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BACKGROUND: Transcranial magnetic stimulation is a relatively new technique for inducing small, localized, and reversible changes in living brain tissue. Although transcranial magnetic stimulation generally results in no immediate changes in plasma corticosterone, prolactin, and testosterone, it normalizes the dexamethasone suppression test in some depressed subjects and has been shown to attenuate stress-induced increases in adrenocorticotropic hormone in rats. METHODS: In this study, serum corticosterone and testosterone concentrations were assayed in male rats immediately and 3, 6, 9, 12, 24, and 48 hours following a single transcranial magnetic stimulation or sham application. Serum prolactin concentrations were determined immediately and 2 hours following a one-time application of either transcranial magnetic stimulation or sham. RESULTS: Transcranial magnetic stimulation animals displayed significantly lower corticosterone concentrations at 6 and 24 hours following a single application compared with sham-control values. Transcranial magnetic stimulation also resulted in lower corticosterone concentrations numerically but not statistically in transcranial magnetic stimulation animals immediately after application (p =.089). No significant differences were found between groups for serum prolactin or testosterone levels at any given collection time point. CONCLUSIONS: These findings 1) suggest that transcranial magnetic stimulation alters the hypothalamic-pituitary-adrenal stress axis and 2) provide time-course data for the implications of the hormonal mechanism that may be involved in the actions of transcranial magnetic stimulation.
\n \n\n \n \nPrevious studies of glucocorticoid receptor (GR) function in COPD lung macrophages have used dexamethasone to evaluate inhibition of cytokine production. We have now used the clinically relevant corticosteroid beclomethasone-17-monopropionate (17-BMP) to assess GR function in COPD lung macrophages, and investigated the transactivation of glucocorticoid sensitive genes and GR phosphorylation in addition to cytokine production. Lung macrophages were purified from surgically acquired lung tissue, from patients with COPD, smokers, and non-smokers. The transactivation of glucocorticoid sensitive genes (FKBP51 and GILZ) by 17-BMP were analysed by polymerase chain reaction. 17-BMP suppression of LPS-induced TNF\u03b1, IL-6 and CXCL8 was measured by ELISA and GR phosphorylation was measured by immunohistochemistry and Western blot. 17-BMP reduced cytokine release in a concentration dependent manner, with >70% inhibition of all cytokines, and no difference between COPD patients and controls. Similarly, the transactivation of FKBP51 and GILZ, and GR phosphorylation was similar between COPD patients and controls. In this context, GR function in COPD lung macrophages is unaltered. 17-BMP effectively suppresses cytokine production in COPD lung macrophages.
\n \n\n \n \nIn clinic studies, altered hypothalamic-pituitary-adrenal (HPA) axis function has been associated with fibromyalgia, a syndrome characterised by chronic widespread body pain. These results may be explained by the associated high rates of psychological distress and somatisation. We address the hypothesis that the latter, rather than the pain, might explain the HPA results. A population study ascertained pain and psychological status in subjects aged 25 to 65 years. Random samples were selected from the following three groups: satisfying criteria for chronic widespread pain; free of chronic widespread pain but with strong evidence of somatisation ('at risk'); and a reference group. HPA axis function was assessed from measuring early morning and evening salivary cortisol levels, and serum cortisol after physical (pain pressure threshold exam) and chemical (overnight 0.25 mg dexamethasone suppression test) stressors. The relationship between HPA function with pain and the various psychosocial scales assessed was modelled using appropriate regression analyses, adjusted for age and gender. In all 131 persons with chronic widespread pain (participation rate 74%), 267 'at risk' (58%) and 56 controls (70%) were studied. Those in the chronic widespread pain and 'at risk' groups were, respectively, 3.1 (95% CI (1.3, 7.3)) and 1.8 (0.8, 4.0) times more likely to have a saliva cortisol score in the lowest third. None of the psychosocial factors measured were, however, associated with saliva cortisol scores. Further, those in the chronic widespread pain (1.9 (0.8, 4.7)) and 'at risk' (1.6 (0.7, 3.6)) groups were also more likely to have the highest serum cortisol scores. High post-stress serum cortisol was related to high levels of psychological distress (p = 0.05, 95% CI (0.02, 0.08)). After adjusting for levels of psychological distress, the association between chronic widespread pain and post-stress cortisol scores remained, albeit slightly attenuated. This is the first population study to demonstrate that those with established, and those psychologically at risk of, chronic widespread pain demonstrate abnormalities of HPA axis function, which are more marked in the former group. Although some aspects of the altered function are related to the psychosocial factors measured, we conclude that the occurrence of HPA abnormality in persons with chronic widespread pain is not fully explained by the accompanying psychological stress.
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