
Background:Prolonged stress during pregnancy is associated with various neurodevelopmental abnormalities and an increased risk of neurological disorders. Although prenatal stress is implicated in altered brain development, its contribution to infant seizures remains unclear. Specifically, the effects of prolonged prenatal stress on seizure susceptibility and the mechanisms underlying this association remain unclear. Purpose:Infantile spasms, also known as West syndrome, are age-specific epileptic seizures. Most affected patients exhibit signs of delayed development. Using a pharmacologically induced N-methyl-D-aspartate (NMDA)-induced spasm-like seizure model, this study aimed to determine whether long-term prenatal stress increases susceptibility to these spasm-like events and examine the associated changes in glial activation and gamma-aminobutyric acid (GABA)ergic signaling. Methods:Pregnant Sprague-Dawley rats were subjected to acute immobilization stress (AIS; single 45-min restraint on gestational day 15) or chronic immobilization stress (CIS; daily 2-hour restraint on gestational days 15-19). Their offspring were assigned to the control, AIS, and CIS groups. NMDA (15 mg/kg, intraperitoneal) was administered to the resulting offspring on postnatal day 15, and spasm-like behavior was scored 75 minutes after the injection by an observer blinded to the group assignment. Immunohistochemical, quantitative reverse transcription polymerase chain reaction, and Sholl analyses were performed to assess glial activation and GABA-related protein expression. Results:We observed that exposure to long-term prenatal stress increased spasm frequency and decreased latency to spasm onset compared to exposure to short-term prenatal stress. Prenatal immobilization stress increased seizure susceptibility to NMDA-triggered spasms on postnatal day 15 and markedly increased microglial activation in the hippocampus. These findings were observed in acute and CIS models and were accompanied by increased microglial and astrocyte activation and decreased GAD67 expression. Conclusion:Long-term prenatal stress, particularly CIS, enhances susceptibility to NMDA-induced spasm-like seizures and is associated with enhanced glial activation and altered GABAergic signaling. As the present findings are associative, further studies are needed to determine whether neuroinflammation and GABAergic dysfunction causally contribute to the increased susceptibility.
The rapid integration of electronic media into daily life has transformed early childhood experiences worldwide. While digital technology offers opportunities for learning, communication, and entertainment, concerns persist regarding its impact on neurodevelopment during the critical early years of life. This narrative review synthesizes current evidence on the association between electronic media exposure and neurodevelopmental outcomes in children under 5 years of age. The literature search of PubMed, Embase, Scopus, Web of Science, and the Cochrane Library identified 21 original studies, 12 review articles (systematic reviews/meta-analyses, scoping reviews, and narrative reviews), and 4 international guidelines/recommendations, which were included in the narrative synthesis. Evidence related to cognitive, language, motor, behavioral, socioemotional development, sleep, and neuroimaging findings was critically reviewed. Overall, excessive and early screen exposure was associated with language delays, impaired attention and executive functioning, socioemotional difficulties, sleep disturbances, and reduced motor activity. Sleep disruption, including shorter sleep duration and delayed sleep onset, may represent an important pathway linking excessive media use with adverse neurodevelopmental outcomes. Neuroimaging studies also suggest reduced white matter integrity in language-related brain pathways, providing biological plausibility for these associations.Developmental outcomes were influenced by parental mediation, content quality, socioeconomic factors, and increased screen exposure during the coronavirus disease 2019 pandemic. Current guidelines from the American Academy of Pediatrics, World Health Organization, and Indian Academy of Pediatrics recommend limiting screen exposure and promoting caregiver-supervised, developmentally appropriate media use. Excessive and unsupervised electronic media use may adversely affect multiple domains of neurodevelopment, particularly when it replaces interactive play, caregiver engagement, and healthy sleep. Further longitudinal studies incorporating objective measures of media exposure, sleep assessment, and neuroimaging are needed to strengthen current evidence and guide pediatric recommendations.
Children with tracheostomy and home ventilation are vulnerable to rapidly evolving airway and equipment emergencies after discharge. Health literacy in this setting is the functional capacity to access, understand, appraise, communicate, and apply child-specific information under stress. This narrative review synthesizes health-literacy literature, American Thoracic Society (ATS) guidance, caregiver education and simulation studies, outpatient emergency-knowledge studies, and health-system data to address the implementation gap between guideline-concordant discharge education and reliable caregiver action. The evidence is heterogeneous and largely observational or based on small educational interventions. In one cohort of 92 children, 44% had an Emergency Department visit with hospital admission within 90 days of discharge, 36% of which were tracheostomy- or respiratory-related. In an outpatient study of 52 caregivers, only 46.2% answered all 3 tracheostomy-emergency scenarios correctly, while 80% reported at least one tracheostomy-related emergency after discharge. We propose an author-derived 6-domain framework-baseline recognition, airway, ventilator/equipment, emergency action, communication, and system navigation-developed by mapping multidimensional health-literacy constructs, ATS safety recommendations, and recurrent caregiver tasks in pediatric tracheostomy/home-ventilation literature. Educational strategies include staged multimodal teaching, teach-back and show-back, simulation, mastery-oriented assessment, and longitudinal reassessment. Korean data illustrate how workforce, geography, and home-care organization modify implementation, but the framework is intended to be adaptable across healthcare systems. Health literacy should be treated as a safety capacity that connects guideline-defined structures to observable caregiver performance.
The incidence of pediatric inflammatory bowel disease (PIBD) has risen worldwide, creating significant challenges for healthcare professionals. Compared with adult-onset inflammatory bowel disease, PIBD often presents with more extensive intestinal involvement, a more aggressive course, and complications affecting growth and puberty, making timely disease control critical for PIBD. However, treatment selection remains largely empirical, and many patients fail to respond to initial therapy. Additionally, conventional experimental models, including 2-dimensional cell culture and animal systems, often fail to reproduce the complexities of human intestinal tissues. These limitations highlight the need for human-relevant experimental platforms capable of capturing patient-specific disease biology and supporting precise therapeutic decision-making in PIBD. In this context, patient-derived intestinal organoids have emerged as valuable tools for studying disease mechanisms and evaluating therapeutic responsiveness in patients with PIBD. Organoid-based systems enable direct investigations of epithelial barrier dysfunction, inflammatory signaling, metabolic alterations, and genotype-associated molecular features that provide insight into tissue-level disease heterogeneity. Emerging data suggest that ex vivo drug responses observed in patient-derived intestinal organoids may parallel clinical treatment outcomes, indicating their potential to support more informed therapy selection in PIBD. Despite these advances, current organoid models have important limitations including the absence of immune, stromal, and vascular components as well as challenges related to standardization, scalability, and cost-effectiveness. To overcome these limitations, next-generation platforms incorporating immune cell coculture systems, microbiota, and microfluidic technologies are being developed to better replicate the complexity of the host intestinal microenvironment. As these integrated systems evolve, intestinalorganoids are expected to become increasingly powerful tools for disease modeling, biomarker discovery, and therapeutic response prediction, ultimately supporting the development of personalized and effective treatment strategies for PIBD.