Journal of Circadian Rhythms最新文献

Shift work is an inconsistent and atypical work schedule. This study aimed to investigate the influence of shift work on the Quality of Sleep (QOS) and Executive Functions (EF). Thirty shift workers and thirty day workers first completed a demographic questionnaire. They then were tested using the Pittsburgh Sleep Quality Index (PSQI) and EF tests, including the Corsi Block-Tapping Task (CBTT), Berg's Card Sorting Task (BCST), and the Continuous Performance Task (CPT). Results were subjected to non-parametric Chi-Square Tests, the Mann-Whitney U Test, and Independent T-Tests. Shift workers had significantly poorer sleep quality than day workers, which was shown in PSQI global scale (p = 0.001), sleep duration (p = 0.042), habitual sleep efficiency (p = 0.021), and sleep disturbance (p = 0.021). Concerning EF tests, shift workers performed significantly poorer on CBTT (p = 0.019) and BCST (p = 0.015, 0.047) compared with day workers. Significant differences were also observed between shift workers and day workers in terms of variables of omission errors (p = 0.037) and commission errors (p = 0.041) on CPT, but no significant difference was found between shift workers and day workers in reaction time (p = 0.561). Shift work impaired EF. These findings are related to shift workers' poorer sleep and its detrimental effects on areas of the brain, which are critical for EF, such as the prefrontal area. Our results suggest the evaluation and implication of practices and policies to assuage the consequences of working in shifts.

Eveningness (a diurnal preference for evening time) is associated with a number of negative health outcomes and risk and prevalence for psychiatric disorder. Our understanding of the anatomical substrates of diurnal preference, however, is limited. The current study used Voxel-Based Morphometry to compare grey matter volume in a large sample (N = 3730) of healthy adults determined by questionnaire to be either definite morning-type or definite evening-type. Eveningness was associated with increased grey matter volume in precuneus, brain regions implicated in risk and reward processing (bilateral nucleus accumbens, caudate, putamen and thalamus) and orbitofrontal cortex. These results indicate an anatomical-basis for diurnal preference which may underlie reported differences in behaviour and brain function observed in these individuals.

Although sleep is ubiquitous, its evolutionary purpose remains elusive. Though every species of animal, as well as many plants sleep, theories of its origin are purely physiological, e.g. to conserve energy, make repairs or to consolidate learning. An evolutionary reason for sleep would answer one of biology's fundamental unanswered questions. When environmental conditions change on a periodic basis (winter/summer, day/night) organisms must somehow confront the change or else be less able to compete in either niche. Seasonal adaptation includes the migration of birds, changes in honeybee physiology and winter abscission in plants. Diurnal adaptation must be more rapid, forcing changes in behavior in addition to physiology. Since organisms must exist in both environments, evolution has created a way to force a change in behavior, in effect creating "different" organisms (one awake, one asleep) adapted separately to two distinct niches. We sleep to allow evolving into two competing niches. The physiology of sleep forces a change to a different state for the second niche. The physiological needs for sleep are mechanisms that have evolved to achieve this goal.

The reproductive function of humans is regulated by several sex hormones which are secreted in synergy with the circadian timing of the body. Sleep patterns produce generic signatures that physiologically drive the synthesis, secretion, and metabolism of hormones necessary for reproduction. Sleep deprivation among men and women is increasingly reported as one of the causes of infertility. In animal models, sleep disturbances impair the secretion of sexual hormones thereby leading to a decrease in testosterone level, reduced sperm motility and apoptosis of the Leydig cells in male rats. Sleep deprivation generates stressful stimuli intrinsically, due to circadian desynchrony and thereby increases the activation of the Hypothalamus-Pituitary Adrenal (HPA) axis, which, consequently, increases the production of corticosterone. The elevated level of corticosteroids results in a reduction in testosterone production. Sleep deprivation produces a commensurate effect on women by reducing the chances of fertility. Sleeplessness among female shift workers suppresses melatonin production as well as excessive HPA activation which results in early pregnancy loss, failed embryo implantation, anovulation and amenorrhea. Sleep deprivation in women has also be found to be associated with altered gonadotropin and sex steroid secretion which all together lead to female infertility. Poor quality of sleep is observed in middle-aged and older men and this also contributes to reduced testosterone concentrations. The influence of sleep disturbances post-menopausal is associated with irregular synthesis and secretion of female sex steroid hormones.

Sleep seems essential to proper functioning of the prefrontal cortex (PFC). The role of different neurotransmitters has been studied, mainly the catecholamines and serotonin. Less attention has been paid to the amino acid transmitters and histamine. Here, we focus on the activity of these molecules in the PFC during sleep and sleep deprivation (SD). We determined extracellular concentrations of histamine and 8 amino acids in the medial PFC before, during and after SD. Additionally, we systematically reviewed the literature on studies reporting microdialysis measurements relating to sleep throughout the brain. In our experiment, median concentrations of glutamate were higher during SD than during baseline (p = 0.013) and higher during the dark-active than during the resting phase (p = 0.003). Glutamine was higher during post-SD recovery than during baseline (p = 0.010). For other compounds, no differences were observed between light and dark circadian phase, and between sleep deprivation, recovery and baseline. We retrieved 13 papers reporting on one or more of the molecules of interest during naturally occurring sleep, 2 during sleep deprivation and 2 during both. Only two studies targeted PFC. Histamine was low during sleep, but high during sleep deprivation and wakefulness, irrespective of brain area. Glu (k = 11) and GABA (k = 8) concentrations in different brain areas were reported to peak during sleep or wakefulness or to lack state-dependency. Aspartate, glycine, asparagine and taurine were less often studied (1-2 times), but peaked exclusively during sleep. Sleep deprivation increased glutamate and GABA exclusively in the cortex. Further studies are needed for drawing solid conclusions.

Introduction: Women diagnosed with breast cancer (BC) are at increased risk of sleep deficiency. Approximately 30-60% of these women report poor sleep during and following surgery, chemotherapy, radiation therapy, and anti-estrogen therapy. The purpose of this study was to examine the relationship between genetic variation in circadian rhythm genes and self-reported sleep quality in women with BC.

Methods: This cross-sectional study recruited women with a first diagnosis of breast cancer at five sites in Nebraska and South Dakota. Sixty women were included in the study. Twenty-six circadian genes were selected for exome sequencing using the Nextera Rapid Capture Expanded Exome kit. 414 variants had a minor allele frequency of ≥5% and were included in the exploratory analysis. The association between Pittsburgh Sleep Quality Index (PSQI) score and genetic variants was determined by two-sample t-test or ANOVA.

Results: Twenty-five variants were associated with the PSQI score at p < 0.10, of which 19 were significant at p<0.05, although the associations did not reach statistical significance after adjustment for multiple comparisons. Variants associated with PSQI were from genes CSNK1D & E, SKP1, BHLHE40 & 41, NPAS2, ARNTL, MYRIP, KLHL30, TIMELESS, FBXL3, CUL1, PER1&2, RORB. Two genetic variants were synonymous or missense variants in the BHLHE40 and TIMELESS genes, respectively.

Conclusions: These exploratory results demonstrate an association of genetic variants in circadian rhythm pathways with self-reported sleep in women with BC. Testing this association is warranted in a larger replication population.

The circadian clock is a biological mechanism that permits some organisms to anticipate daily environmental variations. This clock generates biological rhythms, which can be reset by environmental cues such as cycles of light or temperature, a process known as entrainment. After entrainment, circadian rhythms typically persist with approximately 24 hours periodicity in free-running conditions, i.e. in the absence of environmental cues. Experimental evidence also shows that a free-running period close to 24 hours is maintained across a range of temperatures, a process known as temperature compensation. In the plant Arabidopsis, the effect of light on the circadian system has been widely studied and successfully modelled mathematically. However, the role of temperature in periodicity, and the relationship between entrainment and compensation, are not fully understood. Here we adapt recent models to incorporate temperature dependence by applying Arrhenius equations to the parameters of the models that characterize transcription, translation, and degradation rates. We show that the resulting models can exhibit thermal entrainment and temperature compensation, but that these phenomena emerge from physiologically different sets of processes. Further simulations combining thermal and photic forcing in more realistic scenarios clearly distinguish between the processes of entrainment and compensation, and reveal temperature compensation as an emergent property which can arise as a result of multiple temperature-dependent interactions. Our results consistently point to the thermal sensitivity of degradation rates as driving compensation and entrainment across a range of conditions.