Extended nights, sleep loss, and recovery sleep in adolescents

In summary, this study of sleep in adolescents on an atypical schedule of 18-hour nights showed marked but not unanticipated differences in sleep as function of prior sleep deprivation. Unanticipated was the evidence of "recovery" sleep in adolescents who not only were not sleep deprived, but who had been on a sleep "optimizing" schedule and had been awake for only 10 hours. Extended sleep beginning about 4 hours in advance of entrained sleep onset phase was not associated with a return of SWS, a finding coinciding with predictions from studies in adults. Finally, this study provides an indication that the homeostatic sleep/wake process becomes less robust or sleep responsive during adolescent development, a phenomenon that may influence the delay of sleep common in adolescents.     

Interactions among sleep disordered breathing,obesity, and sleep duration

Sleep and Biological Rhythms -     

Muscle pain, dyskinesia, and sleep

Muscle pain and poor sleep commonly occur together. Whether pain induces poor sleep or vice versa is difficult to know. Muscle pain is also observed in the presence of some types of dyskinesia or movement disorders. The interaction between sleep, movement disorders, and some musculoskeletal pain appears to be complex and may be influenced by various concomitant psychological and (or) biological factors.     

Interfering with theories of sleep and memory: sleep, declarative memory, and associative interference

Mounting behavioral evidence in humans supports the claim that sleep leads to improvements in recently acquired, nondeclarative memories. Examples include motor-sequence learning; visual-discrimination learning; and perceptual learning of a synthetic language. In contrast, there are limited human data supporting a benefit of sleep for declarative (hippocampus-mediated) memory in humans (for review, see). This is particularly surprising given that animal models (e.g.,) and neuroimaging studies (e.g.,) predict that sleep facilitates hippocampus-based memory consolidation. We hypothesized that we could unmask the benefits of sleep by challenging the declarative memory system with competing information (interference). This is the first study to demonstrate that sleep protects declarative memories from subsequent associative interference, and it has important implications for understanding the neurobiology of memory consolidation.     

Effect of fasting during Ramadan on sleep architecture,daytime sleepiness and sleep pattern

Sleep and Biological Rhythms - Fasting during Ramadan is distinct from regular voluntary or experimental fasting. This project was conducted to objectively assess the effect of Ramadan fasting on...     

Stress, cardiac activity and sleep.

An overview is presented of the relationship between cardiovascular activity and sleep, emphasizing the interrelations between stage of sleep and cardiovascular dysfunction. Possible implications of the data are discussed, especially in relation to stress-related factors and possible treatment regimens.     

Hypocretin/orexin, sleep and narcolepsy

The discovery that hypocretins are involved in narcolepsy, a disorder associated with excessive daytime sleepiness, cataplexy and unusually rapid transitions to rapid-eye-movement sleep, opens a new field of investigation in the area of sleep control physiology. Hypocretin-1 and -2 (also called orexin-A and -B) are newly discovered neuropeptides processed from a common precursor, preprohypocretin. Hypocretin-containing cells are located exclusively in the lateral hypothalamus, with widespread projections to the entire neuroaxis. Two known receptors, Hcrtr1 and Hcrtr2, have been reported. The functional significance of the hypocretin system is rapidly emerging in both animals and humans. Hypocretin abnormalities cause narcolepsy in dogs, human and mice. The role of the hypocretin system in normal sleep regulation is more uncertain. We believe hypocretin cells drive cholinergic and monoaminergic activity across the sleep cycle. Input from the suprachiasmatic nucleus to hypocretin-containing neurons may explain the occurrence of clock-dependent alertness. Other functions are suggested by pharmacological and neurochemical experiments. These include regulation of food intake, neuroendocrine function, autonomic nervous system activity and energy balance.     

One's sex,sleep, and posttraumatic stress disorder

Women are approximately twice as likely as men to develop posttraumatic stress disorder (PTSD) after trauma exposure. Mechanisms underlying this difference are not well understood. Although sleep is recognized to have a critical role in PTSD and physical and psychological health more generally, research into the role of sleep in PTSD sex differences has been only recent. In this article, we review both animal and human studies relevant to sex differences in sleep and PTSD with an emphasis on the roles of sex hormones. Sleep impairment including insomnia, trauma-related nightmares, and rapid-eye-movement (REM) sleep fragmentation has been observed in individuals with chronic and developing PTSD, suggesting that sleep impairment is a characteristic of PTSD and a risk factor for its development. Preliminary findings suggested sex specific patterns of sleep alterations in developing and established PTSD. Sleep maintenance impairment in the aftermath of trauma was observed in women who subsequently developed PTSD, and greater REM sleep fragmentation soon after trauma was associated with developing PTSD in both sexes. In chronic PTSD, reduced deep sleep has been found only in men, and impaired sleep initiation and maintenance with PTSD have been found in both sexes. A limited number of studies with small samples have shown that sex hormones and their fluctuations over the menstrual cycle influenced sleep as well as fear extinction, a process hypothesized to be critical to the pathogenesis of PTSD. To further elucidate the possible relationship between the sex specific patterns of PTSD-related sleep alterations and the sexually dimorphic risk for PTSD, future studies with larger samples should comprehensively examine effects of sex hormones and the menstrual cycle on sleep responses to trauma and the risk/resilience for PTSD utilizing various methodologies including fear conditioning and extinction paradigms and animal models.     

Don't worry,sleep well: predictors of sleep loss over worry

Sleep and Biological Rhythms - In this study, our aim was to explore the relationship between sleep quality/quantity, chronotype, pre-sleep arousal, arousability, stress, coping, neuroticism,...     

Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Sleep is understood to possess recuperative properties and, conversely, sleep loss is associated with disease and shortened life span. Despite these critical attributes, the mechanisms and functions by which sleep and sleep loss impact health still are speculative. One of the most consistent, if largely overlooked, signs of sleep loss in both humans and laboratory rats is a progressive increase in circulating phagocytic cells, mainly neutrophils. The destination, if any, of the increased circulating populations has been unknown and, therefore, its medical significance has been uncertain. The purpose of the present experiment was to determine the content and location of neutrophils in liver and lung tissue of sleep-deprived rats. These are two principal sites affected by neutrophil migration during systemic inflammatory illness. The content of neutrophils in the intestine also was determined. Sleep deprivation in rats was produced for 5 and 10 days by the Bergmann-Rechtschaffen disk method, which has been validated for its high selectivity under freely moving conditions and which was tolerated and accompanied by a deep negative energy balance. Comparison groups included basal conditions and 48 h of sleep recovery after 10 days of sleep loss. Myeloperoxidase (MPO), an enzyme constituent of neutrophils, was extracted from liver, lung, and intestinal tissues, and its activity was determined by spectrophotometry. Leukocytes were located in vasculature and interstitial spaces in the liver and the lung by immunohistochemistry. Heme oxygenase-1, also known as heat shock protein-32 and a marker of cellular stress, and corticosterone also were measured. The results indicate neutrophil migration into extravascular liver and lung tissue concurrent with cell stress and consistent with tissue injury or infection induced by sleep loss. Plasma corticosterone was unchanged. Recovery sleep was marked by increased lung heme oxygenase-1, increased intestinal MPO activity, and abnormally low corticosterone, suggesting ongoing reactive processes as a result of prior sleep deprivation.     

MCH levels in the CSF,brain preproMCH and MCHR1 gene expression during paradoxical sleep deprivation,sleep rebound and chronic sleep restriction

Neurons that utilize melanin-concentrating hormone (MCH) as neuromodulator are located in the lateral hypothalamus and incerto-hypothalamic area. These neurons project throughout the central nervous system and play a role in sleep regulation. With the hypothesis that the MCHergic system function would be modified by the time of the day as well as by disruptions of the sleep-wake cycle, we quantified in rats the concentration of MCH in the cerebrospinal fluid (CSF), the expression of the MCH precursor (Pmch) gene in the hypothalamus, and the expression of the MCH receptor 1 (Mchr1) gene in the frontal cortex and hippocampus. These analyses were performed during paradoxical sleep deprivation (by a modified multiple platform technique), paradoxical sleep rebound and chronic sleep restriction, both at the end of the active (dark) phase (lights were turned on at Zeitgeber time zero, ZT0) and during the inactive (light) phase (ZT8).We observed that in control condition (waking and sleep ad libitum), Mchr1 gene expression was larger at ZT8 (when sleep predominates) than at ZT0, both in frontal cortex and hippocampus.In addition, compared to control, disturbances of the sleep–wake cycle produced the following effects: paradoxical sleep deprivation for 96 and 120 h reduced the expression of Mchr1 gene in frontal cortex at ZT0. Sleep rebound that followed 96 h of paradoxical sleep deprivation increased the MCH concentration in the CSF also at ZT0. Twenty-one days of sleep restriction produced a significant increment in MCH CSF levels at ZT8. Finally, sleep disruptions unveiled day/night differences in MCH CSF levels and in Pmch gene expression that were not observed in control (undisturbed) conditions.In conclusion, the time of the day and sleep disruptions produced subtle modifications in the physiology of the MCHergic system.     

Lipid signaling: sleep, synaptic plasticity, and neuroprotection

Increasing evidence indicates that bioactive lipids participate in the regulation of synaptic function and dysfunction. We have demonstrated that signaling mediated by platelet-activating factor (PAF) and cyclooxygenase (COX)-2-synthesized PGE2 is involved in synaptic plasticity, memory, and neuronal protection [Clark GD, Happel LT, Zorumski CF, Bazan NG. Enhancement of hippocampal excitatory synaptic transmission by platelet-activating factor. Neuron 1992; 9:1211; Kato K, Clark GD, Bazan NG, Zorumski CF. Platelet-activating factor as a potential retrograde messenger in CA1 hippocampal long-term potentiation. Nature 1994; 367:175; Izquierdo I, Fin C, Schmitz PK, et al. Memory enhancement by intrahippocampal, intraamygdala or intraentorhinal infusion of platelet-activating factor measured in an inhibitory avoidance. Proc Natl Acad Sci USA 1995; 92:5047; Chen C, Magee CJ, Bazan NG. Cyclooxygenase-2 regulates prostaglandin E2 signaling in hippocampal long-term synaptic plasticity. J Neurophysiol 2002; 87:2851]. Recently, we found that prolonged continuous wakefulness (primarily rapid eye movement (REM)-sleep deprivation, SD) causes impairments in hippocampal long-term synaptic plasticity and hippocampus-dependent memory formation [McDermott CM, LaHoste GJ, Chen C, Musto A, Bazan NG, Magee JC. Sleep deprivation causes behavioral, synaptic, and membrane excitability alterations in hippocampal neurons. J Neurosci 2003; 23:9687]. To explore the mechanisms underlying SD-induced impairments, we have studied several bioactive lipids in the hippocampus following SD. It appears that SD causes increases in prostaglandin D2 (PGD2) and 2-arachidonylglycerol (2-AG), and a decrease in PGE2, suggesting that these lipid messengers participate in memory consolidation during REM sleep. We have also explored the formation of endogenous neuroprotective lipids. Toward this aim, we have used ischemia-reperfusion damage and LC-PDA-ESI-MS-MS-based lipidomic analysis and identified docosanoids derived from synaptic phospholipid-enriched docosahexaenoic acid. Some of the docosanoids exert potent neuroprotective bioactivity [Marcheselli VL, Hong S, Lukiw WJ, et al. Novel docosanoids inhibit brain ischemia-reperfusion-mediated leukocyte infiltration and pro-inflammatory gene expression. J Biol Chem 2003; 278:43807; Mukherjee PK, Marcheselli VL, Serhan CN, Bazan, NG. Neuroprotectin D1: A docosahexaenoic acid-derived docosatriene protects human retinal pigment epithelial cells from oxidative stress. Proc Nat Acad Sci USA 2004; 101:8491). Taken together, these observations that signaling lipids participate in synaptic plasticity, cognition, and survival indicate that lipid signaling is closely associated with several functions (e.g; learning and memory, sleep, and experimental stroke) and pathologic events. Alterations in endogenous signaling lipids or their receptors resulting from drug abuse lead to changes in synaptic circuitry and induce profound effects on these important functions. In the present article, we will briefly review bioactive lipids involved in sleep, synaptic transmission and plasticity, and neuroprotection, focusing mainly on our experimental studies and how these signaling molecules are related to functions and implicated in some neurologic disorders.     

Relationships among sleep timing,sleep duration and glycemic control in Type 2 diabetes in Thailand

There is evidence that the sleep and circadian systems play a role in glucose metabolism. In addition to physiological factors, sleep is also affected by behavioral, environmental, cultural and social factors. In this study, we examined whether morning or evening preference, sleep timing and sleep duration are associated with glycemic control in patients with type 2 diabetes residing in Thailand. Two hundred and ten type 2 diabetes patients who were not shift workers completed an interview and questionnaires to collect information on diabetes history, habitual sleep duration and sleep timing. Chronotype, an individual’s tendency for being a “morning” or “evening” person, was assessed using the Composite Score of Morningness (CSM), which reflects an individual’s subjective preference for activities in the morning or evening, as well as mid-sleep time on weekend nights (MSF), which reflects their actual sleep behavior. Most recent hemoglobin A1c (HbA1c) values were retrieved from medical records. Evening preference (as indicated by lower CSM), later bedtime on weekends, and shorter sleep duration correlated with higher HbA1c (r?=??0.18, p?=?0.01; r?=?0.17, p?=?0.01 and r?=??0.17, p?=?0.01, respectively), while there was no association between MSF or wake up time and glycemic control. In addition, later bedtime on weekends significantly correlated with shorter sleep duration (r?=??0.34, p?<?0.001). Hierarchical regression analyses adjusting for age, sex, body mass index, insulin use and diabetes duration revealed that later bedtime on weekends was significantly associated with poorer glycemic control (B?=?0.018, p?=?0.02), while CSM was not. Mediation analysis revealed that this association was fully mediated by sleep duration. In summary, later bedtime on weekends was associated with shorter sleep duration and poorer glycemic control in patients with type 2 diabetes. It is likely that patients with later weekend bedtimes curtail their sleep by waking up earlier. Exploring the potential reasons for this phenomenon (e.g. cultural influences, metropolitan lifestyle, environmental factors, family and social obligations) specific to a Thai population may help identify behavioral modifications (i.e. earlier bedtime and/or sleep duration extension) that could possibly lead to improved glycemic control in this population.     

Differences in workday sleep fragmentation,rest-activity cycle,sleep quality,and activity level among nurses working different shifts

ABSTRACT

Schedule changes associated with rotating shifts can interfere with the circadian rhythms of nurses and thereby affect their sleep duration, sleep quality, work efficiency, and work performance. The objectives of this study was to investigate differences in workday sleep fragmentation, rest-activity cycle, sleep quality, and activity level among nurses working different shifts. After filling out a basic information questionnaire and completing the Pittsburgh Sleep Quality Index (PSQI) questionnaire, participants were asked to wear an actigraph and keep sleep records for seven consecutive days. Data pertaining to wake after sleep onset (WASO), 24-hour autocorrelation coefficient (r24), and daytime activity mean was collected in order to investigate workday sleep fragmentation, rest-activity cycle, and daytime activity level. We obtained complete questionnaires and data from 191 nurses. Day- and evening-shift nurses had more regular workday rest-activity cycles than did night-shift nurses (F = 51.26, p < .001). After controlling for r24 coefficients, we determined that nurses who experienced greater workday sleep fragmentation had higher PSQI scores (β = .18, p = .008). After controlling for WASO times, we determined that nurses who had more regular rest-activity cycles on workdays had lower PSQI scores (β = – .16, p = .036). After controlling for shift type and WASO times, we determined that nurses with higher PSQI scores displayed lower activity levels (β = – .21, p = .015) and those with higher r24 coefficients displayed higher activity levels (β = .18, p = .040) on workdays. We then examined the causal path relationships. Among the shifts, only the day-shift nurses had a higher r24 (β = ?.59, p < .001) than did the night-shift nurses; WASO exerted a significant impact on PSQI scores (β = .20, p = .002); r24 had a significant and negative influence on PSQI scores (β = ?.38, p < .001), and PSQI scores significantly and negatively influenced workday activity levels (β = ?.20, p = .006). This study determined that day- and evening-shift nurses enjoyed more regular and consistent rest-activity cycles than did night-shift nurses; nurses with greater workday sleep fragmentation and/or more irregular rest-activity cycles experienced poorer sleep quality; and nurses suffering from poorer sleep quality displayed lower daytime activity levels on workdays.     

Neurophysiological, neurochemical, autonomous and chronobiological basics of sleep medicine

The review discusses various mechanisms of the rapidly growing problem of Sleep Medicine. The "Sleep-wakefulness" cycle is a continuum of different functional states and the diseases that these states might prompt to manifest themselves in various ways. In these cases, we must say that change produces the conditions of disease manifestation rather than the disease itself. The paper describes the dynamics of the autonomous parameters during sleep, emphasizes the role and importance of chronobiological aspects of the "sleep-wakefulness" cycle. The holographic principle of the operation I sleep cycle is described which persists even in the cerebral stroke. From the standpoint of neurochemistry, modern hypnotics and drugs of the nearest future can be divided into 2 groups: proS (pro sleep)--for sleeping, and antiW (anti-wakefulness)--vs. wakefulness.     

Facts,meanings, and values of desirable sleep

Sleep and Biological Rhythms -