Bronchopulmonary dysplasia arises when premature infants, often requiring prolonged oxygen therapy and mechanical ventilation, experience disrupted lung development, leading to chronic respiratory issues. These infants face not only physical challenges but also risk impairments in brain development, manifesting as cognitive delays, motor dysfunctions, and behavioral abnormalities. While previous studies have noted cognitive deficits associated with BPD presence, an understanding of how the severity of BPD influences the spectrum of neurodevelopmental outcomes has remained elusive—until now.

The research team hypothesized that as BPD severity escalates, so too does the risk of neurodevelopmental disorders. To test this, they analyzed a robust cohort of preterm infants stratified by standardized severity metrics of BPD—mild, moderate, and severe. By using comprehensive neurodevelopmental assessments conducted longitudinally, the study was able to meticulously track the progression and emergence of developmental anomalies against the backdrop of respiratory health status. This approach allowed for a granular understanding of the nuanced interplay between lung pathology and brain development.

Their findings reveal a striking dose-response relationship: infants classified with severe BPD exhibited substantially higher incidences of neurodevelopmental diagnoses compared to those with milder forms or no BPD at all. These disorders encompass a broad range of cognitive, motor, and behavioral impairments including attention deficit hyperactivity disorder (ADHD), autism spectrum disorders (ASD), and global developmental delays. This discovery underscores the importance of considering BPD beyond pulmonary outcomes, positioning it as a critical determinant of long-term neurological health.

Delving into the mechanistic underpinnings, the study discusses how chronic hypoxia, prolonged inflammation, and oxidative stress—hallmarks of severe BPD—may disrupt critical periods of neurogenesis and synaptic pruning in the developing brain. These pathophysiological processes can interrupt the establishment of vital neural circuits, thereby predisposing infants to cognitive and functional deficits. Furthermore, the frequent need for invasive respiratory support in severe BPD cases may compound brain injury through hemodynamic instability and inflammatory cascades.

An essential aspect of this study is the emphasis on early identification and intervention. By recognizing the direct correlation between BPD severity and NDD risk, clinicians can prioritize neurological monitoring alongside respiratory care in high-risk infants. The research advocates for integrating neurodevelopmental evaluations into routine follow-up protocols for infants diagnosed with moderate to severe BPD, enabling earlier therapeutic strategies to mitigate or ameliorate the impacts of neurodevelopmental disorders.

Technological advances in neuroimaging and biomarker discovery may also play a pivotal role in future approaches. The study highlights the potential for employing advanced MRI techniques to detect subtle brain abnormalities in BPD-affected infants, thereby refining prognostic assessments. Meanwhile, the quest for specific inflammatory or metabolic biomarkers could revolutionize screening, allowing for personalized medicine paradigms tailored to the individual risk profile conferred by BPD severity.

The implications of this research ripple beyond the clinical domain into public health policy and resource allocation. Given the increasing survival rates of extremely preterm infants due to advancements in neonatal care, the burden of chronic morbidities such as BPD and its neurological sequelae is poised to rise. As such, health systems worldwide must brace for a surge in demands for multidisciplinary interventions combining pulmonology, neurology, and developmental pediatrics—a call-to-action underscored by this compelling evidence.

Moreover, the study contributes to the urgent dialogue surrounding the optimization of neonatal intensive care practices. It suggests that minimizing invasive ventilation duration and adopting gentler respiratory support modalities may reduce BPD severity, thereby indirectly mitigating neurodevelopmental risks. This aligns with emerging paradigms focusing on neuroprotective strategies during the critical neonatal window, including caffeine therapy, erythropoietin administration, and targeted oxygen saturation protocols.

This research also fuels an ongoing debate about the precise mechanisms linking pulmonary pathology to brain development. While the inflammatory hypothesis stands prominent, alternative theories propose that shared genetic susceptibilities or environmental exposures such as prenatal infections may simultaneously predispose infants to BPD and NDD. Future investigations building upon this foundational work aim to disentangle these intertwined etiologies to develop more effective preventative and therapeutic interventions.

Importantly, the broad neurodevelopmental spectrum associated with BPD severity reported in this study calls for a holistic view of infant health. Neurodevelopmental disorders manifest variably, affecting speech, motor skills, cognition, and social interactions. Therefore, multidisciplinary rehabilitation programs encompassing physical therapy, speech-language pathology, and behavioral support must be integral components of post-discharge care for infants with significant BPD.

The study’s methodological rigor, employing prospective designs and validated neurodevelopmental instruments, strengthens the validity of its conclusions. However, the authors acknowledge limitations including potential confounders such as socioeconomic status and coexisting morbidities like intraventricular hemorrhage, which also influence developmental trajectories. Future multi-center studies with larger samples and more diverse populations are encouraged to confirm and expand upon these findings.

In sum, this pivotal research revolutionizes the understanding of bronchopulmonary dysplasia by illuminating its direct relationship with neurodevelopmental disorders in a severity-dependent manner. It calls for a paradigm shift in neonatal care where respiratory outcomes are no longer viewed in isolation but recognized as part of a complex interplay impacting lifelong neurological health. This fresh insight opens new avenues for early detection, intervention, and ultimately improved quality of life for vulnerable preterm infants.

As scientific communities and clinicians digest these findings, the quest continues to unravel the nuanced crosstalk between underdeveloped lungs and immature brains. The hope is that through integrated research, precision medicine, and compassionate care, the shadow of bronchopulmonary dysplasia on neurodevelopmental futures can be significantly diminished, offering new horizons of health and potential for the tiniest patients.

Subject of Research: The association between bronchopulmonary dysplasia severity and neurodevelopmental disorders in preterm infants

Article Title: The association between bronchopulmonary dysplasia severity and neurodevelopmental disorders

Article References:
Rueff, D.A., Gee, J., Ruddy-Humphries, A. et al. The association between bronchopulmonary dysplasia severity and neurodevelopmental disorders. J Perinatol (2026). https://doi.org/10.1038/s41372-025-02372-4

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DOI: 10.1038/s41372-025-02372-4

Retinopathy of prematurity is a vasoproliferative disorder primarily affecting the immature retinal vasculature in preterm infants. It is a leading cause of childhood blindness worldwide, driven by a complex interplay of oxygen regulation, vascular growth factors, and systemic physiological stressors. While antecedent research has separately implicated elevated NRBC counts and RBC transfusions as potential risk factors for ROP development, integrating these parameters represents a significant advancement in understanding ROP pathogenesis.

NRBCs are immature erythroid precursors that typically diminish to negligible levels by term gestation but may surge in response to intrauterine hypoxia or stress. Elevated NRBC counts at birth serve as biomarkers of fetal hypoxia and stress, conditions thought to contribute to microvascular dysregulation in the retina. The current study provides compelling evidence linking higher NRBC counts at birth to increased susceptibility to ROP, reinforcing the hypothesis that prenatal hypoxic exposure primes the retina for aberrant neovascularization postnatally.

Equally consequential is the study’s illumination of the role of RBC transfusions. Preterm neonates frequently receive RBC transfusions to counteract anemia of prematurity, but the implications of transfusion volume for ROP risk have been ambiguous. The investigation reveals a dose-dependent relationship whereby larger volumes of RBC transfusions correlate with heightened ROP incidence. This suggests that beyond the intrinsic anemia, exogenous manipulation of circulating red cells impacts retinal angiogenesis, possibly through altered oxygen delivery dynamics or inflammatory responses.

The novelty of this research lies in its simultaneous evaluation of NRBC counts and RBC transfusion volumes within the same cohort, enabling a more granular analysis of their combined effects on ROP risk. The study employed robust statistical models to dissect the independent and interactive contributions of these hematologic factors, accounting for confounders such as gestational age, birth weight, and oxygen supplementation status. This methodological rigor enhances the reliability of the conclusions and sets a benchmark for future investigations.

From a mechanistic standpoint, the findings spotlight the role of perinatal hypoxia as a critical initiator of pathological retinal changes, with NRBC counts serving as a proxy for the degree of hypoxic insult. The subsequent administration of RBC transfusions, although life-saving, may exacerbate oxidative stress or disrupt delicate angiogenic signaling pathways, thereby compounding the risk initiated in utero. This dual-hit paradigm offers a plausible explanatory model integrating prenatal and postnatal factors.

Clinically, these insights carry profound implications. Neonatologists and ophthalmologists must consider the prognostic value of NRBC counts at birth when stratifying ROP risk and tailoring surveillance protocols. Furthermore, optimization of transfusion practices—balancing the necessity to correct anemia with minimizing excess transfusion volumes—emerges as a critical component of ROP prevention. The study advocates for the development of nuanced transfusion guidelines informed by hematologic biomarkers, aligning therapeutic interventions with individualized risk profiles.

This research also calls attention to the broader context of neonatal hematologic management. The interplay between erythropoiesis, oxygen delivery, and vascular development is evidently complex and tightly regulated. Disruptions in this equilibrium, whether from fetal hypoxia or medical interventions, can precipitate cascading effects on organ systems beyond the retina. An integrated approach considering systemic hematologic health may therefore improve outcomes across multiple domains.

Future research building on these findings could explore the molecular mediators that link NRBC elevation and transfusion exposure to retinal vascular pathology. Potential targets include hypoxia-inducible factors, vascular endothelial growth factor signaling, and inflammatory cytokine cascades. Elucidating these pathways could foster the development of targeted therapeutics aimed at mitigating ROP without compromising essential hematologic support.

There is also scope for investigating the timing and thresholds of transfusion interventions in relation to NRBC counts and other biomarkers. Precision medicine approaches leveraging real-time hematologic monitoring could inform safer transfusion strategies, ultimately reducing the incidence and severity of ROP. Additionally, longitudinal studies assessing how early hematologic parameters relate to long-term visual and neurodevelopmental outcomes would enrich our understanding of the broader impact.

The novel utilization of NRBC counts as a predictive marker emphasizes the potential utility of routine blood panels taken at birth to guide neonatal intensive care management. Incorporating NRBC quantification into standard assessments could pave the way for early identification of infants at risk and proactive clinical decision-making. This could revolutionize current neonatal protocols, ushering in an era where hematologic biomarkers guide preventive ophthalmic interventions.

Overall, this pioneering study by Zeiler et al. not only advances the scientific understanding of ROP pathophysiology but also provides actionable insights with real-world clinical relevance. It underscores the importance of a multifactorial perspective, drawing connections between prenatal stress markers and postnatal therapeutic exposures to better predict and prevent debilitating outcomes. The implications for improving neonatal care are profound, promising to reduce the burden of blindness associated with prematurity.

As neonatal intensive care continues to evolve, harmonizing efforts between hematologists, neonatologists, and ophthalmologists will be vital. Collaborative protocols integrating NRBC assessments and judicious transfusion management could become standard practice, informed by the rigorous evidence emerging from this study. Such interdisciplinary strategies embody the future of personalized neonatal medicine, aimed at safeguarding visionary potential from the very first moments of life.

This research also exemplifies the value of comprehensive cohorts and multifaceted analytic frameworks in uncovering subtle yet clinically critical interactions. The sophisticated approach taken here illustrates how revisiting established risk factors in conjunction can yield novel insights with direct translational implications. As a result, it sets a new paradigm for neonatal research methodology, combining biomarker evaluation with therapeutic exposure analysis.

In conclusion, the simultaneous examination of the nucleated red blood cell count at birth and the volume of red cell transfusions represents a leap forward in understanding and mitigating retinopathy of prematurity risk. The study’s revelations not only spotlight actionable biomarkers and modifiable risk factors but also inspire a reevaluation of neonatal transfusion practices. These findings have the potential to catalyze meaningful reductions in ROP-related blindness worldwide, transforming neonatal outcomes through refined, biomarker-driven care strategies.

Subject of Research: The impact of nucleated red blood cell count at birth and red blood cell transfusion volume on the risk of developing retinopathy of prematurity (ROP) in preterm infants.

Article Title: The nucleated red blood cell count at birth, the volume of red cell transfusions received, and the risk of developing retinopathy of prematurity

Article References:
Zeiler, B., Bahr, T.M., Esplin, S.D. et al. The nucleated red blood cell count at birth, the volume of red cell transfusions received, and the risk of developing retinopathy of prematurity. J Perinatol (2025). https://doi.org/10.1038/s41372-025-02519-3

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DOI: 26 November 2025

The study, recently published in the Journal of Perinatology, represents one of the most comprehensive epidemiological investigations into infection exposure and antibiotic treatment among neonates with CDH. Spearheaded by S.J. Flohr and colleagues, this research utilized an extensive cohort, employing meticulous data collection that spanned multiple institutions to capture a holistic picture of infection trends and antimicrobial interventions in this fragile patient population. The results not only underscore the complexity of managing infections in CDH newborns but also highlight the urgent need for refined therapeutic protocols tailored to their unique immunological and physiological profiles.

Congenital diaphragmatic hernia impacts the delicate balance of neonates’ respiratory and gastrointestinal function, often necessitating immediate surgical correction and intensive supportive care. However, the innate vulnerability of these newborns, characterized by compromised pulmonary development and frequent invasive procedures, predisposes them to a spectrum of infections ranging from early-onset sepsis to late nosocomial pathogen colonization. Within this clinical backdrop, antibiotic exposure becomes almost inevitable yet remains a double-edged sword. The study carefully quantifies how such exposure correlates with infection rates, antibiotic resistance emergence, and long-term outcomes.

One of the key findings of the research pertains to the timeline and nature of infections in CDH newborns. The authors reveal a nuanced infection chronology, with early infections primarily driven by vertical transmission or immediate postnatal environmental exposure, thus implicating perinatal management strategies as critical determinants of infection risk. Contrastingly, late infections tend to reflect hospital-acquired pathogens, underscoring the significance of infection control policies within neonatal intensive care units (NICUs). The differentiation between early and late infections informs clinicians about the timing of prophylactic antibiotic use, a topic that elicits considerable debate.

Antibiotic stewardship emerges as a central theme throughout the study. While empirical antibiotic therapy is common practice in the face of suspected infections, indiscriminate use can escalate the risk of antibiotic resistance and disturb the neonate’s developing microbiome. Flohr and colleagues raise pertinent concerns about the balance between adequately treating potential infections and minimizing unnecessary antibiotic exposure. Their epidemiological analysis meticulously documents antibiotic regimens, revealing wide variability in the choice, duration, and intensity of treatment across centers, thereby calling attention to the need for standardized guidelines that can optimize therapeutic outcomes without exacerbating resistance issues.

Technological advancements have enabled the team to leverage state-of-the-art diagnostic tools, combining traditional microbiological cultures with advanced molecular techniques for pathogen identification. This comprehensive approach allowed more accurate delimitation of infectious events and challenged some previously held assumptions about the prevalence and diversity of microbial agents affecting CDH patients. The detection of unexpected viral and fungal pathogens alongside bacteria alters the clinical understanding of infection etiology in this population, indicating the need for broader diagnostic consideration in NICU settings.

Beyond immediate infectious risks, the study explores how antibiotic exposure itself modulates neonatal immune responses. Prolonged or repeated antibiotic courses appear to influence the neonates’ inflammatory profiles and susceptibility to subsequent infections. These findings suggest an immune dysregulation scenario, where the treatment aimed at controlling infections paradoxically predisposes newborns to additional infectious insults or immunological challenges. The authors advocate for further research into immunomodulatory therapies that might complement or replace traditional antibiotic approaches in certain clinical contexts.

Moreover, the research touches upon the long-term implications of antibiotic usage in CDH survivors. Although the neonatal period is critical, the early inflammatory and antimicrobial exposure can have lasting impacts on microbial colonization patterns, allergic sensitization, and chronic respiratory morbidity. By integrating clinical follow-up data, the study provides preliminary evidence linking neonatal antibiotic regimens with developmental trajectories and host-microbiome interactions, emphasizing the profound interconnectedness of early medical management and overall health outcomes.

Another layer of complexity is introduced by the heterogeneity of CDH presentations and associated anomalies. The researchers underscore that infection susceptibility and antibiotic responses are not uniform but instead influenced by factors such as defect size, presence of pulmonary hypertension, and the institution’s clinical protocols. This highlights the importance of individualized care pathways and the potential benefits of predictive models incorporating epidemiological and clinical variables to formulate personalized infection prevention and treatment strategies.

Preventive strategies against infection, gleaned from the epidemiological data, suggest a multipronged approach. Enhancing maternal health and perinatal infection surveillance could reduce early-onset infections, while reinforcing NICU hygiene and cohorting policies may mitigate late infections. The study’s detailed mapping of pathogen prevalence provides a critical resource for optimizing prophylactic antibiotic selection and developing targeted antimicrobial stewardship programs that align with real-world microbial threats encountered in the CDH population.

The authors also advocate collaboration across institutions to facilitate large-scale data sharing, enabling continuous refinement of infection control practices and antibiotic use guidelines. The study sets a precedent for the integration of epidemiological surveillance within newborn surgical care, fostering a learning health system that adapts to emerging resistance patterns and evolving microbial landscapes. Such efforts are pivotal in bridging the gap between bench research and bedside application, ultimately improving survival rates and quality of life for infants suffering from CDH.

Importantly, the study emphasizes that antibiotic stewardship is not just a clinical imperative but an ethical obligation in neonatal care. By balancing the urgency to treat life-threatening infections against the risks of overuse, clinicians can safeguard both individual patients and public health at large. The nuanced insights presented challenge current paradigms and call for dynamic, evidence-based protocols that can be tailored to the specific vulnerabilities inherent to CDH newborns.

This landmark investigation by Flohr et al. ultimately advances our understanding of infection dynamics and antibiotic utilization in a uniquely vulnerable but understudied neonatal population. Through its rigor and scope, the research charts a path toward safer, more effective infection management strategies that may serve as a model for other complex congenital conditions. As neonatal intensive care continues to evolve, such epidemiological insights will be indispensable in optimizing care for our most fragile patients.

By dissecting the epidemiological foundations of infection and treatment in CDH, this study lays critical groundwork for enhanced clinical decision-making and future therapeutic innovation. The findings not only guide immediate clinical practice but also open avenues for translational research into immune modulation, novel antimicrobial agents, and non-antibiotic infection control measures. The study exemplifies the power of interdisciplinary, data-driven approaches to tackling some of neonatology’s most daunting challenges.

In summary, the investigation into antibiotic exposure and infection epidemiology among newborns with congenital diaphragmatic hernia addresses a pivotal gap in neonatal care knowledge. Through comprehensive cohort analysis, the authors elucidate infection timing, pathogen diversity, antibiotic usage patterns, immune impact, and long-term consequences, providing a multifaceted view essential for advancing clinical practice. As the study gains attention within the medical community and beyond, it promises to catalyze improvements in neonatal infection management worldwide, benefitting countless infants and their families.

Subject of Research: Infection epidemiology and antibiotic utilization among newborns with congenital diaphragmatic hernia (CDH).

Article Title: Antibiotic exposure and infection epidemiology among newborns with congenital diaphragmatic hernia.

Article References:

Flohr, S.J., Mathew, L., Hedrick, H.L. et al. Antibiotic exposure and infection epidemiology among newborns with congenital diaphragmatic hernia.
J Perinatol (2025). https://doi.org/10.1038/s41372-025-02389-9

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DOI: https://doi.org/10.1038/s41372-025-02389-9

Preterm Premature Rupture of Membranes refers to the spontaneous breaking of fetal membranes before 37 weeks of gestation and prior to the onset of labor. The condition accounts for nearly 30% of all preterm deliveries, marking it as a critical focus for maternal-fetal medicine and a persistent challenge in obstetrics. While the immediate risks associated with PPROM—such as infection, placental abruption, and preterm labor induction—have been widely studied, the study by Bhullar and colleagues takes an unprecedented approach by exploring its ripple effects on neurodevelopmental outcomes in affected neonates.

Central to their investigation is the premise that disruption of the amniotic sac and ensuing intrauterine environment alterations trigger an inflammatory cascade with profound repercussions on the developing fetal brain. Utilizing advanced neuroimaging techniques alongside longitudinal neurodevelopmental assessments, this research provides compelling evidence that the inflammatory milieu associated with PPROM may lead to subtle yet significant alterations in cortical architecture, connectivity, and ultimately, cognitive and motor functions.

The authors detail how pro-inflammatory cytokines, released during the intra-amniotic infection often secondary to membrane rupture, cross the fetal blood-brain barrier. This biochemical infiltration initiates microglial activation, a cellular immune response within the central nervous system, which, while protective, has been linked to neuropathological changes such as white matter injury and impaired synaptogenesis, critical processes for normal brain maturation. These neuroimmune interactions, the study argues, may underpin the increased incidence of neurodevelopmental disorders observed in the cohort of infants born after PPROM.

Expansion of the sample size and the meticulous stratification of subjects by gestational age allowed the researchers to identify nuanced differences in outcomes based on the timing of membrane rupture. Earlier occurrence of PPROM correlated robustly with more severe neurodevelopmental deficits. Particularly, infants born before 28 weeks demonstrated higher rates of cerebral palsy, cognitive delay, and sensory-processing abnormalities when compared to those whose membranes ruptured nearer to term.

Notably, the research team incorporated state-of-the-art diffusion tensor imaging (DTI) and functional MRI (fMRI) analyses to detect microstructural changes in white matter tracts and alterations in functional connectivity patterns within developing brain networks. This neuroimaging dimension offers a window into the subclinical manifestations of brain injury that standard cranial ultrasounds might overlook. These imaging biomarkers may eventually serve as pivotal tools for early identification of at-risk neonates, enabling timely therapeutic interventions.

In addition to neuroimaging, the longitudinal aspect of the study entailed rigorous neuropsychological evaluations up to the age of five. Emphasizing not only motor skills but language development, executive function, and socio-emotional behavior, the assessments revealed that the impact of PPROM extends beyond physical growth parameters. This revelation urges clinicians to consider extended surveillance and multidisciplinary approaches encompassing pediatric neurology, psychology, and rehabilitation services.

One of the remarkable features of this study is the integration of molecular biology with clinical pediatrics, reflecting a vibrant translational research framework. Genetic analysis of placental tissue samples uncovered potential polymorphisms affecting cytokine regulation, which may confer differential susceptibility to neuroinflammation among infants exposed to PPROM. These findings hold promise for personalized medicine approaches in managing and counseling families facing this high-risk condition.

Furthermore, the investigation revisits longstanding debates regarding the benefit-risk ratios of interventions such as corticosteroid administration and antibiotic therapy in PPROM management. The data suggest that while antenatal corticosteroids remain essential for enhancing pulmonary maturity, their role in modulating neuroinflammatory processes warrants further scrutiny. Similarly, preemptive antibiotic treatment reduces infection risks but may inadvertently influence the fetal microbiome, with yet-unknown implications for neurodevelopment.

The study also shines a light on socioeconomic and environmental factors that may exacerbate or ameliorate the neurodevelopmental trajectory post-PPROM. Maternal stress levels, nutrition, and access to neonatal intensive care significantly influenced the developmental outcomes observed, compelling a holistic view of prevention and care.

In the wider context of preterm birth research, these findings underscore the intricate interplay between obstetric events and lifelong neurological health. The elucidation of mechanisms by which PPROM mediates brain injury invites innovation in both therapeutic targets and clinical protocols, potentially revolutionizing perinatal care. Importantly, the study champions the need for interdisciplinary collaboration and early intervention programs tailored to this vulnerable population.

Looking forward, the authors advocate for expanded multicenter trials to validate their findings across diverse populations and healthcare settings. Additionally, longitudinal tracking into adolescence and adulthood could elucidate the enduring cognitive, behavioral, and psychiatric sequelae attributable to early-life exposure to PPROM. This expanded scope will inform public health strategies aiming not only to improve survival but also quality of life for preterm survivors.

In summary, the seminal work by Bhullar et al. amalgamates cutting-edge neuroimaging, molecular genetics, and clinical evaluation to unravel the profound neurodevelopmental consequences of Preterm Premature Rupture of Membranes. It heralds a paradigm shift in understanding how a seemingly isolated obstetric event orchestrates complex neurobiological cascades, with lifelong ramifications. As neonatal medicine advances into an era of precision diagnostics and personalized therapeutics, this research offers a beacon for enhancing outcomes for some of the most vulnerable members of society.

The implications resonate beyond the academic and clinical realms, highlighting a pressing societal imperative: to invest in research, healthcare infrastructure, and family support systems that together nurture brain development from the earliest moments of life. The journey from membrane rupture to cognitive maturation is fraught with challenges but, armed with such scientific revelations, the medical community is better equipped than ever to chart a hopeful course forward.

Subject of Research: Preterm Premature Rupture of Membranes (PPROM) and its impact on neurodevelopmental outcomes.

Article Title: Preterm Premature Rupture of Membranes (PPROM) and Neurodevelopmental Outcomes.

Article References:
Bhullar, H., Stritzke, A., Makarchuk, S. et al. Preterm Premature Rupture of Membranes (PPROM) and Neurodevelopmental Outcomes. J Perinatol (2025). https://doi.org/10.1038/s41372-025-02360-8

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DOI: https://doi.org/10.1038/s41372-025-02360-8