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What does this paper add to existing knowledge? • This study provides insight into the severity of the problem. It demonstrates the differences in risk factors and OHRQoL between patients diagnosed with a psychotic disorder (first-episode) and the general population. • A negative impact on OHRQoL is more prevalent in patients diagnosed with a psychotic disorder (first-episode) (14.8%) compared to the general population (1.8%). • Patients diagnosed with a psychotic disorder (first-episode) have a considerable increase in odds for low OHRQoL compared to the general population, as dem onstrated by the odds ratio of 9.45, which supports the importance of preven tive oral health interventions in this group. What are the implications for practice? • The findings highlight the need for oral health interventions in patients diagnosed with a psychotic disorder (first-episode). Mental health nurses, as one of the main health professionals supporting the health of patients diagnosed with a mental health disorder, can support oral health (e.g. assess oral health in somatic screening, motivate patients, provide oral health education to increase awareness of risk factors, integration of oral healthcare services) all in order to improve the OHRQoL.

Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E₂ (PGE₂) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE₂ to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE₂ synthesis. PGE₂ in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE₂ in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle.

Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E2 (PGE2) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE2 to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE2 synthesis. PGE2 in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE2 in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle.