Easy Way to Remove Microplastics From Your Drinking Water

Aging Can Spread Through Your Body Via a Single Protein

ReHMGB1. A new study pinpoints this protein as being able to spread the wear and tear that comes with time as it quietly travels through the bloodstream. This adds significantly to our understanding of aging.

Short for reduced high mobility group box 1, ReHMGB1 triggers senescence in cells, permanently disabling them. It doesn't just do this locally; it can send damaging signals throughout the body, particularly in response to injuries or disease.

This study reveals that aging signals are not confined to individual cells but can be systemically transmitted via the blood, with ReHMGB1 acting as a key driver

The findings could help develop ways to keep us healthier for longer. If we can block or control this protein's signals, it might slow the cascade of cellular decline that comes with age.

The researchers were able to identify ReHMGB1 as a critical messenger passing on the senescence signal by analyzing different types of human cells grown in the lab and conducting a variety of tests on mice.

When ReHMGB1 transmission was blocked in mice with muscle injuries, muscle regeneration happened more quickly, while the animals showed improved physical performance, fewer signs of cellular aging, and reduced systemic inflammation.

By blocking this pathway, scientists were able to restore tissue regenerative capacity, suggesting a promising strategy to treat aging-related diseases.

This process is only one contributor to aging out of many, but the signals that ReHMGB1 spreads are particularly important in terms of our bodies becoming dysfunctional over time and less able to carry out repairs.

https://www.metabolismjournal.com/article/S0026-0495(25)00128-3/fulltext

COVID infection ages blood vessels, especially in women, research reveals

A COVID infection, particularly in women, may lead to blood vessels aging around five years, according to research published in the European Heart Journal.

Blood vessels gradually become stiffer with age, but the new study suggests that COVID could accelerate this process. Researchers say this is important since people with stiffer blood vessels face a higher risk of cardiovascular disease, including stroke and heart attack.

Researchers know that COVID can directly affect blood vessels. They think that this may result in what they call early vascular aging, meaning that your blood vessels are older than your chronological age and you are more susceptible to heart disease. If that is happening, we need to identify who is at risk at an early stage to prevent heart attacks and strokes.

The study included 2,390 people from 16 different countries (Austria, Australia, Brazil, Canada, Cyprus, France, Greece, Italy, Mexico, Norway, Turkey, UK and US) who were recruited between September 2020 to February 2022.

They were categorized according to whether they had never had COVID, had recent COVID but were not hospitalized, hospitalized for COVID on a general ward or hospitalized for COVID in an intensive care unit.

Researchers assessed each person's vascular age with a device that measures how quickly a wave of blood pressure travels between the carotid artery (in the neck) and femoral arteries (in the legs), a measure called carotid-femoral pulse wave velocity (PWV). The higher this measurement, the stiffer the blood vessels and the higher the vascular age of a person. Measurements were taken six months after COVID infection and again after 12 months.

Researchers also recorded demographic information such as patient's sex, age and other factors that can influence cardiovascular health.

After taking these factors into consideration, researchers found that all three groups of patients who had been infected with COVID, including those with mild COVID, had stiffer arteries, compared to those who had not been infected. The effect was greater in women than in men and in people who experienced the persistent symptoms of long COVID, such as shortness of breath and fatigue.

The average increase in PWV in women who had mild COVID was 0.55 meters per second, 0.60 in women hospitalized with COVID, and 1.09 for women treated in intensive care. Researchers say an increase of around 0.5 meters per second is "clinically relevant" and equivalent to aging around five years, with a 3% increased risk of cardiovascular disease in a 60-year-old woman.

People who had been vaccinated against COVID generally had arteries that were less stiff than people who were unvaccinated. Over the longer term, the vascular aging associated with COVID infection seemed to stabilize or improve slightly.

Part 1

There are several possible explanations for the vascular effects of COVID. The COVID-19 virus acts on specific receptors in the body, called the angiotensin-converting enzyme 2 receptors, that are present on the lining of the blood vessels. The virus uses these receptors to enter and infect cells.

This may result in vascular dysfunction and accelerated vascular aging. Our body's inflammation and immune responses, which defend against infections, may also be involved.

One of the reasons for the difference between women and men could be differences in the function of the immune system. Women mount a more rapid and robust immune response, which can protect them from infection. However, this same response can also increase damage to blood vessels after the initial infection.

Vascular aging is easy to measure and can be addressed with widely available treatments, such as lifestyle changes, blood pressure-lowering and cholesterol-lowering drugs. For people with accelerated vascular aging, it is important to do whatever possible to reduce the risk of heart attacks and strokes.

The researchers are working now on this aspect.

 Rosa Maria Bruno et al, Accelerated vascular ageing after COVID-19 infection: the CARTESIAN study, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf430

Part 2

Wild birds switch from sound to sight communication in noisy  environments

As anyone who has tried to hold a conversation in a noisy room knows, it is sometimes easier to rely on hand gestures than to shout over the din. White-throated dippers face a similar challenge along the fast-flowing streams they inhabit, where the roar of fast-flowing waters can sometimes drown out their melodic songs. Rather than trying to out-sing the river to defend territory or attract mates, these plump, endearing birds sometimes switch strategy entirely—turning to sight instead of sound, by flashing their bright white eyelids in a striking visual display.

A new study led by researchers is among the first to document this kind of sensory shift in a wild bird. The findings shed light on how dippers adapt their communication depending on social and environmental cues—and how such flexibility may have evolved in response to noise.

Evolution shaped by river noise Using more than one sense to communicate can be a big advantage in noisy environments. However, while many animals are known to adapt within a single sense—for example, by singing louder, changing pitch, or repeating themselves—clear evidence of animals switching between senses to send messages, like moving from sound to sight, or touch to smell, is still surprisingly rare. The white-throated dipper made an ideal test case: it lives year-round beside fast-flowing rivers, where background noise is often high, and it has bright white eyelids that can act as a visual signal. If any species had learned to shift between senses to get its message across, the researchers reasoned, the dipper would be a great candidate.

The study sheds light not just on how dippers communicate, but on how environmental challenges—like noisy rivers—can shape the evolution of signaling.

 Léna de Framond et al, Stream noise induces song plasticity and a shift to visual signals in a riverine songbird, Current Biology (2025). DOI: 10.1016/j.cub.2025.07.049

Brain abnormalities seen in children exposed prenatally to widely used pesticide

A new study reports evidence of a link between prenatal exposure to the widely used insecticide chlorpyrifos (CPF) and structural abnormalities in the brain and poorer motor function in  children and adolescents.

The findings are the first to demonstrate enduring and widespread molecular, cellular, and metabolic effects in the brain, as well as poorer fine motor control among youth with prenatal exposure to the insecticide.

Progressively higher insecticide exposure levels were significantly associated with progressively greater alterations in brain structure, function, and metabolism, as well as poorer measures of motor speed and motor programming. Links between higher CPF and greater anomalies across different neuroimaging measures suggest that prenatal exposure produces enduring disturbances in brain structure, function, and metabolism in direct proportion to the level of exposure.

Residential use was the primary source of CPF exposure in this cohort. Although the EPA banned indoor residential use in 2001, agricultural use continues for non-organic fruits, vegetables, and grains, contributing to toxic exposures carried by outdoor air and dust near agricultural areas.

Current widespread exposures, at levels comparable to those experienced in this sample, continue to place farm workers, pregnant women, and unborn children in harm's way.

The disturbances in brain tissue and metabolism that we observed with prenatal exposure to this one pesticide were remarkably widespread throughout the brain. Other organophosphate pesticides likely produce similar effects, warranting caution to minimize exposures in pregnancy, infancy, and early childhood, when brain development is rapid and especially vulnerable to these toxic chemicals, say the researchers.

Brain Abnormalities in Children Exposed Prenatally to the Pesticide Chlorpyrifos, JAMA Neurology (2025). DOI: 10.1001/jamaneurol.2025.2818

How AI support can go wrong in safety-critical settings

When it comes to adopting artificial intelligence in high-stakes settings like hospitals and airplanes, good AI performance and brief worker training on the technology is not sufficient to ensure systems will run smoothly and patients and passengers will be safe, a new study suggests.

Instead, algorithms and the people who use them in the most safety-critical organizations must be evaluated simultaneously to get an accurate view of AI's effects on human decision making, researchers say.

The team also contends these evaluations should assess how people respond to good, mediocre and poor technology performance to put the AI-human interaction to a meaningful test—and to expose the level of risk linked to mistakes.

During tests, results showed that more accurate AI predictions about whether or not a patient was trending toward a medical emergency improved participant performance by between 50% and 60%. But when the algorithm produced an inaccurate prediction, even when accompanied by explanatory data that didn't support that outcome, human performance collapsed, with an over 100% degradation in proper decision making when the algorithm was the most wrong.

An AI algorithm can never be perfect. So if you want an AI algorithm that's ready for safety-critical systems, that means something about the team, about the people and AI together, has to be able to cope with a poor-performing AI algorithm.

The point is this is not about making really good safety-critical system technology. It's the joint human-machine capabilities that matter in a safety-critical system

While the overall results provided evidence that there is a need for this type of evaluation, the researchers said they were surprised that explanations included in some experimental conditions had very little sway in participant concern—instead, the algorithm recommendation, presented in a solid red bar, overruled everything else.

Whatever effect that those annotations had was roundly overwhelmed by the presence of that indicator that swept everything else away.

Dane A. Morey et al, Empirically derived evaluation requirements for responsible deployments of AI in safety-critical settings, npj Digital Medicine (2025). DOI: 10.1038/s41746-025-01784-y

Vaccines trigger rapid lymph node responses, researchers discover

Lymph nodes are a key part of the human immune system, whose primary function is to combat infections. The effectiveness of vaccines is based on their ability to trigger events in lymph nodes that lead to the development of an immune response that protects the host against pathogens.

Researchers observed that lymphatic endothelial cells and other stromal cells are the first cells in the lymph nodes to come into contact with vaccines. The vaccines induced several changes in stromal cells at the gene and protein levels within the first hours of vaccination, which in turn affected lymph node function.

The changes in the stromal cells were observed before the development of the protective immune response triggered by the vaccine.

The researchers also discovered that different vaccines activate lymph node stromal cells in different ways.  

Ruth Fair-Mäkelä et al, COVID-19 vaccine type controls stromal reprogramming in draining lymph nodes, Science Immunology (2025). DOI: 10.1126/sciimmunol.adr6787

How a Brain Implant and AI Gave a Woman with Paralysis Her Voice Back

Early lead exposure could result in memory issues later in life

A new study has found that people who lived in areas with high levels of leaded gasoline emissions in the 1960s and '70s are more likely to report memory problems today—a finding that researchers say could deepen our understanding of environmental risks tied to dementia.

The study and others presented in July at the 2025 Alzheimer's Association International Conference used data from more than 600,000 participants .

Participants who lived in areas with higher estimated lead emissions—often tied to dense traffic and industrial zones—were significantly more likely to report poor memory. 

Lead has long been known to affect brain development in children. But research into its long-term effects on aging brains is still emerging.

Lead is bad for lots of things. There's been some studies that suggest it's related to IQ generally, and also aggression and lots of other things in animal model studies.

IQ is not the only area where lead exposure damages us. Instead, it often overlaps with other social determinants of health, like poverty and poor housing, making it difficult to isolate one factor. Higher levels of exposure and living near environmental pollutants often correlate to those with lower incomes.

Maize plants use a volatile gas to fight off pests in densely crowded fields

When maize fields become too crowded, the plants signal each other to boost their defenses. A research team found that in crowded conditions, maize plants release a volatile gas called linalool into the air. When it reaches neighboring plants, the gas triggers a defensive response in their roots.

While planting crops close together can increase harvest size, it also increases the risk of pathogens and pests such as caterpillars and the African maize stalk borer. When this happens, maize crops don't stand idly by. It was already known that the plants can change their shape in crowded conditions, such as growing taller to get more sunlight, but less was known about their immune response.

The research team reports that in dense fields, linalool acts like an alarm bell, triggering the roots of neighboring plants to increase production of jasmonate and other plant hormones. This, in turn, leads to more benzoxazinoids leaking into the soil around the roots.

This class of plant chemical defense compounds alters the bacterial composition of the soil, thereby protecting the plants from pests. And the protective response is a speedy one, with increased defense against caterpillars observed after just three days of growth in high-density conditions.

However, as the researchers note from their field studies, there is a catch. This defensive boost comes at the cost of reduced growth as the plants put more of their resources into defense rather than growing.

The scientists also showed that soil modified by densely planted maize crops offered ongoing protection for new crops even against different pests. Later plantings were protected from nematodes and other pathogens, not just insects. This suggests that maize defense readiness persists in the soil long after the initial crop is harvested.

Dongsheng Guo et al, Linalool-triggered plant-soil feedback drives defense adaptation in dense maize plantings, Science (2025). DOI: 10.1126/science.adv6675

Niklas Schandry et al, The scent of a crowd, Science (2025). DOI: 10.1126/science.adz7633

How HPV reprograms immune cells to help cancer grow

The most common cancer-causing strain of human papillomavirus (HPV), HPV16, undermines the body's defenses by reprogramming immune cells surrounding the tumor, according to new research.

In mice, blocking this process boosted the ability of experimental treatments for HPV to eliminate cancer cells. The results were published in the Journal for ImmunoTherapy of Cancer.

HPV16 causes more than half of cervical cancer cases and roughly 90% of HPV-linked throat cancers. It can be neutralized with the preventive vaccine Gardasil-9, but only if vaccination occurs prior to HPV exposure.

Researchers are now working to develop "therapeutic vaccines," which can be taken after HPV exposure—for instance, following an abnormal pap smear or cancer diagnosis—to trigger an immune response against infected cells by T-cells, a type of "fighter" cell that helps defend the body from disease. But these vaccines, now in clinical trials, have limited effectiveness—and the new study helps explain why.

The research focuses on a signalling protein in the immune system with inflammatory properties called Interleukin-23 or IL-23. While IL-23 was previously implicated in cervical and throat cancers, its exact role was unclear.

In a series of tests in mice and cell cultures,  researchers found that two HPV proteins, E6 and E7, prompt nearby cells to release IL-23, which in turn prevents the body's T-cells from attacking the tumor.

In order to eliminate the cancer, T-cells need to proliferate and destroy infected cells. But IL-23 stops them from working effectively, so the tumor keeps growing.

HPV16 E6 and E7 expressing cancer cells suppress the anti-tumor immune response by upregulating KLF2 mediated IL-23 expression in macrophages, Journal for ImmunoTherapy of Cancer (2025). DOI: 10.1136/jitc-2025-011915

Restricted blood flow speeds tumor growth by aging the immune system, study finds

Cutting off blood flow can prematurely age the bone marrow, weakening the immune system's ability to fight cancer, according to a new study .

Published online in JACC-CardioOncology, the study showed that peripheral ischemia–restricted blood flow in the arteries in the legs–caused breast tumors in mice to grow at double the rate seen in mice without restricted flow. These findings build on a 2020 study by the same team that found ischemia during a heart attack to have the same effect.

Ischemia occurs when fatty deposits, such as cholesterol, accumulate in artery walls, leading to inflammation and clotting that restrict the flow of oxygen-rich blood. When this happens in the legs, it causes peripheral artery disease, which affects millions of people, and can increase the risk of heart attack or stroke.

This new study  shows that impaired blood flow drives cancer growth regardless of where it happens in the body.

This link between peripheral artery disease and breast cancer growth underscores the critical importance of addressing metabolic and vascular risk factors as part of a comprehensive cancer treatment strategy.

Importantly, the research team found that restricted blood flow triggers a shift toward immune cell populations that cannot efficiently fight infections and cancer, mirroring changes seen with aging.

Part 1

To examine the mechanisms behind the link between cardiovascular disease and cancer growth, the study authors developed a mouse model with breast tumors and induced temporary ischemia in one hind limb. The team then compared cancer growth in mice with and without impaired blood flow.

Their findings build on the nature of the immune system, which evolved to attack invading bacteria and viruses, and, under normal conditions, to detect and eliminate cancer cells. These protective functions rely on stem cell reserves in the bone marrow, which can be activated as needed to produce key white blood cell populations throughout life.

Normally, the immune system responds to injury or infection by ramping up inflammation to eliminate threats, then scaling back to avoid harm to healthy tissue. This balance is maintained by a mix of immune cells that either activate or suppress inflammation.

The researchers found that reduced blood flow disrupts this equilibrium. It reprograms stem cells in the bone marrow to favor the production of "myeloid" immune cells (monocytes, macrophages, neutrophils) that dampen immune responses, while reducing output of lymphocytes like T cells that help to mount strong anti-tumor responses.

The local environment within tumors showed a similar shift, accumulating more immune-suppressive cells– including Ly6Chi monocytes, M2-like F4/80+ MHCIIlo macrophages, and regulatory T cells—that shield cancer from immune attack.

Further experiments showed that these immune changes were long-lasting. Ischemia not only altered the expression of hundreds of genes, shifting immune cells into a more cancer-tolerant state, but also reorganized the structure of chromatin–the protein scaffolding that controls access to DNA–making it harder for immune cells to activate genes involved in fighting cancer.
results reveal a direct mechanism by which ischemia drives cancer growth, reprogramming stem cells in ways that resemble aging and promote immune tolerance.
These findings open the door to new strategies in cancer prevention and treatment, like earlier cancer screening for patients with peripheral artery disease and using inflammation-modulating therapies to counter these effects."

Moving forward, the research team hopes to help design clinical studies that evaluate whether existing inflammation-targeted therapies can counter post-ischemic changes driving tumor growth.

Ischemic Injury Drives Nascent Tumor Growth via Accelerated Hematopoietic Aging, JACC CardioOncology (2025). DOI: 10.1016/j.jaccao.2025.05.016

Part 2

Hight-salt diet sparks brain inflammation that could explain stubborn high blood pressure

A new study finds that a high-salt diet triggers brain inflammation that drives up blood pressure. 

The research suggests the brain may be a missing link in certain forms of high blood pressure—or hypertension—traditionally attributed to the kidneys.

This is new evidence that high blood pressure can originate in the brain, opening the door for developing treatments that act on the brain.

Hypertension affects two-thirds of people over 60 and contributes to 10 million deaths worldwide each year. Often symptomless, the condition increases the risk of heart disease, stroke and other serious health problems.

About one-third of patients don't respond to standard medications, which primarily target the blood vessels and kidneys based on the long-standing view that hypertension begins there.

The study, published in the journal Neuron, suggests the brain may also be a key driver of the condition, particularly in treatment-resistant cases.

How salt disrupts the brain

To mimic human eating patterns, rats were given water containing 2% salt, comparable to a daily diet high in fast food and items like bacon, instant noodles and processed cheese.

The high-salt diet activated immune cells in a specific brain region, causing inflammation and a surge in the hormone vasopressin, which raises blood pressure. Researchers tracked these changes using cutting-edge brain imaging and lab techniques that only recently became available.

The brain's role in hypertension has largely been overlooked, in part because it's harder to study.

The researchers used rats instead of the more commonly studied mice because rats regulate salt and water more like humans. That makes the findings more likely to apply to people.

Next, the scientists plan to study whether similar processes are involved in other forms of hypertension.

Ning Gu et al, Microglia regulate neuronal activity via structural remodeling of astrocytes, Neuron (2025). DOI: 10.1016/j.neuron.2025.07.024

Imagination won't take you everywhere—study reveals limitations of the mind's eye

Our imagination might not be as powerful as we think when it comes to holding visual images, according to a first-of-its-kind study by psychologists.

 The research found that people can remember more items when they've seen them, compared to when they must imagine them.

While short-term visual memory can hold three to four items at once, our imagination can manage only two items before becoming less accurate.

Across a series of five experiments, more than 150 participants were asked to either remember or imagine the locations of objects on a grid.

Researchers examined how accurately participants could detect changes in specific locations under various conditions, including timing, cueing, display type, and object complexity. They then compared the number of items participants could correctly remember after viewing them with the number they could accurately imagine and recall without having seen them.

Findings showed that even when given more time or simpler images, people still imagined fewer items than they could remember visually.

The study, "The relation between the capacities of imagination and visual memory in the short-term," published in the Journal of Experimental Psychology: Human Perception and Performance, offers the first direct comparison of how much information people can hold in visual imagination versus visual memory.

Imagination and memory use similar parts of the brain, but this is the first time scientists have measured exactly how they differ when it comes to capacity. These findings demonstrate that actually seeing something, even a brief glimpse, gives our brain extra sensory support that bolsters our memory. In fact, researchers estimate that 17–35% of visual memory capacity depends on sensory input. When we imagine something from scratch, we don't have that input from our eyes, so it's harder to hold detailed images.

We use imagination constantly in everyday life, as imagery is seen as essential for navigating and predicting our environment and is involved in decision-making and emotion regulation, but the study reveals that our capacity to visualize is surprisingly limited, and this might affect how we make decisions, remember plans, or follow instructions when we rely on mental imagery alone.

Christopher Atkin et al, The relation between the capacities of imagination and visual memory in the short term., Journal of Experimental Psychology: Human Perception and Performance (2025). DOI: 10.1037/xhp0001364

“Logic will get you from A to B.  Imagination will take you everywhere.” –Albert Einstein

Epigenetic noise: Unappreciated process helps cells change identity

All cells in the body contain the same DNA, but different cell types express different genes; skin cells express genes for the skin, liver cells express liver genes, and so on. This coordination is crucial to help cells differentiate into their assigned roles, but a new study by researchers shows how cells can randomly "shake up" regions of the genome to express genes normally reserved for other cell types.

The study, "Thymic epithelial cells amplify epigenetic noise to promote immune tolerance," published in Nature, suggests that randomness or variability in the way DNA is packaged can create a kind of "epigenetic noise," enabling cells to take on the identity of different cell types. This flexibility plays an important role in tissue repair and the immune system but can also be exploited for the development of tumors.

The researchers worked with an incredibly resourceful group of cells called medullary thymic epithelial cells (mTECs). These cells are found in the thymus, a small, specialized organ of the immune system located just above the heart. They are one of the few cell types in the body that can express a wide variety of genes and alter their identity to mirror cell types from other tissues.

mTECs play an important role in training the immune system to prevent autoimmunity. They present proteins that are normally expressed only in specialized tissues and organs to T cells developing in the thymus. Then, the T cells that react too strongly to molecules from the body's own cells are purged so they don't later trigger an autoimmune response.

The capability to express almost any gene and alter their identities makes mTECs a great candidate for studying how cells can change their fates.

Each individual cell does not express the entire genome. Instead, they express only a unique subset of the tissue-specific genes at any given snapshot. There's a great deal of heterogeneity, so the researchers thought that it was really important to look cell-by-cell to uncover the mechanisms that allow the activation of each subset of tissue-specific genes.

Part 1

Since such heterogeneity is important, they used a series of single cell sequencing techniques to study gene expression and chromatin structure in individual mTECs, instead of using traditional bulk sequencing tools that average the results over thousands of cells.

Chromatin is the complex of DNA and proteins in the nucleus that packages long stretches of DNA into more compact structures. When chromatin is more loosely packed, or open, genes are more poised to be activated than if it's tightly coiled.

When the researchers analyzed the data, they did not find links between peak levels of chromatin accessibility and the expression of tissue-specific genes. Instead, they saw a lot of accessibility "noise" that gave cells the potential to activate genes solely expressed in other specialized tissues. This "ectopic expression" in turn helped train T cells to discriminate between self and non-self.

Chromatin is usually tightly regulated to sequester regions that encode other cell fates and focus accessibility for regions pertinent for the established cell identity.
In this work context, the researchers found the genomic regions that should be tightly packed were more labile or 'jiggly," allowing more opportunities for factors to access and activate genes specific to different cell types."
The team then tried to understand how this "chromatin noise" is amplified in cells. They found that the activity of the tumor suppressor protein p53, known as "the guardian of the genome," is repressed by mTECs prior to their genome becoming noisy. p53 is usually activated when DNA is damaged and can trigger cell death or stop tumor cell growth.

So, it made sense to the researchers that it would be implicated in a process where epithelial cells promiscuously express genes dedicated to other tissues and organs.
When the researchers genetically engineered p53 activity to be enhanced in mTECs, their chromatin became more stable, epigenetic noise was turned down, and the cells could no longer activate tissue-specific genes. This ultimately resulted in the escape of self-reactive T cells from the thymus to cause multi-organ autoimmune disease.
This suggests that thymic epithelial cells adopt deviant states that should normally trigger p53 activation and cell death.But because p53 is downregulated, the cells survive and facilitate this ectopic gene expression to promote the self/non-self discrimination.
It's a fascinating idea to think that cells are programmed to loosen their grip on genes to give them more freedom to get creative and solve problems like preventing T cells from attacking their own tissues.
The researchers extended their studies and found that epigenetic noise also allows lung cancer to sample more of the genome once p53 is deleted. This activates programs specific to other tissues to develop into more aggressive, malignant states. They hope to continue studying whether other cancer types exploit similar mechanisms for tumorigenesis.
Part 2

The team also wants to see if epigenetic noise is amplified for wound healing and tissue repair, and whether or not it can be leveraged to reprogram cells to alternate phenotypes for various clinical contexts, including cancer immunotherapy and treating autoimmunity.

It makes sense that to empower an immune system that uses a random process to recognize virtually any entity in the universe, thymic epithelial cells amplify random noise in the genome to ensure the immune system is focused on pathogens and cancers and not its own tissues. It's fighting fire with fire
Sometimes the random background noise can be just as important as the signal.

Thymic epithelial cells amplify epigenetic noise to promote immune tolerance, Nature (2025). DOI: 10.1038/s41586-025-09424-x

Part 3

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Mitochondria defend cells against infections by competing with pathogens for nutrients

Chronic infections impact a substantial portion of the global population, presenting ongoing challenges to health care systems and compromising patient well-being.

In a new study, researchers have discovered a surprising ally in the fight against infection: the cell's own mitochondria. Best known for providing energy to cells, mitochondria also play a defensive role by competing with pathogens for vital nutrients.

The paper is published in the journal Science.

During infection, mitochondria enter a metabolic tug-of-war with intracellular parasites, like Toxoplasma gondii, battling for access to folate, thereby inhibiting pathogen growth.

This discovery highlights a unique defensive strategy employed by host cells and opens up new possibilities for developing therapies against folate-dependent pathogens, such as Toxoplasma and Plasmodium, which cause toxoplasmosis and malaria respectively.

During infection with the human parasite Toxoplasma gondii, researchers observed the activation of the integrated stress response, which rewires mitochondrial metabolism.

This response enhanced mitochondrial activity, leading to increased demand for folate, a critical nutrient for nucleotide synthesis. Consequently, mitochondria limit the parasite's access to folate, curtailing its growth and proliferation. Mice unable to activate this stress response showed faster parasite growth, confirming the pathway's protective role in vivo.

 Tânia Catarina Medeiros et al, Mitochondria protect against an intracellular pathogen by restricting access to folate, Science (2025). DOI: 10.1126/science.adr6326

Saharan bacteria shield themselves with biofilms to survive dust storm journeys

How do living bacteria survive on the surface of dust particles carried by desert storms from the Sahara and Egypt to Israel?

Researchers  discovered that these bacteria can form microscopic biofilms over dust particles. These protective structures shield the bacteria from desiccation, extreme radiation, and severe nutrient scarcity during their atmospheric journey.

The research, published in Communications Earth and Environment, contributes to the growing field of atmospheric microbiology. This discipline explores the survival and activity of microorganisms while in the atmosphere, sometimes over thousands of kilometers, and their impact on global cycles, ecosystems, and human health. These processes significantly impact disease patterns, atmospheric CO₂ levels, plant diseases, and even antibiotic resistance dispersal.

In this study, the researchers successfully isolated and cultured bacteria brought in by dust storms under atmospheric conditions, focusing on beneficial Bacillus strains known for their positive applications in agriculture, construction, and medical probiotics.

The team thinks that natural selection during dust storms favors more innovative bacterial strains—a phenomenon that could potentially enhance their practical applications. This study also expands the traditional soil microbiome concept to include airborne microbial communities, broadening the known repertoire of survival strategies among these remarkable organisms.

Naama Lang-Yona et al, Bacillus biofilm formation and niche adaptation shape long-distance transported dust microbial community, Communications Earth & Environment (2025). DOI: 10.1038/s43247-025-02534-4

Brain scans reveal action-based organization in people born without hands

Conventional wisdom among neuroscientists suggests that the brain's motor functions are organized around the body, meaning certain brain areas control the hand; others the foot. An emerging alternative theory is that parts of the brain may be organized by the types of action, like reaching or using tools, no matter which body part is used to complete the task.

Researchers  recently set out to understand these theories, because knowing how the brain is organized around function versus body part has profound implications for rehabilitation and a person's return to function following a brain injury.

The findings are published in the Proceedings of the National Academy of Sciences. The work is titled "Action-type mapping principles extend beyond evolutionarily-conserved actions, even in people born without hands."

If motor control is partly based on actions rather than body parts, it's possible the brain can use this flexibility to compensate for the loss of specific limbs.

To gain a deeper understanding of the emerging theory, neuroscientists conducted a novel study with volunteers who were born without hands, and instead use their feet for everyday tasks with and without tools.

Using fMRI brain scans, the researchers showed that in these individuals, brain areas typically involved in hand tool use are still active—even though the individuals were using their feet, not their hands. This finding is consistent with the same action preference for control participants, who perform the action with either their hands or feet.

They  found that some regions in the brain care about the type of action a person is doing and not whether this action was performed with the hand or with the foot.

It appears this organization can arise without typical motor experience, providing evidence for action-type as a core driving factor in motor organization and development.

Interestingly, this was not true for all brain areas.

The primary motor cortex, which is tightly mapped to the body, did not reorganize for foot-based tool use, even in people who have been using tools with their feet their whole lives. This suggests that some brain areas demonstrate more plasticity than others.

Still, the study reveals a kind of brain organization that goes beyond the body—one that is abstract and action-centered, and that develops even without typical experience.

 Florencia Martinez-Addiego et al, Action-type mapping principles extend beyond evolutionarily conserved actions, even in people born without hands, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2503188122

Cancer-associated nerve injury can lead to chronic inflammation and immunotherapy resistance

Cancer cells can break down the protective covers around nerves, causing nerve injury that triggers chronic inflammation, leading to immune exhaustion and eventual resistance to immunotherapy, according to new research .

Tumors can sometimes infiltrate the space around nerves and nervous system fibers that are in close proximity, a process known as perineural invasion, which leads to poor prognosis and treatment escalation in various cancer types. 

The study, published today in Nature, underscores the importance of investigating interactions between cancer and the nervous system—a field known as cancer neuroscience. The results suggest that targeting the signaling pathways involved can reverse this inflammation and improve treatment responses.

These findings uncover novel mechanisms by which the immune system and nerves within the tumor microenvironment interact, revealing actionable targets that could transform the way we approach resistance to immunotherapy in patients with cancer.

 Baruch, E.N. et al, Cancer-induced nerve injury promotes resistance to anti-PD-1 therapy, Nature (2025). DOI: 10.1038/s41586-025-09370-8 www.nature.com/articles/s41586-025-09370-8

What happens in the brain when it learns something new

Memories of significant learning experiences—like the first time a driver gets a speeding ticket—are sharp, compared to the recollection of everyday events—like what someone ate for dinner two weeks ago. That's because the human brain is primed to learn from helpful associations.

Researchers have identified specific neural connections that are especially sensitive to this process of learning about causality. The discovery, while seemingly intuitive, could have widespread implications for understanding how humans learn and inform new ways to address learning challenges.

What's happening inside the brain when experiencing something for the first time—and how it decides if it's meaningful—is the subject of new research which focuses on how memory and learning shape the brain. The study is published in the journal Cell Reports.

 Researchers looked at how the connection between two different types of neurons—cells that transmit information to different parts of the brain—changes in response to new learning experiences. They found that the strength of the connection only changed if an experience was meaningful. These neurons are located in the sensory cortex, a part of the brain that other animals—like cows and dogs—have as well. That means that this finding could have a wider significance and help researchers understand how a broad range of animals learn.

Researchers found this change in the brain if something was useful to learn. If there was nothing to learn, there was no change.

This means that somehow the brain can distinguish whether there is a useful association to make, or there is nothing to learn.

The research shows that the brain is primed to learn new important things and that our brains are very sensitive to things that make sense.

 Eunsol Park et al, Somatostatin neurons detect stimulus-reward contingencies to reduce neocortical inhibition during learning, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.115606

Breast tumors tunnel into fat cells to fuel up

Scientists caught cancer cells in the act of breaking into fat cells and releasing their fat. The energy heist seems to be critical for the growth of deadly breast cancer. The study appears in Nature Communications.

When triple-negative breast cancer grows, the fat cells around it seem to shrink. Researchers have discovered that the cells of these tumors, which are among the deadliest types of breast cancer, build molecular tunnels, called gap junctions, into nearby fat cells. The tumor cells then send instructions that trigger the fat cells to release stores of energy that could feed the cancer.

Blocking the gap junctions stopped tumors from growing.

The findings have immediate clinical implications. Although no one is yet testing drugs that block gap junctions for breast cancer, there are ongoing clinical trials using these drugs for brain cancer.

Nature Communications (2025). DOI: 10.1038/s41467-025-62486-3

What happened before the Big Bang? Computational method may provide answers

We're often told it is "unscientific" or "meaningless" to ask what happened before the Big Bang. But a new paper by astrophysicists and cosmologists published in Living Reviews in Relativity, proposes a way forward: using complex computer simulations to numerically (rather than exactly) solve Einstein's equations for gravity in extreme situations.

The team argues that numerical relativity should be applied increasingly in cosmology to probe some of the universe's biggest questions–including what happened before the Big Bang, whether we live in a multiverse, if our universe has collided with a neighboring cosmos, or whether our universe cycled through a series of bangs and crunches.

Einstein's equations of general relativity describe gravity and the motion of cosmic objects. But wind the clock back far enough and you'll typically encounter a singularity—a state of infinite density and temperature—where the laws of physics collapse.

Cosmologists simply cannot solve Einstein's equations in such extreme environments—their normal simplifying assumptions no longer hold. And the same impasse applies to objects involving singularities or extreme gravity, such as black holes.

One issue might be what cosmologists take for granted. They normally assume that the universe is "isotropic" and "homogeneous"—looking the same in every direction to every observer. This is a very good approximation for the universe we see around us, and one that makes it possible to easily solve Einstein's equations in most cosmic scenarios. But is this a good approximation for the universe during the Big Bang?

Numerical relativity allows you to explore those questions. 

Numerical relativity was first suggested in the 1960s and 1970s to try to work out what kinds of gravitational waves (ripples in the fabric of spacetime) would be emitted if black holes collided and merged. This is an extreme scenario for which it is impossible to solve Einstein's equations with paper and pen alone—sophisticated computer code and numerical approximations are required.

Its development received renewed focus when the LIGO experiment was proposed in the 80s, although the problem was only solved in this way in 2005, raising hopes that the method could also be successfully applied to other puzzles.

Part 1

One longstanding puzzle that researchers are particularly excited about is cosmic inflation, a period of extremely rapid expansion in the early universe. Inflation was initially proposed to explain why the universe looks the way it does today, stretching out an initially small patch, so that the universe looks similar across a vast expanse.
If you don't have inflation, a lot of things fall apart. But while inflation helps explain the state of the universe today, nobody has been able to explain how or why the baby universe had this sudden short-lived growth spurt.

The trouble is, to probe this using Einstein's equations, cosmologists have to assume that the universe was homogeneous and isotropic in the first place—something which inflation was meant to explain. If you instead assume it started out in another state, then you don't have the symmetry to write down your equations easily.
But numerical relativity could help us get around this problem—allowing radically different starting conditions. It isn't a simple puzzle to solve, though, as there's an infinite number of ways spacetime could have been before inflation. Researchers are therefore hoping to use numerical relativity to test the predictions coming from more fundamental theories that generate inflation, such as string theory.
There are other exciting prospects, too. Physicists could use numerical relativity to try to work out what kind of gravitational waves could be generated by hypothetical objects called cosmic strings—long, thin "scars" in spacetime–potentially helping to confirm their existence. They might also be able to predict signatures, or "bruises," on the sky from our universe colliding with neighboring universes (if they even exist), which could help us verify the multiverse theory.
Excitingly, numerical relativity could also help reveal whether there was a universe before the Big Bang. Perhaps the cosmos is cyclic and goes through "bounces" from old universes into new ones—experiencing repeated rebirths, big bangs and big crunches. That's a very hard problem to solve analytically.

"Bouncing universes are an excellent example, because they reach strong gravity where you can't rely on your symmetries. Several groups are already working on them—it used to be that nobody was."
Numerical relativity simulations are so complex that they require supercomputers to run. As the technology of these machines improves, we might expect significant improvement in our understanding of the universe.
Cosmologists who are interested in solving some of the questions they cannot solve, can use numerical relativity, the researchers say.

Josu C. Aurrekoetxea et al, Cosmology using numerical relativity, Living Reviews in Relativity (2025). DOI: 10.1007/s41114-025-00058-z

Part 2

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Novel cement lets buildings cool themselves

When temperatures get too hot to handle, most of us crank up the air conditioning to keep cool. It does the job, but it's expensive and uses a significant amount of energy. But now an innovation by scientists could help us cut our reliance on AC. They've developed a new type of cement that allows buildings to stay cool on their own. Their research is published in the journal Science Advances.

Typically, cement absorbs infrared radiation from the sun and stores it as heat, which increases the temperature inside a building. To address this, a research team modified the building material's formula. They created a cement that reflects light and emits heat instead of absorbing it, using tiny reflective crystals of a mineral called ettringite on its surface.

The scientists developed the material from the ground up, starting with its basic chemical recipe. They ground tiny pellets made from minerals like limestone and gypsum into a fine dust and mixed it with water. The mixture was then poured into a silicon mold covered in holes that created depressions in the cement's surface where the ettringite crystals could grow. The result was a supercool cement that acts like a mirror and a radiator, bouncing away sunlight and emitting heat.

Once the cement was created, it was put to the test on a rooftop at Purdue University. Under a strong midday sun, the cement's surface was 5.4 degrees Celsius cooler than the surrounding air. The material also underwent rigorous mechanical, environmental, and optical durability testing.

Additionally, the team used machine learning to analyze its potential environmental benefits, which revealed that it could potentially lead to a net-negative carbon footprint over a 70-year period.

This breakthrough holds the potential to turn the heavy cement industry into a negative-carbon emission system, where supercool cement could play a key role in driving an energy-efficient, carbon-free future for the construction industry.

Buildings currently account for about 40% of global energy use and 36% of carbon emissions. If the supercool cement is successfully scaled up for commercial use, its benefits could be significant. As well as helping to cool the planet, it could dramatically cut energy bills by reducing our reliance on air conditioning. And by keeping buildings and the surrounding air cooler, this novel cement could also create a more pleasant and healthier urban environment.

Guo Lu et al, Scalable metasurface-enhanced supercool cement, Science Advances (2025). DOI: 10.1126/sciadv.adv2820

New research shows the brain's map of the body remains unchanged after amputation

The brain holds a "map" of the body that remains unchanged even after a limb has been amputated, contrary to the prevailing view that it rearranges itself to compensate for the loss, according to new research.

The findings, published in Nature Neuroscience, have implications for the treatment of "phantom limb" pain, but also suggest that controlling robotic replacement limbs via neural interfaces may be more straightforward than previously thought.

Studies have previously shown that within an area of the brain known as the somatosensory cortex there exists a map of the body, with different regions corresponding to different body parts.

These maps are responsible for processing sensory information, such as touch, temperature and pain, as well as body position. For example, if you touch something hot with your hand, this will activate a particular region of the brain; if you stub your toe, a different region activates.

For decades now, the commonly-accepted view among neuroscientists has been that following amputation of a limb, neighboring regions rearrange and essentially take over the area previously assigned to the now missing limb. This has relied on evidence from studies carried out after amputation, without comparing activity in the brain maps beforehand.

But this has presented a conundrum. Most amputees report phantom sensations, a feeling that the limb is still in place—this can also lead to sensations such as itching or pain in the missing limb. Also, brain imaging studies where amputees have been asked to 'move' their missing fingers have shown brain patterns resembling those of able-bodied individuals.

To investigate this contradiction, researchers followed three individuals due to undergo amputation of one of their hands.

This is the first time a study has looked at the hand and face maps of individuals both before and after amputation. 

Prior to amputation, all three individuals were able to move all five digits of their hands. While lying in a functional magnetic resonance imaging (fMRI) scanner—which measures activity in the brain—the participants were asked to move their individual fingers and to purse their lips. The researchers used the brain scans to construct maps of the hand and lips for each individual. In these maps, the lips sit near to the hand.

The participants repeated the activity three months and again six months after amputation, this time asked to purse their lips and to imagine moving individual fingers. One participant was scanned again 18 months after amputation and a second participant five years after amputation.

The researchers examined the signals from the pre-amputation finger maps and compared them against the maps post-amputation. Analysis of the 'before' and 'after' images revealed a remarkable consistency: even with their hand now missing, the corresponding brain region activated in an almost identical manner.

Bearing in mind that the somatosensory cortex is responsible for interpreting what's going on within the body, it seems astonishing that it doesn't seem to know that the hand is no longer there!

As previous studies had suggested that the body map reorganizes such that neighboring regions take over, the researchers looked at the region corresponding to the lips to see if it had moved or spread. They found that it remained unchanged and had not taken over the region representing the missing hand.

Part 1

To complement their findings, the researchers compared their case studies with 26 participants who had their upper limbs amputated, on average, 23.5 years beforehand. These individuals showed similar brain representations of the hand and lips to those in their three case studies, suggesting long-term evidence for the stability of hand and lip representations despite amputation.

Schone, HR et al. Stable Cortical Body Maps Before and After Arm Amputation, Nature Neuroscience (2025). DOI: 10.1038/s41593-025-02037-7

Part 2

Rising temperatures linked to declining moods around the world

Rising global temperatures affect human activity in many ways. Now, a new study illuminates an important dimension of the problem: very hot days are associated with more negative moods, as shown by a large-scale look at social media postings.

Overall, the study examined 1.2 billion social media posts from 157 countries over the span of a year. The research finds that when the temperature rises above 95 degrees Fahrenheit, or 35 degrees Celsius, expressed sentiments become about 25% more negative in lower-income countries and about 8% more negative in better-off countries. Extreme heat affects people emotionally, not just physically.

This study reveals that rising temperatures don't just threaten physical health or economic productivity—they also affect how people feel, every day, all over the world. 

This work opens up a new frontier in understanding how climate stress is shaping human well-being at a planetary scale.

Unequal Impacts of Rising Temperatures on Global Human Sentiment, One Earth (2025). DOI: 10.1016/j.oneear.2025.101422. www.cell.com/one-earth/fulltex … 2590-3322(25)00248-9

Even I have noticed this around my home. Birds are singing in the night!

Birds in light-polluted areas stay up late into the night

Birds that are active during the day sing later into the night in places with significant light pollution, according to new research.

Researchers analyzed data gathered from around the world, comparing more than 180 million bird vocalizations in a single year with global satellite imagery.

They were shocked by their findings: Under the brightest night skies, a bird's day is extended by nearly an hour. But birds staying up an hour past their normal bedtimes was an average. Actual times varied by species.

What is driving this response bybirds? We had the idea that maybe it was a species' photoreceptor sensitivity—their eyesight. And this turned out to be a key factor. Species with large eyes relative to their body size had a disproportionately stronger response to artificial light at night. They were more sensitive to light at night than species with small eyes.

Birds might have more time to forage for food and to mate, but an hour less sleep could be detrimental to their health.

Brent S. Pease et al, Light pollution prolongs avian activity, Science (2025). DOI: 10.1126/science.adv9472. www.science.org/doi/10.1126/science.adv9472

Viruses hidden within fungi could be secret drivers of deadly lung infections

Researchers have discovered that a virus living inside the fungus Aspergillus fumigatus significantly boosts the fungus's ability to survive stress and cause severe infections in mammals. Removing the virus made the fungus weaker and less virulent, while antiviral treatments improved survival outcomes. This finding reveals a hidden factor driving the deadliness of fungal infections and opens the door to potential new treatments that target the virus rather than the fungus itself.

The research reveals that a virus residing within the Aspergillus fumigatus fungus gives it a powerful survival advantage—making it tougher, more resilient, and ultimately, more dangerous to human health.

Aspergillus fumigatus is already notorious in medical circles. Responsible for the majority of invasive fungal infections in humans, it's especially lethal for people with weakened immune systems. Despite decades of research, mortality rates from infections remain alarmingly high—approaching 50%.

A double-stranded RNA virus, quietly riding along inside the fungus, appears to act like a hidden booster pack for the pathogen. When this virus is present, the fungus becomes far more adept at surviving environmental stress, including the heat and oxidative conditions inside the lungs of mammals.

To test the impact of the virus, the researchers removed it from fungal strains and compared their behavior to their virus-infected counterparts. The difference was striking. The virus-free fungi lost their ability to reproduce effectively, showed weaker defenses like reduced melanin production, and became significantly less dangerous when introduced into mammalian lungs.

The findings suggest that these so-called "mycoviruses" may play a quiet but critical role in the development and progression of fungal diseases in humans—a role that has largely gone unnoticed in the field of medical mycology.

Perhaps most promising of all: when antiviral treatments were used to suppress the virus during infection, survival outcomes improved in the mammalian model. This hints at a whole new treatment avenue—not just targeting the fungus itself, but the virus helping it thrive.

This discovery opens the door to rethinking how fungal infections are treated. By targeting the virus within the fungus, researchers may one day weaken the pathogen enough for the immune system—or existing antifungal drugs—to fight back more effectively.

In a world where fungal pathogens are becoming more drug-resistant and harder to treat, the study provides a rare glimmer of hope: Perhaps we've been overlooking a key player all along.

Marina Campos Rocha et al, Aspergillus fumigatus dsRNA virus promotes fungal fitness and pathogenicity in the mammalian host, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02096-3

How climate change increases air turbulence

For many fliers, air turbulence can be an unnerving experience—and in a world warming under the effects of climate change, it is only set to worsen, according to a growing body of scientific evidence.

Beyond making people uneasy, turbulence is also the leading cause of in-flight weather accidents, according to official data.

The numbers remain relatively small: there were 207 reported injuries on US commercial flights between 2009 and 2024. But high-profile incidents have thrust the issue into the spotlight.

These include an Air Europa flight last year, in which 40 passengers were hurt, and a Singapore Airlines flight where one elderly passenger died and dozens were injured.

Typically injuries occur due to un- belting of passengers or cabin crew rather than structural damage. Modern aircraft withstand turbulence, so the main risk is occupant injury, not loss of the plane.

Still, planes must be inspected after "severe" encounters with turbulence—about 1.5 times the normal force of Earth's gravity. Turbulence also increases fuel consumption when pilots must leave optimal altitudes, alter routes or change speeds.

There are three main types of turbulence: convective, mountain wave and clear-air turbulence (CAT), according to experts.

Researchers find a clear, positive trend—an increase in turbulence frequency over many regions, including the North Atlantic, North America, East Asia, the Middle East and North Africa,with increases ranging from 60% to 155%.
Further analysis attributed the rising turbulence in certain regions to increased greenhouse gas emissions.
A 2023 paper led by Isabel Smith at the University of Reading found that for every degree Celsius of near-surface warming, winters would see an increase of about nine percent in moderate CAT in the North Atlantic, and summers a rise of 14%.

Winter has historically been the roughest season for turbulence, but warming is now amplifying CAT in summer and autumn, closing the gap.

Jet stream disruption is not the only concern: climate change is also fueling stronger storms.

Climate change may also increase the frequency and severity of thunderstorms under future scenarios, and turbulence encounters near thunderstorms are a major component of turbulence accidents.
In terms of mitigation strategies, researchers are working on two studies: optimizing flight routes to avoid turbulence hotspots and improving forecasting accuracy.

Some airlines are moving towards strategies involving passengers wearing seatbelts more often, such as ending cabin service earlier.

Promising technologies are also being tested, including onboard LIDAR, which beams lasers into the atmosphere to detect subtle shifts in air density and wind speed.

Ultimately, cutting greenhouse gas emissions will be essential, say the researchers.
Ironically, aviation is responsible for about 3.5% of human-caused warming.
Source: News agencies

Part 2
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Breast cancer drug side effects: Study reveals how tamoxifen raises risk of secondary tumors in uterus

An international research team has identified a previously unknown mechanism by which the breast cancer drug tamoxifen can increase the risk of secondary tumors in the uterus.

The study shows that tamoxifen directly activates a key cellular signaling pathway (known as PI3K) a central driver in the development of sporadic uterine cancers, thereby challenging previously accepted models of therapy-related cancer development.

Since its introduction in the 1970s, tamoxifen has significantly improved survival rates for millions of patients with estrogen receptor–positive breast cancer. However, alongside its life-saving benefits, tamoxifen has also been linked—though rarely—to an elevated risk of uterine cancer. Until now, the precise molecular cause of this effect has remained unclear.

The new findings, published in Nature Genetics, reveal the mechanism: in tamoxifen-associated uterine carcinomas, mutations in the cancer-related gene PIK3CA—which are very common in spontaneously arising uterine tumors and lead to the activation of the PI3K signaling pathway—occur significantly less frequently. Instead, tamoxifen itself takes on the role of a signal activator of the PI3K pathway, making such mutations unnecessary.

Kirsten Kübler et al, Tamoxifen induces PI3K activation in uterine cancer, Nature Genetics (2025). DOI: 10.1038/s41588-025-02308-w

Rethinking phototherapy: Why skin color matters for infant jaundice treatment

Jaundice is one of the most common medical issues in newborns, affecting nearly 80% of full-term infants in their first days of life. The condition occurs when excess bilirubin, a yellow pigment formed as red blood cells break down, builds up in the body. While mildcases usually resolve on their own, dangerously high bilirubin levels can cause brain damage or even death. The standard treatment, phototherapy, uses blue light to break bilirubin down into forms the body can excrete.

A theoretical study recently published in Biophotonics Discovery used computer modeling to examine how skin color and other skin properties might influence how much therapeutic light reaches target tissues.

Researchers employed advanced computer simulations to model light penetration in newborn skin. The simulations incorporated factors such as skin pigmentation, hemoglobin levels, bilirubin concentration, skin thickness, and treatment light wavelength.  

Since specific data on skin color variations in newborns have not yet been reported, the researchers based their pigmentation parameters on established measurements from adult skin data. The modeling predicted that skin pigmentation would have the largest effect on light penetration.

Compared with light-skinned infants, the simulations suggested dark-skinned infants might receive up to 5.7 times less effective light dose under identical settings. This theoretical difference translated into predicted bilirubin reductions of about 40.8% for light-skinned newborns after 24 hours of phototherapy, versus 25.6% for dark-skinned newborns. The model also predicted that epidermal thickness and bilirubin levels would influence treatment effectiveness, though to a lesser degree.

The simulations further suggested that optimal treatment wavelength might vary by skin color. While light-skinned infants were predicted to respond best at around 460 nanometers (nm), dark-skinned infants showed better theoretical responses at slightly longer wavelengths, around 470 nm. The researchers propose that a compromise wavelength near 465 nm could provide more consistent results across skin tones.

Current phototherapy guidelines use a standardized approach without adjustments for skin tone. While phototherapy generally demonstrates effectiveness across populations, the authors note their theoretical findings suggest it might be less efficient in darker-skinned infants, potentially affecting treatment duration and outcomes.

Highlighting the importance of obtaining more fundamental insight into newborn skin pigmentation, they also emphasize the critical need for clinical studies to validate these computational predictions and determine whether actual bilirubin reduction varies by skin color in real patients.

 Alida Johanna Dam-Vervloet et al, Effect of skin color and other skin properties on the delivered light dose in phototherapy for neonatal hyperbilirubinemia, Biophotonics Discovery (2025). DOI: 10.1117/1.BIOS.2.3.032508

Hidden body fat linked to faster heart aging

Excessive amounts of visceral fat—the hidden fat surrounding organs—is linked with faster aging of the heart, a new study has found.

Aging is the biggest risk factor for heart disease, but why some people age faster than others isn't fully understood. The scientists leading the research say that visceral body fat could play an important role in accelerating aging of the heart and blood vessels. This type of fat is known to be harmful to health and this study now links it to faster heart aging.

In the study, published in the European Heart Journal, the scientists analyzed data from 21,241 participants in the UK Biobank, which includes whole-body imaging to map the amount of fat and where it is located in the body.

The UK Biobank data also includes detailed imaging of the heart and blood vessels. Artificial intelligence was used to analyze these images to capture signs of organ aging—such as tissues becoming stiff and inflamed. An individual was given a "heart age" which can be compared to their actual age at the time of the scan.

The researchers found that faster heart aging was linked to having more visceral adipose tissue. Visceral adipose tissue is fat found deep inside the abdomen around organs such as the stomach, intestines, and liver. This type of fat cannot be seen from the outside, and some people can have large amounts of visceral fat despite having a healthy weight.

The researchers found signs on blood tests that visceral fat is linked to increased inflammation in the body—which is a potential cause of premature aging.

They also found differences between the sexes. Male-type fat distribution (fat around the belly, often called 'apple' shaped) was particularly predictive of early aging in men.

In contrast, a genetic predisposition to female-type fat (fat on the hips and thighs, often called "pear" shaped) was protective against heart aging in women.

The researchers also found a link between higher estrogen levels in premenopausal women and a slowing of heart aging, which they suggest could indicate a role for hormones in protecting against heart aging.

Declan P O'Regan et al, Sex-specific body fat distribution predicts cardiovascular ageing, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf553

Croatian Freediver Shatters Record For Longest-Held Breath
This year, on June 14, Croatian freediver Vitomir Maričić set a world record when he held his breath for 29 minutes and 3 seconds.

That’s longer than a bottlenose dolphin, and 5 minutes longer than the previous Guinness World Record holder.
Nearly half an hour without air is mind boggling. That's roughly twice as long as a bottlenose dolphin is thought to hold its breath.
With each breath, a seal can replace 90 percent of the air in its lungs – but our species can only replace 20 percent. To keep up, we need more breaths to fill our lungs with fresh air.

To get as much oxygen into his body as it could possibly carry, Maričić inhaled pure oxygen for 10 minutes before the attempt.
This increased the oxygen dissolved in his blood plasma, which is a crucial reservoir for the body's tissues.

On an Instagram reel, Maričić explains that he started his record-breaking attempt with nearly five times more oxygen in his body than usual. Without that, he never could have lasted so long.

https://www.sciencealert.com/croatian-freediver-shatters-record-for...

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Scientists Have Just Created The Most Synthetic Life Form Ever

Scientists have created a bacteria with a genetic code more streamlined – and more meddled with – than any other life on Earth. This bacteria, a synthetic Escherichia coli called Syn57, has been engineered to build its body using just 57 of the 64 'codons' that have served all known organisms for billions of years. The recipe for life is written in a language that uses 64 different codons, each composed of a triplet of nucleotides. It's the long sentences of 'three-letter' codons that make up our DNA and RNA. They provide our cells with the essential instructions to translate ordinary matter into the building blocks of life, amino acids, which are threaded in sequence to form proteins. When a cell is building proteins, it 'reads' the codon sequence, written using those 64 nucleotide triplets, to know which amino acids to add next, and when to stop.By engineering the entire genome from scratch, the researchers set out to eliminate four of the six codons associated with the amino acid serine, two of the four alanine codons, and one 'stop' codon. Where these redundant codons appeared in the bacteria's genome, the researchers substituted them with synonymous codons that give the same instructions. This required more than 101,000 changes to the genetic code. These were planned out on the computer first, in 100-kilobyte fragments, and then came the arduous work of assembling the gene. To make sure they weren't inserting fundamentally harmful changes into the microbes, the team tested small fragments of the synthetic genome in living bacteria bit by bit, eventually stitching it all together to form the final, entirely synthetic strain.

https://www.science.org/doi/10.1126/science.ady4368

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Scientists discover rare freshened water beneath the seafloor

How did freshened water end up beneath the New England Shelf miles offshore?

Researchers are attempting to answer the question by studying samples collected from three sites off the coast of Nantucket. Sampling of this offshore freshened groundwater to the extent that they can make comprehensive geochemical assessments of its history, including its age, is unprecedented in scientific ocean drilling.

The salinity levels of sediments below the seafloor are typically close to those in the overlying ocean, yet offshore New England, the subseafloor contains an unusually large reservoir of freshened water.

The sheer freshness of the water, which was close to drinking water limits, was a surprise.

The cores will be archived and made accessible for further scientific research for the scientific community after a one-year moratorium period. All expedition data will be open access and resulting outcomes will be published.

https://www.uri.edu/news/2025/05/gso-professor-joins-expedition-to-...

Earliest evidence discovered of interbreeding between Homo sapiens and Neanderthals

An international study by researchers provides the first scientific evidence that Neanderthals and Homo sapiens had biological and social relations, and even interbred for the first time, in the Land of Israel.

The research team found a combination of Neanderthal and Homo sapiens traits in the skeleton of a five-year-old child discovered about 90 years ago in the Skhul Cave on Mount Carmel. The fossil, estimated to be about 140,000 years old, is the earliest human fossil in the world to display morphological features of both of these human groups, which until recently were considered two separate species.

Genetic studies over the past decade have shown that these two groups exchanged genes.

Even today, 40,000 years after the last Neanderthals disappeared, part of our genome—2% to 6%—is of Neanderthal origin. But these gene exchanges took place much later, between 60,000 to 40,000 years ago.

In the new study, the researchers were dealing with a human fossil that is 140,000 years old. They  show that the child's skull, which in its overall shape resembles that of Homo sapiens—especially in the curvature of the skull vault—has an intracranial blood supply system, a lower jaw, and an inner ear structure typical of Neanderthals.

For years, Neanderthals were thought to be a group that evolved in Europe, migrating to the Land of Israel only about 70,000 years ago, following the advance of European glaciers.

Part 1

This human type, which the researchers called "Nesher Ramla Homo" (after the archaeological site near the Nesher Ramla factory where it was found), encountered Homo sapiens groups that began leaving Africa about 200,000 years ago, and according to the current study's findings, interbred with them.

The child from the Skhul Cave is the earliest fossil evidence in the world of the social and biological ties forged between these two populations over thousands of years. The local Neanderthals eventually disappeared when they were absorbed into the Homo sapiens population, much like the later European Neanderthals.

The researchers reached these conclusions after conducting a series of advanced tests on the fossil.
The fossil they studied is the earliest known physical evidence of mating between Neanderthals and Homo sapiens.
The current study reveals that at least some of the fossils from the Skhul Cave are the result of continuous genetic infiltration from the local—and older—Neanderthal population into the Homo sapiens population.

Bastien Bouvier et al, A new analysis of the neurocranium and mandible of the Skhūl I child: Taxonomic conclusions and cultural implications, L'Anthropologie (2025). DOI: 10.1016/j.anthro.2025.103385

Part 2

Cells from the spleen found to play a surprising role after heart attack

After a person survives a heart attack, the heart has a brief window of time in which it can heal if the right circumstances exist. But most of the time, scar tissue forms in the areas that lacked oxygen during the heart attack. This scar tissue impairs heart function, which can worsen into heart failure, reducing quality of life and increasing the risk of early death.

A new study has identified a surprising role for the spleen—a small organ near the ribs that filters blood and fights infections—in helping the heart heal after a heart attack.

The research, published in Circulation, demonstrated in mice that specific immune cells called marginal metallophilic macrophages, which originate in the spleen, travel from the spleen to the heart and support a healing response after a heart attack.

Using mouse models, single-cell RNA sequencing and other advanced techniques, the researchers established that these specialized macrophages from the spleen help clear damaging immune cells, suppress inflammation and activate genes that help repair the injured cardiac tissue following a heart attack.

To assess whether the same thing occurs in humans, the researchers measured levels of marginal metallophilic macrophages in blood samples collected from people upon their hospital admission due to a heart attack. The researchers compared these levels with those of cardiac patients who had coronary artery disease but had not recently had a heart attack. The researchers  found that levels of the specialized macrophages were higher in patients who had just had a heart attack.

The researchers also demonstrated that they could boost the numbers of these specialized immune cells in mice with an experimental drug, and that doing so improved the healing and anti-inflammatory effects. This medical intervention is not yet in clinical trials, but it suggests a possible future cardiac immunotherapy targeting the spleen to prevent heart failure in patients who survive a heart attack.

 Mohamed Ameen Ismahil et al, Splenic CD169⁺Tim4⁺ Marginal Metallophilic Macrophages Are Essential for Wound Healing After Myocardial Infarction, Circulation (2025). DOI: 10.1161/CIRCULATIONAHA.124.071772

Kidney fibrosis linked to molecule made by gut bacteria

A molecule made by bacteria in the gut can hitch a ride to the kidneys, where it sets off a chain reaction of inflammation, scarring and fibrosis—a serious complication of diabetes and a leading cause of kidney failure—according to a new study from researchers .

After finding high levels of corisin—a small peptide produced by Staphylococcus bacteria in the gut—in the blood of patients with diabetic kidney fibrosis, the researchers used computer simulations and tissue and mouse experiments to track how corisin affects the kidneys, how it gets there from the gut, and a possible method of countering it with antibody treatment.

These  new findings suggest corisin is indeed a hidden culprit behind progressive kidney damage in diabetes, and that blocking it could offer a new way to protect kidney health in patients.

Taro Yasuma et al, Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging, Nature Communications (2025). DOI: 10.1038/s41467-025-61847-2

Positive emotional bias could be an early sign of cognitive decline in aging populations

As people age, they display a bias in recognizing emotions as positive—to the point of improperly labeling neutral or negative emotions as positive.

Some researchers theorize this bias is an adaptive mechanism to support mental and emotional wellness, but new evidence suggests it may be a sign of cognitive decline.

In a JNeurosci paper, researchers advance understanding of what this positive emotional bias that elders exhibit signifies about their brains' health.

A large pool of participants (665) viewed faces in an emotion recognition task. Age-related positivity bias correlated with poorer cognitive performance in two assessments, but not necessarily emotional decline as measured by examining nonclinical depressive symptoms.

The researchers also observed structural changes in brain areas associated with emotional processing and changes in how these areas communicate to another brain region involved in social decisions. Thus, positivity bias from aging impacts the brain in observable ways that could be leveraged clinically to detect early rising signs of age-related neurodegeneration and cognitive decline.

Researchers are now  exploring how these findings relate to older adults with early cognitive decline, particularly those showing signs of apathy, which is often another early sign of dementia.

 Age-Related Positivity Bias in Emotion Recognition is Linked to Lower Cognitive Performance and Altered Amygdala–Orbitofrontal Connectivity, JNeurosci (2025). DOI: 10.1523/JNEUROSCI.0386-25.2025

Exercise intensity could be impacting your gut

While exercise is great for both your mental and physical health, new research from Edith Cowan University (ECU) has found that exercise intensity could result in changes to the internal gut biome.

Researchers undertook research into the impact of high and low training loads on athletes, in the hope of assisting athletes to improve their overall health, well-being and performance by better understanding the gut microbiome.

It appears that athletes have a different gut microbiota when compared with the general population. This includes greater total short chain fatty acid concentrations, alpha diversity, an increased abundance of some bacteria and a lower abundance of others.

 while the differing microbiome between athletes and the public could likely be due to the differences in their dietary intake , fitness markers, which include oxygen uptake, have also been correlated.

Published in the Journal of the International Society of Sports Nutrition, this research uncovered that training load had an influence on gut health markers in athletes, with differences detected in short-chain fatty acid concentrations and the abundance of specific bacteria.

 One of the potential reasons for the change in the gut could be the higher levels of blood lactate which results from higher intensity training. The lactate produced in muscle is transported to the gut to be metabolized, which could potentially result in increased bacteria in the gut.

The changes found in the gut biome when comparing high training loads to low training loads, were also related to diet.

Another observation made during the research was the significant slowing of gut transit times in athletes during low training loads. That slowing of transit time during the low training load appears to also be impacting the gut microbiome for an athlete.

The gut may play a role in lactate metabolism and regulating pH levels, both of which could impact performance and overall athlete health, say the researchers. 

B. Charlesson et al, Training load influences gut microbiome of highly trained rowing athletes, Journal of the International Society of Sports Nutrition (2025). DOI: 10.1080/15502783.2025.2507952

Why Were Dinosaurs So Big?

Metabolic adaptations, air sac-filled bones, and evolutionary pressure likely contributed to dinosaurs’ gigantism.

Scientists have found evidence that the long-necked and long-tailed sauropods had a comparatively slower metabolism relative to today’s large mammals, which indicates that they likely didn’t have to eat as much. (1)

And when sauropods did eat, they likely swallowed most of their food whole: Sauropods’ teeth had very little wear, unlike those of other herbivorous species, such as the duck-billed dinosaurs, and even mammals. (2,3)They could ‘vacuum up’ a lot of food without having to spend a lot of time chewing.

Some sauropod bones were also filled with air sacs, which could make even larger body sizes mechanically feasible.  (4)This adaptive anatomical feature is found in many birds, dinosaurs’ closest living relatives, and it helps reduce their body weight and promote flight.

Sources: 

1. Baumgart SL, et al. The living dinosaur: accomplishments and challenges of reconstructi.... Biol Lett. 2025;21(5):20250126.

2. Whitlock JA. Inferences of diplodocoid (Sauropoda: Dinosauria) feeding behavior .... PLoS One. 2011;6(4):e18304.

3. Fiorillo AR. Dental micro wear patterns of the sauropod dinosaurs camarasaurus a.... Hist Biol. 1998;13(1):1-16.

4. Wedel MJ. Evidence for bird-like air sacs in saurischian dinosaurs. J Exp Zool A Ecol Genet Physiol. 2009;311(8):611-628.

5. https://www.the-scientist.com/why-were-dinosaurs-so-big-73254?utm_c...

Cells 'vomit' waste to promote healing, but it comes with a trade-off

When injured, cells have well-regulated responses to promote healing. These include a long-studied self-destruction process that cleans up dead and damaged cells as well as a more recently identified phenomenon that helps older cells revert to what appears to be a younger state to help grow back healthy tissue.

Now, a new study in mice  reveals a previously unknown cellular purging process that may help injured cells revert to a stem cell-like state more rapidly. The investigators have dubbed this newly discovered response cathartocytosis, taking from Greek root words that mean cellular cleansing.

Published in the journal Cell Reports, the study used a mouse model of stomach injury to provide new insights into how cells heal—or fail to heal—in response to damage, such as from an infection or inflammatory disease.

After an injury, the cell's job is to repair that injury. But the cell's mature cellular machinery for doing its normal job gets in the way. So, this cellular cleanse is a quick way of getting rid of that machinery so it can rapidly become a small, primitive cell capable of proliferating and repairing the injury. Researchers identified this process in the GI tract, but they suspect it is relevant in other tissues as well.

The researchers identified cathartocytosis within an important regenerative injury response called paligenosis. 

In paligenosis, injured cells shift away from their normal roles and undergo a reprogramming process to an immature state, behaving like rapidly dividing stem cells, as happens during development. Originally, the researchers assumed the decluttering of cellular machinery in preparation for this reprogramming happens entirely inside cellular compartments called lysosomes, where waste is digested in a slow and contained process. From the start, though, the researchers noticed debris outside the cells. They initially dismissed this as unimportant, but the more external waste they saw in their early studies, the more they began to suspect that something deliberate was going on. They utilized a model of mouse stomach injury that triggered the reprogramming of mature cells to a stem cell state all at once, making it obvious that the "vomiting" response—now happening in all the stomach cells simultaneously—was a feature of paligenosis, not a bug.

In other words, the vomiting process was not just an accidental spill here and there, but a newly identified, standard way cells behaved in response to injury.

Although they discovered cathartocytosis happening during paligenosis, the researchers said cells could potentially use cathartocytosis to jettison waste in other, more worrisome situations, like giving mature cells that ability to start to act like cancer cells.

While the newly discovered cathartocytosis process may help injured cells proceed through paligenosis and regenerate healthy tissue more rapidly, the trade-off comes in the form of additional waste products that could fuel inflammatory states, making chronic injuries harder to resolve and correlating with an increased risk of cancer development.

 Jeffrey W. Brown et al, Cathartocytosis: Jettisoning of cellular material during reprogramming of differentiated cells, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116070