BackgroundRoutinely conducting case finding (also commonly referred to as screening) in patients with chronic illness for depression in primary care appears to have little impact. We explored the views and experiences of primary care nurses, doctors and managers to understand how the implementation of case finding/screening might impact on its effectiveness.MethodsTwo complementary qualitative focus group studies of primary care professionals including nurses, doctors and managers, in five primary care practices and five Community Health Partnerships, were conducted in Scotland.ResultsWe identified several features of the way case finding/screening was implemented that may lead to systematic under-detection of depression. These included obstacles to incorporating case finding/screening into a clinical review consultation; a perception of replacing individualised care with mechanistic assessment, and a disconnection for nurses between management of physical and mental health. Far from being a standardised process that encouraged detection of depression, participants described case finding/screening as being conducted in a way which biased it towards negative responses, and for nurses, it was an uncomfortable task for which they lacked the necessary skills to provide immediate support to patients at the time of diagnosis.ConclusionThe introduction of case finding/screening for depression into routine chronic illness management is not straightforward. Routinized case finding/screening for depression can be implemented in ways that may be counterproductive to engagement (particularly by nurses), with the mental health needs of patients living with long term conditions. If case finding/screening or engagement with mental health problems is to be promoted, primary care nurses require more training to increase their confidence in raising and dealing with mental health issues and GPs and nurses need to work collectively to develop the relational work required to promote cognitive participation in case finding/screening.

Higher rates of stress-related sickness are found in health care professionals when compared with other sectors. The annual direct cost of absence to the National Health Service is £1.7 billion. Increased clinical demand, long hours, low staffing and a lack of support from colleagues and management are contributing to absenteeism, somatic complaints and mental health problems. Mental health work is inherently stressful and levels of work stress experienced by mental health nurses are especially high. The study investigated mental health nurses' and allied health professionals' (AHPs) awareness and knowledge of the service provided by the Occupational Health Service (OHS) and identified work-related stress and self-care strategies within these two groups. Nurses and AHP staff employed in mental health services in a Scottish healthboard area were invited to complete an anonymous questionnaire. Results demonstrated that staff found their contact with the OHS to be a positive experience. They considered direct patient care to be less stressful than the organizational constraints they work under, and they reported a lack of support from both their peer groups and management. There should be recognition of the increased stress that hospital-based nurses and AHPs experience. These areas should be scrutinized and reviewed further to support staff within these environments in accordance with organizational objectives.

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The proliferative B-13 pancreatic cell line is unique in its ability to generate functional hepatocyte-like (B-13/H) cells in response to exposure to glucocorticoid. In these studies, quantitatively comparable hepatic levels of liver-specific and liver-enriched transcription factor and hepatocyte defining mRNA transcripts were expressed after 10–14 days continuous treatment with glucocorticoid. This conversion in phenotype was associated with increased Gr-α mRNA expression and translation of a functional N-terminally truncated variant protein that localized to the nucleus in B-13/H cells. A short (6 hours) pulse exposure to glucocorticoid was also sufficient to transiently activate the Gr and irreversibly drive near identical conversion to B-13/H cells. Examination of epigenetic-related mechanisms demonstrated that B-13 DNA was rapidly methylated and de-methylated over the initial 2 days in response to both continuous or pulse exposure with glucocorticoid. DNA methylation and glucocorticoid-dependent conversion to an hepatic B-13/H phenotype was blocked by the methylation inhibitor, 5-azacytidine. Conversion to an hepatic B-13/H phenotype was also blocked by histone deacetylase inhibitors. Previous experiments have identified N-terminal Sgk1 variant proteins as pivotal to the mechanism(s) associated with pancreatic–hepatic differentiation. Both continuous and pulse exposure to DEX was sufficient to result in a near-similar robust transcriptional increase in Sgk1c mRNA expression from undetectable levels in B-13 cells. Notably, expression of Sgk1c mRNA remained constitutive 14 days later; including after pulse exposure to glucocorticoid and this induction was inhibited by 5-azacytidine or by histone deacetylase inhibitors. These data therefore suggest that exposing B-13 cells to glucocorticoid results in a Gr-dependent pulse in DNA methylation and likely other epigenetic changes such as histone modifications that leads to constitutive expression of Sgk1c and irreversible reprogramming of B-13 cells into B-13/H cells. Understanding and application of these mechanism(s) may enhance the functionality of stem cell-derived hepatocytes generated in vitro.

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