A urinary tract infection may make memory problems worse after a traumatic brain injury, according to new research in mice. The study raises an important question about whether a common infection could interfere with the brain’s recovery after an injury. Traumatic brain injury, often shortened to TBI, happens when a blow, fall or other force […]

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Parents often notice differences between their first and second child and wonder whether birth order really matters. A massive new study suggests it may be linked to health in unexpected ways, although the differences are much smaller than many people might imagine. The findings were published in Nature Health. Researchers analysed health records from more […]

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Canine sarcoptic mange (scabies) is a skin condition in which microscopic mites (Sarcoptes scabiei) infest dogs' skin. The condition is contagious and zoonotic and can be difficult to detect. If left untreated, it can cause bleeding sores, malnutrition, emaciation and secondary bacterial infections that may eventually lead to a dog's death.

It’s no secret that doctors across the world are using AI tools to do stuff from taking notes to looking up questions. But what about the next generation of doctors still in training? According to two medical professionals on the ground, the situation is looking pretty alarming.

With AI being used by med students, “the danger is not just deskilling but never-skilling,” write Simar Bajaj, a journalist and med student at the Stanford University School of Medicine, and Joseph Sakran, a trauma surgeon and executive vice-chair of surgery at Johns Hopkins Medicine, in an essay for The Guardian.

“Although a doctor who has forgotten how to reason is recoverable,” they added, “one who never learned how may not be.”

Bajaj and Sakran point to two alarming recent findings.

One is internal data showing that around two thirds of doctors in the US are using OpenEvidence, an AI chatbot specifically designed for clinicians. The technology is already prevalent and deeply woven into how medical professionals carry out their jobs.

The next is a new study published in the journal Nature Medicine that evaluated the reliability of these medical-specific large language models. Shockingly, the clinical AI tools performed worse  at answering medical queries than general purpose chatbots like ChatGPT and Claude did, the work found. According to the authors, it performed about on par to Google’s AI Overviews, which are notorious for being wonky and inaccurate.

Even if AI tools may be handy for research — and putting aside the major questions over their reliability — they’re no substitute for relying on your brain, as fallible as it might be, because when you’re learning, “the struggle is the point.”

“For example, trainees once asked to build a list of potential diagnoses might struggle and offer an incomplete set, learning what they missed, sometimes painfully,” Bajaj and Sakran wrote. “Now, trainees can simply ask OpenEvidence and get a nearly perfect answer, complete with possibilities they might have never considered and none of the embarrassment of having overlooked them.”

Where AI is different from medical advances in the past is that it’s “not just expanding what doctors can see,” they wrote, “but inserting itself into the cognitive machinery that training is meant to build.” 

A bevy of research on the “cognitive offloading” that AI encourages, in which users naturally begin to outsource a lot of their thinking onto the tools, backs this diagnosis. Some studies have suggested AI impairs critical thinking, and leads to lower brain activity during cognitive tasks.

It’s a conundrum gripping the medical world. Earlier this year, doctors from top medical schools proposed a stricter framework on how medical students should use AI tools.

“The process of deliberately crafting the note forces us to use our brains to really wrestle with what’s happening,” Jaideep Talwalkar, associate dean of educational technology and innovation at Yale School of Medicine, told Stat News. “There’s an importance in doing that with great repetition.”

Bajaj and Sakran have a few suggestions for how to deal with this. One is requiring trainees to periodically work through cases without any AI help, similar to how the Federal Aviation Administration advises aviators to periodically disengage autopilot and fly by hand. Of course, another powerful deterrent could be shame. A recent John Hopkins student found that doctors who used AI are viewed with scorn and skepticism by their peers.

More on AI: AI Model Invents Completely New Viruses Unknown to Nature

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The Marcus Foundation has awarded $28.7 million to Chuck Murry, MD, PhD, director of the USC Stem Cell Center, to support a clinical trial testing a stem cell-based therapy intended to regenerate heart muscle damaged by a severe heart attack. The award, the largest the foundation has given to the University of Southern California and one of its largest contributions to academic medicine, will fund both the planned human study and a parallel research program examining how the immune system responds to transplanted cardiac cells.

The trial is scheduled to begin in 2027 at Keck Hospital of USC in partnership with the USC Cardiac and Vascular Institute. A second clinical site will be established at the University of Washington, where elements of the technology were originally developed. The first phase will enroll approximately 18 patients who have experienced extensive myocardial infarction, the medical term for a heart attack that destroys part of the heart’s muscular wall.

Patients in the study will receive stem-cell-derived heart muscle cells delivered into regions damaged by the infarction. The primary goals will be to evaluate safety and determine whether the procedure is feasible in people with severe cardiac injury. Investigators will also monitor early biological signals, including whether the transplanted cells remain active, integrate with the injured tissue and produce measurable changes in cardiac performance during recovery and long-term follow-up.

A heart attack occurs when blood flow through a coronary artery is blocked, depriving cardiac muscle of oxygen. Within minutes, cells in the affected region begin to die, and the resulting scar tissue lacks the contractile properties of healthy myocardium. Unlike tissues such as skin or blood, adult human heart muscle has only a limited capacity for self-repair. As a result, a large infarction can weaken the heart’s pumping function, increase the risk of heart failure and leave survivors unable to perform ordinary activities without fatigue or breathlessness.

Current cardiovascular treatments can reopen blocked arteries, limit further injury and help the remaining heart muscle work more efficiently. They cannot, however, routinely replace the cardiomyocytes that have already been lost. Murry’s research program is aimed at addressing that biological gap by producing replacement heart muscle cells in the laboratory and delivering them directly to damaged tissue. The strategy represents a shift from supporting a failing heart to attempting to rebuild part of its contractile apparatus.

The transplanted cells are being developed as a form of cellular therapy, in which living cells act as the therapeutic agent rather than serving merely as a vehicle for a drug. According to Murry, the cells are intended to become active within the injured heart, contribute to repair and synchronize with surrounding muscle. Achieving that outcome requires more than placing new cells into scarred tissue: the cells must survive, connect functionally with the host myocardium and avoid creating dangerous electrical disturbances or abnormal rhythms. The initial trial is therefore designed principally to establish safety before testing therapeutic effectiveness in larger patient groups.

The foundation’s funding will also support research into the immune response triggered by cell transplantation. Even cells created from stem cells can be recognized as foreign by the recipient’s immune system, potentially leading to inflammation or destruction of the transplanted population. Patients who receive cellular grafts may consequently require immunosuppressive drugs, which can increase susceptibility to infection and produce other long-term complications. Researchers will study how immune cells interact with the implanted cardiac cells and investigate methods that could reduce or eventually eliminate the need for chronic immunosuppression.

The work builds on approximately three decades of research by Murry and his collaborators to move regenerative cardiology from laboratory experiments toward clinical treatment. The program includes gene-edited cellular technology, intended to improve the compatibility or performance of therapeutic cells in the human body. The precise effectiveness of the approach will not be known until it is tested in patients, and the small 2027 cohort will not be large enough to determine whether the therapy improves survival or prevents heart failure. Those questions would require subsequent trials involving substantially more participants and longer observation.

The Marcus Foundation described the project as a potential turning point for regenerative medicine, while USC leaders said the investment could create a platform for developing additional cellular therapies. The immediate scientific challenge is to determine whether transplanted heart muscle cells can be delivered safely and function meaningfully within severely damaged human hearts. If the trial meets its safety and feasibility objectives, it could provide the clinical evidence needed to advance a new generation of treatments for myocardial infarction—therapies designed not only to help patients live with damaged cardiac tissue, but to restore some of the function that conventional medicine cannot yet replace.

Subject of Research: Stem cell-based regenerative therapy for heart muscle damaged by myocardial infarction

Article Title: $28.7 Million Award Supports USC Trial of Stem Cell Therapy to Regenerate Heart Muscle After Heart Attack

Web References: The Marcus Foundation: https://marcusfoundation.org/; USC Stem Cell Center: https://stemcell.keck.usc.edu/; Chuck Murry Lab: https://murrylab.usc.edu/charles-chuck-murry-md-phd/; USC Cardiac and Vascular Institute: https://www.keckmedicine.org/services/cardiovascular/; Keck School of Medicine of USC: https://keck.usc.edu/

Image Credits: Steve Cohn

Keywords: Heart disease, myocardial infarction, heart attack, heart muscle, stem cell research, stem cell therapy, cell therapy, regenerative medicine, cardiovascular disorders, heart failure, clinical trial, cardiac regeneration

A research team in Japan has won a US$1 million Milestone 2 award in the XPRIZE Healthspan competition for developing engineered “super exosomes,” microscopic biological delivery vehicles designed to target aging and damaged cells. Led by Professor Keisuke Goda of Tohoku University’s SiRIUS Institute of Medical Research and Graduate School of Medicine, in collaboration with researchers from the University of Tokyo’s Department of Chemistry, the team was selected from more than 600 competitors worldwide.

XPRIZE Healthspan is a seven-year international competition focused on extending the period of life people spend in good health. Participating teams are challenged to develop treatments capable of restoring muscle, cognitive, and immune function in adults between 50 and 90 years old. The competition sets a minimum target of reversing at least 10 years of biological decline, while the most ambitious goal is a 20-year improvement within one year or less of treatment. Goda’s team is now moving forward after receiving recognition for results obtained in aged animal studies.

At the center of the research are exosomes, naturally occurring nanoparticles released by cells. These membrane-bound vesicles normally transport proteins, lipids, messenger RNA, and other molecular signals between cells, functioning as part of the body’s communication network. Because exosomes can carry biological cargo and interact with specific tissues, scientists have been investigating them as potential alternatives to synthetic drug-delivery systems. However, naturally produced exosomes often lack sufficient targeting precision, limiting their ability to reach the cells most relevant to a disease or aging process.

The Tohoku-led group attempted to solve that problem by chemically modifying the surface of exosomes with lanthanide ions. Lanthanides are a family of metallic elements with distinctive electronic and chemical properties. According to the researchers, attaching these ions changes the surface behavior of the exosomes and substantially improves their ability to recognize and bind to senescent cells. The resulting particles have been named “super exosomes,” a term that reflects their enhanced targeting and delivery capabilities rather than a new biological category.

Cellular senescence is one of the major biological processes associated with aging. Senescent cells have generally stopped dividing because of accumulated damage or stress, but they do not necessarily disappear. Instead, some remain metabolically active and release inflammatory molecules, growth regulators, and other signals that can disrupt nearby tissues. This collection of secreted factors, often called the senescence-associated secretory phenotype, can contribute to chronic inflammation, impaired tissue repair, and the deterioration of organs. Precisely influencing these cells has therefore become a major objective in longevity research.

The proposed super-exosome platform is designed to deliver regenerative molecular cargo directly to aging tissues after attaching to senescent cells. Potential cargoes include growth factors, messenger RNA, and other genetic materials capable of altering cellular behavior. Rather than distributing such molecules broadly throughout the body, a targeted exosome could concentrate them near damaged or dysfunctional tissue. In theory, this approach could promote repair while reducing unwanted effects in healthy cells, although the degree of targeting and the durability of the response will need to be confirmed in human studies.

In preclinical experiments involving several groups of aged mice, the researchers reported statistically significant improvements in frailty, physical performance, and multiple functional measures associated with aging. They also described the treatment’s safety profile as excellent in the studies conducted so far. The team says the overall benefit corresponds to more than 15 additional healthy human years when estimated using cross-species lifespan scaling. Such calculations can help compare biological effects between species, but they are not evidence that a mouse treatment will extend human life by a specific number of years. Human biology, dosing, immune responses, and long-term risks could differ substantially.

The award will support the next stage of development: clinical studies planned in collaboration with Tohoku University Hospital and the Tohoku University Healthspan Research Center. These studies will need to establish how the particles behave in humans, how efficiently they reach senescent cells, what cargoes are most effective, and whether the treatment produces measurable improvements in strength, cognition, immunity, or other healthspan indicators. Researchers will also have to monitor possible immune reactions, unintended effects on healthy tissues, changes in tumor risk, and the persistence of engineered exosomes in the body. These questions are essential before claims of age reversal can move beyond the laboratory.

The platform could eventually be investigated for conditions involving muscle decline, cognitive impairment, immune dysfunction, hair loss, skin aging, and reproductive health. The team plans to commercialize the technology through NanoTitan, with the aim of developing scalable manufacturing and international distribution for exosome-based therapeutics produced in Japan. “Advancing to the XPRIZE Healthspan finals is an important milestone, but our ultimate goal is to translate this technology into therapies that allow people to lead healthy, independent, and active lives longer,” Goda said. The research now enters its most demanding phase: determining whether an impressive result in aged mice can become a safe, reproducible, and clinically meaningful treatment for people.

Subject of Research: Engineered “super exosomes” designed to target senescent cells and deliver regenerative molecular cargo for healthy aging.

Article Title: Japanese Research Team Wins US$1 Million XPRIZE Award for “Super Exosome” Aging Technology

Web References: https://mediasvc.eurekalert.org/Api/v1/Multimedia/673c8fb3-268a-4a90-93b4-a0d531624a52/Rendition/low-res/Content/Public

Image Credits: Goda Lab

Keywords: Super exosomes, exosomes, cellular senescence, healthy aging, longevity research, XPRIZE Healthspan, regenerative medicine, Tohoku University, lanthanide ions, aged mice, healthspan, nanomedicine

Lipid nanoparticles (LNPs) have become one of the most important delivery technologies in modern medicine, helping transport messenger RNA into cells for vaccines, protein replacement therapies and experimental treatments. Yet a formulation that performs well in mice can behave very differently in humans. This species gap makes nonhuman primate studies an important step in drug development, but conventional methods for comparing multiple nanoparticles often require euthanasia and extensive tissue collection. A new study reports a way to measure the functional activity of several LNPs in the same animal using only a small blood sample.

Published in Nature Biotechnology, the work introduces a non-invasive nanoparticle barcoding platform called snapCodes. The method is designed to determine which LNP formulation successfully delivers its mRNA cargo and prompts cells to produce the encoded protein. Rather than relying on tissue harvesting, the researchers identify delivery events through DNA barcodes that can be recovered from serum and analyzed by sequencing. The approach could allow scientists to compare many candidate nanoparticles in a single nonhuman primate while reducing both animal use and the logistical burden of downstream analysis.

The central challenge addressed by the study is that nanoparticle delivery is not adequately described by measuring where an LNP travels. An LNP may reach an organ or circulate in the bloodstream without releasing its mRNA in a form that cells can translate. The new system instead records functional mRNA delivery. Each nanoparticle is associated with a distinctive DNA sequence, and the mRNA cargo is engineered to encode a fusion protein containing nanoluciferase and a SNAP-tag. Nanoluciferase is a compact enzyme that produces light in the presence of its substrate, while the SNAP-tag is a protein module capable of forming a covalent bond with specific chemical groups.

For the barcode to become a permanent molecular record of delivery, the researchers modified the DNA tags with benzylguanine. When a cell receives an mRNA molecule encoding the nanoluciferase–SNAP-tag fusion, the resulting protein can react with a benzylguanine-bearing snapCode. This creates a stable DNA–protein complex. The complexes are then exported from cells into the circulation, where they can be isolated from a small serum sample. Sequencing the recovered DNA reveals which barcoded LNPs produced the fusion protein and therefore achieved functional mRNA delivery.

The design turns transient protein expression into a measurable signal that can be collected without sacrificing the animal. This is particularly valuable in studies involving nonhuman primates, where tissue-based nanoparticle profiling can require euthanasia and can limit the number of formulations tested in each subject. A blood-based assay also makes it possible to monitor delivery over time, potentially showing how the activity of a formulation changes after dosing. The study used just 30 microliters of serum, a volume small enough to support repeated sampling and longitudinal measurements.

Before comparing nanoparticle performance, the researchers validated the molecular components of the system, including the activity of the snapCode chemistry and the ability of the fusion protein to participate in the intended covalent reaction. These steps were necessary to establish that the barcode signal reflected genuine expression of the delivered mRNA rather than nonspecific interactions. Once the platform had been characterized, the team used it to evaluate multiple chemically distinct LNPs in living animals.

The investigators intravenously administered six snapCoded LNP formulations to mice and nonhuman primates. Each formulation carried its own molecular identity, allowing all six candidates to be assessed in parallel. Serum collected after administration was analyzed for the DNA–fusion protein complexes, and sequencing was used to quantify the relative delivery activity associated with each barcode. By testing the same barcoded set across species, the researchers could directly examine whether patterns observed in mice were reproduced in nonhuman primates.

Such cross-species comparisons are crucial because LNP composition strongly influences biological behavior. Changes in ionizable lipids, helper lipids, cholesterol, polyethylene glycol-lipid components or particle structure can affect stability, organ distribution, cellular uptake and endosomal escape. These properties may differ substantially between rodents and primates because of differences in blood proteins, immune responses, tissue physiology and cellular trafficking. A method that measures expression from several formulations in the same animal may therefore reveal species-specific delivery patterns more efficiently than traditional one-formulation-per-animal experiments.

The snapCode strategy does not replace every form of nanoparticle analysis. It reports successful expression of a particular engineered mRNA and depends on the recovery and sequencing of the associated molecular complexes. It does not, by itself, provide a complete map of tissue distribution, long-term safety or therapeutic efficacy. Nevertheless, it adds a functional layer to LNP evaluation: scientists can ask not only where particles go, but which particles actually release mRNA that cells translate. In early development, that distinction can help prioritize candidates before more resource-intensive studies begin.

By combining multiplexed dosing with low-volume serum sampling, the researchers aim to make nonhuman primate testing more informative while using fewer animals. The platform could be adapted for screening delivery systems designed for different organs or therapeutic proteins, provided that the encoded reporter and barcode chemistry remain compatible with the intended experiment. As mRNA medicines expand beyond vaccines into gene editing, immunotherapy and protein replacement, tools that connect nanoparticle chemistry to real biological output may become increasingly important. Non-invasive barcoding offers a way to track those differences in living subjects and could help narrow the path from promising LNP design to clinically relevant drug candidate.

Subject of Research: A non-invasive method for comparing functional mRNA delivery by multiple lipid nanoparticles in mice and nonhuman primates using serum-based DNA barcodes.

Article Title: Non-invasive nanoparticle barcoding in nonhuman primates

Article References: Jang, B., Zenhausern, R., Lian, L. et al. Non-invasive nanoparticle barcoding in nonhuman primates. Nat Biotechnol (2026). https://doi.org/10.1038/s41587-026-03262-6

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41587-026-03262-6

Keywords: lipid nanoparticles, mRNA delivery, nanoparticle barcoding, snapCodes, SNAP-tag, nanoluciferase, nonhuman primates, serum sequencing, drug delivery, RNA therapeutics

A new study has brought scientists closer to observing how inflammation during pregnancy may alter the earliest stages of human brain development. Using three-dimensional tissue models made from human fetal brain samples, researchers modeled maternal immune activation and identified the signaling molecule interleukin-17A, or IL-17A, as a major driver of abnormal cortical development. The findings, published in Nature Neuroscience, offer a human-based experimental system for investigating how immune signals outside the brain can influence the formation of neural circuits before birth.

Maternal immune activation refers to the biological response triggered when a pregnant individual experiences infection or significant inflammation. Epidemiological studies have associated certain prenatal inflammatory exposures with an increased likelihood of neurodevelopmental conditions, including autism spectrum disorder, schizophrenia, and intellectual disability. Yet the mechanisms behind these associations have remained difficult to study. Animal models have provided important clues, but differences between species can limit their ability to reproduce the timing, cellular organization, and molecular environment of the developing human cortex.

The researchers addressed this challenge with “brain cerebroids,” three-dimensional, ex vivo models that preserve features of developing human fetal brain tissue. Unlike simplified cultures composed of a single cell type, these structures retain a more complex arrangement of neural progenitors, immature neurons, and supporting cells. Their three-dimensional architecture allows cells to communicate and organize in ways that more closely resemble the fetal cortex, including the production and movement of neurons that ultimately establish the layered structure of the brain’s outer region.

To recreate aspects of maternal immune activation, the team exposed the fetal brain cerebroids to inflammatory conditions associated with immune signaling during pregnancy. The central focus was IL-17A, a cytokine produced primarily by activated immune cells, particularly a subset of T cells known as T helper 17 cells. Cytokines are small signaling proteins that coordinate immune responses, but they can also affect tissues beyond the immune system. In the developing brain, inappropriate or excessive exposure to such signals may influence cell proliferation, migration, differentiation, and the formation of connections between neurons.

The study found that IL-17A exposure was linked to disruptions in cortical development within the human cerebroids. These effects are described as “IL-17A-driven,” indicating that the cytokine was not merely associated with the developmental changes but played a functionally important role in producing them. The disturbances affected the organization and behavior of developing neural cells, processes that are essential for building the cortex. During normal development, neural progenitor cells generate new neurons in tightly regulated sequences, while young neurons migrate to their appropriate positions. Interference with either process can alter the structure and connectivity of later-forming brain tissue.

The results are especially significant because they were observed in human fetal brain material rather than inferred only from animal studies. Previous research in mice has implicated maternal immune activation and IL-17A in changes to cortical organization and behavior in offspring. However, the human cerebroid model provides an opportunity to examine whether similar immune mechanisms operate in human tissue, where the timing of neurogenesis, cell-type composition, and cortical architecture differ from those of rodents. The approach may also help reveal human-specific responses that conventional laboratory animals cannot capture.

The findings do not mean that IL-17A exposure during pregnancy inevitably causes a neurodevelopmental condition, nor do they establish that prenatal inflammation is a single explanation for such conditions. Brain development is shaped by a combination of genetic factors, immune signals, environmental influences, and developmental timing. The experiments also took place in an ex vivo model, outside the full physiological environment of a living pregnancy. Cerebroids cannot reproduce the placenta, maternal circulation, hormonal changes, or the complete immune system, all of which influence how inflammatory signals reach the fetus and how long they remain active.

Nevertheless, the model could become a powerful platform for testing mechanisms and potential interventions. Researchers may use it to determine how IL-17A changes gene activity in neural progenitors, whether it alters communication between neurons and glial cells, and which molecular pathways make some developing cells more vulnerable than others. Because the tissue is human and three-dimensional, it may also support studies of patient-specific genetic risk, allowing investigators to compare how different backgrounds respond to the same inflammatory signal.

The work also highlights a broader shift in neuroscience toward experimental systems that combine human tissue with controlled laboratory manipulation. Understanding prenatal inflammation is difficult in clinical studies because immune exposure cannot be ethically assigned or precisely timed in pregnant people. Brain cerebroids offer a way to isolate individual components of that complex biology while preserving more of the developing tissue’s natural organization than conventional two-dimensional cell cultures. As these models improve, they may help distinguish temporary developmental changes from persistent alterations in cortical circuitry and identify when immune signaling is most consequential.

By showing that IL-17A can disrupt human cortical development in a three-dimensional ex vivo system, the study gives researchers a clearer biological target in the search for links between prenatal inflammation and later neurodevelopment. Its most immediate contribution is not a new diagnosis or treatment, but a more precise experimental framework: one that connects maternal immune signaling to cellular events in the developing human cortex. That connection could guide future work on prevention, therapeutic timing, and the complex origins of developmental differences long before the first symptoms become visible.

Subject of Research: Maternal immune activation and IL-17A-driven disruption of human fetal cortical development in 3D ex vivo brain cerebroids.

Article Title: Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development.

Article References: Assir, M.Z.K., Yanakiev, M., Gim, D.H. et al. Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development. Nature Neuroscience (2026). https://doi.org/10.1038/s41593-026-02400-2

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41593-026-02400-2

Keywords: maternal immune activation, IL-17A, fetal brain development, cortical development, brain cerebroids, neurodevelopment, prenatal inflammation, human brain models, cytokines, neuroscience

The price of saving a newborn’s life can extend far beyond the hospital walls. A new analysis published in the Journal of Perinatology is drawing attention to a largely invisible consequence of neonatal intensive care: the direct medical out-of-pocket costs paid by families. The study, led by researchers Gorka, Profit and Phibbs, examines who carries the greatest financial burden during a neonatal intensive care unit admission and investigates how structural conditions may shape those costs.

Neonatal intensive care is among the most technologically advanced forms of medicine. Infants in NICUs may require mechanical ventilation, incubators that regulate temperature and humidity, continuous heart and oxygen monitoring, intravenous nutrition, specialized medications and repeated laboratory testing. These interventions can be lifesaving, particularly for babies born extremely prematurely or with serious medical complications. Yet the financial consequences of receiving this care are not experienced equally by every household, even when families receive treatment in the same health-care system.

The researchers’ focus is direct medical out-of-pocket spending: the money families must pay themselves for medical services connected to a NICU admission. This can include deductibles, copayments, coinsurance and other forms of cost sharing that remain after insurance has paid its portion. Unlike the total hospital charge or the amount reimbursed by an insurer, out-of-pocket cost reflects the portion that reaches a family’s own budget. For households already coping with an unexpected high-risk birth, even relatively small individual charges can accumulate rapidly.

The study is designed not only to document these expenses, but also to explore the structural forces behind differences in cost burden. In health economics, structural contributions refer to the way institutions and systems distribute risk and resources. Insurance design, employment-linked coverage, household income, geographic location, hospital characteristics and access to public assistance can all affect how much a family ultimately pays. Two infants with similar clinical needs may therefore generate very different financial experiences for their parents, depending on the architecture of coverage surrounding them.

That distinction matters because the effects of a NICU admission are not limited to the newborn’s medical condition. Parents may need to travel long distances to reach a specialized hospital, arrange accommodation near the facility, pay for transportation or meals, and take unpaid leave from work. These expenses may not always appear in estimates of direct medical out-of-pocket costs, but they can intensify the economic shock associated with a prolonged admission. The medical bill is only one component of the broader financial strain that can accompany neonatal illness.

A central question raised by the analysis is whether the families with the fewest financial resources are also the ones most exposed to high cost sharing. A payment that is manageable for a high-income household may consume a substantial share of a lower-income family’s monthly budget. Economists often describe this pattern as a disproportionate cost burden: the absolute amount paid may not be the highest, yet the payment represents a greater fraction of household resources. This distinction can reveal inequities that remain hidden when researchers look only at average dollar amounts.

The findings are expected to be relevant to health-policy debates about medical debt, insurance protection and the financial consequences of premature birth. If structural factors account for meaningful differences in family payments, reducing inequality may require more than improving clinical care. Potential responses could include limits on neonatal cost sharing, stronger protections against unexpected bills, expanded eligibility for public coverage and assistance with transportation or family support services. The analysis may also help hospitals and policymakers identify families at risk of financial hardship while an infant is still receiving care.

The issue has significance beyond individual hospitalizations because NICU care can influence a family’s financial stability long after discharge. Parents may face follow-up appointments, medications, developmental assessments and specialist care for children who experienced complications of prematurity or serious illness. Medical expenses can overlap with reduced work hours, job loss or the need for one parent to become a full-time caregiver. A short period of intensive treatment can therefore produce a long economic aftershock, particularly when families lack savings or paid leave.

By placing family payments at the center of neonatal research, Gorka, Profit and Phibbs emphasize a dimension of NICU care that is often absent from clinical success measures. Survival, complications and length of stay remain essential indicators, but they do not fully describe the experience of families navigating intensive care. Understanding who pays the most, why they pay it and how those payments relate to broader social structures could help redefine quality in neonatal medicine. The study’s message is potentially viral because it connects cutting-edge life-saving technology with a simple but consequential question: when medicine saves a baby, how much of the cost is left for the family to survive?

Subject of Research: Direct medical out-of-pocket costs of neonatal intensive care admissions and structural factors contributing to differences in financial burden among NICU families.

Article Title: Who pays the most for neonatal intensive care? An analysis of the out-of-pocket cost burden borne by NICU families

Article References: Gorka, N., Profit, J. & Phibbs, C.S. “Who pays the most for neonatal intensive care? An analysis of the out-of-pocket cost burden borne by NICU families.” Journal of Perinatology (2026). https://doi.org/10.1038/s41372-026-02869-6

Image Credits: AI Generated

DOI: 10.1038/s41372-026-02869-6

Keywords: neonatal intensive care, NICU, out-of-pocket costs, medical expenses, health-care inequality, premature birth, financial burden, insurance, neonatal health, health policy

Expansion microscopy has spent the past decade changing the rules of super-resolution imaging. Instead of relying solely on increasingly sophisticated optics, the technique physically enlarges biological specimens so that molecules separated by nanometers become easier to distinguish with ordinary fluorescence microscopes. Now, researchers have introduced a method designed to push that concept toward one of the most difficult goals in microscopy: seeing the shapes of individual proteins directly.

The approach, described by Ahmed H. Shaib, Mahmoud M. Alawieh and Stefan O. Rizzoli in Nature Protocols, combines one-step nanoscale expansion microscopy with fluctuation-based super-resolution analysis. The resulting workflow, called ONE microscopy, is intended to make molecular-scale imaging more accessible to laboratories that do not have access to cryo-electron microscopes or specialized high-end optical systems.

Traditional light microscopy is limited by diffraction, a physical effect that causes light from two nearby objects to blur together when they are too close. Even modern super-resolution methods can require complex instruments, intense labeling strategies or extensive computational processing. Expansion microscopy takes a different route. Researchers anchor biological molecules within a swellable polymer network and then expand the material, increasing the physical distance between fluorescent labels.

The expansion step does not automatically reveal every molecular detail. A protein’s structure can still be represented by only a small number of fluorescent signals, and conventional images may contain noise, background fluorescence and motion-related fluctuations. ONE microscopy addresses these limitations by analyzing changes in fluorescence intensity over time. These fluctuations contain information about the presence, position and behavior of labeled molecules that may not be obvious in a single frame.

In practical terms, the method links chemical preparation, physical enlargement and computational analysis into a single workflow. Samples are embedded in a polymer gel, labeled to identify the proteins of interest and then expanded. After expansion, researchers acquire image sequences using conventional fluorescence equipment. Specialized software analyzes the temporal variation in the recorded signals, extracting spatial information beyond what a standard diffraction-limited image would provide.

This combination is significant because it shifts the focus from simply locating a protein to examining its overall shape. For many biological questions, knowing that a protein is present is not enough. Its size, orientation and structural organization can determine how it interacts with membranes, vesicles, organelles or neighboring proteins. Directly observing those features could help researchers investigate molecular machines in their native cellular environments rather than relying exclusively on purified samples or averaged structural models.

The protocol is designed to work across a broad range of biological materials, including purified proteins, cultured cells and tissues. That flexibility could make the technique useful for researchers studying protein organization at multiple scales. A purified protein might provide a controlled test of shape reconstruction, while cells and tissues could reveal how the same protein is arranged amid the crowded and complex environment of living biology.

A major part of the reported advance is the accompanying software package. Fluctuation-based imaging can be powerful, but its usefulness depends on reliable data processing, and computational analysis has often been a barrier for non-specialist users. The authors present the software as stable and user-friendly, with the goal of making the analysis more efficient, reproducible and practical for laboratories using standard fluorescence microscopes.

ONE microscopy does not replace cryo-electron microscopy, which remains capable of resolving structures at atomic or near-atomic scales under appropriate conditions. Nor does it eliminate the challenges associated with labeling, gel chemistry, image quality and sample preparation. Expansion can introduce distortions, and successful imaging depends on preserving the relationship between the fluorescent labels and the underlying structures. Nevertheless, the method offers a complementary strategy: rather than averaging thousands or millions of molecules, it aims to examine individual protein shapes through expanded, fluorescence-labeled specimens.

The researchers describe the workflow as a practical framework for protein imaging on conventional equipment. By combining physical separation of fluorophores with information extracted from fluorescence fluctuations, the method brings nanoscale structural analysis closer to routine biological imaging. Its broader impact may come not from replacing existing forms of super-resolution, but from making a previously specialized capability more reproducible and attainable for laboratories investigating how individual proteins operate inside cells and tissues.

Subject of Research: One-step nanoscale expansion microscopy for visualizing individual protein shapes using conventional fluorescence microscopes.

Article Title: ONE microscopy.

Article References: Shaib, A.H., Alawieh, M.M. & Rizzoli, S.O. ONE microscopy. Nature Protocols (2026). https://doi.org/10.1038/s41596-026-01399-x

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41596-026-01399-x

Keywords: expansion microscopy, ExM, nanoscale imaging, super-resolution microscopy, fluctuation-based analysis, protein structure, fluorescence microscopy, single-protein imaging, cryo-electron microscopy, biological imaging

Foundation models are promising to become the “universal translators” of biomedical data—but a new perspective argues that medicine should resist treating them as all-knowing digital doctors. In a review published in Nature Biomedical Engineering, researchers describe how large, adaptable artificial intelligence systems are reshaping biomedical imaging while warning that impressive benchmark scores can conceal serious weaknesses in clinical environments. Their central message is direct: foundation models are most likely to improve healthcare by augmenting specialists, not replacing them.

Foundation models are designed to learn broad representations from enormous and diverse datasets before being adapted to specific tasks. In biomedical imaging, those data may include magnetic resonance imaging, computed tomography, X-rays, ultrasound, digital pathology slides and ophthalmic images. The same underlying model could theoretically identify tumors, segment organs, estimate disease risk, retrieve similar cases and generate clinical reports. The vision becomes even broader when imaging is combined with pathology, electronic health records and genomic information, creating a composite system intended to analyze a patient across multiple biological scales.

That ambition reflects a major change from traditional medical AI. Earlier systems were generally built for one narrowly defined task, such as detecting pneumonia on chest radiographs or outlining a brain lesion on MRI scans. Foundation models instead attempt to create a reusable backbone that can be transferred across diseases, hospitals and imaging technologies. Technically, they learn statistical patterns in high-dimensional data, often through self-supervised training in which the system predicts missing, transformed or associated information. Afterward, developers fine-tune or prompt the model for particular clinical applications.

But biomedical imaging is not a single, uniform world. Images differ according to scanner manufacturer, acquisition protocol, patient population, disease prevalence and local clinical practice. A model trained primarily on data from large academic hospitals may perform very differently in community clinics, rural settings or countries with limited equipment. This problem, known as domain shift, can occur even when images appear visually similar. Small changes in image quality, contrast, hardware or patient demographics may alter the statistical distribution learned by the model and undermine its predictions.

The authors introduce a framework called real-world evaluation and assessment of foundation models, or REAL-FM, to examine whether these systems are ready for practical use. Rather than focusing only on accuracy scores, REAL-FM considers several dimensions at once, including the quality and representativeness of training data, technical readiness, clinical value, integration into existing workflows and responsible artificial intelligence. The framework is intended to help clinicians interpret claims about new models and to push developers toward evaluations that resemble actual medical practice.

One of the sharpest distinctions in the perspective is between pattern recognition and causal reasoning. Foundation models can become extraordinarily skilled at recognizing visual associations—for example, linking a particular texture or anatomical feature with a diagnosis present in their training data. Yet association is not the same as understanding why a disease occurs, how it will progress or whether a treatment will benefit an individual patient. A model may identify a correlation that is valid in one hospital but reflects a hidden confounder, such as a scanner type, reporting convention or patient-selection pattern, rather than a biological signal.

This limitation becomes especially dangerous when models are moved beyond simplified benchmarks. Many benchmark datasets provide carefully curated images, clear labels and narrowly defined tasks. Clinical care is messier: scans can be incomplete, diagnoses can be uncertain, records may contain contradictory information and several conditions may coexist. The perspective highlights a lack of verified generalization across such conditions, along with a shortage of prospective, outcome-based validation. In a prospective study, an AI system would be evaluated while care is actually being delivered, with researchers measuring whether it improves diagnostic accuracy, treatment decisions, patient outcomes or workflow efficiency.

Data scarcity is another obstacle. The largest foundation models require vast quantities of data, but medical information is difficult to collect, standardize and share. Patient records are fragmented across institutions, imaging data may lack reliable annotations and rare diseases are inherently underrepresented. Privacy regulations and governance requirements further complicate the creation of centralized datasets. As a result, a model may appear broadly capable while remaining poorly tested in the populations and clinical circumstances where errors could have the greatest consequences.

The researchers argue that human oversight therefore remains indispensable. In practical terms, foundation models may be most useful as clinical assistants that prioritize images for review, highlight suspicious regions, summarize longitudinal records or offer a second opinion that specialists can interrogate. Safe deployment will require transparent reporting of uncertainty, monitoring for performance drift, mechanisms for correcting errors and clear accountability when recommendations influence care. The future envisioned by the authors is not a single monolithic medical oracle, but a coordinated ecosystem of specialized AI systems, each evaluated for a defined clinical role and connected to expert-led workflows.

The perspective arrives as the biomedical AI field races toward increasingly general-purpose systems. Its warning is not that foundation models lack value, but that technical scale alone cannot establish clinical reliability. Before these models can be trusted with consequential decisions, they must demonstrate robustness across domains, usefulness in real workflows, safety under unexpected conditions and measurable benefits for patients. The proposed REAL-FM framework offers a way to separate viral demonstrations from durable medical progress—by asking not only what a model can recognize, but where it works, why it works and whether it makes care better.

Subject of Research: Foundation models and their real-world evaluation in biomedical imaging and clinical medicine.

Article Title: Foundation models in biomedical imaging: turning hype into reality

Article References: Muneer, A., Zhang, K., Hamdi, I. et al. Foundation models in biomedical imaging: turning hype into reality. Nature Biomedical Engineering 10, 1557–1575 (2026). https://doi.org/10.1038/s41551-026-01762-z

Image Credits: AI Generated

DOI: 10.1038/s41551-026-01762-z

Keywords: foundation models, biomedical imaging, medical artificial intelligence, clinical AI, multimodal AI, domain shift, causal reasoning, clinical validation, responsible AI, REAL-FM

When you’re feeling sad, angry or stressed, it might be tempting to ask a chatbot for help. In fact, a new survey of 12- to 21-year-olds showed that nearly 1 in 5 of them had turned to AI for mental health support. That’s up from 1 in 8 just a couple years ago.

It’s perhaps not surprising that many teens and young adults are seeking advice. In 2023, a whopping 40 percent of high school students said they felt so sad or hopeless that they couldn’t engage in activities that are normal for them. In 2024, 15 percent of 12- to 17-year-olds had a major depressive episode — many without treatment.

Clearly, there is a big need among young people for mental and emotional support. But as lifelike as they might sound in conversations, chatbots aren’t real people with empathy. And free, general-use chatbots such as ChatGPT, Meta AI and Character.AI weren’t built to support mental health. They don’t earn licenses to offer therapy — or follow rules for treating patients — the way humans do.

So, what should teens know before using AI tools for mental health advice? Science News Explores asked the experts.

Should AI ever be used for mental health help?

A chatbot could help you learn more about mental health issues, says Vaile Wright. A psychologist in Chicago, Ill., she works with the American Psychological Association.

You could use AI to search for information about mental health conditions and resources online, Wright suggests. (Just be sure to double-check its findings. Chatbots sometimes make stuff up.) An AI might even be able to offer “some basic advice if you’re struggling in the moment and don’t know where else to turn,” Wright says.

Treating a chatbot like a therapist, though, is not wise. “It’s really when you’re having these multi-turn, very extended types of conversations where you’re using the chatbot to fill some sort of emotional gap in your life,” Wright says, that you enter risky territory.

Why doesn’t a chatbot make a good therapist?

A real therapist’s goal is to help their patient. Chatbots are different. “They’re purposely engineered to keep people on the platform for as long as possible,” Wright says. “The way they do that is by being exceedingly validating and just telling people exactly what they want to hear.” That might feel good. But it’s not what a therapist would do. And it’s not likely to give you useful advice.

“A therapist is going to validate somebody’s feelings,” Wright says. “But it’s also our role to point out where … someone’s acting, thinking or feeling in ways that’s not maybe helpful to them.”

Plus, a chatbot doesn’t have the same types of information a therapist does, says Darja Djordjevic. She’s a psychiatrist at Stanford University in California. “AI was built to have this encyclopedic knowledge,” she says. “But it doesn’t understand the context of people’s lives.” That well-rounded knowledge of a person is key to aiding their mental health.

What are the risks of treating chatbots like therapists?

“They do not handle any mental health crises or emergencies well,” says Djordjevic. She has studied how AI systems would respond to users with a variety of mental health conditions, such as self-harm, anxiety and eating disorders.

“The models really don’t do a good job of recognizing … situations that would warrant human intervention,” Djordjevic says. “Unfortunately, we have some very tragic, more extreme cases [showing this] that involve young people.” Take Adam Raine, 16, of California. He died by suicide last year after discussing his suicidal thoughts with ChatGPT.

Djordjevic notes how crucial human connection is. “We have very little research right now on what the long-term effects of using AI for mental health would be,” she says. “What we do have a lot of research on is how much social connection and human contact are important for health and flourishing. So we know what’s good for us.” Leaning on AI might get in the way of forming crucial connections with real people.

There also are privacy risks to using AI, adds Wright. “Everything [you] put in these apps is not private. All the chats are maintained.” If a chatbot were hacked, someone else might be able to read your sensitive conversations with a bot.

Any advice for seeking mental health help from people, not chatbots?

“It doesn’t have to be an either-or,” Wright says. “You could use the chatbot to say, ‘I’m nervous about approaching my dad about my concerns. How could I do it?’… Using the chatbot as a tool to connect with human relationships in real life, I think, is probably one of the most impactful things that this technology can do.”

Djordjevic notes that most schools have a counselor students can talk to. The National Alliance for Mental Illness also has lots of resources on its site, she adds. This includes a free, confidential helpline for teens.

Sometimes, it might seem easier or less embarrassing to ask a computer about mental-health issues than a real person. In the new survey, almost two-thirds of young people who used chatbots for mental health didn’t tell anyone they were doing it.

But for anyone nervous about seeking human help: Fear not, Djordjevic says. “A lot more adults and people around you have struggled at some point or struggle with mental health issues than you think.”

Suicide was the third leading cause of death among U.S. teens ages 15-19 in 2024. If you or someone you know is suffering from suicidal thoughts, please seek help. In the United States, you can reach the Suicide Crisis Lifeline 24/7 by calling or texting 988 or chat at 988lifeline.org. Please do not suffer in silence.

Tanya Chapman Griffin was coughing so often that she bought jumbo bags of extra-strong menthol cough drops to quell the nearly constant tickle in her throat. “It must be that Saharan dust storm,” Tanya would tell people, referring to the massive dust plume that travels across the Atlantic to the Caribbean and the southern United […]

The post She Had Blood Clots in Her Lungs. Now She Urges Women To Speak Up for Their Health appeared first on Knowridge Science Report.

What about attempts to test their virulence in humans? The approach in the Stanford lab sure sounds like a new form of gain-of-function research to me.

Source

The National Academies of Sciences, Engineering and Medicine had been under pressure from Republican leaders, including President Trump.

© Andrew Kelly/Reuters

The National Academies of Sciences, Engineering and Medicine had been under pressure from Republican leaders, including President Trump.

Clearing amyloid plaques may break the chain reaction that fuels brain cell destruction in Alzheimer’s disease. One Alzheimer’s brain offered researchers something they almost never get to see: a natural side-by-side experiment. In some regions, years of anti-amyloid treatment had removed most of the sticky plaques associated with Alzheimer’s disease (AD). Those areas contained little [...]

Cancer researchers have reported a new strategy that combines bacterial tumor targeting, nutrient deprivation and immune stimulation in a single therapeutic design. The approach uses an engineered conjugate built from L-asparaginase and flagellin, linked to a system that directs the treatment toward calreticulin-bearing cancer cells. In experiments involving Salmonella-mediated tumor therapy, the conjugate enhanced antitumor activity compared with bacterial treatment alone, according to a study published in Cell Death Discovery.

The work addresses a long-standing challenge in cancer therapy: how to make powerful treatments concentrate inside tumors while limiting damage to healthy tissues. Attenuated strains of Salmonella have attracted interest because they can preferentially accumulate in the abnormal environment of solid tumors. Tumors often contain regions with poor oxygen levels, disorganized blood vessels and local immune suppression, conditions that can support bacterial growth. Once inside these sites, therapeutic Salmonella can act as a biological delivery platform and stimulate immune responses against malignant cells.

The researchers focused on calreticulin, a protein normally found inside the endoplasmic reticulum, where it helps regulate calcium storage and protein folding. Under cellular stress, including stress caused by chemotherapy, radiation or other anticancer treatments, calreticulin can move to the outer surface of a cancer cell. There, it functions as an “eat-me” signal, alerting immune cells that the damaged cell should be engulfed. Because surface-exposed calreticulin is associated with immunogenic forms of cell death, it provides a potential molecular address for directing therapeutic agents toward stressed tumor cells.

The experimental construct combines this targeting concept with L-asparaginase, an enzyme already used in clinical oncology, especially in the treatment of acute lymphoblastic leukemia. L-asparaginase breaks down circulating L-asparagine into aspartic acid and ammonia. Some cancer cells, particularly those with limited capacity to synthesize their own asparagine, depend heavily on the amino acid supplied through the bloodstream. Depleting extracellular asparagine can therefore interrupt protein production, trigger metabolic stress and promote cancer-cell death. The enzyme’s effectiveness, however, can be limited by immune reactions, pharmacological instability and toxicity, making targeted delivery an important goal.

The second component, flagellin, is the structural protein that forms the filament of bacterial flagella. It is also a potent molecular signal for the innate immune system. Immune cells recognize flagellin primarily through Toll-like receptor 5, while intracellular sensing pathways can activate inflammasome components such as NLRC4. These signals can promote the release of inflammatory mediators, stimulate antigen-presenting cells and help convert an immunologically “cold” tumor into one more visible to the immune system. By incorporating flagellin into the therapeutic design, the researchers sought to make the treatment not only directly toxic to tumor cells but also capable of amplifying antitumor immunity.

The study’s central finding was that the calreticulin-targeting L-asparaginase–flagellin conjugate strengthened the antitumor effects of Salmonella-based therapy. Rather than relying on a single mechanism, the treatment brings together several forms of pressure on the tumor. Salmonella can concentrate within the tumor microenvironment, the targeting component can help associate the conjugate with calreticulin-exposing cancer cells, L-asparaginase can deprive vulnerable cells of an essential nutrient, and flagellin can activate immune surveillance. The resulting combination is designed to produce a chain reaction in which metabolic stress and immune stimulation reinforce one another.

This type of combination may be particularly valuable because tumors frequently adapt when exposed to one therapeutic pressure. A cancer cell that survives nutrient deprivation may still be eliminated if immune recognition is intensified. Likewise, an immune response that is too weak to control a tumor may become more effective when bacterial localization and enzyme-mediated damage increase the number of abnormal antigens and danger signals released by dying cells. The researchers’ findings suggest that coordinating these mechanisms can improve the performance of bacteria-assisted cancer treatment in experimental settings.

The approach also reflects a broader shift in cancer research toward programmable biological medicines. Instead of treating bacteria only as infectious threats, scientists are redesigning them as localized delivery vehicles capable of carrying enzymes, immune activators or molecular probes. The advantage is spatial: a therapeutic payload can be produced or concentrated near the tumor rather than distributed uniformly throughout the body. The challenge is equally significant. Any clinical version would need precise control over bacterial attenuation, immune activation, enzyme exposure and potential inflammation, while also demonstrating reliable performance across genetically diverse tumors.

Calreticulin targeting may provide a useful way to address some of that complexity because the protein’s appearance on the cell surface is linked to cellular stress and treatment response. However, the extent and duration of calreticulin exposure can vary between tumor types and individual patients. Future studies will need to determine which cancers are most suitable for this strategy, how calreticulin levels predict treatment response and whether the conjugate can be combined safely with established immunotherapies such as immune-checkpoint inhibitors. Researchers will also need to assess pharmacology, manufacturing consistency and the possibility of immune reactions against the bacterial or enzymatic components.

The findings position the engineered conjugate as a promising experimental platform rather than an immediately available therapy. By merging tumor-homing bacteria with a calreticulin-directed enzyme and an innate immune stimulant, the study illustrates how cancer treatments can be designed to attack malignant cells on multiple biological fronts. If the results are confirmed in further preclinical testing and eventually in carefully controlled clinical trials, this strategy could help turn Salmonella from a passive carrier into an active, multifunctional partner in cancer immunotherapy.

Subject of Research: Calreticulin-targeted L-asparaginase–flagellin conjugate used with Salmonella-mediated cancer therapy.

Article Title: Calreticulin-targeting L-asparaginase-flagellin conjugate enhances Salmonella-mediated antitumor efficacy.

Article References: Nguyen, DH., Afzal, A.R., Nguyen, P.TM. et al. Calreticulin-targeting L-asparaginase-flagellin conjugate enhances Salmonella-mediated antitumor efficacy. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-026-03300-x

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41420-026-03300-x

Keywords: cancer immunotherapy, Salmonella, calreticulin, L-asparaginase, flagellin, tumor targeting, bacterial therapy, antitumor efficacy, immunogenic cell death

A short-term decision to eat fewer or no animal products may begin reshaping the human body at the molecular level far sooner than many people expect, according to a new study published in Nature Communications. Research by A. Simistiras, O. Bocher, C. Emmanouil and colleagues examined how restricting animal-derived foods affects both gene activity and protein production in humans, revealing a complex biological response that unfolds beneath the visible changes on a plate.

The study focuses on proteogenomics, an approach that combines two powerful layers of biological information. Genomics and transcriptomics examine the instructions encoded in DNA and the messenger RNA molecules produced when genes are activated. Proteomics, by contrast, measures the proteins that cells actually manufacture. Because proteins perform most of the body’s day-to-day work—from transporting nutrients to controlling immune reactions—studying them alongside gene activity can provide a more direct picture of how physiology responds to dietary change.

Rather than treating diet as a distant influence on long-term health, the research highlights it as an immediate biological signal. When people reduce their intake of animal products, the body is exposed to a different mixture of amino acids, fats, vitamins, minerals and other bioactive compounds. The quantity and timing of these nutrients can alter metabolic pathways, cellular signaling and the activity of genes involved in maintaining tissues. The researchers’ proteogenomic analysis was designed to capture these interconnected effects during a relatively short dietary intervention.

The significance of the work lies in its ability to distinguish between what cells are instructed to do and what they ultimately do. A gene may become more active without producing a corresponding increase in its protein, while a protein may remain stable because of slower turnover or regulation after translation. By examining both molecular layers, the study offers a more refined view of diet-responsive biology than either gene-expression or protein measurements alone. This is particularly important for nutrition research, where modest changes in multiple pathways can combine to influence health.

The findings indicate that restricting animal products can produce measurable molecular shifts even over a limited period. These changes do not represent a simple biological switch from “animal-based” to “plant-based” physiology. Instead, they appear as a network of coordinated responses involving nutrient processing, energy metabolism and cellular regulation. Some proteins may respond directly to altered nutrient availability, while others may change indirectly as tissues adapt to new metabolic demands. The result is a biological signature of dietary transition rather than a single marker that explains every effect.

Such signatures could eventually help researchers understand why individuals respond differently to the same eating pattern. Two people can consume similar diets yet experience distinct changes in blood chemistry, metabolism or immune activity because of differences in genetics, gut microorganisms, age, lifestyle and baseline health. Proteogenomic profiles may help identify these sources of variation by showing which pathways are activated in each person. In the future, that information could support more individualized nutritional guidance instead of assuming that one dietary pattern produces the same outcome for everyone.

The study also underscores an important distinction between molecular response and clinical benefit. Detecting changes in proteins or gene activity does not automatically prove that a diet will prevent disease, improve performance or extend lifespan. Molecular alterations can be adaptive, neutral or potentially harmful depending on their intensity, duration and biological context. The research therefore provides evidence that the body responds rapidly to dietary restriction, while longer and larger studies will be needed to determine how these responses relate to cardiovascular health, metabolic disease, immune function and other outcomes.

The work arrives as plant-forward diets are drawing increasing interest for environmental, ethical and health reasons. Yet public discussions often reduce the science to competing claims about whether animal products are categorically beneficial or harmful. The proteogenomic perspective offers a more nuanced alternative. It suggests that dietary effects emerge through dozens, perhaps hundreds, of interacting pathways, and that the consequences of removing or reducing a food category depend on what replaces it. A diet rich in minimally processed legumes, grains, nuts, seeds, fruits and vegetables may produce a very different molecular response from one dominated by refined plant-based products.

For scientists, the study demonstrates the value of observing dietary change across multiple biological scales. For the public, its message is both striking and practical: the body does not wait years to notice what people eat. Even short-term restriction of animal products can be reflected in the molecular machinery of human cells. The findings do not settle the broader debate over the ideal diet, but they add a new layer of evidence showing that food choices are rapidly translated into biological signals—and that understanding those signals may be key to designing healthier, more personalized nutrition strategies.

Subject of Research: The proteogenomic effects of short-term restriction of animal products in humans.

Article Title: Diet-responsive proteogenomic effects following short-term restriction of animal products in humans.

Article References: Simistiras, A., Bocher, O., Emmanouil, C. et al. Diet-responsive proteogenomic effects following short-term restriction of animal products in humans. Nature Communications (2026). https://doi.org/10.1038/s41467-026-76379-6

Image Credits: AI Generated

DOI: 10.1038/s41467-026-76379-6

Keywords: proteogenomics, nutrition, animal-product restriction, plant-based diet, gene expression, protein response, human metabolism, dietary intervention, precision nutrition

Fuchs endothelial corneal dystrophy, a progressive disorder that can gradually cloud the cornea and impair vision, may be driven by a cellular process more complex than simple cell loss. A new study published in Cell Death Discovery reports that ultraviolet-A light can induce chronic hyperploidization in corneal endothelial cells, triggering changes associated with fibrosis. The findings connect long-term genome abnormalities in post-mitotic cells to the structural deterioration observed in this increasingly recognized eye disease.

The cornea depends on a thin inner layer of endothelial cells to maintain its transparency. These cells regulate the movement of fluid between the cornea and the anterior chamber of the eye, preventing the tissue from becoming waterlogged. Unlike many cell types, human corneal endothelial cells have limited ability to divide and replenish themselves. When they are damaged or lost, neighboring cells may enlarge and stretch to cover the affected area, but this compensation has limits. In Fuchs endothelial corneal dystrophy, the endothelial layer progressively becomes dysfunctional, allowing fluid accumulation and producing corneal swelling, haze and visual distortion.

The study focuses on hyperploidization, a condition in which cells acquire extra sets or copies of chromosomes. In a healthy cell cycle, DNA is replicated and then evenly distributed when a cell divides. Post-mitotic cells, however, are not expected to continue cycling through repeated rounds of DNA replication. If DNA replication occurs without successful cell division, the result can be a cell with an enlarged genome and multiple chromosome sets. This state, known as polyploidy or hyperploidization depending on its extent and context, can alter cell size, metabolism, gene activity and responses to stress.

The researchers investigated how ultraviolet-A, or UVA, light affects cells associated with Fuchs endothelial corneal dystrophy. UVA has a longer wavelength than ultraviolet-B and can penetrate biological tissues more deeply. Although the eye possesses protective mechanisms, persistent or excessive exposure to light-generated stress can damage cellular components, including DNA, proteins and mitochondria. The study indicates that UVA exposure does not merely cause an acute injury that cells either repair or fail to survive. Instead, it can establish a chronic hyperploid state in cells that no longer divide normally.

That distinction is important because a cell can remain alive while becoming increasingly dysfunctional. Hyperploid cells may continue to produce proteins, communicate with neighboring cells and modify their surrounding environment, even as their enlarged genomes disrupt normal regulation. In the corneal endothelium, such persistent abnormalities could interfere with the machinery responsible for maintaining fluid balance and tissue transparency. The research links this long-lasting cellular state to the activation of fibrotic processes, suggesting that damaged endothelial cells may help remodel the cornea rather than simply disappearing.

Fibrosis is the formation or accumulation of excessive connective-tissue components, particularly extracellular matrix proteins such as collagens. During wound healing, matrix production can provide temporary structural support. When the response persists, however, the tissue can stiffen, become disorganized and lose its normal optical properties. In the context of Fuchs endothelial corneal dystrophy, fibrosis may contribute to the loss of corneal clarity and the progression of visual impairment. The study’s central message is that chronic hyperploidization may act as an upstream signal that pushes post-mitotic cells toward this pathological remodeling.

The findings also help explain why a disease affecting a specialized, non-dividing cell population can progress over time. A conventional view of cellular damage often emphasizes apoptosis, necrosis or the gradual depletion of functional cells. The new work highlights another possibility: injured cells may survive in a permanently altered condition and actively influence disease progression. By retaining metabolic activity while carrying abnormal quantities of DNA, these cells could produce signals that encourage inflammation, matrix deposition or changes in the behavior of nearby cells.

The UVA connection raises questions about how environmental stress interacts with inherited susceptibility. Fuchs endothelial corneal dystrophy has genetic and age-related components, and the disease does not arise from a single universal cause. The study does not establish that UVA exposure alone causes the disorder, but it provides a mechanism through which light-associated stress could worsen cellular instability in vulnerable corneal tissue. This may help researchers examine whether cumulative exposure, cellular antioxidant capacity and pre-existing genetic changes combine to determine how rapidly the disease advances.

From a treatment perspective, the work points toward targets beyond replacing lost endothelial cells. Future strategies might seek to prevent abnormal DNA replication, stabilize genome integrity, suppress the fibrotic signals released by hyperploid cells or protect the corneal endothelium from chronic light-induced stress. Such approaches would require careful testing, because polyploidy can serve useful roles in some normal tissues, and broadly blocking cell-cycle or repair pathways could produce harmful effects. The challenge will be to distinguish pathological hyperploidization from adaptive genome changes that help cells survive.

The study ultimately presents Fuchs endothelial corneal dystrophy as a disease of cellular identity as well as cellular survival. UVA-induced chronic hyperploidization appears to place post-mitotic corneal endothelial cells in a persistent state of genomic imbalance, where they can contribute to fibrosis and tissue failure. By connecting light stress, abnormal DNA content and corneal scarring, the research offers a new framework for understanding why the disease can continue even after the initial injury has passed—and provides a potential roadmap for therapies designed to interrupt the process before vision is permanently compromised.

Subject of Research: Ultraviolet-A light-induced chronic hyperploidization and fibrosis in post-mitotic corneal endothelial cells affected by Fuchs endothelial corneal dystrophy

Article Title: Ultraviolet-A light-induced chronic hyperploidization causes fibrosis in post-mitotic cells affected by Fuchs endothelial corneal dystrophy

Article References: Adhikari, Y., Parekh, M., Deshpande, N. et al. Ultraviolet-A light-induced chronic hyperploidization causes fibrosis in post-mitotic cells affected by Fuchs endothelial corneal dystrophy. Cell Death Discov. (2026). https://doi.org/10.1038/s41420-026-03292-8

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41420-026-03292-8

Keywords: Fuchs endothelial corneal dystrophy, ultraviolet-A, UVA, hyperploidization, polyploidy, corneal endothelial cells, fibrosis, post-mitotic cells, genome instability, corneal disease