22 research outputs found
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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 âat riskâ 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 ”g/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