The Epidemiology of Suicide in Young Men in Greenland: A Systematic Review.

Suicide is the leading cause of death among young men aged 15⁻29 in Greenland, but few epidemiological studies have described this problem. We aimed to summarise descriptive epidemiological studies of suicide in young men in Greenland compared with other demographic groups in Denmark and Greenland to inform future suicide prevention strategy. We searched PubMed, PsycINFO, and Embase using an agreed search strategy to identify English-language papers describing suicide epidemiology in Greenlandic men aged 15⁻29. We followed PRISMA guidelines in screening and appraising eligible publications. Eight articles fulfilled inclusion criteria of 64 meeting search criteria. Findings covering 1970⁻2011 supported a dramatic rise in suicide rates in Greenlandic men aged 15⁻24 from 1976, who remained the highest-ranking demographic group over 1976⁻2011 compared with men and women of all age groups in Denmark and Greenland. Highest rates recorded were almost 600 per 100,000 per year in men aged approximately 20⁻23 over 1977⁻1986. No studies described suicide epidemiology after 2011, and no studies described risk factors for suicide in young men. Given the very high suicide rates recorded for young men over 1976⁻2011, such studies will be essential for informing the development and evaluation of appropriate preventive interventions.

Inflammatory response of porcine epithelial IPEC J2 cells to enterotoxigenic E. coli infection is modulated by zinc supplementation.

Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhoea in pigs and humans. The duration and severity of diarrhoea can be controlled using zinc supplementation, typically pharmacological levels of zinc oxide in pigs. In this study, IPEC J2 cells were used as an in vitro model of intestinal ETEC infection, with separate and simultaneous zinc treatment. Genomic analysis identified increased expression of a variety of innate immune response genes (NF-κB targets) in response to ETEC exposure, and several stress response genes in response to zinc exposure, provided as ZnO. Expression of genes involved in the innate immune response was reduced when cells were simultaneously exposed to ZnO, and it is suggested that ZnO treatment inhibits the induction of NF-κB in response to pathogens, possibly through up-regulated heat shock proteins. A similar response in vivo with consequent down-regulation in the inflammatory response would reduce further pathogen invasion, maintain normal gut function and maintain growth.

Dietary zinc oxide affects the expression of genes associated with inflammation: Transcriptome analysis in piglets challenged with ETEC K88.

The post-weaning growth check in commercial pig production systems is often associated with gastrointestinal infection, in particular that caused by enterotoxigenic Escherichia coli (ETEC) K88. Pharmacological doses of zinc oxide (ZnO) in the post-weaning diet reduce the incidence of diarrhoea and improve piglet performance. In the present study, piglets reared indoors or outdoors and weaned onto diets with or without pharmacological levels of ZnO were orally challenged with ETEC K88. Quantitative real-time PCR was performed on RNA extracted from jejunal lamina propria and Peyer's patch samples, to compare expression of a variety of candidate genes between treatments. Candidate genes were selected from an initial microarray study using pooled RNA to identify differentially expressed genes. Dietary treatment with ZnO was associated with significant differences in the transcript abundance of several genes. Zinc supplementation was associated with a marked decrease in expression of immune response genes concerned with inflammation, and possibly related to the stage of infection. Interestingly, evidence was also obtained that a reduced level of MUC4 (a proposed ETEC K88 receptor) was associated with zinc supplementation suggesting a mechanism that might influence ETEC infection. These findings indicate that zinc oxide supplementation may reduce the level of inflammation caused by ETEC challenge.