Rigid and negative thought patterns linked to increasing political polarization online

The ideological divide between opposing political groups has been drastically increasing in various countries worldwide. This phenomenon, known as political polarization, can lead to greater social division, extremism and political violence.

Researchers  recently carried out a study aimed at better understanding the psychology of political polarization and, more specifically, the thought patterns associated with extreme and opposing political views. Their findings, published in Communications Psychology, unveiled a link between the rising political polarization online and distorted ways of thinking often associated with some mental health disorders, including anxiety and depression.

Distorted thinking appeared to precede polarization in some cases. This suggests that how we think—emotionally and cognitively—may be a key driver of polarization, not just what we believe. Of course, their observations do not imply causality.

Andy Edinger et al, Cognitive distortions are associated with increasing political polarization, Communications Psychology (2025). DOI: 10.1038/s44271-025-00289-4

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Global analysis finds 14.8 million life-years added by COVID-19 vaccinations

A Stanford University-led investigation into the COVID-19 vaccination effort reports that it averted an estimated 2.533 million deaths and 14.8 million life-years worldwide between 2020 and 2024.

Amidst much controversy in the public sphere, a worldwide vaccination campaign took place to counter the novel and deadly COVID-19 virus as it spread to every corner of the globe. As the pandemic spread, so did misinformation, disinformation, and real-time updates on risk and prevention that occasionally changed as events unfolded.

Around 7 million people died as a direct result of the virus. Estimating the human toll prevented by vaccines remains a crucial question, both for  public education and for future public health planning.

In the study, "Global Estimates of Lives and Life-Years Saved by COVID-19 Vaccination During 2020-2024," published in JAMA Health Forum, researchers conducted a comparative-effectiveness analysis to quantify life-saving effects attributable to vaccination from December 2020 through October 1, 2024.

Nearly 8 billion individuals (the 2021 world population) served as the study cohort, partitioned by seven age tiers: community versus long-term-care residence, and pre-omicron versus omicron periods.

Investigators estimated deaths averted by multiplying stratum-specific population, projected infection proportion, infection fatality rate, and vaccine effectiveness; life-year gains combined those results with life expectancy and a health-status adjustment factor.

Findings show 2.533 million lives saved, equating to one death averted per 5,400 vaccine doses. Life-year gains reached 14.8 million, or one life-year per 900 doses.

Part 1

About 82% of deaths averted occurred among individuals vaccinated before any infection and 57% during the omicron period. Persons aged 60 years or older accounted for 89.6% of lives saved, with children and adolescents contributing just 0.01%. Sensitivity analyses yielded a range of 1.4–4.0 million deaths and 7.4–23.6 million life-years saved.

Life-year benefits tracked a similar age gradient with individuals over 60 making up 76% of the total years saved, with negligible contributions (<0.5 %) from those under 30. Long‑term‑care residents, who accounted for 11.8 % of deaths averted, only added 2% to life‑years saved. Authors conclude that vaccination offered a clear mortality benefit during 2020–2024, largely among older adults, and describe their estimates as conservative.

John P. A. Ioannidis et al, Global Estimates of Lives and Life-Years Saved by COVID-19 Vaccination During 2020-2024, JAMA Health Forum (2025). DOI: 10.1001/jamahealthforum.2025.2223

Part 2

Early human ancestors showed extreme size differences between males and females

A newly published study has found that males of some of our earliest known ancestors were significantly larger than females. The pronounced difference in body size present in both Australopithecus afarensis (the East African species that includes the famous fossil "Lucy") and A. africanus (a closely related southern African species) suggests the ancient hominins may have lived in social systems marked by intense competition among males, leading to the substantial size disparity among the sexes.

The research  appears in the July issue of the American Journal of Biological Anthropology. Using a novel approach that overcomes the limitations of incomplete fossil records, the study reveals that both A. afarensis and A. africanus were more sexually dimorphic than modern humans—and in some cases, even more than gorillas.

These weren't modest differences. In the case of A. afarensis, males were dramatically larger than females—possibly more so than in any living great ape. And although both of these extinct hominin species exhibited greater sex-specific size differences than modern humans do, they were also more different from each other in this respect than living ape species are, suggesting a greater diversity of evolutionary pressures acting on these closely related species than we had previously appreciated.

The results add new depth to interpretations of the fossil record. Earlier studies had reached differing conclusions about dimorphism in A. afarensis, with some suggesting it resembled the relatively low levels seen in modern humans. Furthermore, direct comparison between fossil species had not previously been made because investigations were limited by incomplete fossil samples and insufficient statistical power to detect real differences.

This analysis overcomes these issues by using an iterative resampling method that mimics the missing data structure in both fossil species when sampling from skeletal material of living species, allowing the inclusion of multiple fossil individuals even when those individual specimens are fragmentary.

This study provides strong evidence that sex-specific evolutionary pressures—likely involving both male competition for mates and resource stress acting more intensely on female size due to the metabolic constraints of pregnancy and lactation—played a larger role in early hominin evolution than previously thought. 

Part 1

Sexual size dimorphism (SSD) isn't just a physical trait—it reveals something deeper about behavior and evolutionary strategy. Consistent with sexual selection theory, high SSD in living primates typically correlates with strong male–male competition and social structures allowing for polygynous mating systems, where one or a few large males monopolize reproductive access to multiple females.

In contrast, low SSD can be found in any species, but tends to be found in those with pair-bonded social structures and low competition for mating opportunities. Modern human populations exhibit low to moderate SSD, where males tend to be slightly larger than females on average but with substantial overlap in size between the sexes.

High SSD in living primates can also be associated with intense resource stress—when food is scarce, small healthy females can get enough food to meet their own metabolic needs and store energy for reproduction faster than larger females can, leading to more offspring with smaller mothers in the next generation and a resulting greater difference in male and female size.

The high SSD identified in both Australopithecus species suggests a high degree of competition among males, similar to that of chimpanzees or even gorillas, while the difference between the two fossil species may be due to a difference in the intensity of those forces of sexual selection and/or a difference in the intensity of resource stress in their environments (e.g., a difference in the length of dry seasons with low fruit availability) and its impact on female body size.

In any event, the high SSD in these fossil hominins contrasts sharply with the more balanced size seen in modern humans and offers a glimpse into a different model of early hominin life—one where large size may have been a key factor in male reproductive success for competitive reasons, and small size may have been a key factor for females for energetic reasons.

Part 2

Australopithecus afarensis, which lived between 3.9 and 2.9 million years ago, is widely regarded as either a direct ancestor of modern humans or a species very closely related to a direct ancestor.

Yet, its high degree of sexual dimorphism suggests that early hominins may have lived in social systems that were far more hierarchical and competitive than once thought.

Meanwhile, the less dimorphic A. africanus—which overlapped in time with A. afarensis but first shows up and last appears in the fossil record slightly later, between roughly 3.3 and 2.1 million years ago—may represent a different evolutionary branch on the hominin tree, or perhaps a transitional stage in the development of more human-like social behavior.
We typically place these early hominins together in a single group called the gracile australopiths, a group of species that are thought to have interacted with their physical and social environments in very similar ways.
while that's true to a certain extent—the evidence suggests that both these species may have had social organizations more like gorillas than modern people—the significant difference in the amount of dimorphism in these two extinct species suggests that these closely related hominin species were subject to selection pressures more distinct than the selection pressures applied to any pair of similarly closely related living ape species, highlighting the diversity of ways that our extinct ancestors and close relatives interacted with the world.

 Adam D. Gordon, Sexual Size Dimorphism in Australopithecus: Postcranial Dimorphism Differs Significantly Among Australopithecusafarensis, A. africanus, and Modern Humans Despite Low‐Power Resampling Analyses, American Journal of Biological Anthropology (2025). DOI: 10.1002/ajpa.70093

Part 3

Aging dampens lupus by reducing overactive immune genes in older adults

 Researchers have found that certain antiviral genes become less active over time in lupus, revealing why some patients see their symptoms fade as they age.

Lupus, an autoimmune disease, causes the immune system's first-line viral defenses—known as interferons—to attack the body. Nearly every organ is at risk, leading to conditions like kidney and heart disease.

But unlike many other autoimmune or chronic illnesses, lupus can improve as patients reach their 60s and 70s.

By analyzing blood samples from patients across the age spectrum, scientists discovered that aging turns down the activity of certain immune genes in people with lupus, leading to fewer interferons and other inflammatory proteins in the body.

The study found that in healthy adults, inflammation-related genes and proteins rose slowly over the years, a process that has been dubbed "inflammaging." In patients with lupus, however, the expression of these genes and proteins was abnormally high in midlife but decreased as the decades went by.

"Inflammaging seemed to be reversed in the lupus patients", say the researchers.

"But it wasn't fully reversed. The lupus patients still had a greater level of inflammatory signaling compared to healthy adults in older age."

Rithwik Narendra et al, Epigenetic attenuation of interferon signaling is associated with aging-related improvements in systemic lupus erythematosus, Science Translational Medicine (2025). DOI: 10.1126/scitranslmed.adt5550

The brain clocks sickness from a mile off

The brain fires up immune cells when sick people are nearby

At the mere sight of a sick person, the brain kickstarts an immune response mimicking the body’s response to an actual infection. In a study, volunteers donned virtual reality headsets to view human avatars with rashes, coughs or other symptoms of illness. Researchers found that the sight of a sick person activates the brain’s ‘salience network’: a collection of regions involved in recognizing and responding to threats. This activity triggered a surge in innate lymphoid cells, which are part of the body’s first line of defence against invaders.

https://www.nature.com/articles/s41593-025-02008-y?utm_source=Live+...

'One and done': A single shot at birth may shield children from HIV for years

A new study in Nature shows that delivering a single injection of gene therapy at birth may offer years-long protection against HIV, tapping into a critical window in early life that could reshape the fight against pediatric infections in high-risk regions.

This study is among the first to show that the first weeks of life, when the immune system is naturally more tolerant, may be the optimal window for delivering gene therapies that would otherwise be rejected at older ages.

In the study, nonhuman primates received a gene therapy that programs cells to continuously produce HIV-fighting antibodies. Timing proved critical to the one-time treatment offering long-term protection.

Those that received the treatment within their first month of life were protected from infection for at least three years with no need for a booster, potentially signifying coverage into adolescence in humans. In contrast, those treated at 8–12 weeks showed a more developed, less tolerant immune system that did not accept the treatment as effectively.

As long as the treatment is delivered close to birth, the baby's immune system will accept it and believe it's part of itself.

Mauricio Martins, Determinants of successful AAV delivery of HIV-1 bNAbs in early life, Nature (2025). DOI: 10.1038/s41586-025-09330-2. www.nature.com/articles/s41586-025-09330-2

Anticipation of a virtual infectious pathogen is enough to prompt real biological defenses

Researchers  report that neural anticipation of virtual infection triggers an immune response through activation of innate lymphoid cells.

Innate lymphoid cells (ILCs) are a type of immune cell crucial for early immune responses. They do not rely on antigen recognition like adaptive immune cells but respond quickly and effectively to various inflammatory signals and pathogen-associated cues, playing an essential role in early defense.

Protecting the body from pathogens typically involves a multitude of responses after actual contact. An anticipatory biological immune reaction to an infection had not been previously demonstrated.

In the study, "Neural anticipation of virtual infection triggers an immune response," published in Nature Neuroscience, researchers designed a multisensory experiment to test whether human brains could anticipate potential infections through virtual reality (VR) and initiate early immune system reactions.

Participants in the experiments conducted exposed to infectious avatars showed an expansion of peripersonal space (PPS) effects, measurable as faster reaction times to tactile stimulation even at farther avatar distances. EEG analyses, performed on a separate group of 32 participants, revealed anticipatory neural responses in multisensory-motor areas and activation within the salience network, particularly the anterior insula and medial prefrontal cortex.

ILCs were significantly modulated in frequency and activation by virtual infections, resembling immune reactions to real pathogens, assessed through comparison with an influenza vaccine cohort. Specifically, both virtual and real infections induced decreases in ILC1s and increases in ILC2s and ILC precursors, indicative of active immune mobilization.

Researchers concluded that the human immune system activates not only after physical contact but also when infection threats breach the functional boundary of body-environment interaction, represented by PPS. This anticipatory neuro-immune mechanism would have advantages, enabling rapid responses to potential infections, even in virtual contexts.

Sara Trabanelli et al, Neural anticipation of virtual infection triggers an immune response, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02008-y

Deepest-known animal communities found nearly 10 km below sea in Mariana Trench

A submersible has discovered thousands of worms and mollusks nearly 10 kilometers (six miles) below sea level in the Mariana Trench, the deepest colony of creatures ever observed, a study revealed this week.

The discovery in Earth's deepest underwater valley suggests that there could be much more life thriving in the hostile conditions at the bottom of our planet's largely unexplored oceans than previously thought,  scientists said.

The study marked "the discovery of the deepest and the most extensive chemosynthesis-based communities known to exist on Earth.

The researchers who conducted this study  said they also found "compelling evidence" that methane was being produced by microbes, with the tubeworms tending to cluster around microbial mats that resemble snow.

Xiaotong Peng et al, Flourishing chemosynthetic life at the greatest depths of hadal trenches, Nature (2025). DOI: 10.1038/s41586-025-09317-z

Just now I received this information from the initiators of this Prize and I am sharing this with the followers of this network

₹20 Crore National Science Prizes Launched to Champion India’s Leading Scientific Talent

• The initiative was announced by Catalyst funder, Blockchain for Impact, under the aegis of Sandeep Nailwal Academy
• It seeks to incentivize high-impact scientific research and honour distinguished innovators across disciplines, supporting India’s strategic commitment to fostering a robust and globally competitive research ecosystem.

New Delhi, 30 July 2025, Wednesday: In a pivotal initiative to strengthen India’s scientific research landscape, Blockchain For Impact, a catalyst funder and non-profit, has today announced the launch of National Science Prizes, with a total allocation of ₹20 crore. These prestigious awards are designed to incentivize groundbreaking research and celebrate exceptional contributions by scientists and innovators across diverse disciplines for India. By recognizing excellence and fostering a culture of innovation, the initiative supports the nation’s strategic commitment to advancing science and technology as key drivers of economic and societal progress.

Established by Sandeep Nailwal,  a young tech entrepreneur, innovator, and philanthropist - the National Science Prizes reflect his deep commitment to advancing India’s scientific potential and his steadfast intent to give back to the nation.

The awards will be distributed across the following categories ; the Lifetime Achievement Award to two distinguished individuals for their profound contributions to science and health, with each receiving Rs 25 lakh; the Sandeep Nailwal India First Award, supporting three Indian-origin or global researchers, entrepreneurs, and innovators relocating to India to scale solutions in biomedical science or public health, each granted Rs 2.5 crore; the Sandeep Nailwal Award for Global Excellence, given to two individuals whose work has globally reshaped biomedical research and public health, with each awarded Rs 5 crore; and the Sandeep Nailwal Award for Young Indian Scientist Award, recognizing two biomedical scientists, public health pioneers, and cross-sector changemakers under 40 who have built transformative solutions, each receiving Rs 50 lakh.

Using a fan can make older adults hotter in a dry heat

Research has found that older adults using an electric fan at 38 °C and 60% relative humidity experienced a modest fall in core temperature and greater comfort. Fan use at 45 °C and 15% relative humidity raised core temperature and increased discomfort.

CDC guidance warns against fan use above 32 °C because of concerns that added airflow could speed heat gain in vulnerable groups. Modeling studies and small laboratory trials have hinted that airflow may help when humidity is high, but effects at very high temperatures in older adults have remained uncertain. Older individuals face elevated heat-related morbidity, creating an urgent need for practical, low-cost cooling ideas.

In the study, "Thermal and Perceptual Responses of Older Adults With Fan Use in Heat Extremes," published in JAMA Network Open, researchers performed a secondary analysis of a randomized crossover clinical trial to test how fan use and skin wetting influence core temperature, sweating, and thermal perception during extreme-heat exposures.

Study investigators conclude that electric fans can serve as a safe, low-cost cooling option for older adults during hot, humid weather at 38 °C, but should be avoided in very hot, dry conditions. Simple skin wetting offers an additional means to manage heat stress while limiting dehydration. Public health agencies may use these findings to refine summer heat-safety messages for seniors.

Georgia K. Chaseling et al, Thermal and Perceptual Responses of Older Adults With Fan Use in Heat Extremes, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.23810

Car tires are polluting the environment and killing salmon

In the 1990s, scientists restoring streams around Seattle, Wash., noticed that returning coho salmon were dying after rainstorms. The effects were immediate: the fish swam in circles, gasping at the surface, then died in a few hours. Over the next several decades, researchers chipped away at the problem until in 2020 they discovered the culprit: a chemical called 6PPD-quinone that forms when its parent compound, a tire additive called 6PPD, reacts with ozone.

6PPD-quinone kills coho salmon at extraordinarily low concentrations, making it one of the most toxic substances to an aquatic species that scientists have ever found.

Today, a growing body of evidence shows that tire additives and their transformation products, including 6PPD-quinone, are contaminating ecosystems and showing up in people.

Now,  the researchers who made that initial discovery are calling for international regulation of these chemicals to protect people and the environment.

https://pubs.acs.org/doi/10.1021/acs.estlett.5c00453

Modern-day potato originated from hybridization event with tomatoes 9 million years ago, study reveals

An international research team has uncovered that natural interbreeding in the wild between tomato plants and potato-like species from South America about 9 million years ago gave rise to the modern-day potato.

In a study published in the journal Cell, researchers suggest this ancient evolutionary event triggered the formation of the tuber, the enlarged underground structure that stores nutrients found in plants like potatoes, yams, and taros.

These findings show how a hybridization event between species can spark the evolution of new traits, allowing even more species to emerge. 

As one of the world's most important crops, the potato's origin had long puzzled scientists. In appearance, modern potato plants are almost identical to three potato-like species from Chile called Etuberosum. But these plants do not carry tubers. Based on phylogenetic analysis, potato plants are more closely related to tomatoes.

To solve this contradiction, researchers analyzed 450 genomes from cultivated potatoes and 56 of the wild potato species.

They found that every potato species contained a stable, balanced mix of genetic material from both Etuberosum and tomato plants, suggesting that potatoes originated from an ancient hybridization between the two.

While Etuberosum and tomatoes are distinct species, they shared a common ancestor about 14 million years ago. Even after diverging for about 5 million years, they were able to interbreed and gave rise to the earliest potato plants with tubers around 9 million years ago.

The team also traced the origins of the potato's key tuber-forming genes, which are a combination of genetic material from each parent. They found the SP6A gene, which acts like a master switch that tells the plant when to start making tubers, came from the tomato side of the family. Another important gene called IT1, which helps control growth of the underground stems that form tubers, came from the Etuberosum side. Without either piece, the hybrid offspring would be incapable of producing tubers.

This evolutionary innovation coincided with the rapid uplift of the Andes mountains, a period when new ecological environments were emerging. With a tuber to store nutrients underground, early potatoes were able to quickly adapt to the changing environment, surviving harsh weather in the mountains.

 Ancient hybridization underlies tuberization and radiation of the potato lineage, Cell (2025). DOI: 10.1016/j.cell.2025.06.034. www.cell.com/cell/fulltext/S0092-8674(25)00736-6

Changes in diet drove physical evolution in early humans

As early humans spread from lush African forests into grasslands, their need for ready sources of energy led them to develop a taste for grassy plants, especially grains and the starchy plant tissue hidden underground.

But a new study  shows that hominins began feasting on these carbohydrate-rich foods before they had the ideal teeth to do so. The study provides the first evidence from the human fossil record of behavioral drive, wherein behaviors beneficial for survival emerge before the physical adaptations that make it easier, the researchers report in Science.

The study authors analyzed fossilized hominin teeth for carbon and oxygen isotopes left behind from eating plants known as graminoids, which include grasses and sedges. They found that ancient humans gravitated toward consuming these plants far earlier than their teeth evolved to chew them efficiently. It was not until 700,000 years later that evolution finally caught up, in the form of longer molars like those that let modern humans easily chew tough plant fibers.

The findings suggest that the success of early humans stemmed from their ability to adapt to new environments despite their physical limitations.

Isotope analysis overcomes the enduring challenge of identifying the factors that caused the emergence of new behaviors—behavior doesn't fossilize.

Anthropologists often assume behaviors on the basis of morphological traits, but these traits can take a long time—a half-million years or more––to appear in the fossil record.

These chemical signatures are an unmistakable remnant of grass-eating that is independent of morphology. They show a significant lag between this novel feeding behavior and the need for longer molar teeth to meet the physical challenge of chewing and digesting tough plant tissues.

 Luke D. Fannin et al, Behavior drives morphological change during human evolution, Science (2025). DOI: 10.1126/science.ado2359. www.science.org/doi/10.1126/science.ado2359.

Microplastics Alter Predator Preferences of Prey through Associative Learning

Exposure to microplastics can give roundworms (Caenorhabditis elegans) a taste for plastic-contaminated food.

When given the choice of plastic-laced or uncontaminated food, worms initially opted for the cleaner option. But after a few generations of worms were exposed to contaminated food, they developed an attraction to contaminated food. This behavior wasn’t seen in mutated worms that had a learning deficit, meaning that the preference for plastic was probably learned and passed down across generations.

https://pubs.acs.org/doi/10.1021/acs.estlett.5c00492

Exposure to microplastic makes animals want to eat it more

Over multiple generations, small nematode worms began preferring microplastic-contaminated food over cleaner options, which could have consequences for ecosystem health

https://www.newscientist.com/article/2488923-exposure-to-microplast...

COVID and flu can ‘wake up’ cancer
Common respiratory illnesses such as COVID-19 or flu can awaken dormant cancer cells in mice. When a tumour grows, some cells can detach, travel round the body and ‘hide’ in tissues such as the lungs after treatment. Researchers found that the release of an immune molecule called interleukin-6, triggered by respiratory illnesses, wakes up these dormant cells — but only for a short time. This means that the infections do not directly cause cancer, but make it more likely that a future threat could revive the disease.

https://www.nature.com/articles/s41586-025-09332-0?utm_source=Live+...

Scientists shrink the genetic code of E. coli to contain only 57 of its usual 64 codons

The DNA of nearly all life on Earth contains many redundancies, and scientists have long wondered whether these redundancies served a purpose or if they were just leftovers from evolutionary processes. Both DNA and RNA contain codons, which are sequences of three nucleotides that either provide information about how to form a protein with a specific amino acid or tell the cell to stop (a stop signal) during protein synthesis.

Altogether, there are 64 possible codon combinations and these combinations are nearly universal for all life on Earth. But some codons are redundant. There are only 20 amino acids available for a cell to work with, and 61 of the 64 codons are available for protein synthesis, while 3 are used as stop signals. This makes for a lot of redundancy in codons.

Some studies suggest that these redundancies might help prevent mutations in DNA, but reducing the genetic code of certain organisms by removing unnecessary parts can also be beneficial. In 2019, a group of scientists reduced the genome of E. coli to 61 codons from 64 by making 18,214 changes. They called the resulting version Syn61 and this virus-resistant version is being used to create more reliable drugs and for manufacturing novel materials.

Now, another group of scientists, some of whom worked on Syn61, have managed to further reduce the genetic code of E. coli down to 57 codons, making Syn57. They recently published their work in Science.

Part 1

This further reduction was a massive effort to take on. The team made over 101,000 codon changes by dividing up the genome into 38 sections and meticulously swapping out redundant codons with synonymous codons—those that perform the same function. Each time a swap was made, the researchers had to determine if the swap would be detrimental to the viability of the bacteria before moving on.

Mapping and fixing at each stage of the synthesis was often crucial to enabling the next step of the synthesis. These experiments provide a paradigm for integrating 'just in time' defect mapping and fixing of initial designs into synthetic schemes, such that local defects are identified and fixed early in the synthesis and longer range, potentially epistatic or synthetic lethal, defects are identified and fixed as they emerge in the assembly process.

In the end, the research team successfully shortened the genetic code to 57 codons by replacing six sense codons and a stop codon with synonymous codons. The resulting bacteria made with the new code were indeed a living organism, but the researchers found that they grow around four times slower than the parent strain—a problem they hope to eventually fix. However, the new strain shows a distinct gene expression profile, which indicates broad physiological adaptation.

Some possible applications of this new strain include virus-resistant organisms for biotechnology and industry, and the synthesis of proteins and polymers with new properties. Overall, the researchers are optimistic about the potential for this new strain. Their work also raises questions about whether there are limits to reducing the number of codons or creating organisms with entirely novel biochemistries.

Wesley E. Robertson et al, Escherichia coli with a 57-codon genetic code, Science (2025). DOI: 10.1126/science.ady4368

Part 2

When immune commanders misfire: New insights into rheumatoid arthritis inflammation

Rheumatoid arthritis (RA) is a chronic autoimmune disease in which the immune system mistakenly attacks the lining of the joints (the synovium), causing pain, swelling, and progressive damage. Approximately 18 million people worldwide live with RA. Early diagnosis and treatment can relieve symptoms, slow disease progression, and help prevent disability.

Current therapies focus on reducing inflammation and preserving joint function, but up to 30% of patients do not respond well. This underscores the pressing need to better understand its pathology for early diagnosis and the development of more effective therapies.

Helper T cells are a type of white blood cell that act as the "commanders" of the immune system. They play a crucial role by recognizing threats and coordinating immune responses. However, in autoimmune diseases like RA, these commanders become dysregulated and cause the immune system to attack the body's own tissues.

Although helper T cells are known to be major players in RA, the precise molecular mechanisms driving inflammation are still unclear.

Part 1

Now, researchers have discovered a primate-specific cytokine called IGFL2, produced by a subset of helper T cells known as peripheral helper T (Tph) cells in the joints of patients with RA.

Their findings, published in Science Immunology, suggest that IGFL2 helps regulate inflammation in the synovial tissue of affected joints and could serve as both a marker of disease activity and a promising target for new therapies.
Using gene expression data from single-cell analysis and clinical information, researchers analyzed individual helper T cells from the joint tissue of patients with RA. They identified a distinct subgroup known as Tph cells, which are closely linked to more severe disease.

Notably, these cells produce IGFL2 (Insulin-like Growth Factor-Like Family Member 2), a cytokine found only in primates. IGFL2 was exclusively expressed in helper T cells within synovial tissue, with the highest levels seen in Tph cells.

The researchers then explored how IGFL2 drives inflammation in RA. They found that IGFL2 boosts the production of a protein called CXCL13, which promotes the production of autoantibodies. Additionally, IGFL2 activates immune cells known as monocytes and macrophages, further amplifying inflammation and joint damage. This is supported by the fact that blocking IGFL2 reduces the activation of these cells.

To assess its clinical relevance, the team measured IGFL2 levels in blood samples from patients with RA. IGFL2 levels were much higher in patients compared to healthy individuals, and even higher in those with more severe symptoms. Its ability to distinguish patients with RA from healthy individuals was similar to commonly used diagnostic markers.

Taken together, these findings suggest that IGFL2 is not just a marker of disease activity but may also actively drive inflammation in RA, making it a promising target for new treatments.
Because this gene is unique to primates, this discovery wouldn't have been possible using conventional animal models like mice or rats.

Human CD4+ T cells regulate peripheral immune responses in rheumatoid arthritis via insulin-like growth factor like family member 2, Science Immunology (2025). DOI: 10.1126/sciimmunol.adr3838

Part 2

A baby boy from a nearly 31-year-old frozen embryo

A baby boy born last week to a couple developed from an embryo that had been frozen for more than 30 years in what is believed to be the longest storage time before a birth.

In what's known as embryo adoption, Linda and Tim Pierce used a handful of embryos donated in 1994 in pursuit of having a child after fighting infertility for years. Their son was born Saturday from an embryo that had been in storage for 11,148 days, which their  doctor says sets a record.

According to Dr. John David Gordon, the transfer of the nearly 31-year-old embryo marks the longest-frozen embryo to result in a live birth.

Source: News agencies

Spider Venom Prevents Tissue Damage After Heart Attack and Stroke

Researchers are using peptides isolated from spider venom to develop treatments for a range of neurological and cardiovascular disorders.

 While a handful of spider venoms are deadly to humans, most are not, and many can be incredibly useful.

Biochemists discovered chemical compounds that can be used to treat stroke, cardiovascular disease, epilepsy, pain, and many more diseases over the years. They  began to realize that these venoms were extremely complex, and most of the compounds in them targeted a class of receptors called ion channels.

Ion channels are the second most common target of all currently available drugs, and they play a role in a range of diseases—primarily nervous system disorders. Many ion channels are very hard to target with small molecules. They're very complex, and they don't have a lot of real estate outside of the cell membrane, so they're really hard to target with antibodies.

So they  decided that they should use the gold mine of spider venom peptides that target these receptors to develop human therapeutics. 

Out of  the peptides they tested 's web spider’s venom stood out in initial screens against relevant ion channels. 

They found that when they delivered it two or four hours after a stroke, they could reduce the brain damage by 80 percent.

In an ischemic stroke, the oxygen supply to cells and tissues of the brain is cut off, which results in a more acidic pH within the affected tissues. This lower pH activates the acid-sensing ion channel 1a (ASIC1a), which in turn causes cell death and permanent tissue damage. By blocking ASIC1a, the Hi1a prevents brain damage progression following an ischemic stroke—even up to eight hours after the event.

Then they went on to show that they could reduce the injury after a heart attack using [Hi1a] as well. 

Saez NJ, et al. Spider-venom peptides as therapeutics. Toxins. 2010;2(12):2851-2871.

Jiang Y, et al. Pharmacological inhibition of the voltage-gated sodium channel NaV1.... ACS Pharmacol Transl Sci. 2021;4(4):1362-1378.

Scientists design superdiamonds with theoretically predicted hexagonal crystal structure

The brilliantly shiny diamond is more than just pretty; it's one of the hardest minerals on Earth, with a name derived from the Greek word adámas, meaning unbreakable. Scientists have now engineered a harder form of diamond known as bulk hexagonal diamond (HD)—a crystalline structure that has been theorized for over half a century to have physical properties superior to those of conventional diamond.

In a study published in Nature, researchers  synthesized bulk hexagonal diamond, ranging from 100-µm-sized to mm-sized, with a highly ordered structure by compressing and heating high-quality graphite single crystals under pressure conditions as uniform as possible.

The designed material, which was recoverable under ambient conditions, unveiled the previously elusive structural world of HD, opening new avenues for exploring its potential as a technologically superior material.

 Liuxiang Yang et al, Synthesis of bulk hexagonal diamond, Nature (2025). DOI: 10.1038/s41586-025-09343-x

Scientists produce quantum entanglement-like results without entangled particles in new experiment

In the everyday world that humans experience, objects behave in a predictable way, explained by classical physics. One of the important aspects of classical physics is that nothing travels faster than the speed of light. Even information is subject to this rule. However, in the 1930s, scientists discovered that very small particles abide by some very different rules. One of the more mind-boggling behaviors exhibited by these particles was quantum entanglement—which Albert Einstein termed "spooky action at a distance."

In quantum entanglement, two particles can become entangled—meaning their properties are correlated with each other and measuring these properties will always give you opposite results (i.e., if one is oriented up, the other must be down). The strange part is that you still get correlated measurements instantaneously, even if these particles are very far away from each other.

If information cannot travel faster than the speed of light, then there should not be a way for one particle to immediately know the state of the other. This "spooky" quantum property is referred to as "nonlocality"—exhibiting effects that should not be possible at large distances in classical mechanics.

Up until recently, it was thought that only entangled particles could exhibit this nonlocality. But a new study, published in Science Advances, has used Bell's inequality to test whether nonlocal quantum correlations can arise from other non-entanglement quantum features.

The experiment used photons generated by laser light hitting a particular type of crystal in such a way that it is impossible to determine their source. The setup ensures that the photons cannot become entangled before their detection at two separate detectors. The researchers used Bell's inequality to determine if the experiment resulted in violations of local realism.

According to their calculations, the experiment resulted in a violation of the Bell inequality, exceeding the threshold by more than four standard deviations. This kind of violation using unentangled photons had not been seen before. The researchers say these violations of Bell's inequality arise from a property called quantum indistinguishability by path identity, instead of entanglement.

This work establishes a connection between quantum correlation and quantum indistinguishability, providing insights into the fundamental origin of the counterintuitive characteristics observed in quantum physics, the study authors write.

Part 1

While this work might be groundbreaking, there are still some possible issues that need to be ironed out in future studies. For example, the experiment relies on post selection—where only certain photons are detected, possibly giving misleading results.

Another possible issue comes from a locality loophole due to the phase settings of the detectors not being separated properly. However, the study authors are aware of this study's limitations and are eager to find fixes to these issues and try again.

 Kai Wang et al, Violation of Bell inequality with unentangled photons, Science Advances (2025). DOI: 10.1126/sciadv.adr1794

Part 2

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Cells have a second DNA repair toolbox for difficult cases

The human genome consists of 3 billion base pairs, and when a cell divides, it takes about seven hours to complete making a copy of its DNA. That's almost 120,000 base pairs per second. At that breakneck speed, one might expect errors to occur, and they do, at a rate of about two per second in every dividing cell. But cells have a "DNA repair kit" of enzymes that can correct those errors at a rate matching that at which they occur. 

That is amazing!

However, a bigger problem happens when there is a barrier to DNA replication, the process of copying the DNA. It can lead to a break in the chromosome, which will lead to loss of vital genetic information if not repaired. Gaps or breaks in DNA can be potentially harmful or fatal, should they lead to genetic diseases or cancer.

Researchers have  been examining cell DNA repair response to these critical events in yeast cells as an analog to human cells, and has discovered that the process is more elaborate and layered than previously thought.

In a recent study published in Cell Reports,  scientists looked at areas of the DNA that are particularly susceptible to breakage.

Those areas are where the sequence consists of long stretches of repeated triplets like CAGCAGCAG, or couplets like ATATATAT, which continue from just a few to hundreds of units long. When that occurs, the DNA may not always fold neatly into a long double helix, but may twist on itself to form hairpins and cruciform structures—like a tangled electric cord.

This is not a minor issue because repetitive DNA makes up about 10% of our genome, which is even greater than the portion that codes for protein.

When the strands become twisted, the repair proteins that scan the length of DNA can hit a snag and fail to carry out their task. That's when a second set of DNA repair proteins  comes into play.  Scientists are learning that there are backup mechanisms, and now it seems there is a place in the cell where the particularly difficult repairs go to get fixed.

That location is at the inner edge of the cell's nucleus, and a   recent paper by scientists describes how the damaged DNA gets there. The way the DNA gets to the periphery of the nucleus depends on the nature of the damage. For CAG repeats, to use an analogy, it's like adding a shipping label to the damaged goods and sending them out to the repair shop.

Part 1

When the first repair attempt stalls at the separating strands (known as the "replication fork"), a set of proteins tasked with stabilizing the fork adds a phosphate—that's the label—to a "signaling" protein. The signal results in the release of the damaged chromosome from a physical tether, allowing it more freedom to move within the nucleus. This release also triggers the formation of microtubules—long polymerized "tracks" of proteins that lead right to the nuclear periphery. The damaged DNA is carried along those tracks to where repair can be completed.

Having uncovered how this backup mechanism for DNA repair works, the scientists who conducted this work points to a potential strategy for treating cancer: Cancer cells have to replicate their genomes really fast, and they may be relying heavily on these backup mechanisms of DNA repair to survive. If we can target DNA repair vulnerabilities, we might have a way to preferentially kill a cancer cell.
That is why we study everything in detail, to use the knowledge in controlling the situations and curing the diseases!

Isn't this more amazing?

Tyler M. Maclay et al, The DNA replication checkpoint targets the kinetochore to reposition DNA structure-induced replication damage to the nuclear periphery, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116083

Part 2

How the brain constructs emotional experiences

Arousal—how alert or excited one feels—is a basic part of emotions, along with whether those emotions are positive or negative.

A recent study  published in Nature Communications uncovers a brain signature that reveals how emotional intensity is consciously experienced—and whether this experience is distinct from automatic bodily reactions.

Using a powerful combination of AI-driven modeling, advanced brain imaging, and close-to-real-life experimental paradigms, the team was able to uncover a brain signature that precisely measures emotional intensity (arousal) across diverse situations ranging from seeing a loved one to watching a horror movie. Notably, the team was able to disentangle the conscious emotional experience from automatic physiological responses such as sweating or heart racing.

The findings touch on a core debate that has fascinated philosophers and psychologists for more than 150 years, debating whether conscious feelings and bodily reactions can be separated. Such insights could drive the next generation of emotionally intelligent AI systems by indicating that conscious emotional experience can be disentangled from bodily aspects.

Beyond the theoretical implications, this discovery opens new avenues for:

• Developing and designing emotionally intelligent AI systems
• Advancing brain-computer interfaces and affective computing, and
• Designing more precise interventions for emotional disorders such as anxiety and depression.

In short, this research offers a better, more precise way to understand how our brains create emotional arousal, and it could help with future studies and applications in understanding emotions.

Ran Zhang et al, A neurofunctional signature of affective arousal generalizes across valence domains and distinguishes subjective experience from autonomic reactivity, Nature Communications (2025). DOI: 10.1038/s41467-025-61706-0

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Eating earlier linked to long-term weight-loss success

 researchers report that eating earlier in the day blunts the weight gain ordinarily predicted by a high genetic score for obesity.

Meal timing has drawn attention for associated effects on metabolism, energy expenditure, and circadian alignment. Zeitgeber, a rhythmically occurring body phenomenon which acts as a cue in the regulation of the body's circadian rhythms, can also synchronize metabolic tissues such as the liver, pancreas, and adipose tissue.

Changes in food timing can alter zeitgeber, leading to a change in the molecular timing of circadian clock cues and, consequently, rhythms in metabolic function.

Peripheral oscillators in metabolic organs and tissues sensitive to food timing may become desynchronized from the central clock, which is highly sensitive to environmental light. It is hypothesized that such internal circadian misalignment may contribute to adverse cardiometabolic traits and obesity.

In the study, "Early meal timing attenuates high polygenic risk of obesity," published in Obesity, the team performed linear regression analyses to test whether meal timing interacts with a genome-wide polygenic score on BMI and long-term weight-loss maintenance.

Investigators calculated a polygenic risk score for BMI from 900,492 single-nucleotide polymorphisms and assessed the timing of meals. Midpoint of meal intake was calculated as the halfway time between a participant's first and last meals, weighted across weekdays and weekends. Linear regression models adjusted for age, sex, clinic site, and principal ancestry components.

Each hour of later midpoint corresponded to a 0.952 kg/m² higher baseline BMI and a 2.2% rise in body weight at 12 years (± 3 y) after treatment. Within the highest polygenic risk tertile, BMI climbed by about 2.21 kg/m² for every hour of meal delay. No association appeared in lower-risk groups.

The authors conclude that meal timing is associated with weight-loss maintenance and moderates genetic risk, suggesting that early eating could form part of personalized obesity interventions.

R De la Peña‐Armada et al, Early meal timing attenuates high polygenic risk of obesity, Obesity (2025). DOI: 10.1002/oby.24319

Divya Joshi et al, Timing Matters: Early Eating Mitigates Genetic Susceptibility for Obesity, Obesity (2025). DOI: 10.1002/oby.24350

Scientists create gold hydride by combining gold and hydrogen under extreme conditions

An international research team formed solid binary gold hydride, a compound made exclusively of gold and hydrogen atoms.

The researchers were studying how long it takes hydrocarbons, compounds made of carbon and hydrogen, to form diamonds under extremely high pressure and heat.

In their experiments at the European XFEL (X-ray Free-Electron Laser) in Germany, the team studied the effect of those extreme conditions in hydrocarbon samples with an embedded gold foil, which was meant to absorb the X-rays and heat the weakly absorbing hydrocarbons. To their surprise, they not only saw the formation of diamonds, but also discovered the formation of gold hydride.

 Gold is typically chemically very  unreactive—that's why researchers use it as an X-ray absorber in the experiments.

These results suggest there's potentially a lot of new chemistry to be discovered at extreme conditions where the effects of temperature and pressure start competing with conventional chemistry, and you can form these exotic compounds.

The results, published in Angewandte Chemie International Edition, provide a glimpse of how the rules of chemistry change under extreme conditions like those found inside certain planets or hydrogen-fusing stars.

Part1

In their experiment, the researchers first squeezed their hydrocarbon samples to pressures greater than those within Earth's mantle using a diamond anvil cell. Then, they heated the samples to over 3,500 degrees Fahrenheit by hitting them repeatedly with X-ray pulses from the European XFEL.

The team recorded and analyzed how the X-rays scattered off the samples, which allowed them to resolve the structural transformations within. As expected, the recorded scattering patterns showed that the carbon atoms had formed a diamond structure. But the team also saw unexpected signals that were due to hydrogen atoms reacting with the gold foil to form gold hydride. Under the extreme conditions created in the study, the researchers found hydrogen to be in a dense, "superionic" state, where the hydrogen atoms flowed freely through the gold's rigid atomic lattice, increasing the conductivity of the gold hydride.

Mungo Frost et al, Synthesis of Gold Hydride at High Pressure and High Temperature, Angewandte Chemie International Edition (2025). DOI: 10.1002/anie.202505811

Part2

Science in History's help

Napoleon's doomed retreat: DNA from Vilnius mass grave reveals signs of foodborne and lice-borne fever

Institut Pasteur and partner institutions report genetic evidence of Salmonella enterica lineage Para C and Borrelia recurrentis in Napoleonic soldiers from Vilnius, indicating paratyphoid fever and louse-borne relapsing fever were present during the 1812 retreat.

Napoleon assembled about 500,000–600,000 soldiers to invade Russia in 1812. After arriving in Moscow without decisively defeating the Russian army, the Napoleonic forces found themselves isolated in a ruined city and initiated a retreat to establish winter encampments along the border with Poland.

Retreat from Russia spanned October 19 to December 14, 1812 and resulted in massive losses attributed by historians to cold, hunger, and diseases. Physicians and officers documented typhus, diarrhea, dysentery, fevers, pneumonia, and jaundice.

Previous reports described body lice in Vilnius remains and PCR-based claims of Rickettsia prowazekii and Bartonella quintana using short fragments, alongside Anelloviridae in other soldiers from Kaliningrad.

In the study, "Paratyphoid Fever and Relapsing Fever in 1812 Napoleon's Devastated Army," published on the pre-print server bioRxiv, researchers recovered and sequenced ancient DNA from the teeth of soldiers who likely died from infectious diseases to identify pathogens that could have contributed to their deaths.

The sampling drew on 13 intact teeth from different individuals recovered from a mass grave in Vilnius, Lithuania associated with the December 1812 retreat, from a site with a minimum of 3,269 exhumed individuals. No battle trauma was observed at the site.

Initial analysis flagged fourteen possible pathogens. Salmonella enterica and Borrelia recurrentis showed the strongest signals. Four soldiers (87A, 92B, 95A and 97B) yielded between roughly 30 and 970 unique DNA fragments matching the Paratyphi C strain, with read-mismatch patterns indicating authentic ancient bacterial DNA.

Sample 93A produced about 4,060 unique fragments covering the chromosome and all seven plasmids of B. recurrentis, while 92B contributed around 320 unique reads and 18 confirmed hits after detailed filtering.

Phylogenetic placement positioned all Salmonella sequences firmly within the Paratyphi C lineage, a pathogen known to cause paratyphoid fever. No authenticated DNA matches Rickettsia prowazekii or Bartonella quintana. While no authenticated reads for R. prowazekii or B. quintana were found, the authors note this does not rule out their presence due to limitations of ancient DNA preservation.

Authors conclude that paratyphoid fever lineage Para C and louse-borne relapsing fever were present among Napoleonic soldiers during the 1812 retreat.

Historical testimony described widespread diarrhea and consumption of salted beets and brine along the route to Vilnius, consistent with a foodborne route for paratyphoid fever.

A scenario of fatigue, cold, and overlapping infections likely contributed to mortality.

Rémi Barbieri et al, Paratyphoid Fever and Relapsing Fever in 1812 Napoleon's Devastated Army, bioRxiv (2025). DOI: 10.1101/2025.07.12.664512

Study finds Ozempic may weaken muscles even as muscle size remains stable

As use of the popular anti-diabetic and weight-loss drug Ozempic skyrockets, so have concerns about the medication's side effects. One such side effect is loss of "lean mass"—body weight that isn't fat—raising concerns that Ozempic could be reducing muscle mass and strength.

New research in mice suggests that muscle mass changes less than expected, but muscles may still get weaker, pointing out an urgent need for clinical studies to pin down the full effects of the popular medications.

Researchers found that Ozempic-induced weight loss did decrease lean mass by about 10%. Most of this lost weight wasn't from skeletal muscles but instead from other tissues like the liver, which shrank by nearly half. The researchers emphasize that more research is needed to determine whether similar changes to organ size occur in humans—and whether those changes come with any risks.

Interestingly, when the researchers tested the amount of force the mice's muscles could exert, they found that, for some muscles, strength decreased as the mice lost weight, even when the size of the muscle stayed roughly the same. For other muscles, strength was unchanged. It's unknown how weight loss drugs affect this balance in people, the researchers say.

A potential loss of strength when taking Ozempic may be of particular concern for adults over the age of 60, who are at higher baseline risk for muscle loss and reduced mobility. "The loss of physical function is a strong predictor of not just quality of life but longevity," they add.

However,  mice and humans gain and lose weight in different ways and unless tested in humans, we can't apply the same results to human beings. 

Unexpected effects of semaglutide on skeletal muscle mass and force-generating capacity in mice, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2025.07.004. www.cell.com/cell-metabolism/f … 1550-4131(25)00331-6

Bacterial duo eliminates tumors without immune system help in new cancer therapy

A  research team has developed an immune-independent bacterial cancer therapy using a novel microbial consortium called AUN.

Cancer immunotherapy originated in 1868 when the German physician Busch reported a case of a cancer patient who was intentionally infected with bacteria and subsequently cured. In 1893, Dr. William Coley proposed the use of bacteria for cancer treatment, and immunotherapies have been evolving into modern treatments such as checkpoint inhibitors and CAR-T cells for over 150 years. While powerful, these approaches fundamentally depend on immune cells—making them ineffective for many cancer patients with compromised immune systems due to chemotherapy or radiotherapy.

The newly developed AUN therapy overturns this long-standing limitation. The research is published in Nature Biomedical Engineering.

AUN is composed of two naturally occurring bacteria:

• Proteus mirabilis (A-gyo), a tumor-resident microbe
• Rhodopseudomonas palustris (UN-gyo), a photosynthetic bacterium

Working in perfect synergy, these AUN bacteria produce exceptional tumor eradication in both murine and human cancer models, even in immunocompromised environments—all without the help of immune cells. The therapy exhibits high biocompatibility and minimal side effects, including suppression of cytokine release syndrome (CRS).

Part 1

In this study, AUN exhibits transcendent antitumor effects through uniquely orchestrated bacterial mechanisms, including:

Selective destruction of tumor vasculature and cancer cells
Structural transformation of A-gyo (filamentation) triggered by tumor metabolites, enhancing its antitumor potency
Functional optimization via intratumoral population shift—although the initial bacterial mixture is A-gyo : UN-gyo ≈ 3:97, it dramatically shifts to 99:1 within the tumor microenvironment
Suppression of pathogenicity and minimization of side effects, including the avoidance of CRS
Notably, UN-gyo functions as a regulatory partner only when coexisting with A-gyo, helping to suppress the pathogenicity of both strains while simultaneously enhancing their tumor-specific cytotoxicity. This "cooperation of labor" mirrors the Japanese philosophical concept of AUN—perfect harmony between opposites. It is this delicate and dynamic interplay between the two bacterial species that unlocks the remarkable antitumor efficacy—a feat previously unattainable through conventional therapies.

Tumour-resident oncolytic bacteria trigger potent anticancer effects through selective intratumoural thrombosis and necrosis, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01459-9

Part 2

New study shows that E. coli can evolve antibiotic resistance during treatment

Scientists have documented a notable case of antibiotic resistance evolving within a critically ill patient during treatment for an E. coli bloodstream infection, providing genomic evidence of how drug resistance can emerge in real time.

This new study published in the Journal of Medical Microbiology, details the rapid evolution of resistance in an E. coli strain exposed to piperacillin/tazobactam (TZP), a first-line treatment for serious bacterial infections that pairs an antibiotic with a compound that inhibits beta-lactamase enzymes, a widespread antibiotic resistance gene.

While the initial infection appeared treatable, the bacteria quickly developed a mechanism to escape the drug's effects, not by acquiring new resistance genes, but by amplifying one it already carried, overcoming the effects of the resistance inhibitor.

This is a striking example of resistance evolving under antibiotic pressure.

The researchers identified a tenfold increase in copies of a key resistance gene within the bacterial isolate, leading to a 32-fold increase in the level of antibiotic required to kill the bacteria, ultimately causing the treatment to fail, and all within the course of a single patient's illness.

The research team, which included genomic scientists, microbiologists and clinicians used high-resolution whole-genome sequencing to confirm the genetic changes.

The amplified resistance gene in E. coli, named blaTEM-1, produces a beta-lactamase enzyme that breaks down the antibiotic piperacillin. Although the TZP drug combination is meant to inhibit these enzymes, the sheer volume produced following gene duplication overwhelmed its protective effect, allowing the infection to persist. Further lab experiments confirmed that exposure to TZP led E. coli to generate even more copies of the gene.

This form of "within-patient evolution" presents a major diagnostic challenge. Routine resistance tests may underestimate the risk of treatment failure if they don't detect bacteria capable of rapidly increasing enzyme production under antibiotic pressure.

The study also highlights that 40% of new antibiotic candidates in the pipeline are beta-lactamase inhibitor combinations like TZP, raising critical concerns for drug developers and frontline clinicians alike.

This study underscores why relying on static resistance profiles can be misleading.

The findings underscore the need for greater investment in diagnostics and surveillance tools that can detect dynamic, hard-to-spot resistance mechanisms before they undermine treatment.

Alice J. Fraser et al, A high-resolution genomic and phenotypic analysis of resistance evolution of an Escherichia coli strain from a critically unwell patient treated with piperacillin/tazobactam, Journal of Medical Microbiology (2025). DOI: 10.1099/jmm.0.002018

Researchers debunk long-standing concern about flu treatment in children

For decades, medical professionals debated whether a common antiviral medication used to treat flu in children caused neuropsychiatric events or if the infection itself was the culprit.

Now researchers at Monroe Carell Jr. Children's Hospital at Vanderbilt have debunked a long-standing theory about oseltamivir, known as Tamiflu.

According to the study, published in JAMA Neurology, oseltamivir treatment during flu episodes was associated with a reduced risk of serious neuropsychiatric events, such as seizures, altered mental status and hallucination.

These findings demonstrated what many pediatricians have long suspected, that the flu, not the flu treatment, is associated with neuropsychiatric events.

"In fact, oseltamivir treatment seems to prevent neuropsychiatric events rather than cause them."

Key points:

• Influenza itself was associated with an increase in neuropsychiatric events compared to children with no influenza, regardless of oseltamivir use.
• Among children with influenza, those treated with oseltamivir had about 50% reduction in neuropsychiatric events.
• Among children without influenza, those who were treated with oseltamivir prophylactically had the same rate of events as the baseline group with no influenza.

Exposure to nanoplastics could induce spread of Alzheimer's disease from the brain to other organs

A new preclinical study has found exposure to nanoplastics may contribute to the rapid progression of Alzheimer's disease and subsequent spread from the brain to other key organs such as the liver, heart and gut.

The research, "Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics," is published in the journal Environment & Health

The study investigated how environmental-level polystyrene nanoplastic exposure influences the progression of Alzheimer's disease from the brain to other parts of the body. Studies in mice revealed that nanoplastic-induced neurological damage is not confined within the brain, but expands systemically through the gut–liver–brain axis.

In mice exposed to polystyrene nanoplastics, Alzheimer's-like symptoms were shown to stimulate 'microglia' immune cell activation in the brain, leading to neuroinflammation and neurodegeneration. This in turn led to peripheral health implications beyond the brain, including fatty liver disease, abnormal build-up of fat and gut microbiota imbalance.

Humans are involuntarily exposed to plastics through inhalation, dermal contact and the consumption of contaminated food and water, and plastic particles have been detected in human lungs, bloodstream and, very recently, in the human brain.

This, however, is the first study to show how rapidly nanoplastics can evolve from the brain to other parts of the body.

Yue Wang et al, Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics, Environment & Health (2025). DOI: 10.1021/envhealth.5c00160

Study finds drinking coffee at night raises impulsivity, especially in females

 A team of  biologists has discovered that nighttime caffeine consumption can increase impulsive behavior, potentially leading to reckless actions.

The study, published in iScience, examined how nighttime caffeine intake affects inhibition and impulsivity in fruit flies.

Drosophila melanogaster, the fruit fly species used in the study, is a powerful model to study complex behaviors due to its genetic and neural parallels with humans. Caffeine is the most widely consumed psychoactive substance in the world.

Interestingly, caffeine consumed by the flies during the daytime did not lead to the same reckless flying, the team said.

The team warns that the findings could have negative implications for shift workers, health care and military personnel who consume coffee at night, particularly females.

Erick Benjamin Saldes et al, Nighttime caffeine intake increases motor impulsivity, iScience (2025). DOI: 10.1016/j.isci.2025.113197

The world nearly beat polio. But fake records, an imperfect vaccine and missteps aided its comeback

For the past decade, health care workers have traveled door to door in southeastern Pakistan, pleading with parents to allow children to be vaccinated against polio as part of a global campaign to wipe out the paralytic disease. She hears their demands and fears. Some are practical—families need basics like food and water more than vaccines. Others are simply unfounded—the oral doses are meant to sterilize their kids.

Amid rampant misinformation and immense pressure for the campaign to succeed, some managers have instructed workers to falsely mark children as immunized. And the vaccines, which must be kept cold, aren't always stored correctly.

In many places, their work is not done with honesty. The result: Polio raised its ugly head again.

The World Health Organization and partners embarked on their polio campaign in 1988 with the bold goal of eradication—a feat seen only once for human diseases, with smallpox in 1980. They came close several times, including in 2021, when just five cases of the natural virus were reported in Pakistan and Afghanistan. But since then, cases rebounded, hitting 99 last year, and officials have missed at least six self-imposed eradication deadlines.

Afghanistan and Pakistan remain the only countries where transmission of polio—which is highly infectious, affects mainly children under 5, and can cause irreversible paralysis within hours—has never been interrupted. The worldwide campaign has focused most of its attention and funding there for the past decade.

But in its quest to eliminate the disease, the Global Polio Eradication Initiative has been derailed by mismanagement and what insiders describe as blind allegiance to an outdated strategy and a problematic oral vaccine, according to workers, polio experts and internal materials.

Officials have falsified vaccination records, selected unqualified people to dole out drops, failed to send out teams during mass campaigns, and dismissed concerns about the oral vaccine sparking outbreaks, according to documents shared with some news agencies.

The documents flagged multiple cases of falsified vaccination records, health workers being replaced by untrained relatives and workers improperly administering vaccines.

Part 1

Before the first polio vaccine was developed in 1955, the disease—spread mostly from person to person, through contaminated water and via fecal particles—was among the world's most feared, paralyzing hundreds of thousands of children annually. People avoided crowded places during epidemics, and hospital wards filled with children encased in iron lungs after the virus immobilized their breathing muscles.

Polio is mainly spread when people are exposed to water infected with the virus. In countries with poor sanitation, children often become infected when they come into contact with contaminated waste.

WHO says that as long as a single child remains infected, kids everywhere are at risk.
Eradication demands near-perfection—zero polio cases and immunizing more than 95% of children.

But public health leaders and former WHO staffers say campaign efforts are far from perfect, and many question the oral vaccine.
The oral vaccine—proven to be safe and effective—has been given to more than 3 billion children. But there are some extremely rare side effects: Scientists estimate that for every 2.7 million first doses given, one child will be paralyzed by the live polio virus in the vaccine.

In even rarer instances, the live virus can mutate into a form capable of starting new outbreaks among unimmunized people where vaccination rates are low.

Worldwide, several hundred vaccine-derived cases have been reported annually since at least 2021, with at least 98 this year.

Most public health experts agree the oral vaccine should be pulled as soon as possible. But they acknowledge there simply isn't enough injectable vaccine—which uses no live virus and doesn't come with the risks of the oral vaccine—to wipe out polio alone. The injectable vaccine also is more expensive and requires more training to administer.

https://medicalxpress.com/news/2025-08-world-polio-fake-imperfect-v...

Part 2

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Low-oxygen air slows Parkinson's progression and restores movement in mice

Researchers have shown that a low-oxygen environment—similar to the thin air found at Mount Everest base camp—can protect the brain and restore movement in mice with Parkinson's-like disease.

The new research, in Nature Neuroscience, suggests that cellular dysfunction in Parkinson's leads to the accumulation of excess oxygen molecules in the brain, which then fuel neurodegeneration—and that reducing oxygen intake could help prevent or even reverse Parkinson's symptoms.

The fact that researchers actually saw some reversal of neurological damage is really exciting. It tells us that there is a window during which some neurons are dysfunctional but not yet dead—and that we can restore their function if we intervene early enough.

The results raise the possibility of an entirely new paradigm for addressing Parkinson's disease.

Parkinson's disease, which affects more than 10 million people worldwide, causes the progressive loss of neurons in the brain, leading to tremors and slowed movements.

Neurons affected by Parkinson's also gradually accumulate toxic protein clumps called Lewy bodies. Some biochemical evidence has suggested that these clumps interfere with the function of mitochondria—the tiny powerhouses of the cell that Mootha knew were altered in other diseases that could be treated with hypoxia.

Moreover, anecdotally, people with Parkinson's seem to fare better at high altitudes. And long-term smokers—who have elevated levels of carbon monoxide, leading to less oxygen in tissues—also appear to have a lower risk of developing Parkinson's.

Based on this evidence, researchers became very interested in the effect of hypoxia on Parkinson's disease.

The results of their experiments were striking. Three months after receiving α-synuclein protein injections, the mice breathing normal air had high levels of Lewy bodies, dead neurons, and severe movement problems. Mice that had breathed low-oxygen air from the start didn't lose any neurons and showed no signs of movement problems, despite developing abundant Lewy bodies.

The findings show that hypoxia wasn't stopping the formation of Lewy bodies but was protecting neurons from the damaging effects of these protein clumps—potentially suggesting a new mode of treating Parkinson's without targeting α-synuclein or Lewy bodies.

What's more, when hypoxia was introduced six weeks after the injection, when symptoms were already appearing, it still worked. The mice's motor skills rebounded, their anxiety-like behaviors faded, and the loss of neurons in the brain stopped.

However, more work is needed before the findings can be directly used to treat Parkinson's.

 Marutani, E et al. Hypoxia ameliorates neurodegeneration and movement disorder in a mouse model of Parkinson's disease, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02010-4

Anthropic says they've found a new way to stop AI from turning evil

AI is a relatively new tool, and despite its rapid deployment in nearly every aspect of our lives, researchers are still trying to figure out how its "personality traits" arise and how to control them. Large learning models (LLMs) use chatbots or "assistants" to interface with users, and some of these assistants have exhibited troubling behaviors recently, like praising evil dictators, using blackmail or displaying sycophantic behaviors with users. Considering how much these LLMs have already been integrated into our society, it is no surprise that researchers are trying to find ways to weed out undesirable behaviors.

Anthropic, the AI company and creator of the LLM Claude, recently released a paper on the arXiv preprint server discussing their new approach to reining in these undesirable traits in LLMs. In their method, they identify patterns of activity within an AI model's neural network—referred to as "persona vectors"—that control its character traits. Anthropic says these persona vectors are somewhat analogous to parts of the brain that "light up" when a person experiences a certain feeling or does a particular activity.

Anthropic's researchers used two open-source LLMs, Qwen 2.5-7B-Instruct and Llama-3.1-8B-Instruct, to test whether they could remove or manipulate these persona vectors to control the behaviors of the LLMs. Their study focuses on three traits: evil, sycophancy and hallucination (the LLM's propensity to make up information). Traits must be given a name and an explicit description for the vectors to be properly identified.

In their method, a technique called "steering" can be used to control behaviors. They write, "When we steer the model with the 'evil' persona vector, we start to see it talking about unethical acts; when we steer with 'sycophancy,' it sucks up to the user; and when we steer with 'hallucination,' it starts to make up information. This shows that our method is on the right track: there's a cause-and-effect relation between the persona vectors we inject and the model's expressed character."

However, they found that when they made these changes after training, the model loses some of its intelligence. But there was a workaround—the team found that inducing the bad behaviors during training allowed the LLMs to integrate better behavior without reducing their usefulness. Furthermore, they found that they can monitor and predict persona shifts during deployment and training and flag problematic training data that is more likely to produce unwanted traits, even before fine-tuning the model.

Runjin Chen et al, Persona Vectors: Monitoring and Controlling Character Traits in Language Models, arXiv (2025). DOI: 10.48550/arxiv.2507.21509

Researchers discover universal rules of quantum entanglement across all dimensions

A team of theoretical researchers used thermal effective theory to demonstrate that quantum entanglement follows universal rules across all dimensions. Their study was published online in Physical Review Letters.

In classical physics, two particles that are far apart behave independently. However, in quantum physics, two particles can exhibit strong correlations regardless of the distance between them. This quantum correlation is known as quantum entanglement.

Quantum entanglement is a fundamental phenomenon underlying quantum technologies such as quantum computation and quantum communication, and understanding its structure is important both theoretically and practically.

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One of the key measures used to quantify quantum entanglement is the Rényi entropy. Rényi entropy quantifies the complexity of quantum states and the distribution of information, and plays a crucial role in the classification of quantum states and in assessing the feasibility of simulating quantum many-body systems.

Moreover, Rényi entropy serves as a powerful tool in theoretical investigations of the black hole information loss problem, and frequently appears in the context of quantum gravity.

 Most studies to date have been limited to (1+1)-dimensional systems, or 1 spatial dimension plus time dimension. In higher dimensions, analyzing the structure of quantum entanglement becomes significantly more difficult.

A group of researchers has shown the universal features of quantum entanglement structures in higher dimensions by applying theoretical techniques developed in the field of particle physics to quantum information theory.

The research team focused on the thermal effective theory, which has recently led to major advances in the analysis of higher-dimensional theories in particle physics. This is a theoretical framework designed to extract universal behavior from complex systems, based on the idea that observable quantities can often be characterized by only a small number of parameters.

By introducing this framework into quantum information theory, the team analyzed the behavior of Rényi entropy in higher-dimensional quantum systems.

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 Yuya Kusuki et al, Universality of Rényi Entropy in Conformal Field Theory, Physical Review Letters (2025). DOI: 10.1103/fsg7-bs7q

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Why do some birds dance?

Cockatoos perform 30 distinct dance moves and may combine them in unique ways

Captive cockatoos have at least 30 different dance moves in their repertoire, including headbanging and body rolls, according to a new study.

 The moves, of which 17 are newly identified, may be performed with or without music.

Several species of parrot have been anecdotally observed dancing to music in captivity. Dancing results from complex brain processes including imitation, learning and synchronized, rhythmic movement. Spontaneous dancing in time to music has only been reported in humans and parrots, although some wild birds also display rhythmic movements as part of their courtship displays.

Researchers analyzed 45 videos posted on social media that showed cockatoos (Cacatuidae) dancing. They identified a total of 30 distinct dance movements—17 of which had not previously been described scientifically. These newly identified dance moves included headbanging, sidesteps and body rolls.

The researchers found that some birds also performed their own individual dance moves, often by combining several of the movements in unique ways. Closely related species did not display more similar dances, and each species had a unique top 10 most common dance moves.

Human eggs are protected from age-related genetic mutations, mtDNA study finds

As we age, the genes in our cells accumulate more mutations. This is one of the contributory factors to age-related diseases and the aging process. However, in a new study published in Science Advances, researchers have discovered one exception where genetic mutations don't appear to build up as humans get older—the mitochondrial DNA (mtDNA) of human egg cells in women.

Mitochondria are the energy powerhouses of the cell. These oval-shaped organelles supply most of the energy for a cell to function, have their own DNA and are only passed down from mothers to their children. Most mitochondrial DNA mutations are harmless, but some can cause diseases such as Leigh Syndrome in children, which can lead to seizures, loss of previously acquired motor skills and heart problems. It was previously unclear, though, whether these mutations increase with age in immature egg cells known as oocytes.

In this new study, scientists used a DNA-sequencing technique to identify mutations in 80 single oocytes from 22 women, aged 20 to 42. They also studied mitochondrial DNA mutations in the women's blood and saliva.

They found that as women age, mitochondrial DNA mutations increase in blood and saliva cells, but not in egg cells. This suggests that a mechanism may have evolved that protects eggs from age-related genetic damage seen in other parts of the body.

"mtDNA in human oocytes is protected against accumulation of mutations with aging and has functional consequences," wrote the researchers. "These findings are particularly timely as humans tend to reproduce later in life."

The researchers also noted that the few mutations they did find tended to occur in parts of the mtDNA that do not make proteins (non-coding regions). Mutations were much less common in the parts that make proteins (coding regions).

Previous studies have shown that older mothers are more likely to pass on chromosomal abnormalities to their children. It was assumed the same was true for mitochondrial mutations. The new research challenges this assumption, offering a promising sign that delaying motherhood may not increase the risk of passing on mtDNA mutations.

Despite these findings, the study's conclusions are not definitive. It was based on a small sample size and did not cover a woman's full reproductive lifespan.

 Barbara Arbeithuber et al, Allele frequency selection and no age-related increase in human oocyte mitochondrial mutations, Science Advances (2025). DOI: 10.1126/sciadv.adw4954

Peacocks have lasers in their tails

As if the tail of a peacock could get any more flamboyant. Scientists have now discovered yellow-green lasers shooting from the ‘eyes’ of their feathers. These aren’t vaporizing beams of light that can cut a bird in half or anything. We would have probably noticed that during a courtship display… The lasers we’re talking about are completely harmless. The term stands for Light Amplification by Stimulated Emission of Radiation. Essentially, that means if you shine a light on some materials and the atoms excite one another, it can release a flood of photons, producing a faint glow. Biological lasers like these can be found in butterfly wings and marine mammals. But this is the first time scientists have observed the effect in the feathers of peacocks. Even the greatest show-offs in the world have a secret or two up their sleeves.

The researchers found evidence of optical cavities in the form of resonating nanostructures in different parts of the eyespot, all faintly emitting two different wavelengths: green and yellow/orange.

Exactly what kind of structure is responsible for aligning the amplified light at these colors isn't clear. But the fact they are found across the feather, all emitting the same precise wavelengths in a signature fashion, is a sign that something strange is at work.

https://www.nature.com/articles/s41598-025-04039-8

Sunlight-activated material turns PFAS in water into harmless fluoride

Researchers  have developed a sunlight-activated material that can degrade per- and polyfluoroalkyl substances (PFAS) in water, breaking down the pollutant into harmless components, including fluoride. The work is published in the journal Small.

The breakthrough discovery represents a promising low-energy solution for PFAS remediation, with potential applications in water treatment and environmental cleanup.

Many water contaminants are degraded by adding a reactive chemical that binds to the carbon. However, in PFAS molecules, the carbon atoms are protected in such a way that makes this process nearly impossible.

The researchers now have altered conditions and optimized the catalyst to target the PFAS-protective F atoms, which resulted in complete breakdown of the forever chemicals.

The produced fluoride can be isolated and used in health care products such as toothpaste or as additives to fertilizers.

Mahmoud Adel Hamza et al, CdIn2S4 Micro‐Pyramids for Reductive Photocatalytic Degradation of Perfluorooctanesulfonic Acid, Small (2025). DOI: 10.1002/smll.202504601