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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. [ABSTRACT FROM AUTHOR]

Glioblastoma is characterized by diffuse infiltration into the normal brain. Invasive glioma stem cells (GSCs) are an underlying cause of treatment failure. Despite the use of multimodal therapies, the prognosis remains dismal. New therapeutic approach targeting invasive GSCs is required. Here, we show that neural stem cells (NSCs) derived from CRISRP/Cas9‐edited human‐induced pluripotent stem cell (hiPSC) expressing a suicide gene had higher tumor‐trophic migratory capacity compared with mesenchymal stem cells (MSCs), leading to marked in vivo antitumor effects. High migratory capacity in iPSC‐NSCs was related to self‐repulsive action and pathotropism involved in EphB‐ephrinB and CXCL12‐CXCR4 signaling. The gene insertion to ACTB provided higher and stable transgene expression than other common insertion sites, such as GAPDH or AAVS1. Ferroptosis was associated with enhanced antitumor immune responses. The thymidylate synthase and dihydroprimidine dehydrogenase expressions predicted the treatment efficacy of therapeutic hiPSC‐NSCs. Our results indicate the potential benefit of genome‐edited iPS cells based gene therapy for invasive GSCs. Furthermore, the present research concept may become a platform to promote clinical studies using hiPSC. [ABSTRACT FROM AUTHOR]

Although neural stem/progenitor cells derived from human induced pluripotent stem cells (hiPSC-NS/PCs) are expected to be a cell source for cell-based therapy, tumorigenesis of hiPSC-NS/PCs is a potential problem for clinical applications. Therefore, to understand the mechanisms of tumorigenicity in NS/PCs, we clarified the cell populations of NS/PCs. We established single cell-derived NS/PC clones (scNS/PCs) from hiPSC-NS/PCs that generated undesired grafts. Additionally, we performed bioassays on scNS/PCs, which classified cell types within parental hiPSC-NS/PCs. Interestingly, we found unique subsets of scNS/PCs, which exhibited the transcriptome signature of mesenchymal lineages. Furthermore, these scNS/PCs expressed both neural (PSA-NCAM) and mesenchymal (CD73 and CD105) markers, and had an osteogenic differentiation capacity. Notably, eliminating CD73+ CD105+ cells from among parental hiPSC-NS/PCs ensured the quality of hiPSC-NS/PCs. Taken together, the existence of unexpected cell populations among NS/PCs may explain their tumorigenicity leading to potential safety issues of hiPSC-NS/PCs for future regenerative medicine. A single cell-based approach to characterize human induced pluripotent stem cells resistant to differentiation finds cellular properties of neural and mesenchymal origins, pointing at underlying causes for undesired grafts after transplantation. [ABSTRACT FROM AUTHOR]

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, Introduction Numerous studies (1-18) have indicated that a variety of treatments, such as administration of antibodies against myelin-associated neurite growth inhibitors (4, 5, 16) and neurotrophic factors (12, 13), can [...]

Notch signaling plays various key roles in cell fate determination during CNS development in a context-dependent fashion. However, its precise physiological role and the localization of its target cells remain unclear. To address this issue, we developed a new reporter system for assessing the RBP-J-mediated activation of Notch signaling target genes in living cells and tissues using a fluorescent protein Venus. Our reporter system revealed that Notch signaling is selectively activated in neurosphere-initiating multipotent neural stem cells in vitro and in radial glia in the embryonic forebrain in vivo. Furthermore, the activation of Notch signaling occurs during gliogenesis and is required in the early stage of astroglial development. Consistent with these findings, the persistent activation of Notch signaling inhibits the differentiation of GFAP-positive astrocytes. Thus, the development of our RBP-J-dependent live reporter system, which is activated upon Notch activation, together with a stage-dependent gain-of-function analysis allowed us to gain further insight into the complexity of Notch signaling in mammalian CNS development. Keywords: Notch; Hes1; RBP-J; Neural stem ceil; Neural progenitors; Astrocyte; EGFP; Venus; Self-renewal; Gliogenesis

Objective. To examine factors associated with the phenomenon of yonaki, or sleep-related nighttime crying (SRNC), in Japanese children Methods. A cross-sectional design incorporating parental self-report was used to investigate relationships between developmental, psychologic, and constitutional/ physiological factors in the incidence of SRNC. Participants were the parents of 170 infants, 174 toddlers, and 137 children at a well-infant clinic in Tokyo, Japan. Results. The lifetime incidence rates of SRNC were 18.8% (infants), 64.9% (toddlers), and 59.9% (children). At all ages, children were most likely to cosleep with their parents; however, infants with reported SRNC were found to cosleep more frequently, whereas infants without SRNC were more likely to sleep in separate, child-dedicated beds. Toddlers with frequent SRNC were more likely to have irregular bedtimes and to have nonparental day care than were those without SRNC. Preschoolers who typically slept 9.5 to 10.5 hours per night were less likely to report SRNC than were children with longer or shorter nighttime sleep durations. In all groups, children with frequent SRNC were more likely to suffer from chronic eczema, and toddlers and preschoolers with SRNC exhibited bruxism more frequently. Conclusions. The traditional Japanese arrangement of cosleeping represents an environment in which parents are readily accessible to children during waking episodes. Physical proximity to the parents in infancy, but not at other ages, is associated with SRNC. The higher incidence of bruxism, chronic eczema, and day care use among children with frequent SRNC supports the hypothesis that nighttime anxiety may promote SRNC. Pediatrics 2005;115:217-224; sleep-related childhood nighttime crying, night waking, cosleeping, nighttime anxiety, day care, bruxism, infant, children., ABBREVIATIONS. SRNC, sleep-related nighttime crying; GA, gestational age. In Japanese, sleep-related nighttime crying (SRNC) is called yonaki, yo- meaning night and -naki meaning crying. SRNC occurs most often after midnight, [...]