Mathematical Models of the Circadian Sleep-Wake Cycle.

Moore‐Ede, Martin C.

doi:10.21236/ada145712

Cited by 28 publications

(12 citation statements)

References 20 publications

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“…2a) has been reported by others (3-5), although they considered fewer sleep episodes (206 vs. 359 reported here). These sleep duration data have become a benchmark for the testing of models (10)(11)(12)(13), first, because the p:<!> relationship is so clear, and second, because few alternative tests have been available.…”

Section: Discussionmentioning

confidence: 99%

Circadian Regulation Dominates Homeostatic Control of Sleep Length and Prior Wake Length in Humans

Strogatz

Kronauer

Czeisler

1986

Sleep

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Summary: During prolonged temporal isolation in caves or windowless rooms, human subjects often develop complicated sleep-wake patterns. Seeking lawful structure in these patterns, we have reanalyzed the spontaneous timing of 359 sleep-wake cycles recorded from 15 internally desynchronized human subjects. The observed sleep-wake patterns obey a simple rule: The phase of the circadian temperature rhythm at bedtime determines the lengths of both prior wake (ex) and subsequent sleep (p). From this rule we derive an average ex:p relationship that depends on circadian phase. The relationship reconciles the established negative ex:p correlation observed in synchronized subjects with the positive ex:p correlation found in desynchronized subjects. Our most surprising result concerns the residual deviations of ex and p from their circadian phase-adjusted mean values. We report that there is no significant positive correlation between the residuals of ex and p, contrary to the prediction of restorative models of sleep duration. Our findings illuminate the mechanisms underlying sleep regulation and provide much-needed tests of mathematical models of the sleep-wake cycle. Key Words: Circadian-Sleep-wake-Serial correlation -Mathematical model-Humans.To better understand how human sleep is regulated, many researchers have studied the sleep-wake behavior of subjects living for weeks in unscheduled, time-free environments (1-9). These experiments have taken place in underground caves (6)(7)(8), bunkers (1,2,5), or soundproofed, windowless apartments (3,9). A common finding is that subjects frequently go to bed near the minimum of their circadian temperature cycle. The sleep-wake and temperature rhythms then remain synchronized at a period near 25 h. Aschoff (1) reported the striking phenomenon of spontaneous internal desynchronization, in which subjects unintentionally but repeatedly stay up past the temperature minimum, leading to average sleep-wake cycle lengths of 30-40 h. Sleep then occurs at unusual phases in the circadian temperature cycle, with concomitant changes in its internal organization (4).Many mathematical models of the human sleep-wake cycle (10-13) have been proposed recently. Nearly all manage to simulate the qualitative aspects of internal de-

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Section: Discussionmentioning

confidence: 99%

Circadian Regulation Dominates Homeostatic Control of Sleep Length and Prior Wake Length in Humans

Strogatz

Kronauer

Czeisler

1986

Sleep

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“…The human circadian clock has at least two different oscillating systems: one is the circadian clock which is probably the same as the SCN circadian clock and the other is the clock or an hour‐glass oscillator involved in the sleep–wake cycle together with the circadian clock (Moore‐Ede & Czeisler, 1984; Dijk & Franken, 2005). Neither the site nor the mechanism of the latter clock is known.…”

Section: The Scn‐independent Rhythms In Rodents and The Sleep–wake Cymentioning

confidence: 99%

The SCN‐independent clocks, methamphetamine and food restriction

Honma

2009

Eur J of Neuroscience

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The circadian system in mammals consists of the central clock in the hypothalamic suprachiasmatic nucleus (SCN) and the peripheral clocks in a variety of tissues and organs. The SCN clock entrains to a light-dark cycle and resets the peripheral clocks. In addition, there are at least two other clocks in the circadian domain which are independent of the SCN and which entrain to nonphotic time cues: methamphetamine (MAP)-induced and restricted daily feeding (RF)-induced clocks. Neither the site nor the mechanism of SCN-independent clocks is known. Canonical clock genes for circadian oscillation are not required for the expression of either SCN-independent rhythm. The central catecholaminergic system is probably involved in the expression of the SCN-independent rhythms, especially of the MAP-induced rhythm. MAP-induced activity rhythms in rats and the sleep-wake cycles in humans share unique phenomena such as spontaneous internal desynchronization, circabidian rhythm and nonphotic entrainment, suggesting overlapping oscillatory mechanisms. The SCN-independent clock is an adaptation that regulates behavior in response to nonphotic time cues, and seems to be closely related to the arousal mechanism.

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“…Besides the well-characterized 24-h circadian clock, 12-h periodic rhythmicity also has been noted in many intertidal plants and animals, as well as in a cluster of endoplasmic reticulum (ER) and metabolic stress genes in several peripheral mouse tissues [1][2][3][4] . Humans display multiple prominent 12-h oscillations that influence daily food intake, immune function, body temperature, cognitive performance, and various circulating hormones [5][6][7][8][9][10][11][12][13][14][15][16][17] . Many of these 12-h physiological cycles have connections to ER stress and unfolded protein response (UPR) pathways that intimately link to the systemic maintenance of metabolic homeostasis [18][19][20][21][22][23][24] .…”

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confidence: 99%

XBP1 links the 12-hour clock to NAFLD and regulation of membrane fluidity and lipid homeostasis

et al. 2020

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A distinct 12-hour clock exists in addition to the 24-hour circadian clock to coordinate metabolic and stress rhythms. Here, we show that liver-specific ablation of X-box binding protein 1 (XBP1) disrupts the hepatic 12-hour clock and promotes spontaneous non-alcoholic fatty liver disease (NAFLD). We show that hepatic XBP1 predominantly regulates the 12-hour rhythmicity of gene transcription in the mouse liver and demonstrate that perturbation of the 12-hour clock, but not the core circadian clock, is associated with the onset and progression of this NAFLD phenotype. Mechanistically, we provide evidence that the spliced form of XBP1 (XBP1s) binds to the hepatic 12-hour cistrome to directly regulate the 12-hour clock, with a periodicity paralleling the harmonic activation of the 12-hour oscillatory transcription of many rate-limiting metabolic genes known to have perturbations in human metabolic disease. Functionally, we show that Xbp1 ablation significantly reduces cellular membrane fluidity and impairs lipid homeostasis via rate-limiting metabolic processes in fatty acid monounsaturated and phospholipid remodeling pathways. These findings reveal that genetic disruption of the hepatic 12-hour clock links to the onset and progression of NAFLD development via transcriptional regulator XBP1, and demonstrate a role for XBP1 and the 12-hour clock in the modulation of phospholipid composition and the maintenance of lipid homeostasis.

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Mathematical Models of the Circadian Sleep-Wake Cycle.

Cited by 28 publications

References 20 publications

Circadian Regulation Dominates Homeostatic Control of Sleep Length and Prior Wake Length in Humans

Circadian Regulation Dominates Homeostatic Control of Sleep Length and Prior Wake Length in Humans

The SCN‐independent clocks, methamphetamine and food restriction

XBP1 links the 12-hour clock to NAFLD and regulation of membrane fluidity and lipid homeostasis

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