Clocks & Sleep最新文献

During the COVID-19 lockdown, a distortion of time passage has been widely reported in association with a change in daily rhythm. However, several variables related to these changes have not been considered. The purpose of the present study was to assess the changes in dispositional mindfulness, time experience, sleep timing and subjective memory functioning. A longitudinal study was conducted on 39 Italian adults (53.85% males; 35.03 ± 14.02 years) assessing mindfulness, ad hoc questions of sleep habits during workdays and free days, chronotypes, subjective time experience, and memory functioning before (December 2019-March 2020) and during (April 2020-May 2020) the first Italian COVID-19 lockdown. Participants reported delayed sleep timing, a slowdown in the perception of the present time, a decrease of time pressure, and an increase in the feeling of time expansion/boredom. In addition to correlations between mindfulness, memory functioning, and subjective sleep duration during workdays, a mediation model showed that changes in the dispositional mindfulness determined a delay of bedtime during workdays through the mediation effect of increased feeling of time expansion/boredom. This finding highlighted the role of mindfulness in reducing the feeling of time expansion/boredom for regulating the sleep timing. The theoretical and practical implications of the findings are discussed.

In this narrative review article, we discuss the role of sleep deprivation (SD) in memory processing in rodent models. Numerous studies have examined the effects of SD on memory, with the majority showing that sleep disorders negatively affect memory. Currently, a consensus has not been established on which damage mechanism is the most appropriate. This critical issue in the neuroscience of sleep remains largely unknown. This review article aims to elucidate the mechanisms that underlie the damaging effects of SD on memory. It also proposes a scientific solution that might explain some findings. We have chosen to summarize literature that is both representative and comprehensive, as well as innovative in its approach. We examined the effects of SD on memory, including synaptic plasticity, neuritis, oxidative stress, and neurotransmitters. Results provide valuable insights into the mechanisms by which SD impairs memory function.

This article provides an overview of how sleep and circadian rhythm disturbances mutually influence the occurrence of dental caries and how it is possible to reduce the risk of circadian rhythm disturbances, sleep, and associated adverse effects. Dental caries is a global problem worldwide that contributes to sociological limitations. Numerous factors influence the occurrence of dental caries, from socioeconomic factors to cariogenic bacteria, dietary habits, and oral hygiene. However, sleep disorders and circadian rhythm disturbances represent a new approach in the fight against the increasing prevalence of dental caries worldwide. Bacteria in the oral cavity and the oral microbiome are mainly responsible for the development of caries, and saliva plays an important role in their regulation. The circadian rhythm regulates numerous physiological functions, including sleep and saliva production. Disturbances in sleep and circadian rhythms affect saliva production, which impacts the development of dental caries, as saliva is necessary for regulating and maintaining oral health, especially for controlling oral infections. A person's preference for a particular time of day depends on the circadian rhythm called chronotype. Individuals with an evening chronotype have a less healthy lifestyle that can lead to a higher caries risk than individuals with a morning chronotype. Because circadian rhythms are critical to maintaining sleep homeostasis and oral health, sleep disturbances can disrupt circadian rhythms and lead to a vicious cycle.

The biological clock is a molecular oscillator that generates a 24-hour rhythm in accordance with the earth's rotation. Physiological functions and pathophysiological processes such as inflammatory bowel diseases (IBD) are closely linked to the molecular clock. This review summarizes 14 studies in humans and mice on the interactions between the biological clock and IBD. It provides evidence that IBD negatively affect core clock gene expression, metabolism and immune functions. On the other hand, disruption of the clock promotes inflammation. Overexpression of clock genes can lead to inhibition of inflammatory processes, while silencing of clock genes can lead to irreversible disease activity. In both human and mouse studies, IBD and circadian rhythms have been shown to influence each other. Further research is needed to understand the exact mechanisms and to develop potential rhythm-related therapies to improve IBD.

Sleep disturbances are a common yet often overlooked symptom of psychosis that can drastically affect the quality of life and well-being of those living with the condition. Sleep disorders are common in people diagnosed with schizophrenia and have significant negative effects on the clinical course of the illness and the functional outcomes and quality of life of patients. There is a limited number of studies addressing this question in first-episode psychosis (FEP). In this narrative review, we aimed to provide an overview of sleep disorders in populations with FEP and at-risk mental states (ARMS). The review was focused on the various treatments currently used for sleep disorders, including both non-pharmacological and pharmacological treatments. A total of 48 studies were included. We found that sleep disturbances are associated with attenuated psychotic symptoms and other psychopathological symptoms in ARMSs. The association of sleep disturbances with the transition to psychosis has been poorly investigated. Sleep disturbances have an impact on the quality of life and the psychopathological symptoms of people suffering from FEP. The non-pharmacological treatments include cognitive behavioral therapy for insomnia, bright light therapy, cognitive restructuring techniques, sleep restriction therapy, basic sleep hygiene education, and the provision of portable sleep trackers. Other treatments include antipsychotics in acute phases and melatonin. The early intervention in sleep disturbances may improve overall prognosis in emerging psychosis populations.

Research has shown that shiftworkers experience poor sleep and high levels of fatigue. Although considerable research has been performed on fatigue within many shift-work occupations, very little has been done with emergency physicians (EPs). This qualitative study was conducted with the goal of gaining insight into EPs' perceptions of fatigue at work. Twenty EPs from an academic medical center participated in virtual interviews, with nine open-ended questions asked in a semi-structured interview format. Twelve common topics with four main themes emerged from the interviews. Three of these common themes included sources of fatigue (including both work- and home-related sources), consequences of fatigue (including impacts on individuals and performance), and prevention and mitigation strategies to cope with fatigue. The fourth main theme was the belief in the inevitability of fatigue due to high cognitive load, emotionally taxing work experiences, work unpredictability, and the 24/7 shift-work nature of emergency medicine. EPs' experiences with fatigue are consistent with but extend those of other types of shiftworkers. Our findings suggest that EPs tend to incorporate the inevitability of fatigue at work into their identity as EPs and experience a sense of learned helplessness as a result, suggesting areas for future interventions.

Sleep issues are pervasive, and treatment can be difficult to access, if available at all. The purpose of this study was to test whether the delivery modality (online vs. in person) of the SLeep Education for Everyone Program (SLEEP) influenced programmatic outcomes. A total of 60 participants completed the study, 28 in the online group and 32 in the in-person group. Across all participants, SLEEP improved sleep duration, sleep quality, and sleep hygiene behaviors (p < 0.001 for all). When comparing delivery modality, sleep duration and quality improved similarly between groups; however, sleep hygiene behaviors improved more in the in-person group (p = 0.033). Sleep hygiene scores did not correlate with sleep duration or quality after the program. Based on these findings, SLEEP appears to be equally effective in improving sleep duration and quality when delivered online or in person. These findings suggest that SLEEP can be delivered based on the organization's and participant's resources, needs, and preferred style of interaction.

The sleep-wake cycle is a highly regulated behavior in which a circadian clock times sleep and waking, whereas a homeostatic process controls sleep need. Both the clock and the sleep homeostat interact, but to what extent they influence each other is not understood. There is evidence that clock genes, in particular Period2 (Per2), might be implicated in the sleep homeostatic process. Sleep regulation depends also on the proper functioning of neurons and astroglial cells, two cell-types in the brain that are metabolically dependent on each other. In order to investigate clock-driven contributions to sleep regulation we non-invasively measured sleep of mice that lack the Per2 gene either in astroglia, neurons, or all body cells. We observed that mice lacking Per2 in all body cells (Per2^Brdm and TPer2 animals) display earlier onset of sleep after sleep deprivation (SD), whereas neuronal and astroglial Per2 knock-out animals (NPer2 and GPer2, respectively) were normal in that respect. It appears that systemic (whole body) Per2 expression is important for physiological sleep architecture expressed by number and length of sleep bouts, whereas neuronal and astroglial Per2 weakly impacts night-time sleep amount. Our results suggest that Per2 contributes to the timing of the regulatory homeostatic sleep response by delaying sleep onset after SD and attenuating the early night rebound response.

Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity in the United States and is associated with numerous chronic sequelae long after the point of injury. One of the most common long-term complaints in patients with TBI is sleep dysfunction. It is reported that alterations in melatonin follow TBI and may be linked with various sleep and circadian disorders directly (via cellular signaling) or indirectly (via free radicals and inflammatory signaling). Work over the past two decades has contributed to our understanding of the role of melatonin as a sleep regulator and neuroprotective anti-inflammatory agent. Although there is increasing interest in the treatment of insomnia following TBI, a lack of standardization and rigor in melatonin research has left behind a trail of non-generalizable data and ambiguous treatment recommendations. This narrative review describes the underlying biochemical properties of melatonin as they are relevant to TBI. We also discuss potential benefits and a path forward regarding the therapeutic management of TBI with melatonin treatment, including its role as a neuroprotectant, a somnogen, and a modulator of the circadian rhythm.

It has recently been noted that a reduction in sleep reactivity, characterized as the trait-like degree to which exposure to stress interferes with sleep, and anxiety sensitivity are associated with reduced insomnia severity. This study aimed to examine whether sleep reactivity and anxiety sensitivity are associated with insomnia-related depression and anxiety among city government employees in Japan. This cross-sectional study included 1810 city government employees of Koka City, Japan (mean age (standard deviation): 45.33 (12.20) years) who completely answered the scales for sleep reactivity, anxiety sensitivity, anxiety, and depression. Stepwise multiple regression analysis adjusted for demographic data showed that anxiety sensitivity (β = 0.39) was significantly linked to anxiety, and sleep reactivity (β = 0.36) was significantly linked to depression in individuals with insomnia. Additionally, the results of a logistic regression analysis adjusted for demographic data showed that anxiety sensitivity and sleep reactivity were relevant factors for anxious insomnia (OR = 12.69) and depressive insomnia (OR = 8.73), respectively. Whereas both sleep reactivity (OR = 14.67) and anxiety sensitivity (OR = 6.14) were associated with combined insomnia. These findings indicate that sleep reactivity is strongly associated with depressive symptoms, and anxiety sensitivity is strongly associated with anxiety symptoms in individuals with insomnia.