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BACKGROUND: Suicide and risk management protocols in mental health research aim to ensure patient safety, provide vital information on how to assess suicidal ideation, manage risk, and respond to unexpected and expected situations. However, there is a lack of literature that identifies specific components and strategies to include in suicide and risk management protocols (SRMPs) for mental health research. The goal of this scoping review was to review academic and grey literature to determine core components and associated strategies, which can be used to inform SRMPs in mental health research. METHODS AND ANALYSIS: The methodological framework outlined by Arksey and O'Malley was used for this scoping review. The search strategy, conducted by a medical librarian, was multidisciplinary and included seven databases. Two reviewers independently assessed eligibility criteria in each document and used a standardized charting form to extract relevant data. The extracted data were then examined using qualitative content analysis. Specifically, summative content analysis was used to identify the core components and strategies used in SRMPs. The data synthesis process was iterative. RESULTS: This review included 36 documents, specifically 22 peer-reviewed articles and 14 documents from the grey literature. Five core components of SRMPs emerged from the reviewed literature including: training; educational resources for research staff; educational resources for research participants; risk assessment and management strategies; and clinical and research oversight. Potentials strategies for risk mitigation within each of the core components are outlined. CONCLUSIONS: The five core components and associated strategies for inclusion in SRMPs will assist mental health researchers in conducting research safely and rigorously. Findings can inform the development of SRMPs and how to tailor them across various research contexts.
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Saúde Mental , Prevenção do Suicídio , Humanos , Literatura de Revisão como Assunto , Medição de Risco , Ideação SuicidaRESUMO
OBJECTIVE: Overexpression of tissue-nonspecific alkaline phosphatase (TNAP) in endothelium leads to arterial calcification in mice. The purpose of this study was to examine the effect of elevated endothelial TNAP on coronary atherosclerosis. In addition, we aimed to examine endogenous TNAP activity in human myocardium. APPROACH AND RESULTS: A vascular pattern of TNAP activity was observed in human non-failing, ischemic, and idiopathic dilated hearts (5 per group); no differences were noted between groups in this study. Endothelial overexpression of TNAP was achieved in mice harboring a homozygous recessive mutation in the low density lipoprotein receptor (whc allele) utilizing a Tie2-cre recombinase (WHC-eTNAP mice). WHC-eTNAP developed significant coronary artery calcification at baseline compared WHC controls (4312 vs 0µm2 alizarin red area, p<0.001). Eight weeks after induction of atherosclerosis, lipid deposition in the coronary arteries of WHC-eTNAP was increased compared to WHC controls (121633 vs 9330µm2 oil red O area, p<0.05). Coronary lesions in WHC-eTNAP mice exhibited intimal thickening, calcifications, foam cells, and necrotic cores. This was accompanied by the reduction in body weight and left ventricular ejection fraction (19.5 vs. 23.6g, p<0.01; 35% vs. 47%, p<0.05). In a placebo-controlled experiment under atherogenic conditions, pharmacological inhibition of TNAP in WHC-eTNAP mice by a specific inhibitor SBI-425 (30mg*kg-1*d-1, for 5 weeks) reduced coronary calcium (78838 vs.144622µm2) and lipids (30754 vs. 77317µm2); improved body weight (22.4 vs.18.8g) and ejection fraction (59 vs. 47%). The effects of SBI-425 were significant in the direct comparisons with placebo but disappeared after TNAP-negative placebo-treated group was included in the models as healthy controls. CONCLUSIONS: Endogenous TNAP activity is present in human cardiac tissues. TNAP overexpression in vascular endothelium in mice leads to an unusual course of coronary atherosclerosis, in which calcification precedes lipid deposition. The prevalence and significance of this mechanism in human atherosclerosis requires further investigations.