TY - CHAP M1 - Book, Section TI - Circadian Rhythms and Sleep Biology A1 - Pack, Allan I. A2 - Grippi, Michael A. A2 - Elias, Jack A. A2 - Fishman, Jay A. A2 - Kotloff, Robert M. A2 - Pack, Allan I. A2 - Senior, Robert M. A2 - Siegel, Mark D. PY - 2015 T2 - Fishman's Pulmonary Diseases and Disorders, 5e AB - Sleep and circadian rhythm are highly coupled processes. In the original formulation they were considered independent but interacting. Borbely et al.1–4 posited that the circadian process (Process C) had a 24-hour rhythm that interacted with the sleep drive system (Process S) (Fig. 12-1). Process S is envisaged to be like an old-fashioned egg timer. The drive for sleep is at a very low level following the major sleep bout and increases progressively as wakefulness proceeds, that is, the drive to sleep is related to the duration of prior wakefulness. Humans are programmed to sustain wakefulness for 16 hours but beyond this develop progressive performance impairments. During the day the drive to sleep is counteracted by an alertness signal from the clock. When this alertness signal declines later in the evening, the sleep drive is unopposed and sleep ensues. During sleep the drive to sleep progressively declines, that is, the egg timer is flipped and the sands recover (Fig. 12-1). The situation is actually more complex than this since sleepiness occurs twice a day, that is, siesta time in early afternoon and late in the evening. While these processes were initially considered independent, they are not at a molecular level.5,6 Core clock molecules increase their expression in brain when sleep is deprived.7 Moreover, mutations of a clock-associated gene – DEC2, now called BHLEH41 – result in short sleep in humans (<6 hours) without evidence of daytime performance impairment.8,9 SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/03/28 UR - accessmedicine.mhmedical.com/content.aspx?aid=1122355006 ER -