People with a lived experience of mental illness are at a higher risk for developing oral diseases and having poorer oral health than the broader population. This paper explores the role of Australian community mental health services in supporting the prevention and management of poor oral health among people living with mental illness. Through focus groups and semi-structured interviews, participants identified the value of receiving oral health support within a community mental health setting, in particular the delivery of basic education, preventive strategies, assistance with making or attending appointments and obtaining priority access to oral health services. Engagement with Community Health Services and referrals generated through the priority access system were identified as key enablers to addressing oral health issues. This study provides new insight into the importance of undertaking an integrated approach to reducing the oral health disparities experienced by those living with mental illness.
Neuroblastoma is a commonly encountered solid tumor in early childhood with high neuroplasticity, and differentiation therapy is hypothesized to lead to tumor mass shrinkage and/or symptom relief. CgA is a tissue specific protein restricted to the diffuse neuroendocrine system, and widely expressed in neuroblastomas. Using knockdown and knockout approaches to deplete CgA levels, we demonstrated that CgA loss inhibits SH-SY5Y cell proliferation and leads to a morphological shift with increased expression of Schwann and extracellular matrix specific molecules, and suppression of chromaffin features. We further confirmed the effects of CgA in a series of neuroblastoma cells with [BE(2)-M17 and IMR-32] and without (SK-N-SH) N-Myc amplification. We demonstrated that CgA depletion reduced IGF-II and IGFBP-2 expression, increased IGFBP-3 levels, and suppresses IGF downstream signaling as evidenced by reduced AKT/ERK pathway activation. This was further supported by an increased anti-proliferative effect of the ERK inhibitor in the CgA depleted cells. In an
in vivo
xenograft neuroblastoma model, CgA knockdown led to increased S-phenotypic marker expression at both protein and mRNA levels. Together these results suggest that CgA maintains IGF secretion and intracellular signaling to regulate proliferation and differentiation in neuroblastomas.
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