Aggression in children carries a high risk of poor outcomes, and, therefore, a better understanding of treatment options is a high priority. The available literature points to the importance of identifying the underlying disorder, when possible, and using this information to guide treatment selection. Future studies are needed to better inform the treatment of aggression across disorders, and the treatment of different aggression subtypes.
We tested the hypothesis that tumor necrosis factor-alpha (TNF) induces barrier dysfunction of pulmonary microvessel endothelial monolayers (PMEM) mediated by specific tyrosine residues in beta-actin. PMEM were transfected with a wild-type, mutant [tyrosine(198) to phenylalanine(198) (Y198F)], mutant Y218F, or mutant Y306F beta-actin construct tagged with enhanced yellow fluorescent protein (EYFP-beta-actin). The cellular compartmentalization of wild-type and mutant EYFP-beta-actin was displayed using EYFP fluorescence of the tagged beta-actin. beta-Actin was quantified for the EYFP-tagged and native beta-actin using Western blot assay. The effect of the EYFP-beta-actin on a cell junction protein was assessed by association of EYFP-beta-actin with beta-catenin using confocal microscopy and coimmunoprecipitation. The permeability of PMEM was assessed by the clearance rate of Evans blue-labeled albumin. The cellular compartmentalization of wild-type and mutant EYFP-beta-actin was similar to the native beta-actin. Incubation of PMEM with TNF (100 ng/ml) for 0.5 h resulted in increases in permeability to albumin and a decrease in association of the EYFP-beta-actin with beta-catenin. However, the expression of the EYFP-Y198F beta-actin and EYFP-Y218F beta-actin prevented the effect of TNF on beta-catenin and barrier function. The vehicle, wild-type EYFP-beta-actin, and mutant Y306F beta-actin had no affect on the response to TNF. The data indicate that TNF induces an increase in endothelial permeability that is dependent on tyrosine(198) and tyrosine(218) in beta-actin.
Little is known about perceptions surrounding self-management for attention deficit hyperactivity disorder (ADHD), although such interventions appear commonly used and are considered essential components of the chronic care model. Our research is part of a mixed methods study that followed students at high and low risk for ADHD over 11 years. During the final study years, area-representative samples of 148 adolescents (54.8% participation; 97 ADHD high-risk group; 51 low-risk peers) and 161 parents (59.4% participation; 108 parents of high-risk adolescent; 53 parents of low-risk peer) completed a cross-sectional survey on community-identified self-management interventions for ADHD (activity outlets, sleep regulation, dietary restriction, homework help, family rules, and prayer). Respondents also answered open-ended questions addressing undesirable self-management effects, which were analyzed using grounded theory methods. High-risk adolescents expressed significantly lower willingness towards all self-management interventions than did adult respondents, except for increased activity outlets. They also reported lower receptivity towards sleep regulation and dietary restriction than did their low-risk peer group. No gender or race differences in self-management willingness were found, except for higher receptivity to prayer in African American respondents. Cost, perceived ineffectiveness, disruptions to routines, causation of interpersonal conflicts, and reduced future self-reliance were seen as potential undesirable effects. Findings suggest that activity-based ADHD interventions appear particularly acceptable across all demographic and risk groups, unlike sleep regulation and dietary approaches. Further research on self-care effectiveness is needed to incorporate adolescents’ viewpoints about ADHD self-management, as interventions may be acceptable to adults, but resisted by adolescents.
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