EEG use in a tertiary referral centre.

The aim of this study was to retrospectively audit all electroencephalograms (EEGs) done over a 2-month period in 2009 by the Neurophysiology Department at Cork University Hospital. There were 316 EEGs performed in total, of which 176/316 (56%) were done within 24 hours of request. Out of 316 EEGs, 208 (66%) were considered 'appropriate' by SIGN and NICE guidelines; 79/208 (38%) had abnormal EEGs and 28 of these abnormal EEGs had epileptiform features. There were 108/316 (34%) 'inappropriate' requests for EEG; of these 15/108 (14%) were abnormal. Of the 67/316 (21%) patients who had EEGs requested based on a history of syncope/funny turns: none of these patients had epileptiform abnormalities on their EEGs. Our audit demonstrates that EEGs are inappropriately over-requested in our institution in particular for cases with reported 'funny turns' and syncope. The yield from EEGs in this cohort of patients was low as would be expected.

Alteration of actin organization by jaspamide inhibits ruffling, but not phagocytosis or oxidative burst, in HL-60 cells and human monocytes.

Jaspamide, a naturally occurring cyclic peptide isolated from the marine sponge Hemiastrella minor, has fungicidal and growth-inhibiting activities. Exposure of promyelocytic HL-60 cells and human monocytes to jaspamide induces a dramatic reorganization of actin from a typical fibrous network to focal aggregates. HL-60 cells exposed to 5 x 10(-8) mol/L or 10(-7) mol/L jaspamide exhibited a reduced proliferation rate. In addition, 10(-7) mol/L jaspamide induced maturation of HL-60 cells as indicated by the appearance of a lobulated nucleus in 55% +/- 5% of the cells and immunophenotypic maturation of the leukemia cells (upregulation of CD16 and CD14 B antigens). Further characterization has shown that F-actin is aggregated both in HL-60 cells and in human monocytes exposed to 10(-7) mol/L jaspamide. Well-spread cultured human monocytes contracted and adopted round shapes after treatment with jaspamide. Moreover, a dose-dependent increase in both total actin and de novo synthesized portions of the soluble actin was observed in jaspamide-treated HL-60 cells. Jaspamide treatment inhibits ruffling and intracellular movement in HL-60 cells and monocytes, but does not affect phagocytic activity or respiratory burst activity. The consequential effects of jaspamide-induced actin reorganization on ruffling, versus its negligible effect on phagocytosis and oxidative burst, may shed light on molecular mechanisms of actin involvement in these processes. Jaspamide disrupts the actin cytoskeleton of normal and malignant mammalian cells with no significant effect on phagocytic activity and may, therefore, be considered as a novel therapeutic agent.