Are two voices better than one? Predicting permanency in minority youth using multi-informant mental health and strength data.

Among youth in child welfare ages 6-17 years, 40 % meet the criteria for one or more DSM diagnoses. For minority youth in child welfare, poor mental health is compounded by limited access to care and racial disparity bias, leading to poorer outcomes. This paper uses data collected and analyzed by an automated behavioral health assessment system for a multiyear study that focused on ways to improve case planning in child welfare. Youth, their caseworkers, and, in some cases, parents completed assessments that measured and monitored the youths' needs and strengths. More than 60 % of youth participating in the study were African-American; permanency rates after six months of case planning were found to be only one third. Predictive factors related to better behavioral health and permanency outcomes are identified and discussed, as well as the implications for improving case planning by incorporating the views of multiple informants, including the youth.

Revolutionizing child welfare with outcomes management.

Outcomes management technology holds great promise for improving the quality of services provided to youth in the child welfare system. Advantages include better detection of behavioral health and trauma-related issues, early indicators of case progress or risk of failure, and program- and system-level learning. Yet organizational barriers to implementation persist. Attention is spent in this paper on addressing these barriers so the use of outcomes management technology becomes a common practice. A model for predicting resiliency is presented, along with case examples demonstrating its potential use for treatment planning and monitoring progress.

Nuclear interleukin-33 is generally expressed in resting endothelium but rapidly lost upon angiogenic or proinflammatory activation.

Interleukin (IL)-33 is a novel member of the IL-1 family of cytokines that promotes Th2 responses in lymphocytes as well as the activation of both mast cells and eosinophils via the ST2 receptor. Additionally, IL-33 has been proposed to act as a chromatin-associated transcriptional regulator in both endothelial cells of high endothelial venules and chronically inflamed vessels. Here we show that nuclear IL-33 is expressed in blood vessels of healthy tissues but down-regulated at the earliest onset of angiogenesis during wound healing; in addition, it is almost undetectable in human tumor vessels. Accordingly, IL-33 is induced when cultured endothelial cells reach confluence and stop proliferating but is lost when these cells begin to migrate. However, IL-33 expression was not induced by inhibiting cell cycle progression in subconfluent cultures and was not prevented by antibody-mediated inhibition of VE-cadherin. Conversely, IL-33 knockdown did not induce detectable changes in either expression levels or the cellular distribution of either VE-cadherin or CD31. However, activation of endothelial cell cultures with either tumor necrosis factor-alpha or vascular endothelial growth factor and subcutaneous injection of these cytokines led to a down-regulation of vascular IL-33, a response consistent with both its rapid down-regulation in wound healing and loss in tumor endothelium. In conclusion, we speculate that the proposed transcriptional repressor function of IL-33 may be involved in the control of endothelial cell activation.