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Biotech / Medical : Gliatech (GLIA) -- Ignore unavailable to you. Want to Upgrade?

To: scaram(o)uche who wrote (901)	8/6/1999 3:10:00 PM
From: scaram(o)uche	Respond to of 2001

[ just parking ] just parking something, such that I can find it again and hopefully to put stuff up that will allow others to see/explain a part of the puzzle..... J Clin Endocrinol Metab 1999 Jun;84(6):1979-85 Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications. Irwin M, Thompson J, Miller C, Gillin JC, Ziegler M Department of Psychiatry, University of California, and San Diego Veterans Affairs Medical Center, 92161, USA. The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.