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Understanding the etiology of violent juvenile offending is critical for prevention and intervention efforts. The risk factors examined included marital status of parents, marital conflict, substance use, age of first substance use, learning difficulties, and school failure. The protective factors assessed included parenting styles, academic achievement, attitudes unfavorable toward violence, having a mentor, positive relationships with peers, and being involved in extracurricular activities. One hundred and twenty-four participants between the ages 14 and 18 years were assessed. A discriminant functions analysis revealed that multiple risk and protective factors were significant in predicting group membership. The nondelinquent group had significantly more protective factors than the other two groups. Significant gender differences were also found.

Highlights d Multi-omics reveals markers of CDI in pediatric IBD patients d Identification of metabolites reveals distinctive features for IBD and CDI d Isocaproyltaurine is made by C. difficile and associates with active IBD d Identifies biomarkers potentially useful for distinguishing disease processes

Gastric carcinogenesis is mediated by complex interactions among Helicobacter pylori , host, and environmental factors. Here, we demonstrate that H . pylori augmented gastric injury in INS-GAS mice under iron-deficient conditions. Mechanistically, these phenotypes were not driven by alterations in the gastric microbiota; however, discovery-based and targeted metabolomics revealed that bile acids were significantly altered in H . pylori –infected mice with iron deficiency, with significant upregulation of deoxycholic acid (DCA), a carcinogenic bile acid. The severity of gastric injury was further augmented when H . pylori –infected mice were treated with DCA, and, in vitro, DCA increased translocation of the H . pylori oncoprotein CagA into host cells. Conversely, bile acid sequestration attenuated H . pylori –induced injury under conditions of iron deficiency. To translate these findings to human populations, we evaluated the association between bile acid sequestrant use and gastric cancer risk in a large human cohort. Among 416,885 individuals, a significant dose-dependent reduction in risk was associated with cumulative bile acid sequestrant use. Further, expression of the bile acid receptor transmembrane G protein–coupled bile acid receptor 5 (TGR5) paralleled the severity of carcinogenic lesions in humans. These data demonstrate that increased H . pylori –induced injury within the context of iron deficiency is tightly linked to altered bile acid metabolism, which may promote gastric carcinogenesis.

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