emanate from the sun. Because this plasma is far more conductive than the regolith, it provides a pathway for excess charge to dissipate into the surrounding environment. However, this helpful effect can't always be guaranteed.
As the moon travels through the solar wind, it creates a long plasma "wake" on its night-time side, where particle densities drop dramatically. "If the plasma flux levels are reduced, charge dissipation will slow. In essence, it will become increasingly difficult to remediate charge buildups in these plasma-starved regions.
These conditions are also found inside the moon's permanently shadowed polar craters—potential harbors of frozen water and carbon dioxide that could be prime targets for upcoming missions. For rovers operating in these environments, engineers must take steps to prevent triboelectric charging from reaching problematic levels.
Using advanced simulations, researchers modeled the balance between triboelectric charging and plasma-based charge dissipation under realistic lunar conditions. Their results show that keeping a rover's speed extremely low—below about 0.2 cm per second—can prevent charge from accumulating.
If a rover moves faster than this speed limit in the given plasma environment, then the wheel tribocharging currents will exceed plasma dissipation currents and the wheel will build up charge. If the rover moves slower than this speed limit, then the plasma currents will dissipate the charge before it builds up to large levels
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The researchers also found that a rover's approach path into a crater can strongly influence its charging environment. If it enters a crater on the downwind side—facing the sun and solar wind—it can remain in a relatively dense plasma flow. If the rover enters the leeward edge of the crater—moving with the sun at its back—the rover enters a region where the local mini-wake first forms Finally, they examined how a rover's wheels should be electrically connected to its body. While isolating the wheels might seem like a way to protect onboard electronics, the simulations showed that this isolation actually limits the dissipation of charge—only worsening the problem. Instead they recommend that the rover wheel is tested to ensure it is electrically connected to the larger rover structure, ensuring that the wheel has a conductive path to the larger structure. The rover body can then be used to increase the plasma current collection to more quickly dissipate the wheel tribocharge buildup. Together, these findings highlight how space-weather effects on the moon can pose subtle but serious risks to surface operations.
W.M. Farrell et al, Rover wheel tribocharging in lunar shadowed regions: deriving a speed limit for charge accumulation, Advances in Space Research (2026). DOI: 10.1016/j.asr.2025.10.102
Scientists design artificial pain receptor that senses pain intensity and self-heals
All over the body are tiny sensors called nociceptors whose job is to spot potentially harmful stimuli and send warning signals to the brain and spinal cord, helping protect us from injury or tissue damage.
In a recent study, scientists designed a jelly-like artificial nociceptive nerve pathway built using a memristor—a tiny electronic component that controls current flow and retains the memory of how much electricity has flowed through it.
The quantized conductance (QC) phenomenon in memristors, where electricity flows through a material in discrete steps rather than a smooth stream, allowed the pain receptor to go beyond simply turning on and off in response to a stimulus. Instead, it exhibited four distinct levels that correspond to the human pain scale: no pain, mild, moderate, and severe.
The bio-inspired receptor also showed signs of self-healing in terms of repairing physical damage and fading of pain signals.
Xuanyu Shan et al, Bioinspired Artificial Nociceptor Based on Quantized Conductance Memristor With Pain Rating, Self‐Healing, and Neuromodulation Capabilities, Advanced Functional Materials (2025). DOI: 10.1002/adfm.202528900
Tumor cells steal immune mitochondria to aid lymph node spread
Researchers report that tumor cells hijack mitochondria from immune cells, reducing anti-tumor immune function and activating cGAS-STING and type I interferon signaling that promotes lymph node metastasis.
Mitochondrial transfer, the movement of mitochondria between cells, is a mode of intercellular communication that reshapes metabolism, stress responses, and cellular function across diverse physiological and pathological settings. Recruiting outside mitochondria into cancer cells can enhance oxidative phosphorylation, promote survival under metabolic stress, and influence therapy resistance.
Lymph node metastasis is a critical early step in cancer progression that can create a systemic impairment of tumor control.
Previous reports have found that T cells and macrophages can transfer mitochondria to cancer cells. The extent of mitochondrial transfer by other immune cells remains unclear, along with any connections to lymph node colonization.
In the experiments, Tumor cells acquired mitochondria from host cells across colon, breast, and melanoma models. Immune cells were identified as a donor source in bone marrow chimera experiments that restricted the reporter signal to hematopoietic cells. Draining lymph nodes carried a higher fraction of tumor cells with immune-derived mitochondria than primary tumors.
Direct physical contact supported transfer, with higher transfer under hypoxic stress and inflammatory cues. Disruption of transfer structures and knockdown of a transfer-related factor reduced transfer, paired with reduced lymph node metastasis incidence in reported mouse experiments. mtDNA polymorphism tracing added a second line of evidence that donor mitochondrial DNA could be detected in tumor material.
Immune cells that lost mitochondria showed reduced antigen-presentation and co-stimulatory machinery, with reduced activation and cytotoxic capacity reported for natural killer and CD8 T cells. Changes aligned with impaired immune surveillance in the co-culture systems described.
Researchers identify immune-to-tumor cell mitochondrial transfer as a central mechanism that facilitates lymph node colonization through two coordinated effects. Loss of mitochondria disables anti-tumor immunity by diminishing antigen presentation and impairing cytotoxic function across multiple immune lineages, while immune-derived mitochondria activate the cGAS-STING pathway in tumor cells and induce a type I interferon program that promotes immune evasion and lymph node colonization.
Targeting mitochondrial transfer or the resulting cGAS-STING signaling represents a promising strategy to restrict lymph node metastasis, a critical early step in systemic cancer progression.
Azusa Terasaki et al, Mitochondrial transfer from immune to tumor cells enables lymph node metastasis, Cell Metabolism (2026). DOI: 10.1016/j.cmet.2025.12.014
A new anti-biofilm strategy Nanopatterned surfaces with nanoscale protrusions physically disrupt bacterial cells, preventing biofilm formation through mechanical means rather than chemical agents. These surfaces, inspired by insect wings, can kill a broad range of microbes, including bacteria and fungi. Scalability challenges are being addressed with adaptable materials like metal-organic frameworks, enabling more practical applications.
Combining mechanical killing mechanisms with chemical agents or near-infrared light irradiation could enhance efficacy against diverse organisms.
Zhejian Cao et al, Mechano‐Bactericidal Surfaces Achieved by Epitaxial Growth of Metal–Organic Frameworks, Advanced Science (2025). DOI: 10.1002/advs.202505976
Human heart regrows muscle cells after heart attack, researchers discover
Until now we've thought that, because heart cells die after a heart attack, those areas of the heart were irreparably damaged, leaving the heart less able to pump blood to the body's organs.
But Pioneering research by experts has shown that heart muscle cells regrow after a heart attack, opening up the possibility of new regenerative treatments for cardiovascular disease.
This new work shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
Though increased mitosis(a process in which cells divide and reproduce) after a heart attack has been observed in the heart muscles of mice, this is the first time the phenomenon has been demonstrated in humans.
Although this new discovery of regrowing muscle cells is exciting, it isn't enough to prevent the devastating effects of a heart attack. Therefore, in time, the researchers hope to develop therapies that can amplify the heart's natural ability to produce new cells and regenerate the heart after an attack.
Robert D. Hume et al, Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction, Circulation Research (2026). DOI: 10.1161/circresaha.125.327486
Why adapting to the environment is more difficult as people age
Age-related structural changes in specific brain regions reduce adaptability to environmental changes. Older adults rely more on brain structures involved in task switching and updating information, but these structures deteriorate over time, correlating with decreased adaptive behaviour in later adulthood. Researchers characterized changes in the brain across two periods of adulthood that may correspond to changes in adaptive behaviour.
Identifying these changes may help track adaptability decline.
No clear evidence that cannabis-based medicines relieve chronic nerve pain, updated review finds
Current evidence does not support that cannabis-based medicines, including THC, CBD, or balanced THC/CBD products, provide clinically meaningful relief for chronic neuropathic pain compared to placebo. Adverse event data are uncertain, with THC products linked to increased dizziness and drowsiness. Higher-quality, longer-term studies are needed.
Cannabis-based medicines for chronic neuropathic pain in adults, Cochrane Database of Systematic Reviews (2026). DOI: 10.1002/14651858.CD012182.pub3
Scientists discover a hidden RNA 'aging clock' in human sperm
Increasing paternal age has been linked to elevated health risks for the next generation, including higher risks of obesity and stillbirth. So, what drives this increased risk?
Most research into this link focuses on how the DNA inside sperm changes with age. But sperm carries other molecules as well, including a diverse array of molecules called RNAs.
Now, new research has shown that the RNA contents of sperm go through similar shifts over time in both mice and humans, which may lead to a rapid, dramatic shift at midlife. What's more, "old RNA" seems to change cells' metabolism—potentially contributing to the health risks of having kids later in life.
It's like finding a molecular clock that ticks with age in both mice and humans, suggesting a fundamental, conserved molecular signature of sperm aging.
The researchers were only able to detect some of these changes when they looked at RNA from the sperm head alone—the part of the sperm that delivers its contents to the egg. The long tail of the sperm contains other RNA that obscured the pattern until now.
If we can understand the enzymes driving this shift, they could become actionable targets for interventions to potentially improve sperm quality in aging males.
Conserved shifts in sperm small non-coding RNA profiles during mouse and human aging, The EMBO Journal (2026). DOI: 10.1038/s44318-025-00687-8
Exposure to wildfire smoke late in pregnancy may raise autism risk in children
Analysis of over 200,000 births in Southern California indicates that exposure to wildfire smoke during the third trimester of pregnancy is associated with a 23% higher risk of autism diagnosis by age 5. The association is strongest with exposure exceeding 10 days. These findings support concerns about air pollution's impact on fetal neurological development.
Prenatal Exposure to Wildfire and Autism in Children, Environmental Science & Technology (2026). DOI: 10.1021/acs.est.5c08256
Scientists have discovered an answer to the longstanding mystery of why more than half of patients with chronic kidney disease ultimately die of cardiovascular problems: Their kidneys produce a substance that poisons the heart.
Chronic kidney disease leads to the production of circulating extracellular vesicles in the kidneys, which carry toxic miRNA that harm the heart. Blocking these vesicles in animal models improved heart function. This mechanism may enable earlier identification and targeted treatment of heart failure risk in CKD patients.
The researchers say the discovery could let doctors identify people at risk and develop new treatments to help prevent and treat heart failure for these patients.
Xisheng Li et al, Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease, Circulation (2026). DOI: 10.1161/circulationaha.125.075579
Certain antibiotics may may boost immune system Fluoroquinolone antibiotics can directly alter macrophage metabolism by stressing their mitochondria, leading to increased production of nitric oxide and enhanced bacterial clearance. This effect is specific to certain younger macrophage subsets in the lung and gut. While these antibiotics may boost immune cell function, they also carry risks such as microbiome disruption and potential tissue damage from excessive inflammation.
Alexander W Hardgrave et al, Fluoroquinolones directly drive mitochondrial hyperpolarization and modulate iNOS expression in monocyte-derived macrophage populations, Discovery Immunology (2025). DOI: 10.1093/discim/kyaf018
Cancer patients warned popular supplement may interfere with treatment
Biotin supplements, commonly used by cancer patients to address hair loss, lack strong evidence for promoting hair or nail regrowth and can interfere with lab tests, potentially leading to inaccurate results and delayed or altered treatment. Biotin may cause false readings in tests for prostate, thyroid, ovarian, and breast cancers. Minoxidil is a safer, effective alternative for hair loss.
Layna Mager et al, Biotin Supplements for Hair and Nail Regrowth: A Caution for Oncologists, JCO Oncology Practice (2025). DOI: 10.1200/op-25-00693
What the brain's shape and complexity say about a newborn's development
The neonatal period, which is defined as the first 28 days after birth, is known to be a crucial stage in the development of the human brain. During this stage, the brain is known to grow significantly in size, with billions of new connections forming between neurons and supporting basic physiological functions.
Researchers recently carried out a study aimed at further exploring how the human brain's overall shape and size as well as the dimensions of distinct regions are linked to a newborn's development and maturity. Their findings, published in Nature Neuroscience, suggest that the brain's shape is a key marker of development during the neonatal period.
They analyzed publicly available magnetic resonance imaging (MRI) data collected from almost 800 human newborns as part of the developing Human Connectome Project (dHCP). Employing a mathematical method called fractal analysis, they tried to delineate the shape of the newborns' brains.
This approach yields a geometric measure called fractal dimensionality (FD) that describes the shape of a brain region in terms of its structural complexity.
Brain shape predicted the infants' ages significantly better than brain size, say teh researchers. Moreover, brain shape captured signatures of premature birth that were not detected with brain size.
They found that the brains of infants who were related to each other, such as twins, were more similar in shape than those of unrelated infants. The shape of the brains of identical twins, who share almost 100% of genes, was found to be more similar than those of fraternal twins, who share approximately 50% of genes.
Based on this relationship, the researchers were able to predict which babies are twin siblings from their brain shapes with high accuracy (~77% overall, ~97% in identical twins), again outperforming all other studied brain measures.
These results suggest that the early-life formation of brain shape represents a fundamental maturational process in human brain development.
Stephan Krohn et al, Fractal analysis of brain shape formation predicts age and genetic similarity in human newborns, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02107-w
Maternal genetic factors may reveal why pregnancy loss is so common
Pregnancy loss in humans is common, with about 15% of recognized pregnancies resulting in miscarriage and many more conceptions being lost at early stages without people realizing it. Analysis of genetic data from nearly 140,000 IVF embryos demonstrates that common maternal genetic variants, particularly in genes involved in chromosome cohesion and recombination, contribute to individual differences in the risk of pregnancy loss due to chromosomal errors. These findings clarify molecular pathways underlying aneuploidy and suggest potential targets for future therapies.
By studying genetic data from nearly 140,000 IVF embryos, scientists have with unprecedented detail revealed why fewer than half of human conceptions survive to birth. The research uncovered the strongest evidence yet for how common genetic differences leave some individuals more vulnerable to pregnancy loss.
The vast dataset allowed the team to demonstrate robust connections between specific variations in a mother's DNA and their risk of miscarriage.
The findings shed new light on human reproduction and suggest pathways for developing treatments to lower the risk of pregnancy loss.
Most chromosome errors originate in the egg and increase in frequency with a mother's age. More mysterious is how factors beyond age, such as genetic differences, may predispose a person to produce eggs with abnormal numbers of chromosomes in the first place.
Figuring that out requires analyzing genetic data from large numbers of embryos before pregnancy loss, as well as their biological parents.
The strongest associations appear in genes that govern how chromosomes pair, recombine, and are held together during egg formation, including a gene (SMC1B) that encodes part of the ring-shaped structure that encircles and binds chromosomes, the team found. These rings are essential for accurate chromosome segregation and tend to break down as women age.
Strikingly, these same genetic variants that influence the risk of pregnancy loss are also associated with recombination, the genetic shuffling process that generates diversity when eggs and sperm are made, they found.
Female meiosis, or the cell division necessary for reproduction, begins during fetal development, when chromosomes pair and recombine. The process then pauses for decades, until ovulation and fertilization. During this long pause, problems in the machinery that keeps chromosomes together can cause them to separate too soon, leading to an abnormal chromosome count when meiosis resumes. The results demonstrate that inherited differences in these meiotic processes contribute to natural variation in risk of aneuploidy and pregnancy loss between individuals.
Small number of 'highly plastic' cancer cells drive disease progression and treatment resistance A small subset of highly plastic cancer cells, capable of shifting identity and behavior, drives tumor progression and treatment resistance. These cells, which increase in prevalence as tumors advance, exploit injury-repair programs and can survive therapies by adapting rapidly. Targeting them, for example via uPAR-directed CAR T cells, significantly impairs tumor growth and may enhance treatment efficacy.
In healthy tissues, stem cells make new cells to replace those that are lost or damaged through normal wear and tear.
Most organs maintain themselves with resident stem cells tailored to that type of tissue—alveoli or bronchial cells in the lung, skin cells, intestinal cells, and so on.
But when an injury occurs, special injury repair programs get triggered that put stem cells in an even more flexible state—"like a super stem cell." This allows the cell to expand its capabilities and produce a much wider variety of new cells.
The problem is when cancer cells borrow these programs that are normally only available to stem cells.
Indeed, it's these highly flexible—highly plastic—cell states related to injury repair that cancer hijacks. Highly plastic cells become more abundant as these tumors grow, researchers found.
These highly plastic cells aren't necessary to initiate a tumor. But they're critical to cancer's progression, the team found—including its ability to give rise to fast-growing cells, to evolve resistance to treatment, and to potentially help the cancer spread to other parts of the body.
If we kill off these plastic cells very early in the initiation of a tumor, you can basically prevent mutated cells from ever becoming cancers, say teh researchers.
What should you do with unused or expired prescription medications?
Unused or expired prescription medications should be disposed of promptly to prevent accidental ingestion, especially by children. Preferred disposal methods include take-back programs at pharmacies, police stations, or DEA events. If these are unavailable, mix medications with unpalatable substances before discarding in the trash. Some drugs, mainly opioids, may be flushed per FDA guidance. Sharps require separate disposal.
If you have unused or expired medication, the best thing is to dispose of it. Many people hang on to them, and this just creates opportunity for things to go wrong.
Scientists may have discovered a new extinct form of life
Prototaxites are something of a prehistoric mystery. They were the first giant organisms on land, towering over ancient landscapes at heights of up to 8 meters. They had smooth trunk-like pillars and no branches, leaves or flowers. And unlike trees, they had no true root system. Instead, they may have been anchored to the ground by a simple bulbous base.
Since their first fossils were discovered in the mid-19th century, scientists have argued over their place in the tree of life. Are they giant fungi, massive algae or some kind of plant? But new evidence has emerged that may help settle the matter.
According to a new study published in the journal Science Advances, Prototaxites belonged to a previously unknown, now-extinct branch of life.
The researchers studied a specimen of Prototaxites taiti recovered from the Rhynie Chert in northeastern Scotland. This paleontological site is well-known for its exceptionally well-preserved plant, fungal and animal material.
The team used lasers and 3D imaging to look inside the fossils and compared their chemical compositions with those of other fossils found in the same rock. They discovered two significant differences.
While fungi have simple networks of long, tubular structures called hyphae, the Prototaxite specimen had a much more complex internal structure. It comprised three different types of tubes and dense hubs where they branch and connect.
To study its chemical fingerprint (the chemical signature organisms leave behind based on the cells they are made of), the team used artificial intelligence. The protein chitin is often detected in fossilized fungi and insects, but it was completely missing from the Prototaxites sample. They also used artificial intelligence to see if its chemistry matched that of any living organism. It didn't.
The researchers ruled out the giant fossils being fungi or plants, and instead, they conclude that Prototaxites were members of an extinct lineage of eukaryotes (complex-celled organisms).
The findings may have finally solved the long-standing mystery about the true nature of Prototaxites. However, further analysis and fossil discoveries may well be needed before the results are considered conclusive.
Scientists solve 66 million-year-old mystery of how Earth's greenhouse age ended
A 66 million-year-old mystery behind how our planet transformed from a tropical greenhouse to the ice-capped world of today has been unraveled by scientists. Their new study has revealed that Earth's massive drop in temperature after the dinosaurs went extinct could have been caused by a large decrease in calcium levels in the ocean.
An international team of experts discovered that concentrations of calcium in the sea dropped by more than half across the last 66 million years.
The study,publishedinProceedings of the National Academy of Sciences, showed that the dramatic calcium shift may have sucked carbon dioxide—a major greenhouse gas—out of the atmosphere, driving global cooling.
Large changes in the composition of seawater chemistry may have been a key driver for climate change.
Their results show that dissolved calcium levels were twice as high at the start of the Cenozoic Era, shortly after dinosaurs roamed the planet, compared to today.
When these levels were high, the oceans worked differently, acting to store less carbon in seawater and releasing carbon dioxide into the air.
As those levels decreased, CO2was sucked out of the atmosphere, and Earth's temperature followed, dropping our climate by as much as 15 to 20 degrees Celsius.
They used fossilized remains of tiny sea creatures dug up from sediments at the seafloor to construct the most detailed record of ocean chemistry to date. The chemical composition of the fossils, called foraminifera, showed a close link between the amount of calcium in seawater and the level of carbon dioxide in the air.
Using computer-made models, the team showed that high levels of calcium change how much carbon is "fixed" by marine life, such as corals and plankton.
This effectively locked it away from the ocean and atmosphere by storing it in sediments on the seafloor.
As dissolved calcium levels decreased across millions of years, it altered how these organisms produced and buried calcium carbonate on the seafloor. The process effectively pulls carbon dioxide out of the atmosphere and locks it away.
This shift could have changed the composition of the atmosphere, effectively turning down the planet's thermostat.
David Evans et al, The major ion chemistry of seawater was closely coupled to the long-term carbon cycle during the Cenozoic, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2511781122
AI models mirror human 'us vs. them' social biases
Large language models (LLMs), the computational models underpinning the functioning of ChatGPT, Gemini and other widely used artificial intelligence (AI) platforms, can rapidly source information and generate texts tailored for specific purposes. As these models are trained on large amounts of texts written by humans, they could exhibit some human-like biases, which are inclinations to prefer specific stimuli, ideas or groups that deviate from objectivity.
One of these biases, known as the "us vs. them" bias, is the tendency of people to prefer groups they belong to, viewing other groups less favorably. This effect is well-documented in humans.
Researchers at University of Vermont's Computational Story Lab and Computational Ethics Lab recently carried out a study investigating the possibility that LLMs "absorb" the "us vs. them" bias from the texts that they are trained on, exhibiting a similar tendency to prefer some groups over others. Their paper, posted to the arXiv preprint server, suggests that many widely used models tend to express a preference for groups that are referred to favorably in training texts, including GPT-4.1, DeepSeek-3.1, Gemma-2.0, Grok-3.0 and LLaMA-3.1.
The results of this recent study highlight the tendency of AI models to pick up the biases and views expressed in the data used to train them. In their paper, the researchers introduced a strategy that could help to reduce this bias in LLMs, which they dubbed ION.
Tweaking a pattern of wound healing established millions of years ago may enable scar-free injury repair after surgery or trauma, researchers have found. If results from their study, which was conducted in mice, translate to humans, it may be possible to avoid or even treat the formation of scars anywhere on or within the body.
Scarring is more than a cosmetic problem. Scars can interfere with normal tissue function and cause chronic pain, disease and even death.
Scars on the skin's surface, while rarely fatal, are stiffer and weaker than normal skin and they lack sweat glands or hair follicles, making it difficult to compensate for temperature changes.
Surgeons have known for decades that facial wounds heal with less scarring than injuries on other parts of the body. This phenomenon makes evolutionary sense: Rapid healing of body wounds prevents death from blood loss, infection or impaired mobility, but healing of the face requires that the skin maintain its ability to function well.
The face is very important. We need to see and hear and breathe and eat. In contrast, injuries on the body must heal quickly. The resulting scar may not look or function like normal tissue, but you will likely still survive to procreate.
Exactly how this discrepancy happens has remained a mystery, although there were some clues.
The face and scalp are developmentally unique. Tissue from the neck up is derived from a type of cell in the early embryo called a neural crest cell. In the study researchers identified specific healing pathways in scar-forming cells called fibroblasts that originate from the neural crest and found that they drive a more regenerative type of healing.
Activating this pathway in even a subset of fibroblasts around small wounds on the abdomen or backs of mice caused them to heal with much less scarring—similar to untreated facial or scalp wounds.
The researchers in their experiments found that after 14 days, the wounds on the face and scalp expressed lower levels of proteins known to be involved in scar formation as compared with those on the abdomen or back of the animals. The sizes of the scars were also smaller.
The researchers then transplanted skin from the face, scalp, back and abdomen of mice onto the backs of control mice. After the transplants had engrafted, they repeated the experiment on the transplanted skin. As before, wounds in the skin transplanted from the faces of the donor mice expressed lower levels of scarring-associated proteins. They isolated fibroblasts from skin samples from the four body sites in the donor mice and injected them into the backs of control mice. They observed reduced levels of scarring-associated proteins on the recipient animals' backs injected with fibroblasts from the donor animals' faces as compared with fibroblasts from the scalp, back or abdomen. The researchers identified changes in gene expression between facial fibroblasts and those from other parts of the body and followed these clues to identify a signaling pathway involving a protein called ROBO2 that maintains facial fibroblasts in a less-fibrotic state. They also saw something interesting in the genomes of fibroblasts making ROBO2. In general, the DNA of the ROBO2-positive cells is less transcriptionally active, or less available for binding by proteins required for gene expression, These fibroblasts more closely resemble their progenitors, the neural crest cells, and they might be more able to become the many cell types required for skin regeneration." In contrast, the DNA in fibroblasts from other sites of the body allows free access to genes like collagen that are involved in the creation of scar tissue.
"It seems that, in order to scar, the cells must be able to express these pro-fibrotic genes. "And this is the default pathway for much of the body."
ROBO2 doesn't act alone. It triggers a signaling pathway that results in the inhibition of another protein called EP300 that facilitates gene expression. EP300 plays an important role in some cancers, and clinical trials of a small drug molecule that can inhibit its activity are underway. Li and his colleagues found that using this pre-existing small molecule to block EP300 activity in fibroblasts prone to scarring caused back wounds to heal like facial wounds.
Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma, say the researchers.
Chemotherapy rewires gut bacteria to curb metastasis, research reveals
Chemotherapy commonly damages the intestinal lining, a well-known side effect. But this injury does not remain confined to the gut. It reshapes nutrient availability for intestinal bacteria, forcing the microbiota to adapt.
In Nature Communications, researchers report that chemotherapy-induced damage to the intestinal lining alters nutrient availability for gut bacteria, reshaping the microbiota and increasing the production of indole-3-propionic acid (IPA), a tryptophan-derived microbial metabolite.
Rather than acting locally, IPA functions as a systemic messenger. It travels from the gut to the bone marrow, where it rewires immune cell production. Elevated IPA levels reprogram myelopoiesis, reducing the generation of immunosuppressive monocytes that facilitate immune evasion and metastatic growth.
By reshaping the gut microbiota, chemotherapy sets off a cascade of events that rewires immunity and makes the body less permissive to metastasis.
Ludivine Bersier et al, Chemotherapy-driven intestinal dysbiosis and indole-3-propionic acid rewire myelopoiesis to promote a metastasis-refractory state, Nature Communications (2025). DOI: 10.1038/s41467-025-67169-7
Cellular senescence linked to brain structure changes across lifespan
Researchers have characterized how cellular senescence—a biological process in which aging cells change how they function—is associated with human brain structure in both development and late life.
The study, published in Cell, provides new insight into how molecular signatures of cellular senescence that are present during development and aging mirror those associated with brain volume and cortical organization.
Cellular senescence is commonly defined as a state characterized by permanent cell cycle arrest in the absence of cell death, in which cells have altered function.
While cellular senescence has been implicated in aging and disease, its role in shaping human brain structure—both during development and aging—has remained unclear till now.
The research team developed a method to define senescent cells in human brain tissue and used the resource to examine how senescence-related gene expression is associated with brain structure.
Among the study's most striking findings was evidence that cellular senescence plays distinct roles in brain structure depending on cell type and stage of life. Genes associated with senescence in microglia—the primary immune cells in the brain—were linked to larger brain volumes, while senescence-related genes in excitatory neurons were associated with smaller brain volumes in the aging brain. Notably, the excitatory neuron findings were also observed early in life, providing the first evidence that senescence-related processes are at work soon after embryonic development.
The results support brain cellular senescence as an example of 'antagonistic pleiotropy'—the idea that some genes help survival or fertility early in life but cause harm later, contributing to aging and disease.
Domestication has changed the chemicals that squash flowers use to attract bees
Domestication alters the floral scent profiles of squash, resulting in lower overall levels of volatile organic compounds (VOCs) except for 1,4-dimethoxybenzene, which remains prevalent and attracts bees. Specialist squash bees detect and respond differently to VOCs from wild versus domesticated flowers, indicating that domestication changes plant–pollinator interactions.
Avehi Singh et al, Domestication Reduces Floral Volatile Richness in Squash (Cucurbitaceae: Cucurbita) But Conserves Key Compounds Critical for Pollinator Attraction, Journal of Chemical Ecology (2025). DOI: 10.1007/s10886-025-01664-5
Delayed stroke care linked to increased disability risk
Prolonged door-in-door-out (DIDO) times for transferring acute ischemic stroke patients to thrombectomy-capable centers significantly reduce the likelihood of receiving endovascular therapy and increase the risk of post-stroke disability. Only 26% of transfers met the recommended 90-minute window, with longer delays linked to worse functional outcomes and higher complication rates. Systemic improvements are needed to minimize transfer times and optimize patient recovery.
Door-in-door-out times and outcomes in patients with acute ischaemic stroke transferred for endovascular therapy in the U.S.: a retrospective cohort study, The Lancet Neurology (2026). DOI: 10.1016/S1474-4422(25)00478-8
Exhaled breath may carry clues to gut microbiome health
Exhaled breath contains volatile organic compounds produced by gut microbes, allowing noninvasive detection of gut microbiome composition. Breath analysis accurately reflected gut bacteria in both children and mice and predicted the presence of asthma-associated Eubacterium siraeum. This approach may enable rapid, noninvasive monitoring and diagnosis of gut health issues.
Viruses that infect bacteria, called phages, evolve different strategies to infect their targets on the International Space Station than they do on the ground. Researchers found that the phages took longer to infect E. coli in microgravity, and that the viruses developed microgravity-specific mutations, some of which helped them to better cling onto bacterial receptors. Understanding how phages adapt to different conditions could help researchers to optimize them for use against antibiotic-resistant bacteria on Earth.
The bacterium Enterococcus faecalis produces damaging molecules that can prevent chronic wounds such as diabetic foot sores from healing. These reactive molecules, such as hydrogen peroxide, trigger a stress response in keratinocytes, the skin cells responsible for wound healing, which effectively paralyzes them. Researchers found that treating skin cells with the antioxidant enzyme catalase can de-stress keratinocytes, which restores their healing capabilities. The team suggests that dressings infused with antioxidants could be a more effective way to treat chronic wounds than trying to kill E. faecalis with antibiotics.
Barnacle-inspired E. coli could treat IBD Escherichia coli engineered to produce biological ‘glue’ could help to heal damage in the guts of people with inflammatory bowel disease (IBD). Researchers engineered E. coli to produce ‘cement proteins’ — similar to those that barnacles use to stick onto rocks — when they come into contact with blood, and a protein that boosts wound healing. In mouse models of IBD, the team found that the bacteria could stick onto internal wounds for ten days, and after that time the mice’s guts resembled those of healthy mice.
A natural, low-calorie sugar that doesn’t cause a spike in insulin sounds too good to be true. But it really does exist!
It’s called tagatose, and it comes in very small amounts in a few fruits and dairy products.
Now, scientists have figured out how to manufacture the rare sugar at larger scales. The product is 92 percent as sweet as sucrose, and yet it doesn’t spike insulin levels.
Tagatose is mostly fermented in the gut, so only a small portion of it is actually absorbed into the bloodstream.
Unlike high-intensity artificial sweeteners, it can even be used in baked goods.
Scientists observe a 300-million-year-old brain rhythm in several animal species
Sleep is a universal biological state that allows all animals, from mammals to amphibians, fish and even insects, to restore their energy and consolidate knowledge that can contribute to their survival. Neuroscientists and zoologists have been investigating the biological underpinnings of sleep and its vital functions for centuries, more recently by measuring the brain activity of animals or people while they are asleep.
Recorded electrical signals that nerve cells produce while they are communicating with each other, also known as brain rhythms, have provided valuable insight into what happens during sleep. One of these rhythms, the so-called infraslow rhythm, had so far been primarily observed in mammals and was linked to a stage of sleep known as non-rapid eye movement (NREM) sleep.
Researchers recently recorded the brain activity of a wider range of animals and found that this ancient rhythm is common across several species, including reptiles, birds, rodents and humans. Their most recent paper, published in Nature Neuroscience, reports the observation of the infraslow brain rhythm in seven different lizard species.
In addition to brain activity, they also recorded physiological signals such as eye movements, heart rate, breathing rate, and muscle tone.
The large dataset compiled by the researchers over the past decade or so led to an important and interesting discovery. Specifically, the team found that reptiles, mammals, and birds share a common brain rhythm, the so-called infraslow rhythm. This finding suggests the presence of an ancestral mechanism that dates back at least to 300 million years ago, when the earliest known ancestor of the species examined lived.
This rhythm involves not only brain activity but also physiological processes and peripheral vascularization, indicating that it is a global, organism-wide rhythm.
The infraslow rhythm closely resembles a rhythm previously described in mammals during non-REM (NREM) sleep. In mammals, this rhythm has been proposed to play a role in brain 'cleaning' processes by facilitating the elimination of metabolic waste through cerebrospinal fluid flow. Additionally, because this rhythm is associated with fluctuations in vigilance, it may also represent an adaptive mechanism that allows periodic monitoring of the environment during sleep, potentially reducing the risk of predation.
Antoine Bergel et al, Sleep-dependent infraslow rhythms are evolutionarily conserved across reptiles and mammals, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02159-y.
An ultra-thin, wireless retinal implant using a zinc oxide nanowire and silver–bismuth–sulfide nanocrystal assembly enables safe, precise electrical stimulation of retinal neurons via near-infrared light at low intensities. The device shows strong biocompatibility, stability, and negligible heating, making it promising for vision restoration and broader neuromodulation applications.
Tarik S. Kaya et al, Photovoltaic nanoassembly of nanowire arrays sensitized with colloidal nanocrystals for near-infrared retina photostimulation, Science Advances (2026). DOI: 10.1126/sciadv.aea7001
Halley's Comet wrongly named: 11th-century English monk predates British astronomer Evidence indicates that the 11th-century monk Eilmer of Malmesbury recognized the periodicity of Halley's Comet centuries before Edmond Halley. Eilmer linked two appearances of the comet, as described in medieval chronicles, suggesting the comet’s cycle was understood earlier than previously thought. This challenges the appropriateness of the comet’s current name.
Beyond the fear: Scientists test the health impacts of 5G From street-level measurements to long-term health studies, researchers are building a clearer picture of the impact of everyday exposure to 5G signals on human health.
Measurements across multiple European countries indicate that everyday exposure to 5G radiofrequency electromagnetic fields remains well below international safety limits. Short-term laboratory studies found no measurable effects on heart function, stress, skin temperature, or brain activity in healthy adults exposed to 3.5 GHz 5G signals. Ongoing research is examining long-term health and behavioural impacts. More than 800 measurements were taken across urban and rural locations in eight EU countries, plus Switzerland and the UK. The team looked at scenarios from phones in flight mode to data-intensive activities, such as sharing attachments or watching livestreamed video.
The results show that exposure to RF-EMF in everyday environments remains well below international safety limits in all settings measured.
These limits, set by independent scientific bodies, define the maximum exposure levels considered safe for the general public and include large safety margins.
To investigate whether 5G signals have any immediate effects on the body, researchers in France have carried out the first coordinated human laboratory studies focusing on a key 5G frequency band: 3.5 gigahertz.
At INERIS, the French National Institute for Industrial Environment and Risks near Paris, 31 healthy volunteers were exposed to 5G signals for 26 minutes under controlled conditions designed to reflect real-world environmental exposure. They observed no measurable impact on heart function, stress levels, skin temperature or brain activity in healthy young adults. However, the researchers stress that the phone doesn't only bring radio frequency electromagnetic fields exposure. It also brings screen light exposure, mental arousal or device dependency.
Dietary choices can influence stomach cancer risk. Consuming more fruits, vegetables, and whole foods while reducing processed foods, sugar, salt, and inflammatory foods may lower risk. Maintaining a healthy weight, regular exercise, avoiding smoking and excess alcohol, and appropriate cancer screening further support prevention. Genetics remain a major risk factor. Eating fewer processed and preserved foods, which are generally high in sugar and salt and potential nitrites or nitrates is one advice all teh experts give.
Aim to eat more fruits and vegetables. The antioxidant compounds in produce can provide extra protection against diseases like stomach cancer. When meal planning, try to ensure that half your plate is filled with vegetables.
When possible, follow a Mediterranean diet, which emphasizes whole, plant-based foods and healthy fats. Choose high-quality proteins like lean meat, fish and legumes. Avoid foods known to cause inflammation and eat fewer starches, including potatoes and pasta.
Eating smaller meal portions throughout the day—such as four to six smaller meals throughout the day—rather than sticking to three large meals. Compared to eating a big meal, eating smaller meals causes less stomach stretching and stress on your body and allows for smaller insulin responses.
Exercise has a positive effect on reducing cancer risk.
Obesity—especially excess fat around the midsection—can increase the risk of cancer. This type of fat, called visceral fat, can secrete hormones that increase your risk of cancer.
In addition to weight gain, pay attention to unexplained weight loss. Unexplained weight loss can be the first sign of cancer.
Other things to avoid include smoking and alcohol—particularly beer, which has been shown to increase stomach cancer risk.
Are llamas big pharma's secret weapon to find new drugs?
Llama-derived nanobodies, small and easily engineered antibody fragments, are being explored as therapeutic agents for diseases such as cancer, autoimmune disorders, and nerve pain. These nanobodies can access targets inaccessible to conventional antibodies and may cross the blood-brain barrier. While some drugs have reached the market, broader clinical success and commercial impact remain under development.
Scientists have discovered the potential of the animals' antibodies to thwart multiple diseases, and now drug developers are collectively plowing billions of dollars into a field that may yield a fresh generation of life-changing medicines. The targets include some hard-to-treat conditions like cancer, nerve pain and a chronic skin ailment.
The immune system of all mammals produces antibodies to thwart viral and bacterial attacks. Those made by llamas and other members of the camelid family can squeeze into tighter spots and better penetrate tissue than human ones, because they're smaller and simpler. Some have been reported to cross the blood-brain barrier, eliciting hope for neurological diseases.
It's the molecular "deal" ice strikes with everything it touches. Unlike most solids, ice refuses to act like a rigid crystal. Instead, it behaves as a self-made lubricant—especially as temperatures hover near freezing.
Ice has an unusual property: it can melt when you apply pressure to it, whereas most materials behave the other way around—pressure usually makes liquids become solid. For a long time, people thought pressure caused slipperiness. But pressure-induced melting only happens in a very narrow temperature range, while ice remains slippery well outside those limits.
Others suggest friction from sliding—think rubbing your hands in the cold to stay warm or a shoe making contact with ice—heated the ice enough to create a melt layer. But that's sort of a chicken-and-egg problem: generating enough heat requires some extended sliding with high friction—ice is slippery without having to slide hardly at all.
Eventually, researchers realized that ice has another funny property: its surface can pre-melt, meaning it naturally has a thin layer of water on top of it, well below the melting temperature. The layer gets thicker as the temperature gets closer to the melting temperature.
However, this idea—based on ice being self-lubricated—doesn't explain why some materials have lower friction against ice than others; if the water layer is always there, everything should be equally slippery. It's an oversimplification, but that's the basic argument. Recently, researchers in Germany used simulations to show that when something touches ice, the water molecules at the surface rearrange from an ordered crystal into a disordered, amorphous structure. This isn't caused by pressure or friction, but by microscopic electrical charges.
Water molecules have positive and negative ends, and when they touch another surface, they react to the atoms in that material. They believe this electrical "push and pull" disrupts the ice's rigid structure, creating that slippery, disordered layer, which would explain why ice is slippery across different temperatures and why some materials slide on it better than others.
But in short, we don't yet know for sure. As many have observed, despite the commonality of water and ice, their physical properties are remarkably unique.
World not ready for rise in extreme heat, scientists say
By 2050, nearly 3.8 billion people could be exposed to extreme heat, with the greatest impacts in tropical and developing regions lacking adequate cooling infrastructure. Even moderate temperature increases will significantly affect cooler countries unaccustomed to heat. Rising demand for cooling will strain energy systems, highlighting an urgent need for adaptation measures.
Bacteria in the human gut can directly deliver proteins into human cells, actively shaping immune responses. Gut bacteria can inject proteins directly into human cells using type III secretion systems, previously thought unique to pathogens. These proteins interact with human immune and metabolic pathways, modulating immune responses such as NF-κB and cytokine signaling. Genes for these effectors are more common in Crohn’s disease, linking this mechanism to chronic intestinal inflammation.
Researchers have discovered this previously unknown mechanism of communication between gut bacteria and human cells. The findings reveal a new way in which the gut microbiome can influence the human body and may help explain how changes in gut bacteria contribute to inflammatory diseases such as Crohn's disease.
Although the human gut microbiome has long been linked to immune, metabolic, and inflammatory disorders, most evidence is correlative, and the molecular mechanisms behind these connections remain largely unexplored.
The new study shows that many harmless, everyday gut bacteria possess type III secretion systems—microscopic, syringe-like structures that can inject bacterial proteins directly into human cells. Until now, these systems were thought to exist only in pathogenic bacteria such as Salmonella.
It shows that these non-pathogenic bacteria are not just passive residents but can actively manipulate human cells by injecting their proteins into our cells
To understand what these bacterial proteins do in human cells, the researchers mapped more than a thousand interactions between bacterial effector proteins and human proteins, creating a large-scale interaction network. Their analyses showed that bacterial proteins preferentially target human pathways involved in immune regulation and metabolism.
Further laboratory experiments confirmed that these proteins can modulate key immune signaling pathways, including NF-κB and cytokine responses. Cytokines are signaling molecules that help coordinate the immune system and prevent excessive reactions that can lead to autoimmune diseases. For example, inhibiting the activity of the cytokine tumor necrosis factor (TNF) is a widely used treatment for Crohn's disease, an autoimmune disease of the gut.
The researchers also found that genes encoding these bacterial effector proteins are enriched in the gut microbiomes of patients with Crohn's disease. This suggests that direct protein delivery from gut bacteria to human cells may contribute to chronic intestinal inflammation, providing a potential mechanistic explanation for previously observed microbiome–disease links.
Cancer tumors may protect against Alzheimer's by cleaning out protein clumps
Tumor-secreted Cystatin-C (Cyst-C) crosses the blood-brain barrier, binds amyloid-beta oligomers and the TREM2 receptor on microglia, and activates microglial clearance of amyloid plaques in Alzheimer's mouse models. This process reduces plaque burden and improves cognitive performance, suggesting a potential therapeutic approach for Alzheimer's disease by targeting existing plaques.
Previously unknown bacterial component in kidney stone formation discovered
In an unexpected finding, a research team has discovered that bacteria are present inside the most common type of kidney stone, revealing a previously unrecognized component involved in their formation. Bacteria have been identified within calcium oxalate kidney stones, indicating a previously unrecognized microbial role in their formation. This challenges the view that these stones arise solely from chemical and physical processes and suggests that targeting bacterial biofilms could offer new prevention and treatment strategies for kidney stone disease.
The findings, to be published in the journal Proceedings of the National Academy of Sciences, point to a possible therapeutic target that could be used for prevention and treatment for the millions of people who are affected by the frequently painful condition.
This breakthrough challenges the long-held assumption that these stones develop solely through chemical and physical processes, and instead shows that bacteria can reside inside stones and may actively contribute to their formation.
Kidney stones are composed of clumps of small crystals. Their prevalence has risen globally in recent years, so that today about 1 in 11 people will get them in their lifetime. Risk factors include family history, metabolic syndrome, and low fluid intake. The stones start forming when crystals grow in urine and become large enough that they can't be washed out with normal urine flow.
There are several subsets of kidney stones and while one rare stone type is known to contain bacteria, by far the most common stone is calcium oxalate (CaOx), comprising almost 80% of kidney stone cases, which have not been previously known to contain bacteria. While examining data from electron and fluorescence microscopy, the researchers unexpectedly detected live bacteria as well as layers, or biofilms, of bacteria integrated into the crystals.
Researchers found a new mechanism of stone formation that may help to explain why these stones are so common.
These results may also help to explain the connections between recurrent urinary tract infections and recurrent kidney stone formation, and provide insights on potential future treatment for these conditions. The findings suggest that bacteria could also be involved in other kidney stone types.
The study focused on calcium-based stones. How other less common stones form is still in question. More studies are needed to fully understand how bacteria and calcium-based kidney stones interact, the researchers conclude.
Wong, Gerard C. L. et al, Intercalated bacterial biofilms are intrinsic internal components of calcium-based kidney stones, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2517066123. doi.org/10.1073/pnas.2517066123
Inflammation gives mutated blood stem cells an edge in cancer development
Inflammation promotes the expansion of blood stem cells with TP53 mutations, increasing the risk of blood cancers such as leukemia in older individuals. Activation of the NLRP1 inflammasome and persistent inflammatory signaling give mutant cells a survival advantage. Blocking inflammatory signals like IL-1B may reduce this risk and offer a potential preventive strategy.
Sisi Chen et al, Mutant p53 promotes clonal hematopoiesis through generating a chronic inflammatory microenvironment, Journal of Clinical Investigation (2025). DOI: 10.1172/jci184285
Dr. Krishna Kumari Challa
Super agers tend to have at least two key genetic advantages
The gene variant posing the greatest genetic risk of late-onset Alzheimer's disease (AD) is called APOE-ε4. A different variant of the same gene, APOE-ε2, is thought to confer protection against AD.
A comparatively large study reported in Alzheimer's & Dementia by researchers measures the frequency of APOE-ε4 and APOE-ε2 in so-called super agers—people ages 80 or older whose cognitive function is comparable to people 20 or 30 years younger.
Super agers were 68% less likely to harbor the gene nobody wants, APOE-ε4, compared to individuals with AD dementia in the same 80+ age group.
Most notably, super agers were 19% less likely to harbor APOE-ε4 than were cognitively normal participants in the same age group.
Super agers were also found for the first time to have higher frequency of the variant you'd want, APOE-ε2: They were 28% more likely to carry APOE-ε2 than were cognitively normal controls ages 80+, and 103% more likely to carry the variant than were participants with AD dementia aged 80 or older.
Evaluating the association of APOE genotype and cognitive resilience in SuperAgers, Alzheimer's & Dementia (2026). DOI: 10.1002/alz.71024. alz-journals.onlinelibrary.wil … oi/10.1002/alz.71024
Jan 17
Dr. Krishna Kumari Challa
Focusing on variety and balance is the best way to reduce exposure to heavy metals in food while keeping your plate full of nutritious choices.
Mix it up. Eat a variety of grains, proteins, fruits, and vegetables—and even vary the brands you buy. Relying too heavily on one food type, source, or growing location can risk repeated exposure to an element that happens to be particularly high in that food or region. Low levels of heavy metals make their way into foods. A varied, healthy diet can limit exposure and absorption.
Choose safer seafood. Fish is one of the healthiest foods you can eat. Opt for smaller fish, which are lower on the food chain, such as salmon, canned light and skipjack tuna, sardines, pollock, or tilapia. Shellfish like scallops, clams, crab, and shrimp are good choices as well. Limit large predatory fish, like swordfish, orange roughy, and king mackerel.
Cook rice smartly. Cook rice with extra water (like pasta) that you drain off. This simple step can reduce arsenic levels (but it also lowers nutritional value). Try other grains like oats, quinoa, bulgur, or barley for variety.
Check your home. If you have older pipes, test your tap water for lead and consider a certified filter if needed. Paint in houses built before 1978 should be tested for lead. (Test kits can be purchased at home improvement stores and may be available for free through local health departments and/or water utilities.)
Refer to trusted sources. The U.S. Food and Drug Administration and Environmental Protection Agency are tasked with helping to ensure your food and water meet safety standards. If unusually high levels of any heavy metals are discovered in a particular food, the media will be alerted, and recalls will be put in place.
Heavy metals are part of our environment, and small amounts do make their way into foods. But research shows that the benefits of a varied, nutrient-rich diet far outweigh the minimal risks from trace exposure.
What to Know About Heavy Metals in Food | Tufts Now
Jan 17
Dr. Krishna Kumari Challa
This a the first cow ever documented using a tool
Jan 20
Dr. Krishna Kumari Challa
Charge buildup in a lunar rover
As they roll across shadowed regions of the moon's surface, future lunar rovers could develop hazardous buildups of electric charge on their wheels.
With an interest in lunar exploration now reigniting worldwide, several space agencies are considering how the moon's surface could be explored in unprecedented detail using wheeled rovers. One challenge these vehicles will face is the buildup of 'triboelectric charge' as their wheels move across the regolith: a dry, granular, and highly insulating layer of dust and rock that blankets the moon. If allowed to accumulate, this charge could trigger discharges that threaten a rover's sensitive electronics and instruments.
As the moon travels through the solar wind, it creates a long plasma "wake" on its night-time side, where particle densities drop dramatically. "If the plasma flux levels are reduced, charge dissipation will slow. In essence, it will become increasingly difficult to remediate charge buildups in these plasma-starved regions.Under many circumstances, charge buildup is naturally limited by the solar wind—a continuous stream of charged particles that emanate from the sun. Because this plasma is far more conductive than the regolith, it provides a pathway for excess charge to dissipate into the surrounding environment. However, this helpful effect can't always be guaranteed.
These conditions are also found inside the moon's permanently shadowed polar craters—potential harbors of frozen water and carbon dioxide that could be prime targets for upcoming missions. For rovers operating in these environments, engineers must take steps to prevent triboelectric charging from reaching problematic levels.
Using advanced simulations, researchers modeled the balance between triboelectric charging and plasma-based charge dissipation under realistic lunar conditions. Their results show that keeping a rover's speed extremely low—below about 0.2 cm per second—can prevent charge from accumulating.
If a rover moves faster than this speed limit in the given plasma environment, then the wheel tribocharging currents will exceed plasma dissipation currents and the wheel will build up charge. If the rover moves slower than this speed limit, then the plasma currents will dissipate the charge before it builds up to large levels
Part 1
Jan 20
Dr. Krishna Kumari Challa
The researchers also found that a rover's approach path into a crater can strongly influence its charging environment. If it enters a crater on the downwind side—facing the sun and solar wind—it can remain in a relatively dense plasma flow.
If the rover enters the leeward edge of the crater—moving with the sun at its back—the rover enters a region where the local mini-wake first forms
Finally, they examined how a rover's wheels should be electrically connected to its body. While isolating the wheels might seem like a way to protect onboard electronics, the simulations showed that this isolation actually limits the dissipation of charge—only worsening the problem.
Instead they recommend that the rover wheel is tested to ensure it is electrically connected to the larger rover structure, ensuring that the wheel has a conductive path to the larger structure. The rover body can then be used to increase the plasma current collection to more quickly dissipate the wheel tribocharge buildup.
Together, these findings highlight how space-weather effects on the moon can pose subtle but serious risks to surface operations.
W.M. Farrell et al, Rover wheel tribocharging in lunar shadowed regions: deriving a speed limit for charge accumulation, Advances in Space Research (2026). DOI: 10.1016/j.asr.2025.10.102
Part 2**
Jan 20
Dr. Krishna Kumari Challa
Scientists design artificial pain receptor that senses pain intensity and self-heals
All over the body are tiny sensors called nociceptors whose job is to spot potentially harmful stimuli and send warning signals to the brain and spinal cord, helping protect us from injury or tissue damage.
In a recent study, scientists designed a jelly-like artificial nociceptive nerve pathway built using a memristor—a tiny electronic component that controls current flow and retains the memory of how much electricity has flowed through it.
The quantized conductance (QC) phenomenon in memristors, where electricity flows through a material in discrete steps rather than a smooth stream, allowed the pain receptor to go beyond simply turning on and off in response to a stimulus. Instead, it exhibited four distinct levels that correspond to the human pain scale: no pain, mild, moderate, and severe.
The bio-inspired receptor also showed signs of self-healing in terms of repairing physical damage and fading of pain signals.
Xuanyu Shan et al, Bioinspired Artificial Nociceptor Based on Quantized Conductance Memristor With Pain Rating, Self‐Healing, and Neuromodulation Capabilities, Advanced Functional Materials (2025). DOI: 10.1002/adfm.202528900
Jan 20
Dr. Krishna Kumari Challa
Tumor cells steal immune mitochondria to aid lymph node spread
Researchers report that tumor cells hijack mitochondria from immune cells, reducing anti-tumor immune function and activating cGAS-STING and type I interferon signaling that promotes lymph node metastasis.
Mitochondrial transfer, the movement of mitochondria between cells, is a mode of intercellular communication that reshapes metabolism, stress responses, and cellular function across diverse physiological and pathological settings. Recruiting outside mitochondria into cancer cells can enhance oxidative phosphorylation, promote survival under metabolic stress, and influence therapy resistance.
Lymph node metastasis is a critical early step in cancer progression that can create a systemic impairment of tumor control.
Previous reports have found that T cells and macrophages can transfer mitochondria to cancer cells. The extent of mitochondrial transfer by other immune cells remains unclear, along with any connections to lymph node colonization.
In the experiments, Tumor cells acquired mitochondria from host cells across colon, breast, and melanoma models. Immune cells were identified as a donor source in bone marrow chimera experiments that restricted the reporter signal to hematopoietic cells. Draining lymph nodes carried a higher fraction of tumor cells with immune-derived mitochondria than primary tumors.
Direct physical contact supported transfer, with higher transfer under hypoxic stress and inflammatory cues. Disruption of transfer structures and knockdown of a transfer-related factor reduced transfer, paired with reduced lymph node metastasis incidence in reported mouse experiments. mtDNA polymorphism tracing added a second line of evidence that donor mitochondrial DNA could be detected in tumor material.
Immune cells that lost mitochondria showed reduced antigen-presentation and co-stimulatory machinery, with reduced activation and cytotoxic capacity reported for natural killer and CD8 T cells. Changes aligned with impaired immune surveillance in the co-culture systems described.
Researchers identify immune-to-tumor cell mitochondrial transfer as a central mechanism that facilitates lymph node colonization through two coordinated effects. Loss of mitochondria disables anti-tumor immunity by diminishing antigen presentation and impairing cytotoxic function across multiple immune lineages, while immune-derived mitochondria activate the cGAS-STING pathway in tumor cells and induce a type I interferon program that promotes immune evasion and lymph node colonization.
Targeting mitochondrial transfer or the resulting cGAS-STING signaling represents a promising strategy to restrict lymph node metastasis, a critical early step in systemic cancer progression.
Azusa Terasaki et al, Mitochondrial transfer from immune to tumor cells enables lymph node metastasis, Cell Metabolism (2026). DOI: 10.1016/j.cmet.2025.12.014
Jan 20
Dr. Krishna Kumari Challa
A new anti-biofilm strategy
Combining mechanical killing mechanisms with chemical agents or near-infrared light irradiation could enhance efficacy against diverse organisms.Nanopatterned surfaces with nanoscale protrusions physically disrupt bacterial cells, preventing biofilm formation through mechanical means rather than chemical agents. These surfaces, inspired by insect wings, can kill a broad range of microbes, including bacteria and fungi. Scalability challenges are being addressed with adaptable materials like metal-organic frameworks, enabling more practical applications.
https://pubmed.ncbi.nlm.nih.gov/22674670/
Zhejian Cao et al, Mechano‐Bactericidal Surfaces Achieved by Epitaxial Growth of Metal–Organic Frameworks, Advanced Science (2025). DOI: 10.1002/advs.202505976
Jan 20
Dr. Krishna Kumari Challa
Human heart regrows muscle cells after heart attack, researchers discover
Until now we've thought that, because heart cells die after a heart attack, those areas of the heart were irreparably damaged, leaving the heart less able to pump blood to the body's organs.
But Pioneering research by experts has shown that heart muscle cells regrow after a heart attack, opening up the possibility of new regenerative treatments for cardiovascular disease.
This new work shows that while the heart is left scarred after a heart attack, it produces new muscle cells, which opens up new possibilities.
Though increased mitosis(a process in which cells divide and reproduce) after a heart attack has been observed in the heart muscles of mice, this is the first time the phenomenon has been demonstrated in humans.
Although this new discovery of regrowing muscle cells is exciting, it isn't enough to prevent the devastating effects of a heart attack. Therefore, in time, the researchers hope to develop therapies that can amplify the heart's natural ability to produce new cells and regenerate the heart after an attack.
Robert D. Hume et al, Human Hearts Intrinsically Increase Cardiomyocyte Mitosis After Myocardial Infarction, Circulation Research (2026). DOI: 10.1161/circresaha.125.327486
Jan 20
Dr. Krishna Kumari Challa
Why adapting to the environment is more difficult as people age
Age-related structural changes in specific brain regions reduce adaptability to environmental changes. Older adults rely more on brain structures involved in task switching and updating information, but these structures deteriorate over time, correlating with decreased adaptive behaviour in later adulthood.
Researchers characterized changes in the brain across two periods of adulthood that may correspond to changes in adaptive behaviour.
Identifying these changes may help track adaptability decline.
eNeuro (2026). DOI: 10.1523/ENEURO.0179-25.2025
Jan 20
Dr. Krishna Kumari Challa
No clear evidence that cannabis-based medicines relieve chronic nerve pain, updated review finds
Current evidence does not support that cannabis-based medicines, including THC, CBD, or balanced THC/CBD products, provide clinically meaningful relief for chronic neuropathic pain compared to placebo. Adverse event data are uncertain, with THC products linked to increased dizziness and drowsiness. Higher-quality, longer-term studies are needed.
Cannabis-based medicines for chronic neuropathic pain in adults, Cochrane Database of Systematic Reviews (2026). DOI: 10.1002/14651858.CD012182.pub3
Jan 20
Dr. Krishna Kumari Challa
Scientists discover a hidden RNA 'aging clock' in human sperm
Increasing paternal age has been linked to elevated health risks for the next generation, including higher risks of obesity and stillbirth. So, what drives this increased risk?
Most research into this link focuses on how the DNA inside sperm changes with age. But sperm carries other molecules as well, including a diverse array of molecules called RNAs.
Now, new research has shown that the RNA contents of sperm go through similar shifts over time in both mice and humans, which may lead to a rapid, dramatic shift at midlife. What's more, "old RNA" seems to change cells' metabolism—potentially contributing to the health risks of having kids later in life.
It's like finding a molecular clock that ticks with age in both mice and humans, suggesting a fundamental, conserved molecular signature of sperm aging.
The researchers were only able to detect some of these changes when they looked at RNA from the sperm head alone—the part of the sperm that delivers its contents to the egg. The long tail of the sperm contains other RNA that obscured the pattern until now.
If we can understand the enzymes driving this shift, they could become actionable targets for interventions to potentially improve sperm quality in aging males.
Conserved shifts in sperm small non-coding RNA profiles during mouse and human aging, The EMBO Journal (2026). DOI: 10.1038/s44318-025-00687-8
Jan 21
Dr. Krishna Kumari Challa
Exposure to wildfire smoke late in pregnancy may raise autism risk in children
Analysis of over 200,000 births in Southern California indicates that exposure to wildfire smoke during the third trimester of pregnancy is associated with a 23% higher risk of autism diagnosis by age 5. The association is strongest with exposure exceeding 10 days. These findings support concerns about air pollution's impact on fetal neurological development.
Prenatal Exposure to Wildfire and Autism in Children, Environmental Science & Technology (2026). DOI: 10.1021/acs.est.5c08256
Jan 21
Dr. Krishna Kumari Challa
Chronic kidney disease poisons patients' hearts, scientists discover
Scientists have discovered an answer to the longstanding mystery of why more than half of patients with chronic kidney disease ultimately die of cardiovascular problems: Their kidneys produce a substance that poisons the heart.
Chronic kidney disease leads to the production of circulating extracellular vesicles in the kidneys, which carry toxic miRNA that harm the heart. Blocking these vesicles in animal models improved heart function. This mechanism may enable earlier identification and targeted treatment of heart failure risk in CKD patients.
The researchers say the discovery could let doctors identify people at risk and develop new treatments to help prevent and treat heart failure for these patients.
Xisheng Li et al, Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease, Circulation (2026). DOI: 10.1161/circulationaha.125.075579
Jan 21
Dr. Krishna Kumari Challa
Certain antibiotics may may boost immune system
Fluoroquinolone antibiotics can directly alter macrophage metabolism by stressing their mitochondria, leading to increased production of nitric oxide and enhanced bacterial clearance. This effect is specific to certain younger macrophage subsets in the lung and gut. While these antibiotics may boost immune cell function, they also carry risks such as microbiome disruption and potential tissue damage from excessive inflammation.
Alexander W Hardgrave et al, Fluoroquinolones directly drive mitochondrial hyperpolarization and modulate iNOS expression in monocyte-derived macrophage populations, Discovery Immunology (2025). DOI: 10.1093/discim/kyaf018
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Jan 21
Dr. Krishna Kumari Challa
Cancer patients warned popular supplement may interfere with treatment
Biotin supplements, commonly used by cancer patients to address hair loss, lack strong evidence for promoting hair or nail regrowth and can interfere with lab tests, potentially leading to inaccurate results and delayed or altered treatment. Biotin may cause false readings in tests for prostate, thyroid, ovarian, and breast cancers. Minoxidil is a safer, effective alternative for hair loss.
Layna Mager et al, Biotin Supplements for Hair and Nail Regrowth: A Caution for Oncologists, JCO Oncology Practice (2025). DOI: 10.1200/op-25-00693
Cancer patients warned popular supplement may interfere with treatment
Jan 21
Dr. Krishna Kumari Challa
What the brain's shape and complexity say about a newborn's development
The neonatal period, which is defined as the first 28 days after birth, is known to be a crucial stage in the development of the human brain. During this stage, the brain is known to grow significantly in size, with billions of new connections forming between neurons and supporting basic physiological functions.
Researchers recently carried out a study aimed at further exploring how the human brain's overall shape and size as well as the dimensions of distinct regions are linked to a newborn's development and maturity. Their findings, published in Nature Neuroscience, suggest that the brain's shape is a key marker of development during the neonatal period.
They analyzed publicly available magnetic resonance imaging (MRI) data collected from almost 800 human newborns as part of the developing Human Connectome Project (dHCP). Employing a mathematical method called fractal analysis, they tried to delineate the shape of the newborns' brains.
This approach yields a geometric measure called fractal dimensionality (FD) that describes the shape of a brain region in terms of its structural complexity.
Brain shape predicted the infants' ages significantly better than brain size, say teh researchers. Moreover, brain shape captured signatures of premature birth that were not detected with brain size.
They found that the brains of infants who were related to each other, such as twins, were more similar in shape than those of unrelated infants. The shape of the brains of identical twins, who share almost 100% of genes, was found to be more similar than those of fraternal twins, who share approximately 50% of genes.
Based on this relationship, the researchers were able to predict which babies are twin siblings from their brain shapes with high accuracy (~77% overall, ~97% in identical twins), again outperforming all other studied brain measures.
These results suggest that the early-life formation of brain shape represents a fundamental maturational process in human brain development.
Stephan Krohn et al, Fractal analysis of brain shape formation predicts age and genetic similarity in human newborns, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02107-w
Jan 22
Dr. Krishna Kumari Challa
Maternal genetic factors may reveal why pregnancy loss is so common
Pregnancy loss in humans is common, with about 15% of recognized pregnancies resulting in miscarriage and many more conceptions being lost at early stages without people realizing it.
Analysis of genetic data from nearly 140,000 IVF embryos demonstrates that common maternal genetic variants, particularly in genes involved in chromosome cohesion and recombination, contribute to individual differences in the risk of pregnancy loss due to chromosomal errors. These findings clarify molecular pathways underlying aneuploidy and suggest potential targets for future therapies.
By studying genetic data from nearly 140,000 IVF embryos, scientists have with unprecedented detail revealed why fewer than half of human conceptions survive to birth. The research uncovered the strongest evidence yet for how common genetic differences leave some individuals more vulnerable to pregnancy loss.
The vast dataset allowed the team to demonstrate robust connections between specific variations in a mother's DNA and their risk of miscarriage.
The findings shed new light on human reproduction and suggest pathways for developing treatments to lower the risk of pregnancy loss.
Most chromosome errors originate in the egg and increase in frequency with a mother's age. More mysterious is how factors beyond age, such as genetic differences, may predispose a person to produce eggs with abnormal numbers of chromosomes in the first place.
Figuring that out requires analyzing genetic data from large numbers of embryos before pregnancy loss, as well as their biological parents.
The strongest associations appear in genes that govern how chromosomes pair, recombine, and are held together during egg formation, including a gene (SMC1B) that encodes part of the ring-shaped structure that encircles and binds chromosomes, the team found. These rings are essential for accurate chromosome segregation and tend to break down as women age.
Part 1
Jan 22
Dr. Krishna Kumari Challa
Strikingly, these same genetic variants that influence the risk of pregnancy loss are also associated with recombination, the genetic shuffling process that generates diversity when eggs and sperm are made, they found.
Female meiosis, or the cell division necessary for reproduction, begins during fetal development, when chromosomes pair and recombine. The process then pauses for decades, until ovulation and fertilization. During this long pause, problems in the machinery that keeps chromosomes together can cause them to separate too soon, leading to an abnormal chromosome count when meiosis resumes.
The results demonstrate that inherited differences in these meiotic processes contribute to natural variation in risk of aneuploidy and pregnancy loss between individuals.
Rajiv McCoy, Common variation in meiosis genes shapes human recombination and aneuploidy, Nature (2026). DOI: 10.1038/s41586-025-09964-2. www.nature.com/articles/s41586-025-09964-2
Part 2
Jan 22
Dr. Krishna Kumari Challa
Small number of 'highly plastic' cancer cells drive disease progression and treatment resistance
A small subset of highly plastic cancer cells, capable of shifting identity and behavior, drives tumor progression and treatment resistance. These cells, which increase in prevalence as tumors advance, exploit injury-repair programs and can survive therapies by adapting rapidly. Targeting them, for example via uPAR-directed CAR T cells, significantly impairs tumor growth and may enhance treatment efficacy.
In healthy tissues, stem cells make new cells to replace those that are lost or damaged through normal wear and tear.
Most organs maintain themselves with resident stem cells tailored to that type of tissue—alveoli or bronchial cells in the lung, skin cells, intestinal cells, and so on.
But when an injury occurs, special injury repair programs get triggered that put stem cells in an even more flexible state—"like a super stem cell." This allows the cell to expand its capabilities and produce a much wider variety of new cells.
The problem is when cancer cells borrow these programs that are normally only available to stem cells.
Indeed, it's these highly flexible—highly plastic—cell states related to injury repair that cancer hijacks. Highly plastic cells become more abundant as these tumors grow, researchers found.
These highly plastic cells aren't necessary to initiate a tumor. But they're critical to cancer's progression, the team found—including its ability to give rise to fast-growing cells, to evolve resistance to treatment, and to potentially help the cancer spread to other parts of the body.
If we kill off these plastic cells very early in the initiation of a tumor, you can basically prevent mutated cells from ever becoming cancers, say teh researchers.
Tuomas Tammela, Critical role for a high-plasticity cell state in lung cancer, Nature (2026). DOI: 10.1038/s41586-025-09985-x. www.nature.com/articles/s41586-025-09985-x
Jan 22
Dr. Krishna Kumari Challa
What should you do with unused or expired prescription medications?
Unused or expired prescription medications should be disposed of promptly to prevent accidental ingestion, especially by children. Preferred disposal methods include take-back programs at pharmacies, police stations, or DEA events. If these are unavailable, mix medications with unpalatable substances before discarding in the trash. Some drugs, mainly opioids, may be flushed per FDA guidance. Sharps require separate disposal.
If you have unused or expired medication, the best thing is to dispose of it. Many people hang on to them, and this just creates opportunity for things to go wrong.
https://medicalxpress.com/news/2026-01-unused-expired-prescription-...
Jan 22
Dr. Krishna Kumari Challa
Scientists may have discovered a new extinct form of life
Prototaxites are something of a prehistoric mystery. They were the first giant organisms on land, towering over ancient landscapes at heights of up to 8 meters. They had smooth trunk-like pillars and no branches, leaves or flowers. And unlike trees, they had no true root system. Instead, they may have been anchored to the ground by a simple bulbous base.
Since their first fossils were discovered in the mid-19th century, scientists have argued over their place in the tree of life. Are they giant fungi, massive algae or some kind of plant? But new evidence has emerged that may help settle the matter.
According to a new study published in the journal Science Advances, Prototaxites belonged to a previously unknown, now-extinct branch of life.
The researchers studied a specimen of Prototaxites taiti recovered from the Rhynie Chert in northeastern Scotland. This paleontological site is well-known for its exceptionally well-preserved plant, fungal and animal material.
The team used lasers and 3D imaging to look inside the fossils and compared their chemical compositions with those of other fossils found in the same rock. They discovered two significant differences.
While fungi have simple networks of long, tubular structures called hyphae, the Prototaxite specimen had a much more complex internal structure. It comprised three different types of tubes and dense hubs where they branch and connect.
To study its chemical fingerprint (the chemical signature organisms leave behind based on the cells they are made of), the team used artificial intelligence. The protein chitin is often detected in fossilized fungi and insects, but it was completely missing from the Prototaxites sample. They also used artificial intelligence to see if its chemistry matched that of any living organism. It didn't.
The researchers ruled out the giant fossils being fungi or plants, and instead, they conclude that Prototaxites were members of an extinct lineage of eukaryotes (complex-celled organisms).
The findings may have finally solved the long-standing mystery about the true nature of Prototaxites. However, further analysis and fossil discoveries may well be needed before the results are considered conclusive.
Corentin Loron et al, Prototaxites fossils are structurally and chemically distinct from extinct and extant Fungi, Science Advances (2026). DOI: 10.1126/sciadv.aec6277. www.science.org/doi/10.1126/sciadv.aec6277
Jan 23
Dr. Krishna Kumari Challa
Scientists solve 66 million-year-old mystery of how Earth's greenhouse age ended
A 66 million-year-old mystery behind how our planet transformed from a tropical greenhouse to the ice-capped world of today has been unraveled by scientists. Their new study has revealed that Earth's massive drop in temperature after the dinosaurs went extinct could have been caused by a large decrease in calcium levels in the ocean.
An international team of experts discovered that concentrations of calcium in the sea dropped by more than half across the last 66 million years.
The study, published in Proceedings of the National Academy of Sciences, showed that the dramatic calcium shift may have sucked carbon dioxide—a major greenhouse gas—out of the atmosphere, driving global cooling.
Large changes in the composition of seawater chemistry may have been a key driver for climate change.
Their results show that dissolved calcium levels were twice as high at the start of the Cenozoic Era, shortly after dinosaurs roamed the planet, compared to today.
When these levels were high, the oceans worked differently, acting to store less carbon in seawater and releasing carbon dioxide into the air.
As those levels decreased, CO2 was sucked out of the atmosphere, and Earth's temperature followed, dropping our climate by as much as 15 to 20 degrees Celsius.
They used fossilized remains of tiny sea creatures dug up from sediments at the seafloor to construct the most detailed record of ocean chemistry to date. The chemical composition of the fossils, called foraminifera, showed a close link between the amount of calcium in seawater and the level of carbon dioxide in the air.
Using computer-made models, the team showed that high levels of calcium change how much carbon is "fixed" by marine life, such as corals and plankton.
Part1
Jan 23
Dr. Krishna Kumari Challa
This effectively locked it away from the ocean and atmosphere by storing it in sediments on the seafloor.
As dissolved calcium levels decreased across millions of years, it altered how these organisms produced and buried calcium carbonate on the seafloor.
The process effectively pulls carbon dioxide out of the atmosphere and locks it away.
This shift could have changed the composition of the atmosphere, effectively turning down the planet's thermostat.
David Evans et al, The major ion chemistry of seawater was closely coupled to the long-term carbon cycle during the Cenozoic, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2511781122
Part 2
Jan 23
Dr. Krishna Kumari Challa
AI models mirror human 'us vs. them' social biases
Large language models (LLMs), the computational models underpinning the functioning of ChatGPT, Gemini and other widely used artificial intelligence (AI) platforms, can rapidly source information and generate texts tailored for specific purposes. As these models are trained on large amounts of texts written by humans, they could exhibit some human-like biases, which are inclinations to prefer specific stimuli, ideas or groups that deviate from objectivity.
One of these biases, known as the "us vs. them" bias, is the tendency of people to prefer groups they belong to, viewing other groups less favorably. This effect is well-documented in humans.
Researchers at University of Vermont's Computational Story Lab and Computational Ethics Lab recently carried out a study investigating the possibility that LLMs "absorb" the "us vs. them" bias from the texts that they are trained on, exhibiting a similar tendency to prefer some groups over others. Their paper, posted to the arXiv preprint server, suggests that many widely used models tend to express a preference for groups that are referred to favorably in training texts, including GPT-4.1, DeepSeek-3.1, Gemma-2.0, Grok-3.0 and LLaMA-3.1.
The results of this recent study highlight the tendency of AI models to pick up the biases and views expressed in the data used to train them. In their paper, the researchers introduced a strategy that could help to reduce this bias in LLMs, which they dubbed ION.
Tabia Tanzin Prama et al, Us-vs-Them bias in Large Language Models, arXiv (2025). DOI: 10.48550/arxiv.2512.13699
Jan 23
Dr. Krishna Kumari Challa
Why the face scars less than the body
Tweaking a pattern of wound healing established millions of years ago may enable scar-free injury repair after surgery or trauma, researchers have found. If results from their study, which was conducted in mice, translate to humans, it may be possible to avoid or even treat the formation of scars anywhere on or within the body.
Scarring is more than a cosmetic problem. Scars can interfere with normal tissue function and cause chronic pain, disease and even death.
Scars on the skin's surface, while rarely fatal, are stiffer and weaker than normal skin and they lack sweat glands or hair follicles, making it difficult to compensate for temperature changes.
Surgeons have known for decades that facial wounds heal with less scarring than injuries on other parts of the body. This phenomenon makes evolutionary sense: Rapid healing of body wounds prevents death from blood loss, infection or impaired mobility, but healing of the face requires that the skin maintain its ability to function well.
The face is very important. We need to see and hear and breathe and eat. In contrast, injuries on the body must heal quickly. The resulting scar may not look or function like normal tissue, but you will likely still survive to procreate.
Exactly how this discrepancy happens has remained a mystery, although there were some clues.
The face and scalp are developmentally unique. Tissue from the neck up is derived from a type of cell in the early embryo called a neural crest cell. In the study researchers identified specific healing pathways in scar-forming cells called fibroblasts that originate from the neural crest and found that they drive a more regenerative type of healing.
Activating this pathway in even a subset of fibroblasts around small wounds on the abdomen or backs of mice caused them to heal with much less scarring—similar to untreated facial or scalp wounds.
The researchers in their experiments found that after 14 days, the wounds on the face and scalp expressed lower levels of proteins known to be involved in scar formation as compared with those on the abdomen or back of the animals. The sizes of the scars were also smaller.
Part 1
Jan 23
Dr. Krishna Kumari Challa
The researchers then transplanted skin from the face, scalp, back and abdomen of mice onto the backs of control mice. After the transplants had engrafted, they repeated the experiment on the transplanted skin. As before, wounds in the skin transplanted from the faces of the donor mice expressed lower levels of scarring-associated proteins.
They isolated fibroblasts from skin samples from the four body sites in the donor mice and injected them into the backs of control mice. They observed reduced levels of scarring-associated proteins on the recipient animals' backs injected with fibroblasts from the donor animals' faces as compared with fibroblasts from the scalp, back or abdomen.
The researchers identified changes in gene expression between facial fibroblasts and those from other parts of the body and followed these clues to identify a signaling pathway involving a protein called ROBO2 that maintains facial fibroblasts in a less-fibrotic state. They also saw something interesting in the genomes of fibroblasts making ROBO2.
In general, the DNA of the ROBO2-positive cells is less transcriptionally active, or less available for binding by proteins required for gene expression, These fibroblasts more closely resemble their progenitors, the neural crest cells, and they might be more able to become the many cell types required for skin regeneration."
In contrast, the DNA in fibroblasts from other sites of the body allows free access to genes like collagen that are involved in the creation of scar tissue.
"It seems that, in order to scar, the cells must be able to express these pro-fibrotic genes.
"And this is the default pathway for much of the body."
ROBO2 doesn't act alone. It triggers a signaling pathway that results in the inhibition of another protein called EP300 that facilitates gene expression. EP300 plays an important role in some cancers, and clinical trials of a small drug molecule that can inhibit its activity are underway. Li and his colleagues found that using this pre-existing small molecule to block EP300 activity in fibroblasts prone to scarring caused back wounds to heal like facial wounds.
Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma, say the researchers.
Fibroblasts of disparate developmental origins harbor anatomically variant scarring potential, Cell (2026). DOI: 10.1016/j.cell.2025.12.014. www.cell.com/cell/fulltext/S0092-8674(25)01427-8
Part 2
**
Jan 23
Dr. Krishna Kumari Challa
Chemotherapy rewires gut bacteria to curb metastasis, research reveals
Chemotherapy commonly damages the intestinal lining, a well-known side effect. But this injury does not remain confined to the gut. It reshapes nutrient availability for intestinal bacteria, forcing the microbiota to adapt.
In Nature Communications, researchers report that chemotherapy-induced damage to the intestinal lining alters nutrient availability for gut bacteria, reshaping the microbiota and increasing the production of indole-3-propionic acid (IPA), a tryptophan-derived microbial metabolite.
Rather than acting locally, IPA functions as a systemic messenger. It travels from the gut to the bone marrow, where it rewires immune cell production. Elevated IPA levels reprogram myelopoiesis, reducing the generation of immunosuppressive monocytes that facilitate immune evasion and metastatic growth.
By reshaping the gut microbiota, chemotherapy sets off a cascade of events that rewires immunity and makes the body less permissive to metastasis.
Ludivine Bersier et al, Chemotherapy-driven intestinal dysbiosis and indole-3-propionic acid rewire myelopoiesis to promote a metastasis-refractory state, Nature Communications (2025). DOI: 10.1038/s41467-025-67169-7
Jan 23
Dr. Krishna Kumari Challa
Cellular senescence linked to brain structure changes across lifespan
Researchers have characterized how cellular senescence—a biological process in which aging cells change how they function—is associated with human brain structure in both development and late life.
The study, published in Cell, provides new insight into how molecular signatures of cellular senescence that are present during development and aging mirror those associated with brain volume and cortical organization.
Cellular senescence is commonly defined as a state characterized by permanent cell cycle arrest in the absence of cell death, in which cells have altered function.
While cellular senescence has been implicated in aging and disease, its role in shaping human brain structure—both during development and aging—has remained unclear till now.
The research team developed a method to define senescent cells in human brain tissue and used the resource to examine how senescence-related gene expression is associated with brain structure.
Among the study's most striking findings was evidence that cellular senescence plays distinct roles in brain structure depending on cell type and stage of life. Genes associated with senescence in microglia—the primary immune cells in the brain—were linked to larger brain volumes, while senescence-related genes in excitatory neurons were associated with smaller brain volumes in the aging brain. Notably, the excitatory neuron findings were also observed early in life, providing the first evidence that senescence-related processes are at work soon after embryonic development.
The results support brain cellular senescence as an example of 'antagonistic pleiotropy'—the idea that some genes help survival or fertility early in life but cause harm later, contributing to aging and disease.
Establishing the relationship between brain cellular senescence and brain structure, Cell (2026). DOI: 10.1016/j.cell.2025.10.014. www.cell.com/cell/fulltext/S0092-8674(25)01179-1
Jan 23
Dr. Krishna Kumari Challa
Domestication has changed the chemicals that squash flowers use to attract bees
Domestication alters the floral scent profiles of squash, resulting in lower overall levels of volatile organic compounds (VOCs) except for 1,4-dimethoxybenzene, which remains prevalent and attracts bees. Specialist squash bees detect and respond differently to VOCs from wild versus domesticated flowers, indicating that domestication changes plant–pollinator interactions.
Avehi Singh et al, Domestication Reduces Floral Volatile Richness in Squash (Cucurbitaceae: Cucurbita) But Conserves Key Compounds Critical for Pollinator Attraction, Journal of Chemical Ecology (2025). DOI: 10.1007/s10886-025-01664-5
Jan 23
Dr. Krishna Kumari Challa
Delayed stroke care linked to increased disability risk
Prolonged door-in-door-out (DIDO) times for transferring acute ischemic stroke patients to thrombectomy-capable centers significantly reduce the likelihood of receiving endovascular therapy and increase the risk of post-stroke disability. Only 26% of transfers met the recommended 90-minute window, with longer delays linked to worse functional outcomes and higher complication rates. Systemic improvements are needed to minimize transfer times and optimize patient recovery.
Door-in-door-out times and outcomes in patients with acute ischaemic stroke transferred for endovascular therapy in the U.S.: a retrospective cohort study, The Lancet Neurology (2026). DOI: 10.1016/S1474-4422(25)00478-8
Jan 23
Dr. Krishna Kumari Challa
Exhaled breath may carry clues to gut microbiome health
Exhaled breath contains volatile organic compounds produced by gut microbes, allowing noninvasive detection of gut microbiome composition. Breath analysis accurately reflected gut bacteria in both children and mice and predicted the presence of asthma-associated Eubacterium siraeum. This approach may enable rapid, noninvasive monitoring and diagnosis of gut health issues.
The gut microbiota shapes the human and murine breath volatilome, Cell Metabolism (2026). DOI: 10.1016/j.cmet.2025.12.013. www.cell.com/cell-metabolism/f … 1550-4131(25)00544-3
Jan 23
Dr. Krishna Kumari Challa
Phages evolve differently in microgravity
Viruses that infect bacteria, called phages, evolve different strategies to infect their targets on the International Space Station than they do on the ground. Researchers found that the phages took longer to infect E. coli in microgravity, and that the viruses developed microgravity-specific mutations, some of which helped them to better cling onto bacterial receptors. Understanding how phages adapt to different conditions could help researchers to optimize them for use against antibiotic-resistant bacteria on Earth.
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pb...
https://www.livescience.com/health/viruses-infections-disease/virus...
Jan 23
Dr. Krishna Kumari Challa
Chronic wound bacterium prevents healing
The bacterium Enterococcus faecalis produces damaging molecules that can prevent chronic wounds such as diabetic foot sores from healing. These reactive molecules, such as hydrogen peroxide, trigger a stress response in keratinocytes, the skin cells responsible for wound healing, which effectively paralyzes them. Researchers found that treating skin cells with the antioxidant enzyme catalase can de-stress keratinocytes, which restores their healing capabilities. The team suggests that dressings infused with antioxidants could be a more effective way to treat chronic wounds than trying to kill E. faecalis with antibiotics.
https://www.science.org/doi/10.1126/sciadv.aeb5297
https://www.genengnews.com/topics/infectious-diseases/disarming-ant...
Jan 23
Dr. Krishna Kumari Challa
Barnacle-inspired E. coli could treat IBD
Escherichia coli engineered to produce biological ‘glue’ could help to heal damage in the guts of people with inflammatory bowel disease (IBD). Researchers engineered E. coli to produce ‘cement proteins’ — similar to those that barnacles use to stick onto rocks — when they come into contact with blood, and a protein that boosts wound healing. In mouse models of IBD, the team found that the bacteria could stick onto internal wounds for ten days, and after that time the mice’s guts resembled those of healthy mice.
New Scientist
Nature Biotechnology paper
Jan 23
Dr. Krishna Kumari Challa
Sugar Without The Insulin Spike
A natural, low-calorie sugar that doesn’t cause a spike in insulin sounds too good to be true. But it really does exist!
It’s called tagatose, and it comes in very small amounts in a few fruits and dairy products.
Now, scientists have figured out how to manufacture the rare sugar at larger scales.
The product is 92 percent as sweet as sucrose, and yet it doesn’t spike insulin levels.
Tagatose is mostly fermented in the gut, so only a small portion of it is actually absorbed into the bloodstream.
Unlike high-intensity artificial sweeteners, it can even be used in baked goods.
https://www.cell.com/cell-reports-physical-science/fulltext/S2666-3864(25)00592-2?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2666386425005922%3Fshowall%3Dtrue
Jan 23
Dr. Krishna Kumari Challa
Scientists observe a 300-million-year-old brain rhythm in several animal species
Sleep is a universal biological state that allows all animals, from mammals to amphibians, fish and even insects, to restore their energy and consolidate knowledge that can contribute to their survival. Neuroscientists and zoologists have been investigating the biological underpinnings of sleep and its vital functions for centuries, more recently by measuring the brain activity of animals or people while they are asleep.
Recorded electrical signals that nerve cells produce while they are communicating with each other, also known as brain rhythms, have provided valuable insight into what happens during sleep. One of these rhythms, the so-called infraslow rhythm, had so far been primarily observed in mammals and was linked to a stage of sleep known as non-rapid eye movement (NREM) sleep.
Researchers recently recorded the brain activity of a wider range of animals and found that this ancient rhythm is common across several species, including reptiles, birds, rodents and humans. Their most recent paper, published in Nature Neuroscience, reports the observation of the infraslow brain rhythm in seven different lizard species.
In addition to brain activity, they also recorded physiological signals such as eye movements, heart rate, breathing rate, and muscle tone.
The large dataset compiled by the researchers over the past decade or so led to an important and interesting discovery. Specifically, the team found that reptiles, mammals, and birds share a common brain rhythm, the so-called infraslow rhythm. This finding suggests the presence of an ancestral mechanism that dates back at least to 300 million years ago, when the earliest known ancestor of the species examined lived.
This rhythm involves not only brain activity but also physiological processes and peripheral vascularization, indicating that it is a global, organism-wide rhythm.
The infraslow rhythm closely resembles a rhythm previously described in mammals during non-REM (NREM) sleep. In mammals, this rhythm has been proposed to play a role in brain 'cleaning' processes by facilitating the elimination of metabolic waste through cerebrospinal fluid flow. Additionally, because this rhythm is associated with fluctuations in vigilance, it may also represent an adaptive mechanism that allows periodic monitoring of the environment during sleep, potentially reducing the risk of predation.
Antoine Bergel et al, Sleep-dependent infraslow rhythms are evolutionarily conserved across reptiles and mammals, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02159-y.
Jan 24
Dr. Krishna Kumari Challa
Ultra-thin wireless retinal implant offers hope for safely restoring vision signals
An ultra-thin, wireless retinal implant using a zinc oxide nanowire and silver–bismuth–sulfide nanocrystal assembly enables safe, precise electrical stimulation of retinal neurons via near-infrared light at low intensities. The device shows strong biocompatibility, stability, and negligible heating, making it promising for vision restoration and broader neuromodulation applications.
Tarik S. Kaya et al, Photovoltaic nanoassembly of nanowire arrays sensitized with colloidal nanocrystals for near-infrared retina photostimulation, Science Advances (2026). DOI: 10.1126/sciadv.aea7001
Jan 24
Dr. Krishna Kumari Challa
Halley's Comet wrongly named: 11th-century English monk predates British astronomer
Evidence indicates that the 11th-century monk Eilmer of Malmesbury recognized the periodicity of Halley's Comet centuries before Edmond Halley. Eilmer linked two appearances of the comet, as described in medieval chronicles, suggesting the comet’s cycle was understood earlier than previously thought. This challenges the appropriateness of the comet’s current name.
https://www.universiteitleiden.nl/en/news/2026/01/halleys-comet-wro....
Jan 24
Dr. Krishna Kumari Challa
Beyond the fear: Scientists test the health impacts of 5G
From street-level measurements to long-term health studies, researchers are building a clearer picture of the impact of everyday exposure to 5G signals on human health.
Measurements across multiple European countries indicate that everyday exposure to 5G radiofrequency electromagnetic fields remains well below international safety limits. Short-term laboratory studies found no measurable effects on heart function, stress, skin temperature, or brain activity in healthy adults exposed to 3.5 GHz 5G signals. Ongoing research is examining long-term health and behavioural impacts.
More than 800 measurements were taken across urban and rural locations in eight EU countries, plus Switzerland and the UK. The team looked at scenarios from phones in flight mode to data-intensive activities, such as sharing attachments or watching livestreamed video.
The results show that exposure to RF-EMF in everyday environments remains well below international safety limits in all settings measured.
These limits, set by independent scientific bodies, define the maximum exposure levels considered safe for the general public and include large safety margins.
To investigate whether 5G signals have any immediate effects on the body, researchers in France have carried out the first coordinated human laboratory studies focusing on a key 5G frequency band: 3.5 gigahertz.
At INERIS, the French National Institute for Industrial Environment and Risks near Paris, 31 healthy volunteers were exposed to 5G signals for 26 minutes under controlled conditions designed to reflect real-world environmental exposure.
They observed no measurable impact on heart function, stress levels, skin temperature or brain activity in healthy young adults.
However, the researchers stress that the phone doesn't only bring radio frequency electromagnetic fields exposure. It also brings screen light exposure, mental arousal or device dependency.
Source:
https://projectgoliat.eu/
https://cordis.europa.eu/project/id/101057262
Jan 24
Dr. Krishna Kumari Challa
Can certain foods prevent stomach cancer?
Dietary choices can influence stomach cancer risk. Consuming more fruits, vegetables, and whole foods while reducing processed foods, sugar, salt, and inflammatory foods may lower risk. Maintaining a healthy weight, regular exercise, avoiding smoking and excess alcohol, and appropriate cancer screening further support prevention. Genetics remain a major risk factor.
Eating fewer processed and preserved foods, which are generally high in sugar and salt and potential nitrites or nitrates is one advice all teh experts give.
Aim to eat more fruits and vegetables. The antioxidant compounds in produce can provide extra protection against diseases like stomach cancer. When meal planning, try to ensure that half your plate is filled with vegetables.
When possible, follow a Mediterranean diet, which emphasizes whole, plant-based foods and healthy fats. Choose high-quality proteins like lean meat, fish and legumes. Avoid foods known to cause inflammation and eat fewer starches, including potatoes and pasta.
Eating smaller meal portions throughout the day—such as four to six smaller meals throughout the day—rather than sticking to three large meals. Compared to eating a big meal, eating smaller meals causes less stomach stretching and stress on your body and allows for smaller insulin responses.
Exercise has a positive effect on reducing cancer risk.
Obesity—especially excess fat around the midsection—can increase the risk of cancer. This type of fat, called visceral fat, can secrete hormones that increase your risk of cancer.
In addition to weight gain, pay attention to unexplained weight loss. Unexplained weight loss can be the first sign of cancer.
Other things to avoid include smoking and alcohol—particularly beer, which has been shown to increase stomach cancer risk.
Jan 24
Dr. Krishna Kumari Challa
Stones Along Railway Tracks
Jan 25
Dr. Krishna Kumari Challa
Why Does Dust Build Up Even in Closed Spaces?
Jan 25
Dr. Krishna Kumari Challa
Are llamas big pharma's secret weapon to find new drugs?
Llama-derived nanobodies, small and easily engineered antibody fragments, are being explored as therapeutic agents for diseases such as cancer, autoimmune disorders, and nerve pain. These nanobodies can access targets inaccessible to conventional antibodies and may cross the blood-brain barrier. While some drugs have reached the market, broader clinical success and commercial impact remain under development.
Scientists have discovered the potential of the animals' antibodies to thwart multiple diseases, and now drug developers are collectively plowing billions of dollars into a field that may yield a fresh generation of life-changing medicines. The targets include some hard-to-treat conditions like cancer, nerve pain and a chronic skin ailment.
The immune system of all mammals produces antibodies to thwart viral and bacterial attacks. Those made by llamas and other members of the camelid family can squeeze into tighter spots and better penetrate tissue than human ones, because they're smaller and simpler. Some have been reported to cross the blood-brain barrier, eliciting hope for neurological diseases.
Source: News agencies
https://phys.org/news/2026-01-llamas-big-pharma-secret-weapon.html?...
on Tuesday
Dr. Krishna Kumari Challa
Why are icy surfaces slippery?
Why do we lose our grip in icy conditions?
It's the molecular "deal" ice strikes with everything it touches. Unlike most solids, ice refuses to act like a rigid crystal. Instead, it behaves as a self-made lubricant—especially as temperatures hover near freezing.
Ice has an unusual property: it can melt when you apply pressure to it, whereas most materials behave the other way around—pressure usually makes liquids become solid. For a long time, people thought pressure caused slipperiness. But pressure-induced melting only happens in a very narrow temperature range, while ice remains slippery well outside those limits.
Others suggest friction from sliding—think rubbing your hands in the cold to stay warm or a shoe making contact with ice—heated the ice enough to create a melt layer. But that's sort of a chicken-and-egg problem: generating enough heat requires some extended sliding with high friction—ice is slippery without having to slide hardly at all.
Eventually, researchers realized that ice has another funny property: its surface can pre-melt, meaning it naturally has a thin layer of water on top of it, well below the melting temperature. The layer gets thicker as the temperature gets closer to the melting temperature.
However, this idea—based on ice being self-lubricated—doesn't explain why some materials have lower friction against ice than others; if the water layer is always there, everything should be equally slippery. It's an oversimplification, but that's the basic argument.
Recently, researchers in Germany used simulations to show that when something touches ice, the water molecules at the surface rearrange from an ordered crystal into a disordered, amorphous structure. This isn't caused by pressure or friction, but by microscopic electrical charges.
Water molecules have positive and negative ends, and when they touch another surface, they react to the atoms in that material. They believe this electrical "push and pull" disrupts the ice's rigid structure, creating that slippery, disordered layer, which would explain why ice is slippery across different temperatures and why some materials slide on it better than others.
But in short, we don't yet know for sure. As many have observed, despite the commonality of water and ice, their physical properties are remarkably unique.
https://penntoday.upenn.edu/news/penn-engineering-why-are-icy-surfa...
on Tuesday
Dr. Krishna Kumari Challa
World not ready for rise in extreme heat, scientists say
By 2050, nearly 3.8 billion people could be exposed to extreme heat, with the greatest impacts in tropical and developing regions lacking adequate cooling infrastructure. Even moderate temperature increases will significantly affect cooler countries unaccustomed to heat. Rising demand for cooling will strain energy systems, highlighting an urgent need for adaptation measures.
Global gridded dataset of heating and cooling degree days under climate change scenarios, Nature Sustainability (2026). DOI: 10.1038/s41893-025-01754-y , www.nature.com/articles/s41893-025-01754-y
on Tuesday
Dr. Krishna Kumari Challa
How gut bacteria control immune responses
Bacteria in the human gut can directly deliver proteins into human cells, actively shaping immune responses.
Gut bacteria can inject proteins directly into human cells using type III secretion systems, previously thought unique to pathogens. These proteins interact with human immune and metabolic pathways, modulating immune responses such as NF-κB and cytokine signaling. Genes for these effectors are more common in Crohn’s disease, linking this mechanism to chronic intestinal inflammation.
Researchers have discovered this previously unknown mechanism of communication between gut bacteria and human cells. The findings reveal a new way in which the gut microbiome can influence the human body and may help explain how changes in gut bacteria contribute to inflammatory diseases such as Crohn's disease.
Although the human gut microbiome has long been linked to immune, metabolic, and inflammatory disorders, most evidence is correlative, and the molecular mechanisms behind these connections remain largely unexplored.
The new study shows that many harmless, everyday gut bacteria possess type III secretion systems—microscopic, syringe-like structures that can inject bacterial proteins directly into human cells. Until now, these systems were thought to exist only in pathogenic bacteria such as Salmonella.
It shows that these non-pathogenic bacteria are not just passive residents but can actively manipulate human cells by injecting their proteins into our cells
To understand what these bacterial proteins do in human cells, the researchers mapped more than a thousand interactions between bacterial effector proteins and human proteins, creating a large-scale interaction network. Their analyses showed that bacterial proteins preferentially target human pathways involved in immune regulation and metabolism.
Further laboratory experiments confirmed that these proteins can modulate key immune signaling pathways, including NF-κB and cytokine responses. Cytokines are signaling molecules that help coordinate the immune system and prevent excessive reactions that can lead to autoimmune diseases. For example, inhibiting the activity of the cytokine tumor necrosis factor (TNF) is a widely used treatment for Crohn's disease, an autoimmune disease of the gut.
The researchers also found that genes encoding these bacterial effector proteins are enriched in the gut microbiomes of patients with Crohn's disease. This suggests that direct protein delivery from gut bacteria to human cells may contribute to chronic intestinal inflammation, providing a potential mechanistic explanation for previously observed microbiome–disease links.
Veronika Young et al, Effector–host interactome map links type III secretion systems in healthy gut microbiomes to immune modulation, Nature Microbiology (2026). DOI: 10.1038/s41564-025-02241-y. www.nature.com/articles/s41564-025-02241-y
on Tuesday
Dr. Krishna Kumari Challa
Cancer tumors may protect against Alzheimer's by cleaning out protein clumps
Tumor-secreted Cystatin-C (Cyst-C) crosses the blood-brain barrier, binds amyloid-beta oligomers and the TREM2 receptor on microglia, and activates microglial clearance of amyloid plaques in Alzheimer's mouse models. This process reduces plaque burden and improves cognitive performance, suggesting a potential therapeutic approach for Alzheimer's disease by targeting existing plaques.
https://medicalxpress.com/news/2026-01-cancer-tumors-alzheimer-prot...
on Tuesday
Dr. Krishna Kumari Challa
Previously unknown bacterial component in kidney stone formation discovered
In an unexpected finding, a research team has discovered that bacteria are present inside the most common type of kidney stone, revealing a previously unrecognized component involved in their formation.
Bacteria have been identified within calcium oxalate kidney stones, indicating a previously unrecognized microbial role in their formation. This challenges the view that these stones arise solely from chemical and physical processes and suggests that targeting bacterial biofilms could offer new prevention and treatment strategies for kidney stone disease.
The findings, to be published in the journal Proceedings of the National Academy of Sciences, point to a possible therapeutic target that could be used for prevention and treatment for the millions of people who are affected by the frequently painful condition.
This breakthrough challenges the long-held assumption that these stones develop solely through chemical and physical processes, and instead shows that bacteria can reside inside stones and may actively contribute to their formation.
Kidney stones are composed of clumps of small crystals. Their prevalence has risen globally in recent years, so that today about 1 in 11 people will get them in their lifetime. Risk factors include family history, metabolic syndrome, and low fluid intake. The stones start forming when crystals grow in urine and become large enough that they can't be washed out with normal urine flow.
There are several subsets of kidney stones and while one rare stone type is known to contain bacteria, by far the most common stone is calcium oxalate (CaOx), comprising almost 80% of kidney stone cases, which have not been previously known to contain bacteria. While examining data from electron and fluorescence microscopy, the researchers unexpectedly detected live bacteria as well as layers, or biofilms, of bacteria integrated into the crystals.
Researchers found a new mechanism of stone formation that may help to explain why these stones are so common.
These results may also help to explain the connections between recurrent urinary tract infections and recurrent kidney stone formation, and provide insights on potential future treatment for these conditions. The findings suggest that bacteria could also be involved in other kidney stone types.
The study focused on calcium-based stones. How other less common stones form is still in question. More studies are needed to fully understand how bacteria and calcium-based kidney stones interact, the researchers conclude.
Wong, Gerard C. L. et al, Intercalated bacterial biofilms are intrinsic internal components of calcium-based kidney stones, Proceedings of the National Academy of Sciences (2026). DOI: 10.1073/pnas.2517066123. doi.org/10.1073/pnas.2517066123
on Tuesday
Dr. Krishna Kumari Challa
Inflammation gives mutated blood stem cells an edge in cancer development
Inflammation promotes the expansion of blood stem cells with TP53 mutations, increasing the risk of blood cancers such as leukemia in older individuals. Activation of the NLRP1 inflammasome and persistent inflammatory signaling give mutant cells a survival advantage. Blocking inflammatory signals like IL-1B may reduce this risk and offer a potential preventive strategy.
Sisi Chen et al, Mutant p53 promotes clonal hematopoiesis through generating a chronic inflammatory microenvironment, Journal of Clinical Investigation (2025). DOI: 10.1172/jci184285
on Tuesday