Risk Assessment of Self-Injurious Behavior and Suicide Presentation in the Emergency Department: An Integrative Review.

INTRODUCTION: Globally, there is a lack of clarity regarding the best practice to distinguish patients at the highest risk of suicide. This review explores the use of risk assessment tools in emergency departments to identify patients at high risk of repeat self-harm, suicide attempts, or death by suicide. METHODS: The review question ("Does the use of risk assessment tools in emergency departments identify patients at high risk of repeat self-harm, suicide attempts, or death by suicide?") focused on exposure and outcome. Studies of any design were included. The Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines were used. Study characteristics and concepts were extracted, compared, and verified. An integrative approach was used for reporting through narrative synthesis. RESULTS: Nine studies were identified for inclusion. Two risk assessment tools were found to have good predictive ability for suicide ideation and self-harm. Three had modest prediction of patient disposition, but in one study, the clinical impression of nurses had higher predictive ability. One tool showed modest predictive ability for patients requiring admission. DISCUSSION: This review found no strong evidence to indicate that any particular risk tool has a superior predictive ability to identify repeat self-harm, suicide attempts, or death by suicide. Best practice lacks clarity to determine patients at highest risk of suicide, but the use of risk assessment tools has been recommended. Nevertheless, such tools should not be used in isolation from clinical judgment and experience to evaluate patients at risk. Education and training to augment risk assessment within the emergency department are recommended.

Improved Murine MHC-Deficient HLA Transgenic NOD Mouse Models for Type 1 Diabetes Therapy Development.

Improved mouse models for type 1 diabetes (T1D) therapy development are needed. T1D susceptibility is restored to normally resistant NOD.ß2m-/- mice transgenically expressing human disease-associated HLA-A*02:01 or HLA-B*39:06 class I molecules in place of their murine counterparts. T1D is dependent on pathogenic CD8+ T-cell responses mediated by these human class I variants. NOD.ß2m-/--A2.1 mice were previously used to identify ß-cell autoantigens presented by this human class I variant to pathogenic CD8+ T cells and for testing therapies to attenuate such effectors. However, NOD.ß2m-/- mice also lack nonclassical MHC I family members, including FcRn, required for antigen presentation, and maintenance of serum IgG and albumin, precluding therapies dependent on these molecules. Hence, we used CRISPR/Cas9 to directly ablate the NOD H2-Kd and H2-Db classical class I variants either individually or in tandem (cMHCI-/-). Ablation of the H2-Ag7 class II variant in the latter stock created NOD mice totally lacking in classical murine MHC expression (cMHCI/II-/-). NOD-cMHCI-/- mice retained nonclassical MHC I molecule expression and FcRn activity. Transgenic expression of HLA-A2 or -B39 restored pathogenic CD8+ T-cell development and T1D susceptibility to NOD-cMHCI-/- mice. These next-generation HLA-humanized NOD models may provide improved platforms for T1D therapy development.