A conceptual review of interprofessional expertise in child safeguarding.

It is increasingly accepted that practitioners across a range of professional fields must work together in order to promote children's welfare and protect them from harm. However, it has also become apparent that interprofessional working is a challenging area of practice that cannot simply be prescribed through protocols and procedures, nor acquired as a set of technical competences. This article develops the concept of interprofessional expertise in order to explain how practitioners become more proficient at working with others to manage complex child welfare issues. Key principles are outlined with reference to relevant theoretical frameworks, including models of skill acquisition. The article concludes by discussing some potential implications for future research and contemporary developments in child safeguarding practice.

Defining continuity of care from the perspectives of mental health service users and professionals: an exploratory, comparative study.

BACKGROUND: Continuity of care (COC) is central to the organization and delivery of mental health services. Traditional definitions have excluded service users, and this lack of involvement has been linked to poor conceptual clarity surrounding the term. Consequently, very little is known about the differences and similarities in the conceptualization of COC by mental health service users and professionals. OBJECTIVE: To explore and compare mental health service users' and professionals' definitions of COC. METHODS: Using an exploratory, qualitative design, five focus groups with 32 service users each met twice. Data were analysed thematically to generate a service user-defined model of COC. In a cross-sectional survey, health and social care professionals (n = 184) defined COC; responses were analysed thematically. Service user and professional definitions were conceptually mapped and compared to identify similarities and differences. RESULTS: There was crossover between the service user and professional derived models of COC. Both contained temporal, quality, systemic, staff, hospital and needs-related elements of COC. Service users prioritized access, information, peer support and avoiding services; health professionals most frequently referred to staff, cross-sectional and temporal COC. Service users alone identified service avoidance, peer support and day centres as COC elements; professionals alone identified cross-sectional working. CONCLUSIONS: Important similarities and differences exist in service user and professional conceptualizations of COC. Further research is necessary to explore these differences, prior to integrating service user and professional perspectives in a validated COC framework which could enable the development and evaluation of interventions to improve COC, informing policy and practice.

Cytohesin 2/ARF6 regulates preadipocyte migration through the activation of ERK1/2.

Preadipocyte migration is vital for the development of adipose tissue, which plays a crucial role in lipid metabolism. ADP-ribosylation factor 6 (ARF6) small GTPase, which regulates membrane trafficking, is activated by GTP-exchange factors (GEFs) such as cytohesin 2. Cytohesin 2 and ARF6 have previously been implicated in the regulation of 3T3-L1 preadipocyte migration. We investigated here the molecular mechanism underlying the cytohesin 2 and ARF6 mediated regulation of preadipocyte migration. Preadipocyte migration and the activation of ARF6 and ERK1/2 were studied by using a number of approaches, including pharmacological inhibitors, siRNA and the inhibitory peptides. The siRNA mediated down regulation of ARF6 and cytohesin 2 expression confirmed the requirement of both for migration of preadipocytes. Phosphatidylinositol 3-kinase (PI3K) and PI 4,5-bisphosphate (PIP2) have also found to be essential for the cytohesin 2/ARF6 induced preadipocyte migration. Pharmacological inhibition of the activation of ARF6, ERK1/2 or dynamin led to significant reduction in migration of 3T3-L1 preadipocytes. Furthermore, our study revealed the activation of ARF6 and ERK1/2 during migration of preadipocytes. In the migrating preadipocytes, ARF6 activation was inhibited with SecinH3 (cytohesin inhibitor) and LY294002 (PI3K inhibitor) whereas the ERK1/2 phosphorylation was inhibited with SecinH3, LY294002, PBP10 (a PIP2 sequester peptide) and PD98059 (MAPKK inhibitor). However, dynosore (dynamin inhibitor) had inhibited neither ARF6 activation nor ERK1/2 phosphorylation during preadipocyte migration. These results together suggest that cytohesin 2 activates ARF6 in a PI3K dependent manner and then the active ARF6 causes phosphorylation of ERK1/2 during preadipocyte migration.

ADP-ribosylation factor 6 regulates endothelin-1-induced lipolysis in adipocytes.

Endothelin-1 (ET-1) induces lipolysis in adipocytes, where ET-1 chronic exposure results in insulin resistance (IR) through suppression of glucose transporter (GLUT)4 translocation to the plasma membrane and consequently glucose uptake. ARF6 small GTPase, which plays a vital role in cell surface receptors trafficking, has previously been shown to regulate GLUT4 recycling and thereby insulin signalling. ARF6 also plays a role in ET-1 promoted endothelial cell migration. However, ARF6 involvement in ET-1-induced lipolysis in adipocytes is unknown. Therefore, we investigated the role of ARF6 in ET-1-induced lipolysis in 3T3-L1 adipocytes. This was achieved by studying the effect of inhibitors for the activation of ARF6 and other signalling proteins on ET-1 induced lipolysis and ARF6 activation in the adipocytes. Our results indicate that ET-1 induces, through endothelin type A receptor (ETAR), lipolysis, the ARF6 activation and extracellular-signal regulated kinase (ERK) phosphorylation in adipocytes, further ET-1 stimulated lipolysis is inhibited by the inhibitors of ARF6 activation, ERK phosphorylation and dynamin, which is essential for endocytosis. Our studies also revealed that ARF6 acts upstream of ERK in ET-1-indcued lipolysis. In summary, we determined that ET-1 activation of ETAR signalled through ARF6, which is crucial for lipolysis.