An exploratory investigation of teachers\u27 intervention planning and perceived implementation barriers

Increasingly teachers are the primary implementer responsible for providing evidence-based interventions to students. However, there is little knowledge regarding the extent to which teachers plan for intervention implementation, receive implementation support, or identify and address implementation barriers. This study explores survey data from over 1200 preschool through grade 12 teachers from 46 public school districts in a Northeastern state. Results indicate that teachers spend significant time engaging in intervention-related behavior and may be a primary source responsible for selecting student interventions. However, the current extent to which they plan for implementation and present levels of implementation support are inadequate to produce high levels of sustained intervention implementation. In addition, almost 60% of implementation barriers reported related to aspects of the intervention itself. Findings from this study provide guidance for future research and preliminary recommendations for ameliorating implementation barriers and proactively supporting treatment integrity in schools

Galectin-1 Co-clusters CD43/CD45 on Dendritic Cells and Induces Cell Activation and Migration through Syk and Protein Kinase C Signaling*

Galectin-1 is a galactoside-binding lectin expressed in multiple tissues that has pleiotropic immunomodulatory functions. We previously showed that galectin-1 activates human monocyte-derived dendritic cells (MDDCs) and triggers a specific genetic program that up-regulates DC migration through the extracellular matrix, an integral property of mucosal DCs. Here, we identify the galectin-1 receptors on MDDCs and immediate downstream effectors of galectin-1-induced MDDC activation and migration. Galectin-1 binding to surface CD43 and CD45 on MDDCs induced an unusual unipolar co-clustering of these receptors and activates a dose-dependent calcium flux that is abrogated by lactose. Using a kinome screen and a systems biology approach, we identified Syk and protein kinase C tyrosine kinases as mediators of the DC activation effects of galectin-1. Galectin-1, but not lipopolysaccharide, stimulated Syk phosphorylation and recruitment of phosphorylated Syk to the CD43 and CD45 co-cluster on MDDCs. Inhibitors of Syk and protein kinase C signaling abrogated galectin-1-induced DC activation as monitored by interleukin-6 production; and MMP-1, -10, and -12 gene up-regulation; and enhanced migration through the extracellular matrix. The latter two are specific features of galectin-1-activated DCs. Interestingly, we also found that galectin-1 can prime DCs to respond more quickly to low dose lipopolysaccharide stimulation. Finally, we underscore the biological relevance of galectin-1-enhanced DC migration by showing that intradermal injection of galectin-1 in MRL-fas mice, which have a defect in skin DC emigration, increased the in vivo migration of dermal DCs to draining lymph nodes