Abstract

Most, and perhaps all, cells harbour a circadian clock. These clocks regulate hundreds of physiological processes, ranging from body temperature and sleep–wake cycle to serum cortisol and melatonin concentration. All clocks operate using a very similar molecular mechanism; they communicate with each other through a complex and still poorly understood neuroendocrine network 1. In the mammalian brain, for example, a key clock gene known as Bmal is turned on and off in a 24-h rhythm, not only in the suprachiasmatic nucleus of the hypothalamus (the seat of the master clock) but also in the hippocampus and neocortex 1. It is therefore expected that many processes occurring in the neocortex are subject to clock control. The question, then, is how such control is achieved and which neuoendocrine regulators play a role. The study by Burioka et al. 2 presented in the current issue of the European Respiratory Journal ( ERJ ) contributes significantly towards addressing this question. The circadian rhythm of vigilance, blood pressure, sympathetic activity, corticoid biogenesis and metabolism is severely altered in patients with obstructive sleep apnoea (OSA). Given the previously sketched importance of clock genes in the genesis of circadian rhythm, investigation of circadian gene activation in OSA patients seems to hold promise. Burioka et al. 2 have quantified the expression of the clock gene Per1 mRNA in peripheral blood cells using real-time PCR analysis at different points over 24 h. In contrast to the matched …

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