Understanding the behavior of microscopic aerosols expelled during coughing or sneezing has never been more critical, especially in light of ongoing global respiratory disease challenges such as influenza, COVID-19, and tuberculosis. These tiny particles, often invisible to the naked eye, serve as carriers for pathogens, enabling virus and bacteria transmission through the air. Numerous factors influence how these infectious aerosols disperse, including the strength of the exhalation, the intricacies of human respiratory anatomy, and environmental conditions. Recent groundbreaking research from the Universitat Rovira i Virgili (URV) has uncovered another vital element governing aerosol behavior: temperature. This revelation could transform how we understand and mitigate airborne disease spread indoors.

The research team from URV has demonstrated through meticulously controlled experiments that the temperature difference between exhaled air and the surrounding environment plays a significant role in the dispersion pattern and concentration of aerosols. Specifically, when warm exhaled air—mimicking body temperature—is introduced into cooler ambient air, the aerosol cloud maintains higher particle concentrations and travels further distances compared to situations where the temperature disparity is minimal. This relationship becomes more pronounced with increasing temperature gradients, shedding new light on the physical dynamics operating during respiratory emissions.

Central to this innovative study is the use of a sophisticated, three-dimensional-printed human airway model developed by the URV’s ECoMMFiT research group. This device replicates the biomechanics of human exhalation with exceptional stability and precision, allowing the researchers to simulate coughing and sneezing under tightly controlled parameters. By modifying this simulator to heat the exhaled air to 37 degrees Celsius—representing a slight fever condition—the team was able to explore interactions between temperature, respiratory flow dynamics, and aerosol dispersal in unprecedented detail.

Experiments were conducted within a climate-controlled chamber at the Catalonia Institute for Energy Research (IREC), where environmental conditions could be precisely manipulated. The team investigated three distinct ambient temperatures: 27°C, 17°C, and 7°C. These temperatures were combined with varying exhalation intensities and two different modes of nasal airflow: open and closed nasal cavities. This combination resulted in eighteen unique trial configurations, each rigorously repeated ten times for statistical robustness, culminating in a comprehensive dataset derived from 180 individual experiments.

The results reveal that the aerosol clouds generated under these varying conditions behave differently in predictable yet complex ways. As Nicolás Catalán, co-author and URV mechanical engineering researcher, explains, the increased temperature difference augments buoyancy effects. Warm exhaled air, less dense than the surrounding cooler air, rises and carries aerosol particles further and more cohesively. This buoyant lift sustains particle concentrations for longer periods, significantly extending the spatial range of potential pathogen transmission, particularly in colder environments.

A particularly striking finding relates to the role of the nasal cavity in shaping aerosol spread. The study confirms that partial airflow through the nose reduces horizontal propagation but promotes increased vertical dispersion. Conversely, when the simulator mimics mouth-only exhalation, aerosols tend to move more horizontally, covering greater frontline distances. This mechanistic insight highlights how variations in individual respiratory behaviors and anatomical structures can dramatically impact transmission risks.

The technical prowess of the study owes much to the utilization of high-speed videography and laser illumination techniques. These tools unveil the fine-scale structure and temporal evolution of the aerosol clouds. The recorded visualizations underscore how the interplay between ambient temperature gradients and respiratory airflow generates intricate aerosol flow patterns. This mechanistic understanding is crucial for modeling pathogen transport pathways more accurately within indoor environments, where interventions are typically applied.

Notably, the research contributes valuable experimental data that historically has been scarce in aerosol studies. Previous investigations frequently relied on numerical simulations or human trials, each limited in their control over parameters such as flow rate and temperature. In contrast, the URV’s 3D-printed airway simulator enables reproducible and stable experimental conditions, providing crucial validation points for computational fluid dynamic (CFD) models that predict aerosol dissemination and, by extension, infection risk.

From a practical standpoint, these insights hold significant implications for public health and safety. Environments like hospitals, schools, biological labs, and public transportation systems, where pathogen exposure risk is elevated, can benefit from refined ventilation designs and tailored control measures based on thermal considerations. For example, in colder seasons or cooler indoor environments, the increased persistence and reach of respiratory aerosols could warrant enhanced air circulation strategies or modifications to heating systems to mitigate transmission potential.

While the research sheds new light on temperature’s role in aerosol dynamics, the authors caution that respiratory aerosol behavior is inherently multifaceted. Factors such as humidity, indoor ventilation patterns, and the longevity of suspended particles must be further investigated to achieve comprehensive risk assessments. The study encourages continued interdisciplinary research integrating experimental, computational, and epidemiological approaches to fully unravel the variables influencing airborne disease propagation.

The research team’s approach, combining experimental rigor with innovative simulation, establishes a robust framework for future investigations. Their novel use of a temperature-controlled exhalation model advances the field beyond simplistic or static assumptions about aerosol dynamics. This detailed analysis forms a foundational step towards predictive models capable of informing adaptive infection control protocols sensitive to thermal variances across seasons and indoor spaces.

In conclusion, the URV-led study emphasizes that temperature differences between exhaled and ambient air significantly affect bioaerosol transport, influencing both the extent and persistence of pathogen-laden particle clouds. By integrating anatomical realism through a 3D-printed airway model and employing precise climate control, the research advances our scientific understanding of respiratory aerosol physics. These findings promise to inform smarter environmental and public health strategies, reducing airborne transmission risks in indoor settings worldwide.

Subject of Research: Respiratory aerosol dynamics and pathogen transmission influenced by temperature differences.

Article Title: Bioaerosol transport dynamics in cold and warm environments: An experimental study using a three-dimensional-printed human airway model.

News Publication Date: 20-Mar-2026

Web References: http://dx.doi.org/10.1063/5.0303143

References:
Catalán, N., Cito, S., Varela Ballesta, S., Fabregat, A., Vernet, A., Graus, D., & Pallarès, J. (2026). Bioaerosol transport dynamics in cold and warm environments: An experimental study using a three-dimensional-printed human airway model. Physics of Fluids.

Keywords

Respiratory aerosols, airborne pathogens, bioaerosol transport, temperature effects, human airway model, aerosol dispersion, exhalation dynamics, infectious disease transmission, ventilation, computational fluid dynamics, public health, indoor air quality

New findings suggest cell size could sharpen cancer prognosis.

In a groundbreaking study published this June in Experimental & Molecular Medicine, researchers have unveiled pivotal insights into the hitherto elusive process by which iron traverses the abluminal membrane of the blood–brain barrier (BBB). This discovery not only deepens our molecular understanding of nutrient transport within the brain’s tightly regulated environment but also paves the way for innovative therapeutic approaches targeting neurodegenerative diseases linked to iron dysregulation. The blood–brain barrier, a highly selective and dynamic interface, controls the passage of essential molecules, with iron transport posing one of the most intricate biological challenges.

Iron, although vital for numerous cellular processes including oxygen transport, DNA synthesis, and energy metabolism, is a double-edged sword due to its potential to catalyze the formation of deleterious reactive oxygen species. Within the central nervous system (CNS), precise control of iron ingress is critical to both neuronal health and function. This new study elucidates how iron crosses the abluminal—or brain-facing—side of the endothelial cells lining the BBB, a process that had remained largely speculative until now.

Central to the findings is the identification of specialized molecular machineries that mediate the release of iron from endothelial cells into the brain’s extracellular milieu. The researchers demonstrate that beyond the well-characterized transferrin receptor (TfR) system facilitating iron uptake from the bloodstream, a complex network of iron exporters and chaperones on the abluminal membrane orchestrates iron efflux into the brain parenchyma. This multidimensional transport system integrates both canonical and noncanonical pathways, underscoring the sophisticated regulatory environment governing cerebral iron homeostasis.

At the molecular level, the study highlights ferroportin (FPN) as the primary iron exporter at the abluminal membrane, functioning in concert with hephaestin, a ferroxidase enzyme that converts ferrous iron (Fe2+) to its ferric form (Fe3+), thereby facilitating its safe release. Notably, the research uncovers previously unappreciated regulatory interactions between ferroportin and intracellular iron chaperones, such as poly rC-binding proteins (PCBPs), which escort iron within the endothelial cytoplasm, protecting it from catalyzing harmful oxidative reactions before export.

Additionally, researchers unravel the nuanced regulation of these iron transporters by systemic and local factors. Hepcidin, a liver-derived peptide hormone well-known as a master regulator of systemic iron balance, is shown to effectively modulate ferroportin activity at the BBB, leading to retention or release of iron depending on physiological demands. Intriguingly, this modulation occurs in a brain-region-specific manner, suggesting an adaptive mechanism tailored to distinct neuronal metabolic requirements.

The implications of this discovery resonate profoundly with pathologies such as Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative disorders where iron mismanagement contributes to oxidative damage and neuronal death. The ability to delineate and potentially manipulate the molecular actors that govern iron’s journey across the BBB opens new frontiers for therapeutic intervention. Targeting ferroportin and its regulatory partners could serve as a viable strategy to restore iron equilibrium in diseased states.

Methodologically, the study employs a sophisticated blend of in vivo imaging, advanced molecular biology techniques, and high-resolution microscopy to visualize and quantify iron transport dynamics in real time. This multipronged approach enables an unprecedented spatial and temporal resolution of iron flux at the cellular and subcellular levels within the BBB’s microenvironment. Cutting-edge CRISPR-Cas9 gene editing also played a crucial role in selectively knocking down transporter genes, shedding light on their individual contributions to the iron egress cascade.

Beyond its immediate biomedical relevance, the study spotlights the blood–brain barrier as a site of remarkable functional complexity and adaptability. The elucidation of iron trafficking underscores the multifaceted roles endothelial cells perform, not just as passive barriers but as active regulators of brain homeostasis. This challenges traditional paradigms and prompts a reevaluation of transporter networks in other nutrient contexts.

Further research avenues are already emerging from these findings. Investigating how pathological states alter the expression and function of these iron transporters may reveal biomarkers for early diagnosis of neurodegeneration. Moreover, pharmacological modulation of ferroportin and associated proteins offers a tantalizing prospect for mitigating iron-associated oxidative stress without disrupting systemic iron homeostasis.

Collaborative efforts integrating computational modeling with molecular neurobiology will likely accelerate translation of this newfound knowledge into clinical applications. Predictive models simulating iron kinetics through the BBB can identify optimal intervention points, while medicinal chemistry endeavors aim to design small molecules that fine-tune transporter activity.

Ethical and safety considerations will be paramount as future research explores therapeutic manipulation of the BBB iron transport machinery. Given the delicate balance required to maintain cerebral iron levels, unintended consequences of disrupting this equilibrium must be carefully assessed through rigorous preclinical and clinical trials.

Ultimately, this seminal study represents a landmark advance in neuroscience and vascular biology, shedding light on one of the most fundamental physiological processes underpinning brain health. By unlocking the secrets of iron’s passage across the abluminal membrane of the blood–brain barrier, researchers are charting a course toward novel treatments that may alleviate the burden of devastating neurological diseases worldwide.

Such strides underscore the ever-expanding frontiers of science whereby intricate cellular phenomena are dissected, understood, and harnessed to enhance human well-being. As this research ripples through the scientific community, it promises not only to deepen our grasp of brain physiology but also to kindle hope for millions affected by iron-related neuropathologies.

This stunning revelation exemplifies the power of interdisciplinary research — uniting vascular biology, molecular neuroscience, and clinical science — and heralds a new era in brain barrier biology, where the mechanisms of nutrient transport are no longer shrouded in mystery but laid bare with clarity and precision.

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Subject of Research: Iron transport mechanisms across the abluminal membrane of the blood–brain barrier

Article Title: How does iron cross the abluminal membrane of the blood–brain barrier

Article References:
Guo, Q., Wang, T., Qian, ZM. et al. How does iron cross the abluminal membrane of the blood–brain barrier. Exp Mol Med (2026). https://doi.org/10.1038/s12276-026-01734-y

Image Credits: AI Generated

DOI: 10.1038/s12276-026-01734-y

In a groundbreaking study published in the prestigious journal npj Parkinson’s Disease, researchers have unveiled compelling evidence indicating that striatal hyperechogenicity observed through ultrasound imaging may serve as a critical biomarker for the prodromal phase of X-linked dystonia-parkinsonism (XDP). This discovery not only offers unprecedented insight into the pathophysiological underpinnings of XDP but also holds transformative potential for the early diagnosis and management of this debilitating neurodegenerative disorder. The study, led by Pauly et al., signifies a pivotal advance in the ongoing quest to decode the enigmatic progression of XDP through non-invasive imaging modalities.

X-linked dystonia-parkinsonism is a hereditary movement disorder predominantly affecting males, especially those of Filipino descent, characterized by the coexistence of dystonia and parkinsonism symptoms. Traditionally, diagnosis has been reliant on clinical criteria and genetic testing, which often recognize the disease only after the onset of overt motor symptoms. This lag in diagnosis severely limits timely therapeutic intervention. By focusing on striatal hyperechogenicity—an increased echogenic signal in the striatum region detected via transcranial ultrasound—the team has illuminated a novel, early biomarker that could detect the disease during its prodromal, or preclinical, phase.

The study utilized advanced high-resolution transcranial ultrasound techniques to examine the brains of subjects genetically predisposed to XDP but not yet manifesting clinical symptoms. The striatum, a deep brain structure integral to motor control and implicated heavily in movement disorders, showed significant hyperechogenic signals in these prodromal individuals compared to matched controls. This finding suggests that pathological alterations in striatal tissue architecture and composition precede the clinical onset of XDP, providing a window of opportunity for early detection.

Crucially, the research delineates the pathological hallmarks that might contribute to hyperechogenicity in the striatum. The authors posit that iron accumulation within the striatal neurons and surrounding glial cells may alter the acoustic properties of the tissue, creating the hyperechogenic signature observed. This hypothesis aligns with existing studies linking abnormal iron metabolism to various neurodegenerative conditions, including Parkinson’s disease, underscoring a shared pathological pathway that might be exploited for diagnostic purposes across multiple disorders.

Beyond iron deposition, microstructural changes such as gliosis, neuronal loss, and inflammatory processes likely amplify the echogenic signal. The striatum’s vulnerability in XDP, exacerbated by genetic mutations on the X chromosome affecting the TAF1 gene, might trigger progressive neurodegeneration that subtly remodels the tissue even before clinically recognizable symptoms arise. These cumulative microscopic changes form the substrate for the ultrasound imaging markers identified by the study.

The implications of these findings extend far beyond early diagnosis. Striatal hyperechogenicity, as a measurable and quantifiable imaging marker, could allow clinicians to stratify at-risk populations, monitor disease progression objectively, and assess therapeutic responses in clinical trials. This is a critical breakthrough in a field where biomarkers have been sorely lacking, thus impeding efforts to develop targeted treatments and intervene before irreversible neuronal damage occurs.

Importantly, the utilization of transcranial ultrasound presents a highly accessible, cost-effective, and non-invasive diagnostic tool that could be adopted widely, particularly in resource-limited settings where XDP prevalence is highest. Compared to more complex neuroimaging modalities like PET or MRI, ultrasound offers a pragmatic solution suited for routine screening and longitudinal monitoring. This democratization of advanced diagnostic capability could fundamentally reshape the clinical landscape for XDP and similar disorders.

The study’s comprehensive approach involved a multidisciplinary team integrating expertise in neurology, radiology, genetics, and biomedical engineering. By correlating imaging findings with genetic and clinical data, the researchers constructed a robust framework linking striatal hyperechogenicity with the earliest stages of disease pathogenesis. This model provides a template for future investigations aiming to uncover prodromal markers in other neurogenetic disorders.

Furthermore, the temporal dynamics of striatal hyperechogenicity warrant further exploration. Whether this imaging signature remains stable, intensifies, or fluctuates throughout disease progression is a question of paramount clinical importance. Longitudinal studies tracking patients from prodromal to advanced stages will be indispensable in validating striatal hyperechogenicity as a reliable surrogate endpoint for disease activity and guiding optimal timing for intervention.

While the findings herald a promising avenue for early detection of XDP, several challenges remain. The specificity of striatal hyperechogenicity to XDP versus other conditions presenting with similar imaging patterns needs rigorous assessment. Overlapping echogenic profiles in disorders such as Parkinson’s disease and other movement syndromes may complicate differential diagnosis, necessitating the integration of imaging data with genetic and biomolecular markers to enhance diagnostic precision.

Ethical considerations also come to the fore when screening asymptomatic individuals for a progressive neurodegenerative disease. The psychological impact of identifying prodromal markers must be balanced against the current absence of definitive disease-modifying therapies. Nonetheless, as novel treatments emerge, early identification facilitated by imaging biomarkers like striatal hyperechogenicity will become increasingly critical.

In summary, the identification of striatal hyperechogenicity as an ultrasound marker for prodromal X-linked dystonia-parkinsonism represents a significant leap forward in the field of movement disorders. This research not only enriches our understanding of XDP pathophysiology but also confronts longstanding diagnostic challenges with an innovative, accessible imaging approach. Its implications resonate deeply within neurology and underscore the importance of multidisciplinary collaboration in tackling complex neurodegenerative diseases.

The study paves the way for a new era wherein neurodegenerative disorders may be detected, monitored, and ultimately treated earlier and more effectively than ever before. As the field advances, the integration of imaging biomarkers with genetic and clinical assessments promises to revolutionize patient care, transforming the prognosis for affected individuals and offering hope to at-risk families worldwide. The future of XDP diagnosis and management looks increasingly hopeful, propelled by the insights laid out in this pioneering research.

Ultimately, this investigation not only highlights a novel diagnostic avenue for XDP but also exemplifies the broader potential of ultrasound imaging in neurodegeneration. As research continues, it is conceivable that similar hyperechogenic markers could be discovered for other elusive neurological conditions, enhancing early detection strategies and opening new frontiers for therapeutic innovation. The convergence of cutting-edge imaging technology with genetic and molecular sciences heralds a transformative period for neurology, promising profound benefits for patients globally.

This landmark study by Pauly and colleagues sets a new standard in the use of non-invasive imaging to unravel the mysteries of neurodegenerative diseases and challenges researchers to further elucidate the complex interplay between genetic vulnerabilities and brain tissue alterations that underlie these devastating conditions.

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Subject of Research: X-linked dystonia-parkinsonism and its prodromal biomarkers

Article Title: Striatal hyperechogenicity as an ultrasound imaging marker for prodromal X-linked dystonia-parkinsonism

Article References:
Pauly, M.G., Diesta, C.C.E., Cataniag, P. et al. Striatal hyperechogenicity as an ultrasound imaging marker for prodromal X-linked dystonia-parkinsonism. npj Parkinsons Dis. 12, 133 (2026). https://doi.org/10.1038/s41531-026-01418-4

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41531-026-01418-4

In the ever-evolving field of pediatric medicine, necrotizing enterocolitis (NEC) represents one of the most formidable challenges clinicians face in neonatal intensive care units. This devastating intestinal disease primarily affects premature infants, often leading to severe complications or even mortality if not diagnosed and treated promptly. Despite advances in neonatal care, the diagnosis and prediction of the need for surgical intervention in NEC remain mired in uncertainty due to the subtle, variable nature of early signs and limited current diagnostic tools. Scientists and clinicians alike have long sought innovative ways to improve early identification and prognosis to optimize outcomes for these vulnerable patients.

In a groundbreaking development announced this June, a team of researchers led by Wang, Jin, Cai, and colleagues have unveiled a cutting-edge artificial intelligence model that harnesses the power of multimodal data to improve NEC diagnostic accuracy and surgical risk prediction. Published in Pediatric Research, this new approach leverages a dual swin transformer architecture—the first of its kind applied to this specific clinical problem—blending diverse patient data inputs to provide a transparent, interpretable decision-support system. This innovation not only promises to revolutionize how NEC is understood and managed but also sets a new standard for AI’s role in complex clinical decision-making.

Necrotizing enterocolitis is characterized by inflammation and necrosis of the infant’s intestine, the pathogenesis of which remains incompletely understood but is believed to involve a complex interplay of intestinal immaturity, microbial imbalance, and systemic inflammatory responses. Early symptoms such as feeding intolerance, abdominal distension, and bloody stools are often nonspecific, leading to diagnostic ambiguity. Current diagnostic methodologies rely heavily on clinical examination combined with radiographic imaging, which may delay recognition of severe disease requiring urgent surgery. Consequently, there is an urgent need for more sensitive and specific predictive tools to guide timely interventions which can preserve bowel function and improve survival.

The dual swin transformer model introduced by the authors capitalizes on recent advances in machine learning and neural network architectures rooted in natural language processing and computer vision. Swin transformers are hierarchical vision transformers designed to efficiently capture local and global context within medical images and tabular clinical data. By integrating radiologic images with patient-specific clinical metrics—such as laboratory values and vital signs—this dual model concurrently processes and synthesizes multiple modalities. This multimodal fusion enables the AI to discern subtle patterns indicative of disease onset and progression that are often imperceptible to human observers.

Importantly, the model was developed with interpretability at its core. In the current landscape of AI in healthcare, “black box” systems can engender clinician skepticism due to a lack of transparency regarding decision rationale. By employing attention mechanisms and visualization strategies, the model highlights key features driving its predictions. For example, it can indicate which segments of radiographic images or particular blood test trends raised suspicion for NEC or increased the likelihood of surgical necessity. This transparency enhances clinical trust and facilitates a collaborative human-machine diagnostic workflow rather than a replacement of clinical judgment.

The researchers trained and validated the model on a robust dataset comprising hundreds of neonates from multiple tertiary centers, ensuring diverse representation across gestational ages and clinical presentations. The dataset included serial abdominal ultrasound and X-ray imaging paired with longitudinal clinical data capturing inflammatory markers, feeding regimens, and hemodynamic parameters. Such comprehensive data collection was decisive in enabling the model not only to achieve high accuracy rates but also to adapt dynamically to temporal changes reflective of NEC progression. Their results demonstrated significant improvements over traditional scoring systems and single-modality AI tools.

Beyond diagnostic accuracy, the study explored the model’s ability to predict which infants would likely require surgical intervention. NEC surgery typically involves resection of necrotic bowel segments, a procedure associated with considerable risk and long-term complications such as short bowel syndrome. Early prediction of surgical need can enhance resource allocation, optimize timing of consultation with pediatric surgeons, and potentially improve postoperative outcomes. The dual swin transformer demonstrated remarkable prowess in stratifying patients by surgical risk, outperforming established clinical predictors by a wide margin and thus holding potential to reshape surgical decision-making paradigms.

Moreover, the translational potential of this technology is significant. The model’s architecture allows for seamless integration into existing hospital information systems and picture archiving and communication systems (PACS), paving the way for real-time clinical deployment. Its modularity also provides adaptability to other neonatal and pediatric disease contexts characterized by multimodal diagnostic complexity, such as congenital heart diseases or sepsis. This flexibility marks an important step toward personalized medicine driven by AI-enhanced precision diagnostics tailored to the needs of critically ill infants.

However, the authors acknowledge several challenges ahead. The generalizability of the model to different healthcare settings, especially those with limited imaging resources, requires further investigation. Additionally, ensuring data privacy and addressing ethical concerns related to AI-driven decisions in vulnerable populations remains paramount. Prospective clinical trials are needed to validate efficacy and safety in routine practice, alongside strategies to train frontline clinicians in interpreting and effectively incorporating AI output into patient care.

The implications of this research extend beyond NEC, highlighting the transformative role of next-generation AI architectures in neonatal intensive care. By bridging the gap between complex multimodal data and actionable clinical insights, such models have the potential to fundamentally enhance early diagnosis, risk stratification, and outcome prediction across a spectrum of neonatal diseases. The collaborative, transparent design philosophy championed by Wang and colleagues exemplifies the future of AI in medicine—one that empowers human clinicians with unprecedented analytic power while ensuring accountability and interpretability.

As the field of pediatric research embraces AI innovations like the dual swin transformer, the promise of improving survival and quality of life for the most fragile patients comes into sharper focus. This confluence of advanced computational techniques with clinical expertise heralds a new era of neonatal care, offering hope to countless families facing the terrifying specter of NEC. By accelerating timely diagnosis and guiding precise surgical decision-making, this technology stands poised to save lives and reduce the burdens of one of neonatal medicine’s most urgent challenges.

In summary, the dual swin transformer model represents a seminal advancement in applying artificial intelligence to the complex problem of necrotizing enterocolitis diagnosis and surgical prediction. Combining sophisticated multimodal data integration with interpretability, it outperforms existing methods while fostering clinician trust. Continued refinement and validation promise to unlock its full clinical potential, signaling a paradigm shift in how AI supports neonatal critical care.

With this landmark study published in Pediatric Research, Wang, Jin, Cai, and their team have undoubtedly charted a new course for marrying AI innovation with frontline neonatal medicine. The coming years will reveal the extent to which models like theirs become integral to NICU practice, but the trajectory is clear—machine learning and biomedical science are converging to confront NEC with previously unattainable precision and foresight, forever altering the landscape of infant healthcare.

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Subject of Research:
Development of an interpretable multimodal artificial intelligence model for the diagnosis and surgical prediction of necrotizing enterocolitis (NEC) in neonates.

Article Title:
Dual swin transformer for assisting in the diagnosis and surgical prediction of necrotizing enterocolitis.

Article References:
Wang, C., Jin, J., Cai, L. et al. Dual swin transformer for assisting in the diagnosis and surgical prediction of necrotizing enterocolitis. Pediatr Res (2026). https://doi.org/10.1038/s41390-026-05145-7

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05145-7

Attorney Aaron Siri exposes the flawed safety testing of childhood vaccines, claiming that none have been tested against saline placebos. Instead, vaccines are compared to older vaccines, creating a misleading safety profile. He argues that significant adverse event rates exist, asserting that these practices endanger children's health and lack proper testing validation.

New findings suggest cell size could sharpen cancer prognosis.

New findings suggest cell size could sharpen cancer prognosis.

In a groundbreaking multicenter study that challenges conventional therapeutic strategies for chronic psoriasis, researchers from Radboud University Medical Center and Ghent University Hospital have demonstrated that significant dosage reductions in advanced biologic treatments do not compromise clinical efficacy. This international, pragmatic, randomized controlled trial, recently published in The Lancet Regional Health – Europe, proposes a paradigm shift in managing this burdensome skin disease, with profound implications for patient quality of life and healthcare economics.

Psoriasis, an autoimmune inflammatory disorder afflicting approximately half a million individuals in the Netherlands alone, manifests with complex immunopathology involving dysregulated cytokine networks. Over the past two decades, the development of biologics targeting specific interleukins—namely IL-17 and IL-23—has revolutionized disease control, offering patients dramatic symptom relief and improved functional capacity. Nevertheless, these biologics come with hefty price tags, often exceeding €17,000 per patient annually, necessitating exploration of optimized dosing regimens.

The study enrolled 244 patients across 19 Dutch and Belgian hospitals, following them over an 18-month period. By employing a non-inferiority design, the investigators assessed whether tapering the biologics to two-thirds or even half of the standard therapeutic doses could maintain remission or low disease activity without increasing adverse events. Importantly, dose reductions were implemented via gradually extending the intervals between injections, an innovative approach that offered practical advantages in clinical settings.

Findings revealed that 75% of patients responded favorably to the reduced dosing regimens, experiencing symptom control equivalent to those maintained on standard doses. This outcome not only underscores the potency and durability of IL-17 and IL-23 inhibitors but also supports the hypothesis that lower antigenic stimulus suffices to suppress the aberrant immune activation characteristic of psoriasis in many patients. By allowing the immune system to recalibrate under diminished pharmacological pressure, treatment sustainability was notably enhanced.

From a pharmacoeconomic standpoint, the implications are substantial. Reducing dosage effectively halves the frequency of injections for some individuals, translating into annual cost savings nearing €8,500 per patient. This reduction diminishes logistical burdens for both patients and healthcare systems and aligns with global imperatives for more sustainable and efficient medical resource utilization. Moreover, fewer injections potentially lower cumulative immunogenicity and treatment-related side effects, contributing to improved safety profiles.

Patient perspectives garnered during the study highlighted the psychological complexity inherent in tapering biologic therapies. Given psoriasis’s chronicity—with many suffering symptoms for decades before initiating biologics—patients often harbor understandable concerns regarding potential relapse. The study’s pragmatic design allowed participants to revert to standard dosing promptly if symptom control waned, ensuring personalized management and strengthening patient confidence during the dose reduction phase.

Lead dermatologist Elke de Jong emphasized that incorporating flexible dosage adjustments into clinical guidelines could transform routine practice. This adaptive strategy balances maximizing therapeutic benefit and minimizing overtreatment, fostering individualized care paradigms. Such guideline evolution is critical as novel biologics continue to enter the market, driving up costs and challenging healthcare sustainability globally.

The research specifically investigated a range of IL-17 inhibitors—including secukinumab, ixekizumab, bimekizumab, and brodalumab—and IL-23 inhibitors such as guselkumab, risankizumab, and tildrakizumab. These agents employ monoclonal antibody technology to selectively neutralize cytokines pivotal in psoriasis pathogenesis, thereby interrupting inflammatory cascades at a molecular level. The demonstrated feasibility of dosing attenuation with these biologics signifies a major advance in the nuanced application of targeted immunotherapies.

Physician-epidemiologist Juul van den Reek explained that extending injection intervals delivers dual benefits: reduction in iatrogenic trauma and the environmental footprint associated with production, packaging, and distribution of biologic medications. In an era accentuated by climate considerations, such efficiencies present vital contributions toward greener healthcare models without compromising patient outcomes.

This well-powered, rigorously conducted trial represents the first large-scale prospective evidence supporting dose tapering of biologics for psoriasis. Given the rising prevalence of autoimmune diseases and escalating pharmaceutical expenses worldwide, these findings furnish a robust framework for revising treatment algorithms both within the Netherlands and Belgium—and potentially beyond. Such clinical innovation positions the dermatology community at the forefront of precision medicine and value-based care delivery.

Future research avenues may focus on identifying biomarkers predictive of which patients can most safely and effectively sustain reduced biologic dosing, paving the way for even more tailored interventions. Furthermore, long-term observational studies are warranted to monitor sustained remission rates and assess immunological consequences of dose modulation.

In conclusion, this landmark study dispels the long-held notion that maximal drug dosing is invariably required to maintain psoriasis control. By scientifically validating the safety and efficacy of biologic dose reduction, the BeNeBio trial heralds a new chapter in dermatological therapeutics—one characterized by patient empowerment, economic prudence, and informed flexibility in chronic disease management.

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Subject of Research: People

Article Title: Dose reduction of IL-17 and IL-23 inhibitors in psoriasis (BeNeBio study): an international, pragmatic, multicentre, randomised, controlled, non-inferiority trial

News Publication Date: 1-Jun-2026

Web References:
10.1016/j.lanepe.2026.101721

Keywords: Psoriasis, Autoimmune disorders, Skin disorders, Drug costs, Pharmaceuticals

Leishmania parasites appear to evolve through widespread genetic exchange, reshaping assumptions about how they adapt and spread. A parasite long thought to spread mostly by cloning itself may be far more genetically dynamic than scientists once believed. A new international study suggests that Leishmania—a group of microscopic parasites responsible for debilitating tropical diseases—regularly swaps genetic [...]

Sunburn and mosquito bites go together in the summer like a hot dog and ketchup. To keep from becoming a mosquito buffet, most of us turn to bug sprays with DEET.  An acronym built from its scientific identification (diethyltoluamide), DEET was developed for the United States Army in 1946 and entered civilian use in 1957. It is generally considered safe when used as directed. 

However, mosquitoes can learn to associate the repellant with food. They may even become attracted to it. The findings are detailed in a study published today in the Journal of Experimental Biology.

“If someone applies DEET and the concentration fades over time, but a mosquito still manages to feed, the insect may begin associating that smell with a reward,” Clément Vinauger, a study co-author and biochemist at Virginia Tech, said in a statement. “That’s a possibility we should take seriously when we think about how repellents are used in the real world.”

Ace processors

Like it or not, Earth’s over 3,500 known mosquito species are pretty smart and an evolutionary wonder. They use sensory information to find hosts and can adapt to changing environments.

In previous studies, Vinauger’s team has shown that the insects remember and avoid hosts who swat them away, can combine smell and vision to precisely track humans, and even gravitate toward and away from the smell of certain soaps.

“Mosquitoes are remarkable at processing information about their environment,” Vinauger said. “What we are trying to understand is not only how they detect us, but how their brains interpret those cues and turn them into behavior.”

A DEET-covered dinner bell?

In this new study, the team focused on the yellow fever mosquito (Aedes aegypti). This species spreads several diseases to tens of millions of people each year, including dengue fever, Zika, yellow fever, and chikungunya.

The team trained mosquitoes using a form of Pavlovian conditioning. Often called “Pavlov’s dogs,” this training method developed by neurologist and physiologist Ivan Pavlov in the early 20th century was used to teach dogs to associate the sound of a bell ringing with food. 

The mosquitoes were restrained behind a piece of fabric mesh. They then offered the mosquitoes a bag of warm blood (yum) that was just out of the insects’ reach to see how enthusiastically the insects stabbed at it with their proboscises. As expected, the mosquitoes were interested in the blood, particularly when the team rewarded them by lowering the bag within reach. Things changed a bit once DEET entered the experiment. When the team offered the insects blood when surrounded by the scent of DEET, they initially stayed away from the potential feast.  

To see if they could be trained to associate that smell with the dinner bell, the team fed the mosquitoes warm blood for 20 seconds, squirting the scent of DEET into the enclosure in the final 10 seconds of dining. They repeated the procedure three more times before noting how the mosquitoes responded to only the scent of DEET. In this trial, over 60 percent of mosquitoes tried to bite when they smelled DEET.  

To examine further, the mosquitoes were given a choice between two human hands. The hand belonged to study co-author Ayelén Nally of the University of Buenos Aires. One of Nally’s hands was coated with DEET at normal concentrations and the other was bare. The untrained mosquitoes avoided the DEET-treated hand, while the trained mosquitoes were drawn to it.

Interestingly, the mosquitoes could form that same association when sugar, instead of blood, was used as the reward. 

According to the team, they are seeing how the mosquito’s brain can rewrite its response based on their experiences. What they have learned matters just as much as what a chemical like DEET does. 

“If mosquitoes are repeatedly exposed to DEET, it becomes less effective as a repellent,” study co-author Claudio Lazzari from University of Tours in France added.

Keep the bug spray

Importantly, this does not mean you should stop using DEET completely. It is still one of the most effective ways to keep the dangerous insects away, particularly where mosquito-borne disease is common.

“If you’re in tropical regions where disease risk is real, you should use it,” Vinauger said. “Instead of applying a lot at once, you may want to reapply regularly so it’s always active and providing continuous protection.”

Treated clothing may also be a challenge since DEET concentrations in fabric decline over time. Additional study to understand their behavior is crucial for public health as mosquito-borne illnesses increase due to climate change. 

“We need to understand how mosquitoes keep outsmarting our control strategies,” Vinauger concluded. “And that takes understanding how they work—at the molecular level, the neural level, the behavioral level.”

The post Mosquitoes can learn that DEET means dinner is served appeared first on Popular Science.

For a woman in her mid-40s to mid-50s, it arrives without warning. She wakes up, overheated, wondering why it’s so hot in the house—until she sees the thermostat is set for 70 degrees, same as always. Or, she’s midway through a work presentation when heat rises from her chest to her face, and she wonders if the flush on her cheeks is visible to everyone in the room. 

It’s a hot flash—a rite of passage for the majority of women in either perimenopause, the years leading up to menopause, or the years beyond it. Menopause itself is diagnosed after 12 consecutive months without a period, but the hot flashes don’t always get the memo.

Here’s everything doctors currently know about hot flashes.

What is a hot flash, and who gets them?

Hot flashes are a sudden heat flare up often paired with flushed skin and sweating. They don’t usually last long, between a minute and five minutes in duration.

Most women experience a hot flash about four and a half to five years after their last period, Dr. Monica Christmas, an OB/GYN at University of Chicago Medicine and director of its menopause program tells Popular Science. She also is the associate medical director of the nonprofit Menopause Society, which provides healthcare professionals with tools and resources to support women through the transition.

Women have grappled with hot flashes—whether simply annoying or genuinely debilitating—for centuries. In 1582, Dr. Jean Liebault of France was among the first to document the phenomenon. But while we know much more about hot flashes and night sweats than Liebault ever did, one question still stumps experts. 

“What we can’t answer is why doesn’t everybody get them,” Christmas says. “Because everybody doesn’t get them. I have patients that will say, ‘I don’t know,’ if I say, ‘Are you having any hot flashes or night sweats?’ And as soon as they say that, I’m like, ‘You’re not having them.’” 

What’s actually happening inside women’s bodies during a hot flash? 

During a hot flash, a woman might feel like she’s spiking a high fever, but physiologically, that’s not what is happening. As women approach menopause and the ovaries begin to make less estrogen, the brain’s internal thermostat—the hypothalamus—becomes hypersensitive to even small shifts in temperature, Christmas says.

The body “thinks” it’s overheating, even when the actual temperature hasn’t changed much. In response, our bodies try to cool us down. Blood vessels dilate, which is supposed to help dissipate some of that heat, but then that triggers a sweating reflex.

“Many people will say, ‘I feel this out of nowhere, this surge of warmth that typically is from the nipple line up,’” she says. “And then as soon as the heat came on, and I felt like I was internally heated up or on fire, I start to sweat.” 

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How do women experience hot flashes differently? 

Exactly how an individual woman experiences hot flashes varies wildly. Some describe very mild symptoms. Others grapple with profuse sweating. Some experience only hot flashes during the day, while some have regular night sweats. About four in five women experience them at some point during the menopause transition, according to the American College of Obstetricians & Gynecologists.

“There’s a lot of variability,” Christmas says. Common triggers include alcohol, caffeine, high-sugar and highly processed foods, along with stress.

Black women also are more likely to experience more severe and longer-lasting symptoms, sometimes up to 11 years, she says. And research also shows that women with more severe, longer-lasting hot flashes and night sweats appear to be at higher risk of cardiovascular disease.

That doesn’t mean treating hot flashes automatically lowers heart risk, Christmas says. But it does reinforce that these women deserve particularly careful attention to blood pressure, cholesterol, and lifestyle. “I want to make sure I’m doing everything possible to minimize that risk,” she says when she treats her patients. 

There’s more to hot flashes than hormonal changes

For decades, the entire process was blamed purely on estrogen loss, Christmas says. But that explanation left some unanswered questions. 

“That doesn’t explain why every menopausal woman doesn’t have night sweats,” she says. “And it also doesn’t quite explain why we can sometimes start to experience them during the perimenopause transition because during perimenopause, people still have some estrogen.” 

Newer research now is telling a more complex story. When the brain recognizes that a woman’s estrogen levels are low, nerve cells in the hypothalamus called KNDy neurons (pronounced “candy”) become overactive, releasing neurotransmitters, which are chemical signals the brain uses to send messages throughout the body. These neurotransmitters include kisspeptin, dynorphin, and neurokinin B. 

“It’s actually those neurotransmitters that seem to have more of an impact on our ability to regulate our internal temperature,” Christmas says. “They’re not hormones.” 

What to do if you get a hot flash

For women in the middle of their hot flash years—along with the 10 percent of menopausal women who continue to experience them—there are treatments. 

Estrogen-based hormone therapy can help, but not every woman, including those with a history of blood clots or breast cancer, can take hormone therapy. 

Fortunately, researchers’ new understanding about the role of KNDy neurons has allowed for new treatments that block the brain signals that trigger hot flashes in the first place. The FDA approved a new drug called Veozah (it’s chemical name is fezolinetant) in 2023. It targets the neurokinin 3 receptor, which plays a key role in regulating body temperature. 

Lynkuet, another drug (with the chemical name elinzanetant), came along in 2025. It blocks both the neurokinin 1 and neurokinin 3 receptors, interrupting the process that triggers hot flashes at two points instead of one. 

Other medications can also provide relief, though weren’t originally developed for hot flashes, Christmas says. Some SSRIs and SNRIs; gabapentin, a neurologic medication; and oxybutynin, used for overactive bladder, are all used off-label for hot flashes and night sweats. 

Cognitive behavioral therapy and hypnosis also have been shown to reduce hot flashes. “I’m menopausal, too, so I know if I’m under a lot of stress or in a stressful situation, I’m going to probably have more hot flashes than not,” Christmas says. 

“So there’s certainly something about being able to calm our central nervous system down that seems to have an impact, too.”

If you’re struggling with hot flashes, Christmas recommends seeing your healthcare provider for help. Treatments are available. What’s more, in some cases, hot flashes or night sweats could signal other issues, including thyroid disorders, cancer, and infections, among others. 

But bottom line, when it comes to hot flashes, you don’t have to sweat them out.

In Ask Us Anything, Popular Science answers your most outlandish, mind-burning questions, from the everyday things you’ve always wondered to the bizarre things you never thought to ask. Have something you’ve always wanted to know? Ask us.

The post What happens inside your body during a hot flash appeared first on Popular Science.

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