Prevention of anxiety among at-risk children: a systematic review and meta-analysis

Background Anxiety disorders are common, often start in childhood and run a chronic course. As such there is a need for effective prevention. Methods We conducted a systematic review and meta-analyses of randomized, controlled trials to prevent the onset of anxiety disorders in ‘at risk’ young people. Diagnostic and symptom outcomes were examined. Putative moderators were tested as was publication bias. Results We included 16 trials (2545 young people). Two trials reported diagnostic outcomes, and significant effects were found for these at end-of-programme (RR = .09, 95%CI = .02 to .16), 6- (RR = .17, 95%CI = .06 to .27) and 12-month (RR = .31, 95%CI .17 to .45) follow-ups. Based on 16 trials, improved anxiety symptoms were significant compared to nonattention controls only, with small effect sizes reported by young people at the end-of-programmes, 6- and 12-month follow-ups; and by parents at the end of the programmes and 12-, but not 6-, month follow-ups. There was no evidence of significant moderation or publication bias. Conclusions Fourteen studies included children and young people who presented with elevated anxiety symptoms, but anxiety disorder was not ruled out in the participants in these studies. Hence, these studies might be reporting results of mixed prevention/early intervention programmes. Prevention programmes that target developmental risk factors, not only disorder maintaining factors, appear most promising. The clinically meaningful impact of anxiety disorder prevention programmes remains unknown

Electron microscopic analysis of glucose-induced endothelial damage in primary culture: Possible mechanism and prevention

We previously reported that high glucose treated cultured endothelial cells (ECs) showed intercellular gaps by transmission electron microscopy (TEM). These gaps were abrogated with insulin and/or heparin treatment. Our aims were to assess the severity of injury in ECs treated with high glucose for variable duration, and to further study the protective effects of insulin and/or heparin. Cells were also treated with Lbuthionine sulfoximine (BSO), a glutathione inhibitor, to help understand the mechanism of high glucose injury. Primary porcine ECs were treated with high glucose (30 mM) for 2, 6 or 10 days; and glucose plus insulin (1 U/ml), glucose plus heparin (5 µg/ml), glucose plus insulin plus heparin for 6 days. ECs were treated with BSO (0.001-0.05 mM) for 2 days. Pellets from trypsinized cells were processed for TEM. High glucose treatment revealed apoptosis or necrosis showing variable cell size, abnormal nuclei, condensation of nuclear chromatin, few mitochondria, cell membrane disruption and needle-shaped structures. Changes increased with duration of exposure. In high glucose plus heparin or insulin treated cultures at least one-half of the cells appeared normal. Most ECs were intact when treated with high glucose plus insulin plus heparin. BSO treatment showed dose-dependent changes with low doses showing apoptosis whereas higher doses revealed necrosis similar to high glucose treatment for 6 or 10 days. High glucose-induced EC injury increased with duration of exposure. These data demonstrate that high glucose injury resembles that of BSO treatment, suggesting that glutathione depletion may be involved in EC injury. Insulin and/or heparin protect against high glucose-induced injury