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Sample records for acute sleep loss

  1. How Acute Total Sleep Loss Affects the Attending Brain: A Meta-Analysis of Neuroimaging Studies

    PubMed Central

    Ma, Ning; Dinges, David F.; Basner, Mathias; Rao, Hengyi

    2015-01-01

    Study Objectives: Attention is a cognitive domain that can be severely affected by sleep deprivation. Previous neuroimaging studies have used different attention paradigms and reported both increased and reduced brain activation after sleep deprivation. However, due to large variability in sleep deprivation protocols, task paradigms, experimental designs, characteristics of subject populations, and imaging techniques, there is no consensus regarding the effects of sleep loss on the attending brain. The aim of this meta-analysis was to identify brain activations that are commonly altered by acute total sleep deprivation across different attention tasks. Design: Coordinate-based meta-analysis of neuroimaging studies of performance on attention tasks during experimental sleep deprivation. Methods: The current version of the activation likelihood estimation (ALE) approach was used for meta-analysis. The authors searched published articles and identified 11 sleep deprivation neuroimaging studies using different attention tasks with a total of 185 participants, equaling 81 foci for ALE analysis. Results: The meta-analysis revealed significantly reduced brain activation in multiple regions following sleep deprivation compared to rested wakefulness, including bilateral intraparietal sulcus, bilateral insula, right prefrontal cortex, medial frontal cortex, and right parahippocampal gyrus. Increased activation was found only in bilateral thalamus after sleep deprivation compared to rested wakefulness. Conclusion: Acute total sleep deprivation decreases brain activation in the fronto-parietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex). Increased thalamic activation after sleep deprivation may reflect a complex interaction between the de-arousing effects of sleep loss and the arousing effects of task performance on thalamic activity. Citation: Ma N, Dinges DF, Basner M, Rao H. How acute total

  2. Sleep Loss and Inflammation

    PubMed Central

    Simpson, Norah S.; Meier-Ewert, Hans K.; Haack, Monika

    2012-01-01

    Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24 hours, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8 hour sleep amount. While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals. Although the mechanism of this altered inflammatory status in humans undergoing experimental sleep loss is unknown, it is likely that autonomic activation and metabolic changes play key roles. PMID:21112025

  3. Exercise, but not acute sleep loss, increases salivary antimicrobial protein secretion.

    PubMed

    Gillum, Trevor L; Kuennen, Matthew R; Castillo, Micaela N; Williams, Nicole L; Jordan-Patterson, Alex T

    2015-05-01

    Sleep deficiencies may play a role in depressing immune parameters. Little is known about the impact of exercise after sleep deprivation on mucosal immunity. The purpose of this study was to quantify salivary antimicrobial proteins (AMPs) in response to sleep loss before and after exercise. Four men and 4 women (age: 22.8 ± 2; : 49.1 ± 7.1 ml · kg(-1) · min(-1)) completed 2 exercise trials consisting of 45 minutes of running at 75% VO2peak after a normal night of sleep (CON) and after a night without sleep (WS). Exercise trials were separated by 10 ± 3 days. Saliva was collected before, immediately after, and 1 hour after exercise. LL-37, HNP1-3, Lactoferrin (Lac), and Lysozyme (Lys) were measured. Sleep loss did not affect the concentration or secretion rate of AMPs before or in response to exercise. However, exercise increased the concentration from pre- to post-exercise of LL-37 (pre: 15.5 ± 8.7; post: 22.3 ± 16.2 ng · ml(-1)), HNP1-3 (pre: 2.2 ± 2.3; post: 3.3 ± 2.5 µg · ml(-1)), Lac (pre: 5,234 ± 4,202; post: 12,283 ± 10,995 ng · ml(-1)), and Lys (pre: 5,831 ± 4,465; post: 12,542 ± 10,755 ng · ml(-1)), p <= 0.05. The secretion rates were higher immediately after and 1 hour after exercise compared with before exercise for LL-37 (pre: 3.1 ± 2.1; post: 5.1 ± 3.7; +1: 6.9 ± 8.4 ng · min(-1)), HNP1-3 (pre: 0.38 ± 0.38; post: 0.80 ± 0.75; +1: 0.84 ± 0.67 µg · min(-1)), Lac (pre: 1,096 ± 829; post: 2,948 ± 2,923; +1: 2,464 ± 3,785 ng · min(-1)), and Lys (pre: 1,534 ± 1,790; post: 3,042 ± 2,773; +1: 1,916 ± 1,682 ng · min-(1)), p <= 0.05. These data suggest that the major constituents of the mucosal immune system are unaffected by acute sleep loss and by exercise after acute sleep loss. Exercise increased the concentration and secretion rate of each AMP suggesting enhanced immunity and control of inflammation, despite limited sleep. PMID:25915527

  4. Sleep Loss Produces False Memories

    PubMed Central

    Diekelmann, Susanne; Landolt, Hans-Peter; Lahl, Olaf; Born, Jan; Wagner, Ullrich

    2008-01-01

    People sometimes claim with high confidence to remember events that in fact never happened, typically due to strong semantic associations with actually encoded events. Sleep is known to provide optimal neurobiological conditions for consolidation of memories for long-term storage, whereas sleep deprivation acutely impairs retrieval of stored memories. Here, focusing on the role of sleep-related memory processes, we tested whether false memories can be created (a) as enduring memory representations due to a consolidation-associated reorganization of new memory representations during post-learning sleep and/or (b) as an acute retrieval-related phenomenon induced by sleep deprivation at memory testing. According to the Deese, Roediger, McDermott (DRM) false memory paradigm, subjects learned lists of semantically associated words (e.g., “night”, “dark”, “coal”,…), lacking the strongest common associate or theme word (here: “black”). Subjects either slept or stayed awake immediately after learning, and they were either sleep deprived or not at recognition testing 9, 33, or 44 hours after learning. Sleep deprivation at retrieval, but not sleep following learning, critically enhanced false memories of theme words. This effect was abolished by caffeine administration prior to retrieval, indicating that adenosinergic mechanisms can contribute to the generation of false memories associated with sleep loss. PMID:18946511

  5. Maintenance of wakefulness with lisdexamfetamine dimesylate, compared with placebo and armodafinil in healthy adult males undergoing acute sleep loss.

    PubMed

    Gasior, Maria; Freeman, Jon; Zammit, Gary; Donnelly, Patricia; Gao, Joseph; Ferreira-Cornwell, Maria Celeste; Roth, Thomas

    2014-12-01

    This study evaluated daytime alertness and performance with lisdexamfetamine dimesylate during acute sleep loss. In a randomized, double-blind study in healthy adult men (n = 135) undergoing 24-hour sleep loss, the alerting effects of single oral lisdexamfetamine dimesylate doses (20, 50, or 70 mg) were compared with a placebo and an active control (armodafinil 250 mg). Primary end point was mean unequivocal sleep latency on the 30-minute maintenance of wakefulness test taken every 2 hours from midnight to 8:00 A.M. Secondary end points included the Karolinska sleepiness scale and psychomotor vigilance task. Safety assessments included treatment-emergent adverse events (TEAEs) and vital signs. Least squares mean (SE) maintenance of wakefulness test unequivocal sleep latency (in minutes) was longer with lisdexamfetamine dimesylate 20, 50, and 70 mg, or armodafinil 250 mg (23.3 [1.10], 27.9 [0.64], 29.3 [0.44], or 27.6 [0.63], respectively) versus placebo (15.3 [1.00]; P < 0.0001). Longer mean unequivocal sleep latency was seen with lisdexamfetamine dimesylate 70 mg versus armodafinil (P = 0.0351) and armodafinil versus lisdexamfetamine dimesylate 20 mg (P = 0.0014). On Karolinska sleepiness scale, lisdexamfetamine dimesylate 50 and 70 mg improved estimated sleepiness versus placebo (P ≤ 0.0002) and armodafinil (P ≤ 0.03). Active treatments improved psychomotor vigilance task performance versus placebo (P < 0.0001). The TEAEs were mild/moderate. No serious adverse events occurred. The most common TEAE was headache with lisdexamfetamine dimesylate and armodafinil (7.4% each) versus placebo (3.7%). Small mean increases in vital signs were observed with lisdexamfetamine dimesylate and armodafinil. In sleep-deprived healthy men, alertness was greater with lisdexamfetamine dimesylate and armodafinil versus placebo on the primary end point. Studies are needed in clinical populations and using longer durations of administration. PMID:25159886

  6. Neuroimmunologic aspects of sleep and sleep loss

    NASA Technical Reports Server (NTRS)

    Rogers, N. L.; Szuba, M. P.; Staab, J. P.; Evans, D. L.; Dinges, D. F.

    2001-01-01

    The complex and intimate interactions between the sleep and immune systems have been the focus of study for several years. Immune factors, particularly the interleukins, regulate sleep and in turn are altered by sleep and sleep deprivation. The sleep-wake cycle likewise regulates normal functioning of the immune system. Although a large number of studies have focused on the relationship between the immune system and sleep, relatively few studies have examined the effects of sleep deprivation on immune parameters. Studies of sleep deprivation's effects are important for several reasons. First, in the 21st century, various societal pressures require humans to work longer and sleep less. Sleep deprivation is becoming an occupational hazard in many industries. Second, to garner a greater understanding of the regulatory effects of sleep on the immune system, one must understand the consequences of sleep deprivation on the immune system. Significant detrimental effects on immune functioning can be seen after a few days of total sleep deprivation or even several days of partial sleep deprivation. Interestingly, not all of the changes in immune physiology that occur as a result of sleep deprivation appear to be negative. Numerous medical disorders involving the immune system are associated with changes in the sleep-wake physiology--either being caused by sleep dysfunction or being exacerbated by sleep disruption. These disorders include infectious diseases, fibromyalgia, cancers, and major depressive disorder. In this article, we will describe the relationships between sleep physiology and the immune system, in states of health and disease. Interspersed will be proposals for future research that may illuminate the clinical relevance of the relationships between sleeping, sleep loss and immune function in humans. Copyright 2001 by W.B. Saunders Company.

  7. The acute effects of twenty-four hours of sleep loss on the performance of national-caliber male collegiate weightlifters.

    PubMed

    Blumert, Peter A; Crum, Aaron J; Ernsting, Mark; Volek, Jeff S; Hollander, Daniel B; Haff, Erin E; Haff, G Gregory

    2007-11-01

    Currently, the degree to which sleep loss influences weightlifting performance is unknown. This study compared the effects of 24 hours of sleep loss on weightlifting performance and subjective ratings of psychological states pre-exercise and postexercise in national-caliber male collegiate weightlifters. Nine males performed a maximal weightlifting protocol following 24 hours of sleep loss and a night of normal sleep. The subjects participated in a randomized, counterbalanced design with each sleep condition separated by 7 days. Testosterone and cortisol levels were quantified prior to, immediately after, and 1 hour after the resistance training session. Additionally, profile of mood states and subjective sleepiness were evaluated at the same time points. The resistance training protocol consisted of several sets of snatches, clean and jerks, and front squats. Performance was evaluated as individual exercise volume load, training intensity and overall workout volume load, and training intensity. During each training session the maximum weight lifted for the snatch, clean and jerk, and front squat were noted. No significant differences were found for any of the performance variables. A significant decrease following the sleep condition was noted for cortisol concentration immediately after and 1 hour postexercise. Vigor, fatigue, confusion, total mood disturbance, and sleepiness were all significantly altered by sleep loss. These data suggest that 24 hours of sleep loss has no adverse effects on weightlifting performance. If an athlete is in an acute period of sleep loss, as noticed by negative mood disturbances, it may be more beneficial to focus on the psychological (motivation) rather than the physiological aspect of the sport. PMID:18076267

  8. Metabolic consequences of sleep and sleep loss

    PubMed Central

    Van Cauter, Eve; Spiegel, Karine; Tasali, Esra; Leproult, Rachel

    2015-01-01

    Reduced sleep duration and quality appear to be endemic in modern society. Curtailment of the bedtime period to minimum tolerability is thought to be efficient and harmless by many. It has been known for several decades that sleep is a major modulator of hormonal release, glucose regulation and cardiovascular function. In particular, slow wave sleep (SWS), thought to be the most restorative sleep stage, is associated with decreased heart rate, blood pressure, sympathetic nervous activity and cerebral glucose utilization, compared with wakefulness. During SWS, the anabolic growth hormone is released while the stress hormone cortisol is inhibited. In recent years, laboratory and epidemiologic evidence have converged to indicate that sleep loss may be a novel risk factor for obesity and type 2 diabetes. The increased risk of obesity is possibly linked to the effect of sleep loss on hormones that play a major role in the central control of appetite and energy expenditure, such as leptin and ghrelin. Reduced leptin and increased ghrelin levels correlate with increases in subjective hunger when individuals are sleep restricted rather than well rested. Given the evidence, sleep curtailment appears to be an important, yet modifiable, risk factor for the metabolic syndrome, diabetes and obesity. The marked decrease in average sleep duration in the last 50 years coinciding with the increased prevalence of obesity, together with the observed adverse effects of recurrent partial sleep deprivation on metabolism and hormonal processes, may have important implications for public health. PMID:18929315

  9. Sleep Disturbances in Acutely Ill Patients with Cancer.

    PubMed

    Matthews, Ellyn E; Tanner, J Mark; Dumont, Natalie A

    2016-06-01

    Intensive care units may place acutely ill patients with cancer at additional risk for sleep loss and associated negative effects. Research suggests that communication about sleep in patients with cancer is suboptimal and sleep problems are not regularly assessed or adequately treated throughout the cancer trajectory. However, many sleep problems and fatigue can be managed effectively. This article synthesizes the current literature regarding the prevalence, cause, and risk factors that contribute to sleep disturbance in the context of acute cancer care. It describes the consequences of poor sleep and discusses appropriate assessment and treatment options. PMID:27215362

  10. Uncovering Residual Effects of Chronic Sleep Loss on Human Performance

    PubMed Central

    Cohen, Daniel A.; Wang, Wei; Wyatt, James K.; Kronauer, Richard E.; Dijk, Derk-Jan; Czeisler, Charles A.; Klerman, Elizabeth B.

    2010-01-01

    Sleep loss leads to profound performance decrements. Yet many individuals believe they adapt to chronic sleep loss or that recovery requires only a single extended sleep episode. To evaluate this, we designed a protocol whereby the usual sleep:wake ratio was reduced from 1:2 to 1:3.3, while the durations of both sleep and wake episodes were increased to ten hours and 32.85 hours respectively. These sleep and wake episodes were distributed across all circadian phases, enabling measurement of the effects of acute and chronic sleep loss at different times of the circadian day and night. Despite recurrent acute and substantial chronic sleep loss, ten hour sleep opportunities consistently restored vigilance performance for several hours of wakefulness. However, chronic sleep loss increased the rate of deterioration in performance across wakefulness, particularly during the circadian “night”. Thus, extended wake during the circadian night reveals the cumulative detrimental effects of chronic sleep loss on performance, with potential adverse health and safety consequences. PMID:20371466

  11. Acute loss of consciousness.

    PubMed

    Tristán, Bekinschtein; Gleichgerrcht, Ezequiel; Manes, Facundo

    2015-01-01

    Acute loss of consciousness poses a fascinating scenario for theoretical and clinical research. This chapter introduces a simple yet powerful framework to investigate altered states of consciousness. We then explore the different disorders of consciousness that result from acute brain injury, and techniques used in the acute phase to predict clinical outcome in different patient populations in light of models of acute loss of consciousness. We further delve into post-traumatic amnesia as a model for predicting cognitive sequels following acute loss of consciousness. We approach the study of acute loss of consciousness from a theoretical and clinical perspective to conclude that clinicians in acute care centers must incorporate new measurements and techniques besides the classic coma scales in order to assess their patients with loss of consciousness. PMID:25702218

  12. Weight Loss & Acute Porphyria

    MedlinePlus

    ... Sale You are here Home Diet and Nutrition Weight loss & acute Porphyria Being overweight is a particular problem ... one of these diseases before they enter a weight-loss program. Also, they should not participate in a ...

  13. Sleep loss and sleepiness: current issues.

    PubMed

    Balkin, Thomas J; Rupp, Tracy; Picchioni, Dante; Wesensten, Nancy J

    2008-09-01

    Awareness of the consequences of sleep loss and its implications for public health and safety is increasing. Sleep loss has been shown to generally impair the entire spectrum of mental abilities, ranging from simple psychomotor performance to executive mental functions. Sleep loss may also impact metabolism in a manner that contributes to obesity and its attendant health consequences. Although objective measures of alertness and performance remain degraded, individuals subjectively habituate to chronic partial sleep loss (eg, sleep restriction), and recovery from this type of sleep loss is slow, factors that may help to explain the observation that many individuals in the general population are chronically sleep restricted. Individual differences in habitual sleep duration appear to be a trait-like characteristic that is determined by several factors, including genetic polymorphisms. PMID:18779203

  14. Sleep Loss in Resident Physicians: The Cause of Medical Errors?

    PubMed Central

    Kramer, Milton

    2010-01-01

    This review begins with the history of the events starting with the death of Libby Zion that lead to the Bell Commission, that the studied her death and made recommendations for improvement that were codified into law in New York state as the 405 law that the ACGME essentially adopted in putting a cap on work hours and establishing the level of staff supervision that must be available to residents in clinical situations particularly the emergency room and acute care units. A summary is then provided of the findings of the laboratory effects of total sleep deprivation including acute total sleep loss and the consequent widespread physiologic alterations, and of the effects of selective and chronic sleep loss. Generally the sequence of responses to increasing sleep loss goes from mood changes to cognitive effects to performance deficits. In the laboratory situation, deficits resulting from sleep deprivation are clearly and definitively demonstrable. Sleep loss in the clinical situation is usually sleep deprivation superimposed on chronic sleep loss. An examination of questionnaire studies, the literature on reports of sleep loss, studies of the reduction of work hours on performance as well as observational and a few interventional studies have yielded contradictory and often equivocal results. The residents generally find they feel better working fewer hours but improvements in patient care are often not reported or do not occur. A change in the attitude of the resident toward his role and his patient has not been salutary. Decreasing sleep loss should have had a positive effect on patient care in reducing medical error, but this remains to be unequivocally demonstrated. PMID:21188260

  15. Sleep loss, learning capacity and academic performance.

    PubMed

    Curcio, Giuseppe; Ferrara, Michele; De Gennaro, Luigi

    2006-10-01

    At a time when several studies have highlighted the relationship between sleep, learning and memory processes, an in-depth analysis of the effects of sleep deprivation on student learning ability and academic performance would appear to be essential. Most studies have been naturalistic correlative investigations, where sleep schedules were correlated with school and academic achievement. Nonetheless, some authors were able to actively manipulate sleep in order to observe neurocognitive and behavioral consequences, such as learning, memory capacity and school performance. The findings strongly suggest that: (a) students of different education levels (from school to university) are chronically sleep deprived or suffer from poor sleep quality and consequent daytime sleepiness; (b) sleep quality and quantity are closely related to student learning capacity and academic performance; (c) sleep loss is frequently associated with poor declarative and procedural learning in students; (d) studies in which sleep was actively restricted or optimized showed, respectively, a worsening and an improvement in neurocognitive and academic performance. These results may been related to the specific involvement of the prefrontal cortex (PFC) in vulnerability to sleep loss. Most methodological limitations are discussed and some future research goals are suggested. PMID:16564189

  16. Sleep loss and "divergent" thinking ability.

    PubMed

    Horne, J A

    1988-12-01

    Although much is known about the impact of sleep loss on many aspects of psychological performance, the effects on divergent ("creative") thinking has received little attention. Twelve subjects went 32 h without sleep, and 12 others acted as normally sleeping controls. All subjects were assessed on the figural and verbal versions of the Torrance Tests of Creative Thinking. As compared with the control condition, sleep loss impaired performance on all test scales (e.g., "flexibility," the ability to change strategy, and "originality," generation of unusual ideas) for both versions, even on an initial 5-min test component. In an attempt at further understanding of whether these findings might be explained solely by a loss of motivation, two additional short and stimulating tests were also used--a word fluency task incorporating high incentive to do well and a challenging nonverbal planning test. Performance at these tasks was still significantly impaired by sleep loss. Increased perseveration was clearly apparent. Apparently, 1 night of sleep loss can affect divergent thinking. This contrasts with the outcome for convergent thinking tasks, which are more resilient to short-term sleep loss. PMID:3238256

  17. Sleep Loss Activates Cellular Inflammatory Signaling

    PubMed Central

    Irwin, Michael R.; Wang, Minge; Ribeiro, Denise; Cho, Hyong Jin; Olmstead, Richard; Breen, Elizabeth Crabb; Martinez-Maza, Otoniel; Cole, Steve

    2008-01-01

    Background Accumulating evidence suggests that sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. This study was undertaken to test the effects of sleep loss on activation of nuclear factor (NF) -κB, a transcription factor that serves a critical role in the inflammatory signaling cascade. Methods In 14 healthy adults (7 females; 7 males), peripheral blood mononuclear cell NF-κB was repeatedly assessed, along with enumeration of lymphocyte subpopulations, in the morning after baseline sleep, partial sleep deprivation (awake from 23:00 h to 03:00 h), and recovery sleep. Results In the morning after a night of sleep loss, mononuclear cell NF-κB activation was significantly greater compared with morning levels following uninterrupted baseline or recovery sleep, in which the response was found in females but not in males. Conclusions These results identify NF-κB activation as a molecular pathway by which sleep disturbance may influence leukocyte inflammatory gene expression and the risk of inflammation-related disease. PMID:18561896

  18. Sleep Loss as a Factor to Induce Cellular and Molecular Inflammatory Variations

    PubMed Central

    Hurtado-Alvarado, Gabriela; Castillo-García, Stephanie Ariadne; Hernández, María Eugenia; Domínguez-Salazar, Emilio; Velázquez-Moctezuma, Javier; Gómez-González, Beatriz

    2013-01-01

    A reduction in the amount of time spent sleeping occurs chronically in modern society. Clinical and experimental studies in humans and animal models have shown that immune function is impaired when sleep loss is experienced. Sleep loss exerts a strong regulatory influence on peripheral levels of inflammatory mediators of the immune response. An increasing number of research projects support the existence of reciprocal regulation between sleep and low-intensity inflammatory response. Recent studies show that sleep deficient humans and rodents exhibit a proinflammatory component; therefore, sleep loss is considered as a risk factor for developing cardiovascular, metabolic, and neurodegenerative diseases (e.g., diabetes, Alzheimer's disease, and multiple sclerosis). Circulating levels of proinflammatory mediators depend on the intensity and duration of the method employed to induce sleep loss. Recognizing the fact that the concentration of proinflammatory mediators is different between acute and chronic sleep-loss may expand the understanding of the relationship between sleep and the immune response. The aim of this review is to integrate data from recent published reports (2002–2013) on the effects of sleep loss on the immune response. This review may allow readers to have an integrated view of the mechanisms involved in central and peripheral deficits induced by sleep loss. PMID:24367384

  19. Sleep loss and fatigue in medical training.

    PubMed

    Owens, J A

    2001-11-01

    The effects of sleep loss and fatigue in the context of medical training is a topic that has generated considerable interest, as well as controversy, over the past two decades. The sleep deprived state in medical trainees potentially impacts on a variety of domains relevant to medical care, including performance on neurobehavioral and work-related tasks, mood and affect, learning, risk for and commission of medical errors, and the health and well-being of medical students and residents. The following review provides a summary of research conducted on this topic in the past decade, including the relation of sleep loss and fatigue to medical errors and the quality of patient care. Those few studies that have analyzed the use of operational alertness management strategies, countermeasures, and educational interventions to address and mitigate the effects of sleep loss and fatigue are also reviewed. There is clearly a need for additional research to further explore the complex interaction between sleep and fatigue and medical care, and to support the development and implementation of regulatory policies based on sound science. PMID:11706318

  20. Sleep and protein synthesis-dependent synaptic plasticity: impacts of sleep loss and stress

    PubMed Central

    Grønli, Janne; Soulé, Jonathan; Bramham, Clive R.

    2014-01-01

    Sleep has been ascribed a critical role in cognitive functioning. Several lines of evidence implicate sleep in the consolidation of synaptic plasticity and long-term memory. Stress disrupts sleep while impairing synaptic plasticity and cognitive performance. Here, we discuss evidence linking sleep to mechanisms of protein synthesis-dependent synaptic plasticity and synaptic scaling. We then consider how disruption of sleep by acute and chronic stress may impair these mechanisms and degrade sleep function. PMID:24478645

  1. Sleep loss as risk factor for neurologic disorders: a review.

    PubMed

    Palma, Jose-Alberto; Urrestarazu, Elena; Iriarte, Jorge

    2013-03-01

    Sleep loss refers to sleep of shorter duration than the average baseline need of seven to eight hours per night. Sleep loss and sleep deprivation have severe effects on human health. In this article, we review the main aspects of sleep loss, taking into account its effects on the central nervous system. The neurocognitive and behavioral effects of sleep loss are well known. However, there is an increasing amount of research pointing to sleep deprivation as a risk factor for neurologic diseases, namely stroke, multiple sclerosis, Alzheimer's disease, headache, epilepsy, pain, and somnambulism. Conversely, sleep loss has been reported to be a potential protective factor against Parkinson's disease. The pathophysiology involved in this relationship is multiple, comprising immune, neuroendocrine, autonomic, and vascular mechanisms. It is extremely important to identify the individuals at risk, since recognition and adequate treatment of their sleep problems may reduce the risk of certain neurologic disorders. PMID:23352029

  2. Leptin and Hunger Levels in Young Healthy Adults After One Night of Sleep Loss

    PubMed Central

    Pejovic, Slobodanka; Vgontzas, Alexandros N.; Basta, Maria; Tsaoussoglou, Marina; Zoumakis, Emanuel; Vgontzas, Angeliki; Bixler, Edward O.; Chrousos, George P.

    2013-01-01

    Summary Short-term sleep curtailment associated with activation of the stress system in healthy, young adults has been shown to be associated with decreased leptin levels, impaired insulin sensitivity and increased hunger and appetite. To assess the effects of one night of sleep loss in a less stressful environment on hunger, leptin, adiponectin, cortisol, and blood pressure/heart rate and whether a 2-hour mid-afternoon nap reverses the changes associated with sleep loss, 21 young healthy individuals (10 men, 11 women) participated in a 7-day sleep deprivation experiment (4 consecutive nights followed by a night of sleep loss and 2 recovery nights). Half of the subjects were randomly assigned to take a mid-afternoon nap (1400–1600) the day following the night of total sleep loss. Serial 24-hour blood sampling and hunger scales were completed on the fourth (pre-deprivation) and sixth day (post-deprivation). Leptin levels were significantly increased after one night of total sleep loss, whereas adiponectin, cortisol levels, blood pressure/heart rate, and hunger were not affected. Daytime napping did not influence the effects of sleep loss on leptin, adiponectin or hunger. Acute sleep loss, in a less stressful environment, influences leptin levels in an opposite manner from that of short-term sleep curtailment associated with activation of the stress system. It appears that sleep loss associated with activation of the stress system but not sleep loss per se may lead to increased hunger and appetite and hormonal changes which ultimately may lead to increased consumption of “comfort” food and obesity. PMID:20545838

  3. The effect of sleep loss on next day effort.

    PubMed

    Engle-Friedman, Mindy; Riela, Suzanne; Golan, Rama; Ventuneac, Ana M; Davis, Christine M; Jefferson, Angela D; Major, Donna

    2003-06-01

    The study had two primary objectives. The first was to determine whether sleep loss results in a preference for tasks demanding minimal effort. The second was to evaluate the quality of performance when participants, under conditions of sleep loss, have control over task demands. In experiment 1, using a repeated-measures design, 50 undergraduate college students were evaluated, following one night of no sleep loss and one night of sleep loss. The Math Effort Task (MET) presented addition problems via computer. Participants were able to select additions at one of five levels of difficulty. Less-demanding problems were selected and more additions were solved correctly when the participants were subject to sleep loss. In experiment 2, 58 undergraduate college students were randomly assigned to a no sleep deprivation or a sleep deprivation condition. Sleep-deprived participants selected less-demanding problems on the MET. Percentage correct on the MET was equivalent for both the non-sleep-deprived and sleep-deprived groups. On a task selection question, the sleep-deprived participants also selected significantly less-demanding non-academic tasks. Increased sleepiness, fatigue, and reaction time were associated with the selection of less difficult tasks. Both groups of participants reported equivalent effort expenditures; sleep-deprived participants did not perceive a reduction in effort. These studies demonstrate that sleep loss results in the choice of low-effort behavior that helps maintain accurate responding. PMID:12753348

  4. Sleep patterns in three acute combat fatigue cases.

    PubMed

    Schlosberg, A; Benjamin, M

    1978-06-01

    A preliminary report is presented on the sleep patterns of three combat fatigued patients with recurrent nightmares, insomnia, low frustration thresholds and impotence. All the patients had undergone acute partial sleep deprivation prior to their breakdown. The results show severe deficiency in REM sleep and absence of stage 4 sleep. EMG was usually high with numerous body movements and bursts of tachycardia throughout the night. Nightmares occurred in stage 2. Total effective sleep time was between 129' and 250'. Most of the sleep was in stage 2, and patients woke up with the feeling that "they had not slept at all." It is hypothesized that acute partial sleep deprivation prior to breakdown was an important predisposing factor, and that chronic partial sleep deprivation was a constant aggravating factor of combat fatigue. Replacement therapy for the specific deficient sleep states is proposed. PMID:207680

  5. Enhancing Slow Wave Sleep with Sodium Oxybate Reduces the Behavioral and Physiological Impact of Sleep Loss

    PubMed Central

    Walsh, James K.; Hall-Porter, Janine M.; Griffin, Kara S.; Dodson, Ehren R.; Forst, Elizabeth H.; Curry, Denise T.; Eisenstein, Rhody D.; Schweitzer, Paula K.

    2010-01-01

    Study Objectives: To investigate whether enhancement of slow wave sleep (SWS) with sodium oxybate reduces the impact of sleep deprivation. Design: Double-blind, parallel group, placebo-controlled design Setting: Sleep research laboratory Participants: Fifty-eight healthy adults (28 placebo, 30 sodium oxybate), ages 18-50 years. Interventions: A 5-day protocol included 2 screening/baseline nights and days, 2 sleep deprivation nights, each followed by a 3-h daytime (08:00-11:00) sleep opportunity and a recovery night. Sodium oxybate or placebo was administered prior to each daytime sleep period. Multiple sleep latency test (MSLT), psychomotor vigilance test (PVT), Karolinska Sleepiness Scale (KSS), and Profile of Mood States were administered during waking hours. Measurements and Results: During daytime sleep, the sodium oxybate group had more SWS, more EEG spectral power in the 1-9 Hz range, and less REM. Mean MSLT latency was longer for the sodium oxybate group on the night following the first daytime sleep period and on the day following the second day sleep period. Median PVT reaction time was faster in the sodium oxybate group following the second day sleep period. The change from baseline in SWS was positively correlated with the change in MSLT and KSS. During recovery sleep the sodium oxybate group had less TST, SWS, REM, and slow wave activity (SWA) than the placebo group. Conclusions: Pharmacological enhancement of SWS with sodium oxybate resulted in a reduced response to sleep loss on measures of alertness and attention. In addition, SWS enhancement during sleep restriction appears to result in a reduced homeostatic response to sleep loss. Citation: Walsh JK; Hall-Porter JM; Griffin KS; Dodson ER; Forst EH; Curry DT; Eisenstein RD; Schweitzer PK. Enhancing slow wave sleep with sodium oxybate reduces the behavioral and physiological impact of sleep loss. SLEEP 2010;33(9):1217-1225. PMID:20857869

  6. Acute total sleep deprivation potentiates cocaine-induced hyperlocomotion in mice.

    PubMed

    Berro, L F; Santos, R; Hollais, A W; Wuo-Silva, R; Fukushiro, D F; Mári-Kawamoto, E; Costa, J M; Trombin, T F; Patti, C L; Grapiglia, S B; Tufik, S; Andersen, M L; Frussa-Filho, R

    2014-09-01

    Sleep deprivation is common place in modern society. Nowadays, people tend to self-impose less sleep in order to achieve professional or social goals. In the social context, late-night parties are frequently associated with higher availability of recreational drugs with abuse potential. Physiologically, all of these drugs induce an increase in dopamine release in the mesolimbic dopaminergic system, which leads to hyperlocomotion in rodents. Sleep deprivation also seems to play an important role in the events related to the neurotransmission of the dopaminergic system by potentiating its behavioral effects. In this scenario, the aim of the present study was to investigate the effects of total sleep deprivation (6h) on the acute cocaine-induced locomotor stimulation in male mice. Animals were sleep deprived or maintained in their home cages and subsequently treated with an acute i.p. injection of 15mg/kg cocaine or saline and observed in the open field. Total sleep deprivation for 6h potentiated the hyperlocomotion induced by acute cocaine administration. In addition, the cocaine sleep deprived group showed a decreased ratio central/total locomotion compared to the cocaine control group, which might be related to an increase in the impulsiveness of mice. Our data indicate that acute periods of sleep loss should be considered risk factors for cocaine abuse. PMID:25067829

  7. A new mathematical model for the homeostatic effects of sleep loss on neurobehavioral performance

    PubMed Central

    McCauley, Peter; Kalachev, Leonid V.; Smith, Amber D.; Belenky, Gregory; Dinges, David F.; Van Dongen, Hans P.A.

    2009-01-01

    The two-process model of sleep regulation makes accurate predictions of sleep timing and duration for a variety of experimental sleep deprivation and nap sleep scenarios. Upon extending its application to waking neurobehavioral performance, however, the model fails to predict the effects of chronic sleep restriction. Here we show that the two-process model belongs to a broader class of models formulated in terms of coupled non-homogeneous first-order ordinary differential equations, which have a dynamic repertoire capturing waking neurobehavioral functions across a wide range of wake/sleep schedules. We examine a specific case of this new model class, and demonstrate the existence of a bifurcation: for daily amounts of wakefulness less than a critical threshold, neurobehavioral performance is predicted to converge to an asymptotically stable state of equilibrium; whereas for daily wakefulness extended beyond the critical threshold, neurobehavioral performance is predicted to diverge from an unstable state of equilibrium. Comparison of model simulations to laboratory observations of lapses of attention on a psychomotor vigilance test (PVT), in experiments on the effects of chronic sleep restriction and acute total sleep deprivation, suggests that this bifurcation is an essential feature of performance impairment due to sleep loss. We present three new predictions that may be experimentally verified to validate the model. These predictions, if confirmed, challenge conventional notions about the effects of sleep and sleep loss on neurobehavioral performance. The new model class implicates a biological system analogous to two connected compartments containing interacting compounds with time-varying concentrations as being a key mechanism for the regulation of psychomotor vigilance as a function of sleep loss. We suggest that the adenosinergic neuromodulator/receptor system may provide the underlying neurobiology. PMID:18938181

  8. The effects of sleep loss on capacity and effort

    PubMed Central

    Engle-Friedman, Mindy

    2014-01-01

    Sleep loss appears to affect the capacity for performance and access to energetic resources. This paper reviews research examining the physical substrates referred to as resource capacity, the role of sleep in protecting that capacity and the reaction of the system as it attempts to respond with effort to overcome the limitations on capacity caused by sleep loss. Effort is the extent to which an organism will exert itself beyond basic levels of functioning or attempt alternative strategies to maintain performance. The purpose of this review is to bring together research across sleep disciplines to clarify the substrates that constitute and influence capacity for performance, consider how the loss of sleep influences access to those resources, examine cortical, physiological, perceptual, behavioral and subjective effort responses and consider how these responses reflect a system reacting to changes in the resource environment. When sleep deprived, the ability to perform tasks that require additional energy is impaired and the ability of the system to overcome the deficiencies caused by sleep loss is limited. Taking on tasks that require effort including school work, meal preparation, pulling off the road to nap when driving drowsy appear to be more challenging during sleep loss. Sleep loss impacts the effort-related choices we make and those choices may influence our health and safety. PMID:26483932

  9. The effects of sleep loss on capacity and effort.

    PubMed

    Engle-Friedman, Mindy

    2014-12-01

    Sleep loss appears to affect the capacity for performance and access to energetic resources. This paper reviews research examining the physical substrates referred to as resource capacity, the role of sleep in protecting that capacity and the reaction of the system as it attempts to respond with effort to overcome the limitations on capacity caused by sleep loss. Effort is the extent to which an organism will exert itself beyond basic levels of functioning or attempt alternative strategies to maintain performance. The purpose of this review is to bring together research across sleep disciplines to clarify the substrates that constitute and influence capacity for performance, consider how the loss of sleep influences access to those resources, examine cortical, physiological, perceptual, behavioral and subjective effort responses and consider how these responses reflect a system reacting to changes in the resource environment. When sleep deprived, the ability to perform tasks that require additional energy is impaired and the ability of the system to overcome the deficiencies caused by sleep loss is limited. Taking on tasks that require effort including school work, meal preparation, pulling off the road to nap when driving drowsy appear to be more challenging during sleep loss. Sleep loss impacts the effort-related choices we make and those choices may influence our health and safety. PMID:26483932

  10. Acute sleep deprivation increases portion size and affects food choice in young men.

    PubMed

    Hogenkamp, Pleunie S; Nilsson, Emil; Nilsson, Victor C; Chapman, Colin D; Vogel, Heike; Lundberg, Lina S; Zarei, Sanaz; Cedernaes, Jonathan; Rångtell, Frida H; Broman, Jan-Erik; Dickson, Suzanne L; Brunstrom, Jeffrey M; Benedict, Christian; Schiöth, Helgi B

    2013-09-01

    Acute sleep loss increases food intake in adults. However, little is known about the influence of acute sleep loss on portion size choice, and whether this depends on both hunger state and the type of food (snack or meal item) offered to an individual. The aim of the current study was to compare portion size choice after a night of sleep and a period of nocturnal wakefulness (a condition experienced by night-shift workers, e.g. physicians and nurses). Sixteen men (age: 23 ± 0.9 years, BMI: 23.6 ± 0.6 kg/m(2)) participated in a randomized within-subject design with two conditions, 8-h of sleep and total sleep deprivation (TSD). In the morning following sleep interventions, portion size, comprising meal and snack items, was measured using a computer-based task, in both fasted and sated state. In addition, hunger as well as plasma levels of ghrelin were measured. In the morning after TSD, subjects had increased plasma ghrelin levels (13%, p=0.04), and chose larger portions (14%, p=0.02), irrespective of the type of food, as compared to the sleep condition. Self-reported hunger was also enhanced (p<0.01). Following breakfast, sleep-deprived subjects chose larger portions of snacks (16%, p=0.02), whereas the selection of meal items did not differ between the sleep interventions (6%, p=0.13). Our results suggest that overeating in the morning after sleep loss is driven by both homeostatic and hedonic factors. Further, they show that portion size choice after sleep loss depend on both an individual's hunger status, and the type of food offered. PMID:23428257

  11. Sex Chromosomes Regulate Nighttime Sleep Propensity during Recovery from Sleep Loss in Mice

    PubMed Central

    Pinckney, Lennisha; Paul, Ketema N.

    2013-01-01

    Sex differences in spontaneous sleep amount are largely dependent on reproductive hormones; however, in mice some sex differences in sleep amount during the active phase are preserved after gonadectomy and may be driven by non-hormonal factors. In this study, we sought to determine whether or not these sex differences are driven by sex chromosome complement. Mice from the four core genotype (FCG) mouse model, whose sex chromosome complement (XY, XX) is independent of phenotype (male or female), were implanted with electroencephalographic (EEG) and electromyographic (EMG) electrodes for the recording of sleep-wake states and underwent a 24-hr baseline recording followed by six hours of forced wakefulness. During baseline conditions in mice whose gonads remained intact, males had more total sleep and non-rapid eye movement sleep than females during the active phase. Gonadectomized FCG mice exhibited no sex differences in rest-phase sleep amount; however, during the mid-active-phase (nighttime), XX males had more spontaneous non-rapid eye movement (NREM) sleep than XX females. The XY mice did not exhibit sex differences in sleep amount. Following forced wakefulness there was a change in the factors regulating sleep. XY females slept more during their mid-active phase siestas than XX females and had higher NREM slow wave activity, a measure of sleep propensity. These findings suggest that the process that regulates sleep propensity is sex-linked, and that sleep amount and sleep propensity are regulated differently in males and females following sleep loss. PMID:23658713

  12. Cell Injury and Repair Resulting from Sleep Loss and Sleep Recovery in Laboratory Rats

    PubMed Central

    Everson, Carol A.; Henchen, Christopher J.; Szabo, Aniko; Hogg, Neil

    2014-01-01

    Study Objectives: Increased cell injury would provide the type of change in constitution that would underlie sleep disruption as a risk factor for multiple diseases. The current study was undertaken to investigate cell injury and altered cell fate as consequences of sleep deprivation, which were predicted from systemic clues. Design: Partial (35% sleep reduction) and total sleep deprivation were produced in rats for 10 days, which was tolerated and without overtly deteriorated health. Recovery rats were similarly sleep deprived for 10 days, then allowed undisturbed sleep for 2 days. The plasma, liver, lung, intestine, heart, and spleen were analyzed and compared to control values for damage to DNA, proteins, and lipids; apoptotic cell signaling and death; cell proliferation; and concentrations of glutathione peroxidase and catalase. Measurements and Results: Oxidative DNA damage in totally sleep deprived rats was 139% of control values, with organ-specific effects in the liver (247%), lung (166%), and small intestine (145%). Overall and organ-specific DNA damage was also increased in partially sleep deprived rats. In the intestinal epithelium, total sleep deprivation resulted in 5.3-fold increases in dying cells and 1.5-fold increases in proliferating cells, compared with control. Two days of recovery sleep restored the balance between DNA damage and repair, and resulted in normal or below-normal metabolic burdens and oxidative damage. Conclusions: These findings provide physical evidence that sleep loss causes cell damage, and in a manner expected to predispose to replication errors and metabolic abnormalities; thereby providing linkage between sleep loss and disease risk observed in epidemiological findings. Properties of recovery sleep include biochemical and molecular events that restore balance and decrease cell injury. Citation: Everson CA, Henchen CJ, Szabo A, Hogg N. Cell injury and repair resulting from sleep loss and sleep recovery in laboratory rats

  13. Sleep restriction acutely impairs glucose tolerance in rats.

    PubMed

    Jha, Pawan K; Foppen, Ewout; Kalsbeek, Andries; Challet, Etienne

    2016-06-01

    Chronic sleep curtailment in humans has been related to impairment of glucose metabolism. To better understand the underlying mechanisms, the purpose of the present study was to investigate the effect of acute sleep deprivation on glucose tolerance in rats. A group of rats was challenged by 4-h sleep deprivation in the early rest period, leading to prolonged (16 h) wakefulness. Another group of rats was allowed to sleep during the first 4 h of the light period and sleep deprived in the next 4 h. During treatment, food was withdrawn to avoid a postmeal rise in plasma glucose. An intravenous glucose tolerance test (IVGTT) was performed immediately after the sleep deprivation period. Sleep deprivation at both times of the day similarly impaired glucose tolerance and reduced the early-phase insulin responses to a glucose challenge. Basal concentrations of plasma glucose, insulin, and corticosterone remained unchanged after sleep deprivation. Throughout IVGTTs, plasma corticosterone concentrations were not different between the control and sleep-deprived group. Together, these results demonstrate that independent of time of day and sleep pressure, short sleep deprivation during the resting phase favors glucose intolerance in rats by attenuating the first-phase insulin response to a glucose load. In conclusion, this study highlights the acute adverse effects of only a short sleep restriction on glucose homeostasis. PMID:27354542

  14. Youthfulness, inexperience, and sleep loss: the problems young drivers face and those they pose for us

    PubMed Central

    Groeger, J A

    2006-01-01

    Young inexperienced drivers are more likely to be involved in road traffic crashes than drivers who are older and more experienced. This paper argues that neither age nor inexperience are, in and of themselves, sufficient explanations of the association between age, experience, and casualty rates. The aim here is to consider what it is about inexperienced young drivers in particular that may increase crash risk. Evidence is reviewed showing differential sleep loss among different teenage groups, which may relate to recently presented evidence that young teenagers are more crash involved than drivers in their early twenties. Potential acute and chronic effects of sleep loss among teenagers and young adults are described. PMID:16788107

  15. Youthfulness, inexperience, and sleep loss: the problems young drivers face and those they pose for us.

    PubMed

    Groeger, J A

    2006-06-01

    Young inexperienced drivers are more likely to be involved in road traffic crashes than drivers who are older and more experienced. This paper argues that neither age nor inexperience are, in and of themselves, sufficient explanations of the association between age, experience, and casualty rates. The aim here is to consider what it is about inexperienced young drivers in particular that may increase crash risk. Evidence is reviewed showing differential sleep loss among different teenage groups, which may relate to recently presented evidence that young teenagers are more crash involved than drivers in their early twenties. Potential acute and chronic effects of sleep loss among teenagers and young adults are described. PMID:16788107

  16. Postoperative sleep disruptions: a potential catalyst of acute pain?

    PubMed

    Chouchou, Florian; Khoury, Samar; Chauny, Jean-Marc; Denis, Ronald; Lavigne, Gilles J

    2014-06-01

    Despite the substantial advances in the understanding of pain mechanisms and management, postoperative pain relief remains an important health care issue. Surgical patients also frequently report postoperative sleep complaints. Major sleep alterations in the postoperative period include sleep fragmentation, reduced total sleep time, and loss of time spent in slow wave and rapid eye movement sleep. Clinical and experimental studies show that sleep disturbances may exacerbate pain, whereas pain and opioid treatments disturb sleep. Surgical stress appears to be a major contributor to both sleep disruptions and altered pain perception. However, pain and the use of opioid analgesics could worsen sleep alterations, whereas sleep disruptions may contribute to intensify pain. Nevertheless, little is known about the relationship between postoperative sleep and pain. Although the sleep-pain interaction has been addressed from both ends, this review focuses on the impact of sleep disruptions on pain perception. A better understanding of the effect of postoperative sleep disruptions on pain perception would help in selecting patients at risk for more severe pain and may facilitate the development of more effective and safer pain management programs. PMID:24074687

  17. Sleep loss and partner violence victimization.

    PubMed

    Walker, Robert; Shannon, Lisa; Logan, T K

    2011-07-01

    Intimate partner violence victimization has been associated with serious health problems among women, including many disorders that involve sleep disturbances. However, there has been only limited examination of sleep duration among women with victimization experiences. A total of 756 women with a domestic violence order (DVO) against a male intimate partner were interviewed about their health, mental health, substance use, and partner violence victimization. Face-to-face interviews were conducted from February 2001 to November 2003 for data collection in three rural and one urban county representing different jurisdictional settings. Because the current analyses focused on understanding intimate partner victimization in the past year and associations with sleep disturbance, 147 participants were excluded for reporting a relationship with the DVO partner for less than 6 months in the past year. The final sample for this article was 609. The women reported an average of a little above 5.5 hours of sleep per night. For women in the current study, significant predictors of sleep disturbance included race, number of children, number of other symptoms of depression in the past 2 weeks excluding sleep criteria, number of other symptoms of PTSD in the past 2 weeks excluding sleep criteria, number of chronic physical health problems, and severity of physical violence by the DVO partner in the past year. Addressing short sleep duration among partner victims in health care settings might enhance safety planning and prevent the development of health/mental health problems that can arise from victimization. PMID:20587469

  18. Sleep Loss and Partner Violence Victimization

    ERIC Educational Resources Information Center

    Walker, Robert; Shannon, Lisa; Logan, T. K.

    2011-01-01

    Intimate partner violence victimization has been associated with serious health problems among women, including many disorders that involve sleep disturbances. However, there has been only limited examination of sleep duration among women with victimization experiences. A total of 756 women with a domestic violence order (DVO) against a male…

  19. Astrocytic modulation of sleep homeostasis and cognitive consequences of sleep loss

    PubMed Central

    Halassa, Michael M.; Florian, Cedrick; Fellin, Tommaso; Munoz, James R.; Lee, So-Young; Abel, Ted; Haydon, Philip G.; Frank, Marcos G.

    2009-01-01

    Astrocytes modulate neuronal activity by releasing chemical transmitters via a process termed gliotransmission. The role of this process in the control of behavior is unknown. Since one outcome of SNARE-dependent gliotransmission is the regulation of extracellular adenosine and because adenosine promotes sleep, we genetically inhibited the release of gliotransmitters and asked if astrocytes play an unsuspected role in sleep regulation. Inhibiting gliotransmission attenuated the accumulation of sleep pressure, assessed by measuring the slow wave activity of the EEG during NREM sleep and prevented cognitive deficits associated with sleep loss. Since the sleep-suppressing effects of the A1 receptor antagonist CPT were prevented following inhibition of gliotransmission and because intracerebroventricular delivery of CPT to wildtype mice mimicked the transgenic phenotype we conclude that astrocytes modulate the accumulation of sleep pressure and its cognitive consequences through a pathway involving A1 receptors. PMID:19186164

  20. New neurons in the adult brain: The role of sleep and consequences of sleep loss

    PubMed Central

    Meerlo, Peter; Mistlberger, Ralph E.; Jacobs, Barry L.; Heller, H. Craig; McGinty, Dennis

    2009-01-01

    Research over the last few decades has firmly established that new neurons are generated in selected areas of the adult mammalian brain, particularly the dentate gyrus of the hippocampal formation and the subventricular zone of the lateral ventricles. The function of adult-born neurons is still a matter of debate. In the case of the hippocampus, integration of new cells in to the existing neuronal circuitry may be involved in memory processes and the regulation of emotionality. In recent years, various studies have examined how the production of new cells and their development into neurons is affected by sleep and sleep loss. While disruption of sleep for a period shorter than one day appears to have little effect on the basal rate of cell proliferation, prolonged restriction or disruption of sleep may have cumulative effects leading to a major decrease in hippocampal cell proliferation, cell survival and neurogenesis. Importantly, while short sleep deprivation may not affect the basal rate of cell proliferation, one study in rats shows that even mild sleep restriction may interfere with the increase in neurogenesis that normally occurs with hippocampus-dependent learning. Since sleep deprivation also disturbs memory formation, these data suggest that promoting survival, maturation and integration of new cells may be an unexplored mechanism by which sleep supports learning and memory processes. Most methods of sleep deprivation that have been employed affect both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Available data favor the hypothesis that decreases in cell proliferation are related to a reduction in REM sleep, whereas decreases in the number of cells that subsequently develop into adult neurons may be related to reductions in both NREM and REM sleep. The mechanisms by which sleep loss affects different aspects of adult neurogenesis are unknown. It has been proposed that adverse effects of sleep disruption may be mediated by stress and

  1. Sleep quality but not sleep quantity effects on cortisol responses to acute psychosocial stress.

    PubMed

    Bassett, Sarah M; Lupis, Sarah B; Gianferante, Danielle; Rohleder, Nicolas; Wolf, Jutta M

    2015-01-01

    Given the well-documented deleterious health effects, poor sleep has become a serious public health concern and increasing efforts are directed toward understanding underlying pathways. One potential mechanism may be stress and its biological correlates; however, studies investigating the effects of poor sleep on a body's capacity to deal with challenges are lacking. The current study thus aimed at testing the effects of sleep quality and quantity on cortisol responses to acute psychosocial stress. A total of 73 college-aged adults (44 females) were investigated. Self-reported sleep behavior was assessed via the Pittsburgh Sleep Quality Index and salivary cortisol responses to the Trier Social Stress Test were measured. In terms of sleep quality, we found a significant three-way interaction, such that relative to bad sleep quality, men who reported fairly good or very good sleep quality showed blunted or exaggerated cortisol responses, respectively, while women's stress responses were less dependent on their self-reported sleep quality. Contrarily, average sleep duration did not appear to impact cortisol stress responses. Lastly, participants who reported daytime dysfunctions (i.e. having trouble staying awake or keeping up enthusiasm) also showed a trend to blunted cortisol stress responses compared to participants who did not experience these types of daytime dysfunctions. Overall, the current study suggests gender-specific stress reactivity dysfunctions as one mechanism linking poor sleep with detrimental physical health outcomes. Furthermore, the observed differential sleep effects may indicate that while the body may be unable to maintain normal hypothalamic-pituitary-adrenal functioning in an acute psychosocial stress situation after falling prey to low sleep quality, it may retain capacities to deal with challenges during extended times of sleep deprivation. PMID:26414625

  2. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    low MSLT scores (e.g., Sleepy subjects) will show an exaggerated response (performance decrement) to sleep loss compared to subjects who have high MSLT scores (Alert subjects) on a nominal sleep schedule. When permitted to extend sleep-thus discharging their sleep debt-the Sleepy subjects will show a sleep-loss response resembling that of the Alert subjects.

  3. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    scores (e.g., Sleepy subjects) will show an exaggerated response (performance decrement) to sleep loss compared to subjects who have high MSLT scores (Alert subjects) on a nominal sleep schedule. when permitted to extend sleep-thus discharging their sleep debt-the Sleepy subjects will show a sleep-loss response resembling that of the Alert subjects.

  4. Individual Differences in Response to Sleep Deprivation: Assessment of Fatigue Following Sleep Loss

    NASA Technical Reports Server (NTRS)

    Carskadon, Mary A.

    1997-01-01

    response (performance decrement) to sleep loss compared to subjects who have high MSLT scores (Alert subjects) on a nominal sleep schedule; (2) when permitted to extend sleep--thus discharging their sleep debt-the Sleepy subjects will show a sleep-loss response resembling that of the Alert subjects.

  5. Sleep active cortical neurons expressing neuronal nitric oxide synthase are active after both acute sleep deprivation and chronic sleep restriction.

    PubMed

    Zielinski, M R; Kim, Y; Karpova, S A; Winston, S; McCarley, R W; Strecker, R E; Gerashchenko, D

    2013-09-01

    Non-rapid eye movement (NREM) sleep electroencephalographic (EEG) delta power (~0.5-4 Hz), also known as slow wave activity (SWA), is typically enhanced after acute sleep deprivation (SD) but not after chronic sleep restriction (CSR). Recently, sleep-active cortical neurons expressing neuronal nitric oxide synthase (nNOS) were identified and associated with enhanced SWA after short acute bouts of SD (i.e., 6h). However, the relationship between cortical nNOS neuronal activity and SWA during CSR is unknown. We compared the activity of cortical neurons expressing nNOS (via c-Fos and nNOS immuno-reactivity, respectively) and sleep in rats in three conditions: (1) after 18-h of acute SD; (2) after five consecutive days of sleep restriction (SR) (18-h SD per day with 6h ad libitum sleep opportunity per day); (3) and time-of-day matched ad libitum sleep controls. Cortical nNOS neuronal activity was enhanced during sleep after both 18-h SD and 5 days of SR treatments compared to control treatments. SWA and NREM sleep delta energy (the product of NREM sleep duration and SWA) were positively correlated with enhanced cortical nNOS neuronal activity after 18-h SD but not 5days of SR. That neurons expressing nNOS were active after longer amounts of acute SD (18h vs. 6h reported in the literature) and were correlated with SWA further suggest that these cells might regulate SWA. However, since these neurons were active after CSR when SWA was not enhanced, these findings suggest that mechanisms downstream of their activation are altered during CSR. PMID:23685166

  6. Sleep and Cognitive Abnormalities in Acute Minor Thalamic Infarction.

    PubMed

    Wu, Wei; Cui, Linyang; Fu, Ying; Tian, Qianqian; Liu, Lei; Zhang, Xuan; Du, Ning; Chen, Ying; Qiu, Zhijun; Song, Yijun; Shi, Fu-Dong; Xue, Rong

    2016-08-01

    In order to characterize sleep and the cognitive patterns in patients with acute minor thalamic infarction (AMTI), we enrolled 27 patients with AMTI and 12 matched healthy individuals. Questionnaires about sleep and cognition as well as polysomnography (PSG) were performed on days 14 and 90 post-stroke. Compared to healthy controls, in patients with AMTI, hyposomnia was more prevalent; sleep architecture was disrupted as indicated by decreased sleep efficiency, increased sleep latency, and decreased non-rapid eye movement sleep stages 2 and 3; more sleep-related breathing disorders occurred; and cognitive functions were worse, especially memory. While sleep apnea and long-delay memory recovered to a large extent in the patients, other sleep and cognitive function deficit often persisted. Patients with AMTI are at an increased risk for hyposomnia, sleep structure disturbance, sleep apnea, and memory deficits. Although these abnormalities improved over time, the slow and incomplete improvement suggest that early management should be considered in these patients. PMID:27237578

  7. Sleep and athletic performance: the effects of sleep loss on exercise performance, and physiological and cognitive responses to exercise.

    PubMed

    Fullagar, Hugh H K; Skorski, Sabrina; Duffield, Rob; Hammes, Daniel; Coutts, Aaron J; Meyer, Tim

    2015-02-01

    Although its true function remains unclear, sleep is considered critical to human physiological and cognitive function. Equally, since sleep loss is a common occurrence prior to competition in athletes, this could significantly impact upon their athletic performance. Much of the previous research has reported that exercise performance is negatively affected following sleep loss; however, conflicting findings mean that the extent, influence, and mechanisms of sleep loss affecting exercise performance remain uncertain. For instance, research indicates some maximal physical efforts and gross motor performances can be maintained. In comparison, the few published studies investigating the effect of sleep loss on performance in athletes report a reduction in sport-specific performance. The effects of sleep loss on physiological responses to exercise also remain equivocal; however, it appears a reduction in sleep quality and quantity could result in an autonomic nervous system imbalance, simulating symptoms of the overtraining syndrome. Additionally, increases in pro-inflammatory cytokines following sleep loss could promote immune system dysfunction. Of further concern, numerous studies investigating the effects of sleep loss on cognitive function report slower and less accurate cognitive performance. Based on this context, this review aims to evaluate the importance and prevalence of sleep in athletes and summarises the effects of sleep loss (restriction and deprivation) on exercise performance, and physiological and cognitive responses to exercise. Given the equivocal understanding of sleep and athletic performance outcomes, further research and consideration is required to obtain a greater knowledge of the interaction between sleep and performance. PMID:25315456

  8. Role of Sleep and Sleep Loss in Hormonal Release and Metabolism

    PubMed Central

    Leproult, Rachel; Van Cauter, Eve

    2011-01-01

    Compared to a few decades ago, adults, as well as children, sleep less. Sleeping as little as possible is often seen as an admirable behavior in contemporary society. However, sleep plays a major role in neuroendocrine function and glucose metabolism. Evidence that the curtailment of sleep duration may have adverse health effects has emerged in the past 10 years. Accumulating evidence from both epidemiologic studies and well-controlled laboratory studies indicates that chronic partial sleep loss may increase the risk of obesity and weight gain. The present chapter reviews epidemiologic studies in adults and children and laboratory studies in young adults indicating that sleep restriction results in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin and increased hunger and appetite. Altogether, the evidence points to a possible role of decreased sleep duration in the current epidemic of obesity. Bedtime extension in short sleepers should be explored as a novel behavioral intervention that may prevent weight gain or facilitate weight loss. Avoiding sleep deprivation may help to prevent the development of obesity, particularly in children. PMID:19955752

  9. Fatigue, Sleep Loss, and Confidence in Judgment

    ERIC Educational Resources Information Center

    Baranski, Joseph V.

    2007-01-01

    Sixty-four adults participated in a study examining the accuracy of metacognitive judgments during 28 hr of sleep deprivation (SD) and continuous cognitive work. Three tasks were studied (perceptual comparison, general knowledge, and mental addition), collectively spanning a range of cognitive abilities and levels of susceptibility to SD.…

  10. Sleep Loss Activates Cellular Markers of Inflammation: Sex Differences

    PubMed Central

    Irwin, Michael R.; Carrillo, Carmen; Olmstead, Richard

    2009-01-01

    Sleep disturbance is associated with inflammation and related disorders including cardiovascular disease, arthritis, and diabetes mellitus. Given sex differences in the prevalence of inflammatory disorders with stronger associations in females, this study was undertaken to test the effects of sleep loss on cellular mechanisms that contribute to proinflammatory cytokine activity. In 26 healthy adults (11 females; 15 males), monocyte intracellular proinflammatory cytokine production was repeatedly assessed at 08:00, 12:00, 16:00, 20:00, and 23:00 h during a baseline period and after partial sleep deprivation (awake from 11 PM to 3 AM). In the morning after a night of sleep loss, monocyte production of interleukin 6 and tumor necrosis factor- α differentially changed between the two sexes. Whereas both females and males showed a marked increase in the lipopolysaccharide (LPS) - stimulated production of IL-6 and TNF-α in the morning immediately after PSD, production of these cytokines during the early- and late evening was increased in the females as compared to decreases in the males. Sleep loss induces a functional alteration of monocyte proinflammatory cytokine responses with females showing greater cellular immune activation as compared to changes in males. These results have implications for understanding the role of sleep disturbance in the differential risk profile for inflammatory disorders between the sexes. PMID:19520155

  11. Sleep Loss Exacerbates Fatigue, Depression, and Pain in Rheumatoid Arthritis

    PubMed Central

    Irwin, Michael R.; Olmstead, Richard; Carrillo, Carmen; Sadeghi, Nina; FitzGerald, John D.; Ranganath, Veena K.; Nicassio, Perry M.

    2012-01-01

    Study Objectives: Disturbances of sleep are hypothesized to contribute to pain. However, experimental data are limited to healthy pain-free individuals. This study evaluated the effect of sleep loss during part of the night on daytime mood symptoms and pain perceptions in patients with rheumatoid arthritis in comparison with control subjects. Design: A between-groups laboratory study with assessment of mood symptoms and pain perception before and after partial night sleep deprivation (PSD; awake 23:00 hr to 03:00 hr). Setting: General clinical research center. Participants: Patients with rheumatoid arthritis (n = 27) and volunteer comparison control subjects (n = 27). Measurements: Subjective reports of sleep, mood symptoms and pain, polysomnographic assessment of sleep continuity, and subjective and objective assessment of rheumatoid arthritis-specific joint pain. Results: PSD induced differential increases in self-reported fatigue (P < 0.09), depression (P < 0.04), anxiety (P < 0.04), and pain (P < 0.01) in patients with rheumatoid arthritis compared with responses in control subjects, in whom differential increases of self-reported pain were independent of changes in mood symptoms, subjective sleep quality, and objective measures of sleep fragmentation. In the patients with rheumatoid arthritis, PSD also induced increases in disease-specific activity as indexed by self-reported pain severity (P < 0.01) and number of painful joints (P < 0.02) as well as clinician-rated joint counts (P < 0.03). Conclusion: This study provides the first evidence of an exaggerated increase in symptoms of mood and pain in patients with rheumatoid arthritis after sleep loss, along with an activation of rheumatoid arthritis-related joint pain. Given the reciprocal relationship between sleep disturbances and pain, clinical management of pain in patients with rheumatoid arthritis should include an increased focus on the prevention and treatment of sleep disturbance in this clinical

  12. Trait-Like Vulnerability to Total and Partial Sleep Loss

    PubMed Central

    Rupp, Tracy L.; Wesensten, Nancy J.; Balkin, Thomas J.

    2012-01-01

    Objective: To determine the extent to which individual differences in vulnerability to total sleep deprivation also reflect individual differences in vulnerability to multiple nights of sleep restriction. Design: Two sleep loss conditions (order counterbalanced) separated by 2 to 4 weeks: (a) total sleep deprivation (TSD) of 2 nights (63 h continuous wakefulness); (b) sleep restriction (SR) of 7 nights of 3 h nightly time in bed (TIB). Both conditions were preceded by 7 in-laboratory nights with 10 h nightly TIB; and followed by 3 recovery nights with 8 h nightly TIB. Measures of cognitive performance (psychomotor vigilance, working memory [1-Back], and mathematical processing), objective alertness, subjective sleepiness, and mood were obtained at regular intervals under both conditions. Intra-class correlation coefficients (ICC) were computed using outcome metrics averaged over the last day (08:00-20:00) of TSD and SR. Setting: Residential sleep/performance testing facility. Participants: Nineteen healthy adults (ages 18-39; 11 males, 8 females). Interventions: 2 nights of TSD and 7 nights SR (3 h nightly TIB). Results: Volunteers who displayed greater vulnerability to TSD displayed greater vulnerability to SR on cognitive performance tasks (ICC: PVT lapses = 0.89; PVT speed = 0.86; 1-Back = 0.88; mathematical processing = 0.68, Ps < 0.05). In addition, trait-like responsivity to TSD/SR was found for mood variables vigor (ICC = 0.91), fatigue (ICC = 0.73), and happiness (ICC = 0.85) (all Ps < 0.05). Conclusion: Resilience to sleep loss is a trait-like characteristic that reflects an individual's ability to maintain performance during both types of sleep loss (SR and TSD). Whether the findings extend to sleep schedules other than those investigated here (63 h of TSD and 7 nights of 3 h nightly TIB) will be the focus of future studies. Citation: Rupp TL; Wesensten NJ; Balkin TJ. Trait-like vulnerability to total and partial sleep loss. SLEEP 2012

  13. Age, circadian rhythms, and sleep loss in flight crews

    NASA Technical Reports Server (NTRS)

    Gander, Philippa H.; Nguyen, DE; Rosekind, Mark R.; Connell, Linda J.

    1993-01-01

    Age-related changes in trip-induced sleep loss, personality, and the preduty temperature rhythm were analyzed in crews from various flight operations. Eveningness decreased with age. The minimum of the baseline temperature rhythm occurred earlier with age. The amplitude of the baseline temperature rhythm declined with age. Average daily percentage sleep loss during trips increased with age. Among crewmembers flying longhaul flight operations, subjects aged 50-60 averaged 3.5 times more sleep loss per day than subjects aged 20-30. These studies support previous findings that evening types and subjects with later peaking temperature rhythms adapt better to shift work and time zone changes. Age and circadian type may be important considerations for duty schedules and fatigue countermeasures.

  14. Impact of sleep and sleep loss on glucose homeostasis and appetite regulation

    PubMed Central

    Knutson, Kristen L

    2007-01-01

    Synopsis Over the past 30 years there has been an increase in the prevalence of obesity and diabetes, both of which can have serious consequences for longevity and quality of life. Sleep durations may have also decreased over this time period. This chapter reviews laboratory and epidemiologic evidence for an association between sleep loss and impairments in glucose metabolism and appetite regulation, which could increase the risk of diabetes or weight gain. PMID:18516218

  15. Pain Sensitivity and Recovery From Mild Chronic Sleep Loss

    PubMed Central

    Roehrs, Timothy A.; Harris, Erica; Randall, Surilla; Roth, Thomas

    2012-01-01

    Study Objectives: To determine whether an extended bedtime in sleepy and otherwise healthy volunteers would increase alertness and thereby also reduce pain sensitivity. Setting: Outpatient with sleep laboratory assessments. Participants and Interventions: Healthy volunteers (n = 18), defined as having an average daily sleep latency on the Multiple Sleep Latency Test (MSLT) < 8 min, were randomized to 4 nights of extended bedtime (10 hr) (EXT) or 4 nights of their diary-reported habitual bedtimes (HAB). On day 1 and day 4 they received a standard MSLT (10:00, 12:00, 14:00, and 16:00 hr) and finger withdrawal latency pain testing to a radiant heat stimulus (10:30 and 14:30 hr). Results: During the four experimental nights the EXT group slept 1.8 hr per night more than the HAB group and average daily sleep latency on the MSLT increased in the EXT group, but not the HAB group. Similarly, finger withdrawal latency was increased (pain sensitivity was reduced) in the EXT group but not the HAB group. The nightly increase in sleep time during the four experimental nights was correlated with the improvement in MSLT, which in turn was correlated with reduced pain sensitivity. Conclusions: These are the first data to show that an extended bedtime in mildly sleepy healthy adults, which resulted in increased sleep time and reduced sleepiness, reduces pain sensitivity. Citation: Roehrs TA; Harris E; Randall S; Roth T. Pain sensitivity and recovery from mild chronic sleep loss. SLEEP 2012;35(12):1667-1672. PMID:23204609

  16. Impact of sleep loss before learning on cortical dynamics during memory retrieval.

    PubMed

    Alberca-Reina, E; Cantero, J L; Atienza, M

    2015-12-01

    Evidence shows that sleep loss before learning decreases activation of the hippocampus during encoding and promotes forgetting. But it remains to be determined which neural systems are functionally affected during memory retrieval after one night of recovery sleep. To investigate this issue, we evaluated memory for pairs of famous people's faces with the same or different profession (i.e., semantically congruent or incongruent faces) after one night of undisturbed sleep in subjects who either underwent 4hours of acute sleep restriction (ASR, N=20) or who slept 8hours the pre-training night (controls, N=20). EEG recordings were collected during the recognition memory task in both groups, and the cortical sources generating this activity localized by applying a spatial beamforming filter in the frequency domain. Even though sleep restriction did not affect accuracy of memory performance, controls showed a much larger decrease of alpha power relative to a baseline period when compared to sleep-deprived subjects. These group differences affected a widespread frontotemporoparietal network involved in retrieval of episodic/semantic memories. Regression analyses further revealed that associative memory in the ASR group was negatively correlated with alpha power in the occipital regions, whereas the benefit of congruency in the same group was positively correlated with delta power in the left lateral prefrontal cortex. Retrieval-related decreases of alpha power have been associated with the reactivation of material-specific memory representations, whereas increases of delta power have been related to inhibition of interferences that may affect the performance of the task. We can therefore draw the conclusion that a few hours of sleep loss in the pre-training night, though insufficient to change the memory performance, is sufficient to alter the processes involved in retrieving and manipulating episodic and semantic information. PMID:26302671

  17. Maximizing Sensitivity of the Psychomotor Vigilance Test (PVT) to Sleep Loss

    PubMed Central

    Basner, Mathias; Dinges, David F.

    2011-01-01

    Study Objectives: The psychomotor vigilance test (PVT) is among the most widely used measures of behavioral alertness, but there is large variation among published studies in PVT performance outcomes and test durations. To promote standardization of the PVT and increase its sensitivity and specificity to sleep loss, we determined PVT metrics and task durations that optimally discriminated sleep deprived subjects from alert subjects. Design: Repeated-measures experiments involving 10-min PVT assessments every 2 h across both acute total sleep deprivation (TSD) and 5 days of chronic partial sleep deprivation (PSD). Setting: Controlled laboratory environment. Participants: 74 healthy subjects (34 female), aged 22–45 years. Interventions: TSD experiment involving 33 h awake (N = 31 subjects) and a PSD experiment involving 5 nights of 4 h time in bed (N = 43 subjects). Measurements and Results: In a paired t-test paradigm and for both TSD and PSD, effect sizes of 10 different PVT performance outcomes were calculated. Effect sizes were high for both TSD (1.59–1.94) and PSD (0.88–1.21) for PVT metrics related to lapses and to measures of psychomotor speed, i.e., mean 1/RT (response time) and mean slowest 10% 1/RT. In contrast, PVT mean and median RT outcomes scored low to moderate effect sizes influenced by extreme values. Analyses facilitating only portions of the full 10-min PVT indicated that for some outcomes, high effect sizes could be achieved with PVT durations considerably shorter than 10 min, although metrics involving lapses seemed to profit from longer test durations in TSD. Conclusions: Due to their superior conceptual and statistical properties and high sensitivity to sleep deprivation, metrics involving response speed and lapses should be considered primary outcomes for the 10-min PVT. In contrast, PVT mean and median metrics, which are among the most widely used outcomes, should be avoided as primary measures of alertness. Our analyses also suggest

  18. Repeated Exposure to Conditioned Fear Stress Increases Anxiety and Delays Sleep Recovery Following Exposure to an Acute Traumatic Stressor

    PubMed Central

    Greenwood, Benjamin N.; Thompson, Robert S.; Opp, Mark R.; Fleshner, Monika

    2014-01-01

    Repeated stressor exposure can sensitize physiological responses to novel stressors and facilitate the development of stress-related psychiatric disorders including anxiety. Disruptions in diurnal rhythms of sleep–wake behavior accompany stress-related psychiatric disorders and could contribute to their development. Complex stressors that include fear-eliciting stimuli can be a component of repeated stress experienced by human beings, but whether exposure to repeated fear can prime the development of anxiety and sleep disturbances is unknown. In the current study, adult male F344 rats were exposed to either control conditions or repeated contextual fear conditioning for 22 days followed by exposure to no, mild (10), or severe (100) acute uncontrollable tail shock stress. Exposure to acute stress produced anxiety-like behavior as measured by a reduction in juvenile social exploration and exaggerated shock-elicited freezing in a novel context. Prior exposure to repeated fear enhanced anxiety-like behavior as measured by shock-elicited freezing, but did not alter social exploratory behavior. The potentiation of anxiety produced by prior repeated fear was temporary; exaggerated fear was present 1 day but not 4 days following acute stress. Interestingly, exposure to acute stress reduced rapid eye movement (REM) and non-REM (NREM) sleep during the hours immediately following acute stress. This initial reduction in sleep was followed by robust REM rebound and diurnal rhythm flattening of sleep/wake behavior. Prior repeated fear extended the acute stress-induced REM and NREM sleep loss, impaired REM rebound, and prolonged the flattening of the diurnal rhythm of NREM sleep following acute stressor exposure. These data suggest that impaired recovery of sleep/wake behavior following acute stress could contribute to the mechanisms by which a history of prior repeated stress increases vulnerability to subsequent novel stressors and stress-related disorders. PMID

  19. Sleep ability mediates individual differences in the vulnerability to sleep loss: evidence from a PER3 polymorphism.

    PubMed

    Maire, M; Reichert, C F; Gabel, V; Viola, A U; Strobel, W; Krebs, J; Landolt, H P; Bachmann, V; Cajochen, C; Schmidt, C

    2014-03-01

    Sleep deprivation is highly prevalent in our 24/7 society with harmful consequences on daytime functioning on the individual level. Genetically determined, trait-like vulnerability contributes to prominent inter-individual variability in the behavioral responses to sleep loss and adverse circadian phase. We aimed at investigating the effects of differential sleep pressure levels (high vs low) on the circadian modulation of neurobehavioral performance, sleepiness correlates, and nap sleep in individuals genotyped for a polymorphism in the clock gene PERIOD3. Fourteen homozygous long (PER3(5/5)) and 15 homozygous short (PER3(4/4)) allele carriers underwent both a 40-h sleep deprivation and multiple nap protocol under controlled laboratory conditions. We compared genotypes regarding subjective and ocular correlates of sleepiness, unintentional sleep episodes as well as psychomotor vigilance during both protocols. Nap sleep was monitored by polysomnography and visually scored according to standard criteria. The detrimental effects of high sleep pressure on sleepiness correlates and psychomotor vigilance were more pronounced in PER3(5/5) than PER3(4/4) carriers. Under low sleep pressure, both groups showed similar circadian time courses. Concomitantly, nap sleep efficiency and subjective sleep quality across all naps tended to be higher in the more vulnerable PER3(5/5) carriers. In addition, PER3-dependent sleep-loss-related attentional lapses were mediated by sleep efficiency across the circadian cycle. Our data corroborate a greater detrimental impact of sleep deprivation in PER3(5/5) compared to PER3(4/4) carriers. They further suggest that the group with greater attentional performance impairment due to sleep deprivation (PER3(5/5) carriers) is superior at initiating sleep over the 24-h cycle. This higher sleep ability may mirror a faster sleep pressure build-up between the multiple sleep opportunities and thus a greater flexibility in sleep initiation. Finally

  20. The Perilipin Homologue, Lipid Storage Droplet 2, Regulates Sleep Homeostasis and Prevents Learning Impairments Following Sleep Loss

    PubMed Central

    Thimgan, Matthew S.; Suzuki, Yasuko; Seugnet, Laurent; Gottschalk, Laura; Shaw, Paul J.

    2010-01-01

    Extended periods of waking result in physiological impairments in humans, rats, and flies. Sleep homeostasis, the increase in sleep observed following sleep loss, is believed to counter the negative effects of prolonged waking by restoring vital biological processes that are degraded during sleep deprivation. Sleep homeostasis, as with other behaviors, is influenced by both genes and environment. We report here that during periods of starvation, flies remain spontaneously awake but, in contrast to sleep deprivation, do not accrue any of the negative consequences of prolonged waking. Specifically, the homeostatic response and learning impairments that are a characteristic of sleep loss are not observed following prolonged waking induced by starvation. Recently, two genes, brummer (bmm) and Lipid storage droplet 2 (Lsd2), have been shown to modulate the response to starvation. bmm mutants have excess fat and are resistant to starvation, whereas Lsd2 mutants are lean and sensitive to starvation. Thus, we hypothesized that bmm and Lsd2 may play a role in sleep regulation. Indeed, bmm mutant flies display a large homeostatic response following sleep deprivation. In contrast, Lsd2 mutant flies, which phenocopy aspects of starvation as measured by low triglyceride stores, do not exhibit a homeostatic response following sleep loss. Importantly, Lsd2 mutant flies are not learning impaired after sleep deprivation. These results provide the first genetic evidence, to our knowledge, that lipid metabolism plays an important role in regulating the homeostatic response and can protect against neuronal impairments induced by prolonged waking. PMID:20824166

  1. Catechol-O-Methyltransferase Val158Met Polymorphism Associates with Individual Differences in Sleep Physiologic Responses to Chronic Sleep Loss

    PubMed Central

    Goel, Namni; Banks, Siobhan; Lin, Ling; Mignot, Emmanuel; Dinges, David F.

    2011-01-01

    Background The COMT Val158Met polymorphism modulates cortical dopaminergic catabolism, and predicts individual differences in prefrontal executive functioning in healthy adults and schizophrenic patients, and associates with EEG differences during sleep loss. We assessed whether the COMT Val158Met polymorphism was a novel marker in healthy adults of differential vulnerability to chronic partial sleep deprivation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily and persistent basis. Methodology/Principal Findings 20 Met/Met, 64 Val/Met, and 45 Val/Val subjects participated in a protocol of two baseline 10h time in bed (TIB) nights followed by five consecutive 4 h TIB nights. Met/Met subjects showed differentially steeper declines in non-REM EEG slow-wave energy (SWE)—the putative homeostatic marker of sleep drive—during PSD, despite comparable baseline SWE declines. Val/Val subjects showed differentially smaller increases in slow-wave sleep and smaller reductions in stage 2 sleep during PSD, and had more stage 1 sleep across nights and a shorter baseline REM sleep latency. The genotypes, however, did not differ in performance across various executive function and cognitive tasks and showed comparable increases in subjective and physiological sleepiness in response to chronic sleep loss. Met/Met genotypic and Met allelic frequencies were higher in whites than African Americans. Conclusions/Significance The COMT Val158Met polymorphism may be a genetic biomarker for predicting individual differences in sleep physiology—but not in cognitive and executive functioning—resulting from sleep loss in a healthy, racially-diverse adult population of men and women. Beyond healthy sleepers, our results may also provide insight for predicting sleep loss responses in patients with schizophrenia and other psychiatric disorders, since these groups repeatedly experience chronically-curtailed sleep and demonstrate COMT

  2. Dynamic Circadian Modulation in a Biomathematical Model for the Effects of Sleep and Sleep Loss on Waking Neurobehavioral Performance

    PubMed Central

    McCauley, Peter; Kalachev, Leonid V.; Mollicone, Daniel J.; Banks, Siobhan; Dinges, David F.; Van Dongen, Hans P. A.

    2013-01-01

    Recent experimental observations and theoretical advances have indicated that the homeostatic equilibrium for sleep/wake regulation—and thereby sensitivity to neurobehavioral impairment from sleep loss—is modulated by prior sleep/wake history. This phenomenon was predicted by a biomathematical model developed to explain changes in neurobehavioral performance across days in laboratory studies of total sleep deprivation and sustained sleep restriction. The present paper focuses on the dynamics of neurobehavioral performance within days in this biomathematical model of fatigue. Without increasing the number of model parameters, the model was updated by incorporating time-dependence in the amplitude of the circadian modulation of performance. The updated model was calibrated using a large dataset from three laboratory experiments on psychomotor vigilance test (PVT) performance, under conditions of sleep loss and circadian misalignment; and validated using another large dataset from three different laboratory experiments. The time-dependence of circadian amplitude resulted in improved goodness-of-fit in night shift schedules, nap sleep scenarios, and recovery from prior sleep loss. The updated model predicts that the homeostatic equilibrium for sleep/wake regulation—and thus sensitivity to sleep loss—depends not only on the duration but also on the circadian timing of prior sleep. This novel theoretical insight has important implications for predicting operator alertness during work schedules involving circadian misalignment such as night shift work. Citation: McCauley P; Kalachev LV; Mollicone DJ; Banks S; Dinges DF; Van Dongen HPA. Dynamic circadian modulation in a biomathematical model for the effects of sleep and sleep loss on waking neurobehavioral performance. SLEEP 2013;36(12):1987-1997. PMID:24293775

  3. Sleep loss alters synaptic and intrinsic neuronal properties in mouse prefrontal cortex

    PubMed Central

    Winters, Bradley D.; Huang, Yanhua H.; Dong, Yan; Krueger, James M.

    2011-01-01

    Despite sleep-loss-induced cognitive deficits, little is known about the cellular adaptations that occur with sleep loss. We used brain slices obtained from mice that were sleep deprived for 8 h to examine the electrophysiological effects of sleep deprivation (SD). We employed a modified pedestal (flowerpot) over water method for SD that eliminated rapid eye movement sleep and greatly reduced non-rapid eye movement sleep. In layer V/VI pyramidal cells of the medial prefrontal cortex, miniature excitatory post synaptic current amplitude was slightly reduced, miniature inhibitory post synaptic currents were unaffected, and intrinsic membrane excitability was increased after SD. PMID:21962531

  4. Increased impulsivity in response to food cues after sleep loss in healthy young men

    PubMed Central

    Cedernaes, Jonathan; Brandell, Jon; Ros, Olof; Broman, Jan-Erik; Hogenkamp, Pleunie S; Schiöth, Helgi B; Benedict, Christian

    2014-01-01

    Objective To investigate whether acute total sleep deprivation (TSD) leads to decreased cognitive control when food cues are presented during a task requiring active attention, by assessing the ability to cognitively inhibit prepotent responses. Methods Fourteen males participated in the study on two separate occasions in a randomized, crossover within-subject design: one night of TSD versus normal sleep (8.5 hours). Following each nighttime intervention, hunger ratings and morning fasting plasma glucose concentrations were assessed before performing a go/no-go task. Results Following TSD, participants made significantly more commission errors when they were presented “no-go” food words in the go/no-go task, as compared with their performance following sleep (+56%; P<0.05). In contrast, response time and omission errors to “go” non-food words did not differ between the conditions. Self-reported hunger after TSD was increased without changes in fasting plasma glucose. The increase in hunger did not correlate with the TSD-induced commission errors. Conclusions Our results suggest that TSD impairs cognitive control also in response to food stimuli in healthy young men. Whether such loss of inhibition or impulsiveness is food cue-specific as seen in obesity—thus providing a mechanism through which sleep disturbances may promote obesity development—warrants further investigation. PMID:24839251

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

    PubMed Central

    Everson, Carol A.; Thalacker, Christa D.; Hogg, Neil

    2008-01-01

    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

  6. Exercise‐Induced growth hormone during acute sleep deprivation

    PubMed Central

    Ritsche, Kevin; Nindl, Bradly C.; Wideman, Laurie

    2014-01-01

    Abstract The effect of acute (24‐h) sleep deprivation on exercise‐induced growth hormone (GH) and insulin‐like growth factor‐1 (IGF‐1) was examined. Ten men (20.6 ± 1.4 years) completed two randomized 24‐h sessions including a brief, high‐intensity exercise bout following either a night of sleep (SLEEP) or (24‐h) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], minimum power [MinP], time to peak power [TTPP], fatigue index, [FI]) and total work per sprint [TWPS]) was determined from four maximal 30‐sec Wingate sprints on a cycle ergometer. Self‐reported sleep 7 days prior to each session was similar between SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 h, P =0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 h vs. 7.92 ± 0.33 h, respectively) (P =0.166). No differences existed in MP, PP, MinP, TTPP, FI, TWPS, resting GH concentrations, time to reach exercise‐induced peak GH concentration (TTP), or free IGF‐1 between sessions. GH area under the curve (AUC) (825.0 ± 199.8 vs. 2212.9 ± 441.9 μg/L*min, P <0.01), exercise‐induced peak GH concentration (17.8 ± 3.7 vs. 39.6 ± 7.1 μg/L, P <0.01) and ΔGH (peak GH – resting GH) (17.2 ± 3.7 vs. 38.2 ± 7.3 μg/L, P <0.01) were significantly lower during the SLEEP versus SLD session. Our results indicate that the exercise‐induced GH response was significantly augmented in sleep‐deprived individuals. PMID:25281616

  7. Sleep

    MedlinePlus

    ... sleep deprivation? What are sleep myths? What are sleep disorders? Can certain diseases/conditions disrupt sleep? What is ... sleep deprivation? What are sleep myths? What are sleep disorders? Can certain diseases/conditions disrupt sleep? What is ...

  8. Non-invasive Positive Pressure Ventilation during Sleep at 3800m: relationship to Acute Mountain Sickness and sleeping oxyhemoglobin saturation

    PubMed Central

    Johnson, PL; Popa, DA; Prisk, GK; Sullivan, CE; Edwards, N

    2014-01-01

    Background and objectives Ascent to high altitude results in hypobaric hypoxia and some individuals will develop Acute Mountain Sickness, which has been shown to be associated with low oxyhemoglobin saturation during sleep. Previous research has shown that positive end-expiratory pressure by use of expiratory valves in a face mask while awake, results in a reduction in AMS symptoms and higher oxyhemoglobin saturation. We aimed to test whether pressure ventilation during sleep would prevent AMS by keeping oxyhaemoglobin higher during sleep. Methods We compared sleeping oxyhemoglobin saturation and the incidence and severity of Acute Mountain Sickness in seven subjects sleeping for two consecutive nights at 3800m above sea level using either non-invasive positive pressure ventilation that delivered positive inspiratory and expiratory airway pressure via a face mask, or sleeping without assisted ventilation. The presence and severity of Acute Mountain Sickness was assessed by administration of the Lake Louise questionnaire. Results We found significant increases in the mean and minimum sleeping oxyhemoglobin saturation and decreases in AMS symptoms in subjects who used positive pressure ventilation during sleep. Mean and minimum sleeping SaO2 was lower in subjects who developed AMS after the night spent without positive pressure ventilation. Conclusion The use of positive pressure ventilation during sleep at 3800m significantly increased the sleeping oxygen saturation; we suggest that the marked reduction in symptoms of AMS is due to this higher sleeping SaO2. We agree with the findings from previous studies that the development of AMS is associated with a lower sleeping oxygen saturation. PMID:20051046

  9. Medical and Genetic Differences in the Adverse Impact of Sleep Loss on Performance: Ethical Considerations for the Medical Profession

    PubMed Central

    Czeisler, Charles A.

    2009-01-01

    The Institute of Medicine recently concluded that-on average-medical residents make more serious medical errors and have more motor vehicle crashes when they are deprived of sleep. In the interest of public safety, society has required limitations on work hours in many other safety sensitive occupations, including transportation and nuclear power generation. Those who argue in favor of traditional extended duration resident work hours often suggest that there are inter- individual differences in response to acute sleep loss or chronic sleep deprivation, implying that physicians may be more resistant than the average person to the detrimental effects of sleep deprivation on performance, although there is no evidence that physicians are particularly resistant to such effects. Indeed, recent investigations have identified genetic polymorphisms that may convey a relative resistance to the effects of prolonged wakefulness on a subset of the healthy population, although there is no evidence that physicians are over-represented in this cohort. Conversely, there are also genetic polymorphisms, sleep disorders and other inter-individual differences that appear to convey an increased vulnerability to the performance-impairing effects of 24 hours of wakefulness. Given the magnitude of inter-individual differences in the effect of sleep loss on cognitive performance, and the sizeable proportion of the population affected by sleep disorders, hospitals face a number of ethical dilemmas. How should the work hours of physicians be limited to protect patient safety optimally? For example, some have argued that, in contrast to other professions, work schedules that repeatedly induce acute and chronic sleep loss are uniquely essential to the training of physicians. If evidence were to prove this premise to be correct, how should such training be ethically accomplished in the quartile of physicians and surgeons who are most vulnerable to the effects of sleep loss on performance

  10. Medical and genetic differences in the adverse impact of sleep loss on performance: ethical considerations for the medical profession.

    PubMed

    Czeisler, Charles A

    2009-01-01

    The Institute of Medicine recently concluded that-on average-medical residents make more serious medical errors and have more motor vehicle crashes when they are deprived of sleep. In the interest of public safety, society has required limitations on work hours in many other safety sensitive occupations, including transportation and nuclear power generation. Those who argue in favor of traditional extended duration resident work hours often suggest that there are inter- individual differences in response to acute sleep loss or chronic sleep deprivation, implying that physicians may be more resistant than the average person to the detrimental effects of sleep deprivation on performance, although there is no evidence that physicians are particularly resistant to such effects. Indeed, recent investigations have identified genetic polymorphisms that may convey a relative resistance to the effects of prolonged wakefulness on a subset of the healthy population, although there is no evidence that physicians are over-represented in this cohort. Conversely, there are also genetic polymorphisms, sleep disorders and other inter-individual differences that appear to convey an increased vulnerability to the performance-impairing effects of 24 hours of wakefulness. Given the magnitude of inter-individual differences in the effect of sleep loss on cognitive performance, and the sizeable proportion of the population affected by sleep disorders, hospitals face a number of ethical dilemmas. How should the work hours of physicians be limited to protect patient safety optimally? For example, some have argued that, in contrast to other professions, work schedules that repeatedly induce acute and chronic sleep loss are uniquely essential to the training of physicians. If evidence were to prove this premise to be correct, how should such training be ethically accomplished in the quartile of physicians and surgeons who are most vulnerable to the effects of sleep loss on performance

  11. REM Sleep and Its Loss-associated Epigenetic Regulation with Reference to Noradrenaline in Particular

    PubMed Central

    Mehta, Rachna; Singh, Abhishek; Bókkon, István; Nath Mallick, Birendra

    2016-01-01

    Sleep is an essential physiological process, which has been divided into rapid eye movement sleep (REMS) and non-REMS (NREMS) in higher animals. REMS is a unique phenomenon that unlike other sleep-waking states is not under voluntary control. Directly or indirectly it influences or gets influenced by most of the physiological processes controlled by the brain. It has been proposed that REMS serves housekeeping function of the brain. Extensive research has shown that during REMS at least noradrenaline (NA) -ergic neurons must cease activity and upon REMS loss, there are increased levels of NA in the brain, which then induces many of the REMS loss associated acute and chronic effects. The NA level is controlled by many bio-molecules that are regulated at the molecular and transcriptional levels. Similarly, NA can also directly or indirectly modulate the synthesis and levels of many molecules, which in turn may affect physiological processes. The burgeoning field of behavioral neuroepigenetics has gained importance in recent years and explains the regulatory mechanisms underlying several behavioral phenomena. As REMS and its loss associated changes in NA modulate several pathophysiological processes, in this review we have attempted to explain on one hand how the epigenetic mechanisms regulating the gene expression of factors like tyrosine hydroxylase (TH), monoamine oxidase (MAO), noradrenaline transporter (NAT) control NA levels and on the other hand, how NA per se can affect other molecules in neural circuitry at the epigenetic level resulting in behavioral changes in health and diseases. An understanding of these events will expose the molecular basis of REMS and its loss-associated pathophysiological changes; which are presented as a testable hypothesis for confirmation. PMID:26813120

  12. The impact of sleep loss on hippocampal function

    PubMed Central

    Prince, Toni-Moi; Abel, Ted

    2013-01-01

    Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep deprivation to impair memory consolidation and plasticity. In this review, we address these topics with a focus on the detrimental effects of post-learning sleep deprivation on memory consolidation. Obtaining adequate sleep is challenging in a society that values “work around the clock.” Therefore, the development of interventions to combat the negative cognitive effects of sleep deprivation is key. However, there are a limited number of therapeutics that are able to enhance cognition in the face of insufficient sleep. The identification of molecular pathways implicated in the deleterious effects of sleep deprivation on memory could potentially yield new targets for the development of more effective drugs. PMID:24045505

  13. Sleep Apnea Prevalence in Acute Myocardial Infarction - the Sleep Apnea in Post Acute Myocardial Infarction Patients (SAPAMI) Study

    PubMed Central

    Ludka, Ondrej; Stepanova, Radka; Vyskocilova, Martina; Galkova, Lujza; Mikolaskova, Monika; Belehrad, Milos; Kostalova, Jana; Mihalova, Zuzana; Drozdova, Adela; Hlasensky, Jiri; Gacik, Michal; Pudilova, Lucie; Mikusova, Tereza; Fischerova, Blanka; Sert-Kuniyoshi, Fatima; Kara, Tomas; Spinar, Jindrich; Somers, Virend K.

    2014-01-01

    Background While sleep apnea (SA) might be a modifiable cardiovascular risk factor, recent data suggest that SA is severely underdiagnosed in patients after acute myocardial infarction (MI). There is limited evidence about day-night variation of onset of MI on dependence of having SA. We therefore investigated the prevalence of SA and examined the day-night variation of onset of MI in acute MI patients. Methods We prospectively studied 782 consecutive patients admitted to the hospital with the diagnosis of acute MI. All subjects underwent sleep evaluations using a portable device after at least 48 hours post-admission. Using the apnea-hypopnea index (AHI), groups were defined as patients without SA (<5 events/hour), mild SA (5–15 events/hour), moderate SA (15–30 events/hour), and severe SA (≥30 events/hour). Results Almost all patients (98%) underwent urgent coronary angiography and 91% of patients underwent primary PCI. Using a threshold of AHI ≥ 5 events/hour, SA was present in 65.7% of patients after acute MI. Mild SA was present in 32.6%, moderate in 20.4% and severe in 12.7%. The day-night variation in the onset of MI in all groups of SA patients was similar to that observed in non-SA patients. From 6AM–12PM, the frequency of MI was higher in both SA and non-SA patients, as compared to the interval from 12AM–6AM (all p<0.05). Conclusion There is a high prevalence of SA in patients presenting with acute MI. Peak time of MI onset in SA patients was between 6AM–noon, similar to that in the general population. Whether diagnosis and treatment of SA after MI will significantly improve outcomes in these patients remains to be determined. PMID:25064202

  14. Cross-Translational Studies in Human and Drosophila Identify Markers of Sleep Loss

    PubMed Central

    Thimgan, Matthew S.; Gottschalk, Laura; Toedebusch, Cristina; McLeland, Jennifer; Rechtschaffen, Allan; Gilliland-Roberts, Marcia; Duntley, Stephen P.; Shaw, Paul J.

    2013-01-01

    Inadequate sleep has become endemic, which imposes a substantial burden for public health and safety. At present, there are no objective tests to determine if an individual has gone without sleep for an extended period of time. Here we describe a novel approach that takes advantage of the evolutionary conservation of sleep to identify markers of sleep loss. To begin, we demonstrate that IL-6 is increased in rats following chronic total sleep deprivation and in humans following 30 h of waking. Discovery experiments were then conducted on saliva taken from sleep-deprived human subjects to identify candidate markers. Given the relationship between sleep and immunity, we used Human Inflammation Low Density Arrays to screen saliva for novel markers of sleep deprivation. Integrin αM (ITGAM) and Anaxin A3 (AnxA3) were significantly elevated following 30 h of sleep loss. To confirm these results, we used QPCR to evaluate ITGAM and AnxA3 in independent samples collected after 24 h of waking; both transcripts were increased. The behavior of these markers was then evaluated further using the power of Drosophila genetics as a cost-effective means to determine whether the marker is associated with vulnerability to sleep loss or other confounding factors (e.g., stress). Transcript profiling in flies indicated that the Drosophila homologues of ITGAM were not predictive of sleep loss. Thus, we examined transcript levels of additional members of the integrin family in flies. Only transcript levels of scab, the Drosophila homologue of Integrin α5 (ITGA5), were associated with vulnerability to extended waking. Since ITGA5 was not included on the Low Density Array, we returned to human samples and found that ITGA5 transcript levels were increased following sleep deprivation. These cross-translational data indicate that fly and human discovery experiments are mutually reinforcing and can be used interchangeably to identify candidate biomarkers of sleep loss. PMID:23637783

  15. Relationship Between Sleep Quality and Quantity and Weight Loss in Women Participating in a Weight-Loss Intervention Trial

    PubMed Central

    Thomson, Cynthia A.; Morrow, Kelly L.; Flatt, Shirley W.; Wertheim, Betsy C.; Perfect, Michelle M.; Ravia, Jennifer J.; Sherwood, Nancy E.; Karanja, Njeri; Rock, Cheryl L.

    2016-01-01

    Evidence suggests that individuals who report fewer total hours of sleep are more likely to be overweight or obese. Few studies have prospectively evaluated weight-loss success in relation to reported sleep quality and quantity. This analysis sought to determine the association between sleep characteristics and weight loss in overweight or obese women enrolled in a randomized clinical trial of a weight-loss program. We hypothesized that in overweight/obese women, significant weight loss would be demonstrated more frequently in women who report a better Pittsburgh Sleep Quality Index (PSQI) Global Score or sleep >7 h/night as compared to women who report a worse PSQI score or sleep ≤7 h/night. Women of ages 45.5 ± 10.4 (mean ± SD) years and BMI of 33.9 ± 3.3 (n = 245) were randomized and completed PSQI at baseline and 6 months; 198 had weight change assessed through 24 months. At baseline, 52.7% reported PSQI scores above the clinical cutoff of 5. Better subjective sleep quality increased the likelihood of weight-loss success by 33% (relative risk (RR), 0.67; 95% confidence interval (CI), 0.52–0.86), as did sleeping >7 h/night. A worse Global Score at 6 months was associated with a 28% lower likelihood of continued successful weight loss at 18 months, but unassociated by 24 months. These results suggest that sleep quality and quantity may contribute to weight loss in intervention-based studies designed to promote weight control in overweight/obese adult women. PMID:22402738

  16. The Impact of Sleep Loss on Hippocampal Function

    ERIC Educational Resources Information Center

    Prince, Toni-Moi; Abel, Ted

    2013-01-01

    Hippocampal cellular and molecular processes critical for memory consolidation are affected by the amount and quality of sleep attained. Questions remain with regard to how sleep enhances memory, what parameters of sleep after learning are optimal for memory consolidation, and what underlying hippocampal molecular players are targeted by sleep…

  17. Toll-Like Receptor 4 Is a Regulator of Monocyte and Electroencephalographic Responses to Sleep Loss

    PubMed Central

    Wisor, Jonathan P.; Clegern, William C.; Schmidt, Michelle A.

    2011-01-01

    Study Objectives: Sleep loss triggers changes in inflammatory signaling pathways in the brain and periphery. The mechanisms that underlie these changes are ill-defined. The Toll-like receptor 4 (TLR4) activates inflammatory signaling cascades in response to endogenous and pathogen-associated ligands known to be elevated in association with sleep loss. TLR4 is therefore a possible mediator of some of the inflammation-related effects of sleep loss. Here we describe the baseline electroencephalographic sleep phenotype and the biochemical and electroencephalographic responses to sleep loss in TLR4-deficient mice. Design, Measurements and Results: TLR4-deficient mice and wild type controls were subjected to electroencephalographic and electromyographic recordings during spontaneous sleep/wake cycles and during and after sleep restriction sessions of 3, 6, and 24-h duration, during which sleep was disrupted by an automated sleep restriction system. Relative to wild type control mice, TLR4-deficient mice exhibited an increase in the duration of the primary daily waking bout occurring at dark onset in a light/dark cycle. The amount of time spent in non-rapid eye movement sleep by TLR4-deficient mice was reduced in proportion to increased wakefulness in the hours immediately after dark onset. Subsequent to sleep restriction, EEG measures of increased sleep drive were attenuated in TLR4-deficient mice relative to wild-type mice. TLR4 was enriched 10-fold in brain cells positive for the cell surface marker CD11b (cells of the monocyte lineage) relative to CD11b-negative cells in wild type mouse brains. To assess whether this population was affected selectively by TLR4 knockout, flow cytometry was used to count F4/80- and CD45-positive cells in the brains of sleep deprived and time of day control mice. While wild-type mice exhibited a significant reduction in the number of CD11b-positive cells in the brain after 24-h sleep restriction, TLR4-deficient mice did not. Conclusion

  18. A neuron-glia interaction involving GABA Transaminase contributes to sleep loss in sleepless mutants

    PubMed Central

    Chen, Wen-Feng; Maguire, Sarah; Sowcik, Mallory; Luo, Wenyu; Koh, Kyunghee; Sehgal, Amita

    2014-01-01

    Sleep is an essential process and yet mechanisms underlying it are not well understood. Loss of the Drosophila quiver/sleepless (qvr/sss) gene increases neuronal excitability and diminishes daily sleep, providing an excellent model for exploring the underpinnings of sleep regulation. Here, we used a proteomic approach to identify proteins altered in sss brains. We report that loss of sleepless post-transcriptionally elevates the CG7433 protein, a mitochondrial γ-aminobutyric acid transaminase (GABAT), and reduces GABA in fly brains. Loss of GABAT increases daily sleep and improves sleep consolidation, indicating that GABAT promotes wakefulness. Importantly, disruption of the GABAT gene completely suppresses the sleep phenotype of sss mutants, demonstrating that GABAT is required for loss of sleep in sss mutants. While SSS acts in distinct populations of neurons, GABAT acts in glia to reduce sleep in sss flies. Our results identify a novel mechanism of interaction between neurons and glia that is important for the regulation of sleep. PMID:24637426

  19. Sleep-related headaches.

    PubMed

    Rains, Jeanetta C; Poceta, J Steven

    2012-11-01

    Irrespective of diagnosis, chronic daily, morning, or "awakening" headache patterns are soft signs of a sleep disorder. Sleep apnea headache may emerge de novo or may present as an exacerbation of cluster, migraine, tension-type, or other headache. Insomnia is the most prevalent sleep disorder in chronic migraine and tension-type headache, and increases risk for depression and anxiety. Sleep disturbance (e.g., sleep loss, oversleeping, schedule shift) is an acute headache trigger for migraine and tension-type headache. Snoring and sleep disturbance are independent risk factors for progression from episodic to chronic headache. PMID:23099138

  20. Sleep in the Acute Phase of Severe Traumatic Brain Injury: A Snapshot of Polysomnography.

    PubMed

    Wiseman-Hakes, Catherine; Duclos, Catherine; Blais, Hélène; Dumont, Marie; Bernard, Francis; Desautels, Alex; Menon, David K; Gilbert, Danielle; Carrier, Julie; Gosselin, Nadia

    2016-09-01

    Background and Objectives The onset of pervasive sleep-wake disturbances associated with traumatic brain injury (TBI) is poorly understood. This study aimed to (a) determine the feasibility of using polysomnography in patients in the acute, hospitalized stage of severe TBI and (b) explore sleep quality and sleep architecture during this stage of recovery, compared to patients with other traumatic injuries. Methods A cross-sectional case-control design was used. We examined the sleep of 7 patients with severe TBI (17-47 years; 20.3 ± 15.0 days postinjury) and 6 patients with orthopedic and/or spinal cord injuries (OSCI; 19-58 years; 16.9 ± 4.9 days postinjury). One night of ambulatory polysomnography was performed at bedside. Results Compared to OSCI patients, TBI patients showed a significantly longer duration of nocturnal sleep and earlier nighttime sleep onset. Sleep efficiency was low and comparable in both groups. All sleep stages were observed in both groups with normal proportions according to age. Conclusion Patients in the acute stage of severe TBI exhibit increased sleep duration and earlier sleep onset, suggesting that the injured brain enhances sleep need and/or decreases the ability to maintain wakefulness. As poor sleep efficiency could compromise brain recovery, further studies should investigate whether strategies known to optimize sleep in healthy individuals are efficacious in acute TBI. While there are several inherent challenges, polysomnography is a useful means of examining sleep in the early stage of recovery in patients with severe TBI. PMID:26704256

  1. Sleep Loss and the Inflammatory Response in Mice Under Chronic Environmental Circadian Disruption

    PubMed Central

    Castanon-Cervantes, Oscar; Natarajan, Divya; Delisser, Patrick; Davidson, Alec J.; Paul, Ketema N.

    2013-01-01

    Shift work and trans-time zone travel lead to insufficient sleep and numerous pathologies. Here, we examined sleep/wake dynamics during chronic exposure to environmental circadian disruption (ECD), and if chronic partial sleep loss associated with ECD influences the induction of shift-related inflammatory disorder. Sleep and wakefulness were telemetrically recorded across three months of ECD, in which the dark-phase of a light-dark cycle was advanced weekly by 6 h. A three month regimen of ECD caused a temporary reorganization of sleep (NREM and REM) and wake processes across each week, resulting in an approximately 10% net loss of sleep each week relative to baseline levels. A separate group of mice were subjected to ECD or a regimen of imposed wakefulness (IW) aimed to mimic sleep amounts under ECD for one month. Fos-immunoreactivity (IR) was quantified in sleep-wake regulatory areas: the nucleus accumbens (NAc), basal forebrain (BF), and medial preoptic area (MnPO). To assess the inflammatory response, trunk blood was treated with lipopolysaccharide (LPS) and subsequent release of IL-6 was measured. Fos-IR was greatest in the NAc, BF, and MnPO of mice subjected to IW. The inflammatory response to LPS was elevated in mice subjected to ECD, but not mice subjected to IW. Thus, the net sleep loss that occurs under ECD is not associated with a pathological immune response. PMID:23696854

  2. Sleep loss and the inflammatory response in mice under chronic environmental circadian disruption.

    PubMed

    Brager, Allison J; Ehlen, J Christopher; Castanon-Cervantes, Oscar; Natarajan, Divya; Delisser, Patrick; Davidson, Alec J; Paul, Ketema N

    2013-01-01

    Shift work and trans-time zone travel lead to insufficient sleep and numerous pathologies. Here, we examined sleep/wake dynamics during chronic exposure to environmental circadian disruption (ECD), and if chronic partial sleep loss associated with ECD influences the induction of shift-related inflammatory disorder. Sleep and wakefulness were telemetrically recorded across three months of ECD, in which the dark-phase of a light-dark cycle was advanced weekly by 6 h. A three month regimen of ECD caused a temporary reorganization of sleep (NREM and REM) and wake processes across each week, resulting in an approximately 10% net loss of sleep each week relative to baseline levels. A separate group of mice were subjected to ECD or a regimen of imposed wakefulness (IW) aimed to mimic sleep amounts under ECD for one month. Fos-immunoreactivity (IR) was quantified in sleep-wake regulatory areas: the nucleus accumbens (NAc), basal forebrain (BF), and medial preoptic area (MnPO). To assess the inflammatory response, trunk blood was treated with lipopolysaccharide (LPS) and subsequent release of IL-6 was measured. Fos-IR was greatest in the NAc, BF, and MnPO of mice subjected to IW. The inflammatory response to LPS was elevated in mice subjected to ECD, but not mice subjected to IW. Thus, the net sleep loss that occurs under ECD is not associated with a pathological immune response. PMID:23696854

  3. The effects of Dexamethasone on sleep in young children with Acute Lymphoblastic Leukemia

    PubMed Central

    Rosen, Gerald; Harris, Anne K.; Liu, Meixia; Dreyfus, Jill; Krueger, James; Messinger, Yoav H.

    2016-01-01

    Purpose Corticosteroids, which are a mainstay in the treatment of acute lymphoblastic leukemia (ALL), have a well-documented adverse effect on sleep. We sought to characterize the effects of dexamethasone on sleep over an entire 28-day treatment cycle using actigraphy, an objective measure of sleep. Methods The sleep of 25 children aged 2–9 years (mean 4.5 years) with ALL treated with dexamethasone were evaluated during maintenance chemotherapy using a within-subject experimental design, actigraphy, and standardized questionnaires to assess sleep, sleep problems, and fatigue. Results During the five days of dexamethasone treatment, sleep time increased during the night (535 vs. 498 min; p = 0.004) and daytime napping increased the following day (14 vs. 0 min; p = 0.002), and the number of wake episodes during the night was lower (14 vs. 20; p = ≤ 0.001). However, when assessed individually, sleep-onset time, efficiency, and wake after sleep onset during the night were unchanged during dexamethasone treatment; when the cumulative effect of all of these factors was assessed, there was a statistically and clinically significant increase in nighttime sleep duration during dexamethasone treatment. Conclusions During the five days of treatment with dexamethasone, an increase in nighttime sleep as well as daytime napping was observed in young children with ALL. The increases in sleep duration return to baseline one day after the discontinuation of dexamethasone. PMID:25799940

  4. Molecular Mechanisms of Age-Related Sleep Loss in the Fruit Fly

    PubMed Central

    Robertson, Meagan; Keene, Alex C.

    2013-01-01

    Across phyla, aging is associated with reduced sleep duration and efficiency. Both aging and sleep involve complex genetic architecture and diverse cell types and are heavily influenced by diet and environment. Therefore, understanding the molecular mechanisms of age-dependent changes in sleep will require integrative approaches that go beyond examining these two processes independently. The fruit fly, Drosophila melanogaster, provides a genetically amenable system for dissecting the molecular basis of these processes. In this review, we examine the role of metabolism and circadian rhythms in age-dependent sleep loss. PMID:23594925

  5. Associations between sleep loss and increased risk of obesity and diabetes

    PubMed Central

    Knutson, Kristen L.; Van Cauter, Eve

    2015-01-01

    During the past few decades, sleep curtailment has become a very common behavior in industrialized countries. This trend for shorter sleep duration has developed over the same time period as the dramatic increase in the prevalence of obesity and diabetes. There is rapidly accumulating evidence to indicate that chronic partial sleep loss may increase the risk of obesity and diabetes. Laboratory studies in healthy volunteers have shown that experimental sleep restriction is associated with an adverse impact on glucose homeostasis. Insulin sensitivity decreases rapidly and markedly without adequate compensation in beta cell function, resulting in an elevated risk of diabetes. Prospective epidemiologic studies in both children and adults are consistent with a causative role of short sleep in the increased risk of diabetes. Sleep curtailment is also associated with a dysregulation of the neuroendocrine control of appetite, with a reduction of the satiety factor leptin and an increase in the hunger-promoting hormone ghrelin. Thus, sleep loss may alter the ability of leptin and ghrelin to accurately signal caloric need, acting in concert to produce an internal misperception of insufficient energy availability. The adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins that promote both waling and feeding. Consistent with the laboratory evidence, multiple epidemiologic studies have shown an association between short sleep and higher body mass index after controlling for a variety of possible confounders. PMID:18591489

  6. One night of sleep loss impairs innovative thinking and flexible decision making.

    PubMed

    Harrison, Y; Horne, J A

    1999-05-01

    Recent findings with clinically oriented neuropsychological tests suggest that one night without sleep causes particular impairment to tasks requiring flexible thinking and the updating of plans in the light of new information. This relatively little investigated field of sleep deprivation research has real-world implications for decision makers having lost a night's sleep. To explore this latter perspective further, we adapted a dynamic and realistic marketing decision making "game" embodying the need for these skills, and whereby such performance could be measured. As the task relied on the comprehension of a large amount of written information, a critical reasoning test was also administered to ascertain whether any failure at the marketing game might lie with information acquisition rather than with failures in decision making. Ten healthy highly motivated and trained participants underwent two counterbalanced 36 h trials, sleep vs no sleep. The critical reasoning task was unaffected by sleep loss, whereas performance at the game significantly deteri orated after 32-36 h of sleep loss, when sleep deprivation led to more rigid thinking, increased perseverative errors, and marked difficulty in appreciating an updated situation. At this point, and despite the sleep-deprived participants' best efforts to do well, their play collapsed, unlike that of the nonsleep-deprived participants. Copyright 1999 Academic Press. PMID:10329298

  7. β-adrenergic signaling regulates evolutionarily derived sleep loss in the Mexican cavefish.

    PubMed

    Duboué, Erik R; Borowsky, Richard L; Keene, Alex C

    2012-01-01

    Sleep is a fundamental behavior exhibited almost universally throughout the animal kingdom. The required amount and circadian timing of sleep differs greatly between species in accordance with habitats and evolutionary history. The Mexican blind cavefish, Astyanax mexicanus, is a model organism for the study of adaptive morphological and behavioral traits. In addition to loss of eyes and pigmentation, cave populations of A. mexicanus exhibit evolutionarily derived sleep loss and increased vibration attraction behavior, presumably to cope with a nutrient-poor environment. Understanding the neural mechanisms of evolutionarily derived sleep loss in this system may reveal critical insights into the regulation of sleep in vertebrates. Here we report that blockade of β-adrenergic receptors with propranolol rescues the decreased-sleep phenotype of cavefish. This effect was not seen with α-adrenergic antagonists. Treatment with selective β1-, β2-, and β3-antagonists revealed that the increased sleep observed with propranolol could partially be explained via the β1-adrenergic system. Morphological analysis of catecholamine circuitry revealed conservation of gross catecholaminergic neuroanatomy between surface and cave morphs. Taken together, these findings suggest that evolutionarily derived changes in adrenergic signaling underlie the reduced sleep of cave populations. PMID:22922609

  8. Effect of Obstructive Sleep Apnea in Acute Coronary Syndrome.

    PubMed

    Leão, Sílvia; Conde, Bebiana; Fontes, Paulo; Calvo, Teresa; Afonso, Abel; Moreira, Ilídio

    2016-04-01

    The effect of obstructive sleep apnea (OSA) on clinical outcomes after acute coronary syndrome (ACS) is incompletely defined. We sought to determine the prevalence of OSA in patients with ACS and evaluate prognostic impact of OSA and continuous positive airway pressure (CPAP) therapy in these patients. This was a prospective longitudinal cohort study of 73 patients admitted on cardiac intensive care unit for ACS. Cardiorespiratory sleep study and/or polysomnography were performed in all patients. CPAP was recommended if Apnea-Hypopnea Index ≥5. The main study outcome was a composite of death for any cause, myocardial infarction, and myocardial revascularization. OSA was diagnosed in 46 patients (63%). Age and cardiovascular risk factors were not significantly different between groups. OSA was classified as mild (m-OSA) in 14 patients (30%) and as moderate-to-severe (s-OSA) in 32 patients (70%). After a median follow-up of 75 months (interquartile range 71 to 79), patients with s-OSA had lower event-free survival rate. After adjustment for gender, patients with s-OSA showed a significantly higher incidence of the composite end point (hazard ratio 3.58, 95% CI 1.09 to 17.73, p = 0.035). Adherence to CPAP occurred in 19 patients (41%), but compliance to CPAP therapy did not reduce the risk of composite end point (hazard ratio 0.87, 95% CI 0.31 to 2.46, p = 0.798). In conclusion, OSA is an underdiagnosed disease with high prevalence in patients with ACS. It is urgent to establish screening protocols because those have high diagnostic yield and allow identifying a group of patients with manifestly unfavorable prognosis. PMID:26857162

  9. Nonapnea Sleep Disorders and the Risk of Acute Kidney Injury

    PubMed Central

    Lin, Hugo You-Hsien; Chang, Kai-Ting; Chang, Yu-Han; Lu, Tzongshi; Liang, Chan-Jung; Wang, Dean-Chuan; Tsai, Jui-Hsiu; Hsu, Chung-Yao; Hung, Chi-Chih; Kuo, Mei-Chuan; Lin, Chang-Shen; Hwang, Shang-Jyh

    2016-01-01

    Abstract Nonapnea sleep disorders (NASDs) and associated problems, which are highly prevalent in patients with kidney diseases, are associated with unfavorable medical sequelae. Nonetheless, whether NASDs are associated with acute kidney injury (AKI) development has not been thoroughly analyzed. We examined the association between NASD and AKI. We conducted a population-based study by using 1,000,000 representative data from the Taiwan National Health Insurance Research Database for the period from January 1, 2000, to December 31, 2010. We studied the incidence and risk of AKI in 9178 newly diagnosed NASD patients compared with 27,534 people without NASD matched according to age, sex, index year, urbanization level, region of residence, and monthly income at a 1:3 ratio. The NASD cohort had an adjusted hazard ratio (hazard ratio [HR]; 95% confidence interval [CI] = 1.15–2.63) of subsequent AKI 1.74-fold higher than that of the control cohort. Older age and type 2 diabetes mellitus were significantly associated with an increased risk of AKI (P < 0.05). Among different types of NASDs, patients with insomnia had a 120% increased risk of developing AKI (95% CI = 1.38–3.51; P = 0.001), whereas patients with other sleep disorders had a 127% increased risk of subsequent AKI (95% CI = 1.07–4.80; P = 0.033). Men with NASDs were at a high risk of AKI (P < 0.05). This nationwide population-based cohort study provides evidence that patients with NASDs are at higher risk of developing AKI than people without NASDs. PMID:26986132

  10. Maternal Ube3a Loss Disrupts Sleep Homeostasis But Leaves Circadian Rhythmicity Largely Intact

    PubMed Central

    Ehlen, J. Christopher; Jones, Kelly A.; Pinckney, Lennisha; Gray, Cloe L.; Burette, Susan; Weinberg, Richard J.; Evans, Jennifer A.; Brager, Allison J.; Zylka, Mark J.

    2015-01-01

    Individuals with Angelman syndrome (AS) suffer sleep disturbances that severely impair quality of life. Whether these disturbances arise from sleep or circadian clock dysfunction is currently unknown. Here, we explored the mechanistic basis for these sleep disorders in a mouse model of Angelman syndrome (Ube3am−/p+ mice). Genetic deletion of the maternal Ube3a allele practically eliminates UBE3A protein from the brain of Ube3am−/p+ mice, because the paternal allele is epigenetically silenced in most neurons. However, we found that UBE3A protein was present in many neurons of the suprachiasmatic nucleus—the site of the mammalian circadian clock—indicating that Ube3a can be expressed from both parental alleles in this brain region in adult mice. We found that while Ube3am−/p+ mice maintained relatively normal circadian rhythms of behavior and light-resetting, these mice exhibited consolidated locomotor activity and skipped the timed rest period (siesta) present in wild-type (Ube3am+/p+) mice. Electroencephalographic analysis revealed that alterations in sleep regulation were responsible for these overt changes in activity. Specifically, Ube3am−/p+ mice have a markedly reduced capacity to accumulate sleep pressure, both during their active period and in response to forced sleep deprivation. Thus, our data indicate that the siesta is governed by sleep pressure, and that Ube3a is an important regulator of sleep homeostasis. These preclinical findings suggest that therapeutic interventions that target mechanisms of sleep homeostasis may improve sleep quality in individuals with AS. SIGNIFICANCE STATEMENT Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by loss of expression of the maternal copy of the UBE3A gene. Individuals with AS have severe sleep dysfunction that affects their cognition and presents challenges to their caregivers. Unfortunately, current treatment strategies have limited efficacy due to a poor understanding of the

  11. Acute physical exercise under hypoxia improves sleep, mood and reaction time.

    PubMed

    de Aquino-Lemos, Valdir; Santos, Ronaldo Vagner T; Antunes, Hanna Karen Moreira; Lira, Fabio S; Luz Bittar, Irene G; Caris, Aline V; Tufik, Sergio; de Mello, Marco Tulio

    2016-02-01

    This study aimed to assess the effect of two sessions of acute physical exercise at 50% VO2peak performed under hypoxia (equivalent to an altitude of 4500 m for 28 h) on sleep, mood and reaction time. Forty healthy men were randomized into 4 groups: Normoxia (NG) (n = 10); Hypoxia (HG) (n = 10); Exercise under Normoxia (ENG) (n = 10); and Exercise under Hypoxia (EHG) (n = 10). All mood and reaction time assessments were performed 40 min after awakening. Sleep was reassessed on the first day at 14 h after the initiation of hypoxia; mood and reaction time were measured 28 h later. Two sessions of acute physical exercise at 50% VO2peak were performed for 60 min on the first and second days after 3 and 27 h, respectively, after starting to hypoxia. Improved sleep efficiency, stage N3 and REM sleep and reduced wake after sleep onset were observed under hypoxia after acute physical exercise. Tension, anger, depressed mood, vigor and reaction time scores improved after exercise under hypoxia. We conclude that hypoxia impairs sleep, reaction time and mood. Acute physical exercise at 50% VO2peak under hypoxia improves sleep efficiency, reversing the aspects that had been adversely affected under hypoxia, possibly contributing to improved mood and reaction time. PMID:26522742

  12. Sleep Loss and Cytokines Levels in an Experimental Model of Psoriasis

    PubMed Central

    Hirotsu, Camila; Rydlewski, Mariana; Araújo, Mariana Silva; Tufik, Sergio; Andersen, Monica Levy

    2012-01-01

    Up to 80% of people develop a cutaneous condition closely connected to their exposure to stressful life events. Psoriasis is a chronic recurrent inflammatory skin disorder with multifactorial etiology, including genetic background, environmental factors, and immune system disturbances with a strong cytokine component. Moreover, psoriasis is variably associated with sleep disturbance and sleep deprivation. This study evaluated the influence of sleep loss in the context of an animal model of psoriasis by measuring cytokine and stress-related hormone levels. Male adult Balb/C mice with or without psoriasis were subjected to 48 h of selective paradoxical sleep deprivation (PSD). Sleep deprivation potentiated the activities of kallikrein-5 and kallikrein-7 in the skin of psoriatic groups. Also, mice with psoriasis had significant increases in specific pro-inflammatory cytokines (IL-1β, IL-6 and IL-12) and decreases in the anti-inflammatory cytokine (IL-10) after PSD, which were normalized after 48 h of sleep rebound. Linear regression showed that IL-2, IL-6 and IL-12 levels predicted 66% of corticosterone levels, which were selectively increased in psoriasis mice subject to PSD. Kallikrein-5 was also correlated with pro-inflammatory cytokines, explaining 58% of IL-6 and IL-12 variability. These data suggest that sleep deprivation plays an important role in the exacerbation of psoriasis through modulation of the immune system in the epidermal barrier. Thus, sleep loss should be considered a risk factor for the development of psoriasis. PMID:23226485

  13. Circadian Misalignment Augments Markers of Insulin Resistance and Inflammation, Independently of Sleep Loss

    PubMed Central

    Leproult, Rachel; Holmbäck, Ulf; Van Cauter, Eve

    2014-01-01

    Shift workers, who are exposed to irregular sleep schedules resulting in sleep deprivation and misalignment of circadian rhythms, have an increased risk of diabetes relative to day workers. In healthy adults, sleep restriction without circadian misalignment promotes insulin resistance. To determine whether the misalignment of circadian rhythms that typically occurs in shift work involves intrinsic adverse metabolic effects independently of sleep loss, a parallel group design was used to study 26 healthy adults. Both interventions involved 3 inpatient days with 10-h bedtimes, followed by 8 inpatient days of sleep restriction to 5 h with fixed nocturnal bedtimes (circadian alignment) or with bedtimes delayed by 8.5 h on 4 of the 8 days (circadian misalignment). Daily total sleep time (SD) during the intervention was nearly identical in the aligned and misaligned conditions (4 h 48 min [5 min] vs. 4 h 45 min [6 min]). In both groups, insulin sensitivity (SI) significantly decreased after sleep restriction, without a compensatory increase in insulin secretion, and inflammation increased. In male participants exposed to circadian misalignment, the reduction in SI and the increase in inflammation both doubled compared with those who maintained regular nocturnal bedtimes. Circadian misalignment that occurs in shift work may increase diabetes risk and inflammation, independently of sleep loss. PMID:24458353

  14. Distinct gender-related sleep pattern in an acute model of TMJ pain.

    PubMed

    Schütz, T C B; Andersen, M L; Silva, A; Tufik, S

    2009-05-01

    Since it is recognized that acute inflammation of the temporomandibular joint results in sleep disturbances in male rats, and that the orofacial region may display a site-specific effect of ovarian hormones on nociception, we hypothesized that distinct genders would respond differently when subjected to this inflammatory acute orofacial pain. Sleep was monitored after injection of saline/Freund's adjuvant into the temporomandibular joint in male and female (proestrus and diestrus phases) rats. Progesterone and stress-related hormones were also assessed. In males, Freund's adjuvant induced a significant nociceptive response and sleep disturbances. Behavior and sleep architecture in the females remained unaffected. Our results suggest that females and males present distinct responses to an acute model of orofacial pain. PMID:19493893

  15. Effects of hypocretin (orexin) neuronal loss on sleep and extracellular adenosine levels in the basal forebrain

    PubMed Central

    Murillo-Rodriguez, Eric; Liu, Meng; Blanco-Centurion, Carlos; Shiromani, Priyattam J.

    2009-01-01

    Neurons containing the neuropeptide hypocretin (orexin) are localized only in the lateral hypothalamus from where they innervate multiple regions implicated in arousal, including the basal forebrain. HCRT activation of downstream arousal neurons is likely to stimulate release of endogenous factors. One such factor is adenosine (AD), which in the basal forebrain increases with waking and decreases with sleep, and is hypothesized to regulate the waxing and waning of sleep drive. Does loss of HCRT neurons affect AD levels in the basal forebrain? Is the increased sleep that accompanies HCRT loss a consequence of higher AD levels in the basal forebrain? In the present study, we investigate these questions by lesioning the HCRT neurons (hypocretin-2-saporin) and measuring sleep and extracellular levels of AD in the basal forebrain. In separate groups of rats, the neurotoxin HCRT2-SAP or saline were administered locally to the lateral hypothalamus and 80 days later AD and sleep were assessed. Rats given the neurotoxin had a 94% loss of the HCRT neurons. These rats awake less at night, and had more REM sleep, which is consistent with a HCRT hypofunction. These rats also had more sleep after brief periods of sleep deprivation. However, in the lesioned rats, AD levels did not increase with 6h sleep deprivation, whereas such an increase in AD occurred in rats without lesion of the HCRT neurons. These findings indicate that AD levels do not increase with waking in rats with a HCRT lesion, and that the increased sleep in these rats occurs independently of AD levels in the basal forebrain. PMID:18783368

  16. Sleep Loss and Its Effects on Health of Family Caregivers of Individuals with Primary Malignant Brain Tumors

    PubMed Central

    Lee, Shih-Yu; Clark, Patricia C.; Sherwood, Paula R.

    2013-01-01

    Sleep loss places caregivers at risk for poor health. Understanding correlates of sleep loss and relationships to health may enable improvement of health of caregivers of individuals with primary malignant brain tumors (PMBT). In this cross-sectional, descriptive study of 133 caregivers, relationships were examined between sleep loss and physical, mental, emotional, and social health at time of patient diagnosis. Sleep loss was not related to physical health. Shorter total sleep time was associated with greater fatigue and social support. Sleep quality was positively associated with quality of life. Further study is needed of the role of sleep loss in the PMBT caregiving trajectory and its long-term relationship with health outcomes. PMID:23633116

  17. Loss of polyubiquitin gene Ubb leads to metabolic and sleep abnormalities in mice

    PubMed Central

    Ryu, K.-Y.; Fujiki, N.; Kazantzis, M.; Garza, J. C.; Bouley, D. M.; Stahl, A.; Lu, X.-Y.; Nishino, S.; Kopito, R. R.

    2010-01-01

    Aims Ubiquitin performs essential roles in a myriad of signalling pathways required for cellular function and survival. Recently, we reported that disruption of the stress-inducible ubiquitin-encoding gene Ubb reduces ubiquitin content in the hypothalamus and leads to adult-onset obesity coupled with a loss of arcuate nucleus neurones and disrupted energy homeostasis in mice. Neuropeptides expressed in the hypothalamus control both metabolic and sleep behaviours. In order to demonstrate that the loss of Ubb results in broad hypothalamic abnormalities, we attempted to determine whether metabolic and sleep behaviours were altered in Ubb knockout mice. Methods Metabolic rate and energy expenditure were measured in a metabolic chamber, and sleep stage was monitored via electroencephalographic/electromyographic recording. The presence of neurodegeneration and increased reactive gliosis in the hypothalamus were also evaluated. Results We found that Ubb disruption leads to early-onset reduced activity and metabolic rate. Additionally, we have demonstrated that sleep behaviour is altered and sleep homeostasis is disrupted in Ubb knockout mice. These early metabolic and sleep abnormalities are accompanied by persistent reactive gliosis and the loss of arcuate nucleus neurones, but are independent of neurodegeneration in the lateral hypothalamus. Conclusions Ubb knockout mice exhibit phenotypes consistent with hypothalamic dysfunction. Our data also indicate that Ubb is essential for the maintenance of the ubiquitin levels required for proper regulation of metabolic and sleep behaviours in mice. PMID:20002312

  18. Tired and Apprehensive: Anxiety Amplifies the Impact of Sleep Loss on Aversive Brain Anticipation

    PubMed Central

    Goldstein, Andrea N.; Greer, Stephanie M.; Saletin, Jared M.; Harvey, Allison G.; Nitschke, Jack B.

    2013-01-01

    Anticipation is an adaptive process, aiding preparatory responses to potentially threatening events. However, excessive anticipatory responding and associated hyper-reactivity in the amygdala and insula are integral to anxiety disorders. Despite the co-occurrence of sleep disruption and anxiety disorders, the impact of sleep loss on affective anticipatory brain mechanisms, and the interaction with anxiety, remains unknown. Here, we demonstrate that sleep loss amplifies preemptive responding in the amygdala and anterior insula during affective anticipation in humans, especially for cues with high predictive certainty. Furthermore, trait anxiety significantly determined the degree of such neural vulnerability to sleep loss: individuals with highest trait anxiety showed the greatest increase in anticipatory insula activity when sleep deprived. Together, these data support a neuropathological model in which sleep disruption may contribute to the maintenance and/or exacerbation of anxiety through its impact on anticipatory brain function. They further raise the therapeutic possibility that targeted sleep restoration in anxiety may ameliorate excessive anticipatory responding and associated clinical symptomatology. PMID:23804084

  19. Homer1a is a core brain molecular correlate of sleep loss

    PubMed Central

    Maret, Stéphanie; Dorsaz, Stéphane; Gurcel, Laure; Pradervand, Sylvain; Petit, Brice; Pfister, Corinne; Hagenbuchle, Otto; O'Hara, Bruce F.; Franken, Paul; Tafti, Mehdi

    2007-01-01

    Sleep is regulated by a homeostatic process that determines its need and by a circadian process that determines its timing. By using sleep deprivation and transcriptome profiling in inbred mouse strains, we show that genetic background affects susceptibility to sleep loss at the transcriptional level in a tissue-dependent manner. In the brain, Homer1a expression best reflects the response to sleep loss. Time-course gene expression analysis suggests that 2,032 brain transcripts are under circadian control. However, only 391 remain rhythmic when mice are sleep-deprived at four time points around the clock, suggesting that most diurnal changes in gene transcription are, in fact, sleep–wake-dependent. By generating a transgenic mouse line, we show that in Homer1-expressing cells specifically, apart from Homer1a, three other activity-induced genes (Ptgs2, Jph3, and Nptx2) are overexpressed after sleep loss. All four genes play a role in recovery from glutamate-induced neuronal hyperactivity. The consistent activation of Homer1a suggests a role for sleep in intracellular calcium homeostasis for protecting and recovering from the neuronal activation imposed by wakefulness. PMID:18077435

  20. Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss

    PubMed Central

    Nedeltcheva, A. V.; Imperial, J. G.; Penev, P. D.

    2012-01-01

    Insufficient sleep is associated with changes in glucose tolerance, insulin secretion, and insulin action. Despite widespread use of weight-loss diets for metabolic risk reduction, the effects of insufficient sleep on glucose regulation in overweight dieters are not known. To examine the consequences of recurrent sleep restriction on 24-hour blood glucose control during diet-induced weight loss, 10 overweight and obese adults (3F/7M; mean [SD] age 41 [5] y; BMI 27.4 [2.0] kg/m2) completed two 14-day treatments with hypocaloric diet and 8.5 or 5.5-h nighttime sleep opportunity in random order 7 [3] months apart. Oral and intravenous glucose tolerance test (IVGTT) data, fasting lipids and free-fatty acids (FFA), and 24-hour blood glucose, insulin, C-peptide, and counter-regulatory hormone measurements were collected after each treatment. Participants had comparable weight loss (1.0 [0.3] BMI units) during each treatment. Bedtime restriction reduced sleep by 131 [30] min/day. Recurrent sleep curtailment decreased 24-hour serum insulin concentrations (i.e. enhanced 24-hour insulin economy) without changes in oral glucose tolerance and 24-hour glucose control. This was accompanied by a decline in fasting blood glucose, increased fasting FFA which suppressed normally following glucose ingestion, and lower total and LDL cholesterol concentrations. Sleep-loss-related changes in counter-regulatory hormone secretion during the IVGTT limited the utility of the test in this study. In conclusion, sleep restriction enhanced 24-hour insulin economy without compromising glucose homeostasis in overweight individuals placed on a balanced hypocaloric diet. The changes in fasting blood glucose, insulin, lipid and FFA concentrations in sleep-restricted dieters resembled the pattern of human metabolic adaptation to reduced carbohydrate availability. PMID:22513492

  1. Development and Validation of Sleep Disturbance Questionnaire in Patients with Acute Coronary Syndrome

    PubMed Central

    Sepahvand, Elham; Khaledi Paveh, Behnam; Rezaei, Mansour

    2014-01-01

    Background and Objectives. Severe sleep disturbance is a common problem among patients in cardiac care units (CCUs). There are questionnaires to measure sleep disturbances. Therefore, the present study seeks to design a valid and reliable questionnaire to assess sleep disturbance in patients with acute coronary syndrome (ACS) hospitalized in CCUs. Materials and Methods. In the present methodological research, items of the questionnaire were extracted through a systematic review. The validity and reliability of the questionnaires was assessed by face validity, content validity, construct validity, Cronbach's alpha coefficient, and test-retest methods. Results. Factor analysis provided a questionnaire of 23 items on 5 dimensions of sleep disturbance in coronary patients: “sleep onset and continuity disorder,” “disorder in daytime functioning,” “sleep disturbance caused by environmental factors,” “sleep disturbance as a result of cardiac diseases,” and “respiratory disorders during sleep.” Furthermore, test-retest analysis showed a reliability correlation coefficient of r = 0.766 and α Cronbach's reliability (α = 0.855). Conclusion. Sleep disturbance questionnaire for patients with ACS hospitalized in coronary care unit (CCU) was identified in 5 dimensions and assessed for validity and reliability. To control and improve the sleep quality of CCU hospitalized patients, we need to identify and remove predisposing factors.

  2. Sleep Is Increased By Weight Gain and Decreased By Weight Loss in Mice

    PubMed Central

    Guan, Zhiwei; Vgontzas, Alexandros N.; Bixler, Edward O.; Fang, Jidong

    2008-01-01

    Objective: To determine whether weight loss could reverse excessive sleep in high-fat diet-induced obesity. Design: Three groups of mice participated in the study. A weight gain/loss group was fed with high-fat food for 6 weeks (weight gain), and regular food again for 4 weeks (weight loss). A control group and a weight gain only group were fed with regular food and high-fat food, respectively, for 10 weeks after the baseline. Participants: Adult male C57BL/6 mice. Measurements: The amounts of wake, rapid eye movement sleep (REMS) and non-REM sleep (NREMS) were determined at week 0 (baseline), week 6, and week 10. Results: The weight gain/loss group displayed a significant decrease in wakefulness and increases in NREMS and episodes of NREMS during 6 weeks of weight gain, which were reversed during subsequent 4 weeks of weight loss. The weight gain only group displayed significant decrease in wakefulness and increase of NREMS and REMS at both week 6 and week 10. The control group did not show significant sleep alterations during the experiment. Conclusion: These observations indicate that sleep alterations induced by weight gain are reversed by weight loss in obese animals. These data may shed light on the mechanisms underlying the well-established association between obesity and sleepiness in humans and may lead to new therapeutic strategies for these 2 increasingly prevalent problems in the modern societies. Citation: Guan Z; Vgontzas AN; Bixler EO; Fang J. Sleep is increased by weight gain and decreased by weight loss in mice. SLEEP 2008;31(5):627-633. PMID:18517033

  3. Effect of Eye Mask on Sleep Quality in Patients with Acute Coronary Syndrome

    PubMed Central

    Daneshmandi, Mohammad; Neiseh, Fatemeh; SadeghiShermeh, Mehdi; Ebadi, Abbas

    2012-01-01

    Introduction: Sleep is one of the basic human needs and sleep deprivation causes nu-merous adverse effects on the human body and mind. Due to reduced sleep quality in patients with acute coronary syndrome, this study was carried out to determine the effect of eye mask on sleep quality in patients with acute coronary syndrome. Methods: In this two-group controlled clinical trial, sixty patients with acute coronary syndrome in the coronary care units of Baqiyatallah Hospital in Tehran in 2010 were selected by purposeful sampling method and randomly allocated to two groups of case and control. In the case group, in the second night stay, the intervention of eye mask was done per night and by using the Petersburg's sleep quality index; sleep quality was evaluated during and at the end of hospitalization. Then data were analyzed by paired t-test, independent t-test, Spearman and Pearson's correlation coefficient and SPSS software version 19. Results: Total sleep quality score of the case group was significantly decreased after intervention (4.86 ± 1.88) from before intervention (10.46 ± 4.09) (p < 0.000). In addi-tion, total score of sleep quality after intervention in the case group (4.86 ± 1.88) was significant different from the control group (8.43 ± 1.97) (p < 0.005). Conclusion: Using eye mask, as an economical and uncomplicated method, can improve sleep quality in patients with acute coronary syndrome in the coronary care units and can be used as an alternative method of treatment instead of drug therapy. PMID:25276688

  4. Upregulation of gene expression in reward-modulatory striatal opioid systems by sleep loss.

    PubMed

    Baldo, Brian A; Hanlon, Erin C; Obermeyer, William; Bremer, Quentin; Paletz, Elliott; Benca, Ruth M

    2013-12-01

    Epidemiological studies have shown a link between sleep loss and the obesity 'epidemic,' and several observations indicate that sleep curtailment engenders positive energy balance via increased palatable-food 'snacking.' These effects suggest alterations in reward-modulatory brain systems. We explored the effects of 10 days of sleep deprivation in rats on the expression of striatal opioid peptide (OP) genes that subserve food motivation and hedonic reward, and compared effects with those seen in hypothalamic energy balance-regulatory systems. Sleep-deprived (Sleep-Dep) rats were compared with yoked forced-locomotion apparatus controls (App-Controls), food-restricted rats (Food-Restrict), and unmanipulated controls (Home-Cage). Detection of mRNA levels with in situ hybridization revealed a subregion-specific upregulation of striatal preproenkephalin and prodynorhin gene expression in the Sleep-Dep group relative to all other groups. Neuropeptide Y (NPY) gene expression in the hippocampal dentate gyrus and throughout neocortex was also robustly upregulated selectively in the Sleep-Dep group. In contrast, parallel gene expression changes were observed in the Sleep-Dep and Food-Restrict groups in hypothalamic energy-sensing systems (arcuate nucleus NPY was upregulated, and cocaine- and amphetamine-regulated transcript was downregulated), in alignment with leptin suppression in both groups. Together, these results reveal a novel set of sleep deprivation-induced transcriptional changes in reward-modulatory peptide systems, which are dissociable from the energy-balance perturbations of sleep loss or the potentially stressful effects of the forced-locomotion procedure. The recruitment of telencephalic food-reward systems may provide a feeding drive highly resistant to feedback control, which could engender obesity through the enhancement of palatable feeding. PMID:23864029

  5. Upregulation of Gene Expression in Reward-Modulatory Striatal Opioid Systems by Sleep Loss

    PubMed Central

    Baldo, Brian A; Hanlon, Erin C; Obermeyer, William; Bremer, Quentin; Paletz, Elliott; Benca, Ruth M

    2013-01-01

    Epidemiological studies have shown a link between sleep loss and the obesity ‘epidemic,' and several observations indicate that sleep curtailment engenders positive energy balance via increased palatable-food ‘snacking.' These effects suggest alterations in reward-modulatory brain systems. We explored the effects of 10 days of sleep deprivation in rats on the expression of striatal opioid peptide (OP) genes that subserve food motivation and hedonic reward, and compared effects with those seen in hypothalamic energy balance-regulatory systems. Sleep-deprived (Sleep-Dep) rats were compared with yoked forced-locomotion apparatus controls (App-Controls), food-restricted rats (Food-Restrict), and unmanipulated controls (Home-Cage). Detection of mRNA levels with in situ hybridization revealed a subregion-specific upregulation of striatal preproenkephalin and prodynorhin gene expression in the Sleep-Dep group relative to all other groups. Neuropeptide Y (NPY) gene expression in the hippocampal dentate gyrus and throughout neocortex was also robustly upregulated selectively in the Sleep-Dep group. In contrast, parallel gene expression changes were observed in the Sleep-Dep and Food-Restrict groups in hypothalamic energy-sensing systems (arcuate nucleus NPY was upregulated, and cocaine- and amphetamine-regulated transcript was downregulated), in alignment with leptin suppression in both groups. Together, these results reveal a novel set of sleep deprivation-induced transcriptional changes in reward-modulatory peptide systems, which are dissociable from the energy-balance perturbations of sleep loss or the potentially stressful effects of the forced-locomotion procedure. The recruitment of telencephalic food-reward systems may provide a feeding drive highly resistant to feedback control, which could engender obesity through the enhancement of palatable feeding. PMID:23864029

  6. Are parenting behaviors associated with child sleep problems during treatment for acute lymphoblastic leukemia?

    PubMed

    McCarthy, Maria C; Bastiani, Jessica; Williams, Lauren K

    2016-07-01

    Sleep disturbance is a recognized common side effect in children treated for acute lymphoblastic leukemia (ALL). Although associated with treatment factors such as hospitalization and corticosteroids, sleep problems may also be influenced by modifiable environmental factors such as parenting behaviors. The purpose of this study was to examine sleep problems in children undergoing treatment for ALL compared to healthy children and whether parenting practices are associated with sleep difficulties. Parents of 73 children aged 2-6 years who were (1) in the maintenance phase of ALL treatment (ALL group, n = 43) or (2) had no major medical illness (healthy control group, n = 30) participated in the study. Parents completed questionnaires measuring their child's sleep behavior and their own parenting practices. Parents of children undergoing ALL treatment reported significantly more child sleep problems; 48% of children with ALL compared to 23% of healthy children had clinical levels of sleep disturbance. Parents of the ALL group also reported significantly more lax parenting practices and strategies associated with their child's sleep including co-sleeping, comforting activities, and offering food and drink in the bedroom. Results of multivariate regression analysis indicated that, after controlling for illness status, parent-child co-sleeping was significantly associated with child sleep difficulties. Strategies employed by parents during ALL treatment may be a potential modifiable intervention target that could result in improved child sleep behaviors. Future research aimed at developing and testing parenting interventions aimed to improve child sleep in the context of oncology treatment is warranted. PMID:27108598

  7. Impact of Acute Sleep Deprivation on Sarcasm Detection

    PubMed Central

    Mary, Alison; Slama, Hichem; Cleeremans, Axel; Peigneux, Philippe; Kissine, Mikhail

    2015-01-01

    There is growing evidence that sleep plays a pivotal role on health, cognition and emotional regulation. However, the interplay between sleep and social cognition remains an uncharted research area. In particular, little is known about the impact of sleep deprivation on sarcasm detection, an ability which, once altered, may hamper everyday social interactions. The aim of this study is to determine whether sleep-deprived participants are as able as sleep-rested participants to adopt another perspective in gauging sarcastic statements. At 9am, after a whole night of sleep (n = 15) or a sleep deprivation night (n = 15), participants had to read the description of an event happening to a group of friends. An ambiguous voicemail message left by one of the friends on another's phone was then presented, and participants had to decide whether the recipient would perceive the message as sincere or as sarcastic. Messages were uttered with a neutral intonation and were either: (1) sarcastic from both the participant’s and the addressee’s perspectives (i.e. both had access to the relevant background knowledge to gauge the message as sarcastic), (2) sarcastic from the participant’s but not from the addressee’s perspective (i.e. the addressee lacked context knowledge to detect sarcasm) or (3) sincere. A fourth category consisted in messages sarcastic from both the participant’s and from the addressee’s perspective, uttered with a sarcastic tone. Although sleep-deprived participants were as accurate as sleep-rested participants in interpreting the voice message, they were also slower. Blunted reaction time was not fully explained by generalized cognitive slowing after sleep deprivation; rather, it could reflect a compensatory mechanism supporting normative accuracy level in sarcasm understanding. Introducing prosodic cues compensated for increased processing difficulties in sarcasm detection after sleep deprivation. Our findings support the hypothesis that sleep

  8. Impact of Acute Sleep Deprivation on Sarcasm Detection.

    PubMed

    Deliens, Gaétane; Stercq, Fanny; Mary, Alison; Slama, Hichem; Cleeremans, Axel; Peigneux, Philippe; Kissine, Mikhail

    2015-01-01

    There is growing evidence that sleep plays a pivotal role on health, cognition and emotional regulation. However, the interplay between sleep and social cognition remains an uncharted research area. In particular, little is known about the impact of sleep deprivation on sarcasm detection, an ability which, once altered, may hamper everyday social interactions. The aim of this study is to determine whether sleep-deprived participants are as able as sleep-rested participants to adopt another perspective in gauging sarcastic statements. At 9am, after a whole night of sleep (n = 15) or a sleep deprivation night (n = 15), participants had to read the description of an event happening to a group of friends. An ambiguous voicemail message left by one of the friends on another's phone was then presented, and participants had to decide whether the recipient would perceive the message as sincere or as sarcastic. Messages were uttered with a neutral intonation and were either: (1) sarcastic from both the participant's and the addressee's perspectives (i.e. both had access to the relevant background knowledge to gauge the message as sarcastic), (2) sarcastic from the participant's but not from the addressee's perspective (i.e. the addressee lacked context knowledge to detect sarcasm) or (3) sincere. A fourth category consisted in messages sarcastic from both the participant's and from the addressee's perspective, uttered with a sarcastic tone. Although sleep-deprived participants were as accurate as sleep-rested participants in interpreting the voice message, they were also slower. Blunted reaction time was not fully explained by generalized cognitive slowing after sleep deprivation; rather, it could reflect a compensatory mechanism supporting normative accuracy level in sarcasm understanding. Introducing prosodic cues compensated for increased processing difficulties in sarcasm detection after sleep deprivation. Our findings support the hypothesis that sleep deprivation might

  9. Is a purpose of REM sleep atonia to help regenerate intervertebral disc volumetric loss?

    PubMed Central

    Fryer, Jerome CJ

    2009-01-01

    The nature of atonia in sleep continues to be enigmatic. This article discusses a new hypothesis for complete core muscle relaxation in REM sleep, suggesting a bottom-up recuperative perspective. That is, does the atonia in REM sleep provide a utility to help restore the mechanobiology and respective diurnal intervertebral disc hydraulic loss? By combining the effects of gravity with current compressive concepts in spinal stability, this article looks at vertebral approximation as a deleterious experience with an intrinsic biological need to keep vertebrae separated. Methods using polysomnography and recumbent MRI are discussed. PMID:19123938

  10. Eating behavior traits and sleep as determinants of weight loss in overweight and obese adults

    PubMed Central

    Filiatrault, M-L; Chaput, J-P; Drapeau, V; Tremblay, A

    2014-01-01

    Objective: To examine the associations between eating behavior traits and weight loss according to sleep quality and duration in adults enrolled in common weight-loss interventions. Methods: Participants included overweight and obese men and women (n=150) (mean±s.d. age, 38.8±8.6 years; mean±s.d. body mass index (BMI), 33.3±3.5 kg m−2) who were subjected to a dietary intervention over a period of 12–16 weeks. Anthropometric measurements, eating behavior traits (Three-Factor Eating Questionnaire), sleep quality (total Pittsburgh Sleep Quality Index (PSQI) score) and sleep duration (hours per night, self-reported from the PSQI) were assessed at both baseline and post intervention. Linear regression analysis was used to quantify the relationships between eating behavior traits and changes in anthropometric markers for all subjects and by sleep categories (short sleep: <7 h per night vs recommended sleep: ⩾7 h per night; poor sleep quality: ⩾5 PSQI score vs good sleep quality: <5 PSQI score). We adjusted for age, sex and baseline BMI in analyses. Results: Baseline eating behavior traits were modest predictors of weight-loss success, but they were all significantly associated with their changes over the weight-loss intervention (P<0.01). The diet intervention induced significant changes in eating behavior traits and even more for those having a non-favorable eating behavior profile at baseline. We observed that changes in flexible control and strategic dieting behavior were constantly negatively associated with changes in body weight and fat mass (P<0.05) for recommended duration sleepers. The change in situational susceptibility to disinhibition was positively associated with the change in fat mass and body weight for those having healthy sleeping habits (P<0.05). For poor quality sleepers, the change in avoidance of fattening foods was negatively associated with changes in adiposity (P<0.05). Conclusion: Eating behavior traits and sleep may act

  11. Sleep state dependence of ventilatory long-term facilitation following acute intermittent hypoxia in Lewis rats

    PubMed Central

    Nakamura, A.; Olson, E. B.; Terada, J.; Wenninger, J. M.; Bisgard, G. E.

    2010-01-01

    Ventilatory long-term facilitation (vLTF) is a form of respiratory plasticity induced by acute intermittent hypoxia (AIH). Although vLTF has been reported in unanesthetized animals, little is known concerning the effects of vigilance state on vLTF expression. We hypothesized that AIH-induced vLTF is preferentially expressed in sleeping vs. awake male Lewis rats. Vigilance state was assessed in unanesthetized rats with chronically implanted EEG and nuchal EMG electrodes, while tidal volume, frequency, minute ventilation (V̇e), and CO2 production were measured via plethysmography, before, during, and after AIH (five 5-min episodes of 10.5% O2 separated by 5-min normoxic intervals), acute sustained hypoxia (25 min of 10.5% O2), or a sham protocol without hypoxia. Vigilance state was classified as quiet wakefulness (QW), light and deep non-rapid eye movement (NREM) sleep (l-NREM and d-NREM sleep, respectively), or rapid eye movement sleep. Ventilatory variables were normalized to pretreatment baseline values in the same vigilance state. During d-NREM sleep, vLTF was observed as a progressive increase in V̇e post-AIH (27 ± 5% average, 30–60 min post-AIH). In association, V̇e/V̇co2 (36 ± 2%), tidal volume (14 ± 2%), and frequency (7 ± 2%) were increased 30–60 min post-AIH during d-NREM sleep. vLTF was significant but less robust during l-NREM sleep, was minimal during QW, and was not observed following acute sustained hypoxia or sham protocols in any vigilance state. Thus, vLTF is state-dependent and pattern-sensitive in unanesthetized Lewis rats, with the greatest effects during d-NREM sleep. Although the physiological significance of vLTF is not clear, its greatest significance to ventilatory control is most likely during sleep. PMID:20360430

  12. Sleep Loss, Circadian Mismatch, and Abnormalities in Reorienting of Attention in Night Workers with Shift Work Disorder

    PubMed Central

    Gumenyuk, Valentina; Howard, Ryan; Roth, Thomas; Korzyukov, Oleg; Drake, Christopher L.

    2014-01-01

    Study Objectives: Permanent night-shift workers may develop shift-work disorder (SWD). In the current study, we evaluated neurophysiological and behavioral indices of distractibility across times prior to the night shift (T1), during night hours (T2), and after acute sleep deprivation (T3) in permanent hospital night workers with and without SWD. Methods: Ten asymptomatic night workers (NW) and 18 NW with SWD participated in a 25-h sleep deprivation study. Circadian phase was evaluated by dim-light salivary melatonin onset (DLMO). Objective sleepiness was evaluated using the Multiple Sleep Latency Test (MSLT). Electrophysiological distractibility was evaluated by brain event-related potentials (ERP), whereas behavioral distractibility was evaluated by performance on a visual task in an auditory-visual distraction paradigm. Statistical analyses: Comparisons of ERP results were performed by repeated-measures analysis of variance, and t-tests were used where appropriate. A Mann-Whitney U test was used for comparison of variables (MLST, Stanford Sleepiness Scale, and DLMO) that deviated from normal. Results: First, in the SWD group, the reorienting negativity ERP amplitude was significantly attenuated compared to that in the NW group. Second, the SWD group had shorter MSLT during night shift hours (4.8 ± 4.9 min) compared to that in NW (7.8 ± 3.7 min; U = 47; z = -2.1; P < 0.03). Third, NW with SWD had a DLMO at 20:27 ± 5.0 h, whereas healthy NW had a DLMO at 05:00 ± 3.4 h (U = 43.5; z = -2.22, P < 0.03). Finally, acute sleep deprivation impaired behavioral performance and the P3a ERP in both groups. Conclusions: Our results demonstrate specific deficits in neurophysiological activity in the attentional domain among the shift-work disorder group relative to night workers. Citation: Gumenyuk V; Howard R; Roth T; Korzyukov O; Drake CL. Sleep loss, circadian mismatch, and abnormalities in reorienting of attention in night workers with shift work disorder. SLEEP 2014

  13. Loss of Gnas Imprinting Differentially Affects REM/NREM Sleep and Cognition in Mice

    PubMed Central

    Lassi, Glenda; Ball, Simon T.; Maggi, Silvia; Colonna, Giovanni; Nieus, Thierry; Cero, Cheryl; Bartolomucci, Alessandro; Peters, Jo; Tucci, Valter

    2012-01-01

    It has been suggested that imprinted genes are important in the regulation of sleep. However, the fundamental question of whether genomic imprinting has a role in sleep has remained elusive up to now. In this work we show that REM and NREM sleep states are differentially modulated by the maternally expressed imprinted gene Gnas. In particular, in mice with loss of imprinting of Gnas, NREM and complex cognitive processes are enhanced while REM and REM–linked behaviors are inhibited. This is the first demonstration that a specific overexpression of an imprinted gene affects sleep states and related complex behavioral traits. Furthermore, in parallel to the Gnas overexpression, we have observed an overexpression of Ucp1 in interscapular brown adipose tissue (BAT) and a significant increase in thermoregulation that may account for the REM/NREM sleep phenotypes. We conclude that there must be significant evolutionary advantages in the monoallelic expression of Gnas for REM sleep and for the consolidation of REM–dependent memories. Conversely, biallelic expression of Gnas reinforces slow wave activity in NREM sleep, and this results in a reduction of uncertainty in temporal decision-making processes. PMID:22589743

  14. Can Ayahuasca and sleep loss change sexual performance in male rats?

    PubMed

    Alvarenga, T A; Polesel, D N; Matos, G; Garcia, V A; Costa, J L; Tufik, S; Andersen, M L

    2014-10-01

    The ingestion of the beverage Ayahuasca usually occurs in religious ceremonies that are performed during the night leading to sleep deprivation. The purpose of the present study was to characterize the acute effects of Ayahuasca upon the sexual response of sleep deprived male rats. One group of sexually experienced male Wistar rats were submitted to a paradoxical sleep deprivation (PSD) protocol for 96h, while another group spent the same amount of time in the home cage (CTRL). After this period, either saline or Ayahuasca drink (250, 500 and 1000μgmL(-1)) was administered by gavage and sexual behavior and hormonal concentrations were measured. Ayahuasca alone significantly decreased sexual performance at all doses. However, in sleep deprived rats, the lower dose increased sexual performance while the intermediate dose produced a detrimental effect on sexual response compared to the CTRL rats at the same dose. Regarding the hormonal analyses, a lower testosterone concentration was observed in sleep-deprived saline rats in relation to the CTRL group. Progesterone was significantly lower only in PSD rats at the dose 500μgmL(-1) compared with CTRL-500μgmL(-1) group. Corticosterone was unchanged among the groups evaluated. Our results suggest that Ayahuasca intake markedly impaired sexual performance alone, but, when combined with sleep deprivation, had significant, but heterogeneous, effects on male sexual response. PMID:25256159

  15. Overtime work, insufficient sleep, and risk of non-fatal acute myocardial infarction in Japanese men

    PubMed Central

    Liu, Y; Tanaka, H

    2002-01-01

    Objectives: To examine the relation between working hours and hours of sleep and the risk of acute myocardial infarction (AMI), with special reference to the joint effect of these two factors. Method: Case-control study in Japan. Cases were 260 men aged 40–79 admitted to hospitals with AMI during 1996–8. Controls were 445 men free from AMI matched for age and residence who were recruited from the resident registers. Odds ratios of AMI relative to mean weekly working hours and daily hours of sleep in the past year or in the recent past were calculated. Results: Weekly working hours were related to progressively increased odds ratios of AMI in the past year as well as in the past month, with a twofold increased risk for overtime work (weekly working hours ≥61) compared with working hours ≤40. Short time sleep (daily hours of sleep ≤5) and frequent lack of sleep (2 or more days/week with <5 hours of sleep) were also associated with a two to threefold increased risk. Frequent lack of sleep and few days off in the recent past showed greater odds ratios than those in the past year. Conclusions: Overtime work and insufficient sleep may be related to increased risk of AMI. PMID:12107292

  16. Flight Schedule and the Circadian Clock Influence on Sleep Loss During Overnight Cargo Operations

    NASA Technical Reports Server (NTRS)

    Gander, Philippa H.; Gregory, Kevin B.; Rosekind, Mark R.; Shafto, Michael G. (Technical Monitor)

    1995-01-01

    -0300) and were longer (average 19.2 h versus 14.8 h) than those in which they slept only once in the morning. Overnight cargo crew members are working around the time of the circadian nadir with an accumulating sleep debt. Two scheduling factors affect sleep loss during these operations: how long before the circadian wakeup signal crew members come off duty, and whether the layover lasts long enough to permit a second sleep episode in the early evening.

  17. Acute Total and Chronic Partial Sleep Deprivation: Effects on Neurobehavioral Functions, Waking EEG and Renin-Angiotensin System

    NASA Technical Reports Server (NTRS)

    Dijk, Derk-Jan

    1999-01-01

    Total sleep deprivation leads to decrements in neurobehavioral performance and changes in electroencephalographic (EEG) oscillations as well as the incidence of slow eye movements ad detected in the electro-oculogram (EOG) during wakefulness. Although total sleep deprivation is a powerful tool to investigate the association of EEG/EOG and neurobehavioral decrements, sleep loss during space flight is usual only partial. Furthermore exposure to the microgravity environment leads to changes in sodium and volume homeostasis and associated renal and cardio-endocrine responses. Some of these changes can be induced in head down tilt bedrest studies. We integrate research tools and research projects to enhance the fidelity of the simulated conditions of space flight which are characterized by complexity and mutual interactions. The effectiveness of countermeasures and physiologic mechanisms underlying neurobehavioral changes and renal-cardio endocrine changes are investigated in Project 3 of the Human Performance Team and Project 3 of the Cardiovascular Alterations Team respectively. Although the. specific aims of these two projects are very different, they employ very similar research protocols. Thus, both projects investigate the effects of posture/bedrest and sleep deprivation (total or partial) on outcome measures relevant to their specific aims. The main aim of this enhancement grant is to exploit the similarities in research protocols by including the assessment of outcome variables relevant to the Renal-Cardio project in the research protocol of Project 3 of the Human Performance Team and by including the assessment of outcome variables relevant to the Quantitative EEG and Sleep Deprivation Project in the research protocols of Project 3 of the Cardiovascular Alterations team. In particular we will assess Neurobehavioral Function and Waking EEG in the research protocols of the renal-cardio endocrine project and renin-angiotensin and cardiac function in the research

  18. The Impact of Moderate Sleep Loss on Neurophysiologic Signals during Working-Memory Task Performance

    PubMed Central

    Smith, Michael E.; McEvoy, Linda K.; Gevins, Alan

    2006-01-01

    Study Objectives This study examined how sleep loss affects neurophysiologic signals related to attention and working memory. Design Subjective sleepiness, resting-state electroencephalogram, and behavior and electroencephalogram during performance of working-memory tasks were recorded in a within-subject, repeated-measures design. Setting Data collection occurred in a computerized laboratory setting. Participants Sixteen healthy adults (mean age, 26 years; 8 female) Interventions Data from alert daytime baseline tests were compared with data from tests during a late-night, extended-wakefulness session that spanned up to 21 hours of sleep deprivation. Measurements and Results Alertness measured both subjectively and electrophysiologically decreased monotonically with increasing sleep deprivation. A lack of alertness-related changes in electroencephalographic measures of the overall mental effort exerted during task execution indicated that participants attempted to maintain high levels of performance throughout the late-night tests. Despite such continued effort, responses became slower, more variable, and more error prone within 1 hour after participants' normal time of sleep onset. This behavior failure was accompanied by significant degradation of event-related brain potentials related to the transient focusing of attention. Conclusions Moderate sleep loss compromises the function of neural circuits critical to subsecond attention allocation during working-memory tasks, even when an effort is made to maintain wakefulness and performance. Multivariate analyses indicate that combinations of working-memory-related behavior and neurophysiologic measures can be sensitive enough to permit reliable detection of such effects of sleep loss in individuals. Similar methods might prove useful for assessment of functional alertness in patients with sleep disorders. PMID:12405615

  19. Sleep Architecture Following a Weight Loss Intervention in Overweight and Obese Patients with Obstructive Sleep Apnea and Type 2 Diabetes: Relationship to Apnea-Hypopnea Index

    PubMed Central

    Shechter, Ari; St-Onge, Marie-Pierre; Kuna, Samuel T.; Zammit, Gary; RoyChoudhury, Arindam; Newman, Anne B.; Millman, Richard P.; Reboussin, David M.; Wadden, Thomas A.; Jakicic, John M.; Pi-Sunyer, F. Xavier; Wing, Rena R.; Foster, Gary D.

    2014-01-01

    Study Objectives: To determine if weight loss and/or changes in apnea-hypopnea index (AHI) improve sleep architecture in overweight/obese adults with type 2 diabetes (T2D) and obstructive sleep apnea (OSA). Methods: This was a randomized controlled trial including 264 overweight/obese adults with T2D and OSA. Participants were randomized to an intensive lifestyle intervention (ILI) or a diabetes and support education (DSE) control group. Measures included anthropometry, AHI, and sleep at baseline and year-1, year-2, and year-4 follow-ups. Results: Changes in sleep duration (total sleep time [TST]), continuity [wake after sleep onset (WASO)], and architecture stage 1, stage 2, slow wave sleep, and REM sleep) from baseline to year 1, 2, and 4 did not differ between ILI and DSE. Repeated-measure mixed-model analyses including data from baseline through year-4 for all participants demonstrated a significant positive association between AHI and stage 1 sleep (p < 0.001), and a significant negative association between AHI and stage 2 (p = 0.01) and REM sleep (p < 0.001), whereas changes in body weight had no relation to any sleep stages or TST. WASO had a significant positive association with change in body weight (p = 0.009). Conclusions: Compared to control, the ILI did not induce significant changes in sleep across the 4-year follow-up. In participants overall, reduced AHI in overweight/obese adults with T2D and OSA was associated with decreased stage 1, and increased stage 2 and REM sleep. These sleep architecture changes are more strongly related to reductions in AHI than body weight, whereas WASO may be more influenced by weight than AHI. Clinical Trial Registration: ClinicalTrials.gov identifier: NCT00194259 Citation: Shechter A, St-Onge MP, Kuna ST, Zammit G, RoyChoudhury A, Newman AB, Millman RP, Reboussin DM, Wadden TA, Jakicic JM, Pi-Sunyer FX, Wing RR, Foster GD, Sleep AHEAD Research Group of the Look AHEAD Research Group. Sleep architecture following a

  20. Sleep loss changes microRNA levels in the brain: A possible mechanism for state-dependent translational regulation

    PubMed Central

    Davis, Christopher J.; Bohnet, Stewart G.; Meyerson, Joseph M.; Krueger, James M.

    2007-01-01

    MicroRNAs (miRNAs) are small (∼22 nucleotide) non-coding RNA strands that base pair with mRNA to degrade it or inhibit its translation. Because sleep and sleep loss induce changes in many mRNA species, we hypothesized that sleep loss would also affect miRNA levels in the brain. Rats were sleep-deprived for 8 h then decapitated; hippocampus, prefrontal and somatosensory cortices and hypothalamus tissues were harvested and frozen in liquid nitrogen. MiRNA was extracted and then characterized using microarrays. Several let-7 miRNA microarray results using hippocampus and prefrontal cortex samples were verified by PCR. From the array data it was determined that about fifty miRNA species were affected by sleep loss. For example, in the hippocampus of sleep-deprived rats, miRNA expression increased compared to cage control samples. In contrast, the majority of miRNA species in the somatosensory and prefrontal cortices decreased, while in the hypothalamus miRNA species were both up- and down-regulated after sleep deprivation. The number of miRNA species affected by sleep loss, their differential expression in separate brain structures and their predicted targets suggest that they have a role in site-specific sleep mechanisms. Current results are, to our knowledge, the first demonstration of the homeostatic process, sleep, altering brain miRNA levels. PMID:17597302

  1. Transiently Increasing cAMP Levels Selectively in Hippocampal Excitatory Neurons during Sleep Deprivation Prevents Memory Deficits Caused by Sleep Loss

    PubMed Central

    Bruinenberg, Vibeke M.; Tudor, Jennifer C.; Ferri, Sarah L.; Baumann, Arnd; Meerlo, Peter

    2014-01-01

    The hippocampus is particularly sensitive to sleep loss. Although previous work has indicated that sleep deprivation impairs hippocampal cAMP signaling, it remains to be determined whether the cognitive deficits associated with sleep deprivation are caused by attenuated cAMP signaling in the hippocampus. Further, it is unclear which cell types are responsible for the memory impairments associated with sleep deprivation. Transgenic approaches lack the spatial resolution to manipulate specific signaling pathways selectively in the hippocampus, while pharmacological strategies are limited in terms of cell-type specificity. Therefore, we used a pharmacogenetic approach based on a virus-mediated expression of a Gαs-coupled Drosophila octopamine receptor selectively in mouse hippocampal excitatory neurons in vivo. With this approach, a systemic injection with the receptor ligand octopamine leads to increased cAMP levels in this specific set of hippocampal neurons. We assessed whether transiently increasing cAMP levels during sleep deprivation prevents memory consolidation deficits associated with sleep loss in an object–location task. Five hours of total sleep deprivation directly following training impaired the formation of object–location memories. Transiently increasing cAMP levels in hippocampal neurons during the course of sleep deprivation prevented these memory consolidation deficits. These findings demonstrate that attenuated cAMP signaling in hippocampal excitatory neurons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks associated with sleep deprivation. PMID:25411499

  2. Rapid eye movement-sleep is reduced in patients with acute uncomplicated diverticulitis—an observational study

    PubMed Central

    Alamili, Mahdi; Nielsen, Claus Henrik; Rosenberg, Jacob; Gögenur, Ismail

    2015-01-01

    Introduction. Sleep disturbances are commonly found in patients in the postoperative period. Sleep disturbances may give rise to several complications including cardiopulmonary instability, transient cognitive dysfunction and prolonged convalescence. Many factors including host inflammatory responses are believed to cause postoperative sleep disturbances, as inflammatory responses can alter sleep architecture through cytokine-brain interactions. Our aim was to investigate alteration of sleep architecture during acute infection and its relationships to inflammation and clinical symptoms. Materials & Methods. In this observational study, we included patients with acute uncomplicated diverticulitis as a model to investigate the isolated effects of inflammatory responses on sleep. Eleven patients completed the study. Patients were admitted and treated with antibiotics for two nights, during which study endpoints were measured by polysomnography recordings, self-reported discomfort scores and blood samples of cytokines. One month later, the patients, who now were in complete remission, were readmitted and the endpoints were re-measured (the baseline values). Results. Total sleep time was reduced 4% and 7% the first (p = 0.006) and second (p = 0.014) nights of diverticulitis, compared to baseline, respectively. The rapid eye movement sleep was reduced 33% the first night (p = 0.016), compared to baseline. Moreover, plasma IL-6 levels were correlated to non-rapid eye movement sleep, rapid eye movement sleep and fatigue. Conclusion. Total sleep time and rapid eye movement sleep were reduced during nights with active diverticulitis and correlated with markers of inflammation. PMID:26290799

  3. Phenotypic vulnerability of energy balance responses to sleep loss in healthy adults

    PubMed Central

    Spaeth, Andrea M.; Dinges, David F.; Goel, Namni

    2015-01-01

    Short sleep duration is a risk factor for increased hunger and caloric intake, late-night eating, attenuated fat loss when dieting, and for weight gain and obesity. It is unknown whether altered energy-balance responses to sleep loss are stable (phenotypic) over time, and the extent to which individuals differ in vulnerability to such responses. Healthy adults experienced two laboratory exposures to sleep restriction separated by 60–2132 days. Caloric intake, meal timing and weight were objectively measured. Although there were substantial phenotypic differences among participants in weight gain, increased caloric intake, and late-night eating and fat intake, responses within participants showed stability across sleep restriction exposures. Weight change was consistent in both normal-weight and overweight adults. Weight change and increased caloric intake were more stable in men whereas late-night eating was consistent in both genders. This is the first evidence of phenotypic differential vulnerability and trait-like stability of energy balance responses to repeated sleep restriction, underscoring the need for biomarkers and countermeasures to predict and mitigate this vulnerability. PMID:26446681

  4. Phenotypic vulnerability of energy balance responses to sleep loss in healthy adults.

    PubMed

    Spaeth, Andrea M; Dinges, David F; Goel, Namni

    2015-01-01

    Short sleep duration is a risk factor for increased hunger and caloric intake, late-night eating, attenuated fat loss when dieting, and for weight gain and obesity. It is unknown whether altered energy-balance responses to sleep loss are stable (phenotypic) over time, and the extent to which individuals differ in vulnerability to such responses. Healthy adults experienced two laboratory exposures to sleep restriction separated by 60-2132 days. Caloric intake, meal timing and weight were objectively measured. Although there were substantial phenotypic differences among participants in weight gain, increased caloric intake, and late-night eating and fat intake, responses within participants showed stability across sleep restriction exposures. Weight change was consistent in both normal-weight and overweight adults. Weight change and increased caloric intake were more stable in men whereas late-night eating was consistent in both genders. This is the first evidence of phenotypic differential vulnerability and trait-like stability of energy balance responses to repeated sleep restriction, underscoring the need for biomarkers and countermeasures to predict and mitigate this vulnerability. PMID:26446681

  5. Sleep Deprivation Accelerates Delay-Related Loss of Visual Short-Term Memories Without Affecting Precision

    PubMed Central

    Wee, Natalie; Asplund, Christopher L.; Chee, Michael W. L.

    2013-01-01

    Study Objectives: Visual short-term memory (VSTM) is an important measure of information processing capacity and supports many higher-order cognitive processes. We examined how sleep deprivation (SD) and maintenance duration interact to influence the number and precision of items in VSTM using an experimental design that limits the contribution of lapses at encoding. Design: For each trial, participants attempted to maintain the location and color of three stimuli over a delay. After a retention interval of either 1 or 10 seconds, participants reported the color of the item at the cued location by selecting it on a color wheel. The probability of reporting the probed item, the precision of report, and the probability of reporting a nonprobed item were determined using a mixture-modeling analysis. Participants were studied twice in counterbalanced order, once after a night of normal sleep and once following a night of sleep deprivation. Setting: Sleep laboratory. Participants: Nineteen healthy college age volunteers (seven females) with regular sleep patterns. Interventions: Approximately 24 hours of total SD. Measurements and Results: SD selectively reduced the number of integrated representations that can be retrieved after a delay, while leaving the precision of object information in the stored representations intact. Delay interacted with SD to lower the rate of successful recall. Conclusions: Visual short-term memory is compromised during sleep deprivation, an effect compounded by delay. However, when memories are retrieved, they tend to be intact. Citation: Wee N; Asplund CL; Chee MWL. Sleep deprivation accelerates delay-related loss of visual short-term memories without affecting precision. SLEEP 2013;36(6):849-856. PMID:23729928

  6. A single night of partial sleep loss impairs fasting insulin sensitivity but does not affect cephalic phase insulin release in young men.

    PubMed

    Cedernaes, Jonathan; Lampola, Lauri; Axelsson, Emil K; Liethof, Lisanne; Hassanzadeh, Sara; Yeganeh, Adine; Broman, Jan-Erik; Schiöth, Helgi B; Benedict, Christian

    2016-02-01

    The present study sought to investigate whether a single night of partial sleep deprivation (PSD) would alter fasting insulin sensitivity and cephalic phase insulin release (CPIR) in humans. A rise in circulating insulin in response to food-related sensory stimulation may prepare tissues to break down ingested glucose, e.g. by stimulating rate-limiting glycolytic enzymes. In addition, given insulin's anorexigenic properties once it reaches the brain, the CPIR may serve as an early peripheral satiety signal. Against this background, in the present study 16 men participated in two separate sessions: one night of PSD (4.25 h sleep) versus one night of full sleep (8.5 h sleep). In the morning following each sleep condition, subjects' oral cavities were rinsed with a 1-molar sucrose solution for 45 s, preceded and followed by blood sampling for repeated determination of plasma glucose and serum insulin concentrations (-3, +3, +5, +7, +10 and +20 min). Our main result was that PSD, compared with full sleep, was associated with significantly higher peripheral insulin resistance, as indicated by a higher fasting homeostasis model assessment of insulin resistance index (+16%, P = 0.025). In contrast, no CPIR was observed in any of the two sleep conditions. Our findings indicate that a single night of PSD is already sufficient to impair fasting insulin sensitivity in healthy men. In contrast, brief oral cavity rinsing with sucrose solution did not change serum insulin concentrations, suggesting that a blunted CPIR is an unlikely mechanism through which acute sleep loss causes metabolic perturbations during morning hours in humans. PMID:26361380

  7. Gloriosa superba ingestion: Hair loss and acute renal failure

    PubMed Central

    Khanam, P. S.; Sangeetha, B.; Kumar, B. V.; Kiran, U.; Priyadarshini, P. I.; Ram, R.; Sridhar, M. S.; Kumar, V. S.

    2015-01-01

    Gloriosa superba is a plant that grows wild in several parts of South India. Tubers of this plant contain several alkaloids. Acute intoxication following the ingestion of G. superba results in gastrointestinal and haematological abnormalities, hepatic and renal insufficiency, cardiotoxicity and hair loss. We present a case with typical features of G superba toxicity. PMID:26060369

  8. The Influence of Sleep Disordered Breathing on Weight Loss in a National Weight Management Program

    PubMed Central

    Janney, Carol A.; Kilbourne, Amy M.; Germain, Anne; Lai, Zongshan; Hoerster, Katherine D.; Goodrich, David E.; Klingaman, Elizabeth A.; Verchinina, Lilia; Richardson, Caroline R.

    2016-01-01

    Study Objective: To investigate the influence of sleep disordered breathing (SDB) on weight loss in overweight/obese veterans enrolled in MOVE!, a nationally implemented behavioral weight management program delivered by the National Veterans Health Administration health system. Methods: This observational study evaluated weight loss by SDB status in overweight/obese veterans enrolled in MOVE! from May 2008–February 2012 who had at least two MOVE! visits, baseline weight, and at least one follow-up weight (n = 84,770). SDB was defined by International Classification of Diseases, Ninth Revision, Clinical Modification codes. Primary outcome was weight change (lb) from MOVE! enrollment to 6- and 12-mo assessments. Weight change over time was modeled with repeated-measures analyses. Results: SDB was diagnosed in one-third of the cohort (n = 28,269). At baseline, veterans with SDB weighed 29 [48] lb more than those without SDB (P < 0.001). On average, veterans attended eight MOVE! visits. Weight loss patterns over time were statistically different between veterans with and without SDB (P < 0.001); veterans with SDB lost less weight (−2.5 [0.1] lb) compared to those without SDB (−3.3 [0.1] lb; P = 0.001) at 6 months. At 12 mo, veterans with SDB continued to lose weight whereas veterans without SDB started to re-gain weight. Conclusions: Veterans with sleep disordered breathing (SDB) had significantly less weight loss over time than veterans without SDB. SDB should be considered in the development and implementation of weight loss programs due to its high prevalence and negative effect on health. Citation: Janney CA, Kilbourne AM, Germain A, Lai Z, Hoerster KD, Goodrich DE, Klingaman EA, Verchinina L, Richardson CR. The influence of sleep disordered breathing on weight loss in a national weight management program. SLEEP 2016;39(1):59–65. PMID:26350475

  9. Prevalence of Impaired Memory in Hospitalized Adults and Associations with In-Hospital Sleep Loss

    PubMed Central

    Calev, Hila; Spampinato, Lisa M; Press, Valerie G; Meltzer, David O; Arora, Vineet M

    2015-01-01

    Background Effective inpatient teaching requires intact patient memory, but studies suggest hospitalized adults may have memory deficits. Sleep loss among inpatients could contribute to memory impairment. Objective To assess memory in older hospitalized adults, and to test the association between sleep quantity, sleep quality and memory, in order to identify a possible contributor to memory deficits in these patients. Design Prospective cohort study Setting General medicine and hematology/oncology inpatient wards Patients 59 hospitalized adults at least 50 years of age with no diagnosed sleep disorder. Measurements Immediate memory and memory after a 24-hour delay were assessed using a word recall and word recognition task from the University of Southern California Repeatable Episodic Memory Test (USC-REMT). A vignette-based memory task was piloted as an alternative test more closely resembling discharge instructions. Sleep duration and efficiency overnight in the hospital were measured using actigraphy. Results Mean immediate recall was 3.8 words out of 15 (SD=2.1). Forty-nine percent of subjects had poor memory, defined as immediate recall score of 3 or lower. Median immediate recognition was 11 words out of 15 (IQR=9, 13). Median delayed recall score was 1 word and median delayed recognition was 10 words (IQR= 8–12). In-hospital sleep duration and efficiency were not significantly associated with memory. The medical vignette score was correlated with immediate recall (r=0.49, p<0.01) Conclusions About half of inpatients studied had poor memory while in the hospital, signaling that hospitalization might not be an ideal teachable moment. In-hospital sleep was not associated with memory scores. PMID:25872763

  10. [Acute correction of nocturnal hypoxemia and sleep pattern using continuous nasal positive pressure in patients with obstructive sleep apnea syndrome].

    PubMed

    Díaz, M; Rendón, A; Cano, M E

    1998-01-01

    In order to find out the effectiveness of the nasal CPAP in the treatment of obstructive sleep apnea (OSA), we studied 30 patients with this diagnosis corroborated by nocturnal polysomnography. The average age was 46.37 +/- 11.58 years, 97% were males and 90% were overweight, with a weight of 101.24 +/- 15.57 Kg. All the patients were evaluated before and after the application of nasal CPAP with a pressure of 12.9 +/- 4.35 cm of H2O with a FIO2 of 21%. The sleep efficiency index improved from 0.62 +/- 0.03 to 0.84 +/- 0.02 (p < 0.0001). The maximum duration of the apneas diminished from 65.5 +/- 6.5 seconds to 19 +/- 3.7 seconds (p < 0.0001), and the minimum level of O2 saturation of the hemoglobin increased from 56.8 +/- 3.2% to 84.9 +/- 1.9% (p < 00.0001). These findings showed a clear improvement in the majority of the evaluated parameters in all of the patients, and, in many of them, a normalization. We conclude that the nasal CPAP is effective for the acute improvement of the disorders observed during the sleep in patients with OSA, which supports its therapeutic use in this illness. PMID:9927773

  11. Parent-of-origin genetic background affects the transcriptional levels of circadian and neuronal plasticity genes following sleep loss

    PubMed Central

    Tinarelli, Federico; Garcia-Garcia, Celina; Nicassio, Francesco; Tucci, Valter

    2014-01-01

    Sleep homoeostasis refers to a process in which the propensity to sleep increases as wakefulness progresses and decreases as sleep progresses. Sleep is tightly organized around the circadian clock and is regulated by genetic and epigenetic mechanisms. The homoeostatic response of sleep, which is classically triggered by sleep deprivation, is generally measured as a rebound effect of electrophysiological measures, for example delta sleep. However, more recently, gene expression changes following sleep loss have been investigated as biomarkers of sleep homoeostasis. The genetic background of an individual may affect this sleep-dependent gene expression phenotype. In this study, we investigated whether parental genetic background differentially modulates the expression of genes following sleep loss. We tested the progeny of reciprocal crosses of AKR/J and DBA/2J mouse strains and we show a parent-of-origin effect on the expression of circadian, sleep and neuronal plasticity genes following sleep deprivation. Thus, we further explored, by in silico, specific functions or upstream mechanisms of regulation and we observed that several upstream mechanisms involving signalling pathways (i.e. DICER1, PKA), growth factors (CSF3 and BDNF) and transcriptional regulators (EGR2 and ELK4) may be differentially modulated by parental effects. This is the first report showing that a behavioural manipulation (e.g. sleep deprivation) in adult animals triggers specific gene expression responses according to parent-of-origin genomic mechanisms. Our study suggests that the same mechanism may be extended to other behavioural domains and that the investigation of gene expression following experimental manipulations should take seriously into account parent-of-origin effects. PMID:24446504

  12. Obstructive sleep apnea syndrome with bilateral papilledema and vision loss in a 3-year-old child.

    PubMed

    Quinn, Anthony G; Gouws, Pieter; Headland, Sophie; Oades, Patrick; Pople, Ian; Taylor, David; Benton, J Sarah; Buncic, J Raymond; Henderson, John; Fleming, Peter

    2008-04-01

    We describe bilateral papilledema and vision loss in a 3-year-old child with obstructive sleep apnea. Although lumbar puncture initially disclosed a normal opening pressure, cerebrospinal fluid (CSF) pressure monitoring during sleep confirmed intermittent episodes of elevated intracranial pressure corresponding to increased airway resistance. The association of obstructive sleep apnea and raised intracranial pressure is recognized in children with craniosynostosis but has not been reported in its absence. PMID:18289895

  13. Acute stress alters autonomic modulation during sleep in women approaching menopause.

    PubMed

    de Zambotti, Massimiliano; Sugarbaker, David; Trinder, John; Colrain, Ian M; Baker, Fiona C

    2016-04-01

    Hot flashes, hormones, and psychosocial factors contribute to insomnia risk in the context of the menopausal transition. Stress is a well-recognized factor implicated in the pathophysiology of insomnia; however the impact of stress on sleep and sleep-related processes in perimenopausal women remains largely unknown. We investigated the effect of an acute experimental stress (impending Trier Social Stress Task in the morning) on pre-sleep measures of cortisol and autonomic arousal in perimenopausal women with and without insomnia that developed in the context of the menopausal transition. In addition, we assessed the macro- and micro-structure of sleep and autonomic functioning during sleep. Following adaptation to the laboratory, twenty two women with (age: 50.4 ± 3.2 years) and eighteen women without (age: 48.5 ± 2.3 years) insomnia had two randomized in-lab overnight recordings: baseline and stress nights. Anticipation of the task resulted in higher pre-sleep salivary cortisol levels and perceived tension, faster heart rate and lower vagal activity, based on heart rate variability measures, in both groups of women. The effect of the stress manipulation on the autonomic nervous system extended into the first 4 h of the night in both groups. However, vagal tone recovered 4-6 h into the stress night in controls but not in the insomnia group. Sleep macrostructure was largely unaltered by the stress, apart from a delayed latency to REM sleep in both groups. Quantitative analysis of non-rapid eye movement sleep microstructure revealed greater electroencephalographic (EEG) power in the beta1 range (15-≤23 Hz), reflecting greater EEG arousal during sleep, on the stress night compared to baseline, in the insomnia group. Hot flash frequency remained similar on both nights for both groups. These results show that pre-sleep stress impacts autonomic nervous system functioning before and during sleep in perimenopausal women with and without insomnia. Findings also indicate

  14. Effect of Acute Intermittent CPAP Depressurization during Sleep in Obese Patients

    PubMed Central

    Jun, Jonathan C.; Unnikrishnan, Dileep; Schneider, Hartmut; Kirkness, Jason; Schwartz, Alan R.; Smith, Philip L.; Polotsky, Vsevolod Y.

    2016-01-01

    Background Obstructive Sleep Apnea (OSA) describes intermittent collapse of the airway during sleep, for which continuous positive airway pressure (CPAP) is often prescribed for treatment. Prior studies suggest that discontinuation of CPAP leads to a gradual, rather than immediate return of baseline severity of OSA. The objective of this study was to determine the extent of OSA recurrence during short intervals of CPAP depressurization during sleep. Methods Nine obese (BMI = 40.4 ± 3.5) subjects with severe OSA (AHI = 88.9 ± 6.8) adherent to CPAP were studied during one night in the sleep laboratory. Nasal CPAP was delivered at therapeutic (11.1 ± 0.6 cm H20) or atmospheric pressure, in alternating fashion for 1-hour periods during the night. We compared sleep architecture and metrics of OSA during CPAP-on and CPAP-off periods. Results 8/9 subjects tolerated CPAP withdrawal. The average AHI during CPAP-on and CPAP-off periods was 3.6 ± 0.6 and 15.8 ± 3.6 respectively (p<0.05). The average 3% ODI during CPAP-on and CPAP-off was 4.7 ± 2 and 20.4 ± 4.7 respectively (p<0.05). CPAP depressurization also induced more awake (p<0.05) and stage N1 (p<0.01) sleep, and less stage REM (p<0.05) with a trend towards decreased stage N3 (p = 0.064). Conclusion Acute intermittent depressurization of CPAP during sleep led to deterioration of sleep architecture but only partial re-emergence of OSA. These observations suggest carryover effects of CPAP. PMID:26731735

  15. Evidence for Neuroinflammatory and Microglial Changes in the Cerebral Response to Sleep Loss

    PubMed Central

    Wisor, Jonathan P.; Schmidt, Michelle A.; Clegern, William C.

    2011-01-01

    Study Objectives: Sleep loss has pro-inflammatory effects, but the roles of specific cell populations in mediating these effects have not been delineated. We assessed the modulation of the electroencephalographic and molecular responses to sleep deprivation (S-DEP) by minocycline, a compound that attenuates microglial activation occurring in association with neuroinflammatory events. Design: Laboratory rodents were subjected to assessment of sleep and wake in baseline and sleep deprived conditions. Participants: Adult male CD-1 mice (30-35 g) subjected to telemetric electroencephalography. Interventions: Minocycline was administered daily. Mice were subjected to baseline data collection on the first day of minocycline administration and, on subsequent days, 2 S-DEP sessions, 1 and 3 h in duration, followed by recovery sleep. Following EEG studies, mice were euthanized either at the end of a 3 h S-DEP or as time-of day controls for sampling of brain messenger RNAs. Gene expression was measured by real-time polymerase chain reaction. Measurements and Results: Minocycline-treated mice exhibited a reduction in time spent asleep, relative to saline-treated mice, in the 3-h interval immediately after administration. S-DEP resulted in an increase in EEG slow wave activity relative to baseline in saline-treated mice. This response to S-DEP was abolished in animals subjected to chronic minocycline administration. S-DEP suppressed the expression of the microglial-specific transcript cd11b and the neuroinflammation marker peripheral benzodiazepine receptor, in the brain at the mRNA level. Minocycline attenuated the elevation of c-fos expression by S-DEP. Brain levels of pro-inflammatory cytokine mRNAs interleukin-1β (il-1β), interleukin-6 (il-6), and tumor necrosis factor-α (tnfα) were unaffected by S-DEP, but were elevated in minocycline-treated mice relative to saline-treated mice. Conclusions: The anti-neuroinflammatory agent minocycline prevents either the buildup or

  16. Sleep Loss Activates Cellular Inflammation and Signal Transducer and Activator of Transcription (STAT) Family Proteins in Humans

    PubMed Central

    Irwin, Michael R.; Witarama, Tuff; Caudill, Marissa; Olmstead, Richard; Breen, Elizabeth Crabb

    2014-01-01

    Sleep disturbance and short sleep duration are associated with inflammation and related disorders including cardiovascular disease, arthritis, diabetes mellitus, and certain cancers. This study was undertaken to test the effects of experimental sleep loss on spontaneous cellular inflammation and activation of signal transducer and activator of transcription (STAT) family proteins, which together promote an inflammatory microenvironment. In 24 healthy adults (16 females; 8 males), spontaneous production of IL-6 and TNF in monocytes and spontaneous intranuclear expression of activated STAT1, STAT3, and STAT5 in peripheral blood mononuclear cells (PBMC), monocyte-, and lymphocyte populations were measured in the morning after uninterrupted baseline sleep, partial sleep deprivation (PSD, sleep period from 3 a.m. to 7 a.m.), and recovery sleep. Relative to baseline, spontaneous monocytic expression of IL-6 and TNF-α was significantly greater after PSD (P<0.02) and after recovery sleep (P<0.01). Relative to baseline, spontaneous monocytic expression of activated STAT 1 and STAT 5 was significantly greater after recovery sleep (P<0.007P<0.02, respectively) but not STAT 3 (P=0.09). No changes in STAT1, STAT3, or STAT5 were found in lymphocyte populations. Sleep loss induces activation of spontaneous cellular innate immunity and of STAT family proteins, which together map the dynamics of sleep loss on the molecular signaling pathways that regulate inflammatory and other immune responses. Treatments that target short sleep duration have the potential to constrain inflammation and reduce the risk for inflammatory disorders and some cancers in humans. PMID:25451613

  17. Effects of Maintained Weight Loss on Sleep Dynamics and Neck Morphology in Severely Obese Adults

    PubMed Central

    Hernandez, Teri L.; Ballard, Robert D.; Weil, Kathleen M.; Shepard, Trudy Y.; Scherzinger, Ann L.; Stamm, Elizabeth R.; Sharp, Teresa A.; Eckel, Robert H.

    2011-01-01

    The goals of the study were to determine if moderate weight loss in severely obese adults resulted in 1) reduction in apnea/hypopnea index (AHI), 2) improved pharyngeal patency, 3) reduced total body oxygen consumption (VO2) and carbon dioxide production (VCO2) during sleep, and 4) improved sleep quality. The main outcome was the change in AHI from before to after weight loss. Fourteen severely obese (BMI>40 kg/m2) patients (3 males, 11 females) completed a highly controlled weight reduction program which included 3 months of weight loss and 3 months of weight maintenance. At baseline and post-weight loss, patients underwent pulmonary function testing, polysomnography, and MRI to assess neck morphology. Weight decreased from 134±6.6 kg to 118±6.1 kg (mean ± SEM; F=113.763, p<0.0001). There was a significant reduction in the AHI between baseline and post-weight loss (SUBJECT, F=11.11, p=0.007). Moreover, patients with worse sleep disordered breathing (SDB) at baseline had the greatest improvements in AHI (GROUP, F=9.00, p=0.005). Reductions in VO2 (285±12 to 234±16 ml/min; F=24.85, p<0.0001) and VCO2 (231±9 to 186±12 ml/min; F=27.74, p<0.0001) were also observed, and pulmonary function testing showed improvements in spirometry parameters. Sleep studies revealed improved minimum SaO2 (83.4±61.9% to 89.1±1.2%; F=7.59, p=0.016), and mean SaO2 (90.4±1.1% to 93.8±1.0%; F=6.89, p=0.022), and a significant increase in the number of arousals (8.1±1.4 at baseline, to 17.1±3.0 after weight loss; F=18.13, p=0.001). In severely obese patients, even moderate weight loss (~10%) boasts substantial benefit in terms of the severity of SDB and sleep dynamics. PMID:18948968

  18. Sleep Apnea Determines Soluble TNF-α Receptor 2 Response to Massive Weight Loss

    PubMed Central

    Pallayova, Maria; Steele, Kimberley E.; Magnuson, Thomas H.; Schweitzer, Michael A.; Smith, Philip L.; Patil, Susheel P.; Bevans-Fonti, Shannon; Polotsky, Vsevolod Y.

    2015-01-01

    Background The effects of surgical weight loss (WL) on inflammatory biomarkers associated with sleep apnea remain unknown. We sought to determine if any bio-markers can predict amelioration of sleep apnea achieved by bariatric surgery. We hypothesized that surgical WL would substantially reduce severity of sleep apnea and levels of proinflammatory cytokines. Methods Twenty-three morbidly obese adults underwent anthropometric measurements, polysomnography, and serum biomarker profiling prior to and 1 year following bariatric surgery. We examined the effect of WL and amelioration of sleep apnea on metabolic and inflammatory markers. Results Surgical WL resulted in significant decreases in BMI (16.7±5.97 kg/m2/median 365 days), apnea–hypopnea index (AHI), CRP, IL-6, sTNFαR1, sTNFαR2, and leptin levels, while ghrelin, adiponectin, and soluble leptin receptor concentrations increased significantly. Utilizing an AHI cutoff of 15 events/h, we found significantly elevated levels of baseline sTNFαR2 and greater post-WL sTNFαR2 decreases in subjects with baseline AHI ≥15 events/h compared to those with AHI <15 events/h despite no significant differences in baseline BMI, age, and ΔBMI. In a multivariable linear regression model adjusting for sex, age, impaired glucose metabolism, ΔBMI, and follow-up period, the post-WL decreases in AHI were an independent predictor of the decreases in sTNFαR2 and altogether accounted for 46% of the variance of ΔsTNFαR2 (P=0.011) in the entire cohort. Conclusions Of all the biomarkers, the decrease in sTNFαR2 was independently determined by the amelioration of sleep apnea achieved by bariatric surgery. The results suggest that sTNFαR2 may be a specific sleep apnea biomarker across a wide range of body weight. PMID:21298510

  19. Fatigue on the flight deck: the consequences of sleep loss and the benefits of napping.

    PubMed

    Hartzler, Beth M

    2014-01-01

    The detrimental effects of fatigue in aviation are well established, as evidenced by both the number of fatigue-related mishaps and numerous studies which have found that most pilots experience a deterioration in cognitive performance as well as increased stress during the course of a flight. Further, due to the nature of the average pilot's work schedule, with frequent changes in duty schedule, early morning starts, and extended duty periods, fatigue may be impossible to avoid. Thus, it is critical that fatigue countermeasures be available which can help to combat the often overwhelming effects of sleep loss or sleep disruption. While stimulants such as caffeine are typically effective at maintaining alertness and performance, such countermeasures do nothing to address the actual source of fatigue - insufficient sleep. Consequently, strategic naps are considered an efficacious means of maintaining performance while also reducing the individual's sleep debt. These types of naps have been advocated for pilots in particular, as opportunities to sleep either in the designated rest facilities or on the flight deck may be beneficial in reducing both the performance and alertness impairments associated with fatigue, as well as the subjective feelings of sleepiness. Evidence suggests that strategic naps can reduce subjective feelings of fatigue and improve performance and alertness. Despite some contraindications to implementing strategic naps while on duty, such as sleep inertia experienced upon awakening, both researchers and pilots agree that the benefits associated with these naps far outweigh the potential risks. This article is a literature review detailing both the health and safety concerns of fatigue among commercial pilots as well as benefits and risks associated with strategic napping to alleviate this fatigue. PMID:24215936

  20. Sleep disruption and its effect on lymphocyte redeployment following an acute bout of exercise.

    PubMed

    Ingram, Lesley A; Simpson, Richard J; Malone, Eva; Florida-James, Geraint D

    2015-07-01

    Sleep disruption and deprivation are common in contemporary society and have been linked with poor health, decreased job performance and increased life-stress. The rapid redeployment of lymphocytes between the blood and tissues is an archetypal feature of the acute stress response, but it is not known if short-term perturbations in sleep architecture affect lymphocyte redeployment. We examined the effects of a disrupted night sleep on the exercise-induced redeployment of lymphocytes and their subtypes. 10 healthy male cyclists performed 1h of cycling at a fixed power output on an indoor cycle ergometer, following a night of undisrupted sleep (US) or a night of disrupted sleep (DS). Blood was collected before, immediately after and 1h after exercise completion. Lymphocytes and their subtypes were enumerated using direct immunofluorescence assays and 4-colour flow cytometry. DS was associated with elevated concentrations of total lymphocytes and CD3(-)/CD56(+) NK-cells. Although not affecting baseline levels, DS augmented the exercise-induced redeployment of CD8(+) T-cells, with the naïve/early differentiated subtypes (KLRG1(-)/CD45RA(+)) being affected most. While the mobilisation of cytotoxic lymphocyte subsets (NK cells, CD8(+) T-cells γδ T-cells), tended to be larger in response to exercise following DS, their enhanced egress at 1h post-exercise was more marked. This occurred despite similar serum cortisol and catecholamine levels between the US and DS trials. NK-cells redeployed with exercise after DS retained their expression of perforin and Granzyme-B indicating that DS did not affect NK-cell 'arming'. Our findings indicate that short-term changes in sleep architecture may 'prime' the immune system and cause minor enhancements in lymphocyte trafficking in response to acute dynamic exercise. PMID:25582807

  1. Effects of Night Work, Sleep Loss and Time on Task on Simulated Threat Detection Performance

    PubMed Central

    Basner, Mathias; Rubinstein, Joshua; Fomberstein, Kenneth M.; Coble, Matthew C.; Ecker, Adrian; Avinash, Deepa; Dinges, David F.

    2008-01-01

    Study Objectives: To investigate the effects of night work and sleep loss on a simulated luggage screening task (SLST) that mimicked the x-ray system used by airport luggage screeners. Design: We developed more than 5,800 unique simulated x-ray images of luggage organized into 31 stimulus sets of 200 bags each. 25% of each set contained either a gun or a knife with low or high target difficulty. The 200-bag stimuli sets were then run on software that simulates an x-ray screening system (SLST). Signal detection analysis was used to obtain measures of hit rate (HR), false alarm rate (FAR), threat detection accuracy (A′), and response bias (B″D). Setting: Experimental laboratory study Participants: 24 healthy nonprofessional volunteers (13 women, mean age ± SD = 29.9 ± 6.5 years). Interventions: Subjects performed the SLST every 2 h during a 5-day period that included a 35 h period of wakefulness that extended to night work and then another day work period after the night without sleep. Results: Threat detection accuracy A′ decreased significantly (P < 0.001) while FAR increased significantly (P < 0.001) during night work, while both A′ (P = 0.001) and HR decreased (P = 0.008) during day work following sleep loss. There were prominent time-on-task effects on response bias B″D (P = 0.002) and response latency (P = 0.004), but accuracy A′ was unaffected. Both HR and FAR increased significantly with increasing study duration (both P < 0.001), while response latency decreased significantly (P < 0.001). Conclusions: This study provides the first systematic evidence that night work and sleep loss adversely affect the accuracy of detecting complex real world objects among high levels of background clutter. If the results can be replicated in professional screeners and real work environments, fatigue in luggage screening personnel may pose a threat for air traffic safety unless countermeasures for fatigue are deployed. Citation: Basner M; Rubinstein J

  2. Sleep after critical illness: Study of survivors of acute respiratory distress syndrome and systematic review of literature

    PubMed Central

    Dhooria, Sahajal; Sehgal, Inderpaul Singh; Agrawal, Anshu Kumar; Agarwal, Ritesh; Aggarwal, Ashutosh Nath; Behera, Digambar

    2016-01-01

    Background and Aims: This study aims to evaluate the sleep quality, architecture, sleep-related quality of life, and sleep-disordered breathing (SDB) in acute respiratory distress syndrome (ARDS) survivors early after discharge. Materials and Methods: In this prospective, observational study, consecutive patients with ARDS discharged from the Intensive Care Unit (ICU) underwent evaluation with Epworth sleepiness scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Functional Outcomes of Sleep Questionnaire (FOSQ), and overnight polysomnography. Patients having one or more of the following characteristics were classified as having abnormal sleep: ESS>10, PSQI>5, FOSQ <17.9, apnea–hypopnea index (AHI) ≥5, or AHI during rapid eye movement (REM) sleep ≥5. Results: Twenty patients (median interquartile range [IQR] age of 24 [22–28] years, 11 [55%] females) were included in the study. Acute febrile illness of unknown etiology with multi-organ dysfunction syndrome was the most common underlying etiology for ARDS. The median (IQR) PaO2/FiO2 ratio and APACHE II scores on admission were 176 (151–191.5) and 14 (14–16), respectively. The median (IQR) duration of stay in the ICU was 10 days (7.3–19.5). The overall sleep efficiency (median [IQR], 54% [32.3–65.4%]) was poor. None of the patients had ESS>10, seven (35%) had global PSQI>5 and one had FOSQ <17.9. Ten (50%) patients had at least one characteristic that suggested abnormal sleep (4 insomnia, 2 central sleep apnea, 1 obstructive sleep apnea, 1 REM-SDB, and 2 with a high PSQI, but no specific sleep abnormality). Conclusions: Sleep disturbances are common in ARDS survivors early after discharge from the ICU. PMID:27390455

  3. Chronotype, sleep loss, and diurnal pattern of salivary cortisol in a simulated daylong driving.

    PubMed

    Oginska, Halszka; Fafrowicz, Magdalena; Golonka, Krystyna; Marek, Tadeusz; Mojsa-Kaja, Justyna; Tucholska, Kinga

    2010-07-01

    distinct diurnal variation (F = 2.950, p < .019), whereas E types showed a flattened diurnal curve. Cortisol values did not correlate with subjective assessments of workload, arousal, or sleepiness at any time-of-day. Diurnal cortisol pattern parameters (i.e., morning level, mean level, and range of diurnal changes) showed significant positive correlations with sleep length before the experiment (r = .48, .54, and .53, respectively) and with sleep index (r = .63, .64, and .56, respectively). The conclusions of this study are: (i) E-oriented types showed lower salivary cortisol levels and a flattened diurnal curve in comparison with M types; (ii) sleep loss was associated with lower morning cortisol and mean diurnal level, whereas higher cortisol levels were observed in rested individuals. In the context of stress theory, it may be hypothesized that rested subjects perceived the driving task as a challenge, whereas those with reduced sleep were not challenged, but bored/exhausted with the experimental situation. PMID:20636209

  4. Sleep, its regulation and possible mechanisms of sleep disturbances.

    PubMed

    Porkka-Heiskanen, T; Zitting, K-M; Wigren, H-K

    2013-08-01

    The state of sleep consists of different phases that proceed in successive, tightly regulated order through the night forming a physiological program, which for each individual is different but stabile from one night to another. Failure to accomplish this program results in feeling of unrefreshing sleep and tiredness in the morning. The program core is constructed by genetic factors but regulated by circadian rhythm and duration and intensity of day time brain activity. Many environmental factors modulate sleep, including stress, health status and ingestion of vigilance-affecting nutrients or medicines (e.g. caffeine). Acute sleep loss results in compromised cognitive performance, memory deficits, depressive mood and involuntary sleep episodes during the day. Moreover, prolonged sleep curtailment has many adverse health effects, as evidenced by both epidemiological and experimental studies. These effects include increased risk for depression, type II diabetes, obesity and cardiovascular diseases. In addition to voluntary restriction of sleep, shift work, irregular working hours, jet lag and stress are important factors that induce curtailed or bad quality sleep and/or insomnia. This review covers the current theories on the function of normal sleep and describes current knowledge on the physiologic effects of sleep loss. It provides insights into the basic mechanisms of the regulation of wakefulness and sleep creating a theoretical background for understanding different disturbances of sleep. PMID:23746394

  5. Classifying performance impairment in response to sleep loss using pattern recognition algorithms on single session testing

    PubMed Central

    St. Hilaire, Melissa A.; Sullivan, Jason P.; Anderson, Clare; Cohen, Daniel A.; Barger, Laura K.; Lockley, Steven W.; Klerman, Elizabeth B.

    2012-01-01

    There is currently no “gold standard” marker of cognitive performance impairment resulting from sleep loss. We utilized pattern recognition algorithms to determine which features of data collected under controlled laboratory conditions could most reliably identify cognitive performance impairment in response to sleep loss using data from only one testing session, such as would occur in the “real world” or field conditions. A training set for testing the pattern recognition algorithms was developed using objective Psychomotor Vigilance Task (PVT) and subjective Karolinska Sleepiness Scale (KSS) data collected from laboratory studies during which subjects were sleep deprived for 26 – 52 hours. The algorithm was then tested in data from both laboratory and field experiments. The pattern recognition algorithm was able to identify performance impairment with a single testing session in individuals studied under laboratory conditions using PVT, KSS, length of time awake and time of day information with sensitivity and specificity as high as 82%. When this algorithm was tested on data collected under real-world conditions from individuals whose data were not in the training set, accuracy of predictions for individuals categorized with low performance impairment were as high as 98%. Predictions for medium and severe performance impairment were less accurate. We conclude that pattern recognition algorithms may be a promising method for identifying performance impairment in individuals using only current information about the individual’s behavior. Single testing features (e.g., number of PVT lapses) with high correlation with performance impairment in the laboratory setting may not be the best indicators of performance impairment under real-world conditions. Pattern recognition algorithms should be further tested for their ability to be used in conjunction with other assessments of sleepiness in real-world conditions to quantify performance impairment in

  6. Early sleep psychiatric intervention for acute insomnia: implications from a case of obsessive-compulsive disorder.

    PubMed

    Abe, Yuichiro; Nishimura, Go; Endo, Takuro

    2012-04-15

    Insomnia is a common problem among patients with obsessive-compulsive disorder (OCD), and patients suffering from acute insomnia with psychiatric comorbidity are more likely to develop chronic insomnia without appropriate intervention. Here we report a case of obsessive-compulsive disorder with acute insomnia, successfully treated with early sleep psychiatric non-pharmacological intervention. The augmentation of medication runs a risk of exacerbating daytime impairment. Clinicians usually prescribe medication, such as antidepressants and hypnotics without reflections for such complaints. However, the use of these sedative agents is often problematic, especially when patients have kept a good QOL activity in daily life. The rapid recovery from acute insomnia in this case suggests that the appropriate use of actigraphy is a favorable non-pharmacological intervention in acute insomnia. PMID:22505865

  7. Risk of Performance Decrements and Adverse Health Outcomes Resulting from Sleep Loss, Circadian Desynchronization, and Work Overload

    NASA Technical Reports Server (NTRS)

    Evans-Flynn, Erin; Gregory, Kevin; Arsintescu, Lucia; Whitmire, Alexandra; Leveton, Lauren B.; Vessey, William

    2015-01-01

    Sleep loss, circadian desynchronization, and work overload occur to some extent for ground and flight crews, prior to and during spaceflight missions. Ground evidence indicates that such risk factors may lead to performance decrements and adverse health outcomes, which could potentially compromise mission objectives. Efforts are needed to identify the environmental and mission conditions that interfere with sleep and circadian alignment, as well as individual differences in vulnerability and resiliency to sleep loss and circadian desynchronization. Specifically, this report highlights a collection of new evidence to better characterize the risk and reveals new gaps in this risk.

  8. Frontal predominance of a relative increase in sleep delta and theta EEG activity after sleep loss in humans

    NASA Technical Reports Server (NTRS)

    Cajochen, C.; Foy, R.; Dijk, D. J.; Czeisler, C. A. (Principal Investigator)

    1999-01-01

    The effect of sleep deprivation (40 h) on topographic and temporal aspects of electroencephalographic (EEG) activity during sleep was investigated by all night spectral analysis in six young volunteers. The sleep-deprivation-induced increase of EEG power density in the delta and theta frequencies (1-7 Hz) during nonREM sleep, assessed along the antero-posterior axis (midline: Fz, Cz, Pz, Oz), was significantly larger in the more frontal derivations (Fz, Cz) than in the more parietal derivations (Pz, Oz). This frequency-specific frontal predominance was already present in the first 30 min of recovery sleep, and dissipated in the course of the 8-h sleep episode. The data demonstrate that the enhancement of slow wave EEG activity during sleep following extended wakefulness is most pronounced in frontal cortical areas.

  9. Activation of the prostaglandin system in response to sleep loss in healthy humans: Potential mediator of increased spontaneous pain

    PubMed Central

    Haack, Monika; Lee, Erin; Cohen, Daniel; Mullington, Janet M.

    2009-01-01

    Insufficient duration of sleep is a highly prevalent behavioral pattern in society that has been shown to cause an increase in spontaneous pain and sensitivity to noxious stimuli. Prostaglandins (PG), in particular PGE2, are key mediators of inflammation and pain, and we investigated whether PGE2 is a potential mediator in sleep-loss induced changes in nociceptive processing. Twenty-four participants (7 females, age 35. 17.1yrs) stayed for 7 days in the Clinical Research Center. After two baseline days, participants were randomly assigned to either three days of 88 hours of total sleep deprivation (TSD, N=15) or 8 hours of sleep per night (N=9), followed by a night of recovery sleep. Participants rated the intensity of various pain-related symptoms every two hours across waking periods on computerized visual analog scales. PGE2 was measured in 24h-urine collections during baseline and third sleep deprivation day. Spontaneous pain, including headache, muscle pain, stomach pain, generalized body pain, and physical discomfort significantly increased by 5 to 14 units on a 100-unit scale during TSD, compared to the sleep condition. Urinary PGE2 metabolite significantly increased by about 30% in TSD over sleep condition. TSD-induced increase in spontaneous pain, in particular headache and muscle pain, was significantly correlated with increase in PGE2 metabolite. Activation of the PGE2 system appears to be a potential mediator of increased spontaneous pain in response to insufficient sleep. PMID:19560866

  10. Reduced Sleep Acutely Influences Sedentary Behavior and Mood But Not Total Energy Intake in Normal-Weight and Obese Women.

    PubMed

    Romney, Lora; Larson, Michael J; Clark, Tyler; Tucker, Larry A; Bailey, Bruce W; LeCheminant, James D

    2016-01-01

    Using a crossover design, 22 normal-weight and 22 obese women completed two free-living sleep conditions: (a) Normal Sleep: night of ~8 hr time in bed; and (b) Reduced Sleep: night of < 5 hr time in bed). Outcome measures were energy intake, physical activity and sedentary time, and mood. Sleep time was 7.7 ± 0.3 and 4.8 ± 0.2 hrs during the Normal Sleep and Reduced Sleep conditions, respectively (F = 1791.94; p < 0.0001). Energy intake did not differ between groups or as a function of sleep condition (F = 2.46; p = 0.1244). Sedentary time was ~ 30 min higher after the Reduced Sleep condition (F = 4.98; p = 0.0318); other physical activity outcomes were not different by condition (p > 0.05). Total mood score, depression, anger, vigor, fatigue, and confusion were worse after Reduced Sleep (p < 0.05). Reducing sleep acutely and negatively influenced sedentary time and mood in normal-weight and obese women. PMID:26485109

  11. Baseline Delta Sleep Ratio Predicts Acute Ketamine Mood Response in Major Depressive Disorder

    PubMed Central

    Duncan, Wallace C.; Selter, Jessica; Brutsche, Nancy; Sarasso, Simone; Zarate, Carlos A.

    2012-01-01

    Background Electroencephalographic (EEG) sleep slow wave activity (SWA; EEG power between 0.6–4 Hz) has been proposed as a marker of central synaptic plasticity. Decreased generation of sleep slow waves—a core feature of sleep in depression—indicates underlying plasticity changes in the disease. Various measures of SWA have previously been used to predict antidepressant treatment response. This study examined the relationship between baseline patterns of SWA in the first two NREM episodes and antidepressant response to an acute infusion of the N-methyl-D-aspartate (NMDA) antagonist ketamine. Methods Thirty patients (20M, 10F, 18–65) fulfilling DSM-IV criteria for treatment-resistant major depressive disorder (MDD) who had been drug-free for two weeks received a single open-label infusion of ketamine hydrochloride (.5 mg/kg) over 40 minutes. Depressive symptoms were assessed with the Montgomery-Asberg Depression Rating Scale (MADRS) before and after ketamine infusion. Sleep recordings were obtained the night before the infusion and were visually scored. SWA was computed for individual artifact-free NREM sleep epochs, and averaged for each NREM episode. Delta sleep ratio (DSR) was calculated as SWANREM1 / SWANREM2. Results A significant positive correlation was observed between baseline DSR and reduced MADRS scores from baseline to Day 1 (r=.414, p=.02). Limitations The sample size was relatively small (N=30) and all subjects had treatment-resistant MDD, which may limit the generalizability of the findings. Further studies are needed to replicate and extend this observation to other patient groups. Conclusions DSR may be a useful baseline predictor of ketamine response in individuals with treatment-resistant MDD. PMID:22871531

  12. Heritability of Performance Deficit Accumulation During Acute Sleep Deprivation in Twins

    PubMed Central

    Kuna, Samuel T.; Maislin, Greg; Pack, Frances M.; Staley, Bethany; Hachadoorian, Robert; Coccaro, Emil F.; Pack, Allan I.

    2012-01-01

    during acute sleep deprivation in twins. SLEEP 2012;35(9):1223-1233. PMID:22942500

  13. Epigenomics of Total Acute Sleep Deprivation in Relation to Genome-Wide DNA Methylation Profiles and RNA Expression

    PubMed Central

    Boström, Adrian E.; Mwinyi, Jessica; Schiöth, Helgi B.

    2016-01-01

    Abstract Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within-subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total sleep deprivation (TSD) on the genome-wide methylation profile in blood compared with that in normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations. In addition, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of 10 healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69 bp upstream of ING5, which has been shown to be differentially expressed after sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data. PMID:27310475

  14. Epigenomics of Total Acute Sleep Deprivation in Relation to Genome-Wide DNA Methylation Profiles and RNA Expression.

    PubMed

    Nilsson, Emil K; Boström, Adrian E; Mwinyi, Jessica; Schiöth, Helgi B

    2016-06-01

    Despite an established link between sleep deprivation and epigenetic processes in humans, it remains unclear to what extent sleep deprivation modulates DNA methylation. We performed a within-subject randomized blinded study with 16 healthy subjects to examine the effect of one night of total sleep deprivation (TSD) on the genome-wide methylation profile in blood compared with that in normal sleep. Genome-wide differences in methylation between both conditions were assessed by applying a paired regression model that corrected for monocyte subpopulations. In addition, the correlations between the methylation of genes detected to be modulated by TSD and gene expression were examined in a separate, publicly available cohort of 10 healthy male donors (E-GEOD-49065). Sleep deprivation significantly affected the DNA methylation profile both independently and in dependency of shifts in monocyte composition. Our study detected differential methylation of 269 probes. Notably, one CpG site was located 69 bp upstream of ING5, which has been shown to be differentially expressed after sleep deprivation. Gene set enrichment analysis detected the Notch and Wnt signaling pathways to be enriched among the differentially methylated genes. These results provide evidence that total acute sleep deprivation alters the methylation profile in healthy human subjects. This is, to our knowledge, the first study that systematically investigated the impact of total acute sleep deprivation on genome-wide DNA methylation profiles in blood and related the epigenomic findings to the expression data. PMID:27310475

  15. Risk of Performance Decrements and Adverse Health Outcomes Resulting from Sleep Loss, Circadian Desynchronization, and Work Overload

    NASA Technical Reports Server (NTRS)

    Flynn-Evans, Erin; Gregory, Kevin; Arsintescu, Lucia; Whitmire, Alexandra

    2016-01-01

    Sleep loss, circadian desynchronization, and work overload occur to some extent for ground and flight crews, prior to and during spaceflight missions. Ground evidence indicates that such risk factors may lead to performance decrements and adverse health outcomes, which could potentially compromise mission objectives. Efforts are needed to identify the environmental and mission conditions that interfere with sleep and circadian alignment, as well as individual differences in vulnerability and resiliency to sleep loss and circadian desynchronization. Specifically, this report highlights a collection of new evidence to better characterize the risk and reveals new gaps in this risk as follows: Sleep loss is apparent during spaceflight. Astronauts consistently average less sleep during spaceflight relative to on the ground. The causes of this sleep loss remain unknown, however ground-based evidence suggests that the sleep duration of astronauts is likely to lead to performance impairment and short and long-term health consequences. Further research is needed in this area in order to develop screening tools to assess individual astronaut sleep need in order to quantify the magnitude of sleep loss during spaceflight; current and planned efforts in BHP's research portfolio address this need. In addition, it is still unclear whether the conditions of spaceflight environment lead to sleep loss or whether other factors, such as work overload lead to the reduced sleep duration. Future data mining efforts and continued data collection on the ISS will help to further characterize factors contributing to sleep loss. Sleep inertia has not been evaluated during spaceflight. Ground-based studies confirm that it takes two to four hours to achieve optimal performance after waking from a sleep episode. Sleep inertia has been associated with increased accidents and reduced performance in operational environments. Sleep inertia poses considerable risk during spaceflight when emergency

  16. Sleep deprivation alters choice strategy without altering uncertainty or loss aversion preferences

    PubMed Central

    Mullette-Gillman, O'Dhaniel A.; Kurnianingsih, Yoanna A.; Liu, Jean C. J.

    2015-01-01

    Sleep deprivation alters decision making; however, it is unclear what specific cognitive processes are modified to drive altered choices. In this manuscript, we examined how one night of total sleep deprivation (TSD) alters economic decision making. We specifically examined changes in uncertainty preferences dissociably from changes in the strategy with which participants engage with presented choice information. With high test-retest reliability, we show that TSD does not alter uncertainty preferences or loss aversion. Rather, TSD alters the information the participants rely upon to make their choices. Utilizing a choice strategy metric which contrasts the influence of maximizing and satisficing information on choice behavior, we find that TSD alters the relative reliance on maximizing information and satisficing information, in the gains domain. This alteration is the result of participants both decreasing their reliance on cognitively-complex maximizing information and a concomitant increase in the use of readily-available satisficing information. TSD did not result in a decrease in overall information use in either domain. These results show that sleep deprivation alters decision making by altering the informational strategies that participants employ, without altering their preferences. PMID:26500479

  17. Obstructive Sleep Apnea after Weight Loss: A Clinical Trial Comparing Gastric Bypass and Intensive Lifestyle Intervention

    PubMed Central

    Fredheim, Jan Magnus; Rollheim, Jan; Sandbu, Rune; Hofsø, Dag; Omland, Torbjørn; Røislien, Jo; Hjelmesæth, Jøran

    2013-01-01

    Introduction: Few studies have compared the effect of surgical and conservative weight loss strategies on obstructive sleep apnea (OSA). We hypothesized that Roux-en-Y gastric bypass (RYGB) would be more effective than intensive lifestyle intervention (ILI) at reducing the prevalence and severity of OSA (apnea-hypopnea-index [AHI] ≥ 5 events/hour). Methods: A total of 133 morbidly obese subjects (93 females) were treated with either a 1-year ILI-program (n = 59) or RYGB (n = 74) and underwent repeated sleep recordings with a portable somnograph (Embletta). Results: Participants had a mean (SD) age of 44.7(10.8) years, BMI 45.1(5.7) kg/m2, and AHI 17.1(21.4) events/hour. Eighty-four patients (63%) had OSA. The average weight loss was 8% in the ILI-group and 30% in the RYGB-group (p < 0.001). The mean (95%CI) AHI reduced in both treatment groups, although significantly more in the RYGB-group (AHI change -6.0 [ILI] vs -13.1 [RYGB]), between group difference 7.2 (1.3, 13.0), p = 0.017. Twenty-nine RYGB-patients (66%) had remission of OSA, compared to 16 ILI-patients (40%), p = 0.028. At follow-up, after adjusting for age, gender, and baseline AHI, the RYGB-patients had significantly lower adjusted odds for OSA than the ILI-patients—OR (95% CI) 0.33 (0.14, 0.81), p = 0.015. After further adjustment for BMI change, treatment group difference was no longer statistically significant—OR (95% CI) 1.31 (0.32, 5.35), p = 0.709. Conclusion: Our study demonstrates that RYGB was more effective than ILI at reducing the prevalence and severity of OSA. However, our analysis also suggests that weight loss, rather than the surgical procedure per se, explains the beneficial effects. Citation: Fredheim JM; Rollheim J; Sandbu R; Hofsø D; Omland T; Røislien J; Hjelmesaeth J. Obstructive sleep apnea after weight loss: a clinical trial comparing gastric bypass and intensive lifestyle intervention. J Clin Sleep Med 2013;9(5):427-432. PMID:23674932

  18. NR2A at CA1 Synapses Is Obligatory for the Susceptibility of Hippocampal Plasticity to Sleep Loss

    PubMed Central

    Longordo, Fabio; Kopp, Caroline; Mishina, Masayoshi; Luján, Rafael

    2009-01-01

    A loss in the necessary amount of sleep alters expression of genes and proteins implicated in brain plasticity, but key proteins that render neuronal circuits sensitive to sleep disturbance are unknown. We show that mild (4–6 h) sleep deprivation (SD) selectively augmented the number of NR2A subunits of NMDA receptors on postsynaptic densities of adult mouse CA1 synapses. The greater synaptic NR2A content facilitated induction of CA3-CA1 long-term depression in the theta frequency stimulation range and augmented the synaptic modification threshold. NR2A-knock-out mice maintained behavioral response to SD, including compensatory increase in post-deprivation resting time, but hippocampal synaptic plasticity was insensitive to sleep loss. After SD, the balance between synaptically activated and slowly recruited NMDA receptor pools during temporal summation was disrupted. Together, these results indicate that NR2A is obligatory for the consequences of sleep loss on hippocampal synaptic plasticity. These findings could advance pharmacological strategies aiming to sustain hippocampal function during sleep restriction. PMID:19605640

  19. Clock and cycle limit starvation-induced sleep loss in Drosophila

    PubMed Central

    Keene, Alex C.; Duboué, Erik R.; McDonald, Daniel M.; Dus, Monica; Suh, Greg S.B.; Waddell, Scott; Blau, Justin

    2010-01-01

    Summary Neural systems controlling the vital functions of sleep and feeding in mammals are tightly inter-connected: sleep deprivation promotes feeding, while starvation suppresses sleep. Here we show that starvation in Drosophila potently suppresses sleep suggesting that these two homeostatically regulated behaviors are also integrated in flies. The sleep suppressing effect of starvation is independent of the mushroom bodies, a previously identified sleep locus in the fly brain, and therefore is regulated by distinct neural circuitry. The circadian clock genes Clock (Clk) and cycle (cyc) are critical for proper sleep suppression during starvation. However, the sleep suppression is independent of light cues and of circadian rhythms because starved period mutants sleep like wild type flies. By selectively targeting subpopulations of Clk-expressing neurons we localize the observed sleep phenotype to the dorsally located circadian neurons. These findings show that Clk and cyc act during starvation to modulate the conflict of whether flies sleep or search for food. PMID:20541409

  20. The Impact of Sleep Restriction and Simulated Physical Firefighting Work on Acute Inflammatory Stress Responses

    PubMed Central

    Wolkow, Alexander; Ferguson, Sally A.; Vincent, Grace E.; Larsen, Brianna; Aisbett, Brad; Main, Luana C.

    2015-01-01

    Objectives This study investigated the effect restricted sleep has on wildland firefighters’ acute cytokine levels during 3 days and 2 nights of simulated physical wildfire suppression work. Methods Firefighters completed multiple days of physical firefighting work separated by either an 8-h (Control condition; n = 18) or 4-h (Sleep restriction condition; n = 17) sleep opportunity each night. Blood samples were collected 4 times a day (i.e., 06:15, 11:30, 18:15, 21:30) from which plasma cytokine levels (IL-6, IL-8, IL-1β, TNF-α, IL-4, IL-10) were measured. Results The primary findings for cytokine levels revealed a fixed effect for condition that showed higher IL-8 levels among firefighters who received an 8-h sleep each night. An interaction effect demonstrated differing increases in IL-6 over successive days of work for the SR and CON conditions. Fixed effects for time indicated that IL-6 and IL-4 levels increased, while IL-1β, TNF-α and IL-8 levels decreased. There were no significant effects for IL-10 observed. Conclusion Findings demonstrate increased IL-8 levels among firefighters who received an 8-h sleep when compared to those who had a restricted 4-h sleep. Firefighters’ IL-6 levels increased in both conditions which may indicate that a 4-h sleep restriction duration and/or period (i.e., 2 nights) was not a significant enough stressor to affect this cytokine. Considering the immunomodulatory properties of IL-6 and IL-4 that inhibit pro-inflammatory cytokines, the rise in IL-6 and IL-4, independent of increases in IL-1β and TNF-α, could indicate a non-damaging response to the stress of simulated physical firefighting work. However, given the link between chronically elevated cytokine levels and several diseases, further research is needed to determine if firefighters’ IL-8 and IL-6 levels are elevated following repeated firefighting deployments across a fire season and over multiple fire seasons. PMID:26378783

  1. Is There a Relationship Between Obstructive Sleep Apnea (OSA) and Hearing Loss?

    PubMed

    Ekin, Selami; Turan, Mahfuz; Arısoy, Ahmet; Gunbatar, Hulya; Sunnetcioglu, Aysel; Asker, Selvi; Yıldız, Hanifi

    2016-01-01

    BACKGROUND Obstructive sleep apnea (OSA) is a common disorder with an estimated prevalence in the general population of 2-5%. Its main clinical features are loud snoring and breathing stoppage during sleep. Ischemia could be a consequence of noise-induced hearing loss because cochlear oxygen tension is reduced during and after noise exposure. In this study, we evaluated auditory function in patients affected by OSA and simple snoring. MATERIAL AND METHODS A total of 66 participants (male to female ratio: 40:26) were included in the study, of which 21 were in the control group, 18 were in the simple snoring group, and 27 were in the OSA patient group. Polysomnography and audiometric examination were performed in all participants. RESULTS The mean ages of the participants in the control, simple snoring, and OSA groups were 39.14±9.9, 37.28±8.2, and 41.56±8.99 years, respectively. There were no statistically significant differences among groups regarding age or sex; however, there were statistically significant differences among groups in body mass index, apnea-hypopnea index scores, mean saturation, and duration under 90% saturation. In addition, statistically significant differences were found between the patient group and the control and simple snoring groups concerning the mean saturation, duration under 90% saturation, and the extended high frequency of hearing. CONCLUSIONS These data show that snoring may cause hearing loss at extended high frequencies. PMID:27588548

  2. EEG and ocular correlates of circadian melatonin phase and human performance decrements during sleep loss

    NASA Technical Reports Server (NTRS)

    Cajochen, C.; Khalsa, S. B.; Wyatt, J. K.; Czeisler, C. A.; Dijk, D. J.

    1999-01-01

    The aim of this study was to quantify the associations between slow eye movements (SEMs), eye blink rate, waking electroencephalogram (EEG) power density, neurobehavioral performance, and the circadian rhythm of plasma melatonin in a cohort of 10 healthy men during up to 32 h of sustained wakefulness. The time course of neurobehavioral performance was characterized by fairly stable levels throughout the first 16 h of wakefulness followed by deterioration during the phase of melatonin secretion. This deterioration was closely associated with an increase in SEMs. Frontal low-frequency EEG activity (1-7 Hz) exhibited a prominent increase with time awake and little circadian modulation. EEG alpha activity exhibited circadian modulation. The dynamics of SEMs and EEG activity were phase locked to changes in neurobehavioral performance and lagged the plasma melatonin rhythm. The data indicate that frontal areas of the brain are more susceptible to sleep loss than occipital areas. Frontal EEG activity and ocular parameters may be used to monitor and predict changes in neurobehavioral performance associated with sleep loss and circadian misalignment.

  3. Benefits of napping and an extended duration of recovery sleep on alertness and immune cells after acute sleep restriction.

    PubMed

    Faraut, Brice; Boudjeltia, Karim Zouaoui; Dyzma, Michal; Rousseau, Alexandre; David, Elodie; Stenuit, Patricia; Franck, Thierry; Van Antwerpen, Pierre; Vanhaeverbeek, Michel; Kerkhofs, Myriam

    2011-01-01

    Understanding the interactions between sleep and the immune system may offer insight into why short sleep duration has been linked to negative health outcomes. We, therefore, investigated the effects of napping and extended recovery sleep after sleep restriction on the immune and inflammatory systems and sleepiness. After a baseline night, healthy young men slept for a 2-h night followed by either a standard 8-h recovery night (n=12), a 30-min nap (at 1 p.m.) in addition to an 8-h recovery night (n=10), or a 10-h extended recovery night (n=9). A control group slept 3 consecutive 8-h nights (n=9). Subjects underwent continuous electroencephalogram polysomnography and blood was sampled every day at 7 a.m. Leukocytes, inflammatory and atherogenesis biomarkers (high-sensitivity C-reactive protein, interleukin-8, myeloperoxidase, fibrinogen and apolipoproteins ApoB/ApoA), sleep patterns and sleepiness were investigated. All parameters remained unchanged in the control group. After sleep restriction, leukocyte and - among leukocyte subsets - neutrophil counts were increased, an effect that persisted after the 8-h recovery sleep, but, in subjects who had a nap or a 10-h recovery sleep, these values returned nearly to baseline. Inflammatory and atherogenesis biomarkers were unchanged except for higher myeloperoxidase levels after sleep restriction. The increased sleepiness after sleep restriction was reversed better in the nap and extended sleep recovery conditions. Saliva cortisol decreased immediately after the nap. Our results indicate that additional recovery sleep after sleep restriction provided by a midday nap prior to recovery sleep or a sleep extended night can improve alertness and return leukocyte counts to baseline values. PMID:20699115

  4. Sleep Deprivation and Recovery Sleep Prior to a Noxious Inflammatory Insult Influence Characteristics and Duration of Pain

    PubMed Central

    Vanini, Giancarlo

    2016-01-01

    Study Objectives: Insufficient sleep and chronic pain are public health epidemics. Sleep loss worsens pain and predicts the development of chronic pain. Whether previous, acute sleep loss and recovery sleep determine pain levels and duration remains poorly understood. This study tested whether acute sleep deprivation and recovery sleep prior to formalin injection alter post-injection pain levels and duration. Methods: Male Sprague-Dawley rats (n = 48) underwent sleep deprivation or ad libitum sleep for 9 hours. Thereafter, rats received a subcutaneous injection of formalin or saline into a hind paw. In the recovery sleep group, rats were allowed 24 h between sleep deprivation and the injection of formalin. Mechanical and thermal nociception were assessed using the von Frey test and Hargreaves' method. Nociceptive measures were performed at 1, 3, 7, 10, 14, 17 and 21 days post-injection. Results: Formalin caused bilateral mechanical hypersensitivity (allodynia) that persisted for up to 21 days post-injection. Sleep deprivation significantly enhanced bilateral allodynia. There was a synergistic interaction when sleep deprivation preceded a formalin injection. Rats allowed a recovery sleep period prior to formalin injection developed allodynia only in the injected limb, with higher mechanical thresholds (less allodynia) and a shorter recovery period. There were no persistent changes in thermal nociception. Conclusion: The data suggest that acute sleep loss preceding an inflammatory insult enhances pain and can contribute to chronic pain. The results encourage studies in a model of surgical pain to test whether enhancing sleep reduces pain levels and duration. Citation: Vanini G. Sleep deprivation and recovery sleep prior to a noxious inflammatory insult influence characteristics and duration of pain. SLEEP 2016;39(1):133–142. PMID:26237772

  5. Sleep deprivation suppresses aggression in Drosophila

    PubMed Central

    Kayser, Matthew S; Mainwaring, Benjamin; Yue, Zhifeng; Sehgal, Amita

    2015-01-01

    Sleep disturbances negatively impact numerous functions and have been linked to aggression and violence. However, a clear effect of sleep deprivation on aggressive behaviors remains unclear. We find that acute sleep deprivation profoundly suppresses aggressive behaviors in the fruit fly, while other social behaviors are unaffected. This suppression is recovered following post-deprivation sleep rebound, and occurs regardless of the approach to achieve sleep loss. Genetic and pharmacologic approaches suggest octopamine signaling transmits changes in aggression upon sleep deprivation, and reduced aggression places sleep-deprived flies at a competitive disadvantage for obtaining a reproductive partner. These findings demonstrate an interaction between two phylogenetically conserved behaviors, and suggest that previous sleep experiences strongly modulate aggression with consequences for reproductive fitness. DOI: http://dx.doi.org/10.7554/eLife.07643.001 PMID:26216041

  6. Sleep deprivation suppresses aggression in Drosophila.

    PubMed

    Kayser, Matthew S; Mainwaring, Benjamin; Yue, Zhifeng; Sehgal, Amita

    2015-01-01

    Sleep disturbances negatively impact numerous functions and have been linked to aggression and violence. However, a clear effect of sleep deprivation on aggressive behaviors remains unclear. We find that acute sleep deprivation profoundly suppresses aggressive behaviors in the fruit fly, while other social behaviors are unaffected. This suppression is recovered following post-deprivation sleep rebound, and occurs regardless of the approach to achieve sleep loss. Genetic and pharmacologic approaches suggest octopamine signaling transmits changes in aggression upon sleep deprivation, and reduced aggression places sleep-deprived flies at a competitive disadvantage for obtaining a reproductive partner. These findings demonstrate an interaction between two phylogenetically conserved behaviors, and suggest that previous sleep experiences strongly modulate aggression with consequences for reproductive fitness. PMID:26216041

  7. Acute changes in cardiovascular function during the onset period of daytime sleep: comparison to lying awake and standing.

    PubMed

    Zaregarizi, Mohammad; Edwards, Ben; George, Keith; Harrison, Yvonne; Jones, Helen; Atkinson, Greg

    2007-10-01

    The siesta habit is associated with a 37% reduction in coronary mortality, possibly because of reduced cardiovascular stress associated with daytime sleep. Whether the most important behavior is the daytime nap itself, a supine posture, or the expectancy of a nap is unknown. We present the first detailed description on healthy individuals of the acute changes in cardiovascular function during defined phases of the daytime sleep-onset period. These responses were compared with lying awake and standing. Following a night of restricted (4 h) sleep, nine healthy participants (aged 34 +/- 5 yr) were allowed to sleep at 1400 for up to 1 h. Polysomnography was used to calculate three phases of daytime sleep onset: phase 1, a baseline period of relaxed wakefulness before lights out; phase 2, the period between lights out and onset of stage 1 sleep; and phase 3, the period between onsets of stages 1 and 2 sleep. Differences (means +/- SD) in blood pressure, heart rate, and forearm cutaneous vascular conductance (CVC) between phases were analyzed. During the 9.7 +/- 13.8 min of phase 2, systolic and diastolic blood pressure was 4.7 +/- 4.5 and 3.6 +/- 2.8 mmHg lower than baseline, whereas CVC was 9.5 +/- 4.3% higher than baseline (P < 0.05). Subsequent changes in cardiovascular function during the sleep itself were trivial (P > 0.05). The above changes were not observed when subjects stood or laid supine in relaxed wakefulness for 1 h (P > 0.05). Our findings suggest that the period between lights out and sleep onset is associated with the largest acute reduction in blood pressure during one afternoon siesta. PMID:17641220

  8. Changes in sleep, food intake, and activity levels during acute painful episodes in children with sickle cell disease.

    PubMed

    Jacob, Eufemia; Miaskowski, Christine; Savedra, Marilyn; Beyer, Judith E; Treadwell, Marsha; Styles, Lori

    2006-02-01

    As part of a larger study that examined pain experience, pain management, and pain outcomes among children with sickle cell disease, functional status (sleep, food intake, and activity levels) was examined during hospitalization for acute painful episodes. Children were asked to rate the amount of pain they experienced as well as the amount of time they slept, the amount of food they ate, and the amount of activity they had everyday. Children reported high levels of pain, which showed only a small decrease throughout hospitalization, and had disrupted sleep and wake patterns, decreased food intake, and decreased activity levels. Nurses need to routinely monitor functional status during acute painful episodes so that strategies to promote adequate sleep, food intake, and activity may be incorporated to minimize long-term negative outcomes in children with sickle cell disease. PMID:16428011

  9. Effects of Sleep Deprivation on Brain Bioenergetics, Sleep, and Cognitive Performance in Cocaine-Dependent Individuals

    PubMed Central

    Trksak, George H.; Bracken, Bethany K.; Jensen, J. Eric; Plante, David T.; Penetar, David M.; Tartarini, Wendy L.; Maywalt, Melissa A.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.

    2013-01-01

    In cocaine-dependent individuals, sleep is disturbed during cocaine use and abstinence, highlighting the importance of examining the behavioral and homeostatic response to acute sleep loss in these individuals. The current study was designed to identify a differential effect of sleep deprivation on brain bioenergetics, cognitive performance, and sleep between cocaine-dependent and healthy control participants. 14 healthy control and 8 cocaine-dependent participants experienced consecutive nights of baseline, total sleep deprivation, and recovery sleep in the research laboratory. Participants underwent [31]P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, [31]P MRS scans revealed that cocaine-dependent participants exhibited elevated global brain β-NTP (direct measure of adenosine triphosphate), α-NTP, and total NTP levels compared to those of healthy controls. Cocaine-dependent participants performed worse on the Continuous Performance Task and Digit Symbol Substitution Task at baseline compared to healthy control participants, but sleep deprivation did not worsen cognitive performance in either group. Enhancements of brain ATP levels in cocaine dependent participants following recovery sleep may reflect a greater impact of sleep deprivation on sleep homeostasis, which may highlight the importance of monitoring sleep during abstinence and the potential influence of sleep loss in drug relapse. PMID:24250276

  10. Sleepless in Chicago: Tracking the Effects of Adolescent Sleep Loss During the Middle School Years

    ERIC Educational Resources Information Center

    Fredriksen, Katia; Rhodes, Jean; Reddy, Ranjini; Way, Niobe

    2004-01-01

    The influence of the sleep patterns of 2,259 students, aged 11 to 14 years, on trajectories of depressive symptoms, self-esteem, and grades was longitudinally examined using latent growth cross-domain models. Consistent with previous research, sleep decreased over time. Students who obtained less sleep in sixth grade exhibited lower initial…

  11. Electroencephalographic studies of sleep

    NASA Technical Reports Server (NTRS)

    Webb, W. B.; Agnew, H. W., Jr.

    1975-01-01

    Various experimental studies on sleep are described. The following areas are discussed: (1) effect of altered day length on sleep, (2) effect of a partial loss of sleep on subsequent nocturnal sleep; (3) effect of rigid control over sleep-wake-up times; (4) sleep and wakefulness in a time-free environment; (5) distribution of spindles during a full night of sleep; and (6) effect on sleep and performance of swiftly changing shifts of work.

  12. Acute visual loss in a patient with optic disc drusen.

    PubMed

    Tan, Deborah Kl; Tow, Sharon Lc

    2013-01-01

    Here we report a case of sudden, unilateral, painless visual loss in a middle-aged patient. A 45-year-old gentleman with no known past medical history presented with acute painless left visual impairment. Clinically, he was found to have a left optic neuropathy associated with a swollen and hyperemic left optic disc. The right optic disc was noted to be small and crowded, and both optic discs were noted to have irregular margins. Humphrey perimetry revealed a constricted visual field in the left eye. Fundus autofluorescence imaging revealed autofluorescence, and B-scan ultrasonography showed hyperreflectivity within both nerve heads. Blood investigations for underlying ischemic and inflammatory markers revealed evidence of hyperlipidemia but were otherwise normal. A diagnosis of left nonarteritic anterior ischemic optic neuropathy (NAAION) was made, with associated optic disc drusen and hyperlipidemia. NAAION typically occurs in eyes with small, structurally crowded optic discs. The coexistence of optic disc drusen and vascular risk factors may further augment the risk of developing NAAION. PMID:23658477

  13. Effects of sleep loss, time of day, and extended mental work on implicit and explicit learning of sequences

    NASA Technical Reports Server (NTRS)

    Heuer, H.; Spijkers, W.; Kiesswetter, E.; Schmidtke, V.

    1998-01-01

    Tacit knowledge is part of many professional skills and can be studied experimentally with implicit-learning paradigms. The authors explored the effects of 2 different stressors, loss of sleep and mental fatigue, on implicit learning in a serial-response time (RT) task. In the 1st experiment, 1 night of sleep deprivation was shown to impair implicit but not explicit sequence learning. In the 2nd experiment, no impairment of both types of sequence learning was found after 1.5 hr of mental work. Serial-RT performance, in contrast, suffered from both stressors. These findings suggest that sleep deprivation induces specific risks for automatic, skill-based behavior that are not present in consciously controlled performance.

  14. Single night video-game use leads to sleep loss and attention deficits in older adolescents.

    PubMed

    Wolfe, Jasper; Kar, Kellyann; Perry, Ashleigh; Reynolds, Chelsea; Gradisar, Michael; Short, Michelle A

    2014-10-01

    The present study investigated adolescent video-game use prior to bedtime and subsequent sleep, working memory and sustained attention performance. Participants were 21 healthy, good-sleeping adolescents (16 male) aged between 15 and 20 years (M = 17.6 years, SD = 1.8). Time spent video-gaming and subsequent sleep was measured across one night in the sleep laboratory. There were significant correlations between time spent video-gaming and sleep and between video-gaming and sustained attention, but not working memory. Sleep duration, in turn, had a significant negative association with sustained attention performance. Mediation analyses revealed that the relationship between video-gaming and sustained attention was fully mediated by sleep duration. These results indicate that video-gaming affected the ability to sustain attention only in as much as it affected sleep. In order to minimise negative consequences of video-game playing, video-games should be used in moderation, avoiding use close to the sleep period, to obviate detriments to sleep and performance. PMID:25118041

  15. Acute enhancement of non-rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride.

    PubMed

    Unno, Katsuya; Yamoto, Kurumi; Takeuchi, Kouhei; Kataoka, Aya; Ozaki, Tomoya; Mochizuki, Takatoshi; Honda, Kazuki; Miura, Nobuhiko; Ikeda, Masayuki

    2014-02-01

    Cadmium (Cd) is a heavy metal widely used or effused by industries. Serious environmental Cd pollution has been reported over the past two centuries, whereas the mechanisms underlying Cd-mediated diseases are not fully understood. Interestingly, an increase in reactive oxygen species (ROS) after Cd exposure has been shown. Our group has demonstrated that sleep is triggered via accumulation of ROS during neuronal activities, and we thus hypothesize the involvement of Cd poisoning in sleep-wake irregularities. In the present study, we analyzed the effects of Cd intake (1-100 ppm CdCl₂ in drinking water) on rats by monitoring sleep encephalograms and locomotor activities. The results demonstrated that 100 ppm CdCl₂ administration for 28 h was sufficient to increase non-rapid-eye-movement (non-REM) sleep and reduce locomotor activities during the night (the rat active phase). In contrast, free-running locomotor rhythms under constant dim red light and their re-entrainment to 12:12-h light/dark cycles were intact under chronic (1 month) 100 ppm CdCl₂ administrations, suggesting a limited influence on circadian clock movements at this dosage. The relative amount of oxidized glutathione increased in the brain after the 28-h 100 ppm CdCl₂ administrations similar to the levels in cultured astrocytes receiving H₂O₂ or CdCl₂ in culture medium. Therefore, we propose Cd-induced sleep as a consequence of oxidative stress. As oxidized glutathione is an endogenous sleep substance, we suggest that Cd rapidly induces sleepiness and influences activity performance by occupying intrinsic sleep-inducing mechanisms. In conclusion, we propose increased non-REM sleep during the active phase as an index of acute Cd exposure. PMID:23349044

  16. Sleepless in Chicago: tracking the effects of adolescent sleep loss during the middle school years.

    PubMed

    Fredriksen, Katia; Rhodes, Jean; Reddy, Ranjini; Way, Niobe

    2004-01-01

    The influence of the sleep patterns of 2,259 students, aged 11 to 14 years, on trajectories of depressive symptoms, self-esteem, and grades was longitudinally examined using latent growth cross-domain models. Consistent with previous research, sleep decreased over time. Students who obtained less sleep in sixth grade exhibited lower initial self-esteem and grades and higher initial levels of depressive symptoms. Similarly, students who obtained less sleep over time reported heightened levels of depressive symptoms and decreased self-esteem. Sex of the student played a strong role as a predictor of hours of sleep, self-esteem, and grades. This study underscores the role of sleep in predicting adolescents' psychosocial outcomes and highlights the importance of using idiographic methodologies in the study of developmental processes. PMID:15015676

  17. Gray Matter-Specific Changes in Brain Bioenergetics after Acute Sleep Deprivation: A 31P Magnetic Resonance Spectroscopy Study at 4 Tesla

    PubMed Central

    Plante, David T.; Trksak, George H.; Jensen, J. Eric; Penetar, David M.; Ravichandran, Caitlin; Riedner, Brady A.; Tartarini, Wendy L.; Dorsey, Cynthia M.; Renshaw, Perry F.; Lukas, Scott E.; Harper, David G.

    2014-01-01

    Study Objectives: A principal function of sleep may be restoration of brain energy metabolism caused by the energetic demands of wakefulness. Because energetic demands in the brain are greater in gray than white matter, this study used linear mixed-effects models to examine tissue-type specific changes in high-energy phosphates derived using 31P magnetic resonance spectroscopy (MRS) after sleep deprivation and recovery sleep. Design: Experimental laboratory study. Setting: Outpatient neuroimaging center at a private psychiatric hospital. Participants: A total of 32 MRS scans performed in eight healthy individuals (mean age 35 y; range 23-51 y). Interventions: Phosphocreatine (PCr) and β-nucleoside triphosphate (NTP) were measured using 31P MRS three dimensional-chemical shift imaging at high field (4 Tesla) after a baseline night of sleep, acute sleep deprivation, and 2 nights of recovery sleep. Novel linear mixed-effects models were constructed using spectral and tissue segmentation data to examine changes in bioenergetics in gray and white matter. Measurements and Results: PCr increased in gray matter after 2 nights of recovery sleep relative to sleep deprivation with no significant changes in white matter. Exploratory analyses also demonstrated that increases in PCr were associated with increases in electroencephalographic slow wave activity during recovery sleep. No significant changes in β-NTP were observed. Conclusions: These results demonstrate that sleep deprivation and subsequent recovery-induced changes in high-energy phosphates primarily occur in gray matter, and increases in phosphocreatine after recovery sleep may be related to sleep homeostasis. Citation: Plante DT, Trksak GH, Jensen JE, Penetar DM, Ravichandran C, Riedner BA, Tartarini WL, Dorsey CM, Renshaw PF, Lukas SE, Harper DG. Gray matter-specific changes in brain bioenergetics after acute sleep deprivation: a 31P magnetic resonance spectroscopy study at 4 Tesla. SLEEP 2014

  18. Acute sleep deprivation: the effects of the AMPAKINE compound CX717 on human cognitive performance, alertness and recovery sleep.

    PubMed

    Boyle, Julia; Stanley, Neil; James, Lynette M; Wright, Nicola; Johnsen, Sigurd; Arbon, Emma L; Dijk, Derk-Jan

    2012-08-01

    AMPA receptor modulation is a potential novel approach to enhance cognitive performance. CX717 is a positive allosteric modulator of the AMPA receptor that has shown efficacy in rodent and primate cognition models. CX717 (100 mg, 300 mg and 1000 mg) and placebo were studied in 16 healthy male volunteers (18-45 years) in a randomized, crossover study. Cognitive function, arousal and recovery sleep (by polysomnography) were assessed during the extended wakefulness protocol. Placebo condition was associated with significant decrements in cognition, particularly at the circadian nadir (between 03:00 and 05:00). Pre-specified primary and secondary analyses (general linear mixed modelling, GLMM) at each separate time point did not reveal consistent improvements in performance or objective alertness with any dose of CX717. Exploratory repeated measures analysis, a method used to take into account the influence of individual differences, demonstrated an improvement in attention-based task performance following the 1000 mg dose. Analysis of the recovery sleep showed that CX717 1000 mg significantly reduced stage 4 and slow-wave sleep (p ≤ 0.05) with evidence of reduced electroencephalogram (EEG) slow-wave and spindle activity. The study suggests that CX717 only at the 1000 mg dose may counteract effects of sleep deprivation on attention-based tasks and that it may interfere with subsequent recovery sleep. PMID:21940760

  19. Effects of Sleep Fragmentation on Sleep and Markers of Inflammation in Mice

    PubMed Central

    Trammell, Rita A; Verhulst, Steve; Toth, Linda A

    2014-01-01

    Many people in our society experience curtailment and disruption of sleep due to work responsibilities, care-giving, or life style choice. Delineating the health effect of acute and chronic disruptions in sleep is essential to raising awareness of and creating interventions to manage these prevalent concerns. To provide a platform for studying the health impact and underlying pathophysiologic mechanisms associated with inadequate sleep, we developed and characterized an approach to creating chronic disruption of sleep in laboratory mice. We used this method to evaluate how 3 durations of sleep fragmentation (SF) affect sleep recuperation and blood and lung analyte concentrations in male C57BL/6J mice. Mice housed in environmentally controlled chambers were exposed to automated SF for periods of 6, 12, or 24 h or for 12 h daily during the light (somnolent) phase for 4 sequential days. Sleep time, slow-wave amplitude, or bout lengths were significantly higher when uninterrupted sleep was permitted after each of the 3 SF durations. However, mice did not recover all of the lost slow-wave sleep during the subsequent 12- to 24-h period and maintained a net loss of sleep. Light-phase SF was associated with significant changes in serum and lung levels of some inflammatory substances, but these changes were not consistent or sustained. The data indicate that acute light-phase SF can result in a sustained sleep debt in mice and may disrupt the inflammatory steady-state in serum and lung. PMID:24512957

  20. Effects of Exercise and Weight Loss in Older Adults with Obstructive Sleep Apnea

    PubMed Central

    Dobrosielski, Devon A.; Patil, Susheel; Schwartz, Alan R.; Bandeen-Roche, Karen; Stewart, Kerry J.

    2014-01-01

    Purpose Obstructive sleep apnea (OSA) is prevalent among older individuals and is linked to increased cardiovascular disease morbidity. This study examined the change in OSA severity following exercise training and dietary induced weight loss in older adults and the association between the changes in OSA severity, body composition and aerobic capacity with arterial distensibility. Methods Obese adults (n=25) with OSA, aged 60 years or older, were instructed to participate in supervised exercise (3 days/week) and follow a calorie-restricted diet. Baseline assessments of OSA parameters, body weight and composition, aerobic capacity and arterial distensibility were repeated at 12 weeks. Results Nineteen participants completed the intervention. At 12 weeks, there were reductions in body weight (−9%) and percentage total body fat (−5%) and trunk fat (−8%), while aerobic capacity improved by 20% (all p’s<0.01). The apnea-hypopnea index (AHI) decreased by 10 events per hour (p<0.01) and nocturnal SaO2 (mean SaO2) improved from 94.9% at baseline to 95.2% post intervention (p=0.01). Arterial distensibility for the group was not different from baseline (p=0.99), yet individual changes in distensibility were associated with the change in nocturnal desaturations (r=−0.49, p=0.03), but not with the change in body weight, AHI or aerobic capacity. Conclusion The severity of OSA was reduced following an exercise and weight loss program among older adults, suggesting that this lifestyle approach may be an effective first line non-surgical and non-pharmacological treatment for older patients with OSA. PMID:24870569

  1. Sleep disorders and acute nocturnal delirium in the elderly: a comorbidity not to be overlooked.

    PubMed

    Terzaghi, Michele; Sartori, Ivana; Rustioni, Valter; Manni, Raffaele

    2014-04-01

    Delirium is a disturbance of consciousness and cognition that results in a confusional state. It tends to fluctuate in intensity and is often observed in older patients. Sleep is a window of vulnerability for the occurrence of delirium and sleep disorders can play a role in its appearance. In particular, delirious episodes have been associated with obstructive sleep apnoea syndrome, which is reported to be frequent in the elderly. Hereby, we present a case-report documenting the sudden onset of a confusional state triggered by obstructive sleep apnoea-induced arousal, together with a review of the literature on the topic. We emphasise that, among the many pathogenic factors implicated in delirium, it is worth considering the possible link between nocturnal delirium and the occurrence of impaired arousals. Indeed, the complex confusional manifestations of delirium could be due, in part, to persistence of dysfunctional sleep activity resulting in an inability to sustain full arousal during behavioural wakefulness. Arousals can be triggered by sleep disturbances or other medical conditions. Clinicians should be aware that older patients may present disordered sleep patterns, and make investigation of sleep patterns and disorders potentially affecting sleep continuity a key part of their clinical workup, especially in the presence of cognitive comorbidities. Correct diagnosis and optimal treatment of sleep disorders and disrupted sleep can have a significant impact in the elderly, improving sleep quality and reducing the occurrence of abnormal sleep-related behaviours. PMID:24636782

  2. Nonapnea Sleep Disorders and the Risk of Acute Kidney Injury: A Nationwide Population-Based Study.

    PubMed

    Lin, Hugo You-Hsien; Chang, Kai-Ting; Chang, Yu-Han; Lu, Tzongshi; Liang, Chan-Jung; Wang, Dean-Chuan; Tsai, Jui-Hsiu; Hsu, Chung-Yao; Hung, Chi-Chih; Kuo, Mei-Chuan; Lin, Chang-Shen; Hwang, Shang-Jyh

    2016-03-01

    Nonapnea sleep disorders (NASDs) and associated problems, which are highly prevalent in patients with kidney diseases, are associated with unfavorable medical sequelae. Nonetheless, whether NASDs are associated with acute kidney injury (AKI) development has not been thoroughly analyzed. We examined the association between NASD and AKI. We conducted a population-based study by using 1,000,000 representative data from the Taiwan National Health Insurance Research Database for the period from January 1, 2000, to December 31, 2010. We studied the incidence and risk of AKI in 9178 newly diagnosed NASD patients compared with 27,534 people without NASD matched according to age, sex, index year, urbanization level, region of residence, and monthly income at a 1:3 ratio. The NASD cohort had an adjusted hazard ratio (hazard ratio [HR]; 95% confidence interval [CI] = 1.15-2.63) of subsequent AKI 1.74-fold higher than that of the control cohort. Older age and type 2 diabetes mellitus were significantly associated with an increased risk of AKI (P < 0.05). Among different types of NASDs, patients with insomnia had a 120% increased risk of developing AKI (95% CI = 1.38-3.51; P = 0.001), whereas patients with other sleep disorders had a 127% increased risk of subsequent AKI (95% CI = 1.07-4.80; P = 0.033). Men with NASDs were at a high risk of AKI (P < 0.05). This nationwide population-based cohort study provides evidence that patients with NASDs are at higher risk of developing AKI than people without NASDs. PMID:26986132

  3. Loss of Melanopsin Photoreception and Antagonism of the Histamine H3 Receptor by Ciproxifan Inhibit Light-Induced Sleep in Mice.

    PubMed

    Muindi, Fanuel; Colas, Damien; Ikeme, Jesse; Ruby, Norman F; Heller, H Craig

    2015-01-01

    Light has direct effects on sleep and wakefulness causing arousal in diurnal animals and sleep in nocturnal animals. In the present study, we assessed the modulation of light-induced sleep by melanopsin and the histaminergic system by exposing mice to millisecond light flashes and continuous light respectively. First, we show that the induction of sleep by millisecond light flashes is dose dependent as a function of light flash number. We found that exposure to 60 flashes of light occurring once every 60 seconds for 1-h (120-ms of total light over an hour) induced a similar amount of sleep as a continuous bright light pulse. Secondly, the induction of sleep by millisecond light flashes was attenuated in the absence of melanopsin when animals were presented with flashes occurring every 60 seconds over a 3-h period beginning at ZT13. Lastly, the acute administration of a histamine H3 autoreceptor antagonist, ciproxifan, blocked the induction of sleep by a 1-h continuous light pulse during the dark period. Ciproxifan caused a decrease in NREMS delta power and an increase in theta activity during both sleep and wake periods respectively. The data suggest that some form of temporal integration occurs in response to millisecond light flashes, and that this process requires melanopsin photoreception. Furthermore, the pharmacological data suggest that the increase of histaminergic neurotransmission is sufficient to attenuate the light-induced sleep response during the dark period. PMID:26083020

  4. Long-Term Effect of Weight Loss on Obstructive Sleep Apnea Severity in Obese Patients with Type 2 Diabetes

    PubMed Central

    Kuna, Samuel T.; Reboussin, David M.; Borradaile, Kelley E.; Sanders, Mark H.; Millman, Richard P.; Zammit, Gary; Newman, Anne B.; Wadden, Thomas A.; Jakicic, John M.; Wing, Rena R.; Pi-Sunyer, F. Xavier; Foster, Gary D.

    2013-01-01

    Study Objectives: To examine whether the initial benefit of weight loss on obstructive sleep apnea (OSA) severity at 1 year is maintained at 4 years. Design: Randomized controlled trial with follow-up at 1, 2, and 4 years. Setting: 4 Look AHEAD clinical centers. Participants: Two hundred sixty-four obese adults with type 2 diabetes and OSA. Interventions: Intensive lifestyle intervention with a behavioral weight loss program or diabetes support and education. Measurements: Change in apnea-hypopnea index on polysomnogram. Results: The intensive lifestyle intervention group's mean weight loss was 10.7 ± 0.7 (standard error), 7.4 ± 0.7, and 5.2 ± 0.7 kg at 1, 2, and 4 years respectively, compared to a less than 1-kg weight loss for the control group at each time (P < 0.001). Apnea-hypopnea index difference between groups was 9.7 ± 2.0, 8.0 ± 2.0, and 7.7 ± 2.3 events/h at 1, 2 and 4 years respectively (P < 0.001). Change in apnea-hypopnea index over time was related to the amount of weight loss (P < 0.0001) and intervention, independent of weight loss (P = 0.001). Remission of OSA at 4 years was 5 times more common with intensive lifestyle intervention (20.7%) than diabetes support and education (3.6%). Conclusions: Among obese adults with type 2 diabetes and OSA, intensive lifestyle intervention produced greater reductions in weight and apnea-hypopnea index over a 4 year period than did diabetes support and education. Beneficial effects of intensive lifestyle intervention on apneahypopnea index at 1 year persisted at 4 years, despite an almost 50% weight regain. Effect of intensive lifestyle intervention on apnea-hypopnea index was largely, but not entirely, due to weight loss. Citation: Kuna ST; Reboussin DM; Borradaile KE; Sanders MH; Millman RP; Zammit G; Newman AB; Wadden TA; Jakicic JM; Wing RR; Pi-Sunyer FX; Foster GD; Sleep AHEAD Research Group. Long-term effect of weight loss on obstructive sleep apnea severity in obese patients with type 2 diabetes

  5. Do we really need to panic in all acute vision loss in ICU? Acute angle-closure glaucoma.

    PubMed

    Akal, Ali; Kucuk, Ahmet; Yalcin, Funda; Yalcin, Saban

    2014-08-01

    Acute angle closure glaucoma is a sight-threatening situation characterized by a sudden and marked rise in intraocular pressure (IOP) due to obstruction of aqueous humour outflow. Many local (ocular drops, nasal and nebulized agents) and systemic drugs (e.g. atropine, adrenaline, ephedrine, some psychoactive and antiepileptic drugs) that are widely used in intensive care units have the potential to precipitate such an acute attack. In this case report, we describe progressive visual loss due to acute angle-closure glaucoma (AACG) in a 59 year old female patient followed in the ICU due to a massive pulmonary embolism. PMID:25252529

  6. The effect of an acute sleep hygiene strategy following a late-night soccer match on recovery of players.

    PubMed

    Fullagar, Hugh; Skorski, Sabrina; Duffield, Rob; Meyer, Tim

    2016-01-01

    Elite soccer players are at risk of reduced recovery following periods of sleep disruption, particularly following late-night matches. It remains unknown whether improving sleep quality or quantity in such scenarios can improve post-match recovery. Therefore, the aim of this study was to investigate the effect of an acute sleep hygiene strategy (SHS) on physical and perceptual recovery of players following a late-night soccer match. In a randomised cross-over design, two highly-trained amateur teams (20 players) played two late-night (20:45) friendly matches against each other seven days apart. Players completed an SHS after the match or proceeded with their normal post-game routine (NSHS). Over the ensuing 48 h, objective sleep parameters (sleep duration, onset latency, efficiency, wake episodes), countermovement jump (CMJ; height, force production), YoYo Intermittent Recovery test (YYIR2; distance, maximum heart rate, lactate), venous blood (creatine kinase, urea and c-reactive protein) and perceived recovery and stress markers were collected. Sleep duration was significantly greater in SHS compared to NSHS on match night (P = 0.002, d = 1.50), with NSHS significantly less than baseline (P < 0.001, d = 1.95). Significant greater wake episodes occurred on match night for SHS (P = 0.04, d = 1.01), without significant differences between- or within-conditions for sleep onset latency (P = 0.12), efficiency (P = 0.39) or wake episode duration (P = 0.07). No significant differences were observed between conditions for any physical performance or venous blood marker (all P > 0.05); although maximum heart rate during the YYIR2 was significantly higher in NSHS than SHS at 36 h post-match (P = 0.01; d = 0.81). There were no significant differences between conditions for perceptual "overall recovery" (P = 0.47) or "overall stress" (P = 0.17). Overall, an acute SHS improved sleep quantity following a late-night soccer match; albeit without any improvement in physical

  7. Correlates and Escitalopram Treatment Effects on Sleep Disturbance in Patients with Acute Coronary Syndrome: K-DEPACS and EsDEPACS

    PubMed Central

    Kim, Jae-Min; Stewart, Robert; Bae, Kyung-Yeol; Kang, Hee-Ju; Kim, Sung-Wan; Shin, Il-Seon; Hong, Young Joon; Ahn, Youngkeun; Jeong, Myung Ho; Yoon, Jin-Sang

    2015-01-01

    Study Objectives: To investigate the correlates of sleep disturbance and to assess escitalopram treatment effects of depression on sleep disturbance in patients with acute coronary syndrome (ACS). Design: A cross-sectional study in patients with ACS within 2 w post-ACS, and a 24-w double-blind controlled trial of escitalopram against placebo for patients with ACS who have comorbid depressive disorders. Setting: A university hospital in South Korea. Participants: There were 1,152 patients with ACS who were consecutively recruited. Of 446 patients with comorbid depressive disorders, 300 were randomized to the trial. Measurements and Results: Sleep disturbance was evaluated by the Leeds Sleep Evaluation Questionnaire. Demographic and clinical characteristics were assessed, including cardiovascular risk factors, current cardiac status, and depressive symptoms. Depressive symptoms were most strongly and consistently associated with sleep disturbance. In addition, older age, female sex, hypertension, and more severe ACS status were associated with certain aspects of sleep disturbance. Escitalopram was significantly superior to placebo for improving sleep disturbance over the 24-w treatment period. These effects were substantially explained by improvement in depressive symptoms. Conclusions: Depression screening is indicated in patients with acute coronary syndrome with sleep disturbance. Successful treatment of depression has beneficial effects on sleep outcomes in these patients. Clinical Trials Information: ClinicalTrial.gov identifier for the 24-w drug trial, NCT00419471. Citation: Kim JM, Stewart R, Bae KY, Kang HJ, Kim SW, Shin IS, Hong YJ, Ahn Y, Jeong MH, Yoon JS. Correlates and escitalopram treatment effects on sleep disturbance in patients with acute coronary syndrome: K-DEPACS and EsDEPACS. SLEEP 2015;38(7):1105–1111. PMID:25581916

  8. Consequences of sleep deprivation.

    PubMed

    Orzeł-Gryglewska, Jolanta

    2010-01-01

    This paper presents the history of research and the results of recent studies on the effects of sleep deprivation in animals and humans. Humans can bear several days of continuous sleeplessness, experiencing deterioration in wellbeing and effectiveness; however, also a shorter reduction in the sleep time may lead to deteriorated functioning. Sleeplessness accounts for impaired perception, difficulties in keeping concentration, vision disturbances, slower reactions, as well as the appearance of microepisodes of sleep during wakefulness which lead to lower capabilities and efficiency of task performance and to increased number of errors. Sleep deprivation results in poor memorizing, schematic thinking, which yields wrong decisions, and emotional disturbances such as deteriorated interpersonal responses and increased aggressiveness. The symptoms are accompanied by brain tissue hypometabolism, particularly in the thalamus, prefrontal, frontal and occipital cortex and motor speech centres. Sleep deficiency intensifies muscle tonus and coexisting tremor, speech performance becomes monotonous and unclear, and sensitivity to pain is higher. Sleeplessness also relates to the changes in the immune response and the pattern of hormonal secretion, of the growth hormone in particular. The risk of obesity, diabetes and cardiovascular disease increases. The impairment of performance which is caused by 20-25 hours of sleeplessness is comparable to that after ethanol intoxication at the level of 0.10% blood alcohol concentration. The consequences of chronic sleep reduction or a shallow sleep repeated for several days tend to accumulate and resemble the effects of acute sleep deprivation lasting several dozen hours. At work, such effects hinder proper performance of many essential tasks and in extreme situations (machine operation or vehicle driving), sleep loss may be hazardous to the worker and his/her environment. PMID:20442067

  9. Circadian Rhythms, Sleep Deprivation, and Human Performance

    PubMed Central

    Goel, Namni; Basner, Mathias; Rao, Hengyi; Dinges, David F.

    2014-01-01

    Much of the current science on, and mathematical modeling of, dynamic changes in human performance within and between days is dominated by the two-process model of sleep–wake regulation, which posits a neurobiological drive for sleep that varies homeostatically (increasing as a saturating exponential during wakefulness and decreasing in a like manner during sleep), and a circadian process that neurobiologically modulates both the homeostatic drive for sleep and waking alertness and performance. Endogenous circadian rhythms in neurobehavioral functions, including physiological alertness and cognitive performance, have been demonstrated using special laboratory protocols that reveal the interaction of the biological clock with the sleep homeostatic drive. Individual differences in circadian rhythms and genetic and other components underlying such differences also influence waking neurobehavioral functions. Both acute total sleep deprivation and chronic sleep restriction increase homeostatic sleep drive and degrade waking neurobehavioral functions as reflected in sleepiness, attention, cognitive speed, and memory. Recent evidence indicating a high degree of stability in neurobehavioral responses to sleep loss suggests that these trait-like individual differences are phenotypic and likely involve genetic components, including circadian genes. Recent experiments have revealed both sleep homeostatic and circadian effects on brain metabolism and neural activation. Investigation of the neural and genetic mechanisms underlying the dynamically complex interaction between sleep homeostasis and circadian systems is beginning. A key goal of this work is to identify biomarkers that accurately predict human performance in situations in which the circadian and sleep homeostatic systems are perturbed. PMID:23899598

  10. D1 Receptor Activation in the Mushroom Bodies Rescues Sleep Loss Induced Learning Impairments in Drosophila

    PubMed Central

    Seugnet, Laurent; Suzuki, Yasuko; Vine, Lucy; Gottschalk, Laura; Shaw, Paul J

    2008-01-01

    Background Extended wakefulness disrupts acquisition of short term memories in mammals. However, the underlying molecular mechanisms triggered by extended waking and restored by sleep are unknown. Moreover, the neuronal circuits that depend on sleep for optimal learning remain unidentified. Results Learning was evaluated using Aversive Phototaxic Suppression (APS). In this task, flies learn to avoid light that is paired with an aversive stimulus (quinine /humidity). We demonstrate extensive homology in sleep deprivation induced learning impairment between flies and humans. Both 6 h and 12 h of sleep deprivation are sufficient to impair learning in Canton-S (Cs) flies. Moreover, learning is impaired at the end of the normal waking-day in direct correlation with time spent awake. Mechanistic studies indicate that this task requires intact mushroom bodies (MBs) and requires the Dopamine D1-like receptor (dDA1). Importantly, sleep deprivation induced learning impairments could be rescued by targeted gene expression of the dDA1 receptor to the MBs. Conclusion These data provide direct evidence that extended wakefulness disrupts learning in Drosophila. These results demonstrate that it is possible to prevent the effects of sleep deprivation by targeting a single neuronal structure and identify cellular and molecular targets adversely affected by extended waking in a genetically tractable model organism. PMID:18674913

  11. [Equilibrium function in patients with acute sensorineural hearing loss].

    PubMed

    Pal'chun, V T; Ganichkina, I Ia; Luchikhin, L A; Derevianko, S N

    2002-01-01

    Equilibrium function was investigated with computer-assisted stabilography (CS) in patients with acute neurosensory hypoacusis. This new diagnostic tool was employed in combination with extended vestibulometric and audiologic examinations. Correlations were found between stabilographic and vestibulometric findings. CS is recommended as a method of screening diagnosis in examination of patients with imbalanced equilibrium. PMID:12227024

  12. Long-Term Outcomes of Acute Low-Tone Hearing Loss

    PubMed Central

    Roh, Kyung Jin; Lee, Eun Jung; Park, Ah Young; Choi, Byeong Il

    2015-01-01

    Background and Objectives Although acute low-tone hearing loss has been associated with cochlear hydrops or early stage Meniere's disease, its prognosis in the short-term has been reported to be better than sudden hearing loss. However, recurrence of hearing loss and possible progression to Meniere's disease remain important concerns in the clinical setting. This study aims to investigate the long-term audiological outcomes of acute low-tone hearing loss. Subjects and Methods A retrospective review of patients presenting with a first attack of acute low-tone hearing loss was performed. Of the 77 patients, 33 were followed up for more than 3 months. Progression, recovery of hearing loss and recurrence of hearing loss were examined. Also, correlation between long-term outcomes and associated clinical factors were analyzed. Results Twenty-five patients (75.7%) had complete hearing recovery, five patients (15.1%) had partial recovery, two patients (6.0%) had no recovery, and one patient (3.0%) had progression of hearing loss 1 month after initial treatment. Thirty-three patients were followed up for more than 3 months (mean 22 months, range 3-79 months). Recurrences of acute low-tone hearing loss were observed in five patients (15.2%). All of the recurrences occurred during the first 12 months of follow-up. Long-term prognosis correlated with the initial therapy results (R2=0.693). Conclusions Recurrences of hearing loss were documented in five patients (15.2%), and all of these cases occurred within one year of the first attack. Audiological outcomes after initial therapy may predict the recurrence of acute low-tone hearing loss. PMID:26413572

  13. Ghrelin, Sleep Reduction and Evening Preference: Relationships to CLOCK 3111 T/C SNP and Weight Loss

    PubMed Central

    Garaulet, Marta; Sánchez-Moreno, Carmen; Smith, Caren E.; Lee, Yu-Chi; Nicolás, Francisco; Ordovás, Jose M.

    2011-01-01

    Background Circadian Locomotor Output Cycles Kaput (CLOCK), an essential element of the positive regulatory arm in the human biological clock, is involved in metabolic regulation. The aim was to investigate the behavioral (sleep duration, eating patterns and chronobiological characteristics) and hormonal (plasma ghrelin and leptin concentrations) factors which could explain the previously reported association between the CLOCK 3111T/C SNP and weight loss. Methodology/Principal Findings We recruited 1495 overweight/obese subjects (BMI: 25–40 kg/m2) of 20–65 y. who attended outpatient obesity clinics in Murcia, in southeastern Spain. We detected an association between the CLOCK 3111T/C SNP and weight loss, which was particularly evident after 12–14 weeks of treatment (P = 0.038). Specifically, carriers of the minor C allele were more resistant to weight loss than TT individuals (Mean±SEM) (8.71±0.59 kg vs 10.4±0.57 kg) C and TT respectively. In addition, our data show that minor C allele carriers had: 1. shorter sleep duration Mean ± SEM (7.0±0.05 vs 7.3±0.05) C and TT respectively (P = 0.039), 2. higher plasma ghrelin concentrations Mean ± SEM (pg/ml) (1108±49 vs 976±47)(P = 0.034); 3. delayed breakfast time; 4. evening preference and 5. less compliance with a Mediterranean Diet pattern, as compared with TT homozygotes. Conclusions/Significance Sleep reduction, changes in ghrelin values, alterations of eating behaviors and evening preference that characterized CLOCK 3111C carriers could be affecting weight loss. Our results support the hypothesis that the influence of the CLOCK gene may extend to a broad range of variables linked with human behaviors. PMID:21386998

  14. Sleep disruption and the sequelae associated with traumatic brain injury

    PubMed Central

    Lucke-Wold, Brandon P.; Smith, Kelly E.; Nguyen, Linda; Turner, Ryan C.; Logsdon, Aric F.; Jackson, Garrett J.; Huber, Jason D.; Rosen, Charles L.; Miller, Diane B.

    2016-01-01

    Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. PMID:25956251

  15. Sleep disruption and the sequelae associated with traumatic brain injury.

    PubMed

    Lucke-Wold, Brandon P; Smith, Kelly E; Nguyen, Linda; Turner, Ryan C; Logsdon, Aric F; Jackson, Garrett J; Huber, Jason D; Rosen, Charles L; Miller, Diane B

    2015-08-01

    Sleep disruption, which includes a loss of sleep as well as poor quality fragmented sleep, frequently follows traumatic brain injury (TBI) impacting a large number of patients each year in the United States. Fragmented and/or disrupted sleep can worsen neuropsychiatric, behavioral, and physical symptoms of TBI. Additionally, sleep disruption impairs recovery and can lead to cognitive decline. The most common sleep disruption following TBI is insomnia, which is difficulty staying asleep. The consequences of disrupted sleep following injury range from deranged metabolomics and blood brain barrier compromise to altered neuroplasticity and degeneration. There are several theories for why sleep is necessary (e.g., glymphatic clearance and metabolic regulation) and these may help explain how sleep disruption contributes to degeneration within the brain. Experimental data indicate disrupted sleep allows hyperphosphorylated tau and amyloid β plaques to accumulate. As sleep disruption may act as a cellular stressor, target areas warranting further scientific investigation include the increase in endoplasmic reticulum and oxidative stress following acute periods of sleep deprivation. Potential treatment options for restoring the normal sleep cycle include melatonin derivatives and cognitive behavioral therapy. PMID:25956251

  16. Circadian Disruption, Sleep Loss and Prostate Cancer Risk: A Systematic Review of Epidemiological Studies

    PubMed Central

    Sigurdardottir, Lara G.; Valdimarsdottir, Unnur A.; Fall, Katja; Rider, Jennifer R.; Lockley, Steven W.; Schernhammer, Eva S.; Mucci, Lorelei A.

    2012-01-01

    Disruption of the circadian system has been hypothesized to increase cancer risk, either due to direct disruption of the molecular machinery generating circadian rhythms or due to disruption of parameters controlled by the clock such as melatonin levels or sleep duration. This hypothesis has been studied in hormone-dependent cancers among women, but data are sparse regarding potential effects of circadian disruption on the risk of prostate cancer. This review systematically examines available data evaluating the effects of light at night, sleep patterns, and night shift work on prostate cancer risk. PMID:22564869

  17. Evaluating the Workload of On-Call Psychiatry Residents: Which Activities Are Associated with Sleep Loss?

    ERIC Educational Resources Information Center

    Cooke, Brian K.; Cooke, Erinn O.; Sharfstein, Steven S.

    2012-01-01

    Objective: The purpose of this study was to review the workload inventory of on-call psychiatry residents and to evaluate which activities were associated with reductions in on-call sleep. Method: A prospective cohort study was conducted, following 20 psychiatry residents at a 231-bed psychiatry hospital, from July 1, 2008 through June 30, 2009.…

  18. Acute exposure to evening blue-enriched light impacts on human sleep.

    PubMed

    Chellappa, Sarah L; Steiner, Roland; Oelhafen, Peter; Lang, Dieter; Götz, Thomas; Krebs, Julia; Cajochen, Christian

    2013-10-01

    Light in the short wavelength range (blue light: 446-483 nm) elicits direct effects on human melatonin secretion, alertness and cognitive performance via non-image-forming photoreceptors. However, the impact of blue-enriched polychromatic light on human sleep architecture and sleep electroencephalographic activity remains fairly unknown. In this study we investigated sleep structure and sleep electroencephalographic characteristics of 30 healthy young participants (16 men, 14 women; age range 20-31 years) following 2 h of evening light exposure to polychromatic light at 6500 K, 2500 K and 3000 K. Sleep structure across the first three non-rapid eye movement non-rapid eye movement - rapid eye movement sleep cycles did not differ significantly with respect to the light conditions. All-night non-rapid eye movement sleep electroencephalographic power density indicated that exposure to light at 6500 K resulted in a tendency for less frontal non-rapid eye movement electroencephalographic power density, compared to light at 2500 K and 3000 K. The dynamics of non-rapid eye movement electroencephalographic slow wave activity (2.0-4.0 Hz), a functional index of homeostatic sleep pressure, were such that slow wave activity was reduced significantly during the first sleep cycle after light at 6500 K compared to light at 2500 K and 3000 K, particularly in the frontal derivation. Our data suggest that exposure to blue-enriched polychromatic light at relatively low room light levels impacts upon homeostatic sleep regulation, as indexed by reduction in frontal slow wave activity during the first non-rapid eye movement episode. PMID:23509952

  19. Behavioral training promotes multiple adaptive processes following acute hearing loss

    PubMed Central

    Keating, Peter; Rosenior-Patten, Onayomi; Dahmen, Johannes C; Bell, Olivia; King, Andrew J

    2016-01-01

    The brain possesses a remarkable capacity to compensate for changes in inputs resulting from a range of sensory impairments. Developmental studies of sound localization have shown that adaptation to asymmetric hearing loss can be achieved either by reinterpreting altered spatial cues or by relying more on those cues that remain intact. Adaptation to monaural deprivation in adulthood is also possible, but appears to lack such flexibility. Here we show, however, that appropriate behavioral training enables monaurally-deprived adult humans to exploit both of these adaptive processes. Moreover, cortical recordings in ferrets reared with asymmetric hearing loss suggest that these forms of plasticity have distinct neural substrates. An ability to adapt to asymmetric hearing loss using multiple adaptive processes is therefore shared by different species and may persist throughout the lifespan. This highlights the fundamental flexibility of neural systems, and may also point toward novel therapeutic strategies for treating sensory disorders. DOI: http://dx.doi.org/10.7554/eLife.12264.001 PMID:27008181

  20. Acute unilateral vision loss with optic disc oedema in retinitis pigmentosa.

    PubMed

    Patil-Chhablani, Preeti; Tyagi, Mudit; Kekunnaya, Ramesh; Narayanan, Raja

    2015-01-01

    A 36-year-old woman presented with acute vision loss and was found to have disc oedema and retinitis pigmentosa (RP). She presented with a history of acute, painless vision loss in her left eye over a period of 10 days. Her best-corrected visual acuity was 20/50, N6 in the right eye (OD) and 20/160, N6 in the left eye (OS). She was found to have a swollen optic disc and the examination of her fundus showed changes suggestive of RP. The diagnosis of RP was confirmed by electroretinogram, and after ruling out demyelinating changes in the central nervous system and other possible infectious causes of papillitis, she was treated with intravenous steroids followed by a course of oral steroid therapy. Following treatment, her visual acuity improved to 20/60. Acute vision loss may occur in patients with RP and prompt steroid therapy may result in partial visual recovery. PMID:26240107

  1. Effects of a Two-Year Behavioral Weight Loss Intervention on Sleep and Mood in Obese Individuals Treated in Primary Care Practice

    PubMed Central

    Alfaris, Nasreen; Wadden, Thomas A.; Sarwer, David B; Diwald, Lisa; Volger, Sheri; Hong, Patricia; Baxely, Amber; Minnick, Alyssa M.; Vetter, Marion L.; Berkowitz, Robert I.; Chittams, Jesse

    2014-01-01

    Objective To examine the effect of weight loss on sleep duration, sleep quality, and mood in 390 obese men and women who received one of three behavioral weight loss intervention in the Practice-based Opportunities for Weight Reduction trial at the University of Pennsylvania (POWER-UP). Methods Sleep duration and quality were assessed at baseline and months 6 and 24 by the Pittsburgh Sleep Quality Index (PSQI) questionnaire and mood by the Patient Health Questionnaire-8 (PHQ-8). Changes in sleep and mood were examined according to treatment group and based on participants’ having lost ≥5% of initial weight vs <5%. Results There were few significant differences between treatment groups in changes in sleep or mood. At month 6, however, mean (±SD) min of sleep increased significantly more in participants who lost ≥5% vs <5% (21.6±7.2 vs 1.2±6.0 min, p=0.0031). PSQI total scores similarly improved (declined) more in those who lost ≥5% vs <5% (−1.2±0.2 vs −0.4±0.2, p < 0.001), as did PHQ scores (−2.5±0.4 vs −0.1±0.3, p <0.0001). At month 24, only the differences in mood remained statistically significant (p < 0.05). Conclusion Losing ≥ 5% of initial weight was associated with short-term improvements in sleep duration and sleep quality, as well as favorable short- and long-term changes in mood. PMID:25611944

  2. Bile loss in the acute intestinal radiation syndrome in rats

    SciTech Connect

    Geraci, J.P.; Dunston, S.G.; Jackson, K.L.; Mariano, M.S.; Holeski, C.; Eaton, D.L.

    1987-01-01

    The effects of bile duct ligation (BDL), choledochostomy, bile acid sequestering within the intestinal lumen by cholestyramine, and fluid and electrolyte replacement on survival time and development of diarrhea after whole-body exposure to doses of ionizing radiation that result in death from acute intestinal injury were studied. BDL significantly prolonged survival and delayed the onset of diarrhea after exposure to /sup 137/Cs gamma rays, fission neutrons, or cyclotron-produced neutrons in the range of doses that produce intestinal death or death from a combination of intestinal and hematopoietic injuries. Cannulation of the bile duct with exteriorized bile flow (choledochostomy) to protect the irradiated intestine from the mucolytic action of bile salts did not duplicate the effect of BDL in increasing survival time. Choledochostomy without fluid replacement eliminated the occurrence of diarrhea in 15.4 Gy irradiated rats. Diarrhea did occur in irradiated animals with choledochostomy if they received duodenal injections of fluid and electrolytes to replace the fluid lost as a result of bile drainage. Duodenal injection of fluid and electrolytes had no significant effect on survival time in irradiated rats. Injection of fluid and electrolytes into the peritoneal cavity of irradiated rats resulted in an increase in survival time that was comparable to that observed after BDL. Addition of antibiotics to the peritoneally injected fluid and electrolytes further increased survival time (up to 9 days). This survival time approached that seen in animals receiving the same radiation dose but which had the intestine exteriorized and shielded to minimize radiation injury to the intestine. Postmortem histological examinations of the irradiated small intestine showed mucosal regeneration in these long-term survivors receiving fluid and antibiotic therapy.

  3. Alcohol disrupts sleep homeostasis.

    PubMed

    Thakkar, Mahesh M; Sharma, Rishi; Sahota, Pradeep

    2015-06-01

    Alcohol is a potent somnogen and one of the most commonly used "over the counter" sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to unravel the mechanism of alcohol-induced sleep disruptions. We have conducted a series of experiments using two different species, rats and mice, as animal models. We performed microdialysis, immunohistochemical, pharmacological, sleep deprivation and lesion studies which suggest that the sleep-promoting effects of alcohol may be mediated via alcohol's action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Since binge alcohol consumption is a highly prevalent pattern of alcohol consumption and disrupts sleep, we examined the effects of binge drinking on sleep-wakefulness. Our results suggest that disrupted sleep homeostasis may be the primary cause of sleep disruption observed following binge drinking. Finally, we have also shown that sleep disruptions observed during acute withdrawal, are caused due to impaired

  4. Impact of sleep, screen time, depression, and stress on weight change in the intensive weight loss phase of the LIFE study

    PubMed Central

    Elder, Charles R; Gullion, Christina M; Funk, Kristine L; DeBar, Lynn L; Lindberg, Nangel M; Stevens, Victor J

    2011-01-01

    Background The LIFE study is a two-phase randomized clinical trial comparing two approaches to maintaining weight loss following guided weight loss. Phase I provided a nonrandomized intensive 6-month behavioral weight loss intervention to 472 obese (BMI 30–50) adult participants. Phase II is the randomized weight-loss maintenance portion of the study. This paper focuses on Phase I measures of sleep, screen time, depression, and stress. Methods The Phase I intervention consisted of 22 group sessions led over 26 weeks by behavioral counselors. Recommendations included reducing dietary intake by 500 calories per day, adopting the DASH dietary pattern, and increasing physical exercise to at least 180 minutes per week. Measures reported here are sleep time, insomnia, screen time, depression, and stress at entry and post weight loss intervention follow up. Results The mean weight loss for all participants over the intensive Phase I weight loss intervention was 6.3 kg (SD 7.1). Sixty percent (N=285) of participants lost at least 4.5 kg (10 lbs) and were randomized into Phase II. Participants (N=472) attended a mean of 73.1 % (SD 26.7) of sessions, completed 5.1 (SD 1.9) daily food records/week, and reported 195.1 (SD 123.1) minutes of exercise per week. Using logistic regression, sleep time (quadratic trend, p=.030) and lower stress (p=.024) at entry predicted success in the weight loss program, and lower baseline stress predicted greater weight loss during Phase I (p=.021). In addition, weight loss was significantly correlated with declines in stress (p=.048) and depression (p=.035). Conclusion Results suggest that clinicians and investigators might consider targeting sleep, depression, and stress as part of a behavioral weight loss intervention. PMID:21448129

  5. A pilot study: portable out-of-center sleep testing as an early sleep apnea screening tool in acute ischemic stroke

    PubMed Central

    Chernyshev, Oleg Y; McCarty, David E; Moul, Douglas E; Liendo, Cesar; Caldito, Gloria C; Munjampalli, Sai K; Kelley, Roger E; Chesson, Andrew L

    2015-01-01

    Introduction Prompt diagnosis of obstructive sleep apnea (OSA) after acute ischemic stroke (AIS) is critical for optimal clinical outcomes, but in-laboratory conventional polysomnograms (PSG) are not routinely practical. Though portable out-of-center type III cardiopulmonary sleep studies (out-of-center cardiopulmonary sleep testing [OCST]) are widely available, these studies have not been validated in patients who have recently suffered from AIS. We hypothesized that OCST in patients with AIS would yield similar results when compared to conventional PSG. Methods Patients with AIS had simultaneous type III OCST and PSG studies performed within 72 hours from symptom onset. The accuracy of OCST was compared to PSG using: chi-square tests, receiver operatory characteristic curves, Bland–Altman plot, paired Student’s t-test/Wilcoxon signed-rank test, and calculation of sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Results Twenty-one out of 23 subjects with AIS (age 61±9.4 years; 52% male; 58% African-American) successfully completed both studies (9% technical failure). Nearly all (95%) had Mallampati IV posterior oropharynx; the mean neck circumference was 16.8±1.6 in. and the mean body mass index (BMI) was 30±7 kg/m2. The apnea hypopnea index (AHI) provided by OCST was similar to that provided by PSG (19.8±18.0 vs 22.0±22.7, respectively; P=0.49). On identifying subjects by OCST with an AHI ≥5 on PSG, OCST had the following parameters: sensitivity 100%, specificity 85.7%, PPV 93%, and NPV 100%. On identifying subjects with an AHI ≥15 on PSG, OCST parameters were as follows: sensitivity 100%, specificity 83.3%, PPV 81.8%, and NPV 100%. Bland–Altman plotting showed an overall diagnostic agreement between OCST and PSG modalities for an AHI cutoff >5, despite fine-grained differences in estimated AHIs. Conclusion Compared with PSG, OCST provides similar diagnostic information when run simultaneously in AIS

  6. Tinospora cordifolia ameliorates anxiety-like behavior and improves cognitive functions in acute sleep deprived rats

    PubMed Central

    Mishra, Rachana; Manchanda, Shaffi; Gupta, Muskan; Kaur, Taranjeet; Saini, Vedangana; Sharma, Anuradha; Kaur, Gurcharan

    2016-01-01

    Sleep deprivation (SD) leads to the spectrum of mood disorders like anxiety, cognitive dysfunctions and motor coordination impairment in many individuals. However, there is no effective pharmacological remedy to negate the effects of SD. The current study examined whether 50% ethanolic extract of Tinospora cordifolia (TCE) can attenuate these negative effects of SD. Three groups of adult Wistar female rats - (1) vehicle treated-sleep undisturbed (VUD), (2) vehicle treated-sleep deprived (VSD) and (3) TCE treated-sleep deprived (TSD) animals were tested behaviorally for cognitive functions, anxiety and motor coordination. TSD animals showed improved behavioral response in EPM and NOR tests for anxiety and cognitive functions, respectively as compared to VSD animals. TCE pretreatment modulated the stress induced-expression of plasticity markers PSA-NCAM, NCAM and GAP-43 along with proteins involved in the maintenance of LTP i.e., CamKII-α and calcineurin (CaN) in hippocampus and PC regions of the brain. Interestingly, contrary to VSD animals, TSD animals showed downregulated expression of inflammatory markers such as CD11b/c, MHC-1 and cytokines along with inhibition of apoptotic markers. This data suggests that TCE alone or in combination with other memory enhancing agents may help in managing sleep deprivation associated stress and improving cognitive functions. PMID:27146164

  7. Tinospora cordifolia ameliorates anxiety-like behavior and improves cognitive functions in acute sleep deprived rats.

    PubMed

    Mishra, Rachana; Manchanda, Shaffi; Gupta, Muskan; Kaur, Taranjeet; Saini, Vedangana; Sharma, Anuradha; Kaur, Gurcharan

    2016-01-01

    Sleep deprivation (SD) leads to the spectrum of mood disorders like anxiety, cognitive dysfunctions and motor coordination impairment in many individuals. However, there is no effective pharmacological remedy to negate the effects of SD. The current study examined whether 50% ethanolic extract of Tinospora cordifolia (TCE) can attenuate these negative effects of SD. Three groups of adult Wistar female rats - (1) vehicle treated-sleep undisturbed (VUD), (2) vehicle treated-sleep deprived (VSD) and (3) TCE treated-sleep deprived (TSD) animals were tested behaviorally for cognitive functions, anxiety and motor coordination. TSD animals showed improved behavioral response in EPM and NOR tests for anxiety and cognitive functions, respectively as compared to VSD animals. TCE pretreatment modulated the stress induced-expression of plasticity markers PSA-NCAM, NCAM and GAP-43 along with proteins involved in the maintenance of LTP i.e., CamKII-α and calcineurin (CaN) in hippocampus and PC regions of the brain. Interestingly, contrary to VSD animals, TSD animals showed downregulated expression of inflammatory markers such as CD11b/c, MHC-1 and cytokines along with inhibition of apoptotic markers. This data suggests that TCE alone or in combination with other memory enhancing agents may help in managing sleep deprivation associated stress and improving cognitive functions. PMID:27146164

  8. Sleep Loss and Fatigue in Shift Work and Shift Work Disorder

    PubMed Central

    Åkerstedt, Torbjörn; Wright, Kenneth P.

    2010-01-01

    Shift work is highly prevalent in industrialized societies (>20%) but, when it includes night work, it has pronounced negative effects on sleep, subjective and physiological sleepiness, performance, accident risk, as well as on health outcomes such as cardiovascular disease and certain forms of cancer. The reason is the conflict between the day oriented circadian physiology and the requirement for work and sleep at the “wrong” biological time of day. Other factors that negatively impact work shift sleepiness and accident risk include long duration shifts greater than 12 hours and individual vulnerability for phase intolerance that may lead to a diagnosis of shift work disorder; i.e., those shift workers with the greatest sleepiness and performance impairment during the biological night and insomnia during the biological day. Whereas some countermeasures may be used to ameliorate the negative impact of shift work on nighttime sleepiness and daytime insomnia (combined countermeasures may be the best available), there seems at present to be no way to eliminate most of the negative effects of shift work on human physiology and cognition. PMID:20640236

  9. Duplication and loss of chromosome 21 in two children with Down syndrome and acute leukemia

    SciTech Connect

    Rogan, P.K.; Close, P.; Gannutz, L.

    1995-11-06

    Acute leukemia in Down syndrome (DS) is often associated with additional changes in the number of structure of chromosome 21. We present two DS patients whose leukemic karyotypes were associated with changes in chromosome 21 ploidy. Patient 1 developed acute lymphocytic leukemia (type L1); disomy for chromosome 21 was evident in all blast cells examined. Loss of the paternal chromosome in the leukemic clone produced maternal uniparental disomy with isodisomy over a 25-cM interval. The second patient had acute monoblastic leukemia (type M5) with tetrasomy 21 in all leukemic cells. DNA polymorphism analysis showed duplicate paternal chromosomes in the constitutional genotype. The maternal chromosome was subsequently duplicated in the leukemic clone. The distinct inheritance patterns of chromosome 21 in the blast cells of these patients would appear to indicate that leukemogenesis occurred by different genetic mechanisms in each individual. 57 refs., 2 figs., 3 tabs.

  10. Volume regulatory loss of Na, Cl, and K from rat brain during acute hyponatremia

    SciTech Connect

    Melton, J.E.; Patlak, C.S.; Pettigrew, K.D.; Cserr, H.F.

    1987-04-01

    This study quantitatively evaluates the contribution of tissue Na, Cl, and K loss to brain volume regulation during acute dilutional hyponatremia (DH) and examines the mechanism of Na loss. DH was produced in pentobarbital sodium-anesthetized rats by intraperitoneal infusion of distilled water and brain water and electrolytes analyzed 30 min, 1 h, 3 h, 4 h, or 6 h later. The rate of Na and Cl loss was greatest during the first 30 min of DH. Net loss of Na and Cl was maximal after 3 h of DH. K loss was slower, achieving significance after 3 h. Electrolyte loss was sufficient to account for observed brain volume regulation after three or more hours of DH. Measurements of /sup 22/Na influx and efflux across the blood brain barrier showed that barrier permeability to Na is unchanged during DH. Analysis of results using a two-compartment model of plasma-brain exchange suggests that loss of brain Na during DH does not result solely from a shift of electrolyte across the blood-brain barrier to plasma, and thus provides indirect evidence for an additional pathway for Na loss, presumably via cerebrospinal fluid.

  11. Sleep disturbances and inflammatory bowel disease.

    PubMed

    Ali, Tauseef; Orr, William C

    2014-11-01

    With an estimated 70 million Americans suffering, sleep disorders have become a global issue, and discovering their causes and consequences are the focus of many clinical research studies. Sleep is now also considered to be an important environmental and behavioral factor associated with the process of inflammation and the immune system. Increased sleepiness is considered part of the acute phase of response to tissue injury, and sleep loss activates inflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)-α. Clinical studies in many immune-mediated diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and ankylosing spondylitis, have revealed an association of sleep disturbances with disease activity. Recent research suggests that individuals with sleep abnormalities are also at greater risk of serious adverse health, economic consequences, and most importantly increased all-cause mortality. The importance of sleep in inflammatory bowel disease has recently gained attention with some published studies demonstrating the association of sleep disturbances with disease activity, subclinical inflammation, and risk of disease relapse. A comprehensive review of sleep physiology and its association with the immune system is provided here. Experimental and clinical studies exploring this relationship in inflammatory bowel disease are reviewed, and the clinical implications of this relationship and future directions for research are also discussed. PMID:25025716

  12. The Effect of Acute Sleep Deprivation and Fatigue in Cardiovascular Perfusion Students: A Mixed Methods Study

    PubMed Central

    Hodge, Ashley B.; Snyder, Alexandra C.; Fernandez, Adam L.; Boan, Andrea D.; Malek, Angela M.; Sistino, Joseph J.

    2012-01-01

    Abstract: Sleep deprivation as a result of long working hours has been associated with an increased risk of adverse events in healthcare professions but not in cardiovascular perfusion. The purpose of this study is to investigate the impact of sleep deprivation on cardiovascular perfusion students. Testing with highfidelity simulation after 24 hours of sleep deprivation allowed investigators to assess user competency and the effect of fatigue on performance. After informed consent, seven senior perfusion students were enrolled in the study (three declined to participate). The qualitative portion of the study included a focus group session, whereas the quantitative portion included administration of questionnaires, including the Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS), as well as clinical skills assessment using high-fidelity simulation. Subjects were assessed at three different intervals of sleep deprivation over a 24-hour period: baseline (6:00 am), 12 hours (6:00 pm), 16 hours (10:00 pm), and 24 hours (6:00 am) of wakefulness. During each scenario, normally monitored bypass parameters, including mean arterial pressure, activated clotting times, partial pressures of oxygen, partial pressures of carbon dioxide, and venous flow, were manipulated, and the subjects were required to return the parameters to normal levels. In addition, the scenario required calculation of the final protamine dose (using a dose–response curve) and detection of electrocardiography changes. Each task was varied at the different simulation sessions to decrease the effect of learning. Despite any lack of sleep, we hypothesized that, because of repetition, the times to complete the task would decrease at each session. We also hypothesized that the ESS and SSS scores would increase over time. We expected that the students would anticipate which tasks were being evaluated and would react more quickly. The average ESS scores progressively increased at each time

  13. Suppression of preoptic sleep-regulatory neuronal activity during corticotropin-releasing factor-induced sleep disturbance.

    PubMed

    Gvilia, Irma; Suntsova, Natalia; Kumar, Sunil; McGinty, Dennis; Szymusiak, Ronald

    2015-11-01

    Corticotropin releasing factor (CRF) is implicated in sleep and arousal regulation. Exogenous CRF causes sleep suppression that is associated with activation of at least two important arousal systems: pontine noradrenergic and hypothalamic orexin/hypocretin neurons. It is not known whether CRF also impacts sleep-promoting neuronal systems. We hypothesized that CRF-mediated changes in wake and sleep involve decreased activity of hypothalamic sleep-regulatory neurons localized in the preoptic area. To test this hypothesis, we examined the effects of intracerebroventricular administration of CRF on sleep-wake measures and c-Fos expression in GABAergic neurons in the median preoptic nucleus (MnPN) and ventrolateral preoptic area (VLPO) in different experimental conditions. Administration of CRF (0.1 nmol) during baseline rest phase led to delayed sleep onset and decreases in total amount and mean duration of non-rapid eye movement (NREM) sleep. Administration of CRF during acute sleep deprivation (SD) resulted in suppression of recovery sleep and decreased c-Fos expression in MnPN/VLPO GABAergic neurons. Compared with vehicle controls, intracerebroventricular CRF potentiated disturbances of both NREM and REM sleep in rats exposed to a species-specific psychological stressor, the dirty cage of a male conspecific. The number of MnPN/VLPO GABAergic neurons expressing c-Fos was reduced in the CRF-treated group of dirty cage-exposed rats. These findings confirm the involvement of CRF in wake-sleep cycle regulation and suggest that increased CRF signaling in the brain 1) negatively affects homeostatic responses to sleep loss, 2) exacerbates stress-induced disturbances of sleep, and 3) suppresses the activity of sleep-regulatory neurons of the MnPN and VLPO. PMID:26333784

  14. THE TIME COURSE OF ADENOSINE, NITRIC OXIDE (NO) AND INDUCIBLE NO SYNTHASE CHANGES IN THE BRAIN WITH SLEEP LOSS AND THEIR ROLE IN THE NREM SLEEP HOMEOSTATIC CASCADE

    PubMed Central

    Kalinchuk, Anna V.; McCarley, Robert W.; Porkka-Heiskanen, Tarja; Basheer, Radhika

    2011-01-01

    Both adenosine and nitric oxide (NO) are known for their role in sleep homeostasis, with the basal forebrain (BF) wakefulness center as an important site of action. Previously we reported a cascade of homeostatic events, wherein sleep deprivation (SD) induces the production of inducible nitric oxide synthase (iNOS)-dependent NO in BF, leading to enhanced release of extracellular adenosine. In turn, increased BF adenosine leads to enhanced sleep intensity, as measured by increased non-rapid eye movement (NREM) EEG delta activity. However, the presence and time course of similar events in cortex has not been studied, although a frontal cortical role for the increase in NREM recovery sleep EEG delta power is known. Accordingly, we performed simultaneous hourly microdialysis sample collection from BF and frontal cortex (FC) during 11h SD. We observed that both areas showed sequential increases in iNOS and NO, followed by increases in adenosine. BF increases began at 1h SD, while FC increases began at 5h SD. iNOS and Fos-double labeling indicated that iNOS induction occurred in BF and FC wake-active neurons. These data support the role of BF adenosine and NO in sleep homeostasis and indicate the temporal and spatial sequence of sleep homeostatic cascade for NO and adenosine. PMID:21062286

  15. [The specific clinical features of acute sensorineural loss of hearing associated with vertigo].

    PubMed

    Pal'chun, V T; Guseva, A L; Levina, Yu V; Chistov, S D

    2016-01-01

    The objective of the present study was to estimate the prevalence of vertigo and to determine the type of the lesion of the vestibular analyzer in the patients presenting with acute sensorineural loss of hearing (ASNLH). The secondary objective was to evaluate the possibility of the restoration of the auditory thresholds. The results of the examination and treatment of 94 patients suffering from ASNLH are presented. It was shown that the development of acute sensorineural loss of hearing was accompanied by unilateral peripheral vestibulopathy in 22.3% of the patients. In 5.3% of these cases, dizziness could be attributed to benign paroxysmal positional vertigo and canalolythias is of the posterior semicircular canal on the side of hearing impairment. It is concluded that the presence of the clinical signs of lesions of the vestibular analyzer and peripheral vestibular dysfunction in the form of latent spontaneous nystagmus without gaze fixation and/or asymmetric nystagmus with unilateral weakness in the caloric test is a negative prognostic factor for the restoration of the auditory thresholds in the patients presenting with acute sensorineural loss of hearing. PMID:26977560

  16. Weight loss and brown adipose tissue reduction in rat model of sleep apnea

    PubMed Central

    Martinez, Denis; Vasconcellos, Luiz FT; de Oliveira, Patricia G; Konrad, Signorá P

    2008-01-01

    Background - Obesity is related to obstructive sleep apnea-hypopnea syndrome (OSAHS), but its roles in OSAHS as cause or consequence are not fully clarified. Isocapnic intermittent hypoxia (IIH) is a model of OSAHS. We verified the effect of IIH on body weight and brown adipose tissue (BAT) of Wistar rats. Methods Nine-month-old male breeders Wistar rats of two groups were studied: 8 rats submitted to IIH and 5 control rats submitted to sham IIH. The rats were weighed at the baseline and at the end of three weeks, after being placed in the IIH apparatus seven days per week, eight hours a day, in the lights on period, simulating an apnea index of 30/hour. After experimental period, the animals were weighed and measured as well as the BAT, abdominal, perirenal, and epididymal fat, the heart, and the gastrocnemius muscle. Results Body weight of the hypoxia group decreased 17 ± 7 grams, significantly different from the variation observed in the control group (p = 0,001). The BAT was 15% lighter in the hypoxia group and reached marginally the alpha error probability (p = 0.054). Conclusion Our preliminary results justify a larger study for a longer time in order to confirm the effect of isocapnic intermittent hypoxia on body weight and BAT. PMID:18671859

  17. Prediction of Vigilant Attention and Cognitive Performance Using Self-Reported Alertness, Circadian Phase, Hours since Awakening, and Accumulated Sleep Loss

    PubMed Central

    Bermudez, Eduardo B.; Klerman, Elizabeth B.; Czeisler, Charles A.; Cohen, Daniel A.; Wyatt, James K.; Phillips, Andrew J. K.

    2016-01-01

    Sleep restriction causes impaired cognitive performance that can result in adverse consequences in many occupational settings. Individuals may rely on self-perceived alertness to decide if they are able to adequately perform a task. It is therefore important to determine the relationship between an individual’s self-assessed alertness and their objective performance, and how this relationship depends on circadian phase, hours since awakening, and cumulative lost hours of sleep. Healthy young adults (aged 18–34) completed an inpatient schedule that included forced desynchrony of sleep/wake and circadian rhythms with twelve 42.85-hour “days” and either a 1:2 (n = 8) or 1:3.3 (n = 9) ratio of sleep-opportunity:enforced-wakefulness. We investigated whether subjective alertness (visual analog scale), circadian phase (melatonin), hours since awakening, and cumulative sleep loss could predict objective performance on the Psychomotor Vigilance Task (PVT), an Addition/Calculation Test (ADD) and the Digit Symbol Substitution Test (DSST). Mathematical models that allowed nonlinear interactions between explanatory variables were evaluated using the Akaike Information Criterion (AIC). Subjective alertness was the single best predictor of PVT, ADD, and DSST performance. Subjective alertness alone, however, was not an accurate predictor of PVT performance. The best AIC scores for PVT and DSST were achieved when all explanatory variables were included in the model. The best AIC score for ADD was achieved with circadian phase and subjective alertness variables. We conclude that subjective alertness alone is a weak predictor of objective vigilant or cognitive performance. Predictions can, however, be improved by knowing an individual’s circadian phase, current wake duration, and cumulative sleep loss. PMID:27019198

  18. Prediction of Vigilant Attention and Cognitive Performance Using Self-Reported Alertness, Circadian Phase, Hours since Awakening, and Accumulated Sleep Loss.

    PubMed

    Bermudez, Eduardo B; Klerman, Elizabeth B; Czeisler, Charles A; Cohen, Daniel A; Wyatt, James K; Phillips, Andrew J K

    2016-01-01

    Sleep restriction causes impaired cognitive performance that can result in adverse consequences in many occupational settings. Individuals may rely on self-perceived alertness to decide if they are able to adequately perform a task. It is therefore important to determine the relationship between an individual's self-assessed alertness and their objective performance, and how this relationship depends on circadian phase, hours since awakening, and cumulative lost hours of sleep. Healthy young adults (aged 18-34) completed an inpatient schedule that included forced desynchrony of sleep/wake and circadian rhythms with twelve 42.85-hour "days" and either a 1:2 (n = 8) or 1:3.3 (n = 9) ratio of sleep-opportunity:enforced-wakefulness. We investigated whether subjective alertness (visual analog scale), circadian phase (melatonin), hours since awakening, and cumulative sleep loss could predict objective performance on the Psychomotor Vigilance Task (PVT), an Addition/Calculation Test (ADD) and the Digit Symbol Substitution Test (DSST). Mathematical models that allowed nonlinear interactions between explanatory variables were evaluated using the Akaike Information Criterion (AIC). Subjective alertness was the single best predictor of PVT, ADD, and DSST performance. Subjective alertness alone, however, was not an accurate predictor of PVT performance. The best AIC scores for PVT and DSST were achieved when all explanatory variables were included in the model. The best AIC score for ADD was achieved with circadian phase and subjective alertness variables. We conclude that subjective alertness alone is a weak predictor of objective vigilant or cognitive performance. Predictions can, however, be improved by knowing an individual's circadian phase, current wake duration, and cumulative sleep loss. PMID:27019198

  19. Alcohol disrupts sleep homeostasis

    PubMed Central

    Thakkar, Mahesh M.; Sharma, Rishi; Sahota, Pradeep

    2014-01-01

    Alcohol is a potent somnogen and one of the most commonly used “over the counter” sleep aids. In healthy non-alcoholics, acute alcohol decreases sleep latency, consolidates and increases the quality (delta power) and quantity of NREM sleep during the first half of the night. However, sleep is disrupted during the second half. Alcoholics, both during drinking periods and during abstinences, suffer from a multitude of sleep disruptions manifested by profound insomnia, excessive daytime sleepiness, and altered sleep architecture. Furthermore, subjective and objective indicators of sleep disturbances are predictors of relapse. Finally, within the USA, it is estimated that societal costs of alcohol-related sleep disorders exceeds $18 billion. Thus, although alcohol-associated sleep problems have significant economic and clinical consequences, very little is known about how and where alcohol acts to affect sleep. In this review, we have described our attempts to understand how and where alcohol acts to affect sleep. We have conducted a series of experiments using two different species, rats and mice, as animal models, and a combination of multi-disciplinary experimental methodologies to examine and understand anatomical and cellular substrates mediating the effects of acute and chronic alcohol exposure on sleep-wakefulness. The results of our studies suggest that the sleep-promoting effects of alcohol may be mediated via alcohol’s action on the mediators of sleep homeostasis: adenosine (AD) and the wake-promoting cholinergic neurons of the basal forebrain (BF). Alcohol, via its action on AD uptake, increases extracellular AD resulting in the inhibition of BF wake-promoting neurons. Lesions of the BF cholinergic neurons or blockade of AD A1 receptors results in attenuation of alcohol-induced sleep promotion, suggesting that AD and BF cholinergic neurons are critical for sleep-promoting effects of alcohol. Since binge alcohol consumption is a highly prevalent pattern

  20. translin Is Required for Metabolic Regulation of Sleep.

    PubMed

    Murakami, Kazuma; Yurgel, Maria E; Stahl, Bethany A; Masek, Pavel; Mehta, Aradhana; Heidker, Rebecca; Bollinger, Wesley; Gingras, Robert M; Kim, Young-Joon; Ja, William W; Suter, Beat; DiAngelo, Justin R; Keene, Alex C

    2016-04-01

    Dysregulation of sleep or feeding has enormous health consequences. In humans, acute sleep loss is associated with increased appetite and insulin insensitivity, while chronically sleep-deprived individuals are more likely to develop obesity, metabolic syndrome, type II diabetes, and cardiovascular disease. Conversely, metabolic state potently modulates sleep and circadian behavior; yet, the molecular basis for sleep-metabolism interactions remains poorly understood. Here, we describe the identification of translin (trsn), a highly conserved RNA/DNA binding protein, as essential for starvation-induced sleep suppression. Strikingly, trsn does not appear to regulate energy stores, free glucose levels, or feeding behavior suggesting the sleep phenotype of trsn mutant flies is not a consequence of general metabolic dysfunction or blunted response to starvation. While broadly expressed in all neurons, trsn is transcriptionally upregulated in the heads of flies in response to starvation. Spatially restricted rescue or targeted knockdown localizes trsn function to neurons that produce the tachykinin family neuropeptide Leucokinin. Manipulation of neural activity in Leucokinin neurons revealed these neurons to be required for starvation-induced sleep suppression. Taken together, these findings establish trsn as an essential integrator of sleep and metabolic state, with implications for understanding the neural mechanism underlying sleep disruption in response to environmental perturbation. PMID:27020744

  1. Insomnia in somatoform pain disorder: sleep laboratory studies on differences to controls and acute effects of trazodone, evaluated by the Somnolyzer 24 x 7 and the Siesta database.

    PubMed

    Saletu, Bernd; Prause, Wolfgang; Anderer, Peter; Mandl, Magdalena; Aigner, Martin; Mikova, Olya; Saletu-Zyhlarz, Gerda Maria

    2005-01-01

    Patients with chronic pain often suffer from sleep disturbances, specifically decreased deep sleep, and thus may get into a vicious circle which maintains their pain condition. Utilizing polysomnography and psychometry, objective and subjective sleep and awakening quality was investigated in 11 patients with nonorganic insomnia (F51.0) related to somatoform pain disorder (SPD; F45.4) as compared with age- and sex-matched healthy controls of the Siesta normative database. Patients demonstrated a markedly deteriorated Pittsburgh Sleep Quality Index, a decreased Quality of Life Index, slightly increased self-reported anxiety (Zung SAS) and depression scores (Zung SDS), as well as an increased Epworth Sleepiness Scale and International Restless Legs Syndrome Scale score. Subjective sleep and awakening quality was markedly reduced, while somatic complaints were increased. Polysomnographic evaluation by a recently developed automatic sleep classifier (Somnolyzer 24 x 7) based on the rules of Rechtschaffen and Kales demonstrated reduced slow-wave sleep (SWS), the target variable in the present study, a decreased stage shift index, increased SWS latency and stage 4 sleep (S4) latency and an increased frequency of shifts from S2 to wakefulness (W) in patients as compared with controls. Minimal oxygen saturation was found decreased, periodic leg movements (PLMs) were increased. In the morning, patients showed deteriorated well-being, drive, mood and wakefulness. There were no significant noopsychic or psychophysiological differences between patients and controls (except for a reduced numerical memory and a slightly increased morning diastolic blood pressure in patients). Subsequent evaluation of the acute effects of 100 mg of a controlled-release formulation of trazodone (Trittico retard) in the patients demonstrated an increase in the target variable SWS, accompanied by a reduction in the number of awakenings and stage shifts. It normalized the frequency of shifts from S2

  2. Developmental differences in EEG and sleep responses to acute ethanol administration and its withdrawal (hangover) in adolescent and adult Wistar rats.

    PubMed

    Ehlers, Cindy L; Desikan, Anita; Wills, Derek N

    2013-12-01

    Age-related differences in sensitivity to the acute effects of alcohol may play an important role in the increased risk for the development of alcoholism seen in teens that begin drinking at an early age. The present study evaluated the acute and protracted (hangover) effects of ethanol in adolescent (P33-P40) and adult (P100-P107) Wistar rats, using the cortical electroencephalogram (EEG). Six minutes of EEG was recorded during waking, 15 min after administration of 0, 1.5, or 3.0 g/kg ethanol, and for 3 h at 20 h post ethanol, during the rats' next sleep cycle. Significantly higher overall frontal and parietal cortical power was seen in a wide range of EEG frequencies in adolescent rats as compared to adult rats in their waking EEG. Acute administration of ethanol did not produce differences between adolescents and adults on behavioral measures of acute intoxication. However, it did produce a significantly less intense acute EEG response to ethanol in the theta frequencies in parietal cortex in the adolescents as compared to the adults. At 20 h following acute ethanol administration, during the rats' next sleep cycle, a decrease in slow-wave frequencies (1-4 Hz) was seen and the adolescent rats were found to display more reduction in the slow-wave frequencies than the adults did. The present study found that adolescent rats, as compared to adults, demonstrate low sensitivity to acute ethanol administration in the theta frequencies and more susceptibility to disruption of slow-wave sleep during hangover. These studies may lend support to the idea that these traits may contribute to increased risk for alcohol use disorders seen in adults who begin drinking in their early teenage years. PMID:24169089

  3. Course of hearing recovery according to frequency in patients with acute acoustic sensorineural hearing loss.

    PubMed

    Harada, Hirofumi; Ichikawa, Daisuke; Imamura, Akihide

    2008-01-01

    Through pure-tone audiometry, we studied the course of hearing recovery in 24 ears of 20 men (ages 18-48 years) who had acute acoustic sensorineural hearing loss (ASHL). All subjects were members of the Japanese Self-Defense Force. The hearing level in 5 ears returned to normal, the hearing level of 13 ears recovered but was not within the normal range, and the hearing level of 6 ears was unchanged. The time from noise exposure to presentation was longer in patients with unchanged hearing than in other patients. Recovery of hearing was poorest at 4,000 Hz, followed by 8,000 and 2,000 Hz. We concluded that hearing in patients with acute ASHL is likely to return to normal when the hearing level at 4,000 Hz recovers gradually; partial recovery of hearing is expected when the hearing level at 4,000 Hz reaches an early plateau. PMID:18616091

  4. Acute liver injury associated with a newer formulation of the herbal weight loss supplement Hydroxycut.

    PubMed

    Araujo, James L; Worman, Howard J

    2015-01-01

    Despite the widespread use of herbal and dietary supplements (HDS), serious cases of hepatotoxicity have been reported. The popular herbal weight loss supplement, Hydroxycut, has previously been implicated in acute liver injury. Since its introduction, Hydroxycut has undergone successive transformations in its formulation; yet, cases of liver injury have remained an ongoing problem. We report a case of a 41-year-old Hispanic man who developed acute hepatocellular liver injury with associated nausea, vomiting, jaundice, fatigue and asterixis attributed to the use of a newer formulation of Hydroxycut, SX-7 Clean Sensory. The patient required hospitalisation and improved with supportive therapy. Despite successive transformations in its formulation, potential liver injury appears to remain an ongoing problem with Hydroxycut. Our case illustrates the importance of obtaining a thorough medication history, including HDS, regardless of new or reformulated product marketing efforts. PMID:25948859

  5. Analysis of audio-vestibular assessment in acute low-tone hearing loss.

    PubMed

    Im, Gi Jung; Kim, Sung Kyun; Choi, June; Song, Jae Jun; Chae, Sung Won; Jung, Hak Hyun

    2016-07-01

    Conclusion This study demonstrated excellent hearing recovery following the combined treatment of diuretic and oral steroid, and electrocochleography (ECoG) was significantly higher than normal side. This study reports characteristics of acute low-tone hearing loss (ALHL) that show the greater low-tone hearing loss, the higher ECoG, and excellent recovery, even-though low-tone hearing loss is worse, which can be different compared with sudden deafness. Objective To analyze ALHL without vertigo, this study compared the ALHL group with all patients exhibiting low-tone hearing loss and ear fullness. Hearing changes and vestibular functions were analyzed. Materials and methods ALHL was defined as a mean hearing loss of ≥ 30 dB at 125, 250, and 500 Hz, and ≤ 20 dB at 2, 4, and 8 kHz. From 156 cases of low-tone hearing loss of more than 10 dB without vertigo, 31 met the ALHL criteria and were subjected to audio-vestibular assessments including PTA, ECoG, vestibular evoked myogenic potential (VEMP) testing, and caloric testing. Results In ALHL, low-tone hearing loss was 42.7 ± 9.5 dB, and 83.9% of ALHL significantly recovered by more than 10 dB. The ECoG in ALHL was 0.334 ± 0.11 (higher than 0.25 ± 0.08 on the normal side) and ECoG abnormality was 35.5% (the greater low-tone hearing loss, the higher ECoG value). PMID:26963446

  6. Prevention by Regular Exercise of Acute Sleep Deprivation-Induced Impairment of Late Phase LTP and Related Signaling Molecules in the Dentate Gyrus.

    PubMed

    Zagaar, Munder A; Dao, An T; Alhaider, Ibrahim A; Alkadhi, Karim A

    2016-07-01

    The dentate gyrus (DG) and CA1 regions of the hippocampus are intimately related physically and functionally, yet they react differently to insults. The purpose of this study was to determine the protective effects of regular treadmill exercise on late phase long-term potentiation (L-LTP) and its signaling cascade in the DG region of the hippocampus of rapid eye movement (REM) sleep-deprived rats. Adult Wistar rats ran on treadmills for 4 weeks then were acutely sleep deprived for 24 h using the modified multiple platform method. After sleep deprivation, the rats were anesthetized and L-LTP was induced in the DG region. Extracellular field potentials from the DG were recorded in vivo, and levels of L-LTP-related signaling proteins were assessed both before and after L-LTP expression using immunoblot analysis. Sleep deprivation reduced the basal levels of phosphorylated cAMP response element-binding protein (P-CREB) as well as other upstream modulators including calcium/calmodulin kinase IV (CaMKIV) and brain-derived neurotrophic factor (BDNF) in the DG of the hippocampus. Regular exercise prevented impairment of the basal levels of P-CREB and total CREB as well as those of CaMKIV in sleep-deprived animals. Furthermore, regular exercise prevented sleep deprivation-induced inhibition of L-LTP and post-L-LTP downregulation of P-CREB and BDNF levels in the DG. The current findings show that our exercise regimen prevents sleep deprivation-induced deficits in L-LTP as well as the basal and poststimulation levels of key signaling molecules. PMID:25902862

  7. Neurobiological Consequences of Sleep Deprivation

    PubMed Central

    Alkadhi, Karim; Zagaar, Munder; Alhaider, Ibrahim; Salim, Samina; Aleisa, Abdulaziz

    2013-01-01

    Although the physiological function of sleep is not completely understood, it is well documented that it contributes significantly to the process of learning and memory. Ample evidence suggests that adequate sleep is essential for fostering connections among neuronal networks for memory consolidation in the hippocampus. Sleep deprivation studies are extremely valuable in understanding why we sleep and what are the consequences of sleep loss. Experimental sleep deprivation in animals allows us to gain insight into the mechanism of sleep at levels not possible to study in human subjects. Many useful approaches have been utilized to evaluate the effect of sleep loss on cognitive function, each with relative advantages and disadvantages. In this review we discuss sleep and the detrimental effects of sleep deprivation mostly in experimental animals. The negative effects of sleep deprivation on various aspects of brain function including learning and memory, synaptic plasticity and the state of cognition-related signaling molecules are discussed. PMID:24179461

  8. The effect of ‘sleep high and train low’ on weight loss in overweight Chinese adolescents: study protocol for a randomized controlled trial

    PubMed Central

    2014-01-01

    Background Exercise and diet are the cornerstones for the treatment of obesity in obese children and adolescents. However, compensatory changes in appetite and energy expenditure elicited by exercise and dieting make it hard to maintain a reduced weight over the longterm. The anorexic effect of hypoxia can be potentially utilized to counteract this compensatory increase, thereby enhancing the success of weight loss. The purpose of the study is to assess the effectiveness of four week intermittent hypoxia exposure added to a traditional exercise and diet intervention on inducing short- and longterm weight loss in obese adolescents. Methods/Design In this randomized parallel group controlled clinical trial, 40 obese adolescents (20 boys and 20 girls, 11 to 15-years-old), will be recruited from a summer weight loss camp at the Shanghai University of Sport, China. Participants will be stratified by gender and randomly assigned to either the control group or the hypoxia group. During the four-week intervention period, both groups will exercise and eat a balanced diet. Additionally, the control group will sleep in normal conditions, while the hypoxia group will sleep in a normobaric hypoxia chamber (sleep high and train low). The primary outcome will be body composition and the main secondary outcomes will be the circulating levels of appetite regulatory gastrointestinal hormones. All the outcome measures will be assessed at baseline, after the four-week intervention, and at two months follow-up. Discussion Our study will be the first to evaluate the effectiveness of ‘sleep high and train low’ on short- and longterm weight loss among obese adolescents. A potential mechanism for the appetite regulatory effect of hypoxia will also be explored. The results of the study will provide an evidence-based recommendation for the use of hypoxia in a weight loss intervention among obese children and adolescents. Furthermore, the clarification of mechanisms leading to weight loss

  9. Sphenoidal sinus mucocele presenting with acute visual loss in a scuba diver.

    PubMed

    Mowatt, Lizette; Foster, Tecah

    2013-01-01

    A 43-year-old male scuba diver presented with an acute history of painful unilateral visual loss after scuba diving. He had right-sided retrobulbar pain and headache. He was known to have sinusitis and had transient visual loss in two previous episodes after scuba diving. His visual acuity was hand motions and 20/20 in the right and left eye, respectively. There was no proptosis. He had a right relative afferent pupillary defect. Colour vision was normal in the left eye and absent in the right eye. Fundal examination revealed healthy discs and macula bilaterally. He was assessed as a right optic neuropathy, possibly secondary to compression. An MRI of the brain revealed a large sphenoidal mucocele extending into the right optic foramen. He was treated with oral steroids, antibiotics and nasal decongestants. He underwent endoscopic intranasal sphenoidectomy and marsupialisation with return of his visual acuity to 20/25 in that eye. PMID:23964041

  10. Sphenoidal sinus mucocele presenting with acute visual loss in a scuba diver

    PubMed Central

    Mowatt, Lizette; Foster, Tecah

    2013-01-01

    A 43-year-old male scuba diver presented with an acute history of painful unilateral visual loss after scuba diving. He had right-sided retrobulbar pain and headache. He was known to have sinusitis and had transient visual loss in two previous episodes after scuba diving. His visual acuity was hand motions and 20/20 in the right and left eye, respectively. There was no proptosis. He had a right relative afferent pupillary defect. Colour vision was normal in the left eye and absent in the right eye. Fundal examination revealed healthy discs and macula bilaterally. He was assessed as a right optic neuropathy, possibly secondary to compression. An MRI of the brain revealed a large sphenoidal mucocele extending into the right optic foramen. He was treated with oral steroids, antibiotics and nasal decongestants. He underwent endoscopic intranasal sphenoidectomy and marsupialisation with return of his visual acuity to 20/25 in that eye. PMID:23964041

  11. Acupuncture as a primary and independent treatment in the acute phases of sudden sensorineural hearing loss

    PubMed Central

    Jin, Yuanyuan; Lu, Ming

    2016-01-01

    Abstract Sudden sensorineural hearing loss (SSHL) is an otological emergency defined as a rapid hearing loss, seriously affects patient's social life. To data, no study has reported the treatment by acupuncture alone in the acute phase. In this report, Acupuncture and Moxibustion therapy of excitation-focus transfer is outlined. The patient was a 26-year-old young woman who had an SSHL coupled with ear fullness. The patient had no past medical history, but she had undergone variable emotions and had a history of excessive noise exposure. The patient refused to receive any medicine especially steroids and hyperbaric oxygen therapy. She just only received acupuncture treatment. Her symptoms and outcome measurements were improved every week and completely recovered after the last week. Even though the article presents a single case and is based on self-reports, there are very clear trends on how patients with SSHL responded to acupuncture treatments. PMID:27368045

  12. Impaired Recognition of Facially Expressed Emotions in Different Groups of Patients with Sleep Disorders

    PubMed Central

    Crönlein, Tatjana; Langguth, Berthold; Eichhammer, Peter; Busch, Volker

    2016-01-01

    Introduction Recently it has been shown that acute sleep loss has a direct impact on emotional processing in healthy individuals. Here we studied the effect of chronically disturbed sleep on emotional processing by investigating two samples of patients with sleep disorders. Methods 25 patients with psychophysiologic insomnia (23 women and 2 men, mean age: 51.6 SD; 10.9 years), 19 patients with sleep apnea syndrome (4 women and 15 men, mean age: 51.9; SD 11.1) and a control sample of 24 subjects with normal sleep (15women and 9 men, mean age 45.3; SD 8.8) completed a Facial Expressed Emotion Labelling (FEEL) task, requiring participants to categorize and rate the intensity of six emotional expression categories: anger, anxiety, fear, happiness, disgust and sadness. Differences in FEEL score and its subscales among the three samples were analysed using ANOVA with gender as a covariate. Results Both patients with psychophysiologic insomnia and patients with sleep apnea showed significantly lower performance in the FEEL test as compared to the control group. Differences were seen in the scales happiness and sadness. Patient groups did not differ from each other. Conclusion By demonstrating that previously known effects of acute sleep deprivation on emotional processing can be extended to persons experiencing chronically disturbed sleep, our data contribute to a deeper understanding of the relationship between sleep loss and emotions. PMID:27073852

  13. Sleep and adult neurogenesis: implications for cognition and mood.

    PubMed

    Mueller, Anka D; Meerlo, Peter; McGinty, Dennis; Mistlberger, Ralph E

    2015-01-01

    The hippocampal dentate gyrus plays a critical role in learning and memory throughout life, in part by the integration of adult-born neurons into existing circuits. Neurogenesis in the adult hippocampus is regulated by numerous environmental, physiological, and behavioral factors known to affect learning and memory. Sleep is also important for learning and memory. Here we critically examine evidence from correlation, deprivation, and stimulation studies that sleep may be among those factors that regulate hippocampal neurogenesis. There is mixed evidence for correlations between sleep variables and rates of hippocampal cell proliferation across the day, the year, and the lifespan. There is modest evidence that periods of increased sleep are associated with increased cell proliferation or survival. There is strong evidence that disruptions of sleep exceeding 24 h, by total deprivation, selective REM sleep deprivation, and chronic restriction or fragmentation, significantly inhibit cell proliferation and in some cases neurogenesis. The mechanisms by which sleep disruption inhibits neurogenesis are not fully understood. Although sleep disruption procedures are typically at least mildly stressful, elevated adrenal corticosterone secretion is not necessary for this effect. However, procedures that prevent both elevated corticosterone and interleukin 1β signaling have been found to block the effect of sleep deprivation on cell proliferation. This result suggests that sleep loss impairs hippocampal neurogenesis by the presence of wake-dependent factors, rather than by the absence of sleep-specific processes. This would weigh against a hypothesis that regulation of neurogenesis is a function of sleep. Nonetheless, impaired neurogenesis may underlie some of the memory and mood effects associated with acute and chronic sleep disruptions. PMID:24218292

  14. Loss of dorsolateral nigral hyperintensity on 3.0 tesla susceptibility-weighted imaging in idiopathic rapid eye movement sleep behavior disorder.

    PubMed

    De Marzi, Roberto; Seppi, Klaus; Högl, Birgit; Müller, Christoph; Scherfler, Christoph; Stefani, Ambra; Iranzo, Alex; Tolosa, Eduardo; Santamarìa, Joan; Gizewski, Elke; Schocke, Michael; Skalla, Elisabeth; Kremser, Christian; Poewe, Werner

    2016-06-01

    We assessed loss of dorsolateral nigral hyperintensity (DNH) on high-field susceptibility-weighted imaging (SWI), a novel magnetic resonance imaging marker for Parkinson's disease (PD), in 15 subjects with idiopathic rapid eye movement sleep behavior disorder (iRBD) and compared findings to 42 healthy controls (HCs) and 104 PD patients. We found loss of DNH in at least two thirds of iRBD subjects, which approaches the rate observed in PD and is in contrast to findings in HCs. We propose that absence of DNH on high-field SWI could identify prodromal degenerative parkinsonism in iRBD. Ann Neurol 2016;79:1026-1030. PMID:27016314

  15. AICA syndrome with facial palsy following vertigo and acute sensorineural hearing loss.

    PubMed

    Ikegami-Takada, Tomoko; Izumikawa, Masahiko; Doi, Tadashi; Takada, Yohei; Tomoda, Koichi

    2012-04-01

    We report a case of infarction of the anterior inferior cerebellar artery (AICA) with peripheral facial palsy following vertigo and acute sensorineural hearing loss. A 39-year-old female presented with vertigo and sudden hearing loss, tinnitus, and aural fullness of the right ear. An audiogram revealed a severe hearing loss at all tested frequencies in the right ear. Spontaneous nystagmus toward the left side was also observed. Otoneurological examinations showed sensorineural hearing loss of the right ear and horizontal and rotatory gaze nystagmus toward the left side, and a caloric reflex test demonstrated canal paresis. Initially, we diagnosed the patient for sudden deafness with vertigo. However, right peripheral facial palsy appeared 2 days later. An eye tracking test (ETT) and optokinetic pattern test (OKP) showed centralis abnormality. The patient's brain was examined by magnetic resonance imaging (MRI) and magnetic resonance angioglaphy (MRA) and showed an infarction localized in the pons and cerebellum. MRI and MRA revealed infarction of the right cerebellar hemisphere indicating occlusion of the AICA. Consequently, the patient was diagnosed with AICA syndrome but demonstrated regression following steroid and edaravone treatment. We suggest that performing MRI and MRA in the early stage of AICA syndrome is important for distinguishing cerebellar infarction resulting from vestibular disease. PMID:21862260

  16. Acute acoustic trauma: dynamics of hearing loss following cessation of exposure.

    PubMed

    Segal, S; Harell, M; Shahar, A; Englender, M

    1988-07-01

    The natural history of individuals with acute acoustic trauma who ceased to be exposed to impact noise was examined. Retrospective follow-up was carried out for 4 years on patients who were qualified as disabled following acoustic trauma with permanent threshold shift. Eight hundred forty-one individuals (1682 ears) were examined, of which 1514 ears with acoustic trauma were included in the study group; 150 individuals (300 ears) who continued to be exposed to impact noise even after discovery of acoustic trauma comprised the control group. In the latter, as long as exposure to gunfire continued, the severity of acoustic trauma increased. In the study group, during the first year after injury, changes were observed in hearing, whether improvement or deterioration; after this period, hearing loss appeared to be final. We suggest that, after 1 year following acute acoustic trauma, the associated hearing loss be considered as final, provided there is no further exposure to noise. This finding holds great importance from the medicolegal standpoint, an aspect that is unclear in the literature. It clarifies that beyond the period of 1 year after initial exposure, the pathologic process ceases (as long as there is no additional exposure to noise or gunfire). Further hearing deterioration beyond this period is not related to the initial acoustic trauma but rather to other factors. PMID:3177612

  17. Loss of neurovirulence is associated with reduction of cerebral capillary sequestration during acute Babesia bovis infection

    PubMed Central

    2013-01-01

    Background Severe neurological signs that develop during acute infection by virulent strains of Babesia bovis are associated with sequestration of infected erythrocytes in cerebral capillaries. Serial passage of virulent strains in cattle results in attenuated derivatives that do not cause neurologic disease. We evaluated whether serial passage also results in a loss of cerebral capillary sequestration by examining brain biopsies during acute disease and at necropsy. Findings Cerebral biopsies of spleen intact calves inoculated intravenously with a virulent or attenuated strain pair of B. bovis were evaluated for capillary sequestration at the onset of babesiosis and during severe disease. In calves infected with the virulent strain, there was a significant increase in sequestration between the first and second biopsy timepoint. The attenuated strain was still capable of sequestration, but at a reduced level, and did not change significantly between the first and second biopsy. Necropsy examination confirmed the second biopsy results and demonstrated that sequestration identified at necropsy reflects pathologic changes occurring in live animals. Conclusions Loss of neurovirulence after serial in vivo passage of the highly virulent T2Bo strain of B. bovis in splenectomized animals is associated with a significant reduction of cerebral capillary sequestration. Previous genomic analysis of this and two other strain pairs suggests that this observation could be related to genomic complexity, particularly of the ves gene family, rather than consistent gene specific differences. Additional experiments will examine whether differential gene expression of ves genes is also associated with reduced cerebral sequestration and neurovirulence in attenuated strains. PMID:23777713

  18. Predicting risk in space: Genetic markers for differential vulnerability to sleep restriction

    NASA Astrophysics Data System (ADS)

    Goel, Namni; Dinges, David F.

    2012-08-01

    Several laboratories have found large, highly reliable individual differences in the magnitude of cognitive performance, fatigue and sleepiness, and sleep homeostatic vulnerability to acute total sleep deprivation and to chronic sleep restriction in healthy adults. Such individual differences in neurobehavioral performance are also observed in space flight as a result of sleep loss. The reasons for these stable phenotypic differential vulnerabilities are unknown: such differences are not yet accounted for by demographic factors, IQ or sleep need, and moreover, psychometric scales do not predict those individuals cognitively vulnerable to sleep loss. The stable, trait-like (phenotypic) inter-individual differences observed in response to sleep loss—with intraclass correlation coefficients accounting for 58-92% of the variance in neurobehavioral measures—point to an underlying genetic component. To this end, we utilized multi-day highly controlled laboratory studies to investigate the role of various common candidate gene variants—each independently—in relation to cumulative neurobehavioral and sleep homeostatic responses to sleep restriction. These data suggest that common genetic variations (polymorphisms) involved in sleep-wake, circadian, and cognitive regulation may serve as markers for prediction of inter-individual differences in sleep homeostatic and neurobehavioral vulnerability to sleep restriction in healthy adults. Identification of genetic predictors of differential vulnerability to sleep restriction—as determined from candidate gene studies—will help identify astronauts most in need of fatigue countermeasures in space flight and inform medical standards for obtaining adequate sleep in space. This review summarizes individual differences in neurobehavioral vulnerability to sleep deprivation and ongoing genetic efforts to identify markers of such differences.

  19. Duplication and loss of chromosome 21 in two children with Down Syndrome and acute leukemia

    SciTech Connect

    Rogan, P.K.; Close, P.; Seip, J.R.

    1994-09-01

    Acute leukemia in patients with Trisomy 21 (Down Syndrome; DS) may often result in additional karyotypic changes in the number or structure of chromosome 21. We present two DS patients whose immunoblast karyotypes were associated with changes in chromosome 21 ploidy. Patient L.E. developed acute lymphocytic leukemia concomitant with the loss of a single copy of chromosome 21. Trisomy 21 in this individual was due to maternal meiosis I nondisjunction. A recombination event resulted in reduction of maternal alleles to homozygosity distal to D21S167. Loss of the paternal chromosomes in the leukemia clone produced uniparental maternal disomy with isodisomy over a 25cM interval. This could, in theory, permit the unopposed expression of one or more homozygous recessive maternal tumor-associated genes, thus providing an explanation for leukemogenesis in this patient. Patient E.H. was diagnosed with acute monoblastic leukemia and consistently displayed tetrasomy 21 in the blast cell population. The DS karyotype probably arose from a mitotic error in which the paternal chromosome was duplicated. DNA polymorphism analysis indicated that the additional chromosome in the leukemia clone was of maternal origin. The presence of equal numbers of maternal and paternal chromosomes in the tetraploid blast clone would not appear to be consistent with the expression of a mutant tumor suppressor gene in this patient. Although tetrasomy 21 could be a non-specific karyotypic abnormality unrelated to leukemogenesis, it is possible that monoblastic leukemia may be a consequence of increased expression of one or more genes on this chromosome.

  20. Sleeping Beauty transposon screen identifies signaling modules that cooperate with STAT5 activation to induce B cell acute lymphoblastic leukemia

    PubMed Central

    Heltemes-Harris, Lynn M.; Larson, Jon D.; Starr, Timothy K.; Hubbard, Gregory K.; Sarver, Aaron L.; Largaespada, David A.; Farrar, Michael A.

    2015-01-01

    STAT5 activation occurs frequently in human progenitor B cell acute lymphoblastic leukemia (B-ALL). To identify gene alterations that cooperate with STAT5 activation to initiate leukemia we crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) to mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only in B cells. Stat5b-CA mice typically do not develop B-ALL (<2% penetrance); in contrast, 89% of Stat5b–CA mice in which the T2/Onc transposon had been mobilized died of B-ALL by 3 months of age. High-throughput sequencing approaches were used to identify genes frequently targeted by the T2/Onc transposon; these included Sos1 (74%), Kdm2a (35%), Jak1 (26%), Bmi1 (19%), Prdm14 or Ncoa2 (13%), Cdkn2a (10%), Ikzf1 (8%), Caap1 (6%) and Klf3 (6%). Collectively, these mutations target three major cellular processes: (i) the JAK/STAT5 pathway (ii) progenitor B cell differentiation and (iii) the CDKN2A tumor suppressor pathway. Transposon insertions typically resulted in altered expression of these genes, as well as downstream pathways including STAT5, ERK and p38. Importantly, expression of Sos1 and Kdm2a, and activation of p38, correlated with survival, further underscoring the role these genes and associated pathways play in B-ALL. PMID:26500062

  1. A Novel BHLHE41 Variant is Associated with Short Sleep and Resistance to Sleep Deprivation in Humans

    PubMed Central

    Pellegrino, Renata; Kavakli, Ibrahim Halil; Goel, Namni; Cardinale, Christopher J.; Dinges, David F.; Kuna, Samuel T.; Maislin, Greg; Van Dongen, Hans P.A.; Tufik, Sergio; Hogenesch, John B.; Hakonarson, Hakon; Pack, Allan I.

    2014-01-01

    Study Objectives: Earlier work described a mutation in DEC2 also known as BHLHE41 (basic helix-loophelix family member e41) as causal in a family of short sleepers, who needed just 6 h sleep per night. We evaluated whether there were other variants of this gene in two well-phenotyped cohorts. Design: Sequencing of the BHLHE41 gene, electroencephalographic data, and delta power analysis and functional studies using cell-based luciferase. Results: We identified new variants of the BHLHE41 gene in two cohorts who had either acute sleep deprivation (n = 200) or chronic partial sleep deprivation (n = 217). One variant, Y362H, at another location in the same exon occurred in one twin in a dizygotic twin pair and was associated with reduced sleep duration, less recovery sleep following sleep deprivation, and fewer performance lapses during sleep deprivation than the homozygous twin. Both twins had almost identical amounts of non rapid eye movement (NREM) sleep. This variant reduced the ability of BHLHE41 to suppress CLOCK/BMAL1 and NPAS2/BMAL1 transactivation in vitro. Another variant in the same exome had no effect on sleep or response to sleep deprivation and no effect on CLOCK/BMAL1 transactivation. Random mutagenesis identified a number of other variants of BHLHE41 that affect its function. Conclusions: There are a number of mutations of BHLHE41. Mutations reduce total sleep while maintaining NREM sleep and provide resistance to the effects of sleep loss. Mutations that affect sleep also modify the normal inhibition of BHLHE41 of CLOCK/BMAL1 transactivation. Thus, clock mechanisms are likely involved in setting sleep length and the magnitude of sleep homeostasis. Citation: Pellegrino R, Kavakli IH, Goel N, Cardinale CJ, Dinges DF, Kuna ST, Maislin G, Van Dongen HP, Tufik S, Hogenesch JB, Hakonarson H, Pack AI. A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans. SLEEP 2014;37(8):1327-1336. PMID:25083013

  2. Acute Versus Chronic Loss of Mammalian Azi1/Cep131 Results in Distinct Ciliary Phenotypes

    PubMed Central

    Hall, Emma A.; Keighren, Margaret; Ford, Matthew J.; Davey, Tracey; Jarman, Andrew P.; Smith, Lee B.; Jackson, Ian J.; Mill, Pleasantine

    2013-01-01

    Defects in cilium and centrosome function result in a spectrum of clinically-related disorders, known as ciliopathies. However, the complex molecular composition of these structures confounds functional dissection of what any individual gene product is doing under normal and disease conditions. As part of an siRNA screen for genes involved in mammalian ciliogenesis, we and others have identified the conserved centrosomal protein Azi1/Cep131 as required for cilia formation, supporting previous Danio rerio and Drosophila melanogaster mutant studies. Acute loss of Azi1 by knock-down in mouse fibroblasts leads to a robust reduction in ciliogenesis, which we rescue by expressing siRNA-resistant Azi1-GFP. Localisation studies show Azi1 localises to centriolar satellites, and traffics along microtubules becoming enriched around the basal body. Azi1 also localises to the transition zone, a structure important for regulating traffic into the ciliary compartment. To study the requirement of Azi1 during development and tissue homeostasis, Azi1 null mice were generated (Azi1Gt/Gt). Surprisingly, Azi1Gt/Gt MEFs have no discernible ciliary phenotype and moreover are resistant to Azi1 siRNA knock-down, demonstrating that a compensation mechanism exists to allow ciliogenesis to proceed despite the lack of Azi1. Cilia throughout Azi1 null mice are functionally normal, as embryonic patterning and adult homeostasis are grossly unaffected. However, in the highly specialised sperm flagella, the loss of Azi1 is not compensated, leading to striking microtubule-based trafficking defects in both the manchette and the flagella, resulting in male infertility. Our analysis of Azi1 knock-down (acute loss) versus gene deletion (chronic loss) suggests that Azi1 plays a conserved, but non-essential trafficking role in ciliogenesis. Importantly, our in vivo analysis reveals Azi1 mediates novel trafficking functions necessary for flagellogenesis. Our study highlights the importance of both acute

  3. Effects of acute microinjections of thyroid hormone to the preoptic region of hypothyroid adult male rats on sleep, motor activity and body temperature.

    PubMed

    Moffett, Steven X; Giannopoulos, Phillip F; James, Thomas D; Martin, Joseph V

    2013-06-21

    Thyroid hormones induce short-latency nongenomic effects in adult brain tissue, suggesting that their acute administration would affect brain activity in intact animals. The influence on EEG-defined sleep of acute restoration of l-3,3'5-triiodothyronine (T3) to a sleep-regulatory brain region, the preoptic region, was examined in hypothyroid rats. Sleep parameters were monitored for 48 h weekly: for 24 h immediately following a control microinjection and for an additional 24h after a second microinjection including a T3 dose to the preoptic region or lateral ventricle. Male albino rats were implanted with EEG and EMG electrodes, abdominal temperature/activity transponders and unilateral lateral ventricle cannulae or bilateral preoptic region cannulae, and were given 0.02% n-propythiouracil (PTU) in their drinking water for 4 weeks. For histologically-confirmed bilateral preoptic region cannula placements (N=7), effects of T3 (especially a 3 μg dose) were apparent within 10h of injection as decreases in REM, NREM and total sleep and increases in waking and activity. Minimal effects of lateral ventricle T3 microinjection were demonstrated (N=5). Significant effects due to the time of day on the experimental measures were seen in both lateral ventricle and preoptic region groups, but these effects did not interact with the effect of administered hormone dose. These effects of T3 microinjection to the preoptic region were demonstrated after acute injections and within hours of injection rather than after chronic administration over days. PMID:23603414

  4. Effects of acute microinjections of the thyroid hormone derivative 3-iodothyronamine to the preoptic region of adult male rats on sleep, thermoregulation and motor activity.

    PubMed

    James, Thomas D; Moffett, Steven X; Scanlan, Thomas S; Martin, Joseph V

    2013-06-01

    The decarboxylated thyroid hormone derivative 3-iodothyronamine (T1AM) has been reported as having behavioral and physiological consequences distinct from those of thyroid hormones. Here, we investigate the effects of T1AM on EEG-defined sleep after acute administration to the preoptic region of adult male rats. Our laboratory recently demonstrated a decrease in EEG-defined sleep after administration of 3,3',5-triiodo-l-thyronine (T3) to the same brain region. After injection of T1AM or vehicle solution, EEG, EMG, activity, and core body temperature were recorded for 24h. Sleep parameters were determined from EEG and EMG data. Earlier investigations found contrasting systemic effects of T3 and T1AM, such as decreased heart rate and body temperature after intraperitoneal T1AM injection. However, nREM sleep was decreased in the present study after injections of 1 or 3 μg T1AM, but not after 0.3 or 10 μg, closely mimicking the previously reported effects of T3 administration to the preoptic region. The biphasic dose-response observed after either T1AM or T3 administration seems to indicate shared mechanisms and/or functions of sleep regulation in the preoptic region. Consistent with systemic administration of T1AM, however, microinjection of T1AM decreased body temperature. The current study is the first to show modulation of sleep by T1AM, and suggests that T1AM and T3 have both shared and independent effects in the adult mammalian brain. PMID:23702093

  5. [Clinical observations of acute low-tone sensorineural hearing loss considered as cochlear hydrops].

    PubMed

    Yamasoba, T; Sugasawa, T; Yagi, M; Harada, T; Futaki, T

    1990-02-01

    Acute low-tone sensorineural hearing loss (ALHL) has the following three criteria; obscure origin, acute onset and sensorineural hearing loss limited to low frequencies. Sixteen cases of ALHL which were considered as cochlear hydrops using glycerol test and electrocochleogram were studied. All patients visited our department within two weeks after onset and were followed up for one year or more after initial examination. The subjective symptoms, the character of vestibular and hearing impairment and prognosis of 16 cases with ALHL were also investigated. The results were as follows. 1. Patients complained of ear fullness rather than hearing impairment. Four patients were unaware of hearing loss. 2. Recruitment phenomenon was found in all of 15 cases examined. Vestibular findings were mostly normal, except that spontaneous nystagmus was found in two cases and head-shaking nystagmus in one. 3. Recurrence and fluctuation of hearing impairment occurred in 14 cases. Three cases had an attack of rotatory vertigo once and two has diagnosed as Meniere's disease later. 4. During three months prior to last examination, hearing was stabilized in nine cases and continued to fluctuate in seven cases. In the former, hearing was improved in four cases, unchanged in three, and worsened in two. 5. Two patients underwent an endolymphatic sac operation and have had a good prognosis. 6. The authors suggest that most of ALHL should be considered as transient cochlear hydrops because the subjective symptom and audiological and vestibular findings of our cases are similar to those of cases which were reported as ALHL by other investigators. According to the findings of glycerol test and electrocochleogram, endolymphatic hydrops in ALHL is considered to exist in all turns of cochlea. PMID:2348281

  6. On the Need of Objective Vigilance Monitoring: Effects of Sleep Loss on Target Detection and Task-Negative Activity Using Combined EEG/fMRI

    PubMed Central

    Czisch, Michael; Wehrle, Renate; Harsay, Helga A.; Wetter, Thomas C.; Holsboer, Florian; Sämann, Philipp G.; Drummond, Sean P. A.

    2012-01-01

    Sleep loss affects attention by reducing levels of arousal and alertness. The neural mechanisms underlying the compensatory efforts of the brain to maintain attention and performance after sleep deprivation (SD) are not fully understood. Previous neuroimaging studies of SD have not been able to separate the effects of reduced arousal from the effects of SD on cerebral responses to cognitive challenges. Here, we used a simultaneous electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) approach to study the effects of 36 h of total sleep deprivation (TSD). Specifically, we focused on changes in selective attention processes as induced by an active acoustic oddball task, with the ability to isolate runs with objective EEG signs of high (SDalert) or reduced (SDsleepy) vigilance. In the SDalert condition, oddball task-related activity appears to be sustained by compensatory co-activation of insular regions, but task-negative activity in the right posterior node of the default mode network is altered following TSD. In the SDsleepy condition, oddball task-positive activity was massively impaired, but task-negative activation was showing levels comparable with the control condition after a well-rested night. Our results suggest that loss of strict negative correlation between oddball task-positive and task-negative activation reflects the effects of TSD, while the actual state of vigilance during task performance can affects either task-related or task-negative activity, depending on the exact vigilance level. PMID:22557992

  7. On the Need of Objective Vigilance Monitoring: Effects of Sleep Loss on Target Detection and Task-Negative Activity Using Combined EEG/fMRI.

    PubMed

    Czisch, Michael; Wehrle, Renate; Harsay, Helga A; Wetter, Thomas C; Holsboer, Florian; Sämann, Philipp G; Drummond, Sean P A

    2012-01-01

    Sleep loss affects attention by reducing levels of arousal and alertness. The neural mechanisms underlying the compensatory efforts of the brain to maintain attention and performance after sleep deprivation (SD) are not fully understood. Previous neuroimaging studies of SD have not been able to separate the effects of reduced arousal from the effects of SD on cerebral responses to cognitive challenges. Here, we used a simultaneous electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) approach to study the effects of 36 h of total sleep deprivation (TSD). Specifically, we focused on changes in selective attention processes as induced by an active acoustic oddball task, with the ability to isolate runs with objective EEG signs of high (SD(alert)) or reduced (SD(sleepy)) vigilance. In the SD(alert) condition, oddball task-related activity appears to be sustained by compensatory co-activation of insular regions, but task-negative activity in the right posterior node of the default mode network is altered following TSD. In the SD(sleepy) condition, oddball task-positive activity was massively impaired, but task-negative activation was showing levels comparable with the control condition after a well-rested night. Our results suggest that loss of strict negative correlation between oddball task-positive and task-negative activation reflects the effects of TSD, while the actual state of vigilance during task performance can affects either task-related or task-negative activity, depending on the exact vigilance level. PMID:22557992

  8. The Impact of Acute Loss of Weight on Eustachian Tube Function

    PubMed Central

    Pascoto, Gabriela; Abreu, Cassiana; Silva, Maria Laura; Weber, Raimar; Pignatari, Shirley Shizue; Stamm, Aldo

    2014-01-01

    Introduction The eustachian tube is one of the key structures responsible for the functional balance of the middle ear. Some clinical conditions associated with tubal malfunction can cause extremely unpleasant symptoms. These symptoms could be triggered by acute loss of weight, for example, after bariatric surgery. Objective To evaluate the frequency and intensity of auditory tube dysfunction symptoms in obese patients after bariatric surgery. Methods Nineteen patients with accepted formal indications for bariatric surgery underwent a hearing evaluation (otoscopy, tonal and vocal audiometry, and impedanceometry) and a hearing questionnaire before, at the time of, 3 months after surgery (first postoperative evaluation), and 6 months (second postoperative evaluation) after surgery. Patients with a history of ear disease or ear surgery were excluded. Results None of the patients reported tubal dysfunction symptoms before surgery. Postsurgical results showed that 5 (26.3%) patients presented symptoms related to dysfunction of the eustachian tube at the first postoperative evaluation. After the 6-month follow-up, 9 (47.3%) patients reported symptoms of tubal dysfunction. Conclusion This study suggests that bariatric surgery can cause symptoms of eustachian tube dysfunction, probably due to rapid weight loss and the consequent loss of peritubal fat. PMID:25992125

  9. Effects of sleeping with reduced carbohydrate availability on acute training responses.

    PubMed

    Lane, Stephen C; Camera, Donny M; Lassiter, David Gray; Areta, José L; Bird, Stephen R; Yeo, Wee Kian; Jeacocke, Nikki A; Krook, Anna; Zierath, Juleen R; Burke, Louise M; Hawley, John A

    2015-09-15

    We determined the effects of "periodized nutrition" on skeletal muscle and whole body responses to a bout of prolonged exercise the following morning. Seven cyclists completed two trials receiving isoenergetic diets differing in the timing of ingestion: they consumed either 8 g/kg body mass (BM) of carbohydrate (CHO) before undertaking an evening session of high-intensity training (HIT) and slept without eating (FASTED), or consumed 4 g/kg BM of CHO before HIT, then 4 g/kg BM of CHO before sleeping (FED). The next morning subjects completed 2 h of cycling (120SS) while overnight fasted. Muscle biopsies were taken on day 1 (D1) before and 2 h after HIT and on day 2 (D2) pre-, post-, and 4 h after 120SS. Muscle [glycogen] was higher in FED at all times post-HIT (P < 0.001). The cycling bouts increased PGC1α mRNA and PDK4 mRNA (P < 0.01) in both trials, with PDK4 mRNA being elevated to a greater extent in FASTED (P < 0.05). Resting phosphorylation of AMPK(Thr172), p38MAPK(Thr180/Tyr182), and p-ACC(Ser79) (D2) was greater in FASTED (P < 0.05). Fat oxidation during 120SS was higher in FASTED (P = 0.01), coinciding with increases in ACC(Ser79) and CPT1 as well as mRNA expression of CD36 and FABP3 (P < 0.05). Methylation on the gene promoter for COX4I1 and FABP3 increased 4 h after 120SS in both trials, whereas methylation of the PPARδ promoter increased only in FASTED. We provide evidence for shifts in DNA methylation that correspond with inverse changes in transcription for metabolically adaptive genes, although delaying postexercise feeding failed to augment markers of mitochondrial biogenesis. PMID:26112242

  10. Effect of acupressure with valerian oil 2.5% on the quality and quantity of sleep in patients with acute coronary syndrome in a cardiac intensive care unit

    PubMed Central

    Bagheri-Nesami, Masoumeh; Gorji, Mohammad Ali Heidari; Rezaie, Somayeh; Pouresmail, Zahra; Cherati, Jamshid Yazdani

    2015-01-01

    The purpose of this three-group double-blind clinical trial study was to investigate the effect of acupressure (指壓 zhǐ yā) with valerian (纈草 xié cǎo) oil 2.5% on the quality and quantity of sleep in patients with acute coronary syndrome (ACS) in a coronary intensive care unit (CCU). This study was conducted on 90 patients with ACS in Mazandaran Heart Center (Sari, Iran) during 2013. The patients were randomly assigned to one of three groups. Patients in the acupressure with valerian oil 2.5% group (i.e., valerian acupressure group) received bilateral acupoint (穴位 xué wèi) massage with two drops of valerian oil for 2 minutes for three nights; including every point this treatment lasted in total 18 minutes. Patients in the acupressure group received massage at the same points with the same technique but without valerian oil. Patients in the control group received massage at points that were 1–1.5 cm from the main points using the same technique and for the same length of time. The quality and quantity of the patients' sleep was measured by the St. Mary's Hospital Sleep Questionnaire (SMHSQ). After the intervention, there was a significant difference between sleep quality and sleep quantity in the patients in the valerian acupressure group and the acupressure group, compared to the control group (p < 0.05). Patients that received acupressure with valerian oil experienced improved sleep quality; however, this difference was not statistically significant in comparison to the acupressure only group. Acupressure at the ear spirit gate (神門 shén mén), hand Shenmen, glabella (印堂 yìn táng), Wind Pool (風池 fēng chí), and Gushing Spring (湧泉 yǒng quán) acupoints can have therapeutic effects and may improve the quality and quantity of sleep in patients with ACS. Using these techniques in combination with herbal medicines such valerian oil can have a greater impact on improving sleep and reducing waking during the night. PMID:26587395

  11. Effect of acupressure with valerian oil 2.5% on the quality and quantity of sleep in patients with acute coronary syndrome in a cardiac intensive care unit.

    PubMed

    Bagheri-Nesami, Masoumeh; Gorji, Mohammad Ali Heidari; Rezaie, Somayeh; Pouresmail, Zahra; Cherati, Jamshid Yazdani

    2015-10-01

    The purpose of this three-group double-blind clinical trial study was to investigate the effect of acupressure ( zhǐ yā) with valerian ( xié cǎo) oil 2.5% on the quality and quantity of sleep in patients with acute coronary syndrome (ACS) in a coronary intensive care unit (CCU). This study was conducted on 90 patients with ACS in Mazandaran Heart Center (Sari, Iran) during 2013. The patients were randomly assigned to one of three groups. Patients in the acupressure with valerian oil 2.5% group (i.e., valerian acupressure group) received bilateral acupoint ( xué wèi) massage with two drops of valerian oil for 2 minutes for three nights; including every point this treatment lasted in total 18 minutes. Patients in the acupressure group received massage at the same points with the same technique but without valerian oil. Patients in the control group received massage at points that were 1-1.5 cm from the main points using the same technique and for the same length of time. The quality and quantity of the patients' sleep was measured by the St. Mary's Hospital Sleep Questionnaire (SMHSQ). After the intervention, there was a significant difference between sleep quality and sleep quantity in the patients in the valerian acupressure group and the acupressure group, compared to the control group (p < 0.05). Patients that received acupressure with valerian oil experienced improved sleep quality; however, this difference was not statistically significant in comparison to the acupressure only group. Acupressure at the ear spirit gate ( shén mén), hand Shenmen, glabella ( yìn táng), Wind Pool ( fēng chí), and Gushing Spring ( yǒng quán) acupoints can have therapeutic effects and may improve the quality and quantity of sleep in patients with ACS. Using these techniques in combination with herbal medicines such valerian oil can have a greater impact on improving sleep and reducing waking during the night. PMID:26587395

  12. Genetic loss of SH2B3 in acute lymphoblastic leukemia

    PubMed Central

    Perez-Garcia, Arianne; Ambesi-Impiombato, Alberto; Hadler, Michael; Rigo, Isaura; LeDuc, Charles A.; Kelly, Kara; Jalas, Chaim; Paietta, Elisabeth; Racevskis, Janis; Rowe, Jacob M.; Tallman, Martin S.; Paganin, Maddalena; Basso, Giuseppe; Tong, Wei; Chung, Wendy K.

    2013-01-01

    The SH2B adaptor protein 3 (SH2B3) gene encodes a negative regulator of cytokine signaling with a critical role in the homeostasis of hematopoietic stem cells and lymphoid progenitors. Here, we report the identification of germline homozygous SH2B3 mutations in 2 siblings affected with developmental delay and autoimmunity, one in whom B-precursor acute lymphoblastic leukemia (ALL) developed. Mechanistically, loss of SH2B3 increases Janus kinase-signal transducer and activator of transcription signaling, promotes lymphoid cell proliferation, and accelerates leukemia development in a mouse model of NOTCH1-induced ALL. Moreover, extended mutation analysis showed homozygous somatic mutations in SH2B3 in 2 of 167 ALLs analyzed. Overall, these results demonstrate a Knudson tumor suppressor role for SH2B3 in the pathogenesis of ALL and highlight a possible link between genetic predisposition factors in the pathogenesis of autoimmunity and leukemogenesis. PMID:23908464

  13. Diet/Energy Balance Affect Sleep and Wakefulness Independent of Body Weight

    PubMed Central

    Perron, Isaac J.; Pack, Allan I.; Veasey, Sigrid

    2015-01-01

    Study Objectives: Excessive daytime sleepiness commonly affects obese people, even in those without sleep apnea, yet its causes remain uncertain. We sought to determine whether acute dietary changes could induce or rescue wake impairments independent of body weight. Design: We implemented a novel feeding paradigm that generates two groups of mice with equal body weight but opposing energetic balance. Two subsets of mice consuming either regular chow (RC) or high-fat diet (HFD) for 8 w were switched to the opposite diet for 1 w. Sleep recordings were conducted at Week 0 (baseline), Week 8 (pre-diet switch), and Week 9 (post-diet switch) for all groups. Sleep homeostasis was measured at Week 8 and Week 9. Participants: Young adult, male C57BL/6J mice. Measurements and Results: Differences in total wake, nonrapid eye movement (NREM), and rapid eye movement (REM) time were quantified, in addition to changes in bout fragmentation/consolidation. At Week 9, the two diet switch groups had similar body weight. However, animals switched to HFD (and thus gaining weight) had decreased wake time, increased NREM sleep time, and worsened sleep/wake fragmentation compared to mice switched to RC (which were in weight loss). These effects were driven by significant sleep/wake changes induced by acute dietary manipulations (Week 8 → Week 9). Sleep homeostasis, as measured by delta power increase following sleep deprivation, was unaffected by our feeding paradigm. Conclusions: Acute dietary manipulations are sufficient to alter sleep and wakefulness independent of body weight and without effects on sleep homeostasis. Citation: Perron IJ, Pack AI, Veasey S. Diet/energy balance affect sleep and wakefulness independent of body weight. SLEEP 2015;38(12):1893–1903. PMID:26158893

  14. Acute Sleep Deprivation and Circadian Misalignment Associated with Transition onto the First Night of Work Impairs Visual Selective Attention

    PubMed Central

    Santhi, Nayantara; Horowitz, Todd S.; Duffy, Jeanne F.; Czeisler, Charles A.

    2007-01-01

    Background Overnight operations pose a challenge because our circadian biology promotes sleepiness and dissipates wakefulness at night. Since the circadian effect on cognitive functions magnifies with increasing sleep pressure, cognitive deficits associated with night work are likely to be most acute with extended wakefulness, such as during the transition from a day shift to night shift. Methodology/Principal Findings To test this hypothesis we measured selective attention (with visual search), vigilance (with Psychomotor Vigilance Task [PVT]) and alertness (with a visual analog scale) in a shift work simulation protocol, which included four day shifts followed by three night shifts. There was a nocturnal decline in cognitive processes, some of which were most pronounced on the first night shift. The nighttime decrease in visual search sensitivity was most pronounced on the first night compared with subsequent nights (p = .04), and this was accompanied by a trend towards selective attention becoming ‘fast and sloppy’. The nighttime increase in attentional lapses on the PVT was significantly greater on the first night compared to subsequent nights (p<.05) indicating an impaired ability to sustain focus. The nighttime decrease in subjective alertness was also greatest on the first night compared with subsequent nights (p<.05). Conclusions/Significance These nocturnal deficits in attention and alertness offer some insight into why occupational errors, accidents, and injuries are pronounced during night work compared to day work. Examination of the nighttime vulnerabilities underlying the deployment of attention can be informative for the design of optimal work schedules and the implementation of effective countermeasures for performance deficits during night work. PMID:18043740

  15. Pax5 loss imposes a reversible differentiation block in B-progenitor acute lymphoblastic leukemia

    PubMed Central

    Liu, Grace J.; Cimmino, Luisa; Jude, Julian G.; Hu, Yifang; Witkowski, Matthew T.; McKenzie, Mark D.; Kartal-Kaess, Mutlu; Best, Sarah A.; Tuohey, Laura; Liao, Yang; Shi, Wei; Mullighan, Charles G.; Farrar, Michael A.; Nutt, Stephen L.; Smyth, Gordon K.; Zuber, Johannes; Dickins, Ross A.

    2014-01-01

    Loss-of-function mutations in hematopoietic transcription factors including PAX5 occur in most cases of B-progenitor acute lymphoblastic leukemia (B-ALL), a disease characterized by the accumulation of undifferentiated lymphoblasts. Although PAX5 mutation is a critical driver of B-ALL development in mice and humans, it remains unclear how its loss contributes to leukemogenesis and whether ongoing PAX5 deficiency is required for B-ALL maintenance. Here we used transgenic RNAi to reversibly suppress endogenous Pax5 expression in the hematopoietic compartment of mice, which cooperates with activated signal transducer and activator of transcription 5 (STAT5) to induce B-ALL. In this model, restoring endogenous Pax5 expression in established B-ALL triggers immunophenotypic maturation and durable disease remission by engaging a transcriptional program reminiscent of normal B-cell differentiation. Notably, even brief Pax5 restoration in B-ALL cells causes rapid cell cycle exit and disables their leukemia-initiating capacity. These and similar findings in human B-ALL cell lines establish that Pax5 hypomorphism promotes B-ALL self-renewal by impairing a differentiation program that can be re-engaged despite the presence of additional oncogenic lesions. Our results establish a causal relationship between the hallmark genetic and phenotypic features of B-ALL and suggest that engaging the latent differentiation potential of B-ALL cells may provide new therapeutic entry points. PMID:24939936

  16. Total dream loss: a distinct neuropsychological dysfunction after bilateral PCA stroke.

    PubMed

    Bischof, Matthias; Bassetti, Claudio L

    2004-10-01

    The term Charcot-Wilbrand syndrome (CWS) denotes dream loss following focal brain damage. We report the first case of CWS, in whom neuropsychological functions, extension of the underlying lesion, and sleep architecture changes were assessed. A 73-year-old woman reported a total dream loss after acute, bilateral occipital artery infarction (including the right inferior lingual gyrus), which lasted for over 3 months. In the absence of sleep-wake complaints and (other) neuropsychological deficits, polysomnography demonstrated an essentially normal sleep architecture with preservation of REM sleep. Dreaming was denied also after repeated awakenings from REM sleep. This observation suggests that CWS (1) can represent a distinct and isolated neuropsychological manifestation of deep occipital lobe damage, and (2) may occur in the absence of detectable REM sleep abnormalities. PMID:15389890

  17. Sleep and Women

    MedlinePlus

    ... Benefits Side Effects Variations Tips Healthy Sleep Habits Sleep Disorders by Category Insomnias Insomnia Child Insomnia Short Sleeper ... Work SIDS Sleep apnea Sleep Debt Sleep Deprivation Sleep Disorders Sleep history Sleep hygiene sleep length Sleep Need ...

  18. Short-Term Outcomes of Acute Low-Tone Sensorineural Hearing Loss According to Treatment Modality

    PubMed Central

    Chang, Jinkyung; Yum, Gunhwee; Im, Ha-Young; Jung, Jong Yoon; Rah, Yoon Chan

    2016-01-01

    Background and Objectives We compared improvements in hearing thresholds in acute low-tone sensorineural hearing loss (ALHL) patients after two different treatments: steroid alone and steroid and diuretic combined. We analyzed how the duration between the onset of symptoms and the initiation of treatment affected hearing loss improvement and investigated the relation between presence of vertigo in ALHL patients and ALHL progression to Ménière's disease (MD). Subjects and Methods We retrospectively analyzed the medical records of 47 ALHL patients aged 21 to 76 years. Patients received either orally administered steroid alone (n=12) or steroid and diuretic combined (n=35). We compared improvements in the two groups' hearing thresholds at three lower frequencies (125, 250, and 500 Hz) after participants had received one month of each respective treatment. Results Our two treatments did not show any statistical difference in hearing loss improvement after one month. Forty percent of ALHL patients with vertigo developed MD, which was a significantly higher rate than the 12.5% of ALHL patients without vertigo who developed MD. The shorter duration between the onset of symptoms and the initiation of treatment significantly increased improvement in the sum of lower frequency hearing threshold after one month. Conclusions The current study suggests that steroid and diuretic administered together and steroid alone similarly improve the hearing threshold in ALHL patients after one month. We concluded that patients should initiate ALHL treatment as soon as they experience symptoms. ALHL patients should also be notified of their higher risk of developing MD. PMID:27144234

  19. Sleep and obesity

    PubMed Central

    Beccuti, Guglielmo; Pannain, Silvana

    2013-01-01

    Purpose of review This review summarizes the most recent evidence linking decreased sleep duration and poor sleep quality to obesity, focusing upon studies in adults. Recent findings Published and unpublished health examination surveys and epidemiological studies suggest that the worldwide prevalence of obesity has doubled since 1980. In 2008, 1 in 10 adults was obese, with women more likely to be obese than men. This obesity epidemic has been paralleled by a trend of reduced sleep duration. Poor sleep quality, which leads to overall sleep loss has also become a frequent complaint. Growing evidence from both laboratory and epidemiological studies points to short sleep duration and poor sleep quality as new risk factors for the development of obesity. Summary Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result in metabolic and endocrine alterations, including decreased glucose tolerance, decreased insulin sensitivity, increased evening concentrations of cortisol, increased levels of ghrelin, decreased levels of leptin, and increased hunger and appetite. Recent epidemiological and laboratory evidence confirm previous findings of an association between sleep loss and increased risk of obesity. PMID:21659802

  20. Progressive Loss of the Orexin Neurons Reveals Dual Effects on Wakefulness

    PubMed Central

    Branch, Abigail F.; Navidi, William; Tabuchi, Sawako; Terao, Akira; Yamanaka, Akihiro; Scammell, Thomas E.; Diniz Behn, Cecilia

    2016-01-01

    Study Objectives: Narcolepsy is caused by loss of the orexin (also known as hypocretin) neurons. In addition to the orexin peptides, these neurons release additional neurotransmitters, which may produce complex effects on sleep/wake behavior. Currently, it remains unknown whether the orexin neurons promote the initiation as well as the maintenance of wakefulness, and whether the orexin neurons influence initiation or maintenance of sleep. To determine the effects of the orexin neurons on the dynamics of sleep/wake behavior, we analyzed sleep/wake architecture in a novel mouse model of acute orexin neuron loss. Methods: We used survival analysis and other statistical methods to analyze sleep/wake architecture in orexin-tTA ; TetO diphtheria toxin A mice at different stages of orexin neuron degeneration. Results: Progressive loss of the orexin neurons dramatically reduced survival of long wake bouts, but it also improved survival of brief wake bouts. In addition, with loss of the orexin neurons, mice were more likely to wake during the first 30 sec of nonrapid eye movement sleep and then less likely to return to sleep during the first 60 sec of wakefulness. Conclusions: These findings help explain the sleepiness and fragmented sleep that are characteristic of narcolepsy. Orexin neuron loss impairs survival of long wake bouts resulting in poor maintenance of wakefulness, but this neuronal loss also fragments sleep by increasing the risk of awakening at the beginning of sleep and then reducing the likelihood of quickly returning to sleep. Citation: Branch AF, Navidi W, Tabuchi S, Terao A, Yamanaka A, Scammell TE, Diniz Behn C. Progressive loss of the orexin neurons reveals dual effects on wakefulness. SLEEP 2016;39(2):369–377. PMID:26446125

  1. Loss of promoter IV-driven BDNF expression impacts oscillatory activity during sleep, sensory information processing and fear regulation.

    PubMed

    Hill, J L; Hardy, N F; Jimenez, D V; Maynard, K R; Kardian, A S; Pollock, C J; Schloesser, R J; Martinowich, K

    2016-01-01

    Posttraumatic stress disorder is characterized by hyperarousal, sensory processing impairments, sleep disturbances and altered fear regulation; phenotypes associated with changes in brain oscillatory activity. Molecules associated with activity-dependent plasticity, including brain-derived neurotrophic factor (BDNF), may regulate neural oscillations by controlling synaptic activity. BDNF synthesis includes production of multiple Bdnf transcripts, which contain distinct 5' noncoding exons. We assessed arousal, sensory processing, fear regulation and sleep in animals where BDNF expression from activity-dependent promoter IV is disrupted (Bdnf-e4 mice). Bdnf-e4 mice display sensory hyper-reactivity and impaired electrophysiological correlates of sensory information processing as measured by event-related potentials (ERP). Utilizing electroencephalogram, we identified a decrease in slow-wave activity during non-rapid eye movement sleep, suggesting impaired sleep homeostasis. Fear extinction is controlled by hippocampal-prefrontal cortical BDNF signaling, and neurophysiological communication patterns between the hippocampus (HPC) and medial prefrontal cortex (mPFC) correlate with behavioral performance during extinction. Impaired fear extinction in Bdnf-e4 mice is accompanied by increased HPC activation and decreased HPC-mPFC theta phase synchrony during early extinction, as well as increased mPFC activation during extinction recall. These results suggest that activity-dependent BDNF signaling is critical for regulating oscillatory activity, which may contribute to altered behavior. PMID:27552586

  2. Sleep disorders and work performance: findings from the 2008 National Sleep Foundation Sleep in America poll.

    PubMed

    Swanson, Leslie M; Arnedt, J Todd; Rosekind, Mark R; Belenky, Gregory; Balkin, Thomas J; Drake, Christopher

    2011-09-01

    Chronic sleep deprivation is common among workers, and has been associated with negative work outcomes, including absenteeism and occupational accidents. The objective of the present study is to characterize reciprocal relationships between sleep and work. Specifically, we examined how sleep impacts work performance and how work affects sleep in individuals not at-risk for a sleep disorder; assessed work performance outcomes for individuals at-risk for sleep disorders, including insomnia, obstructive sleep apnea (OSA) and restless legs syndrome (RLS); and characterized work performance impairments in shift workers (SW) at-risk for shift work sleep disorders relative to SW and day workers. One-thousand Americans who work 30 h per week or more were asked questions about employment, work performance and sleep in the National Sleep Foundation's 2008 Sleep in America telephone poll. Long work hours were associated with shorter sleep times, and shorter sleep times were associated with more work impairments. Thirty-seven percent of respondents were classified as at-risk for any sleep disorder. These individuals had more negative work outcomes as compared with those not at-risk for a sleep disorder. Presenteeism was a significant problem for individuals with insomnia symptoms, OSA and RLS as compared with respondents not at-risk. These results suggest that long work hours may contribute to chronic sleep loss, which may in turn result in work impairment. Risk for sleep disorders substantially increases the likelihood of negative work outcomes, including occupational accidents, absenteeism and presenteeism. PMID:20887396

  3. Acute Psychophysiological Relationships Between Mood, Inflammatory and Cortisol Changes in Response to Simulated Physical Firefighting Work and Sleep Restriction.

    PubMed

    Wolkow, Alexander; Aisbett, Brad; Reynolds, John; Ferguson, Sally A; Main, Luana C

    2016-06-01

    This study examined how changes in wildland firefighters' mood relate to cytokine and cortisol levels in response to simulated physical firefighting work and sleep restriction. Firefighters completed 3 days of simulated wildfire suppression work separated by an 8-h (control condition; n = 18) or 4-h sleep opportunity (sleep restriction condition; n = 17) each night. Firefighters' mood was assessed daily using the Mood Scale II and Samn-Perelli fatigue scale. Participants also provided samples for the determination of salivary cortisol and pro- (IL-6, IL-8, IL-1β, TNF-α) and anti-inflammatory (IL-4, IL-10) cytokine levels. An increase in the positive mood dimension Happiness was related to a rise in IL-8 and TNF-α in the sleep restriction condition. A rise in the positive mood dimension Activation among sleep restricted firefighters was also related to higher IL-6 levels. An increase in the negative mood dimension Fatigue in the sleep restriction condition was associated with increased IL-6, TNF-α, IL-10 and cortisol levels. In addition, an increase in Fear among sleep restricted firefighters was associated with a rise in TNF-α. Elevated positive mood and immune activation may reflect an appropriate response by the firefighters to these stressors. To further understand this relationship, subsequent firefighting-based research is needed that investigates whether immune changes are a function of affective arousal linked to the expression of positive moods. Positive associations between negative mood and inflammatory and cortisol levels to physical work and restricted sleep provide useful information to fire agencies about subjective fire-ground indicators of physiological changes. PMID:26698865

  4. The Neuroprotective Aspects of Sleep

    PubMed Central

    Eugene, Andy R.; Masiak, Jolanta

    2015-01-01

    Sleep is an important component of human life, yet many people do not understand the relationship between the brain and the process of sleeping. Sleep has been proven to improve memory recall, regulate metabolism, and reduce mental fatigue. A minimum of 7 hours of daily sleep seems to be necessary for proper cognitive and behavioral function. The emotional and mental handicaps associated with chronic sleep loss as well as the highly hazardous situations which can be contributed to the lack of sleep is a serious concern that people need to be aware of. When one sleeps, the brain reorganizes and recharges itself, and removes toxic waste byproducts which have accumulated throughout the day. This evidence demonstrates that sleeping can clear the brain and help maintain its normal functioning. Multiple studies have been done to determine the effects of total sleep deprivation; more recently some have been conducted to show the effects of sleep restriction, which is a much more common occurrence, have the same effects as total sleep deprivation. Each phase of the sleep cycle restores and rejuvenates the brain for optimal function. When sleep is deprived, the active process of the glymphatic system does not have time to perform that function, so toxins can build up, and the effects will become apparent in cognitive abilities, behavior, and judgment. As a background for this paper we have reviewed literature and research of sleep phases, effects of sleep deprivation, and the glymphatic system of the brain and its restorative effect during the sleep cycle. PMID:26594659

  5. The Effects of Acute Blood Loss for Diagnostic Bloodwork and Fluid Replacement in Clinically Ill Mice

    PubMed Central

    Marx, James O; Jensen, JanLee A; Seelye, Stacie; Walton, Raquel M; Hankenson, F Claire

    2015-01-01

    Despite the great value of diagnostic bloodwork for identifying disease in animals, the volume of blood required for these analyses limits its use in laboratory mice, particularly when they are clinically ill. We sought to determine the effects of acute blood loss (ABL) following blood collection for diagnostic bloodwork in healthy mice compared with streptozotocin-induced diabetic and dextran sulfate sodium (DSS)-treated dehydrated mice. ABL caused several mild changes in the control mice, with significant decreases in body weight, temperature, and activity in both experimental groups; increased dehydration and azotemia in the DSS-treated mice; and a significant drop in the blood pressure of the diabetic mice. To determine whether these negative outcomes could be ameliorated, we treated mice with intraperitoneal lactated Ringers solution either immediately after or 30 min before ABL. Notably, preABL administration of fluids helped prevent the worsening of the dehydration and azotemia in the DSS-treated mice and the changes in blood pressure in the diabetic mice. However, fluid administration provided no benefit in control of blood pressure when administered after ABL in the diabetic mice. Furthermore, fluid therapy did not prevent ABL-induced drops in body weight and activity. Although one mouse not receiving fluid therapy became moribund at the 24-h time point, no animals died during the 24-h study. This investigation demonstrates that blood for diagnostic bloodwork can be collected safely from clinically ill mice and that preemptive fluid therapy mitigates some of the negative changes associated with this blood loss. PMID:26141445

  6. p53 loss promotes acute myeloid leukemia by enabling aberrant self-renewal

    PubMed Central

    Zhao, Zhen; Zuber, Johannes; Diaz-Flores, Ernesto; Lintault, Laura; Kogan, Scott C.; Shannon, Kevin; Lowe, Scott W.

    2010-01-01

    The p53 tumor suppressor limits proliferation in response to cellular stress through several mechanisms. Here, we test whether the recently described ability of p53 to limit stem cell self-renewal suppresses tumorigenesis in acute myeloid leukemia (AML), an aggressive cancer in which p53 mutations are associated with drug resistance and adverse outcome. Our approach combined mosaic mouse models, Cre-lox technology, and in vivo RNAi to disable p53 and simultaneously activate endogenous KrasG12D—a common AML lesion that promotes proliferation but not self-renewal. We show that p53 inactivation strongly cooperates with oncogenic KrasG12D to induce aggressive AML, while both lesions on their own induce T-cell malignancies with long latency. This synergy is based on a pivotal role of p53 in limiting aberrant self-renewal of myeloid progenitor cells, such that loss of p53 counters the deleterious effects of oncogenic Kras on these cells and enables them to self-renew indefinitely. Consequently, myeloid progenitor cells expressing oncogenic Kras and lacking p53 become leukemia-initiating cells, resembling cancer stem cells capable of maintaining AML in vivo. Our results establish an efficient new strategy for interrogating oncogene cooperation, and provide strong evidence that the ability of p53 to limit aberrant self-renewal contributes to its tumor suppressor activity. PMID:20595231

  7. Body mass loss correlates with cognitive performance in primates under acute caloric restriction conditions.

    PubMed

    Villain, N; Picq, J-L; Aujard, F; Pifferi, F

    2016-05-15

    Brain functions are known to consume high levels of energy, thus, the integrity of cognitive performance can be drastically impacted by acute caloric restriction. In this study, we tested the impact of a 40% caloric restriction on the cognitive abilities of the grey mouse lemur (Microcebus murinus). Twenty-three male mouse lemurs were divided into two groups: 13 control animals (CTL) that were fed with 105kJ/day and 10calorie restricted (CR) animals that received 40% less food (63kJ/day) than the CTL animals. The animals were fed according to their group for 19days. Before treatment, we assessed baseline associative learning capacities, resting metabolic rates and locomotor performance of both animal groups. After treatment, we tested the same functions as well as long-term memory. Our results showed that CR animals had lower learning performance following caloric restriction. The effects of caloric restriction on memory recall varied and depended on the metabolism of the individual animal. Body mass loss was linked to memory test performance in the CR group, and lower performance was observed in individuals losing the most weight. While CR was observed to negatively impact learning, locomotor capacities were preserved in CR animals, and there were higher resting metabolic rates in the CR group. Our data reinforce the strong link between energy allocation and brain function, and suggest that in the context of food shortage, learning capacities could be a limiting parameter in the adaptation to a changing environment. PMID:26952885

  8. Sleep Problems

    MedlinePlus

    ... For Consumers Consumer Information by Audience For Women Sleep Problems Share Tweet Linkedin Pin it More sharing ... PDF 474KB) En Español Medicines to Help You Sleep Tips for Better Sleep Basic Facts about Sleep ...

  9. Sleep Quiz

    MedlinePlus

    ... on. Photo: iStock Take the National Center on Sleep Disorders Research Sleep Quiz TRUE OR FALSE ? _____1. Sleep ... sleepy during the day, you may have a sleep disorder. _____4. Opening the car window or turning the ...

  10. Sleep Disorders

    MedlinePlus

    ... the day, even if you have had enough sleep? You might have a sleep disorder. The most common kinds are Insomnia - a hard time falling or staying asleep Sleep apnea - breathing interruptions during sleep Restless legs syndrome - ...

  11. Sleep Disorders

    MedlinePlus

    ... have had enough sleep? You might have a sleep disorder. The most common kinds are Insomnia - a hard ... problems called parasomnias. There are treatments for most sleep disorders. Sometimes just having regular sleep habits can help.

  12. Acute Sleep Deprivation Induces a Local Brain Transfer Information Increase in the Frontal Cortex in a Widespread Decrease Context

    PubMed Central

    Alonso, Joan F.; Romero, Sergio; Mañanas, Miguel A.; Alcalá, Marta; Antonijoan, Rosa M.; Giménez, Sandra

    2016-01-01

    Sleep deprivation (SD) has adverse effects on mental and physical health, affecting the cognitive abilities and emotional states. Specifically, cognitive functions and alertness are known to decrease after SD. The aim of this work was to identify the directional information transfer after SD on scalp EEG signals using transfer entropy (TE). Using a robust methodology based on EEG recordings of 18 volunteers deprived from sleep for 36 h, TE and spectral analysis were performed to characterize EEG data acquired every 2 h. Correlation between connectivity measures and subjective somnolence was assessed. In general, TE showed medium- and long-range significant decreases originated at the occipital areas and directed towards different regions, which could be interpreted as the transfer of predictive information from parieto-occipital activity to the rest of the head. Simultaneously, short-range increases were obtained for the frontal areas, following a consistent and robust time course with significant maps after 20 h of sleep deprivation. Changes during sleep deprivation in brain network were measured effectively by TE, which showed increased local connectivity and diminished global integration. TE is an objective measure that could be used as a potential measure of sleep pressure and somnolence with the additional property of directed relationships. PMID:27089346

  13. Acute Sleep Deprivation Induces a Local Brain Transfer Information Increase in the Frontal Cortex in a Widespread Decrease Context.

    PubMed

    Alonso, Joan F; Romero, Sergio; Mañanas, Miguel A; Alcalá, Marta; Antonijoan, Rosa M; Giménez, Sandra

    2016-01-01

    Sleep deprivation (SD) has adverse effects on mental and physical health, affecting the cognitive abilities and emotional states. Specifically, cognitive functions and alertness are known to decrease after SD. The aim of this work was to identify the directional information transfer after SD on scalp EEG signals using transfer entropy (TE). Using a robust methodology based on EEG recordings of 18 volunteers deprived from sleep for 36 h, TE and spectral analysis were performed to characterize EEG data acquired every 2 h. Correlation between connectivity measures and subjective somnolence was assessed. In general, TE showed medium- and long-range significant decreases originated at the occipital areas and directed towards different regions, which could be interpreted as the transfer of predictive information from parieto-occipital activity to the rest of the head. Simultaneously, short-range increases were obtained for the frontal areas, following a consistent and robust time course with significant maps after 20 h of sleep deprivation. Changes during sleep deprivation in brain network were measured effectively by TE, which showed increased local connectivity and diminished global integration. TE is an objective measure that could be used as a potential measure of sleep pressure and somnolence with the additional property of directed relationships. PMID:27089346

  14. The Inevitability of Sleep: Using Manet's Last Paintings to Envision a Pedagogy of Loss and Mourning

    ERIC Educational Resources Information Center

    Otto, Stacy

    2013-01-01

    In this article, the author offers Manet's last paintings as metaphors for a bygone, psychically healthy conception of loss and mourning, what is called the pre-Freudian, Victorian notion of loss (Otto 2008), which contrasts with the post-Freudian, Modern notion of loss and mourning (Otto 2008). Otto argues this liminal, transitional moment…

  15. Sleep and Breathing at High Altitude.

    PubMed

    Wickramasinghe, Himanshu; Anholm, James D.

    1999-01-01

    Sleep at high altitude is characterized by poor subjective quality, increased awakenings, frequent brief arousals, marked nocturnal hypoxemia, and periodic breathing. A change in sleep architecture with an increase in light sleep and decreasing slow-wave and REM sleep have been demonstrated. Periodic breathing with central apnea is almost universally seen amongst sojourners to high altitude, although it is far less common in long-standing high altitude dwellers. Hypobaric hypoxia in concert with periodic breathing appears to be the principal cause of sleep disruption at altitude. Increased sleep fragmentation accounts for the poor sleep quality and may account for some of the worsened daytime performance at high altitude. Hypoxic sleep disruption contributes to the symptoms of acute mountain sickness. Hypoxemia at high altitude is most severe during sleep. Acetazolamide improves sleep, AMS symptoms, and hypoxemia at high altitude. Low doses of a short acting benzodiazepine (temazepam) may also be useful in improving sleep in high altitude. PMID:11898114

  16. Sleep deprivation worsens inflammation and delays recovery in a mouse model of colitis

    PubMed Central

    Tang, Yueming; Preuss, Fabian; Turek, Fred W.; Jakate, Shriram; Keshavarzian, Ali

    2012-01-01

    Background and aim We recently showed that patients with inflammatory bowel disease (IBD) report significantly more sleep disturbances. To determine whether disrupted sleep can affect the severity of inflammation and the course of IBD, we used an animal model of colonic inflammation to determine the effects of acute and chronic intermittent sleep deprivation on the severity of colonic inflammation and tissue damage in colitis and recovery from this damage. Methods Acute sleep deprivation (ASD) consisted of 24 h of forced locomotor activity in a mechanical wheel rotating at a constant speed. Chronic intermittent sleep deprivation (CISD) consisted of an acute sleep deprivation episode, followed by additional sleep deprivation periods in the wheel for 6 h every other day throughout the 10 day study period. To induce colitis, mice were given 2% dextran sodium sulfate (DSS) in their daily drinking water for 7 days. The development and severity of colitis were monitored by measuring weight loss and tissue myeloperoxidase (MPO) activity daily and colon histology scores 10 days after initiation of colitis. Results ASD or CISD did not cause colonic inflammation in vehicle-treated mice. Changes in daily body weight, tissue MPO levels and colon histopathology score were similar between mice that were sleep deprived and controls. Daily DSS ingestion caused colitis in mice. ASD worsened colonic inflammation: tissue MPO levels in ASD/DSS-treated mice were significantly higher than in DSS-treated mice that were not sleep deprived. However, the worsening of colonic inflammation by ASD was not enough to exacerbate clinical manifestations of colitis such as weight loss. In contrast, the deleterious effects of CISD were severe enough to cause worsening of histological and clinical manifestations of colitis. The deleterious effects of sleep deprivation on severity of colitis appeared to be due to both increased colonic inflammation and a decrease in the ability of mice to recover from

  17. Astrocyte-derived Adenosine and A1 Receptor Activity Contribute to Sleep Loss-Induced Deficits in Hippocampal Synaptic Plasticity and Memory in Mice

    PubMed Central

    Florian, Cédrick; Vecsey, Christopher G.; Halassa, Michael M.; Haydon, Philip G.; Abel, Ted

    2011-01-01

    Sleep deprivation (SD) can have a negative impact on cognitive function, but the mechanism(s) by which SD modulates memory remain unclear. We have previously shown that astrocyte-derived adenosine is a candidate molecule involved in the cognitive deficits following a brief period of SD (Halassa et al., 2009). In this study, we examined whether genetic disruption of SNARE-dependent exocytosis in astrocytes (dnSNARE mice) or pharmacological blockade of A1 receptor signaling using an adenosine A1 receptor (A1R) antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT) could prevent the negative effects of 6 hours of SD on hippocampal late-phase long-term potentiation (L-LTP) and hippocampus-dependent spatial object recognition memory. We found that SD impaired L-LTP in wild-type mice but not in dnSNARE mice. Similarly, this deficit in L-LTP resulting from SD was prevented by a chronic infusion of CPT. Consistent with these results, we found that hippocampus-dependent memory deficits produced by SD were rescued in dnSNARE mice and CPT-treated mice. These data provide the first evidence that astrocytic ATP and adenosine A1R activity contribute to the effects of SD on hippocampal synaptic plasticity and hippocampus-dependent memory, and suggest a new therapeutic target to reverse the hippocampus-related cognitive deficits induced by sleep loss. PMID:21562257

  18. [Forensic medical assessment of vascular and neuronal lesions in the brain associated with acute blood loss and anemia].

    PubMed

    Indiaminov, S I

    2010-01-01

    Brain tissues available for examination in the present study were obtained from 30 subjects who died from the blood loss following injuries to blood vessels and internal organs inflicted by sharp objects. The study revealed variable character of tanatogenesis induced by acute blood loss and anemia. Tanatogenesis associated with injuries to the heart and major blood vessels is most likely due to the deficiency of blood in the microcirculatory system developing in the terminal period. The main tanatogenic factors in subjects with multiple injuries to peripheral vessels are vascular dystonia and abnormal rheological properties of blood. PMID:20394188

  19. Impaired sleep and recovery after night matches in elite football players.

    PubMed

    Fullagar, Hugh H K; Skorski, Sabrina; Duffield, Rob; Julian, Ross; Bartlett, Jon; Meyer, Tim

    2016-07-01

    Despite the perceived importance of sleep for elite footballers, descriptions of the duration and quality of sleep, especially following match play, are limited. Moreover, recovery responses following sleep loss remain unclear. Accordingly, the present study examined the subjective sleep and recovery responses of elite footballers across training days (TD) and both day and night matches (DM and NM). Sixteen top division European players from three clubs completed a subjective online questionnaire twice a day for 21 days during the season. Subjective recall of sleep variables (duration, onset latency, time of wake/sleep, wake episode duration), a range of perceptual variables related to recovery, mood, performance and internal training loads and non-exercise stressors were collected. Players reported significantly reduced sleep durations for NM compared to DM (-157 min) and TD (-181 min). In addition, sleep restfulness (SR; arbitrary scale 1 = very restful, 5 = not at all restful) and perceived recovery (PR; acute recovery and stress scale 0 = not recovered at all, 6 = fully recovered) were significantly poorer following NM than both TD (SR: +2.0, PR: -2.6), and DM (SR: +1.5; PR: -1.5). These results suggest that reduced sleep quantity and quality and reduced PR are mainly evident following NM in elite players. PMID:26750446

  20. Effects of acute microinjections of thyroid hormone to the preoptic region of euthyroid adult male rats on sleep and motor activity.

    PubMed

    Martin, Joseph V; Giannopoulos, Phillip F; Moffett, Steven X; James, Thomas D

    2013-06-21

    In adult brain tissue, thyroid hormones are known to have multiple effects which are not mediated by chronic influences of the hormones on heterodimeric thyroid hormone nuclear receptors. Previous work has shown that acute microinjections of l-triiodothyronine (T3) to the preoptic region significantly influence EEG-defined sleep in hypothyroid rats. The current study examined the effects of similar microinjections in euthyroid rats. In 7 rats with histologically confirmed microinjection sites bilaterally placed in the preoptic region, slow-wave sleep time was significantly decreased, but REM and waking were increased as compared to vehicle-injected controls. The EEG-defined parameters were significantly influenced by the microinjections in a biphasic dose-response relationship; the lowest (0.3μg) and highest (10μg) doses tested were without significant effect while intermediate doses (1 and 3μg) induced significant differences from controls. There were significant diurnal variations in the measures, yet no significant interactions between the effect of hormone and time of day were demonstrated. Core body temperature was not significantly altered in the current study. The demonstration of effects of T3 within hours instead of days is consistent with a rapid mechanism of action such as a direct influence on neurotransmission. Since the T3-mediated effects were robust in the current work, euthyroid rats retain thyroid hormone sensitivity which would be needed if sleep-regulatory mechanisms in the preoptic region are continuously modulated by the hormones. This article is part of a Special Issue entitled LInked: BRES-D-12-01552 & BRES-D-12-01363R2. PMID:23348377

  1. Sleep and Rest Requirements: Physiological Considerations

    NASA Technical Reports Server (NTRS)

    Neri, David F.; Rosekind, Mark R. (Technical Monitor)

    1997-01-01

    Sleep is a vital physiological need which must be met to insure optimal functioning. A single night of significantly shortened sleep negatively impacts performance, alertness, and mood. Restricted sleep studies have shown that even a relatively small amount of sleep loss over several consecutive days can be additive and result in a cumulative sleep debt with similar detrimental effects. Compounding the problem of sleep loss in the operational environment is the poor correlation between subjective reports of sleepiness and objective measures of physiological sleep need. Some of the factors determining how sleepy an individual is at a given point in time are: (1) individual characteristics (e.g., amount of prior sleep and wakefulness, circadian phase, age), (2) environmental conditions (e.g., noise, temperature, amount of social interaction), and (3) task variables (e.g., signal rate, workload). Although sleep need can be masked with medications, the only way to reduce it is with sleep itself. The timing of the sleep period can affect sleep duration and quality and thus its restorative strength. The data are clear that increasing sleep time results in improved alertness. This paper will briefly review the scientific findings on sleep need, the effects of sleep loss, napping strategies, and the implications of incorporating physiologically sound sleep and rest strategies into the operational aviation environment.

  2. Sustained Sleep Fragmentation Induces Sleep Homeostasis in Mice

    PubMed Central

    Baud, Maxime O.; Magistretti, Pierre J.; Petit, Jean-Marie

    2015-01-01

    Study Objectives: Sleep fragmentation (SF) is an integral feature of sleep apnea and other prevalent sleep disorders. Although the effect of repetitive arousals on cognitive performance is well documented, the effects of long-term SF on electroencephalography (EEG) and molecular markers of sleep homeostasis remain poorly investigated. To address this question, we developed a mouse model of chronic SF and characterized its effect on EEG spectral frequencies and the expression of genes previously linked to sleep homeostasis including clock genes, heat shock proteins, and plasticity-related genes. Design: N/A. Setting: Animal sleep research laboratory. Participants : Sixty-six C57BL6/J adult mice. Interventions: Instrumental sleep disruption at a rate of 60/h during 14 days Measurements and Results: Locomotor activity and EEG were recorded during 14 days of SF followed by recovery for 2 days. Despite a dramatic number of arousals and decreased sleep bout duration, SF minimally reduced total quantity of sleep and did not significantly alter its circadian distribution. Spectral analysis during SF revealed a homeostatic drive for slow wave activity (SWA; 1–4 Hz) and other frequencies as well (4–40 Hz). Recordings during recovery revealed slow wave sleep consolidation and a transient rebound in SWA, and paradoxical sleep duration. The expression of selected genes was not induced following chronic SF. Conclusions: Chronic sleep fragmentation (SF) increased sleep pressure confirming that altered quality with preserved quantity triggers core sleep homeostasis mechanisms. However, it did not induce the expression of genes induced by sleep loss, suggesting that these molecular pathways are not sustainably activated in chronic diseases involving SF. Citation: Baud MO, Magistretti PJ, Petit JM. Sustained sleep fragmentation induces sleep homeostasis in mice. SLEEP 2015;38(4):567–579. PMID:25325477

  3. Sleep and sleepiness of fishermen on rotating schedules.

    PubMed

    Gander, Philippa; van den Berg, Margo; Signal, Leigh

    2008-04-01

    studies that objectively monitored the sleep of seafarers. It has the strength of operational fidelity but the weakness that large inter- and intra-individual variability in sleep, combined with the small sample size, limited the power of the study to detect statistically significant differences between sleep at home and at sea. The clear preference for sleep at night during the 12 h on/6 h off schedule at sea is consistent with the expectation that this 18 h duty/rest cycle is outside the range of entrainment of the circadian pacemaker. High levels of acute sleep loss, and residual sleepiness after sleep, were much more common at sea than at home. The longer duration of trips during the peak of the fishing season increases the risk of performance impairment due to greater cumulative sleep loss than would be expected on typical three-day trips. Key fatigue management strategies in this environment include that fishermen report to work as well rested as possible. Once at sea, the day-to-day variability in activities due to uncontrollable factors, such as fishing success, repairing gear, and weather conditions, mean that contingency planning is required for managing situations where the entire crew have experienced long periods of intensive work with minimum recovery opportunities. PMID:18533331

  4. Loss of Goosecoid-like and DiGeorge syndrome critical region 14 in interpeduncular nucleus results in altered regulation of rapid eye movement sleep

    PubMed Central

    Funato, Hiromasa; Sato, Makito; Sinton, Christopher M.; Gautron, Laurent; Williams, S. Clay; Skach, Amber; Elmquist, Joel K.; Skoultchi, Arthur I.; Yanagisawa, Masashi

    2010-01-01

    Sleep and wakefulness are regulated primarily by inhibitory interactions between the hypothalamus and brainstem. The expression of the states of rapid eye movement (REM) sleep and non-REM (NREM) sleep also are correlated with the activity of groups of REM-off and REM-on neurons in the dorsal brainstem. However, the contribution of ventral brainstem nuclei to sleep regulation has been little characterized to date. Here we examined sleep and wakefulness in mice deficient in a homeobox transcription factor, Goosecoid-like (Gscl), which is one of the genes deleted in DiGeorge syndrome or 22q11 deletion syndrome. The expression of Gscl is restricted to the interpeduncular nucleus (IP) in the ventral region of the midbrain–hindbrain transition. The IP has reciprocal connections with several cell groups implicated in sleep/wakefulness regulation. Although Gscl−/− mice have apparently normal anatomy and connections of the IP, they exhibited a reduced total time spent in REM sleep and fewer REM sleep episodes. In addition, Gscl−/− mice showed reduced theta power during REM sleep and increased arousability during REM sleep. Gscl−/− mice also lacked the expression of DiGeorge syndrome critical region 14 (Dgcr14) in the IP. These results indicate that the absence of Gscl and Dgcr14 in the IP results in altered regulation of REM sleep. PMID:20921407

  5. Sleep Quiz

    MedlinePlus

    ... Home » About the NHLBI » Organization » National Center on Sleep Disorders Research (NCSDR) » Patient & Public Information » Sleep Quiz National Center on Sleep Disorders Research Research Professional Education Patient & Public Information Communications ...

  6. Sleep Quiz

    MedlinePlus

    Skip Navigation Bar Home Current Issue Past Issues Sleep Quiz Past Issues / Summer 2007 Table of Contents ... on. Photo: iStock Take the National Center on Sleep Disorders Research Sleep Quiz TRUE OR FALSE ? _____1. ...

  7. Modeling Murine Gastric Metaplasia Through Tamoxifen-Induced Acute Parietal Cell Loss.

    PubMed

    Saenz, Jose B; Burclaff, Joseph; Mills, Jason C

    2016-01-01

    Parietal cell loss represents the initial step in the sequential progression toward gastric adenocarcinoma. In the setting of chronic inflammation, the expansion of the mucosal response to parietal cell loss characterizes a crucial transition en route to gastric dysplasia. Here, we detail methods for using the selective estrogen receptor modulator tamoxifen as a novel tool to rapidly and reversibly induce parietal cell loss in mice in order to study the mechanisms that underlie these pre-neoplastic events. PMID:27246044

  8. Aging induced endoplasmic reticulum stress alters sleep and sleep homeostasis.

    PubMed

    Brown, Marishka K; Chan, May T; Zimmerman, John E; Pack, Allan I; Jackson, Nicholas E; Naidoo, Nirinjini

    2014-06-01

    Alterations in the quality, quantity, and architecture of baseline and recovery sleep have been shown to occur during aging. Sleep deprivation induces endoplasmic reticular (ER) stress and upregulates a protective signaling pathway termed the unfolded protein response. The effectiveness of the adaptive unfolded protein response is diminished by age. Previously, we showed that endogenous chaperone levels altered recovery sleep in Drosophila melanogaster. We now report that acute administration of the chemical chaperone sodium 4-phenylbutyrate (PBA) reduces ER stress and ameliorates age-associated sleep changes in Drosophila. PBA consolidates both baseline and recovery sleep in aging flies. The behavioral modifications of PBA are linked to its suppression of ER stress. PBA decreased splicing of X-box binding protein 1 and upregulation of phosphorylated elongation initiation factor 2 α, in flies that were subjected to sleep deprivation. We also demonstrate that directly activating ER stress in young flies fragments baseline sleep and alters recovery sleep. Alleviating prolonged or sustained ER stress during aging contributes to sleep consolidation and improves recovery sleep or sleep debt discharge. PMID:24444805

  9. Atypical Wernicke's syndrome sans encephalopathy with acute bilateral vision loss due to post-chiasmatic optic tract edema

    PubMed Central

    Desai, Soaham Dilip; Shah, Diva Sidharth

    2014-01-01

    A middle aged male presented with acute bilateral vision loss, 4 weeks after undergoing gastric bypass surgery for gastric carcinoma. He had normal sensorium, fundoscopy, normal pupillary reaction to light, but had mild opthalmoparesis and nystagmus with ataxia. Magnetic resonance imaging of the brain revealed post-chiasmatic optic tract edema along with other classical features of Wernicke's syndrome. Thiamine supplementation leads to complete resolution of clinical as well as imaging findings. In appropriate clinical settings, a high index of suspicion and early treatment are essential for managing Wernicke's syndrome even in patients with atypical clinical and imaging presentation. PMID:24753673

  10. [Sleep psychiatry].

    PubMed

    Chiba, Shigeru

    2013-01-01

    Sleep disorders are serious issues in modern society. There has been marked scientific interest in sleep for a century, with the discoveries of the electrical activity of the brain (EEG), sleep-wake system, rapid eye movement (REM) sleep, and circadian rhythm system. Additionally, the advent of video-polysomnography in clinical research has revealed some of the consequences of disrupted sleep and sleep deprivation in psychiatric disorders. Decades of clinical research have demonstrated that sleep disorders are intimately tied to not only physical disease (e. g., lifestyle-related disease) but psychiatric illness. According to The International Classification of Sleep Disorders (2005), sleep disorders are classified into 8 major categories: 1) insomnia, 2) sleep-related breathing disorders, 3) hypersomnias of central origin, 4) circadian rhythm sleep disorders, 5) parasomnias, 6) sleep-related movement disorders, 7) isolated symptoms, and 8) other sleep disorders. Several sleep disorders, including obstructive sleep apnea syndrome, restless legs syndrome, periodic limb movement disorder, sleepwalking, REM sleep behavior disorder, and narcolepsy, may be comorbid or possibly mimic numerous psychiatric disorders, and can even occur due to psychiatric pharmacotherapy. Moreover, sleep disorders may exacerbate underlying psychiatric disorders when left untreated. Therefore, psychiatrists should pay attention to the intimate relationship between sleep disorders and psychiatric symptoms. Sleep psychiatry is an academic field focusing on interrelations between sleep medicine and psychiatry. This mini-review summarizes recent findings in sleep psychiatry. Future research on the bidirectional relation between sleep disturbance and psychiatric symptoms will shed light on the pathophysiological view of psychiatric disorders and sleep disorders. PMID:24050022

  11. Acute bilateral glaucoma and panuveitis as a side effect of topiramate for weight loss treatment.

    PubMed

    Pikkel, Yoav Yechezkel

    2014-01-01

    A 54-year-old male patient presented to our clinic with acute angle-closure glaucoma and panuveitis in both eyes after being treated with topiramate for binge eating and obesity. This case report emphasises the hazardous side effects of treatment with topiramate with unusual indication and the precaution a caretaker must take when treating a patient. PMID:24744070

  12. Sleep and Chronic Disease

    MedlinePlus

    ... CDC Cancel Submit Search The CDC Sleep and Sleep Disorders Note: Javascript is disabled or is not supported ... CDC.gov . Sleep About Us About Sleep Key Sleep Disorders Sleep and Chronic Disease How Much Sleep Do ...

  13. Sleep As A Strategy For Optimizing Performance.

    PubMed

    Yarnell, Angela M; Deuster, Patricia

    2016-01-01

    Recovery is an essential component of maintaining, sustaining, and optimizing cognitive and physical performance during and after demanding training and strenuous missions. Getting sufficient amounts of rest and sleep is key to recovery. This article focuses on sleep and discusses (1) why getting sufficient sleep is important, (2) how to optimize sleep, and (3) tools available to help maximize sleep-related performance. Insufficient sleep negatively impacts safety and readiness through reduced cognitive function, more accidents, and increased military friendly-fire incidents. Sufficient sleep is linked to better cognitive performance outcomes, increased vigor, and better physical and athletic performance as well as improved emotional and social functioning. Because Special Operations missions do not always allow for optimal rest or sleep, the impact of reduced rest and sleep on readiness and mission success should be minimized through appropriate preparation and planning. Preparation includes periods of "banking" or extending sleep opportunities before periods of loss, monitoring sleep by using tools like actigraphy to measure sleep and activity, assessing mental effectiveness, exploiting strategic sleep opportunities, and consuming caffeine at recommended doses to reduce fatigue during periods of loss. Together, these efforts may decrease the impact of sleep loss on mission and performance. PMID:27045502

  14. Neuronal Machinery of Sleep Homeostasis in Drosophila

    PubMed Central

    Donlea, Jeffrey M.; Pimentel, Diogo; Miesenböck, Gero

    2014-01-01

    Summary Sleep is under homeostatic control, but the mechanisms that sense sleep need and correct sleep deficits remain unknown. Here, we report that sleep-promoting neurons with projections to the dorsal fan-shaped body (FB) form the output arm of Drosophila’s sleep homeostat. Homeostatic sleep control requires the Rho-GTPase-activating protein encoded by the crossveinless-c (cv-c) gene in order to transduce sleep pressure into increased electrical excitability of dorsal FB neurons. cv-c mutants exhibit decreased sleep time, diminished sleep rebound, and memory deficits comparable to those after sleep loss. Targeted ablation and rescue of Cv-c in sleep-control neurons of the dorsal FB impair and restore, respectively, normal sleep patterns. Sleep deprivation increases the excitability of dorsal FB neurons, but this homeostatic adjustment is disrupted in short-sleeping cv-c mutants. Sleep pressure thus shifts the input-output function of sleep-promoting neurons toward heightened activity by modulating ion channel function in a mechanism dependent on Cv-c. PMID:24559676

  15. Sleep function: Toward elucidating an enigma.

    PubMed

    Krueger, James M; Frank, Marcos G; Wisor, Jonathan P; Roy, Sandip

    2016-08-01

    Sleep function remains controversial. Individual perspectives frame the issue of sleep function differently. We briefly illustrate how sleep measurement and the evolution, tissue organization levels, molecular mechanisms, and regulation of sleep could influence one's view of sleep function. Then we discuss six viable theories of sleep function. Sleep serves host-defense mechanisms and conserves caloric expenditures, but these functions likely are opportunistic functions evolving later in evolution. That sleep replenishes brain energy stores and that sleep serves a glymphatic function by removing toxic byproducts of waking activity are attractive ideas, but lack extensive supporting experimental evidence. That sleep restores performance is experimentally demonstrated and has obvious evolutionary value. However, this hypothesis lacks experimentally verified mechanisms although ideas relating to this issue are presented. Finally, the ideas surrounding the broad hypothesis that sleep serves a connectivity/plasticity function are many and attractive. There is experimental evidence that connectivity changes with sleep, sleep loss, and with changing afferent input, and that those changes are linked to sleep regulatory mechanisms. In our view, this is the leading contender for the primordial function of sleep. However, much refinement of ideas and innovative experimental approaches are needed to clarify the sleep-connectivity relationship. PMID:26447948

  16. Managing acute phosphorus loss with fertilizer source and placement: Proof of concept

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Surface water eutrophication is a pervasive global problem, with P losses from agriculture often identified as a contributor. This study was conducted to evaluate the implications of fertilizer source and placement on potential soluble P (SP) runoff. National P Runoff Project protocols were used f...

  17. ACUTE EXPOSURE TO TRIS (2-CHLOROETHYL) PHOSPHATE HIPPOCAMPAL NEURONAL LOSS AND IMPAIRS LEARNING IN RATS

    EPA Science Inventory

    Adult female, Fischer 344 rats were exposed to 275 mg/kg of tris(2- chloroethyl)phosphate (TRCP) by gavage. RCP produced consistent signs of convulsive activity within 60-90 minutes after dosing and extensive loss of CA1 hippocampal pyramidal cells when examined 7 days after dosi...

  18. BDNF in sleep, insomnia, and sleep deprivation.

    PubMed

    Schmitt, Karen; Holsboer-Trachsler, Edith; Eckert, Anne

    2016-01-01

    The protein brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors involved in plasticity of neurons in several brain regions. There are numerous evidence that BDNF expression is decreased by experiencing psychological stress and that, accordingly, a lack of neurotrophic support causes major depression. Furthermore, disruption in sleep homeostatic processes results in higher stress vulnerability and is often associated with stress-related mental disorders. Recently, we reported, for the first time, a relationship between BDNF and insomnia and sleep deprivation (SD). Using a biphasic stress model as explanation approach, we discuss here the hypothesis that chronic stress might induce a deregulation of the hypothalamic-pituitary-adrenal system. In the long-term it leads to sleep disturbance and depression as well as decreased BDNF levels, whereas acute stress like SD can be used as therapeutic intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial SD (PSD) induced a fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Key messages Brain-derived neurotrophic factor (BDNF) plays a key role in the pathophysiology of stress-related mood disorders. The interplay of stress and sleep impacts on BDNF level. Partial sleep deprivation (PSD) shows a fast action on BDNF level increase. PMID:26758201

  19. Loss of Ifnar1 in Pancreatic Acinar Cells Ameliorates the Disease Course of Acute Pancreatitis.

    PubMed

    Miller, Katharina J; Raulefs, Susanne; Kong, Bo; Steiger, Katja; Regel, Ivonne; Gewies, Andreas; Kleeff, Jörg; Michalski, Christoph W

    2015-01-01

    Type I interferon constitutes an essential component of the combinational therapy against viral disease. Acute pancreatitis is one side effect of type I interferon-based therapy, implying that activation of type I interferon signaling affects the homeostasis and integrity of pancreatic acinar cells. Here, we investigated the role of type I interferon signaling in pancreatic acinar cells using a caerulein-induced murine model of acute pancreatitis. Pancreas-specific ablation of interferon (alpha and beta) receptor 1 (Ifnar1) partially protected animals from caerulein-induced pancreatitis, as demonstrated by reduced tissue damage. Profiling of infiltrating immune cells revealed that this dampened tissue damage response correlated with the number of macrophages in the pancreas. Pharmacologic depletion of macrophages reversed the protective effect of Ifnar1 deficiency. Furthermore, expression of chemokine (C-C motif) ligand 2 (Ccl2), a potent factor for macrophage recruitment, was significantly increased in the Ifnar1-deficient pancreas. Thus, type I interferon signaling in pancreatic acinar cells controls pancreatic homeostasis by affecting the macrophage-mediated inflammatory response in the pancreas. PMID:26618925

  20. REM sleep homeostasis in the absence of REM sleep: Effects of antidepressants.

    PubMed

    McCarthy, Andrew; Wafford, Keith; Shanks, Elaine; Ligocki, Marcin; Edgar, Dale M; Dijk, Derk-Jan

    2016-09-01

    Most antidepressants suppress rapid eye movement (REM) sleep, which is thought to be important to brain function, yet the resulting REM sleep restriction is well tolerated. This study investigated the impact of antidepressants with different mechanisms of action, such as selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCA), on the regulation of REM sleep in rats. REM sleep was first demonstrated to be homeostatically regulated using 5, 8 and 10 h of REM-sleep specific restriction through EEG-triggered arousals, with an average of 91 ± 10% of lost REM sleep recovered following a 26-29 -hour recovery period. Acute treatment with the antidepressants paroxetine, citalopram and imipramine inhibited REM sleep by 84 ± 8, 84 ± 8 and 69 ± 9% respectively relative to vehicle control. The pharmacologically-induced REM sleep deficits by paroxetine and citalopram were not fully recovered, whereas, after imipramine the REM sleep deficit was fully compensated. Given the marked difference between REM sleep recovery following the administration of paroxetine, citalopram, imipramine and REM sleep restriction, the homeostatic response was further examined by pairing REM sleep specific restriction with the three antidepressants. Surprisingly, the physiologically-induced REM sleep deficits incurred prior to suppression of REM sleep by all antidepressants was consistently recovered. The data indicate that REM sleep homeostasis remains operative following subsequent treatment with antidepressants and is unaffected by additional pharmacological inhibition of REM sleep. PMID:27150557

  1. Comparative genomic hybridization in childhood acute lymphoblastic leukemia: correlation with interphase cytogenetics and loss of heterozygosity analysis.

    PubMed

    Scholz, I; Popp, S; Granzow, M; Schoell, B; Holtgreve-Grez, H; Takeuchi, S; Schrappe, M; Harbott, J; Teigler-Schlegel, A; Zimmermann, M; Fischer, C; Koeffler, H P; Bartram, C R; Jauch, A

    2001-01-15

    We used comparative genomic hybridization (CGH) to study DNA copy number changes in 71 children with acute lymphoblastic leukemia (ALL) including 50 B-lineage and 21 T-ALLs. Forty-two patients (59%) showed genomic imbalances whereby gains were more frequently observed than losses (127 vs. 29). Gains most commonly affected the entire chromosomes 21 and 10 (19.7% each), 6, 14, 18, X (15.5% each), 17 (14.1%) and 4 (11.3%). Highly hyperdiploid karyotypes (chromosome number >50) occurred more frequently in B-lineage than in T-lineage ALL (24% vs. 4.8%). In both cell lineages deletions were mainly detected on 9p (14.1%) and 12p (8.4%), and on 6q in T-lineage ALL (4.2%). These findings were compared with loss of heterozygosity (LOH) of 6q, 9p, 11q, and 12p previously performed in 56 of the 71 patients. Among 54 sites of LOH, CGH revealed losses of the respective chromosome arms in 17 LOH-positive regions (31.5%). G-banding analysis and interphase cytogenetics with subregional probes for 14 loci confirmed the presence of genomic imbalances as detected by CGH. We, therefore, conclude that, in the absence of cytogenetic data, CGH represents a suitable method for identifying hyperdiploid karyotypes as well as prognostically relevant deletions in ALL patients. PMID:11172898

  2. A Case-Crossover Study of Sleep and Work Hours and the Risk of Road Traffic Accidents

    PubMed Central

    Valent, Francesca; Di Bartolomeo, Stefano; Marchetti, Riccardo; Sbrojavacca, Rodolfo; Barbone, Fabio

    2010-01-01

    Study Objectives: Sleepiness, prolonged wakefulness, and extended work hours have been associated with increased risk of injuries and road accidents. The authors' objective was to study the relation between those factors and road accidents using a case-crossover design, effective in estimating the risk of acute events associated with transient, short effect exposures. Design: Five hundred seventy-four injured drivers presenting for care after road accidents to the Emergency Room of Udine, Italy, were enrolled in the study from March 2007 to March 2008. Sleep, work, and driving patterns in the 48 h before the accident were assessed through an interview. Measurements and Results: The relative risk (RR) of accident associated with each exposure was estimated using the case-crossover matched pair interval approach. Sleeping ≥ 11 h daily was associated with a decrease of the RR, as was sleeping less than usual. Being awake ≥ 16 h and, possibly, working > 12 h daily were associated with increases in the RR. Conclusions: Extended work hours and prolonged wakefulness increase the risk of road accidents and suggest that awareness should be raised among drivers. The findings regarding acute sleep amount are less clear, possibly due to an effect of chronic sleep loss. Citation: Valent F; Di Bartolomeo S; Marchetti R; Sbrojavacca R; Barbone F. A case-crossover study of sleep and work hours and the risk of road traffic accidents. SLEEP 2010;33(3):349-354. PMID:20337193

  3. Increased risk of severe vaso-occlusive episodes after initial acute chest syndrome in children with sickle cell anemia less than 4 years old: Sleep and asthma cohort.

    PubMed

    Vance, Leah D; Rodeghier, Mark; Cohen, Robyn T; Rosen, Carol L; Kirkham, Fenella J; Strunk, Robert C; DeBaun, Michael R

    2015-05-01

    Previous studies have shown that the highest incidence of acute chest syndrome (ACS) in sickle cell disease occurs in children <4 years old, and a history of ACS at this age is a risk factor for future ACS episodes. However, the interval associated with the highest risk of subsequent ACS or severe pain is not known. Through this mixed retrospective-prospective observational study, the Sleep and Asthma Cohort, we sought to determine the interval after an initial ACS episode during which the majority of children <4 years old are rehospitalized for ACS or severe pain. The cumulative prevalence of rehospitalization for ACS or severe pain within 6 months, 1 years, and 2 years was calculated for children with an initial ACS episode <4 years old and compared to children with an initial ACS episode ≥4 years old. A total of 44.8% and 55.2% of participants had an initial ACS episode <4 years and ≥4 years old (Range: 4-17.7 years), respectively. At 1 year following the initial ACS episode, children <4 years old had a significantly higher cumulative prevalence of rehospitalizations for ACS or pain as compared to children ≥4 years of age, 62.5 and 39.1%, respectively (P = 0.009). After initial ACS episodes, the majority of children <4 years old will be rehospitalized for ACS or severe pain within one year, suggesting the need for a therapeutic intervention for this high-risk group. PMID:25619382

  4. Sleep and Mechanical Ventilation in Critical Care.

    PubMed

    Blissitt, Patricia A

    2016-06-01

    Sleep disturbances in critically ill mechanically ventilated patients are common. Although many factors may potentially contribute to sleep loss in critical care, issues around mechanical ventilation are among the more complex. Sleep deprivation has systemic effects that may prolong the need for mechanical ventilation and length of stay in critical care and result in worse outcomes. This article provides a brief review of the physiology of sleep, physiologic changes in breathing associated with sleep, and the impact of mechanical ventilation on sleep. A summary of the issues regarding research studies to date is also included. Recommendations for the critical care nurse are provided. PMID:27215357

  5. Carvedilol promotes neurological function, reduces bone loss and attenuates cell damage after acute spinal cord injury in rats.

    PubMed

    Liu, Da; Huang, Ying; Li, Bin; Jia, Changqing; Liang, Feng; Fu, Qin

    2015-02-01

    Acute spinal cord injury (SCI) leads to permanent functional deficits via mechanical injury and secondary mechanisms, but the therapeutic strategy for SCI is limited. Carvedilol has been shown to possess multiple biological and pharmacological properties. The of the present study was to investigate the possible protective effect of carvedilol in SCI rats. An acute SCI rat model was established and neurological function was tested. After carvedilol (10 mg/kg, oral gavage) treatment for 21 days, the status of osteoporosis, neuron damage, astrocyte activation, inflammation, oxidative stress and apoptosis were evaluated in rats. Carvedilol significantly improved locomotor activity that was decreased by SCI. In addition, carvedilol promoted bone growth by regulating the expression of nuclear factor-κB ligand (receptor activator of nuclear factor-κB ligand; RANKL) and osteoprotegerin (OPG), inactivating osteoclasts and thereby increasing bone mineral density in tibias. In addition, carvedilol reduced SCI-induced neural damage, increased neuron number and reduced astrocyte activation in the spinal cord. Furthermore, the production and mRNA expression of tumour necrosis factor-α, interleukin (IL)-1β and IL-6 were significantly reduced, reduced glutathione content and superoxide dismutase activity were markedly increased and malondialdehyde content was markedly decreased in the spinal cords of carvedilol-treated rats. These results indicate that carvedilol exhibits anti-inflammatory and anti-oxidative effects in SCI rats. In addition, the expression of Fas and Fas ligand was reduced by carvedilol treatment, which, in turn, reduced cleaved caspase 3 expression and finally decreased the number of apoptotic cells in the spinal cord. In conclusion, carvedilol promotes neurological function, reduces bone loss and attenuates cell damage after acute SCI in rats. PMID:25424914

  6. Glomerular and tubular adaptive responses to acute nephron loss in the rat. Effect of prostaglandin synthesis inhibition.

    PubMed Central

    Pelayo, J C; Shanley, P F

    1990-01-01

    These studies, using in vivo micropuncture techniques in the Munich-Wistar rat, document the magnitude of changes in glomerular and tubular function and structure 24 h after approximately 75% nephron loss (Nx) and compared these results with those obtained in sham-operated rats. The contribution of either nephron hypertrophy or renal prostaglandin to these adjustments in nephron function was also explored. After acute Nx, single nephron GFR (SNGFR) was increased, on average by approximately 30%, due primarily to glomerular hyperperfusion and hypertension. The approximately 45% reduction in preglomerular and the constancy in postglomerular vascular resistances was entirely responsible for these adaptations. Although increases in fluid reabsorption in proximal convoluted tubules correlated closely with increase in SNGFR, the fractional fluid reabsorption between late proximal and early distal tubular segments was depressed. Nephron hypertrophy could not be substantiated based on either measurements of protein content in renal tissue homogenates or morphometric analysis of proximal convoluted tubules. However, acute Nx was associated with increased urinary excretory rates per functional nephron for 6-keto-PGF1 alpha and TXB2. Prostaglandin synthesis inhibition did not affect function in control nephrons, but this maneuver was associated with normalization of glomerular and tubular function in remnant nephrons. The results suggest that enhanced synthesis of cyclooxygenase-dependent products is one of the earliest responses to Nx, and even before hypertrophy the pathophysiologic effects of prostaglandin may be important contributors to the adaptations in remnant nephron function. PMID:1693376

  7. Sleep Eduction: Treatment & Therapy

    MedlinePlus

    ... Benefits Side Effects Variations Tips Healthy Sleep Habits Sleep Disorders by Category Insomnias Insomnia Child Insomnia Short Sleeper Hypersomnias Narcolepsy Insufficient Sleep Syndrome Long Sleeper Sleep Breathing Disorders Sleep Apnea Snoring Central Sleep Apnea Overview & Facts ...

  8. Sleep Talking (Somniloquy)

    MedlinePlus

    ... Benefits Side Effects Variations Tips Healthy Sleep Habits Sleep Disorders by Category Insomnias Insomnia Child Insomnia Short Sleeper Hypersomnias Narcolepsy Insufficient Sleep Syndrome Long Sleeper Sleep Breathing Disorders Sleep Apnea Snoring Central Sleep Apnea Overview & Facts ...

  9. Sleep Apnea Information Page

    MedlinePlus

    ... is Sleep Apnea? Sleep apnea is a common sleep disorder characterized by brief interruptions of breathing during sleep. ... better ways to prevent, treat, and ultimately cure sleep disorders, such as sleep apnea. NIH Patient Recruitment for ...

  10. Healthy Sleep Habits

    MedlinePlus

    ... Benefits Side Effects Variations Tips Healthy Sleep Habits Sleep Disorders by Category Insomnias Insomnia Child Insomnia Short Sleeper Hypersomnias Narcolepsy Insufficient Sleep Syndrome Long Sleeper Sleep Breathing Disorders Sleep Apnea Snoring Central Sleep Apnea Overview & Facts ...

  11. Changing your sleep habits

    MedlinePlus

    Insomnia - sleep habits; Sleep disorder - sleep habits; Problems falling asleep; Sleep hygiene ... People who have insomnia are often worried about getting enough sleep. The more they try to sleep, the more frustrated and upset they ...

  12. Sleep disorders - overview

    MedlinePlus

    ... Narcolepsy; Hypersomina; Daytime sleepiness; Sleep rhythm; Sleep disruptive behaviors; Jet lag ... a regular sleep schedule (sleep rhythm problem) Unusual behaviors during sleep (sleep-disruptive behaviors) PROBLEMS FALLING AND ...

  13. Sleep and its disorders.

    PubMed

    Vgontzas, A N; Kales, A

    1999-01-01

    Sleep disorders are very prevalent in the general population and are associated with significant medical, psychological, and social disturbances. Insomnia is the most common. When chronic, it usually reflects psychological/behavioral disturbances. Most insomniacs can be evaluated in an office setting, and a multidimensional approach is recommended, including sleep hygiene measures, psychotherapy, and medication. The parasomnias, including sleepwalking, night terrors, and nightmares, have benign implications in childhood but often reflect psychopathology or significant stress in adolescents and adults and organicity in the elderly. Excessive daytime sleepiness is typically the most frequent complaint and often reflects organic dysfunction. Narcolepsy and idiopathic hypersomnia are chronic brain disorders with an onset at a young age, whereas sleep apnea is more common in middle age and is associated with obesity and cardiovascular problems. Therapeutic naps, medications, and supportive therapy are recommended for narcolepsy and hypersomnia; continuous positive airway pressure, weight loss, surgery, and oral devices are the common treatments for sleep apnea. PMID:10073285

  14. Adult obstructive sleep apnoea.

    PubMed

    Jordan, Amy S; McSharry, David G; Malhotra, Atul

    2014-02-22

    Obstructive sleep apnoea is an increasingly common disorder of repeated upper airway collapse during sleep, leading to oxygen desaturation and disrupted sleep. Features include snoring, witnessed apnoeas, and sleepiness. Pathogenesis varies; predisposing factors include small upper airway lumen, unstable respiratory control, low arousal threshold, small lung volume, and dysfunctional upper airway dilator muscles. Risk factors include obesity, male sex, age, menopause, fluid retention, adenotonsillar hypertrophy, and smoking. Obstructive sleep apnoea causes sleepiness, road traffic accidents, and probably systemic hypertension. It has also been linked to myocardial infarction, congestive heart failure, stroke, and diabetes mellitus though not definitively. Continuous positive airway pressure is the treatment of choice, with adherence of 60-70%. Bi-level positive airway pressure or adaptive servo-ventilation can be used for patients who are intolerant to continuous positive airway pressure. Other treatments include dental devices, surgery, and weight loss. PMID:23910433

  15. Acute effects of CPAP and BiPAP breathing on pulmonary haemodynamics in patients with obstructive sleep apnoea.

    PubMed

    Palasiewicz, G; Sliwiński, P; Koziej, M; Zieliński, J

    1997-10-01

    Continuous positive airway pressure (CPAP) breathing increases alveolar and intrathoracic pressures, hampering venous return and pulmonary capillary flow. Bilevel positive airway pressure (BiPAP) breathing assuring lower expiratory pressure should impede less the pulmonary circulation. We aimed to compare the effects of CPAP and BiPAP breathing on pulmonary haemodynamics in patients with obstructive sleep apnoea (OSA). Nine male OSA patients (mean ( +/- SD) apnoea-hypopnoea index (AHD = 46 +/- 22) were studied. In each patient, intravascular and oesophageal pressures were measured and mean transmural pulmonary artery and transmural wedge pressures were calculated. After baseline recordings, patients were submitted to 25 min of CPAP and BiPAP breathing delivered in random order. The pressure of 10 cmH2O for CPAP and 10/4 cmH2O for BiPAP was used. At baseline, subjects presented with normal pulmonary arterial pressures and cardiac output (Q'). CPAP breathing resulted in a slow increase in mean pulmonary intravascular pressure from 13.8 +/- 2.0 mmHg reaching 14.8 +/- 1.8 mmHg at the 25th minute of investigation (p < 0.05). Transmural pressure did not change. There was also no change in the Q' and in the pulmonary vascular resistance. BiPAP breathing had no effect on intravascular and transmural pressures, Q' and pulmonary vascular resistance. We conclude that continuous positive airway pressure breathing increases pulmonary intravascular but not transmural, true, pressure. Bilevel positive airway pressure breathing does not affect central pulmonary haemodynamics. PMID:9510662

  16. The impact of disaster work on community volunteers: The role of peri-traumatic distress, level of personal affectedness, sleep quality and resource loss, on post-traumatic stress disorder symptoms and subjective health.

    PubMed

    Thormar, Sigridur B; Gersons, Berthold P R; Juen, Barbara; Djakababa, Maria Nelden; Karlsson, Thorlakur; Olff, Miranda

    2014-12-01

    Disaster work has shown to cause PTSD symptoms and subjective health complaints in professional emergency personnel. However, very little is known about how disaster work affects community volunteers. This first time longitudinal study examined factors contributing to post-traumatic stress disorder symptoms (PTSD) and subjective health complaints in volunteers working in an earthquake setting. At six and eighteen months post disaster, a sample of 506 Indonesian Red Cross volunteers were assessed using the Impact of Event Scale-Revised and the Subjective Health Complaints Inventory. Factors analyzed in relation to the outcomes included: peri-traumatic distress, level of personal affectedness by the disaster, sleep quality and loss of resources as a consequence of the disaster. At 18 months post-disaster the findings showed high levels of PTSD symptoms and subjective health complaints. Quality of sleep was related to both outcomes but resource loss only to PTSD symptoms. Neither peri-traumatic distress nor level of affectedness by the disaster (external versus directly affected volunteers), were predictive of symptoms. This study indicates that characteristics of disaster work e.g. low quality of sleep, may be an important contributor to PTSD symptoms and subjective health complaints in volunteers. PMID:25445088

  17. Sleep Apnea

    MedlinePlus

    Sleep apnea is a common disorder that causes your breathing to stop or get very shallow. Breathing ... an hour. The most common type is obstructive sleep apnea. It causes your airway to collapse or ...

  18. Sleep Apnea

    MedlinePlus

    Sleep apnea is a common disorder that causes your breathing to stop or get very shallow. Breathing pauses ... an hour. The most common type is obstructive sleep apnea. It causes your airway to collapse or become ...

  19. Orexin receptor antagonist-induced sleep does not impair the ability to wake in response to emotionally salient acoustic stimuli in dogs

    PubMed Central

    Tannenbaum, Pamela L.; Stevens, Joanne; Binns, Jacquelyn; Savitz, Alan T.; Garson, Susan L.; Fox, Steven V.; Coleman, Paul; Kuduk, Scott D.; Gotter, Anthony L.; Marino, Michael; Tye, Spencer J.; Uslaner, Jason M.; Winrow, Christopher J.; Renger, John J.

    2014-01-01

    The ability to awaken from sleep in response to important stimuli is a critical feature of normal sleep, as is maintaining sleep continuity in the presence of irrelevant background noise. Dual orexin receptor antagonists (DORAs) effectively promote sleep across species by targeting the evolutionarily conserved wake-promoting orexin signaling pathway. This study in dogs investigated whether DORA-induced sleep preserved the ability to awaken appropriately to salient acoustic stimuli but remain asleep when exposed to irrelevant stimuli. Sleep and wake in response to DORAs, vehicle, GABA-A receptor modulators (diazepam, eszopiclone and zolpidem) and antihistamine (diphenhydramine) administration were evaluated in telemetry-implanted adult dogs with continuous electrocorticogram, electromyogram (EMG), electrooculogram (EOG), and activity recordings. DORAs induced sleep, but GABA-A modulators and antihistamine induced paradoxical hyperarousal. Thus, salience gating studies were conducted during DORA-22 (0.3, 1, and 5 mg/kg; day and night) and vehicle nighttime sleep. The acoustic stimuli were either classically conditioned using food reward and positive attention (salient stimulus) or presented randomly (neutral stimulus). Once conditioned, the tones were presented at sleep times corresponding to maximal DORA-22 exposure. In response to the salient stimuli, dogs woke completely from vehicle and orexin-antagonized sleep across all sleep stages but rarely awoke to neutral stimuli. Notably, acute pharmacological antagonism of orexin receptors paired with emotionally salient anticipation produced wake, not cataplexy, in a species where genetic (chronic) loss of orexin receptor signaling leads to narcolepsy/cataplexy. DORA-induced sleep in the dog thereby retains the desired capacity to awaken to emotionally salient acoustic stimuli while preserving uninterrupted sleep in response to irrelevant stimuli. PMID:24904334

  20. The Effects of Sleep Continuity Disruption on Positive Mood and Sleep Architecture in Healthy Adults

    PubMed Central

    Finan, Patrick H.; Quartana, Phillip J.; Smith, Michael T.

    2015-01-01

    Objective: The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. Design: Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). Setting: The study was set in an inpatient clinical research suite. Participants: Healthy, good-sleeping men and women were included. Measurement and Results: Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). Conclusions: To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression. Citation: Finan PH, Quartana PJ, Smith MT. The effects of sleep continuity disruption on positive mood and sleep architecture in healthy adults. SLEEP 2015;38(11):1735–1742. PMID:26085289

  1. Sleep deprivation: consequences for students.

    PubMed

    Marhefka, Julie King

    2011-09-01

    During the adolescent years, a delayed pattern of the sleep-wake cycle occurs. Many parents and health care providers are not aware that once established, these poor sleep habits can continue into adulthood. Early school hours start a pattern of sleep loss that begins a cycle of daytime sleepiness, which may affect mood, behavior, and increase risk for accidents or injury. These sleep-deprived habits established in adolescence can often lead to problems during college years. Sleep hygiene can be initiated to help break the cycle, along with education and implementation of a strict regimen. Monitoring all adolescents and college-aged students for sleep insufficiency is imperative to improve both academic and emotional well-being. PMID:21846079

  2. Sleep in the intensive care unit

    PubMed Central

    Beltrami, Flávia Gabe; Nguyen, Xuân-Lan; Pichereau, Claire; Maury, Eric; Fleury, Bernard; Fagondes, Simone

    2015-01-01

    ABSTRACT Poor sleep quality is a consistently reported by patients in the ICU. In such a potentially hostile environment, sleep is extremely fragmented and sleep architecture is unconventional, with a predominance of superficial sleep stages and a limited amount of time spent in the restorative stages. Among the causes of sleep disruption in the ICU are factors intrinsic to the patients and the acute nature of their condition, as well as factors related to the ICU environment and the treatments administered, such as mechanical ventilation and drug therapy. Although the consequences of poor sleep quality for the recovery of ICU patients remain unknown, it seems to influence the immune, metabolic, cardiovascular, respiratory, and neurological systems. There is evidence that multifaceted interventions focused on minimizing nocturnal sleep disruptions improve sleep quality in ICU patients. In this article, we review the literature regarding normal sleep and sleep in the ICU. We also analyze sleep assessment methods; the causes of poor sleep quality and its potential implications for the recovery process of critically ill patients; and strategies for sleep promotion. PMID:26785964

  3. Effect of on-call-related sleep deprivation on physicians’ mood and alertness

    PubMed Central

    Wali, Siraj O.; Qutah, Karimah; Abushanab, Lujain; Basamh, Roa’a; Abushanab, Jolanar; Krayem, Ayman

    2013-01-01

    BACKGROUND AND OBJECTIVE: Physicians may experience periods of acute sleep deprivation while on-call, in addition to baseline chronic sleep deprivation which may affect physicians’ performance and patients’ safety. The purpose of this study was to determine the effect of acute sleep deprivation due to working long on-call shifts on mood and alertness, both of which may impair physicians’ performance. METHODS: Eighty-eight junior physicians working in one university hospital completed a questionnaire, before and after completion of a shift, that collected data regarding socio-demographic factors, patterns of work and sleep, Profile of Mood States (POMS), and Stanford Sleepiness Scale. Based on duration of sleep the physicians had during on-call in comparison to their usual average sleep, the participants were categorized into group 1 (those who slept many fewer hours), group 2 (those who slept fewer hours), or group 3 (those who slept the same number of hours). RESULTS: More than 87% of the participant slept 5 or fewer hours while working an on-call shift. Among all participants, the percentage of physicians who were alert post-on-call was significantly reduced compared to the percentage pre-on-call (P = 0.001). The post-on-call total POMS scores of groups 1 and 2 were significantly worse than their pre-on-call scores (P = 0.001 and 0.038, respectively), while there was no significant difference between the pre- and post-on-call POMS scores of group 3 (P = 0.165). CONCLUSION: Acute sleep loss due to working long on-call shifts significantly decreases daytime alertness and negatively affects the mood state of junior physicians. PMID:23439930

  4. Sleep and Respiration in Microgravity

    NASA Technical Reports Server (NTRS)

    West, John B.; Elliott, Ann R.; Prisk, G. Kim; Paiva, Manuel

    2003-01-01

    Sleep is often reported to be of poor quality in microgravity, and studies on the ground have shown a strong relationship between sleep-disordered breathing and sleep disruption. During the 16-day Neurolab mission, we studied the influence of possible changes in respiratory function on sleep by performing comprehensive sleep recordings on the payload crew on four nights during the mission. In addition, we measured the changes in the ventilatory response to low oxygen and high carbon dioxide in the same subjects during the day, hypothesizing that changes in ventilatory control might affect respiration during sleep. Microgravity caused a large reduction in the ventilatory response to reduced oxygen. This is likely the result of an increase in blood pressure at the peripheral chemoreceptors in the neck that occurs when the normally present hydrostatic pressure gradient between the heart and upper body is abolished. This reduction was similar to that seen when the subjects were placed acutely in the supine position in one-G. In sharp contrast to low oxygen, the ventilatory response to elevated carbon dioxide was unaltered by microgravity or the supine position. Because of the similarities of the findings in microgravity and the supine position, it is unlikely that changes in ventilatory control alter respiration during sleep in microgravity. During sleep on the ground, there were a small number of apneas (cessation of breathing) and hypopneas (reduced breathing) in these normal subjects. During sleep in microgravity, there was a reduction in the number of apneas and hypopneas per hour compared to preflight. Obstructive apneas virtually disappeared in microgravity, suggesting that the removal of gravity prevents the collapse of upper airways during sleep. Arousals from sleep were reduced in microgravity compared to preflight, and virtually all of this reduction was as a result of a reduction in the number of arousals from apneas and hypopneas. We conclude that any sleep

  5. [A case of steroid psychosis caused by treatment for acute sensorineural hearing loss].

    PubMed

    Sato, Yuki; Masuda, Masatsugu; Kohno, Naoyuki

    2013-08-01

    A 36 y/o female presented with the chief complaint of diarrhea and vomiting which had lasted for four days, and with a family history of suicide. The first general examination showed severe dehydration with hyponatremia. After admission, she was diagnosed as having isolated adrenocorticotropic hormone (ACTH) deficiency and mixed connective tissue disease, and the steroid replacement therapy was started with the dose equivalent to 7.5 mg/day of prednisolone (PSL). Three days later, she had right sensorineural hearing loss (SNHL). She was given 40 mg/day PSL in addition to the steroid replacement therapy. On the next day, she developed a persecutory type of paranoid disorder, and then was given psychiatric medication. After tapering off PSL for SNHL, the delusion began to improve with psychiatric medication. Three weeks after the onset of SNHL, her hearing level had partially recovered. Ten months later, she did not show any psychic instability. A family history of psychosis and the present history of malnutrition and connective tissue disease are risk factors of steroid psychosis. It can develop even with 5 mg PSL if the patient has a risk factor. Careful medical history taking and knowledge about the steroid psychosis will prevent the severe side effects associated with steroid treatment. PMID:24044173

  6. Cutaneous warming promotes sleep onset.

    PubMed

    Raymann, Roy J E M; Swaab, Dick F; Van Someren, Eus J W

    2005-06-01

    Sleep occurs in close relation to changes in body temperature. Both the monophasic sleep period in humans and the polyphasic sleep periods in rodents tend to be initiated when core body temperature is declining. This decline is mainly due to an increase in skin blood flow and consequently skin warming and heat loss. We have proposed that these intrinsically occurring changes in core and skin temperatures could modulate neuronal activity in sleep-regulating brain areas (Van Someren EJW, Chronobiol Int 17: 313-54, 2000). We here provide results compatible with this hypothesis. We obtained 144 sleep-onset latencies while directly manipulating core and skin temperatures within the comfortable range in eight healthy subjects under controlled conditions. The induction of a proximal skin temperature difference of only 0.78 +/- 0.03 degrees C (mean +/- SE) around a mean of 35.13 +/- 0.11 degrees C changed sleep-onset latency by 26%, i.e., by 3.09 minutes [95% confidence interval (CI), 1.91 to 4.28] around a mean of 11.85 min (CI, 9.74 to 14.41), with faster sleep onsets when the proximal skin was warmed. The reduction in sleep-onset latency occurred despite a small but significant decrease in subjective comfort during proximal skin warming. The induction of changes in core temperature (delta = 0.20 +/- 0.02 degrees C) and distal skin temperature (delta = 0.74 +/- 0.05 degrees C) were ineffective. Previous studies have demonstrated correlations between skin temperature and sleep-onset latency. Also, sleep disruption by ambient temperatures that activate thermoregulatory defense mechanisms has been shown. The present study is the first to experimentally demonstrate a causal contribution to sleep-onset latency of skin temperature manipulations within the normal nocturnal fluctuation range. Circadian and sleep-appetitive behavior-induced variations in skin temperature might act as an input signal to sleep-regulating systems. PMID:15677527

  7. Increased risk of severe vaso-occlusive episodes after initial acute chest syndrome in children with sickle cell anemia less than 4 years old: Sleep and Asthma Cohort

    PubMed Central

    Vance, Leah D; Rodeghier, Mark; Cohen, Robyn T.; Rosen, Carol L.; Kirham, Fenella J.; Strunk, Robert C.; DeBaun, Michael R.

    2015-01-01

    Previous studies have shown that the highest incidence of acute chest syndrome (ACS) in sickle cell disease (SCD) occurs in children less than 4 years old, and a history of ACS at this age is a risk factor for future ACS episodes. However, the interval associated with the highest risk of subsequent ACS or severe pain is not known. Through this mixed retrospective-prospective observational study, the Sleep and Asthma Cohort, we sought to determine the interval after an initial ACS episode during which the majority of children <4 years old are re-hospitalized for ACS or severe pain. The cumulative prevalence of re-hospitalization for ACS or severe pain within 6 months, 1 years, and 2 years was calculated for children with an initial ACS episode <4 years old and compared to children with an initial ACS episode ≥4 years old. A total of 44.8% and 55.2% of participants had an initial ACS episode <4 years and ≥4 years old (Range: 4-17.7 years), respectively. At 1 year following the initial ACS episode, children <4 years old had a significantly higher cumulative prevalence of re-hospitalizations for ACS or pain as compared to children ≥4 years of age, 62.5% and 39.1%, respectively (P = 0.009). After initial ACS episodes, the majority of children <4 years old will be re-hospitalized for ACS or severe pain within one year, suggesting the need for a therapeutic intervention for this high-risk group. PMID:25619382

  8. Effect of Patient Sex on the Severity of Coronary Artery Disease in Patients with Newly Diagnosis of Obstructive Sleep Apnoea Admitted by an Acute Coronary Syndrome

    PubMed Central

    Sánchez-de-la-Torre, Alicia; Abad, Jorge; Durán-Cantolla, Joaquín; Mediano, Olga; Cabriada, Valentín; Masdeu, María José; Terán, Joaquín; Masa, Juan Fernando; de la Peña, Mónica; Aldomá, Albina; Worner, Fernando; Valls, Joan; Barbé, Ferran; Sánchez-de-la-Torre, Manuel

    2016-01-01

    Background The cardiovascular consequences of obstructive sleep apnoea (OSA) differ by sex. We hypothesized that sex influences the severity of acute coronary syndrome (ACS) in patients with OSA. OSA was defined as an apnoea–hypopnoea index (AHI)>15 events·h-1. We evaluated the severity of ACS according to the ejection fraction, Killip class, number of diseased vessels, number of stents implanted and plasma peak troponin level. Methods We included 663 men (mean±SD, AHI 37±18 events·h-1) and 133 women (AHI 35±18 events·h-1) with OSA. Results The men were younger than the women (59±11 versus 66±11 years, p<0.0001), exhibited a higher neck circumference (p<0.0001), and were more likely to be smokers and alcohol users than women (p<0.0001, p = 0.0005, respectively). Body mass index and percentage of hypertensive patients or diabetics were similar between sexes. We observed a slight tendency for a higher Killip classification in women, although it was not statistically significant (p = 0.055). For men, we observed that the number of diseased vessels and the number of stents implanted were higher (p = 0.02, p = 0.001, respectively), and a decrease in the ejection fraction (p = 0.002). Conclusions This study shows that sex in OSA influences the severity of ACS. Men show a lower ejection fraction and an increased number of diseased vessels and number of stents implanted. PMID:27416494

  9. Sleeping Beauty transposon screen identifies signaling modules that cooperate with STAT5 activation to induce B-cell acute lymphoblastic leukemia.

    PubMed

    Heltemes-Harris, L M; Larson, J D; Starr, T K; Hubbard, G K; Sarver, A L; Largaespada, D A; Farrar, M A

    2016-06-30

    Signal transducer and activator of transcription 5 (STAT5) activation occurs frequently in human progenitor B-cell acute lymphoblastic leukemia (B-ALL). To identify gene alterations that cooperate with STAT5 activation to initiate leukemia, we crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only in B cells. Stat5b-CA mice typically do not develop B-ALL (<2% penetrance); in contrast, 89% of Stat5b-CA mice in which the T2/Onc transposon had been mobilized died of B-ALL by 3 months of age. High-throughput sequencing approaches were used to identify genes frequently targeted by the T2/Onc transposon; these included Sos1 (74%), Kdm2a (35%), Jak1 (26%), Bmi1 (19%), Prdm14 or Ncoa2 (13%), Cdkn2a (10%), Ikzf1 (8%), Caap1 (6%) and Klf3 (6%). Collectively, these mutations target three major cellular processes: (i) the Janus kinase/STAT5 pathway (ii) progenitor B-cell differentiation and (iii) the CDKN2A tumor-suppressor pathway. Transposon insertions typically resulted in altered expression of these genes, as well as downstream pathways including STAT5, extracellular signal-regulated kinase (Erk) and p38. Importantly, expression of Sos1 and Kdm2a, and activation of p38, correlated with survival, further underscoring the role these genes and associated pathways have in B-ALL. PMID:26500062

  10. Spontaneous sleep and homeostatic sleep regulation in ghrelin knockout mice.

    PubMed

    Szentirmai, Eva; Kapás, Levente; Sun, Yuxiang; Smith, Roy G; Krueger, James M

    2007-07-01

    Ghrelin is well known for its feeding and growth hormone-releasing actions. It may also be involved in sleep regulation; intracerebroventricular administration and hypothalamic microinjections of ghrelin stimulate wakefulness in rats. Hypothalamic ghrelin, together with neuropeptide Y and orexin form a food intake-regulatory circuit. We hypothesized that this circuit also promotes arousal. To further investigate the role of ghrelin in the regulation of sleep-wakefulness, we characterized spontaneous and homeostatic sleep regulation in ghrelin knockout (KO) and wild-type (WT) mice. Both groups of mice exhibited similar diurnal rhythms with more sleep and less wakefulness during the light period. In ghrelin KO mice, spontaneous wakefulness and rapid-eye-movement sleep (REMS) were slightly elevated, and non-rapid-eye-movement sleep (NREMS) was reduced. KO mice had more fragmented NREMS than WT mice, as indicated by the shorter and greater number of NREMS episodes. Six hours of sleep deprivation induced rebound increases in NREMS and REMS and biphasic changes in electroencephalographic slow-wave activity (EEG SWA) in both genotypes. Ghrelin KO mice recovered from NREMS and REMS loss faster, and the delayed reduction in EEG SWA, occurring after sleep loss-enhanced increases in EEG SWA, was shorter-lasting compared with WT mice. These findings suggest that the basic sleep-wake regulatory mechanisms in ghrelin KO mice are not impaired and they are able to mount adequate rebound sleep in response to a homeostatic challenge. It is possible that redundancy in the arousal systems of the brain or activation of compensatory mechanisms during development allow for normal sleep-wake regulation in ghrelin KO mice. PMID:17409264

  11. Acute sleep deprivation enhances avoidance learning and spatial memory and induces delayed alterations in neurochemical expression of GR, TH, DRD1, pCREB and Ki67 in rats.

    PubMed

    Azogu, Idu; de la Tremblaye, Patricia Barra; Dunbar, Megan; Lebreton, Marianne; LeMarec, Nathalie; Plamondon, Hélène

    2015-02-15

    The current study investigated the effects of acute versus repeated periods of sleep deprivation on avoidance learning and spatial memory and on the expression of discrete biochemical brain signals involved in stress regulation, motivation and brain plasticity. Male Long-Evans rats were sleep deprived using the platform-over-water method for a single 4 h period (ASD) or for daily 4h RSD period on five consecutive days (CSD). The Y maze passive avoidance task (YM-PAT) and the Morris water maze (MWM) were used to determine learning and memory 1h following the last SD period. Region-specific changes in glucocorticoid receptors (GR), tyrosine hydroxylase (TH), dopamine 1 receptors (DRD1), phospho-CREB (pCREB) and Ki-67 expression were assessed in the hippocampal formation, hypothalamus and mesolimbic regions 72 h following RSD. Behaviorally, our findings revealed increased latency to re-enter the aversive arm in the YM-PAT and reduced distance traveled and latency to reach the platform in the MWM in ASD rats compared to all other groups, indicative of improved avoidance learning and spatial memory, respectively. Acute SD enhanced TH expression in the ventral tegmental area, nucleus accumbens and A11 neurons of the hypothalamus and DRD1 expression in the lateral hypothalamus. Cell proliferation in the subventricular zone and pCREB expression in the dentate gyrus and CA3 regions was also enhanced following acute SD. In contrast, repeated SD significantly elevated GR-ir at the hypothalamic paraventricular nucleus and CA1 and CA3 layers of the hippocampus compared to all other groups. Our study supports that a brief 4h sleep deprivation period is sufficient to induce delayed neurochemical changes. PMID:25433096

  12. Sleep Insufficiency, Sleep Health Problems and Performance in High School Students

    PubMed Central

    Ming, Xue; Koransky, Rebecca; Kang, Victor; Buchman, Sarah; Sarris, Christina E.; Wagner, George C.

    2011-01-01

    A survey on sleep schedule, sleep health, school performance and school start times was conducted in 1,941 adolescents. A high level of early and circadian-disadvantaged sleep/wake schedules during weekdays was observed. Shorter sleep duration on weekdays was reported, especially in upper classmen. Complaints of inadequate sleep and sleepiness during weekdays, alarm clock use, and napping were prevalent. Night awakening and prolonged sleep onset were common and associated with poor school performance. Students with a sleep length of less than 7 hours on both weekdays and weekends exhibited poorer performance, while those who made up this sleep loss on weekends did not. The total number of poor sleep factors in an individual also correlated with poor school performance. Earlier school start times were associated with a perception of poor sleep quality, shorter sleep duration and more sleep health problems. We conclude that sleep inadequacies and sleep health problems were prevalent in this population, especially in those who started school earlier in the morning, and that these poor sleep factors were associated with school performance. PMID:22084618

  13. Mammalian sleep

    NASA Astrophysics Data System (ADS)

    Staunton, Hugh

    2005-05-01

    This review examines the biological background to the development of ideas on rapid eye movement sleep (REM sleep), so-called paradoxical sleep (PS), and its relation to dreaming. Aspects of the phenomenon which are discussed include physiological changes and their anatomical location, the effects of total and selective sleep deprivation in the human and animal, and REM sleep behavior disorder, the latter with its clinical manifestations in the human. Although dreaming also occurs in other sleep phases (non-REM or NREM sleep), in the human, there is a contingent relation between REM sleep and dreaming. Thus, REM is taken as a marker for dreaming and as REM is distributed ubiquitously throughout the mammalian class, it is suggested that other mammals also dream. It is suggested that the overall function of REM sleep/dreaming is more important than the content of the individual dream; its function is to place the dreamer protagonist/observer on the topographical world. This has importance for the developing infant who needs to develop a sense of self and separateness from the world which it requires to navigate and from which it is separated for long periods in sleep. Dreaming may also serve to maintain a sense of ‘I’ness or “self” in the adult, in whom a fragility of this faculty is revealed in neurological disorders.

  14. Sleep stages, memory and learning.

    PubMed

    Dotto, L

    1996-04-15

    Learning and memory can be impaired by sleep loss during specific vulnerable "windows" for several days after new tasks have been learned. Different types of tasks are differentially vulnerable to the loss of different stages of sleep. Memory required to perform cognitive procedural tasks is affected by the loss of rapid-eye-movement (REM) sleep on the first night after learning occurs and again on the third night after learning. REM-sleep deprivation on the second night after learning does not produce memory deficits. Declarative memory, which is used for the recall of specific facts, is not similarly affected by REM-sleep loss. The learning of procedural motor tasks, including those required in many sports, is impaired by the loss of stage 2 sleep, which occurs primarily in the early hours of the morning. These findings have implications for the academic and athletic performance of students and for anyone whose work involves ongoing learning and demands high standards of performance. PMID:8612256

  15. Sleep in disorders of consciousness

    PubMed Central

    Cologan, Victor; Schabus, Manvel; Ledoux, Didier; Moonen, Gustave; Maquet, Pierre; Laureys, Steven

    2010-01-01

    SUMMARY From a behavioral as well as neurobiological point of view, sleep and consciousness are intimately connected. A better understanding of sleep cycles and sleep architecture of patients suffering from disorders of consciousness (DOC) might therefore improve the clinical care for these patients as well as our understanding of the neural correlations of consciousness. Defining sleep in severely brain-injured patients is however problematic as both their electrophysiological and sleep patterns differ in many ways from healthy individuals. This paper discusses the concepts involved in the study of sleep of patients suffering from DOC and critically assesses the applicability of standard sleep criteria in these patients. The available literature on comatose and vegetative states as well as that on locked-in and related states following traumatic or non-traumatic severe brain injury will be reviewed. A wide spectrum of sleep disturbances ranging from almost normal patterns to severe loss and architecture disorganization are reported in cases of DOC and some patterns correlate with diagnosis and prognosis. At the present time the interactions of sleep and consciousness in brain-injured patients are a little studied subject but, the authors suggest, a potentially very interesting field of research. PMID:19524464

  16. Sleep in disorders of consciousness.

    PubMed

    Cologan, Victor; Schabus, Manvel; Ledoux, Didier; Moonen, Gustave; Maquet, Pierre; Laureys, Steven

    2010-04-01

    From a behavioral as well as neurobiological point of view, sleep and consciousness are intimately connected. A better understanding of sleep cycles and sleep architecture of patients suffering from disorders of consciousness (DOC) might therefore improve the clinical care for these patients as well as our understanding of the neural correlations of consciousness. Defining sleep in severely brain-injured patients is however problematic as both their electrophysiological and sleep patterns differ in many ways from healthy individuals. This paper discusses the concepts involved in the study of sleep of patients suffering from DOC and critically assesses the applicability of standard sleep criteria in these patients. The available literature on comatose and vegetative states as well as that on locked-in and related states following traumatic or non-traumatic severe brain injury will be reviewed. A wide spectrum of sleep disturbances ranging from almost normal patterns to severe loss and architecture disorganization are reported in cases of DOC and some patterns correlate with diagnosis and prognosis. At the present time the interactions of sleep and consciousness in brain-injured patients are a little studied subject but, the authors suggest, a potentially very interesting field of research. PMID:19524464

  17. Acute onset of bilateral visual loss during sildenafil therapy in a young infant with congenital heart disease

    PubMed Central

    Gaffuri, Marcella; Cristofaletti, Alessandra; Mansoldo, Caterina; Biban, Paolo

    2014-01-01

    We report a case of posterior non-arteritic ischaemic optic neuropathy (NAION) causing bilateral visual loss in a 7-month-old female infant, after a therapeutic course with sildenafil, a phosphodiesterase type 5 inhibitors (PDE5i). The patient was affected by a complex cyanotic congenital heart defect and had undergone cavopulmonary anastomosis (Glenn operation) 3 months ago. After 2 months of recurring chylothorax, a course of oral sildenafil was administered, with the hypothesis that pulmonary vascular resistances were increased. Approximately 4 weeks later the acute onset of visual worsening and poor pupillary light reflex prompted the diagnosis of posterior NAION. Despite a rapid cessation of PDE5i and systemic treatment with corticosteroids, no visual recovery was noticed at 2-year follow-up. NAION has been associated with PDE5i therapy in adults, but to the best of our knowledge it is almost unheard of in children. We suggest close monitoring of visual function in children undergoing treatment with sildenafil. PMID:24895393

  18. A dynamic deep sleep stage in Drosophila.

    PubMed

    van Alphen, Bart; Yap, Melvyn H W; Kirszenblat, Leonie; Kottler, Benjamin; van Swinderen, Bruno

    2013-04-17

    How might one determine whether simple animals such as flies sleep in stages? Sleep in mammals is a dynamic process involving different stages of sleep intensity, and these are typically associated with measurable changes in brain activity (Blake and Gerard, 1937; Rechtschaffen and Kales, 1968; Webb and Agnew, 1971). Evidence for different sleep stages in invertebrates remains elusive, even though it has been well established that many invertebrate species require sleep (Campbell and Tobler, 1984; Hendricks et al., 2000; Shaw et al., 2000; Sauer et al., 2003). Here we used electrophysiology and arousal-testing paradigms to show that the fruit fly, Drosophila melanogaster, transitions between deeper and lighter sleep within extended bouts of inactivity, with deeper sleep intensities after ∼15 and ∼30 min of inactivity. As in mammals, the timing and intensity of these dynamic sleep processes in flies is homeostatically regulated and modulated by behavioral experience. Two molecules linked to synaptic plasticity regulate the intensity of the first deep sleep stage. Optogenetic upregulation of cyclic adenosine monophosphate during the day increases sleep intensity at night, whereas loss of function of a molecule involved in synaptic pruning, the fragile-X mental retardation protein, increases sleep intensity during the day. Our results show that sleep is not homogenous in insects, and suggest that waking behavior and the associated synaptic plasticity mechanisms determine the timing and intensity of deep sleep stages in Drosophila. PMID:23595750

  19. Obstructive sleep apnea - adults

    MedlinePlus

    Sleep apnea - obstructive - adults; Apnea - obstructive sleep apnea syndrome - adults; Sleep-disordered breathing - adults; OSA - adults ... the upper airway for obstructive sleep apnea in adults. Sleep . 2010;33:1408-1413. PMID: 21061864 www. ...

  20. National Sleep Foundation

    MedlinePlus

    ... Turkish Ukrainian Urdu Vietnamese Welsh Yiddish Choose a Sleep Topic sleep.org Sleep Disorders View More Items ... Recommendations. More Join Now Become a Professional Member Sleep.org Footer Redirect Learn about how sleep impacts ...

  1. Sleep disorders - overview

    MedlinePlus

    Insomnia; Narcolepsy; Hypersomina; Daytime sleepiness; Sleep rhythm; Sleep disruptive behaviors; Jet lag ... excessive daytime sleepiness) Problems sticking to a regular sleep schedule (sleep rhythm problem) Unusual behaviors during sleep ( ...

  2. Sleep Environment Recommendations for Future Spaceflight Vehicles

    NASA Technical Reports Server (NTRS)

    Flynn-Evans, Erin; Caddick, Zachary

    2016-01-01

    Current evidence demonstrates that astronauts experience sleep loss and circadian desynchronization during spaceflight. Ground-based evidence demonstrates that these conditions lead to reduced performance, increased risk of injuries and accidents and short and long-term health consequences. Many of the factors contributing to these conditions relate to the habitability of the sleep environment. Noise, inadequate temperature and airflow, and inappropriate lighting and light pollution have each been associated with sleep loss and circadian misalignment during spaceflight operations and on Earth. As NASA prepares to send astronauts on long-duration, deep space missions, it is critical that the habitability of the sleep environment provide adequate mitigations for potential sleep disruptors. We conducted a comprehensive literature review summarizing optimal sleep hygiene parameters for lighting, temperature, airflow, humidity, comfort, intermittent and erratic sounds, and privacy and security in the sleep environment. We reviewed the design and use of sleep environments in a wide range of cohorts including among aquanauts, expeditioners, pilots, military personnel and ship operators. We also reviewed the specifications and sleep quality data arising from every NASA spaceflight mission, beginning with Gemini. Finally, we conducted structured interviews with individuals experienced in sleeping in non-traditional spaces including oilrig workers, Navy personnel, astronauts, and expeditioners. We also interviewed the engineers responsible for the design of the sleeping quarters presently deployed on the International Space Station. We found that the optimal sleep environment is cool, dark, quiet, and is perceived as safe and private. There are wide individual differences in the preferred sleep environment; therefore modifiable sleeping compartments are necessary to ensure all crewmembers are able to select personalized configurations for optimal sleep. A sub-optimal sleep

  3. Sleep Interacts with Aβ to Modulate Intrinsic Neuronal Excitability

    PubMed Central

    Tabuchi, Masashi; Lone, Shahnaz R.; Liu, Sha; Liu, Qili; Zhang, Julia; Spira, Adam P.; Wu, Mark N.

    2015-01-01

    SUMMARY Background Emerging data suggest an important relationship between sleep and Alzheimer’s Disease (AD), but how poor sleep promotes the development of AD remains unclear. Results Here, using a Drosophila model of AD, we provide evidence suggesting that changes in neuronal excitability underlie the effects of sleep loss on AD pathogenesis. β-amyloid (Aβ) accumulation leads to reduced and fragmented sleep, while chronic sleep deprivation increases Aβ burden. Moreover, enhancing sleep reduces Aβ deposition. Increasing neuronal excitability phenocopies the effects of reducing sleep on Aβ, and decreasing neuronal activity blocks the elevated Aβ accumulation induced by sleep deprivation. At the single neuron level, we find that chronic sleep deprivation, as well as Aβ expression, enhances intrinsic neuronal excitability. Importantly, these data reveal that sleep loss exacerbates Aβ–induced hyperexcitability and suggest that defects in specific K+ currents underlie the hyperexcitability caused by sleep loss and Aβ expression. Finally, we show that feeding levetiracetam, an anti-epileptic medication, to Aβ-expressing flies suppresses neuronal excitability and significantly prolongs their lifespan. Conclusions Our findings directly link sleep loss to changes in neuronal excitability and Aβ accumulation and further suggest that neuronal hyperexcitability is an important mediator of Aβ toxicity. Taken together, these data provide a mechanistic framework for a positive feedback loop, whereby sleep loss and neuronal excitation accelerate the accumulation of Aβ, a key pathogenic step in the development of AD. PMID:25754641

  4. Sleep Loss Reduces the DNA-Binding of BMAL1, CLOCK, and NPAS2 to Specific Clock Genes in the Mouse Cerebral Cortex

    PubMed Central

    Curie, Thomas; Franken, Paul

    2011-01-01

    We have previously demonstrated that clock genes contribute to the homeostatic aspect of sleep regulation. Indeed, mutations in some clock genes modify the markers of sleep homeostasis and an increase in homeostatic sleep drive alters clock gene expression in the forebrain. Here, we investigate a possible mechanism by which sleep deprivation (SD) could alter clock gene expression by quantifying DNA-binding of the core-clock transcription factors CLOCK, NPAS2, and BMAL1 to the cis-regulatory sequences of target clock genes in mice. Using chromatin immunoprecipitation (ChIP), we first showed that, as reported for the liver, DNA-binding of CLOCK and BMAL1 to target clock genes changes in function of time-of-day in the cerebral cortex. Tissue extracts were collected at ZT0 (light onset), −6, −12, and −18, and DNA enrichment of E-box or E'-box containing sequences was measured by qPCR. CLOCK and BMAL1 binding to Cry1, Dbp, Per1, and Per2 depended on time-of-day, with maximum values reached at around ZT6. We then observed that SD, performed between ZT0 and −6, significantly decreased DNA-binding of CLOCK and BMAL1 to Dbp, consistent with the observed decrease in Dbp mRNA levels after SD. The DNA-binding of NPAS2 and BMAL1 to Per2 was also decreased by SD, although SD is known to increase Per2 expression in the cortex. DNA-binding to Per1 and Cry1 was not affected by SD. Our results show that the sleep-wake history can affect the clock molecular machinery directly at the level of chromatin binding thereby altering the cortical expression of Dbp and Per2 and likely other targets. Although the precise dynamics of the relationship between DNA-binding and mRNA expression, especially for Per2, remains elusive, the results also suggest that part of the reported circadian changes in DNA-binding of core clock components in tissues peripheral to the suprachiasmatic nuclei could, in fact, be sleep-wake driven. PMID:22039518

  5. Sleep loss reduces the DNA-binding of BMAL1, CLOCK, and NPAS2 to specific clock genes in the mouse cerebral cortex.

    PubMed

    Mongrain, Valérie; La Spada, Francesco; Curie, Thomas; Franken, Paul

    2011-01-01

    We have previously demonstrated that clock genes contribute to the homeostatic aspect of sleep regulation. Indeed, mutations in some clock genes modify the markers of sleep homeostasis and an increase in homeostatic sleep drive alters clock gene expression in the forebrain. Here, we investigate a possible mechanism by which sleep deprivation (SD) could alter clock gene expression by quantifying DNA-binding of the core-clock transcription factors CLOCK, NPAS2, and BMAL1 to the cis-regulatory sequences of target clock genes in mice. Using chromatin immunoprecipitation (ChIP), we first showed that, as reported for the liver, DNA-binding of CLOCK and BMAL1 to target clock genes changes in function of time-of-day in the cerebral cortex. Tissue extracts were collected at ZT0 (light onset), -6, -12, and -18, and DNA enrichment of E-box or E'-box containing sequences was measured by qPCR. CLOCK and BMAL1 binding to Cry1, Dbp, Per1, and Per2 depended on time-of-day, with maximum values reached at around ZT6. We then observed that SD, performed between ZT0 and -6, significantly decreased DNA-binding of CLOCK and BMAL1 to Dbp, consistent with the observed decrease in Dbp mRNA levels after SD. The DNA-binding of NPAS2 and BMAL1 to Per2 was also decreased by SD, although SD is known to increase Per2 expression in the cortex. DNA-binding to Per1 and Cry1 was not affected by SD. Our results show that the sleep-wake history can affect the clock molecular machinery directly at the level of chromatin binding thereby altering the cortical expression of Dbp and Per2 and likely other targets. Although the precise dynamics of the relationship between DNA-binding and mRNA expression, especially for Per2, remains elusive, the results also suggest that part of the reported circadian changes in DNA-binding of core clock components in tissues peripheral to the suprachiasmatic nuclei could, in fact, be sleep-wake driven. PMID:22039518

  6. Chronic Stress is Prospectively Associated with Sleep in Midlife Women: The SWAN Sleep Study

    PubMed Central

    Hall, Martica H.; Casement, Melynda D.; Troxel, Wendy M.; Matthews, Karen A.; Bromberger, Joyce T.; Kravitz, Howard M.; Krafty, Robert T.; Buysse, Daniel J.

    2015-01-01

    Study Objectives: Evaluate whether levels of upsetting life events measured over a 9-y period prospectively predict subjective and objective sleep outcomes in midlife women. Design: Prospective cohort study. Setting: Four sites across the United States. Participants: 330 women (46–57 y of age) enrolled in the Study of Women's Health Across the Nation (SWAN) Sleep Study. Interventions: N/A. Measurements and Results: Upsetting life events were assessed annually for up to 9 y. Trajectory analysis applied to life events data quantitatively identified three distinct chronic stress groups: low stress, moderate stress, and high stress. Sleep was assessed by self-report and in-home polysomnography (PSG) during the ninth year of the study. Multivariate analyses tested the prospective association between chronic stress group and sleep, adjusting for race, baseline sleep complaints, marital status, body mass index, symptoms of depression, and acute life events at the time of the Sleep Study. Women characterized by high chronic stress had lower subjective sleep quality, were more likely to report insomnia, and exhibited increased PSG-assessed wake after sleep onset (WASO) relative to women with low to moderate chronic stress profiles. The effect of chronic stress group on WASO persisted in the subsample of participants without baseline sleep complaints. Conclusions: Chronic stress is prospectively associated with sleep disturbance in midlife women, even after adjusting for acute stressors at the time of the sleep study and other factors known to disrupt sleep. These results are consistent with current models of stress that emphasize the cumulative effect of stressors on health over time. Citation: Hall MH, Casement MD, Troxel WM, Matthews KA, Bromberger JT, Kravitz HM, Krafty RT, Buysse DJ. Chronic stress is prospectively associated with sleep in midlife women: the SWAN Sleep Study. SLEEP 2015;38(10):1645–1654. PMID:26039965

  7. Continued improvement in survival of acute myeloid leukemia patients: an application of the loss in expectation of life.

    PubMed

    Bower, H; Andersson, T M-L; Björkholm, M; Dickman, P W; Lambert, P C; Derolf, Å R

    2016-01-01

    We evaluated temporal trends in survival of Swedish acute myeloid leukemia (AML) patients diagnosed between 1973 and 2011 using relative survival ratios (RSRs) and a measure called the loss in expectation of life (LEL). RSRs increased most for patients <60 years at diagnosis during the first calendar periods, but between 1997-2005 and 2006-2011 the most pronounced increase was for those aged 61-70 years at diagnosis; RSR changed from 0.16 (95% confidence interval (CI): 0.13-0.19) to 0.28 (95% CI: 0.23-0.33), respectively. The LEL for males aged 35 years at diagnosis was 41.0 (95% CI: 40.1-41.8) years in 1975 and 19.5 (95% CI: 16.4-22.5) years in 2011. For males aged 65 years, the corresponding figures were 13.8 (95% CI: 13.7-14.0) and 12.0 (95% CI: 11.3-12.8). Conditional LEL estimates suggested that patients who survive 5 years postdiagnosis have shorter remaining lifespan than the general population. The proportion of expected life lost (PELL) suggested that male 65-year-old patients lost 75% of their life expectancy in 2005 and 66% if they were diagnosed in 2011. Survival continued to increase to 2011, with larger improvements in those aged 61-70 years at diagnosis. The LEL and PELL are intuitive measures that may be useful in communicating survival statistics to patients, clinicians and health-care providers. PMID:26849011

  8. Continued improvement in survival of acute myeloid leukemia patients: an application of the loss in expectation of life

    PubMed Central

    Bower, H; Andersson, T M-L; Björkholm, M; Dickman, P W; Lambert, P C; Derolf, Å R

    2016-01-01

    We evaluated temporal trends in survival of Swedish acute myeloid leukemia (AML) patients diagnosed between 1973 and 2011 using relative survival ratios (RSRs) and a measure called the loss in expectation of life (LEL). RSRs increased most for patients <60 years at diagnosis during the first calendar periods, but between 1997–2005 and 2006–2011 the most pronounced increase was for those aged 61–70 years at diagnosis; RSR changed from 0.16 (95% confidence interval (CI): 0.13–0.19) to 0.28 (95% CI: 0.23–0.33), respectively. The LEL for males aged 35 years at diagnosis was 41.0 (95% CI: 40.1–41.8) years in 1975 and 19.5 (95% CI: 16.4–22.5) years in 2011. For males aged 65 years, the corresponding figures were 13.8 (95% CI: 13.7–14.0) and 12.0 (95% CI: 11.3–12.8). Conditional LEL estimates suggested that patients who survive 5 years postdiagnosis have shorter remaining lifespan than the general population. The proportion of expected life lost (PELL) suggested that male 65-year-old patients lost 75% of their life expectancy in 2005 and 66% if they were diagnosed in 2011. Survival continued to increase to 2011, with larger improvements in those aged 61–70 years at diagnosis. The LEL and PELL are intuitive measures that may be useful in communicating survival statistics to patients, clinicians and health-care providers. PMID:26849011

  9. Loss of activator of G-protein signaling 3 impairs renal tubular regeneration following acute kidney injury in rodents

    PubMed Central

    Regner, Kevin R.; Nozu, Kandai; Lanier, Stephen M.; Blumer, Joe B.; Avner, Ellis D.; Sweeney, William E.; Park, Frank

    2011-01-01

    The intracellular mechanisms underlying renal tubular epithelial cell proliferation and tubular repair following ischemia-reperfusion injury (IRI) remain poorly understood. In this report, we demonstrate that activator of G-protein signaling 3 (AGS3), an unconventional receptor-independent regulator of heterotrimeric G-protein function, influences renal tubular regeneration following IRI. In rat kidneys exposed to IRI, there was a temporal induction in renal AGS3 protein expression that peaked 72 h after reperfusion and corresponded to the repair and recovery phase following ischemic injury. Renal AGS3 expression was localized predominantly to the recovering outer medullary proximal tubular cells and was highly coexpressed with Ki-67, a marker of cell proliferation. Kidneys from mice deficient in the expression of AGS3 exhibited impaired renal tubular recovery 7 d following IRI compared to wild-type AGS3-expressing mice. Mechanistically, genetic knockdown of endogenous AGS3 mRNA and protein in renal tubular epithelial cells reduced cell proliferation in vitro. Similar reductions in renal tubular epithelial cell proliferation were observed following incubation with gallein, a selective inhibitor of Gβγ subunit activity, and lentiviral overexpression of the carboxyl-terminus of G-protein-coupled receptor kinase 2 (GRK2ct), a scavenger of Gβγ subunits. In summary, these data suggest that AGS3 acts through a novel receptor-independent mechanism to facilitate renal tubular epithelial cell proliferation and renal tubular regeneration.—Regner, K. R., Nozu, K., Lanier, S. M., Blumer, J. B., Avner, E. D., Sweeney, Jr., W. E., Park, F. Loss of activator of G-protein signaling 3 impairs renal tubular regeneration following acute kidney injury in rodents. PMID:21343176

  10. Differential loss of natural killer cell activity in patients with acute myocardial infarction and stable angina pectoris

    PubMed Central

    Yan, Wenwen; Zhou, Lin; Wen, Siwan; Duan, Qianglin; Huang, Feifei; Tang, Yu; Liu, Xiaohong; Chai, Yongyan; Wang, Lemin

    2015-01-01

    Background: To evaluate the activity of natural killer cells through their inhibitory and activating receptors and quantity in peripheral blood mononuclear cells extracted from patients with acute myocardial infarction, stable angina pectoris and the controls. Methods: 100 patients with myocardial infarction, 100 with stable angina, and 20 healthy volunteers were recruited into the study. 20 randomly chosen people per group were examined for the whole human genome microarray analysis to detect the gene expressions of all 40 inhibitory and activating natural killer cell receptors. Flow cytometry analysis was applied to all 200 patients to measure the quantity of natural killer cells. Results: In myocardial infarction group, the mRNA expressions of six inhibitory receptors KIR2DL2, KIR3DL3, CD94, NKG2A, KLRB1, KLRG1, and eight activating receptors KIR2DS3, KIR2DS5, NKp30, NTB-A, CRACC, CD2, CD7 and CD96 were significantly down-regulated (P<0.05) compared with both angina patients and the controls. There was no statistical difference in receptor expressions between angina patients and control group. The quantity of natural killer cells was significantly decreased in both infarction and angina patients compared with normal range (P<0.001). Conclusions: The significant mRNAs down-regulation of several receptors in myocardial infarction group and reduction in the quantity of natural killer cells in both myocardial infarction and angina patients showed a quantitative loss and dysfunction of natural killer cells in myocardial infarction patients. PMID:26823790

  11. Sleep in thyrotoxicosis

    PubMed Central

    Sridhar, G. R.; Putcha, Venkata; Lakshmi, G.

    2011-01-01

    Objective: Pattern of sleep in hyperthyroid state / thyrotoxicosis has not been systematically studied. It is being characterized as poor without further elaboration. We analyzed the pattern of sleep in a large sample of individuals with thyrotoxicosis who came to our endocrine center in southern India. Materials and Methods: We identified individuals with the diagnosis of ‘thyrotoxicosis’ from our electronic medical record database, and evaluated clinical parameters and pattern of their sleep: difficulty in falling asleep (DFA), difficulty in maintaining sleep (DMS), excess daytime sleepiness). In the first phase, univariate analysis with logistic regression was performed. Multivariate logistic regression was performed in the next phase on variables with a P-value < 0.1: these were considered as potential categories/ variables. Results: In model response variable with DFA, multivariate logistic regression predicted that subjects with abnormal appetite (more 1.7 or less 2.2), change in bowel motion (loose 1.5 or constipation 2.8), in mood (easy loss of temper 3.4), change of voice -- hoarse 7.4 or moderately hoarse 3.1), tended to have higher chances of difficulty in falling asleep (DFA). Patients with tremor (yes = 5.4) had greater likelihood of difficulty in maintaining sleep (DMS). Conclusions: Individuals with hyperthyroidism/thyrotoxicosis principally had difficulty in falling asleep DFA, which was related to hyperkinetic features. PMID:21584162

  12. [CHANGING OF THE MORPHOMETRIC AND CYTOLOGICAL INDEXES OF THE SPLEEN IN THE CONDITION OF ACUTE BLOOD LOSS ON THE BACKGROUND OF STEM CELLS INSERTION].

    PubMed

    Maklakova, I Yu; Yastrebov, A P; Grebnev, D Yu

    2015-01-01

    The objective of the work was to study morphometric and cytological indexes of the spleen in mature and old laboratory animals after acute blood loss on the background of allogenic transplantation of placenta MMSC and GSC. The study proved that 5 days after acute blood loss on the background of stem cells transplantations to the mature animals there was a reduction of lymphoid follicles area due to reduction in thymus independent area. There were no immunosuppressive effects to the white pulp of the spleen in old animals. The increase of leucocytes' and erythrocytes' elements in red pulp in the mature animals was noted. In old animals, the increase of cells' density in red pulp is mainly due to increased number of erythroid cells. PMID:26856082

  13. Joint bleeding in factor VIII deficient mice causes an acute loss of trabecular bone and calcification of joint soft tissues which is prevented with aggressive factor replacement

    PubMed Central

    Lau, Anthony G.; Sun, Junjiang; Hannah, William B.; Livingston, Eric W.; Heymann, Dominique; Bateman, Ted A.; Monahan, Paul E.

    2015-01-01

    Introduction While chronic degenerative arthropathy is the main morbidity of hemophilia, a very high prevalance of low bone density is also seen in men and boys with hemophilia. The current study investigates bone degradation in the knee joint of hemophilic mice resulting from hemarthrosis and the efficacy of aggressive treatment with factor VIII in the period surrounding injury to prevent bone pathology. Methods Skeletally mature factor VIII knock-out mice were subjected to knee joint hemorrhage induced by puncture of the left knee joint capsule. Mice received either intravenous Factor VIII treatment or placebo immediately prior to injury and at hours 4, 24, 48, 72 and 96 after hemorrhage. Mice were euthanized two-weeks after injury and the joint morphology and loss of bone in the proximal tibia was assessed using microCT imaging. Results Quantitative microCT imaging of the knee joint found acute bone loss at the proximal tibia following injury including loss of trabecular bone volumetric density and bone mineral density, as well as trabecular connectivity density, number, and thickness. Unexpectedly, joint injury also resulted in calcification of the joint soft tissues including the tendons, ligaments, menisci, and cartilage. Treatment with factor VIII prevented this bone and soft tissue degeneration. Conclusion Knee joint hemorrhage resulted in acute changes of adjacent bone including loss of bone density and mineralization of joint soft tissues. The rapid calcification and loss of bone has implications for the initiation and progression of osteoarthritic degradation following joint bleeding. PMID:24712867

  14. Joint bleeding in factor VIII deficient mice causes an acute loss of trabecular bone and calcification of joint soft tissues which is prevented with aggressive factor replacement.

    PubMed

    Lau, A G; Sun, J; Hannah, W B; Livingston, E W; Heymann, D; Bateman, T A; Monahan, P E

    2014-09-01

    While chronic degenerative arthropathy is the main morbidity of haemophilia, a very high prevalence of low bone density is also seen in men and boys with haemophilia. This study investigates bone degradation in the knee joint of haemophilic mice resulting from haemarthrosis and the efficacy of aggressive treatment with factor VIII in the period surrounding injury to prevent bone pathology. Skeletally mature factor VIII knock-out mice were subjected to knee joint haemorrhage induced by puncture of the left knee joint capsule. Mice received either intravenous factor VIII treatment or placebo immediately prior to injury and at hours 4, 24, 48, 72 and 96 after haemorrhage. Mice were killed 2-weeks after injury and the joint morphology and loss of bone in the proximal tibia was assessed using microCT imaging. Quantitative microCT imaging of the knee joint found acute bone loss at the proximal tibia following injury including loss of trabecular bone volumetric density and bone mineral density, as well as trabecular connectivity density, number and thickness. Unexpectedly, joint injury also resulted in calcification of the joint soft tissues including the tendons, ligaments, menisci and cartilage. Treatment with factor VIII prevented this bone and soft tissue degeneration. Knee joint haemorrhage resulted in acute changes in adjacent bone including loss of bone density and mineralization of joint soft tissues. The rapid calcification and loss of bone has implications for the initiation and progression of osteoarthritic degradation following joint bleeding. PMID:24712867

  15. Sleep and Aging

    MedlinePlus

    ... There are two types of sleep: non-rapid eye movement -- or NREM sleep -- and rapid eye movement -- or REM sleep. NREM sleep includes four stages, ranging from light to deep sleep. Then we go into REM sleep, the most active ... During REM sleep, the eyes move back and forth beneath the eyelids and ...

  16. Loss of extracellular superoxide dismutase leads to acute lung damage in the presence of ambient air: a potential mechanism underlying adult respiratory distress syndrome.

    PubMed

    Gongora, Maria Carolina; Lob, Heinrich E; Landmesser, Ulf; Guzik, Tomasz J; Martin, W David; Ozumi, Kiyoski; Wall, Susan M; Wilson, David Scott; Murthy, Niren; Gravanis, Michael; Fukai, Tohru; Harrison, David G

    2008-10-01

    The extracellular superoxide dismutase 3 (SOD3) is highly expressed in both blood vessels and lungs. In different models of pulmonary injury, SOD3 is reduced; however, it is unclear whether this contributes to lung injury. To study the role of acute SOD3 reduction in lung injury, the SOD3 gene was deleted in adult mice by using the Cre-Lox technology. Acute reduction of SOD3 led to a fivefold increase in lung superoxide, marked inflammatory cell infiltration, a threefold increase in the arterial-alveolar gradient, respiratory acidosis, histological changes similar to those observed in adult respiratory distress syndrome, and 85% mortality. Treatment with the SOD mimetic MnTBAP and intranasal administration of SOD-containing polyketal microparticles reduced mortality, prevented the histological alterations, and reduced lung superoxide levels. To understand how mice with the SOD3 embryonic deletion survived without lung injury, gene array analysis was performed. These data demonstrated the up-regulation of 37 genes and down-regulation of nine genes, including those involved in cell signaling, inflammation, and gene transcription in SOD3-/- mice compared with either mice with acute SOD3 reduction or wild-type controls. These studies show that SOD3 is essential for survival in the presence of ambient oxygen and that acute loss of this enzyme can lead to severe lung damage. Strategies either to prevent SOD3 inactivation or to augment its levels might prove useful in the treatment of acute lung injury. PMID:18787098

  17. Sleep and REM sleep disturbance in the pathophysiology of PTSD: the role of extinction memory.

    PubMed

    Pace-Schott, Edward F; Germain, Anne; Milad, Mohammed R

    2015-01-01

    Post-traumatic stress disorder (PTSD) is accompanied by disturbed sleep and an impaired ability to learn and remember extinction of conditioned fear. Following a traumatic event, the full spectrum of PTSD symptoms typically requires several months to develop. During this time, sleep disturbances such as insomnia, nightmares, and fragmented rapid eye movement sleep predict later development of PTSD symptoms. Only a minority of individuals exposed to trauma go on to develop PTSD. We hypothesize that sleep disturbance resulting from an acute trauma, or predating the traumatic experience, may contribute to the etiology of PTSD. Because symptoms can worsen over time, we suggest that continued sleep disturbances can also maintain and exacerbate PTSD. Sleep disturbance may result in failure of extinction memory to persist and generalize, and we suggest that this constitutes one, non-exclusive mechanism by which poor sleep contributes to the development and perpetuation of PTSD. Also reviewed are neuroendocrine systems that show abnormalities in PTSD, and in which stress responses and sleep disturbance potentially produce synergistic effects that interfere with extinction learning and memory. Preliminary evidence that insomnia alone can disrupt sleep-dependent emotional processes including consolidation of extinction memory is also discussed. We suggest that optimizing sleep quality following trauma, and even strategically timing sleep to strengthen extinction memories therapeutically instantiated during exposure therapy, may allow sleep itself to be recruited in the treatment of PTSD and other trauma and stress-related disorders. PMID:26034578

  18. Acute alertness-promoting effects of a novel histamine subtype-3 receptor inverse agonist in healthy sleep-deprived male volunteers.

    PubMed

    Iannone, R; Palcza, J; Renger, J J; Calder, N; Cerchio, K; Gottesdiener, K; Hargreaves, R; Dijk, D J; Boyle, J; Murphy, M G

    2010-12-01

    The alertness-promoting effect of MK-0249 (10 or 50 mg), a histamine subtype-3 receptor (HRH3) inverse agonist (IA), was evaluated in the stimulant reference sleep deprivation model (SRSDM) using a double-blind, double-dummy, placebo- and modafinil- (200 mg) controlled, four-period crossover design in 24 healthy young men. The two primary hypotheses were related to sleep latency (first appearance of one epoch of stage 2, 3, or 4 or REM sleep, as detected using polysomnography (PSG)) at 8:00 AM on day 2. Statistically significant increases in sleep latency were observed in association with the use of modafinil 200 mg (9.07 min; P < 0.0001), MK-0249 50 mg (5.17 min; P = 0.008), and MK-0249 10 mg (5.45 min; P = 0.005) at the maintenance of wakefulness test (MWT) at 8:00 AM. Sleep latency was higher when averaged over all MWT time points (P < 0.0001 for modafinil and for both doses of MK-0249). The alertness-promoting effect with the use of MK-0249 in the SRSDM suggests that HRH3 IAs may be effective in disorders involving excessive somnolence. PMID:20981000

  19. Effects of cumulative stressful and acute variation episodes of farm climate conditions on late embryo/early fetal loss in high producing dairy cows

    NASA Astrophysics Data System (ADS)

    Santolaria, Pilar; López-Gatius, Fernando; García-Ispierto, Irina; Bech-Sàbat, Gregori; Angulo, Eduardo; Carretero, Teresa; Sánchez-Nadal, Jóse Antonio; Yániz, Jesus

    2010-01-01

    The aim of this study was to determine possible relationships between farm climate conditions, recorded from day 0 to day 40 post-artificial insemination (AI), and late embryo/early fetal loss in high producing dairy cows. Pregnancy was diagnosed by rectal ultrasonography between 28 and 34 days post-AI. Fetal loss was registered when a further 80- to 86-day diagnosis proved negative. Climate variables such as air temperature and relative humidity (RH) were monitored in the cubicles area for each 30-min period. Temperature-humidity indices (THI); cumulative stressful values and episodes of acute change (defined as the mean daily value 1.2 times higher or lower than the mean daily values of the 10 previous days) of the climate variables were calculated. The data were derived from 759 cows in one herd. A total of 692 pregnancies (91.2%) carried singletons and 67 (8.8%) carried twins. No triplets were recorded. Pregnancy loss was recorded in 6.7% (51/759) of pregnancies: 5.6% (39/692) in single and 17.9% (12/67) in twin pregnancies. Using logistic regression procedures, a one-unit increase in the daily cumulative number of hours for the THI values higher than 85 during days 11-20 of gestation caused a 1.57-fold increase in the pregnancy loss, whereas the likelihood of fetal loss increased by a factor of 1.16 for each additional episode of acute variation for the maximum THI values during gestation days 0-40. THI values higher than 85 and episodes of acute variation for the maximum THI values were only recorded during the warm and cool periods, respectively. The presence of twins led to a 3.98-fold increase in pregnancy loss. In conclusion, our findings show that cumulative stressful and episodes of acute variation of climatic conditions can compromise the success of gestation during both the cool and warm periods of the year. Twin pregnancy was confirmed as a main factor associated with pregnancy loss.

  20. Sleep schedules and daytime functioning in adolescents.

    PubMed

    Wolfson, A R; Carskadon, M A

    1998-08-01

    Sleep and waking behaviors change significantly during the adolescent years. The objective of this study was to describe the relation between adolescents' sleep/wake habits, characteristics of students (age, sex, school), and daytime functioning (mood, school performance, and behavior). A Sleep Habits Survey was administered in homeroom classes to 3,120 high school students at 4 public high schools from 3 Rhode Island school districts. Self-reported total sleep times (school and weekend nights) decreased by 40-50 min across ages 13-19, ps < .001. The sleep loss was due to increasingly later bedtimes, whereas rise times were more consistent across ages. Students who described themselves as struggling or failing school (C's, D's/F's) reported that on school nights they obtain about 25 min less sleep and go to bed an average of 40 min later than A and B students, ps < .001. In addition, students with worse grades reported greater weekend delays of sleep schedule than did those with better grades. Furthermore, this study examined a priori defined adequate sleep habit groups versus less than adequate sleep habit groups on their daytime functioning. Students in the short school-night total sleep group (< 6 hr 45 min) and/or large weekend bedtime delay group (> 120 min) reported increased daytime sleepiness, depressive mood, and sleep/wake behavior problems, ps < .05, versus those sleeping longer than 8 hr 15 min with less than 60 min weekend delay. Altogether, most of the adolescents surveyed do not get enough sleep, and their sleep loss interferes with daytime functioning. PMID:9768476

  1. Troubled sleep

    PubMed Central

    Haig, David

    2014-01-01

    Disrupted sleep is probably the most common complaint of parents with a new baby. Night waking increases in the second half of the first year of infant life and is more pronounced for breastfed infants. Sleep-related phenotypes of infants with Prader-Willi and Angelman syndromes suggest that imprinted genes of paternal origin promote greater wakefulness whereas imprinted genes of maternal origin favor more consolidated sleep. All these observations are consistent with a hypothesis that waking at night to suckle is an adaptation of infants to extend their mothers’ lactational amenorrhea, thus delaying the birth of a younger sib and enhancing infant survival. PMID:24610432

  2. Pathophysiology of Sleep Apnea

    PubMed Central

    Veasey, Sigrid C.; Morgan, Barbara J.; O'Donnell, Christopher P.

    2010-01-01

    Sleep-induced apnea and disordered breathing refers to intermittent, cyclical cessations or reductions of airflow, with or without obstructions of the upper airway (OSA). In the presence of an anatomically compromised, collapsible airway, the sleep-induced loss of compensatory tonic input to the upper airway dilator muscle motor neurons leads to collapse of the pharyngeal airway. In turn, the ability of the sleeping subject to compensate for this airway obstruction will determine the degree of cycling of these events. Several of the classic neurotransmitters and a growing list of neuromodulators have now been identified that contribute to neurochemical regulation of pharyngeal motor neuron activity and airway patency. Limited progress has been made in developing pharmacotherapies with acceptable specificity for the treatment of sleep-induced airway obstruction. We review three types of major long-term sequelae to severe OSA that have been assessed in humans through use of continuous positive airway pressure (CPAP) treatment and in animal models via long-term intermittent hypoxemia (IH): 1) cardiovascular. The evidence is strongest to support daytime systemic hypertension as a consequence of severe OSA, with less conclusive effects on pulmonary hypertension, stroke, coronary artery disease, and cardiac arrhythmias. The underlying mechanisms mediating hypertension include enhanced chemoreceptor sensitivity causing excessive daytime sympathetic vasoconstrictor activity, combined with overproduction of superoxide ion and inflammatory effects on resistance vessels. 2) Insulin sensitivity and homeostasis of glucose regulation are negatively impacted by both intermittent hypoxemia and sleep disruption, but whether these influences of OSA are sufficient, independent of obesity, to contribute significantly to the “metabolic syndrome” remains unsettled. 3) Neurocognitive effects include daytime sleepiness and impaired memory and concentration. These effects reflect

  3. Exercise & Sleep

    MedlinePlus

    ... on. Feature: Back to School, the Healthy Way Exercise & Sleep Past Issues / Fall 2012 Table of Contents ... helps kids. Photo: iStock 6 "Bests" About Kids' Exercise At least one hour of physical activity a ...

  4. Sleeping sickness

    MedlinePlus

    Human African trypanosomiasis ... Kirchoff LV. Agents of African trypanosomiasis (sleeping sickness). In: Mandell GL, Bennett JE, Dolan R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases . 8th ...

  5. Isolated sleep paralysis

    MedlinePlus

    ... from sleep. It is not associated with another sleep disorder. ... Sleep paralysis can be a symptom of narcolepsy . But if you do not have other symptoms of narcolepsy, there is usually no need to have sleep studies done.

  6. Brain Basics: Understanding Sleep

    MedlinePlus

    ... Many of the body's cells also show increased production and reduced breakdown of proteins during deep sleep. ... deep sleep, REM sleep is associated with increased production of proteins. One study found that REM sleep ...

  7. Snoring and Sleep Apnea

    MedlinePlus

    ... Find an ENT Doctor Near You Snoring and Sleep Apnea Snoring and Sleep Apnea Patient Health Information ... newsroom@entnet.org . Insight into sleeping disorders and sleep apnea Forty-five percent of normal adults snore ...

  8. Pediatric sleep apnea

    MedlinePlus

    Sleep apnea - pediatric; Apnea - pediatric sleep apnea syndrome; Sleep-disordered breathing - pediatric ... Untreated pediatric sleep apnea may lead to: High blood pressure Heart or lung problems Slow growth and development

  9. Isolated sleep paralysis

    MedlinePlus

    ... from sleep. It is not associated with another sleep disorder. Symptoms Episodes of isolated sleep paralysis last from ... A.M. Editorial team. Related MedlinePlus Health Topics Sleep Disorders Browse the Encyclopedia A.D.A.M., Inc. ...

  10. American Sleep Association

    MedlinePlus

    ... of sleep. Why we sleep. Why do we dream? Sleep Hygiene Tips Get good sleep now. What ... Forum Posts 90 minute rule. _ Re: Insomnia question _ Artificial foods acting as stimulant and causing insomnia _ DNP ...

  11. Pediatric sleep apnea

    MedlinePlus

    Sleep apnea - pediatric; Apnea - pediatric sleep apnea syndrome; Sleep-disordered breathing - pediatric ... During sleep, all of the muscles in the body become more relaxed. This includes the muscles that help keep ...

  12. Obstructive sleep apnea - adults

    MedlinePlus

    Sleep apnea - obstructive - adults; Apnea - obstructive sleep apnea syndrome - adults; Sleep-disordered breathing - adults; OSA - adults ... When you sleep, all of the muscles in your body become more relaxed. This includes the muscles that help keep your ...

  13. American Sleep Apnea Association

    MedlinePlus

    American Sleep Apnea Association Learn About the CPAP Assistance Program About ASAA News about ASAA Who we are Leadership Team Supporting the ASAA Financials Learn Healthy sleep Sleep apnea Other sleep disorders Personal stories Treat Test Yourself ...

  14. Refreshing Sleep and Sleep Continuity Determine Perceived Sleep Quality

    PubMed Central

    Fichten, Catherine; Creti, Laura; Conrod, Kerry; Tran, Dieu-Ly; Grad, Roland; Jorgensen, Mary; Amsel, Rhonda; Rizzo, Dorrie; Baltzan, Marc; Pavilanis, Alan; Bailes, Sally

    2016-01-01

    Sleep quality is a construct often measured, employed as an outcome criterion for therapeutic success, but never defined. In two studies we examined appraised good and poor sleep quality in three groups: a control group, individuals with obstructive sleep apnea, and those with insomnia disorder. In Study 1 we used qualitative methodology to examine good and poor sleep quality in 121 individuals. In Study 2 we examined sleep quality in 171 individuals who had not participated in Study 1 and evaluated correlates and predictors of sleep quality. Across all six samples and both qualitative and quantitative methodologies, the daytime experience of feeling refreshed (nonrefreshed) in the morning and the nighttime experience of good (impaired) sleep continuity characterized perceived good and poor sleep. Our results clarify sleep quality as a construct and identify refreshing sleep and sleep continuity as potential clinical and research outcome measures. PMID:27413553

  15. Refreshing Sleep and Sleep Continuity Determine Perceived Sleep Quality.

    PubMed

    Libman, Eva; Fichten, Catherine; Creti, Laura; Conrod, Kerry; Tran, Dieu-Ly; Grad, Roland; Jorgensen, Mary; Amsel, Rhonda; Rizzo, Dorrie; Baltzan, Marc; Pavilanis, Alan; Bailes, Sally

    2016-01-01

    Sleep quality is a construct often measured, employed as an outcome criterion for therapeutic success, but never defined. In two studies we examined appraised good and poor sleep quality in three groups: a control group, individuals with obstructive sleep apnea, and those with insomnia disorder. In Study 1 we used qualitative methodology to examine good and poor sleep quality in 121 individuals. In Study 2 we examined sleep quality in 171 individuals who had not participated in Study 1 and evaluated correlates and predictors of sleep quality. Across all six samples and both qualitative and quantitative methodologies, the daytime experience of feeling refreshed (nonrefreshed) in the morning and the nighttime experience of good (impaired) sleep continuity characterized perceived good and poor sleep. Our results clarify sleep quality as a construct and identify refreshing sleep and sleep continuity as potential clinical and research outcome measures. PMID:27413553

  16. [REM sleep behavior disorder (RBD) and dissociated REM sleep].

    PubMed

    Watanabe, T; Sugita, Y

    1998-02-01

    REM sleep behavior disorder (RBD) is characterized by the appearance of somnambulism-like behavior associated with dream mentation, and the intermittent loss of muscle atonia during REM sleep (stage 1-REM with tonic EMG; stage 1-REM). RBD is caused symptomatically or idiopathically, and its manifestation of symptoms sometimes associated with psychosocial stress. Muscle tone is often augmented during impared REM sleep observed in RBD patients. Animal experimental studies suggest that dysfunction or lesions of muscle inhibitory system in brain stem is rerated with pathogenesis of RBD. Clonazepam is effective for organic behavior and nightmare, but not remarkable for dissociated REM sleep. Other benzodiazepines and tricyclic antidepressants can be one of the choices of medications. Directions for safe-bedroom and psychotherapy is sometimes necessary. PMID:9503847

  17. Obstructive sleep apnea and other sleep-related syndromes.

    PubMed

    Paiva, Teresa; Attarian, Hrayr

    2014-01-01

    Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by repetitive episodes of breathing cessation due to complete or partial collapse of the upper airway therefore affecting ventilation. It is quite common, with a prevalence of about 2-4%, has a strong genetic component, and creates a proinflammatory state with elevated TNFα and other cytokines. If untreated, OSA can lead to significant neurological problems that include stroke, cognitive decline, depression, headaches, peripheral neuropathy, and nonarteritic ischemic optic neuropathy (NAION). Treatment reverses some of these neurological problems. Treatment includes continuous positive airway pressure and its variants, oral appliances, weight loss, upper airway surgery, and rarely maxillofacial procedures. Other sleep breathing disorders such as hypoventilation, central sleep apnea, complex sleep apnea, and Cheyne-Stokes respiration are less common and are sometimes associated with neuromuscular disorders causing diaphragmatic paralysis, but can also be seen in opiate exposure and severe obesity. PMID:24365301

  18. Sleep Time: Media Hype vs. Diary Data

    ERIC Educational Resources Information Center

    Michelson, William

    2011-01-01

    Sleep duration has figured into claims of two trends promoted recently as dysfunctional in the mass media. One is the observation that the population at large is sleeping less than before. The second is that the annual change from Standard Time to Daylight Savings (or summer) Time causes adverse effects, largely through the loss of an hour's…

  19. The Neurobiology of Orofacial Pain and Sleep and Their Interactions.

    PubMed

    Lavigne, G J; Sessle, B J

    2016-09-01

    This article provides an overview of the neurobiology of orofacial pain as well as the neural processes underlying sleep, with a particular focus on the mechanisms that underlie pain and sleep interactions including sleep disorders. Acute pain is part of a hypervigilance system that alerts the individual to injury or potential injury of tissues. It can also disturb sleep. Disrupted sleep is often associated with chronic pain states, including those that occur in the orofacial region. The article presents many insights that have been gained in the last few decades into the peripheral and central mechanisms involved in orofacial pain and its modulation, as well as the circuits and processes in the central nervous system that underlie sleep. Although it has become clear that sleep is essential to preserve and maintain health, it has also been found that pain, particularly chronic pain, is commonly associated with disturbed sleep. In the presence of chronic pain, a circular relationship may prevail, with mutual deleterious influences causing an increase in pain and a disruption of sleep. This article also reviews findings that indicate that reducing orofacial pain and improving sleep need to be targeted together in the management of acute to chronic orofacial pain states in order to improve an orofacial pain patient's quality of life, to prevent mood alterations or exacerbation of sleep disorder (e.g., insomnia, sleep-disordered breathing) that can negatively affect their pain, and to promote healing and optimize their health. PMID:27154736

  20. Effect of sleep deprivation on the human metabolome.

    PubMed

    Davies, Sarah K; Ang, Joo Ern; Revell, Victoria L; Holmes, Ben; Mann, Anuska; Robertson, Francesca P; Cui, Nanyi; Middleton, Benita; Ackermann, Katrin; Kayser, Manfred; Thumser, Alfred E; Raynaud, Florence I; Skene, Debra J

    2014-07-22

    Sleep restriction and circadian clock disruption are associated with metabolic disorders such as obesity, insulin resistance, and diabetes. The metabolic pathways involved in human sleep, however, have yet to be investigated with the use of a metabolomics approach. Here we have used untargeted and targeted liquid chromatography (LC)/MS metabolomics to examine the effect of acute sleep deprivation on plasma metabolite rhythms. Twelve healthy young male subjects remained in controlled laboratory conditions with respect to environmental light, sleep, meals, and posture during a 24-h wake/sleep cycle, followed by 24 h of wakefulness. Two-hourly plasma samples collected over the 48 h period were analyzed by LC/MS. Principal component analysis revealed a clear time of day variation with a significant cosine fit during the wake/sleep cycle and during 24 h of wakefulness in untargeted and targeted analysis. Of 171 metabolites quantified, daily rhythms were observed in the majority (n = 109), with 78 of these maintaining their rhythmicity during 24 h of wakefulness, most with reduced amplitude (n = 66). During sleep deprivation, 27 metabolites (tryptophan, serotonin, taurine, 8 acylcarnitines, 13 glycerophospholipids, and 3 sphingolipids) exhibited significantly increased levels compared with during sleep. The increased levels of serotonin, tryptophan, and taurine may explain the antidepressive effect of acute sleep deprivation and deserve further study. This report, to our knowledge the first of metabolic profiling during sleep and sleep deprivation and characterization of 24 h rhythms under these conditions, offers a novel view of human sleep/wake regulation. PMID:25002497

  1. Cytotoxic chemotherapy increases sleep and sleep fragmentation in non-tumor-bearing mice.

    PubMed

    Borniger, Jeremy C; Gaudier-Diaz, Monica M; Zhang, Ning; Nelson, Randy J; DeVries, A Courtney

    2015-07-01

    Sleep disruption ranks among the most common complaints of breast cancer patients undergoing chemotherapy. Because of the complex interactions among cancer, treatment regimens, and life-history traits, studies to establish a causal link between chemotherapy and sleep disruption are uncommon. To investigate how chemotherapy acutely influences sleep, adult female c57bl/6 mice were ovariectomized and implanted with wireless biotelemetry units. EEG/EMG biopotentials were collected over the course of 3days pre- and post-injection of 13.5mg/kg doxorubicin and 135mg/kg cyclophosphamide or the vehicle. We predicted that cyclophosphamide+doxorubicin would disrupt sleep and increase central proinflammatory cytokine expression in brain areas that govern vigilance states (i.e., hypothalamus and brainstem). The results largely support these predictions; a single chemotherapy injection increased NREM and REM sleep during subsequent active (dark) phases; this induced sleep was fragmented and of low quality. Mice displayed marked increases in low theta (5-7Hz) to high theta (7-10Hz) ratios following chemotherapy treatment, indicating elevated sleep propensity. The effect was strongest during the first dark phase following injection, but mice displayed disrupted sleep for the entire 3-day duration of post-injection sleep recording. Vigilance state timing was not influenced by treatment, suggesting that acute chemotherapy administration alters sleep homeostasis without altering sleep timing. qPCR analysis revealed that disrupted sleep was accompanied by increased IL-6 mRNA expression in the hypothalamus. Together, these data implicate neuroinflammation as a potential contributor to sleep disruption after chemotherapy. PMID:25449581

  2. Effect of illicit recreational drugs upon sleep: cocaine, ecstasy and marijuana.

    PubMed

    Schierenbeck, Thomas; Riemann, Dieter; Berger, Mathias; Hornyak, Magdolna

    2008-10-01

    The illicit recreational drugs cocaine, ecstasy and marijuana have pronounced effects upon sleep. Administration of cocaine increases wakefulness and suppresses REM sleep. Acute cocaine withdrawal is often associated with sleep disturbances and unpleasant dreams. Studies have revealed that polysomnographically assessed sleep parameters deteriorate even further during sustained abstinence, although patients report that sleep quality remains unchanged or improves. This deterioration of objective sleep measures is associated with a worsening in sleep-related cognitive performance. Like cocaine, 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy") is a substance with arousing properties. Heavy MDMA consumption is often associated with persistent sleep disturbances. Polysomnography (PSG) studies have demonstrated altered sleep architecture in abstinent heavy MDMA users. Smoked marijuana and oral Delta-9-tetrahydrocannabinol (THC) reduce REM sleep. Moreover, acute administration of cannabis appears to facilitate falling asleep and to increase Stage 4 sleep. Difficulty sleeping and strange dreams are among the most consistently reported symptoms of acute and subacute cannabis withdrawal. Longer sleep onset latency, reduced slow wave sleep and a REM rebound can be observed. Prospective studies are needed in order to verify whether sleep disturbances during cocaine and cannabis withdrawal predict treatment outcome. PMID:18313952

  3. Sleep-wake disorders and dermatology.

    PubMed

    Gupta, Madhulika A; Gupta, Aditya K

    2013-01-01

    Sleep is an active process that occupies about one-third of the lives of humans; however, there are relatively few studies of skin disorders during sleep. Sleep disruption in dermatologic disorders can significantly affect the quality of life and mental health of the patient and in some situations may even lead to exacerbations of the dermatologic condition. Sleep and skin disorders interface at several levels: (1) the role of the skin in normal sleep physiology, such as thermoregulation, core body temperature control, and sleep onset; (2) the effect of endogenous circadian rhythms and peripheral circadian "oscillators" on cutaneous symptoms, such as the natural trough in cortisol levels during the evening in patients with inflammatory dermatoses, which most likely results in increased pruritus during the evening and night; (3) the effect of symptoms such as pruritus, hyperhidrosis, and problems with thermoregulation, on sleep and sleep-related quality of life of the patients and their families; (4) the possible effect of primary sleep disorders, such as insomnia, sleep apnea, sleep deprivation, and circadian rhythm disorders, on dermatologic disorders; for example, central nervous system arousals from sleep in sleep apnea can result in increased sympathetic neural activity and increased inflammation; and (5) comorbidity of some dermatologic disorders with stress and psychiatric disorders, for example, major depressive disorder and attention deficit hyperactivity disorder (ADHD) that are also associated with sleep-related complaints. Sleep loss in atopic dermatitis (AD) is likely involved in the pathogenesis of ADHD-like symptoms in AD. Scratching during sleep, which may be proportional to the overall level of sympathetic nervous activity during the respective stages of sleep, usually occurs most frequently during non-rapid eye movement (NREM) stages 1 and 2 (vs stages 3 and 4 which are the deeper stages of sleep), and in rapid eye movement (REM) sleep, where the

  4. Chronic sleep disturbance impairs glucose homeostasis in rats.

    PubMed

    Barf, R Paulien; Meerlo, Peter; Scheurink, Anton J W

    2010-01-01

    Epidemiological studies have shown an association between short or disrupted sleep and an increased risk for metabolic disorders. To assess a possible causal relationship, we examined the effects of experimental sleep disturbance on glucose regulation in Wistar rats under controlled laboratory conditions. Three groups of animals were used: a sleep restriction group (RS), a group subjected to moderate sleep disturbance without restriction of sleep time (DS), and a home cage control group. To establish changes in glucose regulation, animals were subjected to intravenous glucose tolerance tests (IVGTTs) before and after 1 or 8 days of sleep restriction or disturbance. Data show that both RS and DS reduce body weight without affecting food intake and also lead to hyperglycemia and decreased insulin levels during an IVGTT. Acute sleep disturbance also caused hyperglycemia during an IVGTT, yet, without affecting the insulin response. In conclusion, both moderate and severe disturbances of sleep markedly affect glucose homeostasis and body weight control. PMID:20339560

  5. [The use of a vitamin and metabolite complex for correcting the disorders in systemic and organ hemodynamics during liver resection under conditions of acute blood loss].

    PubMed

    Shcherban', A N; Korkhov, S I; Nazarov, N V; Krivitskiĭ, N M; Kislukhin, V V; Kopytov, S V; Kholodov, I G

    1990-01-01

    The efficacy of some infusion media, vitamins, and metabolites in resection of the liver in acute blood loss was studied in experiments on dogs. Inclusion of vitamins B1, B2, and B6, lipoic acid, calcium pantothenate, nicotinamide, solution of alpha-glutamate and gamma-aminobutyric acid (aminalone) in the infusion led to a sharp increase of myocardial contractility, increase of cardiac output and total hepatic blood flow, normalization of biochemical blood values, and restoration of the activity of hepatocyte enzymes. PMID:2080080

  6. Mobile phones and sleep - A review

    NASA Astrophysics Data System (ADS)

    Supe, Sanjay S.

    2010-01-01

    The increasing use of mobile phones has raised concerns regarding the potential health effects of exposure to the radiofrequency electromagnetic fields. An increasing amount research related to mobile phone use has focussed on the possible effects of mobile phone exposure on human brain activity and function. In particular, the use of sleep research has become a more widely used technique for assessing the possible effects of mobile phones on human health and wellbeing especially in the investigation of potential changes in sleep architecture resulting from mobile phone use. Acute exposure to a mobile phone prior to sleep significantly enhances electroencephalogram spectral power in the sleep spindle frequency range. This mobile phone-induced enhancement in spectral power is largely transitory and does not linger throughout the night. Furthermore, a reduction in rapid eye movement sleep latency following mobile phone exposure was also found, although interestingly, neither this change in rapid eye movement sleep latency or the enhancement in spectral power following mobile phone exposure, led to changes in the overall quality of sleep. In conclusion, a short exposure to the radiofrequency electromagnetic fields emitted by a mobile phone handset immediately prior to sleep is sufficient to induce changes in brain activity in the initial part of sleep. The consequences or functional significance of this effect are currently unknown and it would be premature to draw conclusions about possible health consequences.

  7. [Sleep disturbances in critically ill patients].

    PubMed

    Walder, B; Haase, U; Rundshagen, I

    2007-01-01

    Sleep is an essential part of life with many important roles which include immunologic, cognitive and muscular functions. Of the working population 20% report sleep disturbances and in critically ill patients an incidence of more than 50% has been shown. However, sleep disturbances in the intensive care unit (ICU) population have not been investigated in detail. Sleep disturbances in ICU patients have a variety of reasons: e.g. patient-related pathologies like sepsis, acute or chronic pulmonary diseases, cardiac insufficiency, stroke or epilepsy, surgery, therapeutical interventions like mechanical ventilation, noise of monitors, pain or medication. Numerous scales and questionnaires are used to quantify sleep and the polysomnogramm is used to objectify sleep architecture. To improve sleep in ICU patients concepts are needed which include in addition to pharmacological treatment (pain reduction and sedation) synchronization of ICU activities with daylight, noise reduction and music for relaxation. In order to establish evidence-based guidelines, research activities about sleep and critical illness should be intensified. Questions to be answered are: 1) Which part of sleep disturbances in critically ill patients is directly related to the illness or trauma? 2) Is the grade of sleep disturbance correlated with the severity of the illness or trauma? 3) Which part is related to the medical treatment and can be modified or controlled? In order to define non-pharmacological and pharmacological concepts to improve sleep quality, studies need to be randomized and to include different ICU populations. The rate of nosocomial infections, cognitive function and respiratory muscle function should be considered in these studies as well. This will help to answer the question, whether it is useful to monitor sleep in ICU patients as a parameter to indicate therapeutical success and short-term quality of life. Follow-up needs to be long enough to detect adverse effects of

  8. Is sleep deprivation a contributor to obesity in children?

    PubMed

    Chaput, Jean-Philippe

    2016-03-01

    Chronic lack of sleep (called "sleep deprivation") is common in modern societies with 24/7 availability of commodities. Accumulating evidence supports the role of reduced sleep as contributing to the current obesity epidemic in children and youth. Longitudinal studies have consistently shown that short sleep duration is associated with weight gain and the development of obesity. Recent experimental studies have reported that sleep restriction leads to weight gain in humans. Increased food intake appears to be the main mechanism by which insufficient sleep results in weight gain. Voluntary sleep restriction has been shown to increase snacking, the number of meals eaten per day, and the preference for energy-dense foods. Although the causes of sleep loss in the pediatric population are numerous, more research looking at screen exposure before bedtime and its effects on sleep is needed given the pervasiveness of electronic media devices in today's environment. Health professionals should routinely ask questions about sleep and promote a good night's sleep because insufficient sleep impacts activity and eating behaviors. Future research should examine the clinical benefits of increasing sleep duration on eating behaviors and body weight control and determine the importance of adequate sleep to improve the treatment of obesity. PMID:26576804

  9. Sleep alterations in mammals: did aquatic conditions inhibit rapid eye movement sleep?

    PubMed

    Madan, Vibha; Jha, Sushil K

    2012-12-01

    Sleep has been studied widely in mammals and to some extent in other vertebrates. Higher vertebrates such as birds and mammals have evolved an inimitable rapid eye movement (REM) sleep state. During REM sleep, postural muscles become atonic and the temperature regulating machinery remains suspended. Although REM sleep is present in almost all the terrestrial mammals, the aquatic mammals have either radically reduced or completely eliminated REM sleep. Further, we found a significant negative correlation between REM sleep and the adaptation of the organism to live on land or in water. The amount of REM sleep is highest in terrestrial mammals, significantly reduced in semi-aquatic mammals and completely absent or negligible in aquatic mammals. The aquatic mammals are obligate swimmers and have to surface at regular intervals for air. Also, these animals live in thermally challenging environments, where the conductive heat loss is approximately ~90 times greater than air. Therefore, they have to be moving most of the time. As an adaptation, they have evolved unihemispheric sleep, during which they can rove as well as rest. A condition that immobilizes muscle activity and suspends the thermoregulatory machinery, as happens during REM sleep, is not suitable for these animals. It is possible that, in accord with Darwin's theory, aquatic mammals might have abolished REM sleep with time. In this review, we discuss the possibility of the intrinsic role of aquatic conditions in the elimination of REM sleep in the aquatic mammals. PMID:23225315

  10. Age-related changes in sleep spindles characteristics during daytime recovery following a 25-hour sleep deprivation

    PubMed Central

    Rosinvil, T.; Lafortune, M.; Sekerovic, Z.; Bouchard, M.; Dubé, J.; Latulipe-Loiselle, A.; Martin, N.; Lina, J. M.; Carrier, J.

    2015-01-01

    Objectives: The mechanisms underlying sleep spindles (~11–15 Hz; >0.5 s) help to protect sleep. With age, it becomes increasingly difficult to maintain sleep at a challenging time (e.g., daytime), even after sleep loss. This study compared spindle characteristics during daytime recovery and nocturnal sleep in young and middle-aged adults. In addition, we explored whether spindles characteristics in baseline nocturnal sleep were associated with the ability to maintain sleep during daytime recovery periods in both age groups. Methods: Twenty-nine young (15 women and 14 men; 27.3 y ± 5.0) and 31 middle-aged (19 women and 13 men; 51.6 y ± 5.1) healthy subjects participated in a baseline nocturnal sleep and a daytime recovery sleep after 25 hours of sleep deprivation. Spindles were detected on artifact-free Non-rapid eye movement (NREM) sleep epochs. Spindle density (nb/min), amplitude (μV), frequency (Hz), and duration (s) were analyzed on parasagittal (linked-ears) derivations. Results: In young subjects, spindle frequency increased during daytime recovery sleep as compared to baseline nocturnal sleep in all derivations, whereas middle-aged subjects showed spindle frequency enhancement only in the prefrontal derivation. No other significant interaction between age group and sleep condition was observed. Spindle density for all derivations and centro-occipital spindle amplitude decreased whereas prefrontal spindle amplitude increased from baseline to daytime recovery sleep in both age groups. Finally, no significant correlation was found between spindle characteristics during baseline nocturnal sleep and the marked reduction in sleep efficiency during daytime recovery sleep in both young and middle-aged subjects. Conclusion: These results suggest that the interaction between homeostatic and circadian pressure modulates spindle frequency differently in aging. Spindle characteristics do not seem to be linked with the ability to maintain daytime recovery sleep. PMID

  11. Enhancements to the multiple sleep latency test

    PubMed Central

    Meza-Vargas, Sonia; Giannouli, Eleni; Younes, Magdy

    2016-01-01

    Introduction The utility of multiple sleep latency tests (MSLTs) is limited to determining sleep onset latency (SOL) and rapid eye movement sleep latency. The odds ratio product (ORP) is a continuous index of sleep depth with values of 0, 1.0, and 2.5 reflecting very deep sleep, light sleep, and full wakefulness, respectively. We determined the time course of sleep depth during MSLT naps expecting that this would enhance the test’s clinical utility. Methods Thirty MSLTs (150 naps) were performed for excessive somnolence. Patients indicated whether they slept (yes/no) after each nap. SOL was scored by two experienced technologists. Time course of ORP was determined with a commercial system. We determined ORP at SOL (ORPSOL), times ORP decreased <2.0, <1.5, <1.0 and <0.5 during the entire nap duration, and the integral of decrease in ORP over nap duration (ΔORPINT). Results SOL occurred almost invariably when ORP was between 1.0 and 2.0. Of 47 naps (21 patients) with SOL <5 minutes, ORP decreased <1.0 (light sleep) in <5 minutes in only 13 naps (nine patients) and <0.5 (deep sleep) in only two naps in one patient. The relation between ORPINT and frequency of sleep perception was well defined, allowing determination of a threshold for sleep perception. This threshold ranged widely (5–50 ΔORP*epoch). Conclusion As currently identified, SOL reflects transition into a highly unstable state between wakefulness and sleep. Reporting the times of attaining different sleep depths may help better identify patients at high risk of vigilance loss. Furthermore, an ORPSOL outside the range 1.0–2.0 can help identify scoring errors. PMID:27274327

  12. A pilot study investigating the effects of continuous positive airway pressure treatment and weight-loss surgery on autonomic activity in obese obstructive sleep apnea patients☆, ☆☆

    PubMed Central

    Bakker, Jessie P.; Campana, Lisa M.; Montesi, Sydney B.; Balachandran, Jayshankar; DeYoung, Pamela N.; Smales, Erik; Patel, Sanjay R.; Malhotra, Atul

    2015-01-01

    Background We have previously demonstrated that severity of obstructive sleep apnea (OSA) as measured by the apnea–hypopnea index (AHI) is a significant independent predictor of readily-computed time-domain metrics of short-term heart rate variability (HRV). Methods We aimed to assess time-domain HRV measured over 5-min while awake in a trial of obese subjects undergoing one of two OSA therapies: weight-loss surgery (n = 12, 2 males, median and interquartile range (IQR) for BMI 43.7 [42.0, 51.4] kg/m2, and AHI 18.1 [16.3, 67.5] events/h) or continuous positive airway pressure (CPAP) (n = 15, 11 males, median BMI 33.8 [31.3, 37.9] kg/m2, and AHI 36.5 [24.7, 77.3] events/h). Polysomnography was followed by electrocardiography during wakefulness; measurements were repeated at 6 and 12–18 months post-intervention. Results Despite similar measurements at baseline, subjects who underwent surgery exhibited greater improvement in short-term HRV than those who underwent CPAP (p = 0.04). Conclusions Our data suggest a possible divergence in autonomic function between the effects of weight loss resulting from bariatric surgery, and the amelioration of obstructive respiratory events resulting from CPAP treatment. Randomized studies are necessary before clinical recommendations can be made. PMID:24636793

  13. Herpes simplex virus/Sleeping Beauty vector-based embryonic gene transfer using the HSB5 mutant: loss of apparent transposition hyperactivity in vivo.

    PubMed

    de Silva, Suresh; Mastrangelo, Michael A; Lotta, Louis T; Burris, Clark A; Izsvák, Zsuzsanna; Ivics, Zoltán; Bowers, William J

    2010-11-01

    The Sleeping Beauty (SB) transposon system has been successfully used as a gene delivery tool in nonviral and viral vector platforms. Since its initial reconstruction, a series of hyperactive mutants of SB have been generated. Questions remain as to whether the enhanced in vitro activities of these SB transposase mutants translate to the in vivo setting, and whether such increased integration efficiencies will ultimately compromise the safety profile of the transposon platform by raising the risk of genomic insertional mutagenesis. Herein, we compared the in vivo impact of a herpes simplex virus (HSV) amplicon-vectored "wild-type" SB transposase (SB10) and a "hyperactive" SB mutant (HSB5), codelivered in utero with the HSVT-βgeo transposable reporter amplicon vector to embryonic day 14.5 C57BL/6 mice. The SB10 and HSB5 transposases do not disparately affect the viability and development of injected mouse embryos. Quantitation of brain-resident βgeo expression on postnatal day 21 revealed that mice receiving HSB5 exhibited only a trending increase in transgene expression compared with the SB10-infused group, an outcome that did not mirror the marked enhancement of HSB5-mediated transposition observed in vitro. These findings indicate that in vivo application of hyperactive SB mutants, although not differentially genotoxic to the developing mouse embryo, does not necessarily provide a significant therapeutic advantage over the employment of a lesser active SB when delivered in the context of the HSV/SB amplicon platform. PMID:20507234

  14. Sleep and Recovery in Team Sport: Current Sleep-Related Issues Facing Professional Team-Sport Athletes.

    PubMed

    Fullagar, Hugh H K; Duffield, Rob; Skorski, Sabrina; Coutts, Aaron J; Julian, Ross; Meyer, Tim

    2015-11-01

    While the effects of sleep loss on performance have previously been reviewed, the effects of disturbed sleep on recovery after exercise are less reported. Specifically, the interaction between sleep and physiological and psychological recovery in team-sport athletes is not well understood. Accordingly, the aim of the current review was to examine the current evidence on the potential role sleep may play in postexercise recovery, with a tailored focus on professional team-sport athletes. Recent studies show that team-sport athletes are at high risk of poor sleep during and after competition. Although limited published data are available, these athletes also appear particularly susceptible to reductions in both sleep quality and sleep duration after night competition and periods of heavy training. However, studies examining the relationship between sleep and recovery in such situations are lacking. Indeed, further observational sleep studies in team-sport athletes are required to confirm these concerns. Naps, sleep extension, and sleep-hygiene practices appear advantageous to performance; however, future proof-of-concept studies are now required to determine the efficacy of these interventions on postexercise recovery. Moreover, more research is required to understand how sleep interacts with numerous recovery responses in team-sport environments. This is pertinent given the regularity with which these teams encounter challenging scenarios during the course of a season. Therefore, this review examines the factors that compromise sleep during a season and after competition and discusses strategies that may help improve sleep in team-sport athletes. PMID:25756787

  15. Sleep in Neurodegenerative Diseases.

    PubMed

    Iranzo, Alex

    2016-03-01

    Disorders of sleep are an integral part of neurodegenerative diseases and include insomnia, sleep-wake cycle disruption, excessive daytime sleepiness that may be manifested as persistent somnolence or sudden onset of sleep episodes, obstructive and central sleep apnea, rapid eye movement sleep behavior disorder, and restless legs syndrome. The origin of these sleep disorders is multifactorial including degeneration of the brain areas that modulate sleep, the symptoms of the disease, and the effect of medications. Treatment of sleep disorders in patients with neurodegenerative diseases should be individualized and includes behavioral therapy, sleep hygiene, bright light therapy, melatonin, hypnotics, waking-promoting agents, and continuous positive airway pressure. PMID:26972029

  16. Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses

    PubMed Central

    Aho, Vilma; Ollila, Hanna M.; Kronholm, Erkki; Bondia-Pons, Isabel; Soininen, Pasi; Kangas, Antti J.; Hilvo, Mika; Seppälä, Ilkka; Kettunen, Johannes; Oikonen, Mervi; Raitoharju, Emma; Hyötyläinen, Tuulia; Kähönen, Mika; Viikari, Jorma S.A.; Härmä, Mikko; Sallinen, Mikael; Olkkonen, Vesa M.; Alenius, Harri; Jauhiainen, Matti; Paunio, Tiina; Lehtimäki, Terho; Salomaa, Veikko; Orešič, Matej; Raitakari, Olli T.; Ala-Korpela, Mika; Porkka-Heiskanen, Tarja

    2016-01-01

    Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and serum metabolome were analysed. Sleep loss decreased the expression of genes encoding cholesterol transporters and increased expression in pathways involved in inflammatory responses in both paradigms. Metabolomic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting insufficient sleep, while circulating LDL decreased in the experimental sleep restriction study. These findings suggest that prolonged sleep deprivation modifies inflammatory and cholesterol pathways at the level of gene expression and serum lipoproteins, inducing changes toward potentially higher risk for cardiometabolic diseases. PMID:27102866

  17. Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses.

    PubMed

    Aho, Vilma; Ollila, Hanna M; Kronholm, Erkki; Bondia-Pons, Isabel; Soininen, Pasi; Kangas, Antti J; Hilvo, Mika; Seppälä, Ilkka; Kettunen, Johannes; Oikonen, Mervi; Raitoharju, Emma; Hyötyläinen, Tuulia; Kähönen, Mika; Viikari, Jorma S A; Härmä, Mikko; Sallinen, Mikael; Olkkonen, Vesa M; Alenius, Harri; Jauhiainen, Matti; Paunio, Tiina; Lehtimäki, Terho; Salomaa, Veikko; Orešič, Matej; Raitakari, Olli T; Ala-Korpela, Mika; Porkka-Heiskanen, Tarja

    2016-01-01

    Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and serum metabolome were analysed. Sleep loss decreased the expression of genes encoding cholesterol transporters and increased expression in pathways involved in inflammatory responses in both paradigms. Metabolomic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting insufficient sleep, while circulating LDL decreased in the experimental sleep restriction study. These findings suggest that prolonged sleep deprivation modifies inflammatory and cholesterol pathways at the level of gene expression and serum lipoproteins, inducing changes toward potentially higher risk for cardiometabolic diseases. PMID:27102866

  18. Sleep deprivation amplifies striatal activation to monetary reward

    PubMed Central

    Mullin, Benjamin C.; Phillips, Mary L.; Siegle, Greg J.; Buysse, Daniel J.; Forbes, Erika E.; Franzen, Peter L.

    2013-01-01

    Background Sleep loss produces abnormal increases in reward-seeking, though the mechanisms underlying this phenomenon are poorly understood. The present study examined the influence of one night of sleep deprivation on neural responses to a monetary reward task in a sample of late adolescents/young adults. Methods Using a within-subjects crossover design, 27 healthy, right-handed late-adolescents/young adults (16 females, 11 males; mean age 23.1 years) completed functional magnetic resonance imaging following a night of sleep deprivation and following a night of normal sleep. Participants’ recent sleep history was monitored using actigraphy for one week prior to each sleep condition. Results Following sleep deprivation, participants exhibited increased activity in the ventral striatum and reduced deactivation in medial prefrontal cortex during the winning of monetary reward, relative to the same task following normal sleep conditions. Shorter total sleep time over the five nights before the sleep deprived testing condition was associated with reduced deactivation in the medial prefrontal cortex during reward. Conclusions These findings support the hypothesis that sleep loss produces aberrant functioning in reward neural circuitry, increasing the salience of positively-reinforcing stimuli. Aberrant reward functioning related to insufficient sleep may contribute to the development and maintenance of reward dysfunction-related disorders, such as compulsive gambling, eating, substance abuse, and mood disorders. PMID:23286303

  19. Cardiovascular, Inflammatory and Metabolic Consequences of Sleep Deprivation

    PubMed Central

    Mullington, Janet M.; Haack, Monika; Toth, Maria; Serrador, Jorge; Meier-Ewert, Hans

    2009-01-01

    That insufficient sleep is associated with poor attention and performance deficits is becoming widely recognized. Fewer people are aware that chronic sleep complaints in epidemiological studies have also been associated with an increase in overall mortality and morbidity. This article summarizes findings of known effects of insufficient sleep on cardiovascular risk factors including blood pressure, glucose metabolism, hormonal regulation and inflammation with particular emphasis on experimental sleep loss, using models of total and partial sleep deprivation, in healthy individuals who normally sleep in the range of 7-8 hours and have no sleep disorders. These studies show that insufficient sleep alters established cardiovascular risk factors in a direction that is known to increase the risk of cardiac morbidity. PMID:19110131

  20. Identification of SLEEPLESS, a novel sleep-promoting factor#

    PubMed Central

    Koh, Kyunghee; Joiner, William J.; Wu, Mark N.; Yue, Zhifeng; Smith, Corinne J.; Sehgal, Amita

    2008-01-01

    Sleep is an essential process conserved from flies to humans. The importance of sleep is underscored by its tight homeostatic control. Here, through a forward-genetic screen, we identify a novel gene, sleepless, required for sleep in Drosophila. sleepless encodes a brain-enriched, glycosyl-phosphatidylinositol-anchored protein. Loss of SLEEPLESS protein causes an extreme (>80%) reduction in sleep. Furthermore, a moderate reduction in SLEEPLESS protein has minimal effects on baseline sleep, but markedly reduces recovery sleep following sleep deprivation. Genetic and molecular analyses reveal that quiver, a mutation that impairs Shaker-dependent K+ current, is an allele of sleepless. Consistent with this finding, Shaker protein level is reduced in sleepless mutants. We propose that SLEEPLESS is a signaling molecule that connects sleep drive to lowered membrane excitability. PMID:18635795

  1. Short neuropeptide F is a sleep-promoting inhibitory modulator

    PubMed Central

    Shang, Yuhua; Donelson, Nathan C.; Vecsey, Christopher G.; Guo, Fang; Rosbash, Michael; Griffith, Leslie C.

    2013-01-01

    SUMMARY To advance the understanding of sleep regulation, we screened for sleep-promoting cells and identified neurons expressing neuropeptide Y-like short neuropeptide F (sNPF). Sleep-induction by sNPF meets all relevant criteria. Rebound sleep following sleep deprivation is reduced by activation of sNPF neurons and flies even experience negative sleep rebound upon cessation of sNPF neuronal stimulation, indicating that sNPF provides an important signal to the sleep homeostat. Only a subset of sNPF-expressing neurons, which includes the small ventrolateral clock neurons, is sleep-promoting. Their release of sNPF increases sleep consolidation in part by suppressing the activity of wake-promoting large ventrolateral clock neurons, and suppression of neuronal firing may be the general response to sNPF receptor activation. sNPF acutely increases sleep without altering feeding behavior, which it affects only on a much longer time scale. The profound effect of sNPF on sleep indicates that it is an important sleep-promoting molecule. PMID:24094110

  2. Treatment issues related to sleep and depression.

    PubMed

    Thase, M E

    2000-01-01

    In the management of depression, the role of sleep and sleep disturbances is important for several reasons. The same neurotransmitter systems that regulate mood, interest, energy, and other functions that may be disturbed in depression also regulate sleep. Sleep disturbances may be responsive to treatment with some antidepressants and may be worsened during treatment with other antidepressants. Serotonergic neurons play a critical role in modulating the onset and maintenance of sleep, and it is thought that insomnia in depression is caused by dysfunction of serotonergic systems. For a significant minority, SSRIs can have negative effects on sleep patterns resulting in insomnia that requires concomitant sedatives or anxiolytics. By contrast, agents that block the serotonin type 2 (5-HT2) receptor have beneficial effects on depressive insomnia. For example, a recent 8-week study comparing the effects of nefazodone and fluoxetine on sleep disturbances in outpatients with nonpsychotic depression and insomnia found that fluoxetine was associated with approximately a 30% increase in the number of nocturnal awakenings whereas nefazodone was associated with about a 15% decrease, a net difference of 45%. Long-term studies must be conducted to determine whether sleep benefits provided by the newer antidepressants will continue past the acute treatment phase. PMID:10926055

  3. Sustained sleep fragmentation affects brain temperature, food intake and glucose tolerance in mice.

    PubMed

    Baud, Maxime O; Magistretti, Pierre J; Petit, Jean-Marie

    2013-02-01

    Sleep fragmentation is present in numerous sleep pathologies and constitutes a major feature of patients with obstructive sleep apnea. A prevalence of metabolic syndrome, diabetes and obesity has been shown to be associated to obstructive sleep apnea. While sleep fragmentation has been shown to impact sleep homeostasis, its specific effects on metabolic variables are only beginning to emerge. In this context, it is important to develop realistic animal models that would account for chronic metabolic effects of sleep fragmentation. We developed a 14-day model of instrumental sleep fragmentation in mice, and show an impact on both brain-specific and general metabolism. We first report that sleep fragmentation increases food intake without affecting body weight. This imbalance was accompanied by the inability to adequately decrease brain temperature during fragmented sleep. In addition, we report that sleep-fragmented mice develop glucose intolerance. We also observe that sleep fragmentation slightly increases the circadian peak level of glucocorticoids, a factor that may be involved in the observed metabolic effects. Our results confirm that poor-quality sleep with sustained sleep fragmentation has similar effects on general metabolism as actual sleep loss. Altogether, these results strongly suggest that sleep fragmentation is an aggravating factor for the development of metabolic dysfunctions that may be relevant for sleep disorders such as obstructive sleep apnea. PMID:22734931

  4. Healthcare Providers' Knowledge of Disordered Sleep, Sleep Assessment Tools, and Nonpharmacological Sleep Interventions for Persons Living with Dementia: A National Survey

    PubMed Central

    Brown, Cary A.; Jones, Allyson; Crick, Katelyn

    2014-01-01

    A large proportion of persons with dementia will also experience disordered sleep. Disordered sleep in dementia is a common reason for institutionalization and affects cognition, fall risk, agitation, self-care ability, and overall health and quality of life. This report presents findings of a survey of healthcare providers' awareness of sleep issues, assessment practices, and nonpharmacological sleep interventions for persons with dementia. There were 1846 participants, with the majority being from nursing and rehabilitation. One-third worked in long-term care settings and one-third in acute care. Few reported working in the community. Findings revealed that participants understated the incidence of sleep deficiencies in persons with dementia and generally lacked awareness of the relationship between disordered sleep and dementia. Their knowledge of sleep assessment tools was limited to caregiver reports, self-reports, and sleep diaries, with few using standardized tools or other assessment methods. The relationship between disordered sleep and comorbid conditions was not well understood. The three most common nonpharmacological sleep interventions participants identified using were a regular bedtime routine, increased daytime activity, and restricted caffeine. Awareness of other evidence-based interventions was low. These findings will guide evidence-informed research to develop and test more targeted and contextualized sleep and dementia knowledge translation strategies. PMID:24851185

  5. REM sleep - by default?

    PubMed

    Horne, J A

    2000-12-01

    Elements of three old, overlapping theories of REM sleep (REM) function, the Ontogenetic, Homeostatic and Phylogenetic hypotheses, together still provide a plausible framework - that REM (i) is directed towards early cortical development, (ii) "tones up" the sleeping cortex, (iii) can substitute for wakefulness, (iv) has a calming effect. This framework is developed in the light of recent findings. It is argued that the "primitiveness" of REM and its similarity to wakefulness liken it to a default state of "non-wakefulness" or a waking antagonist, anteceding "true" (non-REM) sleep. The "toning up" is reflected by inhibition of motor, sensory and (importantly) emotional systems, together pointing to integrated "flight or fight" activity, that preoccupies/distracts the organism when non-REM is absent and wakefulness unnecessary. Dreaming facilitates this distraction. In rodents, REM can provide stress coping and calming, but REM deprivation procedures incorporating immobility may further enhance stress and confound outcomes. REM "pressure" (e.g. REM rebounds) may be a default from a loss of inhibition of REM by non-REM. REM can be reduced and/or replaced by wakefulness, without adverse effects. REM has little advantage over wakefulness in providing positive cerebral recovery or memory consolidation. PMID:11118606

  6. REM sleep Behaviour Disorder.

    PubMed

    Ferini-Strambi, Luigi; Rinaldi, Fabrizio; Giora, Enrico; Marelli, Sara; Galbiati, Andrea

    2016-01-01

    Rapid Eye Movement (REM) sleep Behaviour Disorder (RBD) is a REM sleep parasomnia characterized by loss of the muscle atonia that typically occurs during REM sleep, therefore allowing patients to act out their dreams. RBD manifests itself clinically as a violent behaviour occurring during the night, and is detected at the polysomnography by phasic and/or tonic muscle activity on the electromyography channel. In absence of neurological signs or central nervous system lesions, RBD is defined as idiopathic. Nevertheless, in a large number of cases the development of neurodegenerative diseases in RBD patients has been described, with the duration of the follow-up representing a fundamental aspect. A growing number of clinical, neurophysiologic and neuropsychological studies aimed to detect early markers of neurodegenerative dysfunction in RBD patients. Anyway, the evidence of impaired cortical activity, subtle neurocognitive dysfunction, olfactory and autonomic impairment and neuroimaging brain changes in RBD patients is challenging the concept of an idiopathic form of RBD, supporting the idea of RBD as an early manifestation of a more complex neurodegenerative process. PMID:26427638

  7. Sleep and Nutritional Deprivation and Performance of House Officers.

    ERIC Educational Resources Information Center

    Hawkins, Michael R.; And Others

    1985-01-01

    A study to compare cognitive functioning in acutely and chronically sleep-deprived house officers is described. A multivariate analysis of variance revealed significant deficits in primary mental tasks involving basic rote memory, language, and numeric skills. (Author/MLW)

  8. Sleep Changes in Older Adults

    MedlinePlus

    ... ages can have a sleep disorder such as sleep apnea. Restless legs syndrome or periodic limb movement disorder ... that can cause problems with sleep. What is sleep apnea? Sleep apnea is a disorder in which a ...

  9. Stress-free automatic sleep deprivation using air puffs

    PubMed Central

    Gross, Brooks A.; Vanderheyden, William M.; Urpa, Lea M.; Davis, Devon E.; Fitzpatrick, Christopher J.; Prabhu, Kaustubh; Poe, Gina R.

    2015-01-01

    Background Sleep deprivation via gentle handling is time-consuming and personnel-intensive. New Method We present here an automated sleep deprivation system via air puffs. Implanted EMG and EEG electrodes were used to assess sleep/waking states in six male Sprague-Dawley rats. Blood samples were collected from an implanted intravenous catheter every 4 hours during the 12-hour light cycle on baseline, 8 hours of sleep deprivation via air puffs, and 8 hours of sleep deprivation by gentle handling days. Results The automated system was capable of scoring sleep and waking states as accurately as our offline version (~90% for sleep) and with sufficient speed to trigger a feedback response within an acceptable amount of time (1.76 s). Manual state scoring confirmed normal sleep on the baseline day and sleep deprivation on the two manipulation days (68% decrease in non-REM, 63% decrease in REM, and 74% increase in waking). No significant differences in levels of ACTH and corticosterone (stress hormones indicative of HPA axis activity) were found at any time point between baseline sleep and sleep deprivation via air puffs. Comparison with Existing Method There were no significant differences in ACTH or corticosterone concentrations between sleep deprivation by air puffs and gentle handling over the 8-hour period. Conclusions Our system accurately detects sleep and delivers air puffs to acutely deprive rats of sleep with sufficient temporal resolution during the critical 4-5 h post learning sleep-dependent memory consolidation period. The system is stress-free and a viable alternative to existing sleep deprivation techniques. PMID:26014662

  10. Medicines for sleep

    MedlinePlus

    ... this page: //medlineplus.gov/ency/patientinstructions/000758.htm Medicines for sleep To use the sharing features on ... or illegal drug use Over-the-counter sleep medicines Most over-the-counter (OTC) sleeping pills contain ...

  11. Treatments for Sleep Changes

    MedlinePlus

    ... Contributing medical factors Non-drug strategies Medications Common sleep changes Many people with Alzheimer’s experience changes in ... at night. Subscribe now Non-drug treatments for sleep changes Non-drug treatments aim to improve sleep ...

  12. Good Night's Sleep

    MedlinePlus

    ... symptoms to see if you might have a sleep disorder like insomnia, sleep apnea, or a movement disorder. ... periodic limb movement disorder, and rapid eye movement sleep behavior disorder are common in older adults. These movement disorders ...

  13. Sleep and your health

    MedlinePlus

    ... and awake, even when you are very tired. Sleep disorders Sleep problems are a big reason why many ... through the night. It is the most common sleep disorder. Insomnia can last for a night, a couple ...

  14. Aging changes in sleep

    MedlinePlus

    ... CHANGES Sleeping difficulty is an annoying problem. Chronic insomnia is a major cause of auto accidents and ... health condition is affecting your sleep. COMMON PROBLEMS Insomnia is one of the more common sleep problems ...

  15. Sleep Apnea Detection

    MedlinePlus

    ... Prenatal Baby Bathing & Skin Care Breastfeeding Crying & Colic Diapers & Clothing Feeding & Nutrition Preemie Sleep Teething & Tooth Care Toddler Preschool Gradeschool Teen Young Adult Healthy Children > Ages & Stages > Baby > Sleep > Sleep Apnea ...

  16. Overview of sleep disorders.

    PubMed

    Roldan, Glenn; Ang, Robert C

    2006-03-01

    Sleep disorders are common and can affect anyone, from every social class and every ethnic background. It is estimated that more than 70 million Americans are afflicted by chronic sleep disorders. Currently about 88 sleep disorders are described by the International Classification of Sleep Disorders as established by The American Academy of Sleep Medicine. This article describes the dyssomnias and parasomnias most commonly seen in the clinical setting of the sleep disorder clinic or laboratory. PMID:16530646

  17. Interactions between sleep, stress, and metabolism: From physiological to pathological conditions

    PubMed Central

    Hirotsu, Camila; Tufik, Sergio; Andersen, Monica Levy

    2015-01-01

    Poor sleep quality due to sleep disorders and sleep loss is highly prevalent in the modern society. Underlying mechanisms show that stress is involved in the relationship between sleep and metabolism through hypothalamic–pituitary–adrenal (HPA) axis activation. Sleep deprivation and sleep disorders are associated with maladaptive changes in the HPA axis, leading to neuroendocrine dysregulation. Excess of glucocorticoids increase glucose and insulin and decrease adiponectin levels. Thus, this review provides overall view of the relationship between sleep, stress, and metabolism from basic physiology to pathological conditions, highlighting effective treatments for metabolic disturbances. PMID:26779321

  18. Loss of CD28 on Peripheral T Cells Decreases the Risk for Early Acute Rejection after Kidney Transplantation

    PubMed Central

    Dedeoglu, Burç; Meijers, Ruud W. J.; Klepper, Mariska; Hesselink, Dennis A.; Baan, Carla C.; Litjens, Nicolle H. R.; Betjes, Michiel G. H.

    2016-01-01

    Background End-stage renal disease patients have a dysfunctional, prematurely aged peripheral T-cell system. Here we hypothesized that the degree of premature T-cell ageing before kidney transplantation predicts the risk for early acute allograft rejection (EAR). Methods 222 living donor kidney transplant recipients were prospectively analyzed. EAR was defined as biopsy proven acute allograft rejection within 3 months after kidney transplantation. The differentiation status of circulating T cells, the relative telomere length and the number of CD31+ naive T cells were determined as T-cell ageing parameters. Results Of the 222 patients analyzed, 30 (14%) developed an EAR. The donor age and the historical panel reactive antibody score were significantly higher (p = 0.024 and p = 0.039 respectively) and the number of related donor kidney transplantation was significantly lower (p = 0.018) in the EAR group. EAR-patients showed lower CD4+CD28null T-cell numbers (p<0.01) and the same trend was observed for CD8+CD28null T-cell numbers (p = 0.08). No differences regarding the other ageing parameters were found. A multivariate Cox regression analysis showed that higher CD4+CD28null T-cell numbers was associated with a lower risk for EAR (HR: 0.65, p = 0.028). In vitro, a significant lower percentage of alloreactive T cells was observed within CD28null T cells (p<0.001). Conclusion Immunological ageing-related expansion of highly differentiated CD28null T cells is associated with a lower risk for EAR. PMID:26950734

  19. Effects of sleep deprivation on cognition.

    PubMed

    Killgore, William D S

    2010-01-01

    Sleep deprivation is commonplace in modern society, but its far-reaching effects on cognitive performance are only beginning to be understood from a scientific perspective. While there is broad consensus that insufficient sleep leads to a general slowing of response speed and increased variability in performance, particularly for simple measures of alertness, attention and vigilance, there is much less agreement about the effects of sleep deprivation on many higher level cognitive capacities, including perception, memory and executive functions. Central to this debate has been the question of whether sleep deprivation affects nearly all cognitive capacities in a global manner through degraded alertness and attention, or whether sleep loss specifically impairs some aspects of cognition more than others. Neuroimaging evidence has implicated the prefrontal cortex as a brain region that may be particularly susceptible to the effects of sleep loss, but perplexingly, executive function tasks that putatively measure prefrontal functioning have yielded inconsistent findings within the context of sleep deprivation. Whereas many convergent and rule-based reasoning, decision making and planning tasks are relatively unaffected by sleep loss, more creative, divergent and innovative aspects of cognition do appear to be degraded by lack of sleep. Emerging evidence suggests that some aspects of higher level cognitive capacities remain degraded by sleep deprivation despite restoration of alertness and vigilance with stimulant countermeasures, suggesting that sleep loss may affect specific cognitive systems above and beyond the effects produced by global cognitive declines or impaired attentional processes. Finally, the role of emotion as a critical facet of cognition has received increasing attention in recent years and mounting evidence suggests that sleep deprivation may particularly affect cognitive systems that rely on emotional data. Thus, the extent to which sleep deprivation

  20. Weight-loss surgery and children

    MedlinePlus

    ... and blood pressure Fewer sleep problems In the United States, weight loss operations have been used with success ... is not yet approved for teenagers in the United States. All weight loss operations can be performed through ...

  1. Cyclosporine Does Not Prevent Microvascular Loss in Transplantation but Can Synergize With a Neutrophil Elastase Inhibitor, Elafin, to Maintain Graft Perfusion During Acute Rejection.

    PubMed

    Jiang, X; Nguyen, T T; Tian, W; Sung, Y K; Yuan, K; Qian, J; Rajadas, J; Sallenave, J-M; Nickel, N P; de Jesus Perez, V; Rabinovitch, M; Nicolls, M R

    2015-07-01

    The loss of a functional microvascular bed in rejecting solid organ transplants is correlated with fibrotic remodeling and chronic rejection; in lung allografts, this pathology is predicted by bronchoalveolar fluid neutrophilia which suggests a role for polymorphonuclear cells in microcirculatory injury. In a mouse orthotopic tracheal transplant model, cyclosporine, which primarily inhibits T cells, failed as a monotherapy for preventing microvessel rejection and graft ischemia. To target neutrophil action that may be contributing to vascular injury, we examined the effect of a neutrophil elastase inhibitor, elafin, on the microvascular health of transplant tissue. We showed that elafin monotherapy prolonged microvascular perfusion and enhanced tissue oxygenation while diminishing the infiltration of neutrophils and macrophages and decreasing tissue deposition of complement C3 and the membrane attack complex, C5b-9. Elafin was also found to promote angiogenesis through activation of the extracellular signal-regulated kinase (ERK) signaling pathway but was insufficient as a single agent to completely prevent tissue ischemia during acute rejection episodes. However, when combined with cyclosporine, elafin effectively preserved airway microvascular perfusion and oxygenation. The therapeutic strategy of targeting neutrophil elastase activity alongside standard immunosuppression during acute rejection episodes may be an effective approach for preventing the development of irreversible fibrotic remodeling. PMID:25727073

  2. Cyclosporine does not prevent microvascular loss in transplantation but can synergize with a neutrophil elastase inhibitor, elafin, to maintain graft perfusion during acute rejection

    PubMed Central

    Jiang, Xinguo; Nguyen, Tom T.; Tian, Wen; Sung, Yon K.; Yuan, Ke; Qian, Jin; Rajadas, Jayakumar; Sallenave, Jean-Michel; Nickel, Nils P.; de Jesus Perez, Vinicio; Rabinovitch, Marlene; Nicolls, Mark R.

    2015-01-01

    The loss of a functional microvascular bed in rejecting solid organ transplants is correlated with fibrotic remodeling and chronic rejection; in lung allografts, this pathology is predicted by bronchoalveolar fluid neutrophilia which suggests a role for polymorphonuclear cells in microcirculatory injury. In a mouse orthotopic tracheal transplant model, cyclosporine, which primarily inhibits T cells, failed as a monotherapy for preventing microvessel rejection and graft ischemia. To target neutrophil action that may be contributing to vascular injury, we examined the effect of a neutrophil elastase inhibitor, elafin, on the microvascular health of transplant tissue. We showed that elafin monotherapy prolonged microvascular perfusion and enhanced tissue oxygenation while diminishing the infiltration of neutrophils and macrophages and decreasing tissue deposition of complement C3 and the membrane attack complex, C5b-9. Elafin was also found to promote angiogenesis through activation of the extracellular signal-regulated kinase (ERK) signaling pathway but was insufficient as a single agent to completely prevent tissue ischemia during acute rejection episodes. However, when combined with cyclosporine, elafin effectively preserved airway microvascular perfusion and oxygenation. The therapeutic strategy of targeting neutrophil elastase activity alongside standard immunosuppression during acute rejection episodes may be an effective approach for preventing the development of irreversible fibrotic remodeling. PMID:25727073

  3. Toxicokinetic toxicodynamic (TKTD) modeling of Ag toxicity in freshwater organisms: whole-body sodium loss predicts acute mortality across aquatic species.

    PubMed

    Veltman, Karin; Hendriks, A Jan; Huijbregts, Mark A J; Wannaz, Cédric; Jolliet, Olivier

    2014-12-16

    ToxicoKinetic ToxicoDynamic (TKTD) models are considered essential tools to further advance acute toxicity prediction of metals for a range of species and exposure conditions, but they are currently underutilized. We present a mechanistic TKTD model for acute toxicity prediction of silver (Ag) in freshwater organisms. In this new approach, we explicitly link relevant TKTD processes to species (physiological) characteristics, which facilitates model application to other untested freshwater organisms. The model quantifies the reduction in whole-body sodium concentration over time as a function of the target site inhibition over time, the target site density and the species-specific sodium turnover rate. Freshwater species are assumed to die instantly when they have lost a critical amount of their initial whole-body sodium concentration. Results show that mortality is significantly related to sodium loss (r(2) = 0.86) for various aquatic organisms and exposure durations. The model accurately predicts lethal effect concentrations for different freshwater organisms, including Daphnia magna, rainbow trout and juvenile crayfish, and is able to capture the observed size-specific variation of nearly 2 orders of magnitude in empirical LC50s. PMID:25420046

  4. Sleep-disordered breathing as a delayed complication of iatrogenic vocal cord trauma.

    PubMed

    Faiz, Saadia A; Bashoura, Lara; Kodali, Lavanya; Hessel, Amy C; Evans, Scott E; Balachandran, Diwakar D

    2016-06-01

    A case of a 55-year-old woman with iatrogenic vocal cord trauma and sleep-related symptoms is reported. In particular, this case highlights sleep-disordered breathing as a delayed complication after iatrogenic vocal cord trauma. The patient developed acute stridor from a contralateral vocal cord hematoma following vocal fold injection for right vocal cord paralysis. Acute respiratory symptoms resolved with oxygen, steroids, and nebulized therapy, but nocturnal symptoms persisted and polysomnography revealed sleep-related hypoventilation and mild obstructive sleep apnea. Positive pressure therapy was successfully used to ameliorate her symptoms and treat sleep-disordered breathing until her hematoma resolved. In addition to the typically acute respiratory symptoms that may result from vocal cord dysfunction, sleep-disordered breathing may also present as a significant subacute or chronic problem. Management of the acute respiratory symptoms is relatively well established, but clinicians should be alert for more subtle nocturnal symptoms that may require further study with polysomnography. PMID:27544828

  5. Sleep and sleep disorders in older adults.

    PubMed

    Crowley, Kate

    2011-03-01

    A common but significant change associated with aging is a profound disruption to the daily sleep-wake cycle. It has been estimated that as many as 50% of older adults complain about difficulty initiating or maintaining sleep. Poor sleep results in increased risk of significant morbidity and mortality. Moreover, in younger adults, compromised sleep has been shown to have a consistent effect on cognitive function, which may suggest that sleep problems contribute to the cognitive changes that accompany older age. The multifactorial nature of variables affecting sleep in old age cannot be overstated. Changes in sleep have been thought to reflect normal developmental processes, which can be further compromised by sleep disturbances secondary to medical or psychiatric diseases (e.g., chronic pain, dementia, depression), a primary sleep disorder that can itself be age-related (e.g., Sleep Disordered Breathing and Periodic Limb Movements During Sleep), or some combination of any of these factors. Given that changes in sleep quality and quantity in later life have implications for quality of life and level of functioning, it is imperative to distinguish the normal age-related sleep changes from those originating from pathological processes. PMID:21225347

  6. Heightened sexual interest and sleep disturbance

    NASA Technical Reports Server (NTRS)

    Zarcone, V.; De La Pena, A.; Dement, W. C.

    1974-01-01

    The study demonstrates a behavioral effect of selective sleep disturbance in normal human subjects. Ten male subjects were selectively REM-deprived for two nights by awakening them at the onset of REM sleep. In addition, there were baseline and non-REM awakening conditions. Heightened sexual interest was defined by the number of film frames (using a Mackworth camera) in which subjects fixated on parts of the female figure in photographs. The largest mean difference in sexual interest was found between baseline and REM-deprivation. Both the non-REM awakenings and REM-sleep deprivation enhanced sexual interest. The failure to demonstrate a significant difference between REM-deprivation and non-REM awakenings may be due to the fact that subjects were REM-sleep-deprived in both conditions. It is suggested that REM-sleep loss may lead to increased selective attention and preoccupation with any cues which are usually interesting.

  7. Sleep restriction alters the hypothalamic-pituitary-adrenal response to stress

    NASA Technical Reports Server (NTRS)

    Meerlo, P.; Koehl, M.; van der Borght, K.; Turek, F. W.

    2002-01-01

    Chronic sleep restriction is an increasing problem in many countries and may have many, as yet unknown, consequences for health and well being. Studies in both humans and rats suggest that sleep deprivation may activate the hypothalamic-pituitary-adrenal (HPA) axis, one of the main neuroendocrine stress systems. However, few attempts have been made to examine how sleep loss affects the HPA axis response to subsequent stressors. Furthermore, most studies applied short-lasting total sleep deprivation and not restriction of sleep over a longer period of time, as often occurs in human society. Using the rat as our model species, we investigated: (i) the HPA axis activity during and after sleep deprivation and (ii) the effect of sleep loss on the subsequent HPA response to a novel stressor. In one experiment, rats were subjected to 48 h of sleep deprivation by placing them in slowly rotating wheels. Control rats were placed in nonrotating wheels. In a second experiment, rats were subjected to an 8-day sleep restriction protocol allowing 4 h of sleep each day. To test the effects of sleep loss on subsequent stress reactivity, rats were subjected to a 30-min restraint stress. Blood samples were taken at several time points and analysed for adrenocorticotropic hormone (ACTH) and corticosterone. The results show that ACTH and corticosterone concentrations were elevated during sleep deprivation but returned to baseline within 4 h of recovery. After 1 day of sleep restriction, the ACTH and corticosterone response to restraint stress did not differ between control and sleep deprived rats. However, after 48 h of total sleep deprivation and after 8 days of restricted sleep, the ACTH response to restraint was significantly reduced whereas the corticosterone response was unaffected. These results show that sleep loss not only is a mild activator of the HPA axis itself, but also affects the subsequent response to stress. Alterations in HPA axis regulation may gradually appear under

  8. Beneficial Impact of Sleep Extension on Fasting Insulin Sensitivity in Adults with Habitual Sleep Restriction

    PubMed Central

    Leproult, Rachel; Deliens, Gaétane; Gilson, Médhi; Peigneux, Philippe

    2015-01-01

    Study Objectives: A link between sleep loss and increased risk for the development of diabetes is now well recognized. The current study investigates whether sleep extension under real-life conditions is a feasible intervention with a beneficial impact on glucose metabolism in healthy adults who are chronically sleep restricted. Design: Intervention study. Participants: Sixteen healthy non-obese volunteers (25 [23, 27.8] years old, 3 men). Intervention: Two weeks of habitual time in bed followed by 6 weeks during which participants were instructed to increase their time in bed by one hour per day. Measurements and Results: Continuous actigraphy monitoring and daily sleep logs during the entire study. Glucose and insulin were assayed on a single morning blood sample at the end of habitual time in bed and at the end of sleep extension. Home polysomnography was performed during one weekday of habitual time in bed and after 40 days of sleep extension. Sleep time during weekdays increased (mean actigraphic data: +44 ± 34 minutes, P < 0.0001; polysomnographic data: +49 ± 68 minutes, P = 0.014), without any significant change during weekends. Changes from habitual time in bed to the end of the intervention in total sleep time correlated with changes in glucose (r = +0.53, P = 0.041) and insulin levels (r = −0.60, P = 0.025), as well as with indices of insulin sensitivity (r = +0.76, P = 0.002). Conclusions: In healthy adults who are chronically sleep restricted, a simple low cost intervention such as sleep extension is feasible and is associated with improvements in fasting insulin sensitivity. Citation: Leproult R, Deliens G, Gilson M, Peigneux P. Beneficial impact of sleep extension on fasting insulin sensitivity in adults with habitual sleep restriction. SLEEP 2015;38(5):707–715. PMID:25348128

  9. Sleep: A Health Imperative

    PubMed Central

    Luyster, Faith S.; Strollo, Patrick J.; Zee, Phyllis C.; Walsh, James K.

    2012-01-01

    Chronic sleep deficiency, defined as a state of inadequate or mistimed sleep, is a growing and underappreciated determinant of health status. Sleep deprivation contributes to a number of molecular, immune, and neural changes that play a role in disease development, independent of primary sleep disorders. These changes in biological processes in response to chronic sleep deficiency may serve as etiological factors for the development and exacerbation of cardiovascular and metabolic diseases and, ultimately, a shortened lifespan. Sleep deprivation also results in significant impairments in cognitive and motor performance which increase the risk of motor vehicle crashes and work-related injuries and fatal accidents. The American Academy of Sleep Medicine and the Sleep Research Society have developed this statement to communicate to national health stakeholders the current knowledge which ties sufficient sleep and circadian alignment in adults to health. Citation: Luyster FS; Strollo PJ; Zee PC; Walsh JK. Sleep: a health imperative. SLEEP 2012;35(6):727-734. PMID:22654183

  10. Sleep Discrepancy, Sleep Complaint, and Poor Sleep Among Older Adults

    PubMed Central

    2013-01-01

    Objectives. Discrepancy between self-report- and actigraphy-measured sleep, often considered an artifact of measurement error, has been well documented among insomnia patients. Sleep problems are common among older adults, and this discrepancy may represent meaningful sleep-related phenomenon, which could have clinical and research significance. Method. Sleep discrepancy was examined in 4 groups of older adults (N = 152, mean age = 71.93 years) based on sleep complaint versus no complaint and presence versus absence of insomnia symptoms. Participants completed the Beck Depression Inventory-second edition (BDI-II) and 14 nights of sleep diaries and actigraphy. Results. Controlling for covariates, group differences were found in the duration and frequency of discrepancy in sleep onset latency (SOLd) and wake after sleep onset (WASOd). Those with insomnia symptoms and complaints reported greater duration and frequency of WASOd than the other 3 groups. Quantities of SOLd and WASOd were related to BDI-II score and group status, indicating that sleep discrepancy has meaningful clinical correlates. Discussion. Discrepancy occurred across all groups but was pronounced among the group with both insomnia symptoms and complaints. This discrepancy may provide a means of quantifying and conceptualizing the transition from wake to sleep among older adults, particularly those with sleeping problems. PMID:23804432

  11. Sleep for cognitive enhancement

    PubMed Central

    Diekelmann, Susanne

    2014-01-01

    Sleep is essential for effective cognitive functioning. Loosing even a few hours of sleep can have detrimental effects on a wide variety of cognitive processes such as attention, language, reasoning, decision making, learning and memory. While sleep is necessary to ensure normal healthy cognitive functioning, it can also enhance performance beyond the boundaries of the normal condition. This article discusses the enhancing potential of sleep, mainly focusing on the domain of learning and memory. Sleep is known to facilitate the consolidation of memories learned before sleep as well as the acquisition of new memories to be learned after sleep. According to a widely held model this beneficial effect of sleep relies on the neuronal reactivation of memories during sleep that is associated with sleep-specific brain oscillations (slow oscillations, spindles, ripples) as well as a characteristic neurotransmitter milieu. Recent research indicates that memory processing during sleep can be boosted by (i) cueing memory reactivation during sleep; (ii) stimulating sleep-specific brain oscillations; and (iii) targeting specific neurotransmitter systems pharmacologically. Olfactory and auditory cues can be used, for example, to increase reactivation of associated memories during post-learning sleep. Intensifying neocortical slow oscillations (the hallmark of slow wave sleep (SWS)) by electrical or auditory stimulation and modulating specific neurotransmitters such as noradrenaline and glutamate likewise facilitates memory processing during sleep. With this evidence in mind, this article concludes by discussing different methodological caveats and ethical issues that should be considered when thinking about using sleep for cognitive enhancement in everyday applications. PMID:24765066

  12. Selective REM Sleep Deprivation Improves Expectation-Related Placebo Analgesia

    PubMed Central

    Chouchou, Florian; Chauny, Jean-Marc; Rainville, Pierre; Lavigne, Gilles J.

    2015-01-01

    The placebo effect is a neurobiological and psychophysiological process known to influence perceived pain relief. Optimization of placebo analgesia may contribute to the clinical efficacy and effectiveness of medication for acute and chronic pain management. We know that the placebo effect operates through two main mechanisms, expectations and learning, which is also influenced by sleep. Moreover, a recent study suggested that rapid eye movement (REM) sleep is associated with modulation of expectation-mediated placebo analgesia. We examined placebo analgesia following pharmacological REM sleep deprivation and we tested the hypothesis that relief expectations and placebo analgesia would be improved by experimental REM sleep deprivation in healthy volunteers. Following an adaptive night in a sleep laboratory, 26 healthy volunteers underwent classical experimental placebo analgesic conditioning in the evening combined with pharmacological REM sleep deprivation (clonidine: 13 volunteers or inert control pill: 13 volunteers). Medication was administered in a double-blind manner at bedtime, and placebo analgesia was tested in the morning. Results revealed that 1) placebo analgesia improved with REM sleep deprivation; 2) pain relief expectations did not differ between REM sleep deprivation and control groups; and 3) REM sleep moderated the relationship between pain relief expectations and placebo analgesia. These results support the putative role of REM sleep in modulating placebo analgesia. The mechanisms involved in these improvements in placebo analgesia and pain relief following selective REM sleep deprivation should be further investigated. PMID:26678391

  13. Impact of Obstructive Sleep Apnea on the Levels of Placental Growth Factor (PlGF) and Their Value for Predicting Short-Term Adverse Outcomes in Patients with Acute Coronary Syndrome

    PubMed Central

    Barcelo, Antonia; Bauça, Josep Miquel; Yañez, Aina; Fueyo, Laura; Gomez, Cristina; de la Peña, Monica; Pierola, Javier; Rodriguez, Alberto; Sanchez-de-la-Torre, Manuel; Abad, Jorge; Mediano, Olga; Amilibia, Jose; Masdeu, Maria Jose; Teran, Joaquin; Montserrat, Josep Maria; Mayos, Mercè; Sanchez-de-la-Torre, Alicia; Barbé, Ferran

    2016-01-01

    Background Placental growth factor (PlGF) induces angiogenesis and promotes tissue repair, and plasma PlGF levels change markedly during acute myocardial infarction (AMI). Currently, the impact of obstructive sleep apnea (OSA) in patients with AMI is a subject of debate. Our objective was to evaluate the relationships between PlGF levels and both the severity of acute coronary syndrome (ACS) and short-term outcomes after ACS in patients with and without OSA. Methods A total of 538 consecutive patients (312 OSA patients and 226 controls) admitted for ACS were included in this study. All patients underwent polygraphy in the first 72 hours after hospital admission. The severity of disease and short-term prognoses were evaluated during the hospitalization period. Plasma PlGF levels were measured using an electrochemiluminescence immunoassay. Results Patients with OSA were significantly older and more frequently hypertensive and had higher BMIs than those without OSA. After adjusting for age, smoking status, BMI and hypertension, PlGF levels were significantly elevated in patients with OSA compared with patients without OSA (19.9 pg/mL, interquartile range: 16.6–24.5 pg/mL; 18.5 pg/mL, interquartile range: 14.7–22.7 pg/mL; p<0.001), and a higher apnea-hypopnea index (AHI) was associated with higher PlGF concentrations (p<0.003). Patients with higher levels of PlGF had also an increased odds ratio for the presence of 3 or more diseased vessels and for a Killip score>1, even after adjustment. Conclusions The results of this study show that in patients with ACS, elevated plasma levels of PlGF are associated with the presence of OSA and with adverse outcomes during short-term follow-up. Trial Registration ClinicalTrials.gov NCT01335087 PMID:26930634

  14. Exposure to acute severe hypoxia leads to increased urea loss and disruptions in acid-base and ionoregulatory balance in dogfish sharks (Squalus acanthias).

    PubMed

    Zimmer, Alex M; Wood, Chris M

    2014-01-01

    The effects of acute moderate (20% air O2 saturation; 6-h exposure) and severe (5% air O2 saturation; 4-h exposure) hypoxia on N-waste, acid-base, and ion balance in dogfish sharks (Squalus acanthias suckleyi) were evaluated. We predicted that the synthesis and/or retention of urea, which are active processes, would be inhibited by hypoxia. Exposure to moderate hypoxia had negligible effects on N-waste fluxes or systemic physiology, except for a modest rise in plasma lactate. Exposure to severe hypoxia led to a significant increase in urea excretion (Jurea), while plasma, liver, and muscle urea concentrations were unchanged, suggesting a loss of urea retention. Ammonia excretion (Jamm) was elevated during normoxic recovery. Moreover, severe hypoxia led to disruptions in acid-base balance, indicated by a large increase in plasma [lactate] and substantial decreases in arterial pHa and plasma [Formula: see text], as well as loss of ionic homeostasis, indicated by increases in plasma [Mg(2+)], [Ca(2+)], and [Na(+)]. We suggest that severe hypoxia in dogfish sharks leads to a reduction in active gill homeostatic processes, such as urea retention, acid-base regulation and ionoregulation, and/or an osmoregulatory compromise due to increased functional gill surface area. Overall, the results provide a comprehensive picture of the physiological responses to a severe degree of hypoxia in an ancient fish species. PMID:25244375

  15. Adolescents' Sleep Behaviors and Perceptions of Sleep

    ERIC Educational Resources Information Center

    Noland, Heather; Price, James H.; Dake, Joseph; Telljohann, Susan K.

    2009-01-01

    Background: Sleep duration affects the health of children and adolescents. Shorter sleep durations have been associated with poorer academic performance, unintentional injuries, and obesity in adolescents. This study extends our understanding of how adolescents perceive and deal with their sleep issues. Methods: General education classes were…

  16. A mathematical model of the sleep/wake cycle.

    PubMed

    Rempe, Michael J; Best, Janet; Terman, David

    2010-05-01

    We present a biologically-based mathematical model that accounts for several features of the human sleep/wake cycle. These features include the timing of sleep and wakefulness under normal and sleep-deprived conditions, ultradian rhythms, more frequent switching between sleep and wakefulness due to the loss of orexin and the circadian dependence of several sleep measures. The model demonstrates how these features depend on interactions between a circadian pacemaker and a sleep homeostat and provides a biological basis for the two-process model for sleep regulation. The model is based on previous "flip-flop" conceptual models for sleep/wake and REM/NREM and we explore whether the neuronal components in these flip-flop models, with the inclusion of a sleep-homeostatic process and the circadian pacemaker, are sufficient to account for the features of the sleep/wake cycle listed above. The model is minimal in the sense that, besides the sleep homeostat and constant cortical drives, the model includes only those nuclei described in the flip-flop models. Each of the cell groups is modeled by at most two differential equations for the evolution of the total population activity, and the synaptic connections are consistent with those described in the flip-flop models. A detailed analysis of the model leads to an understanding of the mathematical mechanisms, as well as insights into the biological mechanisms, underlying sleep/wake dynamics. PMID:19557415

  17. Elevated ghrelin predicts food intake during experimental sleep restriction

    PubMed Central

    Broussard, Josiane L.; Kilkus, Jennifer M.; Delebecque, Fanny; Abraham, Varghese; Day, Andrew; Whitmore, Harry R.; Tasali, Esra

    2015-01-01

    Objective Sleep curtailment has been linked to obesity, but underlying mechanisms remain to be elucidated. We assessed whether sleep restriction alters 24-hour profiles of appetite-regulating hormones ghrelin, leptin and pancreatic polypeptide during a standardized diet, and whether these hormonal alterations predict food intake during ad libitum feeding. Methods Nineteen healthy, lean men were studied under normal sleep and sleep restriction in a randomized crossover design. Blood samples were collected for 24-hours during standardized meals. Subsequently, participants had an ad libitum feeding opportunity (buffet meals and snacks) and caloric intake was measured. Results Ghrelin levels were increased after sleep restriction as compared to normal sleep (p<0.01). Overall, sleep restriction did not alter leptin or pancreatic polypeptide profiles. Sleep restriction was associated with an increase in total calories from snacks by 328 ± 140 Kcal (p=0.03), primarily from carbohydrates (p=0.02). The increase in evening ghrelin during sleep restriction was correlated with higher consumption of calories from sweets (r=0.48, p=0.04). Conclusions Sleep restriction as compared to normal sleep significantly increases ghrelin levels. The increase in ghrelin is associated with more consumption of calories. Elevated ghrelin may be a mechanism by which sleep loss leads to increased food intake and the development of obesity. PMID:26467988

  18. Sleep deprivation attenuates inflammatory responses and ischemic cell death.

    PubMed

    Weil, Zachary M; Norman, Greg J; Karelina, Kate; Morris, John S; Barker, Jacqueline M; Su, Alan J; Walton, James C; Bohinc, Steven; Nelson, Randy J; DeVries, A Courtney

    2009-07-01

    Although the biological function of sleep remains uncertain, the consequences of sleep deprivation are well-described and are reported to be detrimental to cognitive function and affective well-being. Sleep deprivation also is strongly associated with elevated risk factors for cardiovascular disease. We used a mouse model of cardiac arrest/cardiopulmonary resuscitation to test the hypothesis that acute sleep deprivation would exacerbate neuroinflammation and neurodegeneration after global ischemia. The resulting data led to a rejection of our hypothesis that sleep deprivation is necessarily detrimental. Indeed, acute sleep deprivation (ASD) was associated with a reduction in ischemia-induced interleukin 1beta (IL-1beta) gene expression and attenuation of neuronal damage in the hippocampus. Further, sleep deprivation increased gene expression of two anti-inflammatory cytokines, IL-6 and IL-10 that are associated with improved ischemic outcome. To determine whether the anti-inflammatory properties of ASD were specific to ischemia, mice were treated systemically with lipopolysaccharide (LPS), a potent inflammogen. Acute sleep deprivation attenuated the central and peripheral increase in tumor necrosis factor-alpha (TNFalpha) and increased IL-10 expression. Together, the ischemia and LPS data suggest that, ASD produces an anti-inflammatory bias that could be exploited to improve medical procedures that are compromised by inflammation. PMID:19409382

  19. Sleep deprivation: Impact on cognitive performance

    PubMed Central

    Alhola, Paula; Polo-Kantola, Päivi

    2007-01-01

    Today, prolonged wakefulness is a widespread phenomenon. Nevertheless, in the field of sleep and wakefulness, several unanswered questions remain. Prolonged wakefulness can be due to acute total sleep deprivation (SD) or to chronic partial sleep restriction. Although the latter is more common in everyday life, the effects of total SD have been examined more thoroughly. Both total and partial SD induce adverse changes in cognitive performance. First and foremost, total SD impairs attention and working memory, but it also affects other functions, such as long-term memory and decision-making. Partial SD is found to influence attention, especially vigilance. Studies on its effects on more demanding cognitive functions are lacking. Coping with SD depends on several factors, especially aging and gender. Also interindividual differences in responses are substantial. In addition to coping with SD, recovering from it also deserves attention. Cognitive recovery processes, although insufficiently studied, seem to be more demanding in partial sleep restriction than in total SD. PMID:19300585

  20. Behavioral Sleep-Wake Homeostasis and EEG Delta Power Are Decoupled By Chronic Sleep Restriction in the Rat

    PubMed Central

    Stephenson, Richard; Caron, Aimee M.; Famina, Svetlana

    2015-01-01

    Study Objectives: Chronic sleep restriction (CSR) is prevalent in society and is linked to adverse consequences that might be ameliorated by acclimation of homeostatic drive. This study was designed to test the hypothesis that the sleep-wake homeostat will acclimatize to CSR. DESIGN: A four-parameter model of proportional control was used to quantify sleep homeostasis with and without recourse to a sleep intensity function. Setting: Animal laboratory, rodent walking-wheel apparatus. Subjects: Male Sprague-Dawley rats. Interventions: Acute total sleep deprivation (TSD, 1 day × 18 or 24 h, N = 12), CSR (10 days × 18 h TSD, N = 6, or 5 days × 20 h TSD, N = 5). Measurements and Results: Behavioral rebounds were consistent with model predictions for proportional control of cumulative times in wake, nonrapid eye movement sleep (NREM) and rapid eye movement sleep (REM). Delta (Δ) energy homeostasis was secondary to behavioral homeostasis; a biphasic NREM Δ power rebound contributed to the dynamics (rapid response) but not to the magnitude of the rebound in Δ energy. REM behavioral homeostasis was little affected by CSR. NREM behavioral homeostasis was attenuated in proportion to cumulative NREM deficit, whereas the biphasic NREM Δ power rebound was only slightly suppressed, indicating decoupled regulatory mechanisms following CSR. Conclusions: We conclude that sleep homeostasis is achieved through behavioral regulation, that the nonrapid eye movement sleep behavioral homeostat is susceptible to attenuation during chronic sleep restriction and that the concept of sleep intensity is not essential in a model of sleep-wake regulation. Citation: Stephenson R, Caron AM, Famina S. Behavioral sleep-wake homeostasis and EEG delta power are decoupled by chronic sleep restriction in the rat. SLEEP 2015;38(5):685–697. PMID:25669184

  1. Loss of DNAM-1 ligand expression by acute myeloid leukemia cells renders them resistant to NK cell killing.

    PubMed

    Kearney, Conor J; Ramsbottom, Kelly M; Voskoboinik, Ilia; Darcy, Phillip K; Oliaro, Jane

    2016-08-01

    Acute myeloid leukemia (AML) is associated with poor natural killer (NK) cell function through aberrant expression of NK-cell-activating receptors and their ligands on tumor cells. These alterations are thought to promote formation of inhibitory NK-target cell synapses, in which killer cell degranulation is attenuated. Allogeneic stem cell transplantation can be effective in treating AML, through restoration of NK cell lytic activity. Similarly, agents that augment NK-cell-activating signals within the immunological synapse may provide some therapeutic benefit. However, the receptor-ligand interactions that critically dictate NK cell function in AML remain undefined. Here, we demonstrate that CD112/CD155 expression is required for DNAM-1-dependent killing of AML cells. Indeed, the low, or absent, expression of CD112/CD155 on multiple AML cell lines resulted in failure to stimulate optimal NK cell function. Importantly, isolated clones with low CD112/155 expression were resistant to NK cell killing while those expressing abundant levels of CD112/155 were highly susceptible. Attenuated NK cell killing in the absence of CD112/CD155 originated from decreased NK-target cell conjugation. Furthermore, we reveal by time-lapse microscopy, a significant increase in NK cell 'failed killing' in the absence of DNAM-1 ligands. Consequently, NK cells preferentially lysed ligand-expressing cells within heterogeneous populations, driving clonal selection of CD112/CD155-negative blasts upon NK cell attack. Taken together, we identify reduced CD155 expression as a major NK cell escape mechanism in AML and an opportunity for targeted immunotherapy. PMID:27622064

  2. Time-dependent retinal ganglion cell loss, microglial activation and blood-retina-barrier tightness in an acute model of ocular hypertension.

    PubMed

    Trost, A; Motloch, K; Bruckner, D; Schroedl, F; Bogner, B; Kaser-Eichberger, A; Runge, C; Strohmaier, C; Klein, B; Aigner, L; Reitsamer, H A

    2015-07-01

    Glaucoma is a group of neurodegenerative diseases characterized by the progressive loss of retinal ganglion cells (RGCs) and their axons, and is the second leading cause of blindness worldwide. Elevated intraocular pressure is a well known risk factor for the development of glaucomatous optic neuropathy and pharmacological or surgical lowering of intraocular pressure represents a standard procedure in glaucoma treatment. However, the treatment options are limited and although lowering of intraocular pressure impedes disease progression, glaucoma cannot be cured by the currently available therapy concepts. In an acute short-term ocular hypertension model in rat, we characterize RGC loss, but also microglial cell activation and vascular alterations of the retina at certain time points. The combination of these three parameters might facilitate a better evaluation of the disease progression, and could further serve as a new model to test novel treatment strategies at certain time points. Acute ocular hypertension (OHT) was induced by the injection of magnetic microbeads into the rat anterior chamber angle (n = 22) with magnetic position control, leading to constant elevation of IOP. At certain time points post injection (4d, 7d, 10d, 14d and 21d), RGC loss, microglial activation, and microvascular pericyte (PC) coverage was analyzed using immunohistochemistry with corresponding specific markers (Brn3a, Iba1, NG2). Additionally, the tightness of the retinal vasculature was determined via injections of Texas Red labeled dextran (10 kDa) and subsequently analyzed for vascular leakage. For documentation, confocal laser-scanning microscopy was used, followed by cell counts, capillary length measurements and morphological and statistical analysis. The injection of magnetic microbeads led to a progressive loss of RGCs at the five time points investigated (20.07%, 29.52%, 41.80%, 61.40% and 76.57%). Microglial cells increased in number and displayed an activated morphology

  3. Retino-hypothalamic regulation of light-induced murine sleep

    PubMed Central

    Muindi, Fanuel; Zeitzer, Jamie M.; Heller, Horace Craig

    2014-01-01

    The temporal organization of sleep is regulated by an interaction between the circadian clock and homeostatic processes. Light indirectly modulates sleep through its ability to phase shift and entrain the circadian clock. Light can also exert a direct, circadian-independent effect on sleep. For example, acute exposure to light promotes sleep in nocturnal animals and wake in diurnal animals. The mechanisms whereby light directly influences sleep and arousal are not well understood. In this review, we discuss the direct effect of light on sleep at the level of the retina and hypothalamus in rodents. We review murine data from recent publications showing the roles of rod-, cone- and melanopsin-based photoreception on the initiation and maintenance of light-induced sleep. We also present hypotheses about hypothalamic mechanisms that have been advanced to explain the acute control of sleep by light. Specifically, we review recent studies assessing the roles of the ventrolateral preoptic area (VLPO) and the suprachiasmatic nucleus (SCN). We also discuss how light might differentially promote sleep and arousal in nocturnal and diurnal animals respectively. Lastly, we suggest new avenues for research on this topic which is still in its early stages. PMID:25140132

  4. Sleep Apnea Facts

    MedlinePlus

    ... Apnea Facts Sleep Apnea Links Sleep Apnea Facts Sleep apnea affects up to 18 million Americans The condition was ... member is the first to notice signs of sleep apnea in someone with the ... diagnosed. The condition affects about 4 percent of middle-aged men and ...

  5. Sleep and Infant Learning

    ERIC Educational Resources Information Center

    Tarullo, Amanda R.; Balsam, Peter D.; Fifer, William P.

    2011-01-01

    Human neonates spend the majority of their time sleeping. Despite the limited waking hours available for environmental exploration, the first few months of life are a time of rapid learning about the environment. The organization of neonate sleep differs qualitatively from adult sleep, and the unique characteristics of neonatal sleep may promote…

  6. Sleep Disorders (PDQ)

    MedlinePlus

    ... The two main phases of sleep are rapid eye movement (REM) and non-rapid eye movement (NREM): REM sleep, also known as "dream sleep," ... taken during sleep that show: Brain wave changes. Eye movements. Breathing rate. Blood pressure . Heart rate and electrical ...

  7. How (and why) the immune system makes us sleep

    PubMed Central

    Imeri, Luca; Opp, Mark R.

    2010-01-01

    Good sleep is necessary for physical and mental health. For example, sleep loss impairs immune function, and sleep is altered during infection. Immune signalling molecules are present in the healthy brain, where they interact with neurochemical systems to contribute to the regulation of normal sleep. Animal studies have shown that interactions between immune signalling molecules (such as the cytokine interleukin 1) and brain neurochemical systems (such as the serotonin system) are amplified during infection, indicating that these interactions might underlie the changes in sleep that occur during infection. Why should the immune system cause us to sleep differently when we are sick? We propose that the alterations in sleep architecture during infection are exquisitely tailored to support the generation of fever, which in turn imparts survival value. PMID:19209176

  8. Total sleep deprivation decreases flow experience and mood status

    PubMed Central

    Kaida, Kosuke; Niki, Kazuhisa

    2014-01-01

    Background The purpose of this study was to examine the effect of sleep deprivation on flow experience. Methods Sixteen healthy male volunteers of mean age 21.4±1.59 (21–24) years participated in two experimental conditions, ie, sleep-deprivation and normal sleep. In the sleep-deprived condition, participants stayed awake at home for 36 hours (from 8 am until 10 pm the next day) beginning on the day prior to an experimental day. In both conditions, participants carried out a simple reaction time (psychomotor vigilance) task and responded to a questionnaire measuring flow experience and mood status. Results Flow experience was reduced after one night of total sleep deprivation. Sleep loss also decreased positive mood, increased negative mood, and decreased psychomotor performance. Conclusion Sleep deprivation has a strong impact on mental and behavioral states associated with the maintenance of flow, namely subjective well-being. PMID:24376356

  9. Promoting healthy sleep.

    PubMed

    Price, Bob

    2016-03-01

    Nurses are accustomed to helping others with their sleep problems and dealing with issues such as pain that may delay or interrupt sleep. However, they may be less familiar with what constitutes a healthy night's sleep. This article examines what is known about the process and purpose of sleep, and examines the ways in which factors that promote wakefulness and sleep combine to help establish a normal circadian rhythm. Theories relating to the function of sleep are discussed and research is considered that suggests that sleep deficit may lead to metabolic risks, including heart disease, obesity, type 2 diabetes mellitus and several types of cancer. PMID:26959472

  10. Occupational Sleep Medicine.

    PubMed

    Cheng, Philip; Drake, Christopher

    2016-03-01

    Sleep and circadian rhythms significantly impact almost all aspects of human behavior and are therefore relevant to occupational sleep medicine, which is focused predominantly around workplace productivity, safety, and health. In this article, 5 main factors that influence occupational functioning are reviewed: (1) sleep deprivation, (2) disordered sleep, (3) circadian rhythms, (4) common medical illnesses that affect sleep and sleepiness, and (5) medications that affect sleep and sleepiness. Consequences of disturbed sleep and sleepiness are also reviewed, including cognitive, emotional, and psychomotor functioning and drowsy driving. PMID:26972034

  11. Sleep and Stroke.

    PubMed

    Mims, Kimberly Nicole; Kirsch, Douglas

    2016-03-01

    Evidence increasingly suggests sleep disorders are associated with higher risk of cardiovascular events, including stroke. Strong data correlate untreated sleep apnea with poorer stroke outcomes and more recent evidence implicates sleep disruption as a possible etiology for increased cerebrovascular events. Also, sleep duration may affect incidence of cardiovascular events. In addition, sleep-disordered breathing, insomnia, restless legs syndrome, and parasomnias can occur as a result of cerebrovascular events. Treatment of sleep disorders improve sleep-related symptoms and may also improve stroke recovery and risk of future events. PMID:26972032

  12. Caffeine Consuming Children and Adolescents Show Altered Sleep Behavior and Deep Sleep

    PubMed Central

    Aepli, Andrina; Kurth, Salome; Tesler, Noemi; Jenni, Oskar G.; Huber, Reto

    2015-01-01

    Caffeine is the most commonly ingested psychoactive drug worldwide with increasing consumption rates among young individuals. While caffeine leads to decreased sleep quality in adults, studies investigating how caffeine consumption affects children’s and adolescents’ sleep remain scarce. We explored the effects of regular caffeine consumption on sleep behavior and the sleep electroencephalogram (EEG) in children and adolescents (10–16 years). While later habitual bedtimes (Caffeine 23:14 ± 11.4, Controls 22:17 ± 15.4) and less time in bed were found in caffeine consumers compared to the control group (Caffeine 08:10 ± 13.3, Controls 09:03 ± 16.1), morning tiredness was unaffected. Furthermore, caffeine consumers exhibited reduced sleep EEG slow-wave activity (SWA, 1–4.5 Hz) at the beginning of the night compared to controls (20% ± 9% average reduction across all electrodes and subjects). Comparable reductions were found for alpha activity (8.25–9.75 Hz). These effects, however, disappeared in the morning hours. Our findings suggest that caffeine consumption in adolescents may lead to later bedtimes and reduced SWA, a well-established marker of sleep depth. Because deep sleep is involved in recovery processes during sleep, further research is needed to understand whether a caffeine-induced loss of sleep depth interacts with neuronal network refinement processes that occur during the sensitive period of adolescent development. PMID:26501326

  13. Caffeine Consuming Children and Adolescents Show Altered Sleep Behavior and Deep Sleep.

    PubMed

    Aepli, Andrina; Kurth, Salome; Tesler, Noemi; Jenni, Oskar G; Huber, Reto

    2015-01-01

    Caffeine is the most commonly ingested psychoactive drug worldwide with increasing consumption rates among young individuals. While caffeine leads to decreased sleep quality in adults, studies investigating how caffeine consumption affects children's and adolescents' sleep remain scarce. We explored the effects of regular caffeine consumption on sleep behavior and the sleep electroencephalogram (EEG) in children and adolescents (10-16 years). While later habitual bedtimes (Caffeine 23:14 ± 11.4, Controls 22:17 ± 15.4) and less time in bed were found in caffeine consumers compared to the control group (Caffeine 08:10 ± 13.3, Controls 09:03 ± 16.1), morning tiredness was unaffected. Furthermore, caffeine consumers exhibited reduced sleep EEG slow-wave activity (SWA, 1-4.5 Hz) at the beginning of the night compared to controls (20% ± 9% average reduction across all electrodes and subjects). Comparable reductions were found for alpha activity (8.25-9.75 Hz). These effects, however, disappeared in the morning hours. Our findings suggest that caffeine consumption in adolescents may lead to later bedtimes and reduced SWA, a well-established marker of sleep depth. Because deep sleep is involved in recovery processes during sleep, further research is needed to understand whether a caffeine-induced loss of sleep depth interacts with neuronal network refinement processes that occur during the sensitive period of adolescent development. PMID:26501326

  14. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation

    NASA Technical Reports Server (NTRS)

    Van Dongen, Hans P A.; Maislin, Greg; Mullington, Janet M.; Dinges, David F.

    2003-01-01

    OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness

  15. Impact of a nursing-driven sleep hygiene protocol on sleep quality.

    PubMed

    Faraklas, Iris; Holt, Brennen; Tran, Sally; Lin, Hsin; Saffle, Jeffrey; Cochran, Amalia

    2013-01-01

    The purpose of this study was to evaluate the impact on sleep quality of a nursing-driven sleep hygiene protocol (SHP) instituted in a single burn-trauma intensive care unit. Criteria for eligibility were adult patients admitted to the Burn Service who were not delirious, able to respond verbally, and had not received general anesthesia in the prior 24 hours. Patients were surveyed using the validated Richards-Campbell Sleep Questionnaire prior to implementation ("PRE"; May to December 2010) and following implementation ("POST"; January to August 2011) of a SHP that sought to minimize environmental stimuli and limit disruptions during the night. This analysis includes only initial survey responses from each patient. A total of 130 patients were surveyed, 81 PRE and 49 POST; 60% were burn admissions. There was no significant difference in responses to the questionnaire between burn and nonburn patients. All patients in the POST group were significantly older and more frequently endorsed taking sleep medication at home. Although not significant, POST patients reported falling asleep somewhat more quickly, but no other differences were identified between the two groups. Among patients who reported having sleep difficulties prior to admission, POST patients not only reported a significantly higher pain score than PRE patients, but also reported significant improvement in falling asleep and being able to go back to sleep. Frequency of complaints of sleep disruption was unchanged between PRE and POST patients. POST patients did complain significantly less than PRE patients about sleep disruptions by clinicians. Implementation of the SHP permitted acutely injured or ill patients in our intensive care unit to fall asleep more quickly and to experience fewer sleep disruptions. A sleep protocol may be helpful in improving sleep and overall well-being of burn center patients. PMID:23412331

  16. Sleep disorders in children.

    PubMed

    Ward, Teresa; Mason, Thornton B A

    2002-12-01

    Sleep disorders are common in childhood, and may affect multiple aspects of a child's life and the lives of other family members. A sleep disorder assessment should begin with detailed sleep history and a review of interrelated health issues. Factors contributing to disturbed sleep may be discovered or confirmed by a thorough physical examination. Thereafter, appropriate ancillary testing can provide support for a specific clinical diagnosis. The spectrum of childhood sleep disorders includes OSA, narcolepsy, RLS/PLMD, sleep onset association disorder, and parasomnias. Diagnosing sleep disorders in children remains a challenge; however, a multidisciplinary approach may provide an opportunity for productive collaboration and, thereby, more effective patient management. Centers treating pediatric sleep disorders may include providers from a variety of disciplines in pediatric healthcare, such as child psychology, pulmonology, neurology, psychiatry, nursing, and otolaryngology. Over the last decade, research in pediatric sleep disorders has expanded greatly, paralleled by an increased awareness of the importance of adequate, restorative sleep in childhood. PMID:12587368

  17. Call it Worm Sleep.

    PubMed

    Trojanowski, Nicholas F; Raizen, David M

    2016-02-01

    The nematode Caenorhabditis elegans stops feeding and moving during a larval transition stage called lethargus and following exposure to cellular stressors. These behaviors have been termed 'sleep-like states'. We argue that these behaviors should instead be called sleep. Sleep during lethargus is similar to sleep regulated by circadian timers in insects and mammals, and sleep in response to cellular stress is similar to sleep induced by sickness in other animals. Sleep in mammals and Drosophila shows molecular and functional conservation with C. elegans sleep. The simple neuroanatomy and powerful genetic tools of C. elegans have yielded insights into sleep regulation and hold great promise for future research into sleep regulation and function. PMID:26747654

  18. Isolated sleep paralysis elicited by sleep interruption.

    PubMed

    Takeuchi, T; Miyasita, A; Sasaki, Y; Inugami, M; Fukuda, K

    1992-06-01

    We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy. PMID:1621022

  19. Sleep disorders and aortic dissection in a working population.

    PubMed

    Hata, Mitsumasa; Yoshitake, Isamu; Wakui, Shinji; Unosawa, Satoshi; Takahashi, Kana; Kimura, Haruka; Hata, Hiroaki; Shiono, Motomi

    2012-04-01

    The aim of the present study was to assess the relationship between acute aortic dissection (AAD) and sleep disorders in a working population. Seventy (50.4%) of 139 younger subjects with AAD suffered from sleep disorders. Insomnia was reported by 35 patients (50%), sleep deprivation by 31 patients (44.3%), and sleep apnea syndrome was present in 43 patients (61.4%). The average apnea-hypopnea index was 22.0 ± 7.5 points, requiring appropriate treatment. Most of these patients had irregular daily schedules due to job pressure. Sixty-six (94.3%) complained of severe mental and physical stress in daily life. Sleep disorders are considered one of the risk factors for the occurrence of AAD at younger active ages. In primary care for patients with mental or physical stress due to their daily life, it is important to assess these individuals for the presence of sleep disorders. PMID:22127533

  20. Ostriches Sleep like Platypuses

    PubMed Central

    Lesku, John A.; Meyer, Leith C. R.; Fuller, Andrea; Maloney, Shane K.; Dell'Omo, Giacomo

    2011-01-01

    Mammals and birds engage in two distinct states of sleep, slow wave sleep (SWS) and rapid eye movement (REM) sleep. SWS is characterized by slow, high amplitude brain waves, while REM sleep is characterized by fast, low amplitude waves, known as activation, occurring with rapid eye movements and reduced muscle tone. However, monotremes (platypuses and echidnas), the most basal (or ‘ancient’) group of living mammals, show only a single sleep state that combines elements of SWS and REM sleep, suggesting that these states became temporally segregated in the common ancestor to marsupial and eutherian mammals. Whether sleep in basal birds resembles that of monotremes or other mammals and birds is unknown. Here, we provide the first description of brain activity during sleep in ostriches (Struthio camelus), a member of the most basal group of living birds. We found that the brain activity of sleeping ostriches is unique. Episodes of REM sleep were delineated by rapid eye movements, reduced muscle tone, and head movements, similar to those observed in other birds and mammals engaged in REM sleep; however, during REM sleep in ostriches, forebrain activity would flip between REM sleep-like activation and SWS-like slow waves, the latter reminiscent of sleep in the platypus. Moreover, the amount of REM sleep in ostriches is greater than in any other bird, just as in platypuses, which have more REM sleep than other mammals. These findings reveal a recurring sequence of steps in the evolution of sleep in which SWS and REM sleep arose from a single heterogeneous state that became temporally segregated into two distinct states. This common trajectory suggests that forebrain activation during REM sleep is an evolutionarily new feature, presumably involved in performing new sleep functions not found in more basal animals. PMID:21887239

  1. Acute responses to opioidergic blockade as a biomarker of hedonic eating among obese women enrolled in a mindfulness-based weight loss intervention trial.

    PubMed

    Mason, Ashley E; Lustig, Robert H; Brown, Rashida R; Acree, Michael; Bacchetti, Peter; Moran, Patricia J; Dallman, Mary; Laraia, Barbara; Adler, Nancy; Hecht, Frederick M; Daubenmier, Jennifer; Epel, Elissa S

    2015-08-01

    There are currently no commonly used or easily accessible 'biomarkers' of hedonic eating. Physiologic responses to acute opioidergic blockade, indexed by cortisol changes and nausea, may represent indirect functional measures of opioid-mediated hedonic eating drive and predict weight loss following a mindfulness-based intervention for stress eating. In the current study, we tested whether cortisol and nausea responses induced by oral ingestion of an opioidergic antagonist (naltrexone) correlated with weight and self-report measures of hedonic eating and predicted changes in these measures following a mindfulness-based weight loss intervention. Obese women (N = 88; age = 46.7 ± 13.2 years; BMI = 35.8 ± 3.8) elected to complete an optional sub-study prior to a 5.5-month weight loss intervention with or without mindfulness training. On two separate days, participants ingested naltrexone and placebo pills, collected saliva samples, and reported nausea levels. Supporting previous findings, naltrexone-induced cortisol increases were associated with greater hedonic eating (greater food addiction symptoms and reward-driven eating) and less mindful eating. Among participants with larger cortisol increases (+1 SD above mean), mindfulness participants (relative to control participants) reported greater reductions in food addiction symptoms, b = -0.95, SE(b) = 0.40, 95% CI [-1.74, -0.15], p = .0