Scientists reveal how senses work together in the brain

It has long been understood that experiencing two senses simultaneously, like seeing and hearing, can lead to improved responses relative to those seen when only one sensory input is experienced by itself. For example, a potential prey that gets visual and auditory clues that it is about to be attacked by a snake in the grass has a better chance of survival.

Precisely how multiple senses are integrated or work together in the brain has been an area of fascination for neuroscientists for decades. New research has revealed some new key insights.

Research participants were asked to watch a simple dot animation while listening to a series of tones and press a button when they noticed a change in the dots, the tones, or both.

Using EEG, the scientists were able to infer that when changes happened in both the dots and tones, auditory and visual decision processes unfolded in parallel but came together in the motor system. This allowed participants to speed up their reaction times.

Researchers found that the EEG accumulation signal reached very different amplitudes when auditory versus visual targets were detected, indicating that there are distinct auditory and visual accumulators.

Using computational models, the researchers then tried to explain the decision signal patterns as well as reaction times. In one model, the auditory and visual accumulators race against each other to trigger a motor reaction, while the other model integrates the auditory and visual accumulators and then sends the information to the motor system. Both models worked until researchers added a slight delay to either the audio or visual signals.

Then the integration model did a much better job at explaining all the data, suggesting that during a multisensory (audiovisual) experience, the decision signals may start on their own sensory-specific tracks but then integrate when sending the information to areas of the brain that generate movement.

The research provides a concrete model of the neural architecture through which multisensory decisions are made. It clarifies that distinct decision processes gather information from different modalities, but their outputs converge onto a single motor process where they combine to meet a single criterion for action.

 Distinct audio and visual accumulators co-activate motor preparation for multisensory detection, Nature Human Behaviour (2025). DOI: 10.1038/s41562-025-02280-9

Exceeding functional biosphere integrity limits: Study finds 60% of the world's land area is in a precarious state

A new study maps the planetary boundary of "functional biosphere integrity" in spatial detail and over centuries. It finds that 60% of global land areas are now already outside the locally defined safe zone, and 38% are even in the high-risk zone.

Functional biosphere integrity refers to the plant world's ability to co-regulate the state of the Earth system. This requires that the plant world is able to acquire enough energy through photosynthesis to maintain the material flows of carbon, water and nitrogen that support the ecosystems and their many networked processes, despite today's massive human interference.

Together with biodiversity loss and climate change, functional integrity forms the core of the Planetary Boundaries analytical framework for a safe operating space for humanity.

There is an enormous need for civilization to utilize the biosphere—for food, raw materials and, in future, also for climate protection.

Human demand for biomass continues to grow—and on top of that, the cultivation of fast-growing grasses or trees for producing bioenergy with carbon capture and storage is considered by many to be an important supporting strategy for stabilizing climate.

It is therefore becoming even more important to quantify the strain we're already putting on the biosphere—in a regionally differentiated manner and over time—to identify overloads. This new research is paving the way for this.

The study builds on the latest update of the Planetary Boundaries framework published in 2023.

The framework now squarely puts energy flows from photosynthesis in the world's vegetation at the center of those processes that co-regulate planetary stability. These energy flows drive all of life—but humans are now diverting a sizable fraction of them to their own purposes, disturbing nature's dynamic processes.

The stress this causes in the Earth system can be measured by the proportion of natural biomass productivity that humanity channels into its own uses—through harvested crops, residues and timber—but also the reduction in photosynthetic activity caused by land cultivation and sealing.

The study added to this measure a second powerful indicator of biosphere integrity: An indicator of risk of ecosystem destabilization records complex structural changes in vegetation and in the biosphere's water, carbon and nitrogen balances.

Part 1

Based on the global biosphere model LPJmL, which simulates water, carbon and nitrogen flows on a daily basis at a resolution of half a degree of longitude/latitude, the study provides a detailed inventory for each individual year since 1600, based on changes in climate and human land use.
The research team not only computed, mapped and compared the two indicators for functional integrity of the biosphere, but also evaluated them by conducting a mathematical comparison with other measures from the literature for which "critical thresholds" are known.

This resulted in each area being assigned a status based on local tolerance limits of ecosystem change: Safe Operating Space, Zone of Increasing Risk or High Risk Zone.

The model calculation shows that worrying developments began as early as 1600 in the mid-latitudes. By 1900, the proportion of global land area where ecosystem changes went beyond the locally defined safe zone, or were even in the high-risk zone, was 37% and 14% respectively, compared to the 60% and 38% we see today.

Industrialization was beginning to take its toll; land use affected the state of the Earth system much earlier than climate warming. At present, this biosphere boundary has been transgressed on almost all land surface—primarily in Europe, Asia and North America—that underwent strong land cover conversion, mainly due to agriculture.

This first world map showing the overshoot of the boundary for functional integrity of the biosphere, depicting both human appropriation of biomass and ecological disruption, is a breakthrough from a scientific perspective, offering a better overall understanding of planetary boundaries.
It also provides an important impetus for the further development of international climate policy. This is because it points to the link between biomass and natural carbon sinks, and how they can contribute to mitigating climate change. Governments must treat it as a single overarching issue: comprehensive biosphere protection together with strong climate action.

 Breaching planetary boundaries: Over half of global land area suffers critical losses in functional biosphere integrity, One Earth (2025). DOI: 10.1016/j.oneear.2025.101393. www.cell.com/one-earth/fulltex … 2590-3322(25)00219-2

Part 2

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How human protein ACE2 modulation could stop the entry of coronavirus

Early in the pandemic, most research focused on designing drugs that could block the virus's spike protein. This was a logical first step, but as we've seen, the virus is a moving target. It was rapidly evolving, and new variants acquired resistance due to changes in the surface spike glycoprotein (S protein).

This highlighted a critical challenge: would our treatments still work as the virus continued to change? Instead of constantly chasing new variants, scientists began to ask, what if they focused on how the human body responds to the virus, rather than only targeting the virus itself?

Instead of pursuing the virus directly, researchers decided to explore a new idea: targeting the human protein that mediates the virus's entry into cells in our body. This led them to angiotensin converting enzyme-2 (ACE2), the critical "gateway" protein the virus hijacks to begin its invasion. ACE2 is present on the surface of many human cells, especially in the lungs, and plays a crucial role in regulating blood pressure and heart health. Unfortunately, SARS-CoV-2 hijacks this protein as its entry point into cells.

This poses a significant challenge: blocking ACE2 entirely isn't a good option, as it's far too important for normal body functions. So the scientists' goal was: can they  make it harder for the virus to use ACE2 without disturbing its vital role in our bodies?

The researchers, in their experiments, found that when a suitable small molecule binds to  allosteric pocket of hACE2, it causes a conformational change in ACE2. This change primarily affects the global allostery, which is critical for the protein's interaction with the viral spike glycoprotein. This conformational shift weakens the binding between ACE2 and the viral spike protein, making it tougher for the virus to latch on and infect a cell.

The real innovation, however, is that this conformational change does not inhibit ACE2's normal function; in fact, their simulations and calculations confirmed that it enhances it.

Pratyush Pani et al, Modulating functional allostery of the host-cell receptor protein hACE2 to inhibit viral entry of SARS-CoV-2, Physical Chemistry Chemical Physics (2025). DOI: 10.1039/D5CP01740H

Dementia-like protein buildup found in pancreas cells before cancer develops

Multiple cancer types, including pancreatic cancer, are linked to a faulty mutation in a gene called KRAS, but scientists are increasingly learning that genetic changes are not the whole story.

Scientists have uncovered dementia-like behavior in pancreas cells at risk of turning into cancer. The findings provide clues that could help in the treatment and prevention of pancreatic cancer, a difficult-to-treat disease.

The research was published in the journal Developmental Cell in a paper titled "ER-phagy and proteostasis defects prime pancreatic epithelial state changes in KRAS-mediated oncogenesis."

Researchers studied pancreas cells in mice over time, to see what was causing healthy cells to turn into cancer cells. They discovered that pancreatic cells at risk of becoming cancerous, known as pre-cancers, develop faults in the cell's recycling process (known as "autophagy"). 

In pre-cancer cells, the researchers noticed excess "problem protein" molecules forming clumps—behavior seen in neurological diseases such as dementia. The researchers also noticed similar clumping occurring in human pancreas samples, suggesting this happens during pancreatic cancer development.

This  research shows the potential role autophagy disruption plays in the beginnings of pancreatic cancer. While early stage, we can potentially learn from research into other diseases where we see protein clumping, such as dementia, to better understand this aggressive type of cancer and how to prevent it.

One of the ways cells keep people healthy is by breaking down excess molecules they no longer need, through a recycling process called "autophagy." Autophagy is particularly important in the pancreas to control the level of digestive proteins and hormones the pancreas produces to help break down food.

Scientists have studied autophagy in detail over many years and are learning the key role it plays in diseases such as cancer. In some cases, cancer cells can become "addicted" to autophagy, hijacking the recycling process to help cancer cells divide and grow more quickly.

This research, on the other hand, suggests the combined effect of the faulty KRAS gene and disrupted autophagy could be driving the development of pancreatic cancer.

 ER-phagy and proteostasis defects prime pancreatic epithelial state changes in KRAS-mediated oncogenesis, Developmental Cell (2025). DOI: 10.1016/j.devcel.2025.07.016. www.cell.com/developmental-cel … 1534-5807(25)00473-3.

Scientist uncover hidden immune 'hubs' that drive joint damage in rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune disease that affects millions worldwide and can have a devastating impact on patients' lives. Yet, about one in three patients respond poorly to existing treatments.

Researchers have shed new light on this challenge by discovering that peripheral helper T cells (Tph cells), a key type of immune cell involved in RA, exist in two forms: stem-like Tph cells and effector Tph cells. The stem-like Tph cells reside in immune "hubs" called tertiary lymphoid structures within inflamed joints, where they multiply and activate B cells.

Some of these then become effector Tph cells that leave the hubs and cause inflammation. This continuous supply of effector Tph cells may explain why inflammation persists in some patients despite treatment.

Targeting the stem-like Tph cells at the source could offer a new therapeutic strategy, bringing hope for more effective symptom relief and improved quality of life for patients living with RA.

The findings are published online in Science Immunology.

Yuki Mauso et al, Stem-like and effector peripheral helper T cells comprise distinct subsets in rheumatoid arthritis, Science Immunology (2025). DOI: 10.1126/sciimmunol.adt3955. www.science.org/doi/10.1126/sciimmunol.adt3955

Genetic study shows that common blood cancer includes subtypes

A new study  published in Cell Reports Medicine shows that follicular lymphoma (FL), a common type of blood cancer, is not one single disease but consists of three genetically distinct subtypes. The findings may help doctors diagnose and treat patients more accurately in the future.

Follicular lymphoma (FL) is a slow-growing cancer that affects white blood cells. Until now, it has been treated as one disease. However, by analyzing tumor samples from patients using whole-genome and transcriptomic sequencing, researchers  found that FL comprises three subtypes with distinct genetic profiles, biological features, and clinical outcomes.

These subtypes differ in how they develop and may respond differently to treatment. This means that patients could benefit from more personalized care based on the specific characteristics of their cancer, say the researchers.

The study employed advanced computational methods to investigate patterns in DNA mutations, gene expression, and immune cell behavior. The results showed that each subtype has its own cell of origin and interacts differently with the surrounding tissue. This could affect how the disease progresses and how well it responds to therapy.

Weicheng Ren et al, Whole-genome sequencing reveals three follicular lymphoma subtypes with distinct cell of origin and patient outcomes, Cell Reports Medicine (2025). DOI: 10.1016/j.xcrm.2025.102278

Bioengineered platform uses bacteria to sneak viruses into tumors

Researchers have built a cancer therapy that makes bacteria and viruses work as a team. In a study published in Nature Biomedical Engineering, the Synthetic Biological Systems Lab shows how their system hides a virus inside a tumor-seeking bacterium, smuggles it past the immune system, and unleashes it inside cancerous tumors.

The new platform combines the bacteria's tendency to find and attack tumors with the virus's natural preference for infecting and killing cancerous cells.

The researchers think that this technology—validated in mice—represents the first example of directly engineered cooperation between bacteria and cancer-targeting viruses.

The approach combines the bacteria's instinct for homing in on tumors with a virus's knack for infecting and killing cancer cells.

By bridging bacterial engineering with synthetic virology, the goal is to open a path toward multi-organism therapies that can accomplish far more than any single microbe could achieve alone.

The researchers, therefore,  programmed the bacteria to act as an invisibility cloak, hiding the virus from circulating antibodies, and ferrying the virus to where it is needed. This  system demonstrates that bacteria can potentially be used to launch an oncolytic virus to treat solid tumors in patients who have developed immunity to these viruses.

Singer, Z.S., et al. Engineered bacteria launch and control an oncolytic virus, Nature Biomedical Engineering (2025). DOI: 10.1038/s41551-025-01476-8 www.nature.com/articles/s41551-025-01476-8

Genetically modified immune cell could help organ transplant patients who are prone to rejection

A medical research team  reports in Frontiers in Immunology that it has engineered a new type of genetically modified immune cell that can precisely target and neutralize antibody-producing cells complicit in organ rejection.

Similar strategies have been used to stimulate the immune system against certain cancers, but this research team is the first to show its utility in tamping down immune responses that can lead to organ rejection.

While often lifesaving, these organ transplant procedures depend on a precise match between donor and recipient genes to avoid rejection. When the immune system detects foreign tissue, it can attack the transplanted organ.

For decades, doctors have used immunosuppressant drugs to lower the risk of rejection. But these drugs work broadly, suppressing the entire immune system. This can lead to side effects and shorten the life of the transplanted organ.

This new work showed the feasibility of targeted immunosuppression after transplant that could one day reduce rejection without leaving patients vulnerable to infection and other side effects. This strategy could also level the playing field for patients who have limited eligibility for organs because they are especially prone to rejection.

Part 1

Balancing the immune system

When in working balance, the immune system protects the body against outside invaders without attacking its own tissues. B-cells release antibodies that attack pathogens and infected cells. Regulatory T-cells, or Tregs, keep the immune response from going too far, preventing tissue damage and autoimmune diseases.

When you prick your finger, it is important to mount a strong immune response to kill all the bacteria that entered your finger. But it's also important to bring that immune response to a halt when all the bacteria have been killed. Otherwise, you could lose your finger in the process, and the cure would be as bad as the disease.

A key target for B-cells are human leukocyte antigen (HLA) proteins, which help the immune system to tell self from non-self. Doctors try to match donor and recipient HLA proteins as closely as possible, but with more than 40,000 HLA variants, perfect matches are rare.

One variant, HLA-A2, is found in nearly one-third of the global population. Patients who have had previous exposure to HLA-A2 are considered "pre-sensitized," meaning their immune systems are primed to respond to it and release very large amounts of anti-HLA-A2 antibodies.

These include previous transplant patients; women who, during pregnancy, carried a child with HLA-A2 inherited from their partners; and recipients of HLA-A2-positive blood transfusions. Pre-sensitized patients have a much more difficult time finding a compatible donor organ.
In this new work, researchers developed a novel way for the Tregs to find and neutralize specifically the B-cells producing anti-HLA-A2 antibodies. They have fitted the Tregs with a CHAR—short for chimeric anti-HLA antibody receptor—which detects the appropriate B-cells and alerts the Tregs to suppress them.

When CHARs detect and attach to B-cells secreting anti-HLA-A2 antibodies, they alert the Tregs to neutralize these problematic B-cells, essentially signaling the immune system to stand down and not attack the organ. In this way, not only do CHARs act like heat-seeking missiles to find the right B-cells to target, but they also hold the key to the Treg's ignition, activating its machinery to elicit a more precise immunosuppressive response and prevent it from going overboard.
Researchers now took patients' cells that have been shown to make an extremely strong response against HLA-A2-expressing cells, and showed that the novel CHAR-Tregs calmed them down.

Chimeric anti-HLA antibody receptor engineered human regulatory T cells suppress alloantigen-specific B cells from pre-sensitized transplant recipients.v, Frontiers in Immunology (2025). DOI: 10.3389/fimmu.2025.1601385

Part 2

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How gut microbiota makes genetically identical mice go different ways structurally and functionally while dealing with immune system

Genetically identical, but not the same: How gut microbiota composition shapes the immune system in mice

Laboratory mice are often considered the scientific equivalent of identical twins—genetically identical and expected to look and behave the same. But new research shows that this assumption doesn't always hold true. Researchers discovered that the composition of the gut microbiota can dramatically influence the structure and function of the immune system—even in genetically identical animals.

Researchers were surprised by how much the absence of microbiota increased phenotypic variability. Germ-free mice were each a little different, while those with a normal microbiota were much more alike.

They found that mice with a complex microbiota were more similar to each other than GF or OMM12-colonized mice, and the absence of microbiota dramatically increased variability in the shape and size of gut immune organs. While OMM12 partly restored gut morphology, it failed to restore physiological immune cell numbers or fully replicate the functional immune status of conventional mice.
Along the way, the team also described a previously unknown immune structure—the immunovillus. This densely immune cell–packed villus-like projection was found mainly in mice with restricted microbiota and may represent an adaptation to a specific microbial environment.

Published in the journal Gut Microbes, the study highlights the need to consider microbial context—not just genetics—when interpreting results from laboratory mouse models. Standardizing microbiota is essential for reproducibility, but current simplified microbial consortia such as OMM12 are not yet a perfect substitute for a natural complex microbiota.

Pačes Jan et al, Microbiota modulate immune cell populations and drive dynamic structural changes in gut-associated lymphoid tissue, Gut Microbes (2025). DOI: 10.1080/19490976.2025.2543908

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