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Identifying factors that predict higher levels of children's subjective well-being (SWB) is imperative for practice and policy implications. The current study explored latent subgroups of risks characterized by various dimensions of child well-being and investigated whether the latent risk groups were associated with children's SWB across 16 nations. The moderating role of subjective child rights as a protective factor in the relationship between latent risk profiles and children's SWB was also examined. Data of children aged 12 years from the second wave of the International Survey of Children's Well-Being (N = 19,212) was analyzed. Latent profile analysis was used to identify risk profiles based on children's different risk experiences, and subsequently, multilevel regression analysis was used to identify whether group membership predicted SWB. Five latent profiles were identified: low, moderate, dual, material, and victimization risk groups. Findings revealed the concurrent nature of risks in children's lives, as they are often exposed to deficiencies across multiple domains, rather than just one. Multilevel regression analysis results signified that membership in any risk profile is linked with lower SWB of children when compared to the low risk group and highlighted the significant conditioning role of subjective child rights in the relationship between the risk profiles and SWB. Policymakers should be aware of the co-experience of multiple risk factors and devise policies that meet the needs of various groups of children at risk and advocate children as rights holders to further help children with co-occurring risks attain a higher level of SWB., Author(s): Jisu Park [sup.1] , Hi Jae Jung [sup.2] , Yoonsun Han [sup.3] Author Affiliations: (1) grid.31501.36, 0000 0004 0470 5905, Institute of Social Welfare, Seoul National University, , Seoul, [...]

We examined COVID-19 symptoms and infection rates, disruptions to functioning, and moderators of pandemic response for 620 youth with ADHD and 614 individually matched controls (70% male; M age = 12.4) participating in the Adolescent Brain and Cognitive Development study. There were no group differences in COVID-19 infection rate; however, youth with ADHD were more likely to exhibit COVID-19 symptoms (d = 0.25), greater sleep problems (d = −0.52), fear and negative emotions to infection risk (d = −0.56), trouble with remote learning (d = −0.54), rule-breaking behavior related to COVID-19 restrictions (d = −0.23), family conflict (d = −0.13), and were less prepared for the next school year (d = 0.38). Youth with ADHD were less responsive to protective environmental variables (e.g., parental monitoring, school engagement) during the pandemic and may need more specialized support with return to in-person schooling and daily activities. [ABSTRACT FROM AUTHOR]

Respiratory syncytial virus (RSV) is a leading cause of respiratory tract infections in infants. Macroautophagy/autophagy is a catalytic metabolic process required for cellular homeostasis. Although intracellular metabolism is important for immune responses in dendritic cells, the link between autophagy and immunometabolism remains unknown. Here, we show that the autophagy-related protein ATG5 regulates immunometabolism. Atg5-deficient mouse dendritic cells showed increased CD8A+ T-cell response and increased secretion of proinflammatory cytokines upon RSV infection. Transcriptome analysis showed that Atg5 deficiency alters the expression of metabolism-related genes. Atg5-deficient dendritic cells also showed increased activation of glycolysis and the AKT-MTOR-RPS6KB1 pathway and decreased mitochondrial activity, all of which are cellular signatures for metabolic activation. These cells also showed elevated CD8A+ T-cell priming and surface major histocompatibility complex (MHC) class I expression. Our results suggested that ATG5 regulated host immune responses by modulating dendritic cell metabolism. These findings may help develop potential antiviral therapies that alter host immunity by regulating autophagy and immunometabolism. Abbreviations : 2-DG: 2-deoxyglucose; AAK1: AP2 associated kinase 1; AKT: AKT serine/threonine kinase; AM: alveolar macrophage; ATG: autophagy; ATP: adenosine triphosphate; BAL: bronchoalveolar lavage; BMDC: bone marrow dendritic cell; CSF2/GM-CSF: colony-stimulating factor 2 (granulocyte-macrophage); CTL: cytotoxic T lymphocyte; ELISA: enzyme-linked immunosorbent assay; GFP: green fluorescent protein; GSEA: gene-set enrichment analysis; H-2Db: H-2 class I histocompatibility antigen, D-B alpha chain; H-2Kb: MHC class I H2-K-b; HIF1A: hypoxia-inducible factor 1 alpha; IFNG: interferon-gamma; IL: interleukin; ITGAX: integrin alpha X; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MHC: major histocompatibility complex; MTORC1: mammalian target of rapamycin kinase complex 1; PBS: phosphate-buffered saline; PFU: plaque-forming unit; RLR: retinoic acid-inducible-I-like receptor; ROS: reactive oxygen species; RPMI: Roswell Park Memorial Institute; RPS6KB1/S6K: ribosomal protein S6 kinase, polypeptide 1; RSV: respiratory syncytial virus; Th: T helper; TLR: toll-like receptor; Treg: regulatory T cells; UMAP: uniform manifold approximation and projection. [ABSTRACT FROM AUTHOR]