Barriers and facilitators of physical activity in adolescents with intellectual disabilities: An analysis informed by the COM-B model

BACKGROUND: Adolescents with intellectual disabilities are insufficiently physically active. Where interventions have been developed and delivered, these have had limited effectiveness, and often lack a theoretical underpinning. AIM: Through application of the COM‐B model, our aim is to explore the factors influencing adolescent physical activity within schools. METHODS: A qualitative methodology, using focus groups with students who have mild/moderate intellectual disabilities, their parents'/carers' and teachers'. The COM‐B model provided the lens through which the data were collected and analysed. RESULTS: We identified of a range of individual, interpersonal, and environmental factors influencing physical activity, across all six COM‐B constructs, within the context of the ‘school‐system’. CONCLUSION: This is the first study to use the COM‐B model to explore school‐based physical activity behaviour, for adolescents with intellectual disabilities. Identification of such physical activity behavioural determinants can support the development of effective and sustainable interventions

Efficacy of treatment in an opioid –dependent population group using the Maudsley Addiction Profile (MAP) tool

A pilot study was performed to assess the effectiveness of treatment in an opioid dependent population using the Maudsley Addiction Profile (MAP) tool1

Secretory leucoprotease inhibitor binds to NF-κB binding sites in monocytes and inhibits p65 binding

Secretory leucoprotease inhibitor (SLPI) is a nonglycosylated protein produced by epithelial cells. In addition to its antiprotease activity, SLPI has been shown to exhibit antiinflammatory properties, including down-regulation of tumor necrosis factor α expression by lipopolysaccharide (LPS) in macrophages and inhibition of nuclear factor (NF)-κB activation in a rat model of acute lung injury. We have previously shown that SLPI can inhibit LPS-induced NF-κB activation in monocytic cells by inhibiting degradation of IκBα without affecting the LPS-induced phosphorylation and ubiquitination of IκBα. Here, we present evidence to show that upon incubation with peripheral blood monocytes (PBMs) and the U937 monocytic cell line, SLPI enters the cells, becoming rapidly localized to the cytoplasm and nucleus, and affects NF-κB activation by binding directly to NF-κB binding sites in a site-specific manner. SLPI can also prevent p65 interaction with the NF-κB consensus region at concentrations commensurate with the physiological nuclear levels of SLPI and p65. We also demonstrate the presence of SLPI in nuclear fractions of PBMs and alveolar macrophages from individuals with cystic fibrosis and community-acquired pneumonia. Therefore, SLPI inhibition of NF-κB activation is mediated, in part, by competitive binding to the NF-κB consensus-binding site

The Ability of Secretory Leukocyte Protease Inhibitor to Inhibit Apoptosis in Monocytes Is Independent of Its Antiprotease Activity

Secretory Leukocyte Protease Inhibitor (SLPI) is a serine protease inhibitor produced by epithelial and myeloid cells with anti-inflammatory properties. Research has shown that SLPI exerts its anti-inflammatory activity by directly binding to NF-κB DNA binding sites and, in so doing, prevents binding and subsequent transcription of proinflammatory gene expression. In the current study, we demonstrate that SLPI can inhibit TNF-α-induced apoptosis in U937 cells and peripheral blood monocytes. Specifically, SLPI inhibits TNF-α-induced caspase-3 activation and DNA degradation associated with apoptosis. We go on to show that this ability of SLPI to inhibit apoptosis is not dependent on its antiprotease activity as antiprotease deficient variants of SLPI can also inhibit TNF-α-induced apoptosis. This reduction in monocyte apoptosis may preserve monocyte function during inflammation resolution and promote infection clearance at mucosal sites

Secretory Leucoprotease Inhibitor Impairs Toll-Like Receptor 2- and 4-Mediated Responses in Monocytic Cells

Secretory leucoprotease inhibitor (SLPI) is an anti-inflammatory antiprotease which can inhibit lipopolysaccharide-induced NF-κB activation. We examined its ability to inhibit NF-κB activation induced by lipoteichoic acid and investigated the effects of oxidation or complex formation with neutrophil elastase on SLPI's anti-inflammatory properties in U937 myelomonocytic cells and macrophages