When people die

Mitler, Merrill M.; R, Hajduković; Shafor, Renata; Hahn, Pierre M.; Kripke, Daniel F.

doi:10.1016/0002-9343(87)90067-2

Cited by 110 publications

(16 citation statements)

References 20 publications

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“…In regards to mortality, in general, rates from all causes increase 30% during the night, and for those aged 65 and over, the excess deaths typically occur between the hours of 2 am and 8 am (Mitler et al 1987). The presence of unrecognized or untreated SDB may partially account for these findings as several studies have found an association between SDB in the elderly and increased mortality rates (Bliwise et al 1988; He et al 1988), although some studies of community dwelling, nondemented elderly subjects have not found AHI to be an independent predictor of mortality (Ancoli-Israel et al 1996; Mant et al 1995).…”

Section: Primary Sleep Disordersmentioning

confidence: 99%

Normal and abnormal sleep in the elderly

Cooke

Ancoli‐Israel

2011

Handbook of Clinical Neurology

147

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Section: Primary Sleep Disordersmentioning

confidence: 99%

Normal and abnormal sleep in the elderly

Cooke

Ancoli‐Israel

2011

Handbook of Clinical Neurology

147

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“…Circadian rhythms are self-sustaining, 24-hour cycles in molecular, biochemical, and behavioral parameters that help an organism prepare for anticipated changes in physiological demand. In humans the incidence of adverse cardiac events, such as myocardial infarction, ventricular tachycardia, and death from ischemic heart disease, vary according to the time of day (25, 46, 52, 82), and forced changes in circadian rhythm, such as shift work or sleep apnea, are associated with increased risk for heart failure. Many tissues, including heart, display a circadian rhythm in autophagic activity (47, 63).…”

Section: Introductionmentioning

confidence: 99%

Targets, trafficking, and timing of cardiac autophagy

Rotter

Rothermel

2012

Pharmacological Research

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Heart failure is the major case of death in developed countries, and its prevalence is growing worldwide. Autophagy is a fundamental cellular mechanism through which intracellular components can be removed, recycled and repaired. Studies in humans and animal models demonstrate a marked increase in cardiac autophagic activity under a wide range of disease states and in response to diverse stimuli. Recently, autophagy has been widely promoted as a potential therapeutic target for the treatment of cardiovascular disease and heart failure. An important challenge to achieving this goal is the dual nature of cardiac autophagy, sometimes acting to help preserve cardiac function, other times appearing to promote cardiac decline. Numerous control points regulating autophagic activity and cargo selection provide a diversity of opportunities for drug targeting. In addition there is an innate circadian rhythm to the systemic regulation of autophagy that is often overlooked but provides potential opportunities to target and optimize pharmacological intervention.

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“…Circadian rhythms modulate human behavior and physiology, including cognitive function,1 as well as the timing and treatment of several neurological and medical disorders, including hemorrhagic2 and ischemic3 stroke, amyloid‐β secretion,4 epilepsy,5 myocardial infarction,6 ventricular arrhythmias,7 cancer,8 and even time of death 9. Moreover, circadian misalignment, as seen in shift work, predisposes not only to accidents and lost productivity, but also to common diseases, such as diabetes 10.…”

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confidence: 99%

A common polymorphism near PER1 and the timing of human behavioral rhythms

Lim

Chang

Liu

et al. 2012

Annals of Neurology

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Objective Circadian rhythms influence the timing of behavior, neurological diseases, and even death. Rare mutations in homologs of evolutionarily conserved clock genes are found in select pedigrees with extreme sleep timing, and there is suggestive evidence that certain common polymorphisms may be associated with self-reported day/night preference. However, no common polymorphism has been associated with the timing of directly observed human behavioral rhythms or other physiological markers of circadian timing at the population level. Methods We performed a candidate-gene association study with replication, evaluating associations between polymorphisms in homologs of evolutionarily conserved clock genes and the timing of behavioral rhythms measured by actigraphy. For validated polymorphisms, we evaluated associations with transcript expression and time of death in additional cohorts. Results rs7221412, a common polymorphism near period homolog 1 (PER1), was associated with the timing of activity rhythms in both the discovery and replication cohorts (joint p=2·1×10−7). Mean activity timing was delayed by 67 minutes in rs7221412GG vs. rs7221412AA homozygotes. rs7221412 also showed a suggestive time-dependent relationship with both cerebral cortex (p=0.05) and CD14+CD16− monocyte (p=0.02) PER1 expression and an interesting association with time of death (p=0.015) in which rs7221412GG individuals had a mean time of death nearly seven hours later than rs7221412AA/AG. Interpretation A common polymorphism near PER1 is associated with the timing of human behavioral rhythms, and shows evidence of association with time of death. This may be mediated by differential PER1 expression. These results may facilitate individualized scheduling of shift-work, medical treatments, or monitoring of vulnerable patient populations.

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When people die

Cited by 110 publications

References 20 publications

Normal and abnormal sleep in the elderly

Normal and abnormal sleep in the elderly

Targets, trafficking, and timing of cardiac autophagy

A common polymorphism near PER1 and the timing of human behavioral rhythms

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