Journal of Biological Rhythms最新文献

Augmentation index and pulse wave velocity are markers of vascular compromise and independent predictors of cardiovascular risk and mortality. While the link between shift work and heightened cardiovascular risk is established, the intricate genesis of early cardiovascular outcomes in shift workers remains incompletely understood. However, there is evidence that sleep duration plays a role in this regard. Here we evaluate the association of total sleep time with pulse wave velocity, augmentation index, and central blood pressure in night shift workers. This study cross-sectionally evaluated the association of total sleep time evaluated by 10-day monitoring actigraphy with augmentation index, pulse wave velocity, and brachial and central blood pressure evaluated by oscillometry in nursing professionals, 63 shift workers (89% women; age = 45.0 ± 10.5 years), and 17 (100% women; age = 41.8 ± 15.6) day workers. There were no differences in the studied variables between shift workers and day workers. Results of correlation analysis demonstrated that pulse wave velocity, central systolic blood pressure, central diastolic blood pressure, brachial systolic blood pressure, and brachial diastolic blood pressure tended to have significant correlation with each other, while these measures did not have a significant relationship with augmentation index in both groups. However, results of adjusted restricted cubic spline analysis showed a U-shaped-curve association between total sleep time and augmentation index (p < 0.001 for trend) with a nadir at 300-360 min of total sleep time in shift workers. The present study showed that total sleep time, assessed by actigraphy, had a U-shaped association with augmentation index in shift workers, which indicated better characteristics of vascular functionality when sleep time was 5-6 h in the workers studied.

The objective of the present study was to test the effects of an inpatient management system (CircadianCare) aimed at limiting the negative impact of hospitalization on sleep by enhancing circadian rhythmicity. Fifty inpatients were randomized to either CircadianCare (n = 25; 18 males, 62.4 ± 1.9 years) or standard of care (n = 25; 14 males, 64.5 ± 2.3 years). On admission, all underwent a full sleep-wake evaluation; they then completed daily sleep diaries and wore an actigraph for the whole length of hospitalization. On days 1 (T0), 7 (T1), and 14 (T2, if still hospitalized), salivary melatonin for dim light melatonin onset (DLMO) and 24-h skin temperature were recorded. In addition, environmental noise, temperature, and illuminance were monitored. Patients in the CircadianCare arm followed 1 of 3 schedules for light/dark, meal, and physical activity timings, based on their diurnal preference/habits. They wore short-wavelength-enriched light-emitting glasses for 45 min after awakening and short-wavelength light filter shades from 18:00 h until sleep onset. While the first, primary registered outcome (reduced sleep-onset latency on actigraphy or diary) was not met, based on sleep diaries, there was a trend (0.05 < p < 0.1) toward an advance in bedtime for CircadianCare compared to standard of care patients between T0 and T1. Similarly, DLMO time significantly advanced in the small group of patients for whom it could be computed on both occasions, with untreated ones starting from earlier baseline values. Patients sleeping near the window had significantly higher sleep efficiency, regardless of treatment arm. As noise fluctuation increased, so did the number of night awakenings, regardless of treatment arm. In conclusion, the CircadianCare management system showed positive results in terms of advancing sleep timing and the circadian rhythm of melatonin. Furthermore, our study identified a combination of environmental noise and lighting indices, which could be easily modulated to prevent hospitalization-related insomnia.

Surely most chronobiologists believe circadian clocks are an adaptation of organisms that enhances fitness, but are we certain that this focus of our research effort really confers a fitness advantage? What is the evidence, and how do we evaluate it? What are the best criteria? These questions are the topic of this review. In addition, we will discuss selective pressures that might have led to the historical evolution of circadian systems while considering the intriguing question of whether the ongoing climate change is modulating these selective pressures so that the clock is still evolving.

It has been 50 years since the suprachiasmatic nucleus (SCN) was first identified as the central circadian clock and 25 years since the last overview of developments in the field was published in the Journal of Biological Rhythms. Here, we explore new mechanisms and concepts that have emerged in the subsequent 25 years. Since 1997, methodological developments, such as luminescent and fluorescent reporter techniques, have revealed intricate relationships between cellular and network-level mechanisms. In particular, specific neuropeptides such as arginine vasopressin, vasoactive intestinal peptide, and gastrin-releasing peptide have been identified as key players in the synchronization of cellular circadian rhythms within the SCN. The discovery of multiple oscillators governing behavioral and physiological rhythms has significantly advanced our understanding of the circadian clock. The interaction between neurons and glial cells has been found to play a crucial role in regulating these circadian rhythms within the SCN. Furthermore, the properties of the SCN network vary across ontogenetic stages. The application of cell type-specific genetic manipulations has revealed components of the functional input-output system of the SCN and their correlation with physiological functions. This review concludes with the high-risk effort of identifying open questions and challenges that lie ahead.

Accurate assessment of the intrinsic period of the human circadian pacemaker is essential for a quantitative understanding of how our circadian rhythms are synchronized to exposure to natural and man-made light-dark (LD) cycles. The gold standard method for assessing intrinsic period in humans is forced desynchrony (FD) which assumes that the confounding effect of lights-on assessment of intrinsic period is removed by scheduling sleep-wake and associated dim LD cycles to periods outside the range of entrainment of the circadian pacemaker. However, the observation that the mean period of free-running blind people is longer than the mean period of sighted people assessed by FD (24.50 $\pm$ 0.17 h vs 24.15 $\pm$ 0.20 h, p $<$0.001) appears inconsistent with this assertion. Here, we present a mathematical analysis using a simple parametric model of the circadian pacemaker with a sinusoidal velocity response curve (VRC) describing the effect of light on the speed of the oscillator. The analysis shows that the shorter period in FD may be explained by exquisite sensitivity of the human circadian pacemaker to low light intensities and a VRC with a larger advance region than delay region. The main implication of this analysis, which generates new and testable predictions, is that current quantitative models for predicting how light exposure affects entrainment of the human circadian system may not accurately capture the effect of dim light. The mathematical analysis generates new predictions which can be tested in laboratory experiments. These findings have implications for managing healthy entrainment of human circadian clocks in societies with abundant access to light sources with powerful biological effects.

Prior research indicates that sleep restriction, sleep deprivation, and circadian misalignment diminish positive affect, whereas effects on negative affect are inconsistent. One potential factor that may influence an individual's affective response to sleep restriction, sleep deprivation, and circadian misalignment is chronotype. Later chronotypes generally report higher negative affect and lower positive affect under typical sleep conditions; however, there is mixed evidence for an influence of chronotype on affective responses to sleep restriction and sleep deprivation. The present study examined the effect of chronotype on positive and negative affect during sleep restriction and subsequent total sleep deprivation. Sixteen healthy adults (M_age = 28.2 years, SD_age = 11.6 years) were classified as earlier or later chronotypes using multiple chronotype definitions: morningness-eveningness (MEQ), mid-sleep on free days corrected (MSFsc), habitual mid-sleep timing, dim light melatonin onset (DLMO), and phase relationship between DLMO and bedtime. Participants completed a 10-day protocol with one night of sleep restriction and subsequent 28 h total sleep deprivation. Affect was assessed hourly during scheduled wakefulness with the Positive and Negative Affect Schedule (PANAS). Data were analyzed with mixed-model analyses of variance (ANOVAs). During sleep restriction and subsequent sleep deprivation, positive affect decreased and negative affect increased. Across all chronotype measures, relatively later chronotypes demonstrated vulnerability to increased negative affect during sleep loss. The influence of chronotype on positive affect during sleep loss varied by chronotype measure. These findings suggest later chronotypes are more vulnerable to affective impairments during sleep loss and circadian misalignment, even when late chronotype is not extreme.

This study examines population-level daily patterns of time-stamped emergency medical service (EMS) dispatches to establish their situational predictability. Using visualization, sinusoidal regression, and statistical tests to compare empirical cumulative distributions, we analyzed 311,848,450 emergency medical call records from the US National Emergency Medical Services Information System (NEMSIS) for years 2010 through 2022. The analysis revealed a robust daily pattern in the hourly distribution of distress calls across 33 major categories of medical emergency dispatch types. Sinusoidal regression coefficients for all types were statistically significant, mostly at the p < 0.0001 level. The coefficient of determination $\left(R^2\right)$ ranged from 0.84 and 0.99 for all models, with most falling in the 0.94 to 0.99 range. The common sinusoidal pattern, peaking in mid-afternoon, demonstrates that all major categories of medical emergency dispatch types appear to be influenced by an underlying daily rhythm that is aligned with daylight hours and common sleep/wake cycles. A comparison of results with previous landmark studies revealed new and contrasting EMS patterns for several long-established peak occurrence hours-specifically for chest pain, heart problems, stroke, convulsions and seizures, and sudden cardiac arrest/death. Upon closer examination, we also found that heart attacks, diagnosed by paramedics in the field via 12-lead cardiac monitoring, followed the identified common daily pattern of a mid-afternoon peak, departing from prior generally accepted morning tendencies. Extended analysis revealed that the normative pattern prevailed across the NEMSIS data when reorganized to consider monthly, seasonal, daylight-savings versus civil time, and pre-/post-COVID-19 periods. The predictable daily EMS patterns provide impetus for more research that links daily variation with causal risk and protective factors. Our methods are straightforward and presented with detail to provide accessible and replicable implementation for researchers and practitioners.

Misalignment of behavior and circadian rhythms due to night work can impair sleep and waking function. While both simulated and field-based studies suggest that circadian adaptation to a nocturnal schedule is slow, the rates of adaptation in real-world shift-work conditions are still largely unknown. The aim of this study was to evaluate the extent of adaptation of 24-h rhythms with 6-sulfatoxymelatonin (aMT6s) and cortisol in police officers working rotating shifts, with a special attention to night shifts. A total of 76 police officers (20 women; aged 32 ± 5.4 years, mean ± SD) from the province of Quebec, Canada, participated in a field study during their 28- or 35-day work cycle. Urine samples were collected for ~32 h before a series of day, evening, and night shifts to assess circadian phase. Before day, evening, and night shifts, 60%-89% of officers were adapted to a day schedule based on aMT6 rhythms, and 71%-78% were adapted based on cortisol rhythms. To further quantify the rate of circadian adaptation to night shifts, initial and final phases were determined in a subset of 37 officers with suitable rhythms for both hormones before and after 3-8 consecutive shifts (median = 7). Data were analyzed with circular and linear mixed-effects models. After night shifts, 30% and 24% of officers were adapted to a night-oriented schedule for aMT6s and cortisol, respectively. Significantly larger phase-delay shifts (aMT6s: -7.3 ± 0.9 h; cortisol: -6.3 ± 0.8 h) were observed in police officers who adapted to night shifts than in non-adapted officers (aMT6s: 0.8 ± 0.9 h; cortisol: 0.2 ± 1.1 h). Consistent with prior research, our results from both urinary aMT6s and cortisol midpoints indicate that a large proportion of police officers remained in a state of circadian misalignment following a series of night shifts in dim-light working environments.