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Sleep is one of the basic physiological processes for human survival. Both sleep quantity and sleep quality are fundamental components of sleep. This review looks at both sleep quantity and sleep quality, considering how to manage the complex but probably unavoidable physiological phenomenon of sleep. The need for sleep has marked variations between individuals, in addition to the effects of variable conditions. Studies on sleep quality started later than those on sleep quantity, beginning in 1989 when Ford and Kamerow revealed that insomnia increases the risk of psychiatric disorders. According to the nationwide research team on the quality of sleep (19FA0901), sleep quality is superior to sleep quantity as an index for assessing sleep, and that restfulness obtained through sleep is a useful index for assessing sleep quality. We should pay more attention to obtaining sleep of good quality (restfulness, no sleepiness, no need for more sleep, sufficient objective sleep depth, etc.), although there have not been enough studies on the associations between sleep quality and health or disorders in children and adolescents. Further studies using the deviation from an individual’s optimal sleep quantity may show us another aspect of the effects of sleep quantity on various life issues.

A significant number of adolescents experience sleepiness, primarily due to sleep deprivation. The detrimental effects of inadequate sleep on both physical and mental health are well documented, particularly during adolescence—a critical developmental stage that has far-reaching implications for later life outcomes. The International Classification of Diseases 11th Revision recently introduced the disorder termed ‘insufficient sleep syndrome,’ characterized by a persistent reduction in sleep quantity. However, diagnosing this condition based solely on sleep duration is challenging due to significant individual variation in what constitutes optimal sleep. Despite this, managing sleep debt remains difficult without a clear understanding of individual optimal sleep needs. This review aims to reassess recommended sleep durations, with a focus on enhancing sleep literacy. Beginning with an exploration of insufficient sleep syndrome, this review delves into research on optimal sleep duration and examines foundational studies on sleep debt’s impact on the developing brain. Finally, it addresses the challenges inherent in sleep education programs from the perspective of sleep literacy. By doing so, this review seeks to contribute to a deeper understanding of the chronic sleep debt issues faced by adolescents, particularly those affected by insufficient sleep syndrome.

In this Special Issue of Children, entitled \"Insufficient Sleep Syndrome in Children and Adolescents\", recent advances in pediatric sleep medicine are explored through several diverse and thought-provoking perspectives on insufficient sleep syndrome (ISS) across developmental stages and clinical contexts [...].

This narrative review examines the issue of sleep deprivation among children and adolescents in Japan, exploring its cultural origins and evaluating the current state of sleep education and interventions. It emphasizes the profound influence of the Bushidō spirit, with its focus on self-sacrifice and asceticism, as a core factor in the undervaluation of sleep in Japanese society. While educational initiatives and interventions highlighting the importance of sleep exist, significant limitations remain in improving sleep habits. Sleep deprivation continues to affect children and adolescents, despite its considerable impact on mental health and academic performance. This review presents a method for personalized sleep duration estimation and assesses its potential impact on improving sleep health by using optimal sleep duration calculations. The review also proposes practical steps to improve sleep duration through individualized strategies, integrating cultural context to mitigate the serious health risks associated with insufficient sleep. Ultimately, it underscores the need for targeted strategies to improve sleep among children and adolescents—particularly through personalized optimal sleep duration estimation—while advocating for a shift in cultural perspective beyond self-sacrifice and asceticism. The review highlights the importance of cultural transformation and suggests future research directions and practical applications.

Sleep quality is difficult to define objectively [...]

Letter to the Editor General Pediatrics

Mutations in the ATRX genes cause alpha-thalassemia X-linked intellectual disability (ATR-X) syndrome. Here, we show that ATRX influences the fate of human neural progenitor cells (hNPCs) by forming condensates through liquid-liquid phase separation (LLPS). The intrinsically disordered region (IDR) of ATRX is essential for LLPS and enables ATRX to form dynamic condensates that recruit co-activators. These condensates are necessary for ATRX localization at super-enhancers (SEs) in hNPCs, linking its compartmentalization to transcriptional regulation. Disruption of ATRX condensates alters gene expression and impairs neuronal differentiation. Our findings support a model in which ATRX phase separation regulates gene networks required for hNPC identity. These findings extend current understanding of ATRX function beyond its roles in chromatin structure and suggest that LLPS is a key regulatory mechanism by which ATRX supports neurodevelopment. This study opens avenues for further investigation into how dysregulation of ATRX and its phase-separation ability may contribute to the pathogenesis of ATR-X syndrome and related neurodevelopmental disorders. Tomooka et al . demonstrate that phase-separated ATRX condensates play an essential role in maintaining human neural progenitor identity through chromatin regulation and transcriptional control.

The body's capacity to restore damaged neural networks in the injured CNS is severely limited. Although various treatment regimens can partially alleviate spinal cord injury (SCI), the mechanisms responsible for symptomatic improvement remain elusive. Here, using a mouse model of SCI, we have shown that transplantation of neural stem cells (NSCs) together with administration of valproic acid (VPA), a known antiepileptic and histone deacetylase inhibitor, dramatically enhanced the restoration of hind limb function. VPA treatment promoted the differentiation of transplanted NSCs into neurons rather than glial cells. Transsynaptic anterograde corticospinal tract tracing revealed that transplant-derived neurons reconstructed broken neuronal circuits, and electron microscopic analysis revealed that the transplant-derived neurons both received and sent synaptic connections to endogenous neurons. Ablation of the transplanted cells abolished the recovery of hind limb motor function, confirming that NSC transplantation directly contributed to restored motor function. These findings raise the possibility that epigenetic status in transplanted NSCs can be manipulated to provide effective treatment for SCI.

Bone marrow endothelial cells (BMECs) play a key role in bone formation and haematopoiesis. Although recent studies uncovered the cellular taxonomy of stromal compartments in the bone marrow (BM), the complexity of BMECs is not fully characterized. In the present study, using single-cell RNA sequencing, we defined a spatial heterogeneity of BMECs and identified a capillary subtype, termed type S (secondary ossification) endothelial cells (ECs), exclusively existing in the epiphysis. Type S ECs possessed unique phenotypic characteristics in terms of structure, plasticity and gene expression profiles. Genetic experiments showed that type S ECs atypically contributed to the acquisition of bone strength by secreting type I collagen, the most abundant bone matrix component. Moreover, these cells formed a distinct reservoir for haematopoietic stem cells. These findings provide the landscape for the cellular architecture in the BM vasculature and underscore the importance of epiphyseal ECs during bone and haematopoietic development. Iga et al. perform single-cell RNA sequencing and identify a distinct bone marrow endothelial cell subtype that contributes to the acquisition of bone strength and offers a distinct haematopoietic stem cell niche.

Chronic complete spinal cord injury (SCI) is difficult to treat because of scar formation and cavitary lesions. While human iPS cell-derived neural stem/progenitor cell (hNS/PC) therapy shows promise, its efficacy is limited without the structural support needed to address cavitary lesions. Our study investigated a combined approach involving surgical scar resection, decellularized extracellular matrix (dECM) hydrogel as a scaffold, and hNS/PC transplantation. To mitigate risks such as prion disease associated with spinal cord-derived dECM, we used kidney-derived dECM hydrogel. This material was chosen for its biocompatibility and angiogenic potential. In vitro studies with dorsal root ganglia (DRG) confirmed its ability to support axonal growth. In a chronic SCI rat model, scar resection enhanced the local microenvironment by increasing neuroprotective microglia and macrophages, while reducing inhibitory factors that prevent axonal regeneration. The combination of scar resection and dECM hydrogel further promoted vascular endothelial cell migration. These changes improved the survival of transplanted hNS/PCs and facilitated host axon regeneration. Overall, the integrated approach of scar resection, dECM hydrogel scaffolding, and hNS/PC transplantation has been proven to be a more effective treatment strategy for chronic SCI. However, despite histological improvements, no functional recovery occurred and further research is needed to enhance functional outcomes.