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Most children who receive pocket money have no idea how to manage it as they have never been taught financial literacy. However, the existing literature does not focus on the level of financial education and guidance children receive or the degree to which parents supervise their children in making decisions about pocket money. This research aims to fill the gap. This study focuses on the financial decisions of children aged 12–16, comparing 105 parent–child dyads in which the child gets pocket money to 101 parent–child dyads in which the child does not get pocket money. The study's results demonstrate that, unlike previous studies, getting pocket money has no impact on children's excessive consumption of fast food and sweets, whereas society's impact on children's consumer decisions increases when they are given pocket money. In contrast, if children believe their parents make good financial decisions and if parents share the household financial decisions with them, children will make better financial decisions themselves. In addition, consistent with previous research, girls – more than boys – see themselves as influenced by their friends in the context of consumer decisions and perceive of themselves as excessive consumers. Implications for parents as well as government policy are discussed. [ABSTRACT FROM AUTHOR]

Background: Eosinophilic esophagitis (EoE) is a chronic, food‐driven allergic disease, characterized by eosinophil‐rich inflammation in the esophagus. The histopathological and clinical features of EoE have been attributed to overproduction of the type 2 cytokines IL‐4 and IL‐13, which mediate profound alterations in the esophageal epithelium and neutralizing of their shared receptor component (IL‐4Rα) with a human antibody drug (dupilumab) demonstrates clinical efficacy. Yet, the relative contribution of IL‐4 and IL‐13 and whether the type II IL‐4 receptor (comprised of the IL‐4Rα chain in association with IL‐13Rα1) mediates this effect has not been determined. Methods: Experimental EoE was induced in WT, Il13ra1−/−, and Krt14Cre/Il13ra1fl/fl mice by skin‐sensitized using 4‐ethoxymethylene‐2‐phenyl‐2‐oxazolin (OXA) followed by intraesophageal challenges. Esophageal histopathology was determined histologically. RNA was extracted and sequenced for transcriptome analysis and compared with human EoE RNAseq data. Results: Induction of experimental EoE in mice lacking Il13ra1 and in vivo IL‐13 antibody‐based neutralization experiments blocked antigen‐induced esophageal epithelial and lamina propria thickening, basal cell proliferation, eosinophilia, and tissue remodeling. In vivo targeted deletion of Il13ra1 in esophageal epithelial cells rendered mice protected from experimental EoE. Single‐cell RNA sequencing analysis of human EoE biopsies revealed predominant expression of IL‐13Rα1 in epithelial cells and that EoE signature genes correlated with IL‐13 expression compared with IL‐4. Conclusions: We demonstrate a definitive role for IL‐13 signaling via IL‐13Rα1 in EoE. These data provide mechanistic insights into the mode of action of current therapies in EoE and highlight the type II IL‐4R as a future therapeutic target. [ABSTRACT FROM AUTHOR]