ABSTRACT
Midwives and visiting medical officers have a unique relationship within private hospital maternity settings. The effective exchange of accurate information between them is a fundamental element of patient safety and is vital to the success of the clinical handover process. The SHARED (situation, history, assessment, risk, expectation, documentation) project developed, implemented and evaluated a framework and support tools for improving clinical handover in two private maternity hospitals. The project included a pre- and post-study design using clinician surveys, chart audits, patient satisfaction surveys and a review of clinical incident data. A standardised approach to handover, using the SHARED framework with a standardised minimum dataset, improves the accuracy and appropriateness of information.
Subject(s)
Communication , Continuity of Patient Care/organization & administration , Patient-Centered Care/organization & administration , Australia , Female , Hospitals, Maternity , Hospitals, Private , Humans , Medical Staff, Hospital , Midwifery , Nursing Staff, Hospital , Patient Satisfaction , Program Evaluation , Quality Assurance, Health Care/organization & administration , SafetyABSTRACT
Cytokines are known to induce apoptosis of pancreatic beta-cells. Impaired expression of the anti-apoptotic gene bcl-2 is one of the mechanisms involved. In this study, we identified a defect involving transcription factor cAMP-response element-binding protein (CREB) in the expression of bcl-2. Exposure of mouse pancreatic beta-cell line, MIN6 cells, to cytokines (interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma) led to a significant (p < 0.01) decrease in Bcl-2 protein and mRNA levels. Cytokines decreased (56%) the activity of the bcl-2 promoter that contains a cAMP-response element (CRE) site. Similar decreases were seen with a luciferase reporter gene driven by tandem repeats of CRE and a CREB-specific Gal4-luciferase reporter, suggesting a defect at the level of CREB. The active phospho form (serine 133) of CREB diminished significantly (p < 0.01) in cells exposed to cytokines. Examination of signaling pathways upstream of CREB revealed a reduction in the active form of Akt. Cytokine-induced decrease of bcl-2 promoter activity was partially restored when cells were cotransfected with a constitutively active form of Akt. Several end points of cytokine action including decreases in phospho-CREB, phospho-Akt, and BCl-2 levels and activation of caspase-9 were observed in isolated mouse islets. Overexpression of wild-type CREB in MIN6 cells by plasmid transfection and adenoviral infection led to protection against cytokine-induced apoptosis. Adenoviral transfer of dominant-negative forms of CREB, on the other hand, resulted in activation of caspase-9 and exaggeration of cytokine-induced beta-cell apoptosis. Together, these results point to CREB as a novel target for strategies aimed at improving the survival of beta-cells.
