Autoimmune diseases linked to cancers of the digestive tract

In a comprehensive study, researchers have provided reliable evidence for a link between chronic inflammatory diseases and the development of tumors in the digestive tract. The results were recently published in eClinicalMedicine.

Using data from over 1.5 million patients from 47 studies, the researchers analyzed the association between four autoimmune diseases, most of which are acquired in childhood or younger adulthood, and cancers of the gastrointestinal tract, liver and pancreas.

The study shows that celiac disease, systemic lupus erythematosus and type 1 diabetes increase the risk of several types of cancer of the digestive tract. These include stomach and bowel cancer. In particular, the risk of small bowel cancer increases by a factor of 4.2 if celiac disease is present.

Multiple sclerosis, on the other hand, is associated with a lower risk of certain types of cancer, such as pancreatic, esophageal and rectal cancer.

These results underline the need for targeted monitoring of patients with autoimmune diseases and the development of personalized cancer prevention programs.

Julia Reizner et al, Evaluating the risk of digestive system cancer in autoimmune disease patients: a systematic review and meta-analysis focusing on bias assessment, eClinicalMedicine (2025). DOI: 10.1016/j.eclinm.2025.103410

How noise, air pollution, heat and chemicals act together to damage the cardiovascular system

Cardiovascular diseases comprise a broad range of disorders affecting the heart and blood vessels, including myocardial infarction, stroke, coronary artery disease (CAD), hypertension, heart failure, and arrhythmias. These conditions remain the number one cause of death worldwide.

Therefore, the demand for effective preventive strategies is substantial, and understanding the relevant risk factors is essential. Well-established contributors include obesity, diabetes, smoking, physical inactivity, and an unhealthy diet.

An international research team now warns in a comprehensive review about another group of risk factors that have thus far received limited attention in current prevention strategies: environmental stressors. The authors report in Cardiovascular Research that chronic exposure to noise, fine particulate matter,  heat waves, and chemical pollutants in soil and water can exert harmful effects on the cardiovascular system.

Of particular concern is the combination of multiple environmental stressors: the multimodal exposome can magnify the detrimental effects of individual exposures.

Noise can intensify the impact of air pollutants, and heat can act as a catalyst for vascular damage caused by toxins.
The overlapping biological mechanisms range from oxidative stress and activation of the pro-inflammatory enzyme NOX-2 to endothelial dysfunction—all of which are early precursors of myocardial infarction and stroke.
The exposome concept offers a holistic framework that integrates the lifetime accumulation of environmental exposures and their biological interactions into cardiovascular risk assessment, enabling the development of more targeted preventive strategies. The researchers  stress that stricter environmental and noise protection laws, sustainable urban planning, and green infrastructure can help reduce exposure to these stressors.

Thomas Friedrich Münzel et al, A comprehensive review/expert statement on environmental risk factors of cardiovascular disease, Cardiovascular Research (2025). DOI: 10.1093/cvr/cvaf119. academic.oup.com/cardiovascres … /cvr/cvaf119/8230112

Party 2

How small changes in walking technique may help treat knee osteoarthritis

Gait analysis and pain measures show that subtly adjusting the angle of the foot during walking may reduce knee pain caused by osteoarthritis. This approach may also slow progression of the condition, an incurable disease in which the cartilage cushion inside a joint breaks down.

A new study explored whether changing the way patients position their feet when walking could lessen extra loading—stress on the joint during motion—and help treat the disease.

For the investigation, the scientists tested this intervention in 68 men and women with mild to moderate knee osteoarthritis and then used advanced MRI scans to track how well it worked.

The results suggest that those trained to angle their feet slightly inward or outward from their natural alignment experienced slower cartilage degeneration in the inner part of their knee compared with those who were encouraged to walk more frequently without changing their foot position. A report on the study is published online in the journal The Lancet Rheumatology.

The findings also revealed that those who adjusted their foot angle reduced their pain score by 2.5 points on a 10-point scale, an effect equivalent to that of over-the-counter pain medications. By contrast, those who did not change their gait reduced their pain scores by little more than a point.

 Personalised gait retraining for medial compartment knee osteoarthritis: a randomised controlled trial, The Lancet Rheumatology (2025). DOI: 10.1016/S2665-9913(25)00151-1

A genetic twist that sets human brains apart

Research  has shed new light on an age-old question: what makes the human brain unique? The study is published online in Science Advances.

The  discovery comes from their investigation of human-accelerated regions (HARs)—sections of the human genome that have accumulated an unusually high level of mutations as humans have evolved. There is a lot of scientific interest in HARs, as they are hypothesized to play an essential role in conferring human-specific traits, and also have links to neurodevelopmental disorders, such as autism.

One reason why scientists think that HARs confer human-specific traits is they have undergone rapid changes in their genetic sequences since we split from our closest living relative—the chimpanzee—approximately 5 million years ago.

Now researchers have identified one particular HAR—called HAR123—that appears to be instrumental in shaping the human brain. The researchers found that HAR123 itself is not a gene, but is instead a type of molecular "volume control" known as a transcriptional enhancer. Transcriptional enhancers control which genes are activated, how much they are activated, and at what times they are activated during an organism's development.

Through its role as a transcriptional enhancer, HAR123 promotes the development of neural progenitor cells, the cells that give rise to the two main types of brain cells—neurons and glial cells. HAR123 also influences the ratio of neurons and glial cells that form from neural progenitor cells. 

Part 1

Ultimately, HAR123 promotes a particularly advanced human trait called cognitive flexibility, or the ability to unlearn and replace previous knowledge.
In addition to providing new insights into the biology of the human brain, the results also offer a molecular explanation for some of the radical changes that have occurred in the human brain over the course of our evolution. This is supported, for example, by the authors' finding that the human version of HAR123 exerts different molecular and cellular effects than the chimpanzee version in both stem cells and neuron precursor cells in a petri dish.

 Kun Tan et al, An ancient enhancer rapidly evolving in the human lineage promotes neural development and cognitive flexibility, Science Advances (2025). DOI: 10.1126/sciadv.adt0534. www.science.org/doi/10.1126/sciadv.adt0534

Part 2

In-mouth hydrogel releases artificial saliva to treat dry mouth

Saliva is more than spit. It helps with chewing and swallowing, protects teeth and gums, and even has antimicrobial and digestive properties. However, certain conditions or medical treatments, such as hemodialysis, chemotherapy and radiation therapy, reduce natural saliva production. Now, researchers publishing in ACS Applied Polymer Materials have created a reusable hydrogel that releases artificial saliva over time, which could help provide sustained relief from dry mouth.

Dry mouth is a condition whereby the salivary glands do not produce enough saliva. Many medications to treat dry mouth boost natural saliva production, but they either provide temporary relief or have unwanted side effects, including mouth irritation and tooth erosion. Previous research identified that artificial saliva, often used in laboratory studies, could be a promising alternative to current medications.

Like natural saliva, artificial saliva is mostly water and contains mucins—a class of compounds that lubricate the mouth and have antimicrobial properties.

To create the reservoir, the researchers mixed artificial saliva with a biocompatible polymer poly(hydroxyethyl methacrylate), which is commonly used in medical applications such as contact lenses. The resulting hydrogel is a clear blob roughly the size of a U.S. quarter and small enough to fit in the inner cheek or below the tongue.

To determine how much artificial saliva a single reservoir could absorb, the researchers submerged it in artificial saliva for 6 hours. The saliva gel expanded up to 400% of its original volume, indicating that the gel has a high saliva storage capacity.

Next, the researchers tested the reservoir's ability to release stored saliva. The gel released all stored saliva over a 4-hour time span at 98.6 degrees Fahrenheit (37 degrees Celsius), starting off a little faster and then slowing over time. This demonstrates that human body temperature helps initiate saliva release from the hydrogel.

The researchers also report consistent saliva release rates across five consecutive tests with a single reservoir, demonstrating its potential as a reusable treatment option. Lastly, cultured cells in contact with the gel had no change to their survival or growth rates, indicating the reservoir's biocompatibility.

 Suman Debnath et al, Poly(hydroxyethyl methacrylate) Saliva-Gel: A Polymer-Based Solution for Xerostomia Treatment, ACS Applied Polymer Materials (2025). DOI: 10.1021/acsapm.5c00881

Researchers uncover surprising limit on human imagination

Human beings can juggle up to 10 balls at once. But how many can they move through the air with their imaginations?

The answer, published in Nature Communications, astonished even the researchers pursuing the question. The cognitive psychologists found people could easily imagine the trajectory of a single ball after it disappeared. But the imagination couldn't simultaneously keep tabs on two moving balls that fell from view.

The researchers set out to test the capacity limits of the imagination, and they found that it was just one!

Halely Balaban et al, The capacity limits of moving objects in the imagination, Nature Communications (2025). DOI: 10.1038/s41467-025-61021-8

Maternal microbes play a significant role in shaping early brain development, study suggests

Research finds that microbes play an important role in shaping early brain development, specifically in a key brain region that controls stress, social behaviour, and vital body functions.

The study, published in Hormones and Behavior, used a mouse model to highlight how natural microbial exposure not only impacts brain structure immediately after birth but may even begin influencing development while still in the womb. A mouse model was chosen because mice share significant biological and behavioural similarities with humans and there are no other alternatives to study the role of microbes on brain development. 

This work is of significance because modern obstetric practices, like peripartum antibiotic use and Cesarean delivery, disrupt maternal microbes.

At birth, a newborn body is colonized by microbes as it travels through the birth canal. Birth also coincides with important developmental events that shape the brain.

The research team focused on a brain region called the paraventricular nucleus of the hypothalamus (PVN), which plays a central role in regulating stress, blood pressure, water balance, and even social behavior. Their previous work had shown that mice raised without microbes, or germ-free mice, had more dying neurons in the PVN during early development. The new study set out to determine whether this increased cell death translated to changes in neuron number in the long run, and if any effects could be caused by the arrival of microbes at birth or if they began in the womb via signals from maternal microbes.

. The researchers used a cross-fostering approach. Germ-free newborn mice were placed with mothers that had microbes and compared them to control groups. When the brains of these mice were examined just three days after birth, the results were striking: All mice gestated by germ-free mothers had fewer neurons in the PVN, regardless of whether they received microbes after birth. The team also found that germ-free adult mice had fewer neurons in the PVN.

This study shows that microbes play an important role in sculpting a brain region that is paramount for body functions and social behavior. In addition, the study indicates that microbial effects start in the womb via signaling from maternal microbes.

Rather than shunning our microbes, we should recognize them as partners in early life development. They're helping build our brains from the very beginning, say the researchers

 Yvonne C. Milligan et al, The microbiota shapes the development of the mouse hypothalamic paraventricular nucleus, Hormones and Behavior (2025). DOI: 10.1016/j.yhbeh.2025.105742

Why some wounds heal without scars
Some parts of our bodies — such as the insides of the mouth and uterus — heal without scarring. Now researchers are delving into why this happens, and how it might help to head off some of the downsides of scars. The team compared mouth and face skin and found that, in mice, specialized skin cells communicate differently during healing: in mouth cells, a cell signaling pathway and a protein seem to prevent the formation of scars. Samples of human skin biopsies seem to back up the findings.

https://www.science.org/doi/10.1126/scitranslmed.adk2101?utm_source...

Electrical implant approved for arthritis
A 2-centimetre implant that suppresses the symptoms of rheumatoid arthritis is the first electrical device approved to treat an autoimmune condition. The chip, called a Setpoint System, is implanted into a person’s neck and sends electrical pulses through the vagus nerve. In people with rheumatoid arthritis, these signals tell the immune system to stop attacking the joints. Similar implants are now in clinical trials for other autoimmune conditions, including lupus and inflammatory bowel disease.

https://www.smithsonianmag.com/smart-news/new-implanted-device-coul...

A Case of Bromism Influenced by Use of Artificial Intelligence

Man Hospitalized With Psychiatric Symptoms Following AI Advice

A man who followed a chatbot's health plan ended up in hospital after giving himself a rare form of toxicity.

The story began when the patient decided to improve his health by reducing his intake of salt, or sodium chloride. To find a substitute, he did what so many other people do nowadays: he asked ChatGPT on line.

OpenAI's chatbot apparently suggested sodium bromide, which the man ordered online and incorporated into his diet.

While it is true that sodium bromide can be a substitute for sodium chloride, that's usually if you're trying to clean a hot tub, not to make your fries tastier. But the AI neglected to mention this crucial context.

Three months later, the patient presented to the emergency department with paranoid delusions, believing his neighbour was trying to poison him.

In the first 24 hours of admission, he expressed increasing paranoia and auditory and visual hallucinations, which, after attempting to escape, resulted in an involuntary psychiatric hold for grave disability.

After he was treated with anti-psychosis drugs, the man calmed down enough to explain his AI-inspired dietary regime. This information, along with his test results, allowed the medical staff to diagnose him with bromism, a toxic accumulation of bromide. Bromide levels are typically less than around 10 mg/L in most healthy individuals; this patient's levels were measured at 1,700 mg/L. Bromism was a relatively common condition in the early 20th century, and is estimated to have once been responsible for up to 8 percent of psychiatric admissions. But cases of the condition drastically dropped in the 1970s and 1980s, after medications containing bromides began to be phased out.

Following diagnosis, the patient was treated over the course of three weeks and released with no major issues.

It is important to consider that ChatGPT and other AI systems can generate scientific inaccuracies, lack the ability to critically discuss results, and ultimately fuel the spread of misinformation.

https://www.acpjournals.org/doi/10.7326/aimcc.2024.1260

Scientists reverse immunotherapy-resistance by suppressing EPIC1 in mouse model of breast cancer

Immunotherapy employs patients' own immune systems to fight cancer, and it has shown itself to be an effective treatment in many cases. However, some cancers, like triple-negative breast cancer (TNBC), show resistance to immunotherapy. This occurs when tumor cells find ways to evade immune detection—like suppressing immune signaling pathways. One such mechanism is the use of long noncoding RNAs (lncRNAs), which have been found to regulate cancer biology and immune evasion. These lncRNAs render immunotherapies, like the PD-1 inhibitor, pembrolizumab, ineffective.

To test out the effect of EPIC1 knockdown, the researchers used "humanized mice"—mice with human immune systems implanted to mimic the effect of the mechanism in a human. Using these mouse models along with RNA interference to knock down EPIC1 in various cancer cell lines, they found that targeting EPIC1 enabled reduced tumor growth and increased T cell and inflammatory macrophage infiltration. This led to a significant improvement in the efficacy of pembrolizumab in TNBC.

"EPIC1 can be a potential therapeutic target in combination with immunotherapy. Coculture assays of T cells or monocytes with cancer cells showed that EPIC1 knockdown could significantly increase the therapeutic effect of pembrolizumab through antitumor T cell and macrophage activation," the researchers write.

This is a promising result, offering hope for more effective treatments for aggressive cancers with limited options. However, the study authors note that these results still need to be tested out in human models and with other types of cancers to determine how best to improve immunotherapy outcomes in the future.

 Dhamotharan Pattarayan et al, The lncRNA EPIC1 suppresses dsRNA-induced type I IFN signaling and is a therapeutic target to enhance TNBC response to PD-1 inhibition, Science Signaling (2025). DOI: 10.1126/scisignal.adr9131

**

Part 2

Astronomers discover new type of supernova triggered by black hole-star interaction

Astronomers have discovered what may be a massive star exploding while trying to swallow a black hole companion, offering an explanation for one of the strangest stellar explosions ever seen.

The discovery was made by an Astrophysicist team. The results are published in The Astrophysical Journal.

The blast, named SN 2023zkd, was first discovered in July 2023 by the Zwicky Transient Facility. A new AI algorithm designed to scan for unusual explosions in real time first detected the explosion, and that early alert allowed astronomers to begin follow-up observations immediately—an essential step in capturing the full story of the explosion. By the time the explosion was over, it had been observed by a large set of telescopes, both on the ground and from space.

The scientists think the most likely interpretation is that the massive star was locked in a deadly orbit with the black hole. As energy was lost from the orbit, their separation decreased until the supernova was triggered by the star's gravitational stress as it partially swallowed the black hole.

Analysis shows that the blast was sparked by a catastrophic encounter with a black hole companion, and is the strongest evidence to date that such close interactions can actually detonate a star.

An alternative interpretation considered by the team is that the black hole completely tore the star apart before it could explode on its own. In that case, the black hole quickly pulled in the star's debris and supernova emission was generated when the debris crashed into the gas surrounding it. In both cases, a single, heavier black hole is left behind.

A. Gagliano et al, Evidence for an Instability-induced Binary Merger in the Double-peaked, Helium-rich Type IIn Supernova 2023zkd, The Astrophysical Journal (2025). DOI: 10.3847/1538-4357/adea38. iopscience.iop.org/article/10. … 847/1538-4357/adea38.

Human embryo implantation recorded in real time for the first time

Researchers have captured unparalleled images of a human embryo implanting. This is the first time that the process has been recorded in real time and in 3D.

Failure of the implantation process in the uterus is one of the main causes of infertility, accounting for 60% of spontaneous abortions. Until now, it had not been possible to observe this process in humans in real time, and the limited available information came from still images taken at specific moments during the process.

The researchers have observed that human embryos burrow into the uterus, exerting considerable force during the process. These forces are necessary because the embryos must be able to invade the uterine tissue, becoming completely integrated with it. It is a surprisingly invasive process. Although it is known that many women experience abdominal pain and slight bleeding during implantation, the process itself had never been observed before. 

To advance during implantation, the embryo releases enzymes that break down the surrounding tissue. However, it is also known that force is required in order to penetrate the underlying layers of the uterus. This fibrous tissue is filled with collagen, a rigid protein that also forms tendons and cartilage.

The embryo opens a path through this structure and begins to form specialized tissues that connect to the mother's blood vessels in order to feed.

The research team's results reveal that human embryos exert traction forces on their environment, remodeling it. The embryo pulls on the uterine matrix, moving and reorganizing it. It also reacts to external force cues. Researchers hypothesize that contractions occurring in vivo may influence embryo implantation.Thus, effective embryo invasion is associated with optimal matrix displacement, highlighting the importance of these forces in the implantation process.

Improving our understanding of the implantation process could have a significant impact on fertility rates, embryo quality and the time taken to conceive through assisted reproduction.

Traction force and mechanosensitivity mediate species-specific implantation patterns in human and mouse embryos, Science Advances (2025). DOI: 10.1126/sciadv.adr5199

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

**

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

**

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

**

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