Science Simplified!

                       JAI VIGNAN

All about Science - to remove misconceptions and encourage scientific temper

Communicating science to the common people

'To make  them see the world differently through the beautiful lense of  science'

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  • Dr. Krishna Kumari Challa

    Next, to test mitochondrial transfer from neurons to cancer cells, the team engineered neurons to express mitochondria tagged with fluorescent markers with a novel tracking system called MitoTRACER. The system allowed researchers to monitor cancer cells after mitochondrial transfer, enabling detailed tracing of their fate during disease progression.

    Direct mitochondrial transfer was observed via tunneling nanotubes, initiated by neurons towards the cancer cells. Rho-zero cancer cells regained oxidative phosphorylation and uridine-independent growth after acquiring neuronal mitochondria, confirming functional rescue.

    MitoTRACER revealed that recipient cancer cells displayed enhanced respiration, higher ATP, improved redox balance, and greater resistance to oxidative and mechanical stress.

    In animal models, these labeled recipient cells were significantly enriched in metastases, especially in the brain and liver, indicating that neuronal mitochondria confer a selective advantage during dissemination.

    Together, these two experimental arms show that nerves both sustain tumor energetics broadly and act as direct donors of functional mitochondria, a dual mechanism that promotes cancer survival and spread.
    Denervation experiments established that disrupting nerve input deprives cancer cells of essential bioenergetic capacity, reducing their invasiveness. Cancer cells that had received neuronal mitochondria more readily survived metastatic stressors such as oxidative damage and mechanical shear forces, common hurdles faced during cancer dissemination.

    Gregory Hoover et al, Nerve-to-cancer transfer of mitochondria during cancer metastasis, Nature (2025). DOI: 10.1038/s41586-025-09176-8

    Part 2

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  • Dr. Krishna Kumari Challa

    Psilocybin rewires brain circuits to boost fear extinction and behavioural flexibility in mice

    Psilocybin, a psychedelic compound contained in some varieties of mushrooms, has recently been found to be promising for the treatment of some neuropsychiatric disorders, including depression, some anxiety disorders and post-traumatic stress disorder(PTSD). Some studies suggest that the consumption of this compound may be particularly advantageous for individuals who struggle to adapt their behavior in helpful ways when facing unexpected events or changes in their environment.

    While a growing pool of research has been assessing the therapeutic benefits of psilocybin  the neural mechanisms through which it promotes long-lasting psychological changes remain poorly understood. If it does prompt greater behavioral flexibility in individuals diagnosed with some psychiatric disorders, the processes through which it does so are not yet clear.

    Researchers  recently carried out a new study on mice, which was aimed at better understanding how psilocybin could increase adaptability and potentially ease symptoms of anxiety disorders or PTSD. Their findings, published in Nature Neuroscience, suggest that the compound prompts the reorganization of neural circuits in the retrosplenial cortex , a part of the brain located in the posterior region of the cerebral cortex (i.e., the outermost layer of the mammalian brain).

    Researchers, in their experiments,   found that a single dose of psilocybin altered cortical ensemble turnover and oppositely modulated fear- and extinction-active neurons. Suppression of fear-active neurons and recruitment of extinction-active neurons predicted psilocybin-enhanced fear extinction.

    These results suggested that psilocybin enhances behavioral flexibility by recruiting new neuronal populations and suppressing fear-active populations in the retrosplenial cortex.

    Sophie A. Rogers et al, Psilocybin-enhanced fear extinction linked to bidirectional modulation of cortical ensembles, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-01964-9.

  • Dr. Krishna Kumari Challa

    Engineered bacterial vesicles created to combat antimicrobial resistance

    Bacteria are ubiquitous microscopic organisms capable of rapid growth. While beneficial strains like lactic acid bacteria (LAB) promote gut health and food preservation, pathogenic bacteria such as Escherichia coli and Staphylococcus aureus can cause severe infections. These harmful microbes produce toxins and enzymes that compromise health and, increasingly, show resistance to conventional antibiotics.

    In recent years, scientists have explored alternative approaches to tackle pathogenic bacteria. Among them, endolysins—enzymes that degrade bacterial cell walls—have emerged as potent tools. These proteins, often derived from bacteriophages or engineered microbes, offer specificity in targeting pathogens. However, their widespread use is limited by challenges such as high production costs, instability during storage or circulation, and susceptibility to enzymatic degradation.

    To address this research gap, researchers have turned their attention to extracellular vesicles (EVs)—membrane-bound nanoparticles released by cells that transport biologically active molecules like proteins or nucleic acids. They engineered EVs derived from LAB to carry pathogen-specific endolysins on their surface.

    Their findings were published in the Chemical Engineering Journal on 15 May, 2025. The research outlines the discovery and application of a novel surface-displaying protein found on EVs from Lacticaseibacillus paracasei.

    Jeongmin Lee et al, Surface-displaying protein from Lacticaseibacillus paracasei–derived extracellular vesicles: Identification and utilization in the fabrication of an endolysin-displaying platform against Staphylococcus aureus, Chemical Engineering Journal (2025). DOI: 10.1016/j.cej.2025.162196

  • Dr. Krishna Kumari Challa

    Air pollution is linked to adverse birth outcomes in India

    Prenatal exposure to ambient fine particulate matter and climatic factors, such as temperature and rainfall, are associated with adverse birth outcomes in India, according to a study published in PLOS Global Public Health 

    Ambient air pollution poses a global threat to human health, with a disproportionate burden of its detrimental effects falling on those residing in low and middle-income countries. Referred to as the silent killer, ambient air pollution is among the top five risk factors for mortality in both males and females.

    With a diameter of less than 2.5 microns, ambient fine particulate matter 2.5 (PM2.5), which primarily originates from the burning of fossil fuels and biomass, is considered the most harmful air pollutant. In the 2023 World Air Quality Report, India was ranked as the third-most polluted country out of 134 nations based on its average yearly PM2.5 levels.

    Ambient air pollution has been associated with a range of pediatric morbidities, including adverse birth outcomes, asthma, cancer, and an increased risk of chronic diseases.

    To address the knowledge gap, the researchers investigated the impact of ambient air pollution on adverse birth outcomes at the national level, focusing on  low birth weight and preterm birth, and used different geospatial models to highlight vulnerable areas. The analysis provided evidence of the association between in-utero exposure to PM2.5 and adverse birth outcomes by leveraging satellite data and large-scale survey data.

    The individual-level analysis revealed that an increase in ambient PM2.5 is associated with a greater likelihood of low birth weight and preterm birth. Climatic factors such as rainfall and temperature were also linked to adverse birth outcomes. Children residing in the Northern districts of India appeared to be more susceptible to the adverse effects of ambient air pollution.

    PLOS Global Public Health (2025). DOI: 10.1371/journal.pgph.0003798

  • Dr. Krishna Kumari Challa

    Unlocking the mystery behind Barrett's esophagus

    A research team has shed light on the process that drives Barrett's esophagus formation. This condition affects the lining of the esophagus—the tube that carries food from the mouth to the stomach—and increases the risk of developing esophageal adenocarcinoma, a serious and often deadly cancer.

    The study, published in the Journal of Clinical Investigation, reveals that two important genes involved in guiding and maintaining the identity of the esophagus and intestine, SOX2 and CDX2, are altered in Barrett's esophagus. The findings not only deepen our understanding of how the disease develops but also open the door to new ways of identifying people at risk and potentially preventing the condition from progressing to cancer.

    It is known that Barrett's esophagus usually develops after long-term exposure to acid and bile reflux, which transforms the cells of the lining of the esophagus into cells that look more like those in the stomach and the intestine.

    The esophagus, which is not normally exposed to acid, adapts to acid reflux by becoming more like the stomach or the intestine, organs that are used to an acidic or bile-rich environment.

    Eliminating acid reflux with medication does not heal Barrett's esophagus; the cells do not revert to their typical esophagus characteristics.

    Under the microscope, Barrett's lesions show increased cell proliferation and a disorganized tissue with stomach-like and intestine-like cells where only esophageal cells should be.

    To gain insight into what drives the transformation of esophageal cells into stomach and intestinal cells, the team investigated transcription factors SOX2 and CDX2, which are proteins that regulate the identity of esophageal and intestinal cells, respectively.

    The findings support the idea that Barrett's esophagus may arise from the acid- and bile-triggered reprogramming of normal esophageal cells by altering the balance of SOX2 and CDX2. This new understanding could help scientists find strategies to intervene earlier in the disease process as well as develop new ways to provide an early diagnosis.

    Ramon U. Jin et al, SOX2 regulates foregut squamous epithelial homeostasis and is lost during Barrett's esophagus development, Journal of Clinical Investigation (2025). DOI: 10.1172/JCI190374

  • Dr. Krishna Kumari Challa

    Food contact articles as source of micro- and nanoplastics

  • Dr. Krishna Kumari Challa

    At the frontier between two lives—the evolutionary origins of pregnancy

    An international research team  has uncovered new insights into how specialized cell types and communication networks at the interface between mother and fetus evolved over millions of years. These discoveries shed light on one of nature's most remarkable innovations—the ability to sustain a successful pregnancy. The findings have just been published in Nature Ecology & Evolution.

    Pregnancy that lasts long enough to support full fetal development is a hallmark evolutionary breakthrough of placental mammals—a group that includes humans. At the center of this is the fetal-maternal interface: the site in the womb where a baby's placenta meets the mother's uterus, and where two genetically distinct organisms—mother and fetus—are in intimate contact and constant interaction.

    This interface has to strike a delicate balance: intimate enough to exchange nutrients and signals, but protected enough to prevent the maternal immune system from rejecting the genetically "foreign" fetus.

    To uncover the origins and mechanisms behind this intricate structure, the team analyzed single-cell transcriptomes—snapshots of active genes in individual cells—from six mammalian species representing key branches of the mammalian evolutionary tree. These included mice and guinea pigs (rodents), macaques and humans (primates), and two more unusual mammals: the tenrec (an early placental mammal) and the opossum (a marsupial that split off from placental mammals before they evolved complex placentas).

    By analyzing cells at the fetal-maternal interface, the researchers were able to trace the evolutionary origin and diversification of the key cell types involved. Their focus was on two main players: placenta cells, which originate from the fetus and invade maternal tissue, and uterine stromal cells, which are of maternal origin and respond to this invasion.

    Using molecular biology tools, the team identified distinct genetic signatures—patterns of gene activity unique to specific cell types and their specialized functions. Notably, they discovered a genetic signature associated with the invasive behavior of fetal placenta cells that has been conserved in mammals for more than 100 million years.

    Part 1

  • Dr. Krishna Kumari Challa

    This finding challenges the traditional view that invasive placenta cells are unique to humans, and reveals instead that they are a deeply conserved feature of mammalian evolution. During this time, the maternal cells weren't static, either. Placental mammals, but not marsupials, were found to have acquired new forms of hormone production, a pivotal step toward prolonged pregnancies and complex gestation, and a sign that the fetus and the mother could be driving each other's evolution.
    To better understand how the fetal-maternal interface functions, the study tested two influential theories about the evolution of cellular communication between mother and fetus.

    The first, the "Disambiguation Hypothesis," predicts that over evolutionary time, hormonal signals became clearly assigned to either the fetus or the mother—a possible safeguard to ensure clarity and prevent manipulation. The results confirmed this idea: certain signals, including WNT proteins, immune modulators, and steroid hormones, could be clearly traced back to one source tissue.
    The second, the "Escalation Hypothesis" (or "genomic conflict"), suggests an evolutionary arms race between maternal and fetal genes—with, for example, the fetus boosting growth signals while the maternal side tries to dampen them. This pattern was observed in a small number of genes, notably IGF2, which regulates growth. On the whole, evidence pointed to fine-tuned cooperative signaling.

    These findings suggest that evolution may have favored more coordination between mother and fetus than previously assumed.
    The so-called mother-fetus power struggle appears to be limited to specific genetic regions and there absolutely isn't any conflict.

    Daniel J. Stadtmauer et al, Cell type and cell signalling innovations underlying mammalian pregnancy, Nature Ecology & Evolution (2025). DOI: 10.1038/s41559-025-02748-x

    Part 2

  • Dr. Krishna Kumari Challa

    This material emits infrared light better than it absorbs it, without violating the laws of physics

    New results published in the journal Physical Review Letters detail how a specially designed metamaterial was able to tip the normally equal balance between thermal absorption and emission, enabling the material to better emit infrared light than absorb it.

    At first glance, these findings appear to violate Kirchhoff's law of thermal radiation, which states that—under specific conditions—an object will absorb infrared light (absorptivity) in one direction and emit it (emissivity) with equal intensity in another, a phenomenon known as reciprocity.

    Over the past decade, however, scientists have begun exploring theoretical designs that, under the right conditions, could allow materials to break reciprocity. Understanding how a material absorbs and emits infrared light (heat) is central to many fields of science and engineering. Controlling how a material absorbs and emits infrared light could pave the way for advances in solar energy harvesting, thermal cloaking devices, and other technologies.

    Pioneering experiments conducted by a team of researchers in 2023 yielded tantalizing results. By using a single layer of the magneto-optical material indium arsenide (InAs) and subjecting it to a powerful magnetic field of about one tesla (slightly less powerful than an MRI machine but about 100,000 times more powerful than Earth's magnetic field), the team successfully achieved nonreciprocity. Though this confirmed theoretical predictions, the effect was weak and only operated under a very narrow set of conditions.

    The newly reported design succeeded in doubling the effect seen previously, making it the first reported observation of "strong" nonreciprocal thermal emission.

    To achieve this record-breaking result, researchers created a metamaterial made of five, 440-nanometer-thick layers of electron-doped indium gallium arsenide (InGaAs). The doping concentration increased as the depth increased. The InGaAs layers were then transferred to a silicon substrate.

    The sample was then studied with a custom-designed angle-resolved magnetic thermal emission spectroscopy (ARMTES) set up, which heated the sample to 540 Kelvin (512 Fahrenheit) and subjected it to a 5 tesla magnetic field.

    The researchers then measured the nonreciprocity of the material, demonstrating that it exhibited twice the effect previously reported. This effect persisted over a wide range of angles and a broad range of infrared wavelengths (from 13 to 23 microns).

    This experiment for the first time realizes strong nonreciprocal emission, with nonreciprocity as high as 0.43, which is much higher than nonreciprocity in literature.

    Zhenong Zhang et al, Observation of Strong Nonreciprocal Thermal Emission, Physical Review Letters (2025). DOI: 10.1103/PhysRevLett.135.016901

  • Dr. Krishna Kumari Challa

    New neurons continue to form in the adult human hippocampus: Study

    A study in the journal Science presents compelling new evidence that neurons in the brain's memory center, the hippocampus, continue to form well into late adulthood. The research from Karolinska Institutet in Sweden provides answers to a fundamental and long-debated question about the human brain's adaptability.

    The hippocampus is a brain region that is essential for learning and memory and involved in emotion regulation. Back in 2013, a research group showed in a high-profile study that new neurons can form in the hippocampus of adult humans. The researchers then measured carbon-14 levels in DNA from brain tissue, which made it possible to determine when the cells were formed.

    In the new study, the researchers combined several advanced methods to examine brain tissue from people aged 0 to 78 years from several international biobanks. They used a method called single-nucleus RNA sequencing, which analyzes gene activity in individual cell nuclei, and flow cytometry to study cell properties. By combining this with machine learning, they were able to identify different stages of neuronal development, from stem cells to immature neurons, many of which were in the division phase.

    To localize these cells, the researchers used two techniques that show where in the tissue different genes are active: RNAscope and Xenium. These methods confirmed that the newly formed cells were located in a specific area of the hippocampus called the dentate gyrus. This area is important for memory formation, learning and cognitive flexibility.

    The results show that the progenitors of adult neurons are similar to those of mice, pigs and monkeys, but that there are some differences in which genes are active. There were also large variations between individuals—some adult humans had many neural progenitor cells, others hardly any at all.

    This gives us an important piece of the puzzle in understanding how the human brain works and changes during life.

     Ionut Dumitru et al, Identification of proliferating neural progenitors in the adult human hippocampus, Science (2025). DOI: 10.1126/science.adu9575.

  • Dr. Krishna Kumari Challa

    A single genetic mutation may have made humans more vulnerable to cancer than chimpanzees

    New research has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This insight could lead to more powerful cancer treatments.

    The study was published in Nature Communications. It revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates.

    This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumor-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.

    The evolutionary mutation in FasL may have contributed to the larger brain size in humans. But in the context of cancer, it was an unfavorable trade-off because the mutation gives certain tumors a way to disarm parts of our immune system.

    FasL is an immune cell membrane protein that triggers a programmed cell death called apoptosis. Activated immune cells, including CAR-T cells made from a patient's immune system, use apoptosis to kill cancer cells.
    The UC Davis team discovered that in human genes, a single evolutionary amino acid change—serine instead of proline at position 153—makes FasL more susceptible to being cut and inactivated by plasmin.

    Plasmin is a protease enzyme that is often elevated in aggressive solid tumors like triple negative breast cancer, colon cancer and ovarian cancer.

    This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons—FasL—can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies.

    The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumors. Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer rely heavily on plasmin to spread the cancer.

    Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.

    By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

    Brice E. N. Wamba et al, Evolutionary regulation of human Fas ligand (CD95L) by plasmin in solid cancer immunotherapy, Nature Communications (2025). DOI: 10.1038/s41467-025-60990-0

  • Dr. Krishna Kumari Challa

    Burns and fireworks injuries: What to do when seconds count

    This is what experts advice....

    From a barbecue explosion to a severe firework injury, a lot can go wrong when celebrating.

    When it does, minutes—even seconds—can significantly impact the extent of the injury. Although prevention is key,  response is also essential.

    Alcohol impairs your reaction time. 

    If a firework or sparkler injures an eye, immediately protect it from pressure or further trauma by placing a cup or makeshift device over it. Don't try to cover it with a towel or anything that touches the eye.

    More than a third of firework burns are to the hands and fingers. Should a firework go off in your hand, wrap it in a clean towel and keep it covered until you get to the hospital.

    If you catch on fire, from a firework, bonfire, barbecue or cooking incident,  immediately stop, drop and roll.

    A lot of people like to run and jump in the water. That's not always the best thing. Unless you're standing on a dock or on the edge of a pool, those few seconds it's going to take you to run to the water, you're burning that whole time. It's much more effective to stop, drop, and roll.

    Experts also advise against icing a burn, which can cause further damage.

    You can run normal temperature water over it, and then if it's very serious, of course, call emergency ambulance or seek medical care.

    If running water isn't accessible, a cool, wet cloth can be used as an alternative. However, once the initial pain subsides, you should replace the damp towel with a clean, dry cloth to prevent the burn from becoming infected.

  • Dr. Krishna Kumari Challa

    Missing beneficial bacteria in infant guts linked to rising asthma and allergy cases

    Nearly one in four infants lacks enough healthy gut bacteria essential for training their immune systems, putting them at greater risk of developing non-communicable diseases (NCDs) such as allergies, asthma, and eczema by age 2.

    Bifidobacteria are among the first group of good bacteria to colonize the human gut, and their presence has been linked to positive health outcomes for the host, including protection against metabolic diseases, gastrointestinal tract infections, and inflammation.

    A recent study published in Communications Biology analyzed the gut microbiomes of 412 infants, selected to represent the diverse demographics of the U.S, and found a widespread deficit of Bifidobacteria in infants. Long-term health data from the infants suggested that a lack of detectable Bifidobacteria in infants may contribute to the development of atopy, a genetic predisposition to developing allergic diseases.

    Global estimates suggest that up to 40% of the population has some form of allergy to substances present in the environment—pollen, dust, mites, or animal dander. The last few decades have also witnessed a growing prevalence of allergic conditions among children, ranging from seasonal allergies with mild symptoms, such as a runny nose, sneezing, and itchy eyes, to severe eczema and life-threatening food allergies that can send someone into an anaphylactic shock.

    Emerging data suggests that the rise in such NCDs actually begins during the first 1,000 days of a child's life—inside the mother's womb and through the first two years of life. Scientists think that while environmental and lifestyle changes play a role, a key factor may be disruptions in the gut microbiome. In infants, this disruption includes the widespread loss of certain beneficial strains of Bifidobacterium that are essential for early immune development and long-term health.

    A baby's mode of delivery (C-section or vaginal birth), whether they were breastfed or formula-fed, and exposure to antibiotics can shape the diversity of their gut microbiome, a factor that has been linked to health issues later in life, including allergies, autoimmune diseases, obesity.

    Data analysis revealed that 25% of  infants between 1 and 3 months of age were deficient in Bifidobacterium, and the deficiency was more pronounced in C-section births (35%) than in vaginal births (19%). In C-section infants, the beneficial bacteria were often replaced by potentially pathogenic bacteria that are known to use up human milk oligosaccharides, components in breast milk that shape the infant gut microbiome.
    They also found that microbiomes rich in Bifidobacterium had fewer antimicrobial-resistant and disease-causing genes, along with more beneficial metabolic profiles.

    The researchers highlight that while the term dysbiosis or imbalance in the microbiome is still up for debate, the strong correlation between microbiome composition and infant health suggests that the absence of these key Bifidobacterium strains represents a true dysbiosis in early life.

    John B. Jarman et al, Bifidobacterium deficit in United States infants drives prevalent gut dysbiosis, Communications Biology (2025). DOI: 10.1038/s42003-025-08274-7

  • Dr. Krishna Kumari Challa

    Scientists use lightning to make ammonia out of thin air

     Researchers have harnessed human-made lightning to develop a more efficient method of generating ammonia—one of the world's most important chemicals. Ammonia is also the main ingredient of fertilizers that account for almost half of all global food production.

    The research was published in Angewandte Chemie International edition.

    The team have successfully developed a more straightforward method to produce ammonia (NH3) in gas form. Previous efforts by other laboratories produced ammonia in a solution (ammonium, NH4+), which requires more energy and processes to transform it into the final gas product.

    The current method to generate ammonia, the Haber-Bosch process, comes at great climate cost, leaving a huge carbon footprint. It also needs to happen on a large scale and close to sources of cheap natural gas to make it cost-effective.

    Naturally occurring ammonia (mostly in the form of bird droppings) was once so high in demand it fueled wars.

    The invention of the Haber-Bosch process in the 19th century made human-made ammonia possible and revolutionized modern agriculture and industry. Currently, 90% of global ammonia production relies on the Haber-Bosch process.

    Industry's appetite for ammonia is only growing. For the past decade, the global scientific community has wanted to uncover a more sustainable way to produce ammonia that doesn't rely on fossil fuels.

    In this new research scientists have successfully developed a method that allows air to be converted to ammonia in its gaseous form using electricity. 

    Part 1

  • Dr. Krishna Kumari Challa

    The plasma-based method this team developed uses electricity to excite nitrogen and oxygen molecules in the air. The team then passes these excited molecules to the membrane-based electrolyzer to convert the excited molecules to ammonia.

    The researchers said this is a more straightforward pathway for ammonia production. This new approach is a two-step process, namely combining plasma and electrolysis.

     Wanping Xu et al, Regulating Multifunctional Oxygen Vacancies for Plasma‐Driven Air‐to‐Ammonia Conversion, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202508240

    Part 2

  • Dr. Krishna Kumari Challa

    Circadian disruption by night light linked to multiple cardiovascular outcomes

    Researchers have linked brighter night-time light exposure to elevated risks of five major cardiovascular diseases.

    Circadian rhythms govern fluctuations in blood pressure, heart rate, platelet activation, hormone secretion, and glucose metabolism. Long-term disruption of those rhythms in animal and human studies have produced myocardial fibrosis, hypertension, inflammation, and impaired autonomic balance.

    In the study, "Personal night light exposure predicts incidence of cardiovascular diseases in >88,000 individuals," posted on medRxiv, researchers conducted a prospective cohort analysis to assess whether day and night light exposure predicts incidence of cardiovascular diseases and whether relationships vary with genetic susceptibility, sex, and age.

    Brighter nights showed dose-response associations with higher risk across all five outcomes. Participants classified in the 90–100th percentile of night-time light exposure experienced 23–32% higher hazard for coronary artery disease, 42–47% for myocardial infarction, 45–56% for heart failure, 28–32% for atrial fibrillation, and 28–30% for stroke compared with those in the 0-50th percentile.

    Relationships persisted after controlling for physical activity, smoking, alcohol, diet, sleep duration, socioeconomic status, and genetic risk. Women displayed stronger associations for heart failure and coronary artery disease whereas younger participants showed stronger associations for heart failure and atrial fibrillation.

    Authors propose circadian misalignment induced by unnatural light may trigger metabolic and vascular perturbations that elevate cardiovascular risk. Impaired glucose tolerance and heightened diabetes susceptibility may foster endothelial dysfunction and atherosclerosis.
    Light-driven hypercoagulability could increase thromboembolic events, while sustained elevation of 24-hour blood pressure may damage vascular endothelium and provoke myocardial hypertrophy. Conflicting timing signals to sinoatrial and atrioventricular nodes may amplify arrhythmic vulnerability.

    Avoiding bright light during habitual sleep times may serve as a practical addition to established cardiovascular prevention strategies, according to the authors, who call for circadian-informed lighting guidance in homes, hospitals, and urban planning.

     Daniel P Windred et al, Personal night light exposure predicts incidence of cardiovascular diseases in >88,000 individuals, medRxiv (2025). DOI: 10.1101/2025.06.20.25329961

  • Dr. Krishna Kumari Challa

    Massive study detects AI fingerprints in millions of scientific papers

    Chances are that you have unknowingly encountered compelling online content that was created, either wholly or in part, by some version of a Large Language Model (LLM). As these AI resources, like ChatGPT and Google Gemini, become more proficient at generating near-human-quality writing, it has become more difficult to distinguish between purely human writing from content that was either modified or entirely generated by LLMs.

    This spike in questionable authorship has raised concerns in the academic community that AI-generated content has been quietly creeping into peer-reviewed publications.

    To shed light on just how widespread LLM content is in academic writing, a team of researchers analyzed more than 15 million biomedical abstracts on PubMed to determine if LLMs have had a detectable impact on specific word choices in journal articles.

    Their investigation revealed that since the emergence of LLMs there has been a corresponding increase in the frequency of certain stylist word choices within the academic literature. These data suggest that at least 13.5% of the papers published in 2024 were written with some amount of LLM processing. The results appear in the open-access journal Science Advances.

    The team also identified notable differences in LLM usage between research fields, countries, and venues.

    Dmitry Kobak et al, Delving into LLM-assisted writing in biomedical publications through excess vocabulary, Science Advances (2025). DOI: 10.1126/sciadv.adt3813

  • Dr. Krishna Kumari Challa

    Metabolic differences in male and female muscles may explain diabetes variations

    The skeletal muscles of men and women process glucose and fats in different ways. A study conducted recently provides the first comprehensive molecular analysis of these differences. The results, published in Molecular Metabolism, possibly give an explanation for why metabolic diseases such as diabetes manifest differently in women and men—and why they respond differently to physical activity.

    Skeletal muscles are far more than just "movement driving motors." They play a central role in glucose metabolism and therefore also in the development of type 2 diabetes. This is due to the fact that around 85% of insulin-dependent glucose uptake takes place in the muscles. This means that if muscle cells react less sensitively to insulin, for example in the case of insulin resistance, glucose is less easily absorbed from the blood. This process is specifically counteracted by physical activity.

    The degree to which muscles work differently in women and men has long been underestimated. It is precisely this issue which has now been investigated by researchers now. 

    The result of the work: The first training session triggered a stronger stress response at the molecular level in men, which became manifest in the increased activation of stress genes and the increase in the muscle protein myoglobin in the blood. In addition, male muscles showed a distinct pattern of what are called fast-twitch fibers, which are designed for short-term, intensive exercise and preferably use glucose as an energy source.

    Women had significantly higher amounts of proteins that are responsible for the absorption and storage of fatty acids: an indication of more efficient fat utilization. After eight weeks of regular endurance training, the muscles of both sexes matched and the muscle fiber-specific differences decreased. At the same time, women and men produced more proteins that promote the utilization of glucose and fat in the mitochondria, the "power plants of the cells."

    These adjustments indicate an overall improvement in metabolic performance, which can help to reduce the risk of type 2 diabetes. 

    Simon I. Dreher et al, Sex differences in resting skeletal muscle and the acute and long-term response to endurance exercise in individuals with overweight and obesity, Molecular Metabolism (2025). DOI: 10.1016/j.molmet.2025.102185

  • Dr. Krishna Kumari Challa

     Image rotation in plasma observed

    Light sometimes appears to be "dragged" by the motion of the medium through which it is traveling. This phenomenon, referred to as "light dragging," is typically imperceptible when light is traveling in most widely available materials, as the movement is significantly slower than the speed of light. So far, it has thus proved difficult to observe in experimental settings.

    Physicists recently observed a specific type of light dragging known as image rotation in a plasma-based system.

    Their observation, outlined in a paper published in Physical Review Letters, was made using magnetohydrodynamic (MHD) waves that propagate in a magnetized plasma, known as Alfvén waves.

    Using recently demonstrated plasma rotation control capabilities in the Large Plasma Device at UCLA, the researhcers managed to show that they can indeed rotate the wave pattern left and right by some tens of degrees by controlling the plasma rotation.

    To realize image rotation in plasma, the researchers leveraged the naturally slow velocity with which Alfvén waves travel. They specifically employed a system in which Alfvén waves are launched in a plasma whose rotation can be controlled using electrically charged electrodes brought in contact with the plasma.

    Their efforts led to the observation of image rotation. In other words, they found that the Alfvén waves' transverse structure appeared to twist.

    Interestingly, they also found that these effects surprisingly matched those predicted by theories explaining light dragging in isotropic systems, media far simpler than plasmas that exhibit the same properties irrespective of the directions they are observed from, demonstrating a broader validity of these results.

     Renaud Gueroult et al, Image Rotation in Plasmas, Physical Review Letters (2025). DOI: 10.1103/swrn-w3yf. On arXivarxiv.org/html/2505.18062v1

  • Dr. Krishna Kumari Challa

    A pointless fashion trend or something else? Chimpanzees wear blades of grass in their ears and rears

    A team of researchers from Utrecht University, Durham University, and other institutions have observed something remarkable at a chimpanzee sanctuary in Zambia. Several chimpanzees from one particular group were seen dangling blades of grass from their ear holes or their behinds, for no apparent reason. The behavior was not seen in other chimpanzee groups at the same sanctuary, despite similar living conditions.

    This shows that like humans, other animals also copy seemingly pointless behaviors from one another. And that, in turn, may offer insights into the evolutionary roots of human culture.

    People regularly do arbitrary things that seem to have no immediate use, like shaving a line into their eyebrow or putting a fashionable scarf on themselves or their dog. Most people do not come up with these things themselves, but copy them from others.

    Other animals also adopt behaviours from one another. Often, though, this is useful behaviour, like chimpanzees learning from each other how to find food. But sometimes, animals develop habits that seem to serve no clear purpose. For instance, a fashion trend among orcas, who were seen wearing a dead salmon on their heads, drew quite a bit of media attention last year. Still, these kinds of "useless" trends in animals have rarely been studied in a systematic way.

    In 2010, researchers discovered that a female chimpanzee at the Chimfunshi Wildlife Orphanage Trust sanctuary repeatedly stuck a blade of grass in her ear and left it there, for no apparent reason. Later, seven of her group members adopted the behaviour. And even after the female trendsetter died, the behaviour continued, and some chimps in the group still do it today. Researchers therefore interpreted this behaviour as a cultural tradition.

    Part 1

  • Dr. Krishna Kumari Challa

    More than a decade later, chimpanzees in another group at the same sanctuary also began sticking blades of grass in their ears. They did not copy this behavior from the earlier group, since they had no contact with them. But in the new group, the grass-in-orifice trend did not stop there. While five of the eight chimpanzees in the new group stuck grass in their ears, six of the eight also let a blade of grass dangle from their behinds.

    The researchers found no evidence that the chimpanzees were bothered by their ears or behinds and used the blades of grass, for example, for relieving an itch.
    By carefully tracking which animals displayed the behavior over time, the researchers showed it was likely that the animals did not each invent the behavior on their own, but copied it from one another. When the researchers looked deeper into how the behavior started, they found something striking.

    Both groups, where chimps put blades of grass in their ears, had the same caretakers. These caretakers reported that they sometimes put a blade of grass or a matchstick in their own ears to clean them. Caretakers in the other groups said they did not do this. The chimps in one group then figured out how to stick the blade of grass in another place as well.

    In the wild, similar "useless" trends have not been seen in chimpanzees. So why do they do it in captivity?
    In captivity, they have more free time than in the wild. They don't have to stay as alert or spend as much time searching for food, say the researchers.
    The question of why humans are more culturally evolved than other animals is still being debated by scientists. Some scientists think the key lies in humans' unique ability to copy, including small, seemingly useless details. Other animals would not be able to do this and would have to constantly reinvent the wheel, which limits their cultural evolution.
    But this study shows that chimpanzees are able to copy small, useless behaviours from each other.
    And this behaviour could also serve a social purpose. By copying someone else's behavior, you show that you notice and maybe even like that individual. So, it might help strengthen social bonds and create a sense of belonging within the group, just like it does in humans.

     Edwin J.C. van Leeuwen et al, Chimpanzees socially learn non-instrumental behaviour from conspecifics, Behaviour (2025). DOI: 10.1163/1568539X-bja10313

    Part 2

  • Dr. Krishna Kumari Challa

    Vampire bats’ mutual grooming helps spread innovative rabies vaccine

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

    Bat vaccine can be spread lickety-split

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Scientists use AI to create protein that kills E. coli

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

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

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

    Part 2

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

    Part 2

  • Dr. Krishna Kumari Challa

    Global vaccine stockpiles prevented more than 5.8 million cases

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

  • Dr. Krishna Kumari Challa

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

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

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

    It could be more than 7 billion years old.

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

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Premenstrual symptoms linked to increased risk of cardiovascular disease

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    How do rivers choose their path?

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Artificial sweeteners leave bitter aftertaste for the environment

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

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

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    How the genome defends itself against internal enemies

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

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

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

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

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

    Part 1

  • Dr. Krishna Kumari Challa

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

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

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

    Part 2

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  • Dr. Krishna Kumari Challa

    Late eating is associated with impaired glucose metabolism

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

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

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

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

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

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

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

    This work was done on identical and fraternal twin pairs. 

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

  • Dr. Krishna Kumari Challa

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

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

    About 2 billion tons of dust are emitted yearly.

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

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

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

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

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

    Source: News Agencies

    **

  • Dr. Krishna Kumari Challa

    A few bright buildings light up the entire night sky

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Chronological age determined within 1.36 years using DNA methylation patterns

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Comparing first-trimester UTI antibiotics and congenital malformations

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

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

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Built-in extinguishers can prevent battery fires and explosions

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

    Tool use declines with age in wild chimpanzees

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

  • Dr. Krishna Kumari Challa

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

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

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

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

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

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

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

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

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

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

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

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

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