Developing risk-adjusted quality indicators for pressure ulcers in long-term care hospitals in the Republic of Korea.

Pressure ulcers result in financial losses, including the cost of unnecessary medical expenses because of extended hospital stays, treatment, and examination. This was a retrospective, observational, methodological study to develop quality indicators related to pressure ulcer development and validate risk adjustment factors for pressure ulcer development. We performed a literature review to develop risk adjustment factors, and an expert group performed a content validity test. To validate risk adjustment factors for pressure ulcer development using electronic medical records, 127 patients admitted to a long-term care hospital in South Korea from June to September 2015 were enrolled in the study. Pressure ulcer risk factors were peripheral vascular disease, end-stage disease, past pressure ulcer history, high risk group for pressure ulcer development, fever, haemoglobin, and albumin (all P < 0.05); only albumin (odds ratio: 0.210, P < 0.001) was significantly associated with pressure ulcer development as an independent risk factor. Further research with a large sample size is needed for the validation of risk adjustment factors. Risk-adjusted quality indicators for pressure ulcer development can be used to evaluate the quality of nursing care and compare outcomes after preventive pressure ulcer care activities or between long-term care hospitals.

Temporal variability of glucocorticoid receptor activity is functionally important for the therapeutic action of fluoxetine in the hippocampus.

Previous studies have shown inconsistent results regarding the actions of antidepressants on glucocorticoid receptor (GR) signalling. To resolve these inconsistencies, we used a lentiviral-based reporter system to directly monitor rat hippocampal GR activity during stress adaptation. Temporal GR activation was induced significantly by acute stress, as demonstrated by an increase in the intra-individual variability of the acute stress group compared with the variability of the non-stress group. However, the increased intra-individual variability was dampened by exposure to chronic stress, which was partly restored by fluoxetine treatment without affecting glucocorticoid secretion. Immobility in the forced-swim test was negatively correlated with the intra-individual variability, but was not correlated with the quantitative GR activity during fluoxetine therapy; this highlights the temporal variability in the neurobiological links between GR signalling and the therapeutic action of fluoxetine. Furthermore, we demonstrated sequential phosphorylation between GR (S224) and (S232) following fluoxetine treatment, showing a molecular basis for hormone-independent nuclear translocation and transcriptional enhancement. Collectively, these results suggest a neurobiological mechanism by which fluoxetine treatment confers resilience to the chronic stress-mediated attenuation of hypothalamic-pituitary-adrenal axis activity.