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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. 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

  4. 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.

  5. 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.

  6. 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

  7. 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

  8. 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

  9. Acute Vision Loss.

    PubMed

    Bagheri, Nika; Mehta, Sonia

    2015-09-01

    Acute vision loss can be transient (lasting <24 hours) or persistent (lasting >24 hours). When patients present with acute vision loss, it is important to ascertain the duration of vision loss and whether it is a unilateral process affecting one eye or a bilateral process affecting both eyes. This article focuses on causes of acute vision loss in the nontraumatic setting and provides management pearls to help health care providers better triage these patients.

  10. Acute Vision Loss.

    PubMed

    Bagheri, Nika; Mehta, Sonia

    2015-09-01

    Acute vision loss can be transient (lasting <24 hours) or persistent (lasting >24 hours). When patients present with acute vision loss, it is important to ascertain the duration of vision loss and whether it is a unilateral process affecting one eye or a bilateral process affecting both eyes. This article focuses on causes of acute vision loss in the nontraumatic setting and provides management pearls to help health care providers better triage these patients. PMID:26319342

  11. 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 ...

  12. 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

  13. Sleep Modifications in Acute Transient Global Amnesia

    PubMed Central

    Della Marca, Giacomo; Mazza, Marianna; Losurdo, Anna; Testani, Elisa; Broccolini, Aldobrando; Frisullo, Giovanni; Marano, Giuseppe; Morosetti, Roberta; Pilato, Fabio; Profice, Paolo; Vollono, Catello; Di Lazzaro, Vincenzo

    2013-01-01

    Study Objective: Transient global amnesia (TGA) is a temporary memory loss characterized by an abrupt onset of antero-grade and retrograde amnesia, totally reversible. Since sleep plays a major role in memory consolidation, and in the storage of memory-related traces into the brain cortex, the aims of the present study were: (1) to evaluate changes in sleep macro-structure in TGA; (2) to assess modifications in sleep micro-structure in TGA, with particular reference to the arousal EEG and to cyclic alternating pattern (CAP); (3) to compare sleep parameters in TGA patients with a control group of patients with acute ischemic events (“minor stroke” or transient ischemic attack [TIA]) clinically and neuroradiologically “similar” to the TGA. Methods: TGA group: 17 patients, (8 men and 9 women, 60.2 ± 12.5 years). Stroke or TIA (SoT) group: 17 patients hospitalized in the Stroke Unit for recent onset of minor stroke or TIA with hemispheric localization; healthy controls (HC) group: 17 healthy volunteers, matched for age and sex. Patients and controls underwent full-night polysomnography. Results: In the multivariate analysis (conditions TGA, SoT, and HC) a significant effect of the condition was observed for sleep efficiency index, number of awakenings longer 1 min, REM latency, CAP time, and CAP rate. TGA and SoT differed only for CAP time and CAP rate, which were lower in the TGA group. Conclusions: Microstructural modification associated with TGA could be consequent to: (1) hippocampal dysfunction and memory impairment; (2) impairment of arousal-related structures (in particular, cholinergic pathways); (3) emotional distress. Citation: Della Marca G; Mazza M; Losurdo A; Testani E; Broccolini A; Frisullo G; Marano G; Morosetti R; Pilato F; Profice P; Vollono C; Di Lazzaro V. Sleep modifications in acute transient global amnesia. J Clin Sleep Med 2013;9(9):921-927. PMID:23997704

  14. 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

  15. Countermeasures for sleep loss and deprivation.

    PubMed

    Kushida, Clete A

    2006-09-01

    Sleep deprivation is ubiquitous and carries profound consequences in terms of personal and public health and safety. There is no substitute for a good night's sleep. Sleep that is optimal in quality and quantity for individuals, factoring in their age and personal sleep requirements, will minimize sleep debt and maximize daytime performance. Therefore, setting aside an adequate amount of time for sleep should be a priority; sleep should not be sacrificed at the expense of other activities of daily living. Nevertheless, there are certain therapeutic countermeasures available for individuals who are unable to obtain adequate sleep because of medical or sleep-related conditions (eg, narcolepsy, obstructive sleep apnea) when excessive daytime sleepiness is the main feature of the condition, or residual sleepiness despite treatment for the main conditions is present. These therapeutic countermeasures may also be considered in situations in which occupational constraints (eg, rotating shift work, military duty) dictate that constant or heightened vigilance is important or critical to work performance, crucial decision making, and/or survival. Exploration of the causes of sleep loss or deprivation, whether it is voluntary, or work or family induced, and/or the effects of a medical or sleep disorder, is a necessary first step in the evaluation of a patient who has significant daytime fatigue or sleepiness. Wake-promoting substances and medications such as caffeine, modafinil, methylphenidate, and dextroamphetamine may be considered in situations in which sleep loss is unavoidable or persists despite treatment of an underlying disorder that is characterized by or associated with daytime fatigue or sleepiness.

  16. 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

  17. 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

  18. 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

  19. 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

  20. 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

  1. 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

  2. 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

  3. Acute, painless vision loss.

    PubMed

    Beran, David I; Murphy-Lavoie, Heather

    2009-01-01

    This article provides a review of various conditions causing sudden, painless vision loss. The conditions of amaurosis fugax, central retinal artery occlusion (CRAO), central retinal vein occlusion (CRVO), vitreous hemorrhage, ischemic optic neuropathies (ION), posterior cerebrovascular accidents, and retinal detachment (RD) are discussed. The history, physical, pathophysiology, and treatment of each disease state are discussed along with possible preventative measures for each. An emphasis is made on early ophthalmologic involvement for potential vision restoration and the importance of a thorough history and physical for all patients with ocular complaints. PMID:19785313

  4. Loss of Sleep Affects the Ultrastructure of Pyramidal Neurons in the Adolescent Mouse Frontal Cortex

    PubMed Central

    de Vivo, Luisa; Nelson, Aaron B.; Bellesi, Michele; Noguti, Juliana; Tononi, Giulio; Cirelli, Chiara

    2016-01-01

    Study Objective: The adolescent brain may be uniquely affected by acute sleep deprivation (ASD) and chronic sleep restriction (CSR), but direct evidence is lacking. We used electron microscopy to examine how ASD and CSR affect pyramidal neurons in the frontal cortex of adolescent mice, focusing on mitochondria, endosomes, and lysosomes that together perform most basic cellular functions, from nutrient intake to prevention of cellular stress. Methods: Adolescent (1-mo-old) mice slept (S) or were sleep deprived (ASD, with novel objects and running wheels) during the first 6–8 h of the light period, chronically sleep restricted (CSR) for > 4 days (using novel objects, running wheels, social interaction, forced locomotion, caffeinated water), or allowed to recover sleep (RS) for ∼32 h after CSR. Ultrastructural analysis of 350 pyramidal neurons was performed (S = 82; ASD = 86; CSR = 103; RS = 79; 4 to 5 mice/group). Results: Several ultrastructural parameters differed in S versus ASD, S versus CSR, CSR versus RS, and S versus RS, although the different methods used to enforce wake may have contributed to some of the differences between short and long sleep loss. Differences included larger cytoplasmic area occupied by mitochondria in CSR versus S, and higher number of secondary lysosomes in CSR versus S and RS. We also found that sleep loss may unmask interindividual differences not obvious during baseline sleep. Moreover, using a combination of 11 ultrastructural parameters, we could predict in up to 80% of cases whether sleep or wake occurred at the single cell level. Conclusions: Ultrastructural analysis may be a powerful tool to identify which cellular organelles, and thus which cellular functions, are most affected by sleep and sleep loss. Citation: de Vivo L, Nelson AB, Bellesi M, Noguti J, Tononi G, Cirelli C. Loss of sleep affects the ultrastructure of pyramidal neurons in the adolescent mouse frontal cortex. SLEEP 2016;39(4):861–874. PMID:26715225

  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. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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

  14. 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…

  15. 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

  16. 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

  17. A new likelihood ratio metric for the psychomotor vigilance test and its sensitivity to sleep loss.

    PubMed

    Basner, Mathias; Mcguire, Sarah; Goel, Namni; Rao, Hengyi; Dinges, David F

    2015-12-01

    The Psychomotor Vigilance Test (PVT) is a widely used assay of behavioural alertness sensitive to the effects of sleep loss and circadian misalignment. However, there is currently no accepted PVT composite outcome metric that captures response slowing, attentional lapses and compensatory premature reactions observed typically in sleep-deprived subjects. We developed a novel likelihood ratio metric (LRM) based on relative frequency distributions in 50 categories of reaction times (RT) and false starts in alert and sleep-deprived subjects (acute total sleep deprivation: n = 31 subjects). The LRM had the largest effect size both in a 33-h total sleep deprivation protocol [1.96; 95% confidence interval (CI): 1.61-2.44; followed by response speed 1/RT, effect size 1.93, 95% CI: 1.55-2.65] and in a chronic partial sleep restriction protocol (1.22; 95% CI: 0.96-1.59; followed by response speed 1/RT, effect size 1.21, 95% CI: 0.94-1.59; 5 nights at 4 h sleep per night; n = 43 subjects). LRM scores correlated highly with response speed (R(2 ) = 0.986), and less well with five other common PVT outcome metrics (R(2 ) = 0.111-0.886). In conclusion, the new LRM is a sensitive PVT outcome metric with high statistical power that takes subtle sleep loss-related changes in the distribution of reaction times (including false starts) into account, is not prone to outliers, does not require baseline data and can be calculated and interpreted easily. Congruence between LRM and PVT response speed and their similar effect size rankings support the use of response speed as the primary, most sensitive and most parsimonious standard PVT outcome metric for determining neurobehavioural deficits from sleep loss. PMID:26118830

  18. 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.

  19. 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.

  20. 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.

  1. 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

  2. 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

  3. 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.

  4. 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.…

  5. 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.

  6. Baroreflex control of heart rate during sleep in severe obstructive sleep apnoea: effects of acute CPAP.

    PubMed

    Bonsignore, M R; Parati, G; Insalaco, G; Castiglioni, P; Marrone, O; Romano, S; Salvaggio, A; Mancia, G; Bonsignore, G; Di Rienzo, M

    2006-01-01

    Baroreflex control of heart rate during sleep (baroreflex sensitivity; BRS) has been shown to be depressed in obstructive sleep apnoea (OSA), and improved after treatment with continuous positive airway pressure (CPAP). Whether CPAP also acutely affects BRS during sleep in uncomplicated severe OSA is still debatable. Blood pressure was monitored during nocturnal polysomnography in 18 patients at baseline and during first-time CPAP application. Spontaneous BRS was analysed by the sequence method, and estimated as the mean sequence slope. CPAP did not acutely affect mean blood pressure or heart rate but decreased cardiovascular variability during sleep. Mean BRS increased slightly during CPAP application (from 6.5+/-2.4 to 7.5+/-2.9 ms x mmHg(-1)), mostly in response to decreasing blood pressure. The change in BRS did not correlate with changes in arterial oxygen saturation or apnoea/hypopnoea index. The small change in baroreflex control of heart rate during sleep at first application of continuous positive airway pressure in severe obstructive sleep apnoea was unrelated to the acute resolution of nocturnal hypoxaemia, and might reflect autonomic adjustments to positive intrathoracic pressure, and/or improved sleep architecture. The small increase in baroreflex control of heart rate during sleep may be of clinical relevance as it was accompanied by reduced cardiovascular variability, which is acknowledged as an independent cardiovascular risk factor.

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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.

  12. 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

  13. 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

  14. 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

  15. 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

  16. Effects of Partial and Acute Total Sleep Deprivation on Performance across Cognitive Domains, Individuals and Circadian Phase

    PubMed Central

    Lo, June C.; Groeger, John A.; Santhi, Nayantara; Arbon, Emma L.; Lazar, Alpar S.; Hasan, Sibah; von Schantz, Malcolm; Archer, Simon N.; Dijk, Derk-Jan

    2012-01-01

    Background Cognitive performance deteriorates during extended wakefulness and circadian phase misalignment, and some individuals are more affected than others. Whether performance is affected similarly across cognitive domains, or whether cognitive processes involving Executive Functions are more sensitive to sleep and circadian misalignment than Alertness and Sustained Attention, is a matter of debate. Methodology/Principal Findings We conducted a 2 × 12-day laboratory protocol to characterize the interaction of repeated partial and acute total sleep deprivation and circadian phase on performance across seven cognitive domains in 36 individuals (18 males; mean ± SD of age = 27.6±4.0 years). The sample was stratified for the rs57875989 polymorphism in PER3, which confers cognitive susceptibility to total sleep deprivation. We observed a deterioration of performance during both repeated partial and acute total sleep deprivation. Furthermore, prior partial sleep deprivation led to poorer cognitive performance in a subsequent total sleep deprivation period, but its effect was modulated by circadian phase such that it was virtually absent in the evening wake maintenance zone, and most prominent during early morning hours. A significant effect of PER3 genotype was observed for Subjective Alertness during partial sleep deprivation and on n-back tasks with a high executive load when assessed in the morning hours during total sleep deprivation after partial sleep loss. Overall, however, Subjective Alertness and Sustained Attention were more affected by both partial and total sleep deprivation than other cognitive domains and tasks including n-back tasks of Working Memory, even when implemented with a high executive load. Conclusions/Significance Sleep loss has a primary effect on Sleepiness and Sustained Attention with much smaller effects on challenging Working Memory tasks. These findings have implications for understanding how sleep debt and circadian rhythmicity

  17. Dynamic circadian modulation in a biomathematical model for the effects of sleep and sleep loss on waking neurobehavioral performance.

    PubMed

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

    2013-12-01

    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.

  18. Blood-Brain Barrier Disruption Induced by Chronic Sleep Loss: Low-Grade Inflammation May Be the Link

    PubMed Central

    Velázquez-Moctezuma, J.

    2016-01-01

    Sleep is a vital phenomenon related to immunomodulation at the central and peripheral level. Sleep deficient in duration and/or quality is a common problem in the modern society and is considered a risk factor to develop neurodegenerative diseases. Sleep loss in rodents induces blood-brain barrier disruption and the underlying mechanism is still unknown. Several reports indicate that sleep loss induces a systemic low-grade inflammation characterized by the release of several molecules, such as cytokines, chemokines, and acute-phase proteins; all of them may promote changes in cellular components of the blood-brain barrier, particularly on brain endothelial cells. In the present review we discuss the role of inflammatory mediators that increase during sleep loss and their association with general disturbances in peripheral endothelium and epithelium and how those inflammatory mediators may alter the blood-brain barrier. Finally, this manuscript proposes a hypothetical mechanism by which sleep loss may induce blood-brain barrier disruption, emphasizing the regulatory effect of inflammatory molecules on tight junction proteins. PMID:27738642

  19. 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

  20. 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

  1. 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

  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. 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

  4. CPAP, Weight Loss, or Both for Obstructive Sleep Apnea

    PubMed Central

    Chirinos, Julio A.; Gurubhagavatula, Indira; Teff, Karen; Rader, Daniel J.; Wadden, Thomas A.; Townsend, Raymond; Foster, Gary D.; Maislin, Greg; Saif, Hassam; Broderick, Preston; Chittams, Jesse; Hanlon, Alexandra L.; Pack, Allan I.

    2014-01-01

    BACKGROUND Obesity and obstructive sleep apnea tend to coexist and are associated with inflammation, insulin resistance, dyslipidemia, and high blood pressure, but their causal relation to these abnormalities is unclear. METHODS We randomly assigned 181 patients with obesity, moderate-to-severe obstructive sleep apnea, and serum levels of C-reactive protein (CRP) greater than 1.0 mg per liter to receive treatment with continuous positive airway pressure (CPAP), a weight-loss intervention, or CPAP plus a weight-loss intervention for 24 weeks. We assessed the incremental effect of the combined interventions over each one alone on the CRP level (the primary end point), insulin sensitivity, lipid levels, and blood pressure. RESULTS Among the 146 participants for whom there were follow-up data, those assigned to weight loss only and those assigned to the combined interventions had reductions in CRP levels, insulin resistance, and serum triglyceride levels. None of these changes were observed in the group receiving CPAP alone. Blood pressure was reduced in all three groups. No significant incremental effect on CRP levels was found for the combined interventions as compared with either weight loss or CPAP alone. Reductions in insulin resistance and serum triglyceride levels were greater in the combined-intervention group than in the group receiving CPAP only, but there were no significant differences in these values between the combined-intervention group and the weight-loss group. In per-protocol analyses, which included 90 participants who met prespecified criteria for adherence, the combined interventions resulted in a larger reduction in systolic blood pressure and mean arterial pressure than did either CPAP or weight loss alone. CONCLUSIONS In adults with obesity and obstructive sleep apnea, CPAP combined with a weight-loss intervention did not reduce CRP levels more than either intervention alone. In secondary analyses, weight loss provided an incremental reduction

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

    PubMed

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

    2008-12-01

    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

  7. 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

  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. 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 ...

  10. 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

  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. 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

  14. 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

  15. Relationship between sleep quality and quantity and weight loss in women participating in a weight-loss intervention trial.

    PubMed

    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

    2012-07-01

    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.

  16. Sleep loss reduces diurnal rhythm amplitude of leptin in healthy men.

    PubMed

    Mullington, J M; Chan, J L; Van Dongen, H P A; Szuba, M P; Samaras, J; Price, N J; Meier-Ewert, H K; Dinges, D F; Mantzoros, C S

    2003-09-01

    The aim of the current study was to investigate the effects of sleep loss on the diurnal rhythm of circulating leptin levels. An indwelling forearm catheter was used to sample blood at 90-min intervals for a total of 120 h, which included 88 h of sustained sleeplessness, in 10 healthy men. The diurnal amplitude of leptin was reduced during total sleep deprivation and returned toward normal during the period of recovery sleep. This finding provides evidence that sleep influences the nocturnal leptin profile, and may have implications for the understanding of the role of sleep in metabolic regulation and the aetiologies of obesity and the night eating syndrome.

  17. 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…

  18. 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

  19. Effects of acute sleep deprivation on motor and reversal learning in mice.

    PubMed

    Varga, Andrew W; Kang, Mihwa; Ramesh, Priyanka V; Klann, Eric

    2014-10-01

    Sleep supports the formation of a variety of declarative and non-declarative memories, and sleep deprivation often impairs these types of memories. In human subjects, natural sleep either during a nap or overnight leads to long-lasting improvements in visuomotor and fine motor tasks, but rodent models recapitulating these findings have been scarce. Here we present evidence that 5h of acute sleep deprivation impairs mouse skilled reach learning compared to a matched period of ad libitum sleep. In sleeping mice, the duration of total sleep time during the 5h of sleep opportunity or during the first bout of sleep did not correlate with ultimate gain in motor performance. In addition, we observed that reversal learning during the skilled reaching task was also affected by sleep deprivation. Consistent with this observation, 5h of sleep deprivation also impaired reversal learning in the water-based Y-maze. In conclusion, acute sleep deprivation negatively impacts subsequent motor and reversal learning and memory.

  20. 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

  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. Acute nicotine treatment prevents REM sleep deprivation-induced learning and memory impairment in rat.

    PubMed

    Aleisa, A M; Helal, G; Alhaider, I A; Alzoubi, K H; Srivareerat, M; Tran, T T; Al-Rejaie, S S; Alkadhi, K A

    2011-08-01

    Rapid eye movement (REM) sleep deprivation (SD) is implicated in impairment of spatial learning and memory and hippocampal long-term potentiation (LTP). An increase in nicotine consumption among habitual smokers and initiation of tobacco use by nonsmokers was observed during SD. Although nicotine treatment was reported to attenuate the impairment of learning and memory and LTP associated with several mental disorders, the effect of nicotine on SD-induced learning and memory impairment has not been studied. Modified multiple platform paradigm was used to induce SD for 24 or 48 h during which rats were injected with saline or nicotine (1 mg kg(-1) s.c.) twice a day. In the radial arm water maze (RAWM) task, 24- or 48-h SD significantly impaired learning and short-term memory. In addition, extracellular recordings from CA1 and dentate gyrus (DG) regions of the hippocampus in urethane anesthetized rats showed a significant impairment of LTP after 24- and 48-h SD. Treatment of normal rats with nicotine for 24 or 48 h did not enhance spatial learning and memory or affect magnitude of LTP in the CA1 and DG regions. However, concurrent, acute treatment of rats with nicotine significantly attenuated SD-induced impairment of learning and STM and prevented SD-induced impairment of LTP in the CA1 and DG regions. These results show that acute nicotine treatment prevented the deleterious effect of sleep loss on cognitive abilities and synaptic plasticity.

  3. 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

  4. Effects of acute administration of brotizolam in subjects with disturbed sleep

    PubMed Central

    Roehrs, T.; Zorick, F.; Koshorek, G. L.; Wittig, R.; Roth, T.

    1983-01-01

    1 Effects of ingestion of brotizolam (0.25 and 0.50 mg) over 1-3 days on polysomnographic measures of sleep were assessed in patients complaining of insomnia. 2 Brotizolam reduced latency to sleep, number of awakenings and wake during sleep, and increased total sleep time. It also increased stage 2 sleep and decreased slow wave and rapid eye movement sleep. 3 Increasing the dose from 0.25 to 0.50 mg increased hypnotic efficacy, and there was a more consistent and reliable effect. 4 Discontinuation of brotizolam had minimal effects on sleep compared with placebo over the 3 nights after acute administration. 5 No side-effects or disruption of daytime function was found using questionnaires and objective tests of performance. PMID:6661383

  5. Intact brown adipose tissue thermogenesis is required for restorative sleep responses after sleep loss.

    PubMed

    Szentirmai, Éva; Kapás, Levente

    2014-03-01

    Metabolic signals related to feeding and body temperature regulation have profound effects on vigilance. Brown adipose tissue (BAT) is a key effector organ in the regulation of metabolism in several species, including rats and mice. Significant amounts of active BAT are also present throughout adulthood in humans. The metabolic activity of BAT is due to the tissue-specific presence of the uncoupling protein-1 (UCP-1). To test the involvement of BAT thermogenesis in sleep regulation, we investigated the effects of two sleep-promoting stimuli in UCP-1-deficient mice. Sleep deprivation by gentle handling increased UCP-1 mRNA expression in BAT and elicited rebound increases in non-rapid-eye-movement sleep and rapid-eye-movement sleep accompanied by elevated slow-wave activity of the electroencephalogram. The rebound sleep increases were significantly attenuated, by ~ 35-45%, in UCP-1-knockout (KO) mice. Wild-type (WT) mice with capsaicin-induced sensory denervation of the interscapular BAT pads showed similar impairments in restorative sleep responses after sleep deprivation, suggesting a role of neuronal sleep-promoting signaling from the BAT. Exposure of WT mice to 35 °C ambient temperature for 5 days led to increased sleep and body temperature and suppressed feeding and energy expenditure. Sleep increases in the warm environment were significantly suppressed, by ~ 50%, in UCP-1-KO animals while their food intake and energy expenditure did not differ from those of the WTs. These results suggest that the metabolic activity of the BAT plays a role in generating a metabolic environment that is permissive for optimal sleep. Impaired BAT function may be a common underlying cause of sleep insufficiency and metabolic disorders.

  6. 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

  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. 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.

  9. Polysomnographic measures of sleep in cocaine dependence and alcohol dependence: Implications for age‐related loss of slow wave, stage 3 sleep

    PubMed Central

    Bjurstrom, Martin F.; Olmstead, Richard

    2016-01-01

    Abstract Background and aims Sleep disturbance is a prominent complaint in cocaine and alcohol dependence. This controlled study evaluated differences of polysomnographic (PSG) sleep in cocaine‐ and alcohol‐dependent subjects, and examined whether substance dependence interacts with age to alter slow wave sleep and rapid eye movement (REM) sleep. Design Cross‐sectional comparison. Setting Los Angeles and San Diego, CA, USA. Participants Abstinent cocaine‐dependent subjects (n = 32), abstinent alcohol‐dependent subjects (n = 73) and controls (n = 108); mean age 40.3 years recruited 2005–12. Measurements PSG measures of sleep continuity and sleep architecture primary outcomes of Stage 3 sleep and REM sleep. Covariates included age, ethnicity, education, smoking, body mass index and depressive symptoms. Findings Compared with controls, both groups of substance dependent subjects showed loss of Stage 3 sleep (P < 0.001). A substance dependence × age interaction was found in which both cocaine‐ and alcohol‐dependent groups showed loss of Stage 3 sleep at an earlier age than controls (P < 0.05 for all), and cocaine‐dependent subjects showed loss of Stage 3 sleep at an earlier age than alcoholics (P < 0.05). Compared with controls, REM sleep was increased in both substance‐dependent groups (P < 0.001), and cocaine and alcohol dependence were associated with earlier age‐related increase in REM sleep (P < 0.05 for all). Conclusions Cocaine and alcohol dependence appear to be associated with marked disturbances of sleep architecture, including increased rapid eye movement sleep and accelerated age‐related loss of slow wave, Stage 3 sleep. PMID:26749502

  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.

  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. 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

  15. 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

  16. Sleep loss and its effects on health of family caregivers of individuals with primary malignant brain tumors.

    PubMed

    Pawl, Jean D; Lee, Shih-Yu; Clark, Patricia C; Sherwood, Paula R

    2013-08-01

    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.

  17. 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

  18. 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

  19. 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

  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. 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

  2. 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

  3. REM sleep loss and recovery regulates blood-brain barrier function.

    PubMed

    Gómez-González, Beatriz; Hurtado-Alvarado, Gabriela; Esqueda-León, Enrique; Santana-Miranda, Rafael; Rojas-Zamorano, José Ángel; Velázquez-Moctezuma, Javier

    2013-08-01

    The functions of rapid eye movement (REM) sleep have remained elusive since more than 50 years. Previous reports have identified several independent processes affected by the loss and subsequent recovery of REM sleep (hippocampal neurogenesis, brain stem neuronal cell death, and neurotransmitter content in several brain regions); however, a common underlying mechanism has not been found. We propose that altered brain homeostasis secondary to blood-brain barrier breakdown may explain all those changes induced by REM sleep loss. Therefore, the present report aimed to study the consequences of REM sleep restriction upon blood-brain barrier permeability to Evans blue. REM sleep restriction was induced by the multiple platform technique; male rats were REM sleep restricted 20h daily (with 4h sleep opportunity) during 10 days; control groups included large platform and intact rats. To study blood-brain barrier permeability Evans blue was intracardially administered; stained brains were sliced and photographed for optical density quantification. An independent experiment was carried out to elucidate the mechanism of blood-brain breakdown by transmission electron microscopy. REM sleep restriction increased blood-brain barrier permeability to Evans blue in the whole brain as compared to both control groups. Brief periods of sleep recovery rapidly and effectively restored the severe alteration of blood-brain barrier function by reducing blood-to-brain transfer of Evans blue. The mechanism of blood-brain barrier breakdown involved increased caveolae formation at brain endothelial cells. In conclusion, our data suggest that REM sleep regulates the physical barrier properties of the blood-brain barrier.

  4. What drives sleep-dependent memory consolidation: greater gain or less loss?

    PubMed

    Fenn, Kimberly M; Hambrick, David Z

    2013-06-01

    When memory is tested after a delay, performance is typically better if the retention interval includes sleep. However, it is unclear what accounts for this well-established effect. It is possible that sleep enhances the retrieval of information, but it is also possible that sleep protects against memory loss that normally occurs during waking activity. We developed a new research approach to investigate these possibilities. Participants learned a list of paired-associate items and were tested on the items after a 12-h interval that included waking or sleep. We analyzed the number of items gained versus the number of items lost across time. The sleep condition showed more items gained and fewer items lost than did the wake condition. Furthermore, the difference between the conditions (favoring sleep) in lost items was greater than the difference in gain, suggesting that loss prevention may primarily account for the effect of sleep on declarative memory consolidation. This finding may serve as an empirical constraint on theories of memory consolidation.

  5. 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

  6. Quantity and quality of nocturnal sleep affect morning glucose measurement in acutely burned children.

    PubMed

    Mayes, Theresa; Gottschlich, Michele M; Khoury, Jane; Simakajornboon, Narong; Kagan, Richard J

    2013-01-01

    Hyperglycemia after severe burn injury has long been recognized, whereas sleep deprivation after burns is a more recent finding. The postburn metabolic effects of poor sleep are not clear despite reports in other populations demonstrating the association between sleep insufficiency and deleterious endocrine consequences. The aim of this study was to determine whether a relationship between sleep and glucose dynamics exists in acutely burned children. Two overnight polysomnography runs (2200 to 0600) per subject were conducted in 40 patients with a mean (± SEM) age of 9.4 ± 0.7 years, 50.1 ± 2.9% TBSA burn, and 43.2 ± 3.6% full-thickness injury. Serum glucose was drawn in the morning (0600) immediately after the sleep test. Insulin requirements during the 24-hour period preceding the 0600 glucose measurement were recorded. Generalized linear models were used by the authors to evaluate percent time in each stage of sleep, percent wake time, total sleep time, sleep efficiency, and morning serum glucose, accounting for insulin use. Increased time awake (P = .04, linear; P = .02, quadratic) and reduced time spent in stage 1 sleep (P = .03, linear) were associated with higher glucose levels. Sleep efficiency (P = .01, linear; P = .02, quadratic) and total sleep time (P = .01 linear; P = .02, quadratic) were inversely associated with glucose level. Morning glucose levels appear to be affected by the quality and quantity of overnight sleep in children who have sustained extensive burn injuries. Future research is needed to elucidate the metabolic and neuroendocrine consequences of sleep deprivation on metabolism after burns.

  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. 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

  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. Effects of Positive Airway Pressure on Patients with Obstructive Sleep Apnea during Acute Ascent to Altitude

    PubMed Central

    Nishida, Katsufumi; Cloward, Tom V.; Weaver, Lindell K.; Brown, Samuel M.; Bell, James E.; Grissom, Colin K.

    2015-01-01

    Rationale: In acute ascent to altitude, untreated obstructive sleep apnea (OSA) is often replaced with central sleep apnea (CSA). In patients with obstructive sleep apnea who travel to altitude, it is unknown whether their home positive airway pressure (PAP) settings are sufficient to treat their obstructive sleep apnea, or altitude-associated central sleep apnea. Methods: Ten participants with positive airway pressure–treated obstructive sleep apnea, who reside at 1,320 m altitude, underwent polysomnography on their home positive airway pressure settings at 1,320 m and at a simulated altitude of 2,750 m in a hypobaric chamber. Six of the participants were subsequently studied without positive airway pressure at 2,750 m. Measurements and Main Results: At 1,320 m, all participants’ sleep apnea was controlled with positive airway pressure on home settings; at 2,750, no participants’ sleep apnea was controlled. At higher altitude, the apnea–hypopnea index was higher (11 vs. 2 events/h; P < 0.01), mostly due to hypopneas (10.5 vs. 2 events/h; P < 0.01). Mean oxygen saturations were lower (88 vs. 93%; P < 0.01) and total sleep time was diminished (349 vs. 393 min; P = 0.03). Four of six participants without positive airway pressure at 2,750 m required supplemental oxygen to prevent sustained oxygen saturation (as determined by pulse oximetry) less than 80%. Positive airway pressure also was associated with reduced central sleep apnea (0 vs. 1; P = 0.03), improved sleep time (358 vs. 292 min; P = 0.06), and improved sleep efficiency (78 vs. 63%; P = 0.04). Conclusions: Acute altitude exposure in patients with obstructive sleep apnea treated with positive airway pressure is associated with hypoxemia, decreased sleep time, and increased frequency of hypopneas compared with baseline altitude. Application of positive airway pressure at altitude is associated with decreased central sleep apnea and increased sleep efficiency. PMID:25884271

  12. Individual differences in vulnerability to sleep loss in the work environment.

    PubMed

    Van Dongen, Hans P A; Belenky, Gregory

    2009-10-01

    There are considerable individual differences in cognitive performance deficits resulting from extended work hours and shift work schedules. Recent progress in sleep and performance research has yielded new insights into the causes and consequences of these individual differences. Neurobiological processes of sleep/wake regulation underlie trait individual variability in vulnerability to performance impairment due to sleep loss. Trait vulnerability to sleep loss is observed in the laboratory and in the work environment, even in occupational settings where (self-)selection pressures are high. In general, individuals do not seem to accurately assess the magnitude of their own vulnerability. Methods for identifying workers who are most at risk of sleep loss-related errors and accidents would therefore be helpful to target fatigue countermeasure interventions at those needing them most. As yet, no reliable predictors of vulnerability to sleep loss have been identified, although candidate genetic predictors have been proposed. However, a Bayesian forecasting technique based on closed-loop feedback of measured performance has been developed for individualized prediction of future performance impairment during ongoing operations. Judiciously selecting or monitoring individuals in specific tasks or occupations, within legally and ethically acceptable boundaries, has the potential to improve operational performance and productivity, reduce errors and accidents, and save lives. Trait individual variability in responses to sleep loss represents a major complication in the application of one-size-fits-all hours of service regulations--favoring instead modern fatigue risk management strategies, because these allow flexibility to account for individual vulnerability or resilience to the performance consequences of extended work hours and shift work schedules.

  13. Sleep-related breathing disorders in acute lacunar stroke.

    PubMed

    Bonnin-Vilaplana, Marc; Arboix, Adrià; Parra, Olga; García-Eroles, Luis; Montserrat, Josep M; Massons, Joan

    2009-12-01

    The purpose was to examine the occurrence of sleep-related breathing disorders (SRBD) and variables related to SRBD in patients with acute lacunar stroke. In 68 consecutive patients with radiologically proven lacunes, respiratory polygraphy within the first 48 h of stroke onset was performed. SRBDs were classified according to mutually exclusive cutoff values of the apnea/hypopnea index (AHI) as mild (AHI ≥ 10), moderate (AHI ≥ 20), and severe (AHI ≥ 30). Variables independently associated with SRBDs were assessed by logistic regression analysis. The mean (standard deviation) AHI was 21.9 (17.4). A total of 69.1% of patients showed AHI ≥ 10, 44.1% AHI ≥ 20, and 25% AHI ≥ 30. Cheyne-Stokes respiration (CSR) was present in 20.6% of patients. Smoking (>20 cigarettes/day) or location of lacunes in the internal capsule or the pons was significantly more frequent in the AHI ≥ 10 group than in the remaining AHI groups (80.9% vs. 57.1%, P = 0.041). AHI ≥ 20 and AHI ≥ 30 occurred more frequently in smokers or in capsular or pontine lacunes than in the remaining patients (20% vs. 2.6%, P = 0.053; 29.4% vs. 3.9%, P = 0.01, respectively). In the multivariate analysis, smoking or capsular or pontine topographies were associated with AHI ≥ 10 [odds ratio (OR) = 3.17, 95% confidence interval (CI) 1.02–9.79; P = 0.045]. Lacunes in the internal capsule or the pons in smokers were associated with AHI ≥ 20 (OR = 9.25, 95% CI 1.05–81.70; P = 0.045). Smoking (OR = 19.64, 95% CI 1.68–229.85; P = 0.010) and body mass index (OR = 1.68, 95% CI 1.13–2.50; P = 0.010) were associated with AHI ≥ 30. Smoker patients with capsular or pontine acute lacunar stroke should be screened for SRDB.

  14. Bone Loss in Obesity and Obstructive Sleep Apnea: A Review of Literature

    PubMed Central

    Chakhtoura, Marlene; Nasrallah, Mona; Chami, Hassan

    2015-01-01

    Introduction: Obstructive sleep apnea (OSA) is a common sleep-related respiratory disorder. It is associated with many endocrinopathies including hypogonadotropic hypogonadism, hypercortisolism, and glucose intolerance that may lead to bone loss with secondary osteoporosis. Methods: We report the case of a 41-year-old man who presented with bilateral 9th rib fractures and was found to have obstructive sleep apnea and osteoporosis. We also present a literature review on this topic. Results: OSA can lead to bone loss through various mechanisms. Some are shared with obesity, including hypogonadism, altered adrenergic tone, inflammation, oxidative stress, vitamin D deficiency and diabetes mellitus; others are specific to OSA, such as hypoxia and altered glucocorticoids regulation. Conclusion: There are no guidelines on screening for osteoporosis in OSA. Further research is needed to assess the incidence of bone loss and fractures in OSA. Citation: Chakhtoura M, Nasrallah M, Chami H. Bone loss in obesity and obstructive sleep apnea: a review of literature. J Clin Sleep Med 2015;11(5):575–580. PMID:25580607

  15. 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

  16. 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

  17. 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

  18. 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.

  19. 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

  20. Complete Vision Loss following Orbital Cellulitis Secondary to Acute Dacryocystitis

    PubMed Central

    Pfeiffer, Margaret L.; Hacopian, Alexander; Merritt, Helen

    2016-01-01

    We present a case of a 50-year-old woman with acute dacryocystitis that was complicated by posterior rupture of the lacrimal sac causing an orbital cellulitis with subsequent visual acuity of no light perception. Upon presentation, she was immediately started on broad-spectrum antibiotics and underwent surgical incision and drainage of the lacrimal sac abscess but never regained vision. There are 4 cases in the literature of permanent severe vision loss from acute dacryocystitis. Prompt diagnosis and close monitoring of acute dacryocystitis are therefore essential to prevent extension into the orbit and possible optic nerve compromise. PMID:27803829

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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.

  6. 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

  7. 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

  8. 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

  9. Acute placebo-controlled sleep laboratory studies and clinical follow-up with pramipexole in restless legs syndrome.

    PubMed

    Saletu, M; Anderer, P; Saletu-Zyhlarz, G; Hauer, C; Saletu, B

    2002-08-01

    In a single-blind, placebo-controlled crossover trial, the acute efficacy of the dopamine agonist pramipexole was investigated in 11 restless legs syndrome (RLS) patients by sleep laboratory methods, with a clinical follow-up for 4 weeks. In 3 nights (pre-treatment, placebo and drug night), objective sleep quality was determined by polysomnography (PSG), subjective sleep and awakening quality by rating scales, objective awakening quality by psychometry. Clinical follow-up consisted of completion of the International RLS Study Group (IRLSSG) Scale, Zung Depression (SDS) and Anxiety (SAS) Scale, Quality of Life Index, Pittsburgh Sleep Quality Index and Epworth Sleepiness Scale. Concerning acute effects, an omnibus significance test for PSG variables demonstrated a global difference between placebo and pramipexole, but none between pre-treatment and placebo. Pramipexole 0.27 mg significantly decreased the target variable periodic leg movements (PLM)/h of sleep as well as all other RLS/PLM variables and improved objective sleep efficiency and subjective sleep quality as compared with placebo. In sleep architecture, sleep stages S1 and S2 and stage shifts increased, while slow-wave sleep and SREM decreased. After 4 weeks of therapy, the total scores of the IRLSSG questionnaire, sleep quality and daytime sleepiness, depression and quality of life also improved. Thus, acute pramipexole markedly reduced PLM measures and slightly improved objective and subjective sleep quality. Follow-up ratings showed a moderate improvement of RLS and sleep quality, and to a lesser extent of daytime sleepiness, depression and quality of life. The psychopathological findings as well as acute sleep architecture changes are reminiscent of those seen after activating antidepressants.

  10. 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

  11. 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

  12. Acute unilateral loss of vestibular function.

    PubMed

    Fetter, M

    2016-01-01

    Sudden unilateral loss of vestibular function is the most severe condition that can occur in the vestibular system. The clinical syndrome is caused by the physiologic properties of the vestibulo-ocular reflex (VOR) arc. In the normal situation, the two peripheral vestibular end organs are connected to a functional unit in coplanar pairs of semicircular canals working in a push-pull mode. "Push-pull" mode means that, when one side is excited, the other side is inhibited, and vice versa due to two mechanisms. First, first-order vestibular afferents are bipolar cells. They have a tonic firing rate that is modulated up or down depending on the direction of rotation. Second, via inhibitory neural connections of second-order vestibular neurons between the vestibular nuclei (vestibular commissural system), the excited side inhibits further the contralateral side. The neural signals are encoded as the difference of the change in firing rate of the vestibular neurons modulating the tonic firing rate on both sides in opposite directions (one side up, the contralateral side down). When the head is not moving, the two peripheral vestibular end organs generate a resting firing rate, which is exactly equal on both sides. When the head is rotated, for example, to the right, the right-sided first-order vestibular afferents increase their discharge rate and the left-sided ones decrease their firing rate. This leads to increase in firing rate of also the type I second-order vestibular neurons in the vestibular nuclei, which synapse with inhibitory type II neurons on the contralateral side, further decreasing the firing rate in the second-order vestibular neurons in the contralateral vestibular nucleus. When the direction of head rotation is reversed, the behavior of the type I neurons on the two sides of the head is reversed. The same relation exists between the coplanar vertical canal afferents on the two sides of the head. When there is unilateral damage to the end organ or the

  13. Acute Sleep Restriction Effects on Emotion Responses in 30- to 36-Month-Old Children

    PubMed Central

    Berger, Rebecca H.; Miller, Alison L.; Seifer, Ronald; Cares, Stephanie R.; LeBourgeois, Monique K.

    2011-01-01

    SUMMARY Early childhood is a period of dramatic change in sleep and emotion processing, as well as a time when disturbance in both domains are first detected. Although sleep is recognized as central in emotion processing and psychopathology, the great majority of experimental data have been collected in adults. We examined the effects of acute sleep restriction (nap deprivation) on toddlers’ emotion expression. Ten healthy children (7 females; 30–36 months) followed a strict sleep schedule (≥12.5 hrs time in bed/24 hrs) for 5 days before each of two randomly-assigned afternoon emotion assessments following Nap and No-Nap conditions (resulting in an 11-day protocol). Children viewed emotion-eliciting pictures (5 positive, 3 neutral, 3 negative) and completed puzzles (1 solvable, 1 unsolvable). Children’s faces were video-recorded, and emotion displays were coded. When sleep restricted, children displayed less confusion in response to neutral pictures, more negativity to neutral and negative pictures, and less positivity to positive pictures. Sleep restriction also resulted in a 34% reduction in positive emotion responses (solvable puzzle), as well as a 31% increase in negative emotion responses and a 39% decrease in confused responses (unsolvable puzzle). These findings suggest sleep is a key factor in how young children respond to their world. When sleep restricted, toddlers are neither able to take full advantage of positive experiences nor are they as adaptive in challenging contexts. If insufficient sleep consistently “taxes” young children’s emotion responses, they may not manage emotion regulation challenges effectively, potentially placing them at risk for future emotional/behavioral problems. PMID:21988087

  14. Acute sleep restriction effects on emotion responses in 30- to 36-month-old children.

    PubMed

    Berger, Rebecca H; Miller, Alison L; Seifer, Ronald; Cares, Stephanie R; LeBourgeois, Monique K

    2012-06-01

    Early childhood is a period of dramatic change in sleep and emotion processing, as well as a time when disturbance in both domains are first detected. Although sleep is recognized as central in emotion processing and psychopathology, the great majority of experimental data have been collected in adults. We examined the effects of acute sleep restriction (nap deprivation) on toddlers' emotion expression. Ten healthy children (seven females; 30-36 months old) followed a strict sleep schedule (≥12.5 h time in bed per 24-h) for 5 days, before each of two randomly assigned afternoon emotion assessments following Nap and No-Nap conditions (resulting in an 11-day protocol). Children viewed emotion-eliciting pictures (five positive, three neutral, three negative) and completed puzzles (one solvable, one unsolvable). Children's faces were video-recorded, and emotion displays were coded. When sleep restricted, children displayed less confusion in response to neutral pictures, more negativity to neutral and negative pictures, and less positivity to positive pictures. Sleep restriction also resulted in a 34% reduction in positive emotion responses (solvable puzzle), as well as a 31% increase in negative emotion responses and a 39% decrease in confused responses (unsolvable puzzle). These findings suggest sleep is a key factor in how young children respond to their world. When sleep restricted, toddlers are neither able to take full advantage of positive experiences nor are they as adaptive in challenging contexts. If insufficient sleep consistently 'taxes' young children's emotion responses, they may not manage emotion regulation challenges effectively, potentially placing them at risk for future emotional/behavioral problems.

  15. Acute sleep restriction effects on emotion responses in 30- to 36-month-old children.

    PubMed

    Berger, Rebecca H; Miller, Alison L; Seifer, Ronald; Cares, Stephanie R; LeBourgeois, Monique K

    2012-06-01

    Early childhood is a period of dramatic change in sleep and emotion processing, as well as a time when disturbance in both domains are first detected. Although sleep is recognized as central in emotion processing and psychopathology, the great majority of experimental data have been collected in adults. We examined the effects of acute sleep restriction (nap deprivation) on toddlers' emotion expression. Ten healthy children (seven females; 30-36 months old) followed a strict sleep schedule (≥12.5 h time in bed per 24-h) for 5 days, before each of two randomly assigned afternoon emotion assessments following Nap and No-Nap conditions (resulting in an 11-day protocol). Children viewed emotion-eliciting pictures (five positive, three neutral, three negative) and completed puzzles (one solvable, one unsolvable). Children's faces were video-recorded, and emotion displays were coded. When sleep restricted, children displayed less confusion in response to neutral pictures, more negativity to neutral and negative pictures, and less positivity to positive pictures. Sleep restriction also resulted in a 34% reduction in positive emotion responses (solvable puzzle), as well as a 31% increase in negative emotion responses and a 39% decrease in confused responses (unsolvable puzzle). These findings suggest sleep is a key factor in how young children respond to their world. When sleep restricted, toddlers are neither able to take full advantage of positive experiences nor are they as adaptive in challenging contexts. If insufficient sleep consistently 'taxes' young children's emotion responses, they may not manage emotion regulation challenges effectively, potentially placing them at risk for future emotional/behavioral problems. PMID:21988087

  16. 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

  17. 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

  18. 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

  19. Sleep Disturbance and Altered Expression of Circadian Clock Genes in Patients With Sudden Sensorineural Hearing Loss.

    PubMed

    Yang, Chao-Hui; Hwang, Chung-Feng; Lin, Pai-Mei; Chuang, Jiin-Haur; Hsu, Cheng-Ming; Lin, Sheng-Fung; Yang, Ming-Yu

    2015-07-01

    The cause of sudden sensorineural hearing loss (SSNHL) remains unclear and therefore it is often considered as idiopathic. Sleep disturbance has been linked to SSNHL and circadian rhythm disruption, but the link between circadian rhythm disruption and SSNHL has never been investigated.In this study, we surveyed the sleep quality of 38 patients with SSNHL using a simple insomnia sleep questionnaire. The expression of circadian clock genes in peripheral blood (PB) leukocytes from 38 patients with SSNHL and 71 healthy subjects was accessed using real-time quantitative reverse transcriptase-polymerase chain reaction and validated using immunocytochemical staining.We found that 61.8% of patients with SSNHL suffered from insomnia before the insult of hearing loss. Besides, significantly decreased expression of PER1, CRY1, CRY2, CLOCK, BMAL1, and CKlε was found in PB leukocytes of patients with SSNHL when compared with healthy subjects. SSNHL patients with vertigo had significantly lower expression of CRY1 and CKlε than patients without vertigo symptoms. Our results imply the association of sleep disturbance and disrupted circadian rhythm in SSNHL.

  20. REM sleep deprivation of rats induces acute phase response in liver.

    PubMed

    Pandey, Atul Kumar; Kar, Santosh Kumar

    2011-07-01

    REM sleep is essential for maintenance of body physiology and its deprivation is fatal. We observed that the levels of ALT and AST enzymes and pro-inflammatory cytokines like IL-1 β, IL-6 and IL-12 circulating in the blood of REM sleep deprived rats increased in proportion to the extent of sleep loss. But in contrast the levels of IFN-γ and a ∼200 kDa protein, identified by N-terminal sequencing to be alpha-1-inhibitor-3(A1I3), decreased significantly. Quantitative PCR analysis confirmed that REM sleep deprivation down regulates AII3 gene and up regulates IL1 β, IL6 and their respective receptors gene expression in the liver initiating its inflammation.

  1. 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

  2. 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

  3. 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

  4. 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

  5. Acute and subchronic administration of anandamide or oleamide increases REM sleep in rats.

    PubMed

    Herrera-Solís, Andrea; Vásquez, Khalil Guzmán; Prospéro-García, Oscar

    2010-03-01

    Anandamide and oleamide, induce sleep when administered acutely, via the CB1 receptor. Their subchronic administration must be tested to demonstrate the absence of tolerance to this effect, and that the sudden withdrawal of these endocannabinoids (eCBs) does not affect sleep negatively. The sleep-waking cycle of rats was evaluated for 24h, under the effect of an acute or subchronic administration of eCBs, and during sudden eCBs withdrawal. AM251, a CB1 receptor antagonist (CB1Ra) was utilized to block eCBs effects. Our results indicated that both acute and subchronic administration of eCBs increase REMS. During eCBs withdrawal, rats lack the expression of an abstinence-like syndrome. AM251 was efficacious to prevent REMS increase caused by both acute and subchronic administration of these eCBs, suggesting that this effect is mediated by the CB1 receptor. Our data further support a role of the eCBs in REMS regulation.

  6. 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

  7. 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

  8. 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

  9. 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.

  10. Excess diuresis and natriuresis during acute sleep deprivation in healthy adults.

    PubMed

    Kamperis, Konstantinos; Hagstroem, Soren; Radvanska, Eva; Rittig, Soren; Djurhuus, Jens Christian

    2010-08-01

    The transition from wakefulness to sleep is associated with a pronounced decline in diuresis, a necessary physiological process that allows uninterrupted sleep. The aim of this study was to assess the effect of acute sleep deprivation (SD) on urine output and renal water, sodium, and solute handling in healthy young volunteers. Twenty young adults (10 male) were recruited for two 24-h studies under standardized dietary conditions. During one of the two admissions, subjects were deprived of sleep. Urine output, electrolyte excretions, and osmolar excretions were calculated. Activated renin, angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide were measured in plasma, whereas prostaglandin E(2) and melatonin were measured in urine. SD markedly increased the diuresis and led to excess renal sodium excretion. The effect was more pronounced in men who shared significantly higher diuresis levels during SD compared with women. Renal water handling and arginine vasopressin levels remained unaltered during SD, but the circadian rhythm of the hormones of the renin-angiotensin-aldosterone system was significantly affected. Urinary melatonin and prostaglandin E(2) excretion levels were comparable between SD and baseline night. Hemodynamic changes were characterized by the attenuation of nocturnal blood pressure dipping and an increase in creatinine clearance. Acute deprivation of sleep induces natriuresis and osmotic diuresis, leading to excess nocturnal urine production, especially in men. Hemodynamic changes during SD may, through renal and hormonal processes, be responsible for these observations. Sleep architecture disturbances should be considered in clinical settings with nocturnal polyuria such as enuresis in children and nocturia in adults.

  11. 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.

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

    PubMed

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

    2013-01-01

    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 26-52h. 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 response to sleep loss.

  13. 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

  14. 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.

  15. Tooth loss and obstructive sleep apnea signs and symptoms in the US population

    PubMed Central

    Akinkugbe, Aderonke A.; Slade, Gary D.; Essick, Greg K.

    2016-01-01

    Purpose The aim of this study is to investigate the relationship between tooth loss and signs and symptoms of obstructive sleep apnea (OSA) in a representative sample of the general US population. Methods Data were from 7305 men and women aged ≥25 years participating in the 2005–2008 National Health and Nutrition Examination Survey. Tooth loss, occlusal contacts, and denture use were determined by dental examination. Four cardinal OSA signs and symptoms were evaluated by questions based on American Academy of Sleep Medicine criteria. Adults with ≥2 signs/symptoms of OSA were classified at high-risk of OSA. Prevalence ratios (PR) and 95 % confidence limits (CL) from log binomial regression models estimated the strength of association between tooth loss and high-risk for OSA, adjusting for demographic characteristics, body mass index, dentures, and sleep duration. Results Prevalence of high-risk for OSA increased 2 % for each additional lost tooth (PR = 1.02, 95 % CL, 1.01, 1.03) among adults aged 25 to 65 years. When tooth loss was modeled as an ordinal variable with 0–4 lost teeth as the referent category, adjusted prevalence of high-risk for OSA was as follows: 25 % greater in those missing 5–8 teeth (PR = 1.25, 95 % CL, 1.07, 1.46); 36 % greater in those missing 9–31 teeth (PR = 1.36, 95 % CL, 1.06, 1.73); and 61 % greater in the edentulous (PR = 1.61, 95 % CL, 1.11, 2.33). Conclusion Tooth loss may be an independent risk factor for OSA. PMID:26779902

  16. 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.

  17. 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

  18. The effect of weight loss on sleep-disordered breathing in obese teenagers.

    PubMed

    Verhulst, Stijn L; Franckx, Hilde; Van Gaal, Luc; De Backer, Wilfried; Desager, Kristine

    2009-06-01

    The objective of this study was to assess the effect of weight loss on sleep-disordered breathing (SDB) in obese teenagers attending a residential treatment center. We also assessed whether the presence of SDB at the start of the weight management therapy was correlated with the amount of weight loss achieved. Obese teenagers were recruited and underwent anthropometry and sleep screening. Subjects with SDB (apnea hypopnea index (AHI)>or=2) received a follow-up screening after weight loss therapy. Sixty-one obese subjects were included (age=14.8+/-2.3; BMI z score=2.7+/-0.4). Thirty-one subjects were diagnosed with SDB with 38% continuing to have residual SDB after a median weight loss of 24.0 kg. Subjects with SDB had a higher median relative decrease in BMI z score compared to subjects without SDB which was 30.5, 33.6, and 50.4% in the group with AHI of the baseline screening study<2, 2or=5, respectively (P=0.02). AHI of the baseline screening study correlated significantly with the relative decrease in BMI z score (partial r=0.37; P=0.003), controlling for gender, age, initial BMI z score, and time between both studies. In conclusion, weight loss was successful in treating SDB in obese teenagers. In addition, there was a positive association between the severity of SDB at the start of the treatment and the amount of weight loss achieved. These findings are in favor of considering weight loss as a first-line treatment for SDB in obese children and adolescents.

  19. 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

  20. Acute psychosis associated with dissociated sleep-wakefulness state after mirtazapine treatment.

    PubMed

    Felthous, Alan R; Wenger, Philip J; Hoevet, Rod

    2010-04-01

    Tricyclic antidepressants decrease rapid eye movement (REM) sleep and may suppress sleep atonia. Reports indicate that these agents can induce visual hallucinations, sometimes characterized as hypnopompic or associated with a dissociated sleep-wakefulness state. In addition, disturbing dreams and confusional states were reported during clinical trials and in subsequent studies. To our knowledge, only two cases of nightmares associated with mirtazapine, a tetracyclic antidepressant, have been previously reported. We describe a 43-year-old Caucasian man with major depressive disorder who started mirtazapine 15 mg at bedtime because he had poor symptom control with other antidepressant drugs. Three days later, vivid dream activity was noted, evolving into realistic nightmares that the patient was not able to distinguish from reality on awakening. Acute paranoia was suspected, and haloperidol was started. The dream activity then ended, and within 3 days the patient was able to identify the dreams as unreality. Haloperidol was discontinued, but mirtazapine was continued, and the vivid dream activity persisted; however, reality testing when awake was intact. A short course of haloperidol restored the patient's reality testing, and mirtazapine was eventually replaced with bupropion. The unusual nocturnal activity resolved as a result. Clinicians should be aware of the possible transition from exceptionally vivid dreams to REM sleep behavior disorder and psychosis based on dream content as an adverse effect of mirtazapine.

  1. 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

  2. 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

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

    PubMed

    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.

  4. 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

  5. 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

  6. Total sleep deprivation, chronic sleep restriction and sleep disruption.

    PubMed

    Reynolds, Amy C; Banks, Siobhan

    2010-01-01

    Sleep loss may result from total sleep deprivation (such as a shift worker might experience), chronic sleep restriction (due to work, medical conditions or lifestyle) or sleep disruption (which is common in sleep disorders such as sleep apnea or restless legs syndrome). Total sleep deprivation has been widely researched, and its effects have been well described. Chronic sleep restriction and sleep disruption (also known as sleep fragmentation) have received less experimental attention. Recently, there has been increasing interest in sleep restriction and disruption as it has been recognized that they have a similar impact on cognitive functioning as a period of total sleep deprivation. Sleep loss causes impairments in cognitive performance and simulated driving and induces sleepiness, fatigue and mood changes. This review examines recent research on the effects of sleep deprivation, restriction and disruption on cognition and neurophysiologic functioning in healthy adults, and contrasts the similarities and differences between these three modalities of sleep loss.

  7. 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

  8. 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

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

    PubMed Central

    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/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

  10. 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.

  11. Acute Optogenetic Silencing of Orexin/Hypocretin Neurons Induces Slow-Wave Sleep in Mice

    PubMed Central

    Tsunematsu, Tomomi; Kilduff, Thomas S.; Boyden, Edward S.; Takahashi, Satoru; Tominaga, Makoto; Yamanaka, Akihiro

    2013-01-01

    Orexin/hypocretin neurons have a crucial role in the regulation of sleep and wakefulness. To help determine how these neurons promote wakefulness, we generated transgenic mice in which orexin neurons expressed halorhodopsin (orexin/Halo mice), an orange light-activated neuronal silencer. Slice patch-clamp recordings of orexin neurons that expressed halorhodopsin demonstrated that orange light photic illumination immediately hyperpolarized membrane potential and inhibited orexin neuron discharge in proportion to illumination intensity. Acute silencing of orexin neurons in vivo during the day (the inactive period) induced synchronization of the electroencephalogram and a reduction in amplitude of the electromyogram that is characteristic of slow-wave sleep (SWS). In contrast, orexin neuron photoinhibition was ineffective during the night (active period). Acute photoinhibition of orexin neurons during the day in orexin/Halo mice also reduced discharge of neurons in an orexin terminal field, the dorsal raphe (DR) nucleus. However, serotonergic DR neurons exhibited normal discharge rates in mice lacking orexin neurons. Thus, although usually highly dependent on orexin neuronal activity, serotonergic DR neuronal activity can be regulated appropriately in the chronic absence of orexin input. Together, these results demonstrate that acute inhibition of orexin neurons results in time-of-day-dependent induction of SWS and in reduced firing rate of neurons in an efferent projection site thought to be involved in arousal state regulation. The results presented here advance our understanding of the role of orexin neurons in the regulation of sleep/wakefulness and may be relevant to the mechanisms that underlie symptom progression in narcolepsy. PMID:21775598

  12. 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

  13. 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.

  14. 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

  15. 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

  16. 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.

  17. 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

  18. Sleep disordered breathing and post-discharge mortality in patients with acute heart failure

    PubMed Central

    Khayat, Rami; Jarjoura, David; Porter, Kyle; Sow, Angela; Wannemacher, Jacob; Dohar, Robert; Pleister, Adam; Abraham, William T.

    2015-01-01

    Background Hospitalizations for heart failure are associated with a high post-discharge risk for mortality. Identification of modifiable predictors of post-discharge mortality during hospitalization may improve outcome. Sleep disordered breathing (SDB) is the most common co-morbidity in heart failure patients. Design, setting, and participants Prospective cohort study of patients hospitalized with acute heart failure (AHF) in a single academic heart hospital. Between January 2007 and December 2010, all patients hospitalized with AHF who have left ventricular ejection fraction (LVEF) ≤ 45% and were not already diagnosed with SDB were the target population. Main outcomes and measures Patients underwent in-hospital attended polygraphy testing for SDB and were followed for a median of 3 years post-discharge. Mortality was recorded using national and state vital statistics databases. Results During the study period, 1117 hospitalized AHF patients underwent successful sleep testing. Three hundred and forty-four patients (31%) had central sleep apnoea (CSA), 525(47%) patients had obstructive sleep apnoea (OSA), and 248 had no or minimal SDB (nmSDB). Of those, 1096 patients survived to discharge and were included in the mortality analysis. Central sleep apnoea was independently associated with mortality. The multivariable hazard ratio (HR) for time to death for CSA vs. nmSDB was 1.61 (95% CI: 1.1, 2.4, P = 0.02). Obstructive sleep apnoea was also independently associated with mortality with a multivariable HR vs. nmSDB of 1.53 (CI: 1.1, 2.2, P = 0.02). The Cox proportional hazards model adjusted for the following covariates: LVEF, age, BMI, sex, race, creatinine, diabetes, type of cardiomyopathy, coronary artery disease, chronic kidney disease, discharge systolic blood pressure <110, hypertension, discharge medications, initial length of stay, admission sodium, haemoglobin, and BUN. Conclusions This is the largest study to date to evaluate the effect of SDB on post

  19. Exploring Sleep-Wake Experiences of Mothers during Maintenance Therapy for Their Child’s Acute Lymphoblastic Leukemia

    PubMed Central

    Neu, Madalynn; Matthews, Ellyn; King, Nancy

    2014-01-01

    A qualitative study was designed to explore sleep-wake experience of mothers of children in maintenance treatment for Acute Lymphocytic Leukemia. Interviews were conducted with 20 participants using open-ended, semi-structured questions and were transcribed verbatim. Two main themes emerged: “It’s a whole new cancer world” and “I don’t remember what it’s like to have sleep.” Mothers experience difficulty sleeping during their children’s treatment, and expressed several serious issues. Although the mothers were able to employ various mechanisms to address sleep deprivation and disruption, interventions such as social support, journaling, spiritual guidance, and/or self-talk may be most beneficial. PMID:24486174

  20. 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…

  1. Sleeping to fuel the immune system: mammalian sleep and resistance to parasites.

    PubMed

    Opp, Mark R

    2009-01-09

    Sleep is an enigma. Why animals forgo eating and reproducing, while potentially increasing their risk of predation remains unknown. Although some may question whether all animals sleep, it is clear that all living organisms possess defenses against attack by pathogens. Immune responses of humans and animals are impaired by sleep loss, and responses to immune challenge include altered sleep. Thus, sleep is hypothesized to be a component of the acute phase response to infection and to function in host defense. Examining phylogenetic relationships among sleep parameters, components of the mammalian immune system and resistance to infection may provide insight into the evolution of sleep and lead to a greater appreciation for the role of sleep in host defense.

  2. 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

  3. Effects of sleep deprivation on brain bioenergetics, sleep, and cognitive performance in cocaine-dependent individuals.

    PubMed

    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 ³¹P magnetic resonance spectroscopy (MRS) brain imaging, polysomnography, Continuous Performance Task, and Digit Symbol Substitution Task. Following recovery sleep, ³¹P 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

  4. The spread of sleep loss influences drug use in adolescent social networks.

    PubMed

    Mednick, Sara C; Christakis, Nicholas A; Fowler, James H

    2010-01-01

    Troubled sleep is a commonly cited consequence of adolescent drug use, but it has rarely been studied as a cause. Nor have there been any studies of the extent to which sleep behavior can spread in social networks from person to person to person. Here we map the social networks of 8,349 adolescents in order to study how sleep behavior spreads, how drug use behavior spreads, and how a friend's sleep behavior influences one's own drug use. We find clusters of poor sleep behavior and drug use that extend up to four degrees of separation (to one's friends' friends' friends' friends) in the social network. Prospective regression models show that being central in the network negatively influences future sleep outcomes, but not vice versa. Moreover, if a friend sleeps sleeps < or =7 hours by 11%. If a friend uses marijuana, it increases the likelihood of marijuana use by 110%. Finally, the likelihood that an individual uses drugs increases by 19% when a friend sleeps < or =7 hours, and a mediation analysis shows that 20% of this effect results from the spread of sleep behavior from one person to another. This is the first study to suggest that the spread of one behavior in social networks influences the spread of another. The results indicate that interventions should focus on healthy sleep to prevent drug use and targeting specific individuals may improve outcomes across the entire social network. PMID:20333306

  5. Sleep laboratory studies in periodic limb movement disorder (PLMD) patients as compared with normals and acute effects of ropinirole.

    PubMed

    Saletu, M.; Anderer, P.; Saletu, B.; Hauer, C.; Mandl, M.; Semler, B.; Saletu-Zyhlarz, G.

    2001-03-01

    Periodic limb movement disorder (PLMD) occurs in a variety of sleep disorders and can cause insomnia as well as hypersomnia with daytime somnolence. The aim of this study was to investigate 12 untreated PLMD patients as compared with 12 normal controls and to measure the acute effects of 0.5 mg ropinirole (Requip((R))) - a non-ergoline dopamine agonist - as compared with placebo. In three nights (adaptation, placebo, ropinirole night) objective and subjective sleep and awakening quality were evaluated. In the target variable 'periodic leg movements per hour of sleep' (PLM/(hTST)) PLMD patients showed an increased value of 42/h (normal 0-5/h) with a greater number of arousals due to periodic leg movements (PLM) in sleep. They further demonstrated an increased number of awakenings, sleep stage S1, S4, stage shifts and decreased S2, but there were no significant differences concerning total sleep time, sleep efficiency (SE), subjective sleep quality and morning measures of mood, drive and drowsiness. However, measures of attention variability, numerical memory, fine motor activity and reaction time performance were impaired. Ropinirole 0.5 mg was shown to significantly improve the index PLM/(hTST) by 64% and arousals due to PLM, increase spontaneous arousals, REM-latency, stage 2 and stage shifts and decrease SREM. In the morning attention variability was attenuated and numerical memory augmented. Thus, ropinirole improved some sleep architecture and early morning measures of performance but specifically all PLM variables, which suggests a dopaminergic pathogenesis in PLMD. Copyright 2001 John Wiley & Sons, Ltd.

  6. Amount of weight loss or gain influences the severity of respiratory events in sleep apnea.

    PubMed

    Kulkas, A; Leppänen, T; Sahlman, J; Tiihonen, P; Mervaala, E; Kokkarinen, J; Randell, J; Seppä, J; Töyräs, J; Tuomilehto, H

    2015-10-01

    Severity of obstructive sleep apnea (OSA) is estimated based on respiratory events per hour [i.e., apnea-hypopnea index (AHI)]. The aim of this study was to investigate effects of weight change on the severity of respiratory events. Respiratory event severity, including duration and morphology, was estimated by determining parameters quantifying obstruction and desaturation event lengths and areas, respectively. Respiratory events of 54 OSA patients treated with dietary intervention were evaluated at baseline and after 5-year follow-up in subgroups with different levels of weight change. AHI, oxygen desaturation index (ODI) and obstruction event severities decreased during weight loss. In lower level weight loss, the decrease was milder in obstruction severity than in AHI and ODI, indicating that the decrease in the number of events is more focused on less severe events. In weight gain groups, parameters incorporating obstruction event severity, AHI and ODI increased, although increase was greater in parameters incorporating obstruction event severity. The number and severity of respiratory events were modulated differently by the level of weight change. AHI misses this change in the severity of respiratory events. Therefore, parameters incorporating information on the respiratory event severities may bring additional information on the health effects obtained with dietary treatment of OSA.

  7. Post-learning REM sleep deprivation impairs long-term memory: reversal by acute nicotine treatment.

    PubMed

    Aleisa, A M; Alzoubi, K H; Alkadhi, K A

    2011-07-15

    Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. We now report the interactive effects of post-learning REM-SD and/or nicotine. The animals were first trained on the radial arm water maze (RAWM) task, then they were REM-sleep deprived using the modified multiple platform paradigm for 24h. During REM-SD period, the rats were injected with saline or nicotine (1mg/kg s.c. every 12h: a total of 3 injections). The animals were tested for long-term memory in the RAWM at the end of the REM-SD period. The 24h post-learning REM-SD significantly impaired long-term memory. However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.

  8. 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.

  9. 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.

  10. 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.

  11. [Acute unilateral deafness and contralateral hearing loss following inguinal hernia repair under controlled anesthesia].

    PubMed

    Constantinidis, J; Mertzlufft, F; Steinhart, H

    1999-10-01

    Acute hearing loss following non-otologic surgery and general anesthesia is a rare occurrence. Deafness following anesthesia has more commonly been associated with spinal anesthesia or cardiopulmonary bypass surgical procedures. We present a case with unilateral cochlear dysfunction and sensorineural hearing loss after inguinal hernia operation. The literature is reviewed and the mechanisms causing hearing loss during anesthesia are discussed.

  12. Chronic Sleep Restriction Disrupts Sleep Homeostasis and Behavioral Sensitivity to Alcohol by Reducing the Extracellular Accumulation of Adenosine

    PubMed Central

    Clasadonte, Jerome; McIver, Sally R.; Schmitt, Luke I.; Halassa, Michael M.

    2014-01-01

    Sleep impairments are comorbid with a variety of neurological and psychiatric disorders including depression, epilepsy, and alcohol abuse. Despite the prevalence of these disorders, the cellular mechanisms underlying the interaction between sleep disruption and behavior remain poorly understood. In this study, the impact of chronic sleep loss on sleep homeostasis was examined in C57BL/6J mice following 3 d of sleep restriction. The electroencephalographic power of slow-wave activity (SWA; 0.5–4 Hz) in nonrapid eye movement (NREM) sleep and adenosine tone were measured during and after sleep restriction, and following subsequent acute sleep deprivation. During the first day of sleep restriction, SWA and adenosine tone increased, indicating a homeostatic response to sleep loss. On subsequent days, SWA declined, and this was accompanied by a corresponding reduction in adenosine tone caused by a loss of one source of extracellular adenosine. Furthermore, the response to acute sleep deprivation (6 h) was significantly attenuated in sleep-restricted mice. These effects were long-lasting with reduced SWA and adenosine tone persisting for at least 2 weeks. To investigate the behavioral consequences of chronic sleep restriction, sensitivity to the motor-impairing effects of alcohol was also examined. Sleep-restricted mice were significantly less sensitive to alcohol when tested 24 h after sleep restriction, an effect that persisted for 4 weeks. Intracerebroventricular infusion of an adenosine A1 receptor antagonist produced a similar decrease in sensitivity to alcohol. These results suggest that chronic sleep restriction induces a sustained impairment in adenosine-regulated sleep homeostasis and consequentially impacts the response to alcohol. PMID:24478367

  13. Socially Isolated Mice Exhibit a Blunted Homeostatic Sleep Response to Acute Sleep Deprivation Compared to Socially Paired Mice

    PubMed Central

    Kaushal, Navita; Nair, Deepti; Gozal, David; Ramesh, Vijay

    2012-01-01

    Sleep is an important physiological process underlying maintenance of physical, mental and emotional health. Consequently, sleep deprivation (SD) is associated with adverse consequences and increases the risk for anxiety, immune, and cognitive disorders. SD is characterized by increased energy expenditure responses and sleep rebound upon recovery that are regulated by homeostatic processes, which in turn are influenced by stress. Since all previous studies on SD were conducted in a setting of social isolation, the impact of the social contextual setting is unknown. Therefore, we used a relatively stress-free SD paradigm in mice to assess the impact of social isolation on sleep, wakefulness and delta electroencephalogram (EEG) power during non-rapid eye movement (NREM) sleep. Paired or isolated C57BL/6J adult chronically-implanted male mice were exposed to SD for 6 hours and telemetric polygraphic recordings were conducted, including 18 hours recovery. Recovery from SD in the paired group showed a significant decrease in wake and significant increase in NREM sleep and rapid eye movement (REM), and a similar, albeit less robust response occurred in the isolated mice. Delta power during NREM sleep was increased in both groups immediately following SD, but paired mice exhibited significantly higher delta power throughout the dark period. The increase in body temperature and gross motor activity observed during the SD procedure was decreased during the dark period. In both open field and elevated plus maze tests, socially isolated mice showed significantly higher anxiety than paired mice. The homeostatic processes altered by SD are differentially affected in paired and isolated mice, suggesting that the social context of isolation stress may adversely affect the quantity and quality of sleep in mice. PMID:22498175

  14. Acute sleep fragmentation induces tissue-specific changes in cytokine gene expression and increases serum corticosterone concentration.

    PubMed

    Dumaine, Jennifer E; Ashley, Noah T

    2015-06-15

    Sleep deprivation induces acute inflammation and increased glucocorticosteroids in vertebrates, but effects from fragmented, or intermittent, sleep are poorly understood. Considering the latter is more representative of sleep apnea in humans, we investigated changes in proinflammatory (IL-1β, TNF-α) and anti-inflammatory (TGF-β1) cytokine gene expression in the periphery (liver, spleen, fat, and heart) and brain (hypothalamus, prefrontal cortex, and hippocampus) of a murine model exposed to varying intensities of sleep fragmentation (SF). Additionally, serum corticosterone was assessed. Sleep was disrupted in male C57BL/6J mice using an automated sleep fragmentation chamber that moves a sweeping bar at specified intervals (Lafayette Industries). Mice were exposed to bar sweeps every 20 s (high sleep fragmentation, HSF), 120 s (low sleep fragmentation, LSF), or the bar remained stationary (control). Trunk blood and tissue samples were collected after 24 h of SF. We predicted that HSF mice would exhibit increased proinflammatory expression, decreased anti-inflammatory expression, and elevated stress hormones in relation to LSF and controls. SF significantly elevated IL-1β gene expression in adipose tissue, heart (HSF only), and hypothalamus (LSF only) relative to controls. SF did not increase TNF-α expression in any of the tissues measured. HSF increased TGF-β1 expression in the hypothalamus and hippocampus relative to other groups. Serum corticosterone concentration was significantly different among groups, with HSF mice exhibiting the highest, LSF intermediate, and controls with the lowest concentration. This indicates that 24 h of SF is a potent inducer of inflammation and stress hormones in the periphery, but leads to upregulation of anti-inflammatory cytokines in the brain.

  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. Behavioral and physiological consequences of sleep restriction.

    PubMed

    Banks, Siobhan; Dinges, David F

    2007-08-15

    Adequate sleep is essential for general healthy functioning. This paper reviews recent research on the effects of chronic sleep restriction on neurobehavioral and physiological functioning and discusses implications for health and lifestyle. Restricting sleep below an individual's optimal time in bed (TIB) can cause a range of neurobehavioral deficits, including lapses of attention, slowed working memory, reduced cognitive throughput, depressed mood, and perseveration of thought. Neurobehavioral deficits accumulate across days of partial sleep loss to levels equivalent to those found after 1 to 3 nights of total sleep loss. Recent experiments reveal that following days of chronic restriction of sleep duration below 7 hours per night, significant daytime cognitive dysfunction accumulates to levels comparable to that found after severe acute total sleep deprivation. Additionally, individual variability in neurobehavioral responses to sleep restriction appears to be stable, suggesting a trait-like (possibly genetic) differential vulnerability or compensatory changes in the neurobiological systems involved in cognition. A causal role for reduced sleep duration in adverse health outcomes remains unclear, but laboratory studies of healthy adults subjected to sleep restriction have found adverse effects on endocrine functions, metabolic and inflammatory responses, suggesting that sleep restriction produces physiological consequences that may be unhealthy.

  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.

  19. 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.

  20. Effects of sleep fragmentation on sleep and markers of inflammation in mice.

    PubMed

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

    2014-02-01

    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.

  1. Linkage of sleep-disordered breathing and acute aortic dissection with patent false lumen.

    PubMed

    Inami, Toru; Seino, Yoshihiko; Shimura, Tetsuro; Kurihara, Osamu; Kimata, Nakahisa; Murakami, Daisuke; Munakata, Ryo; Takano, Masamichi; Ohba, Takayoshi; Shimizu, Wataru

    2016-07-01

    Sleep-disordered breathing (SDB) is known as a cardiovascular risk factor and has high prevalence in hypertension, which is a major risk factor of aortic dissection (AD). However, the impact of SDB on AD has not been fully clarified. The aim of this study is to elucidate the impact of SDB on AD, especially on the type of false lumen in AD. We enrolled twenty-three consecutive patients with acute AD (mean age: 66 ± 13 years). All subjects were evaluated by an ambulatory polygraphic sleep monitoring within 1 month from the onset. AD was evaluated by axial images of computed tomography. We comparatively analyzed SDB and AD. 35 % of the subjects presented severe OSA (apnea-hypopnea index: AHI ≥30). The patent false lumen group showed significantly higher systolic and diastolic blood pressure (BP) on arrival and AHI, and lower percutaneous oxygen saturation (SaO2) compared with those in the thrombosed false lumen group. The prevalence of severe SDB was higher in the patent false lumen group (60 vs 15 %, p = 0.039). Systolic BP on arrival was significantly correlated with AHI (r = 0.457, p = 0.033) and the minimum SaO2 (r = -0.537, p = 0.010). The present study revealed close linkage between SDB and AD, and a high prevalence of SDB among AD patients. Severe SDB was related to the development of AD, especially for the patent false lumen type through highly elevated BP which might be easily evoked in the presence of severe SDB. Repetitive occurrence of intrathoracic negative pressure also might influence the repair or closure of false lumen of AD, although the present analysis did not reach statistical significance.

  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. Inter-individual differences in the effects of acute stress on the sleep-wakefulness cycle in the rat.

    PubMed

    Bouyer, J J; Deminière, J M; Mayo, W; Le Moal, M

    1997-04-11

    It has been described that an acute immobilization stress (IS) modifies subsequent paradoxical sleep (PS). However, its effects are complex because some subjects remain unaffected. This discrepancy might result from constitutive inter-individual psychobiological differences. In order to test this hypothesis, an inter-individual analysis of sleep patterns and their modifications after 60 min IS has been performed. Even though global analysis showed a PS increase after IS, inter-individual analysis evidenced different PS reactivity; subjects which had the least PS during control recordings were those with the largest PS increase. Unlike global analysis, an inter-individual study evidenced different modifications of wakefulness and slow wave sleep according to individuals. Subjects presenting the highest amount of wakefulness in control conditions (the lowest amount of slow wave sleep) decreased their wakefulness amount, while subjects with the lowest amount of wakefulness increased it. Thus, individual characteristics of the sleep-wakefulness cycle should be considered while studying its modifications induced by different treatments. PMID:9147403

  4. [Acute perceptive hearing loss. Importance of tuning fork test in primary care].

    PubMed

    Verburg, A F E Arianne; Alkhateeb, W H F Waiel; Merkus, Paul

    2011-01-01

    A 56-year-old woman presented with acute right-sided hearing loss. At first presentation she was diagnosed as having otitis media with effusion. No tuning fork test was performed. After four weeks she was finally correctly diagnosed as having a right-sided sensorineural hearing loss of 90 dB. As a result of the delay no treatment was started. Her hearing loss did not show any improvement after three months. Sensorineural hearing loss is a rare, potentially invalidating condition with a considerable psychological impact. The treatment consists of systemic steroids, which may only be useful if started within 14 days after symptoms start. Some patients are initially treated for conductive hearing loss. Routine performance of the tuning fork test helps in differentiating between conductive and perceptive hearing loss. In cases of acute perceptive hearing loss, patients should be referred to the otorhinolaryngologist to exclude possible causes and start treatment and guidance.

  5. 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.

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

    PubMed Central

    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

  7. 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

  8. Impaired motor memory for a pursuit rotor task following Stage 2 sleep loss in college students.

    PubMed

    Smith; MacNeill

    1994-12-01

    It has recently been reported that selective REM sleep deprivation (REMD) in college students results in memory impairment of the application of a set of rules in a logic task, but not recall of a paired associate task. The present experiments were designed to examine the effects of Total Sleep Deprivation (TSD) and (REMD) following acquisition of a pure motor task, the pursuit rotor. In Experiment 1, subjects (N = 90) were exposed to TSD for one of several nights following training. Results showed that TSD on the same night as training resulted in poorer performance on retest one week later. In Experiment 2, subjects (N = 42) were exposed to various kinds of sleep deprivation on the night of task acquisition. One group was subjected to REMD. Other groups included a non-REM awakening control group (NREMA), a TSD group, a normally rested Control group and a group allowed the first 4 h of sleep in the night before being subjected to TSD (LH - TSD) for the rest of the night. Results showed the REMD and Control groups to have excellent memory for this task while the TSD and LH - TSD subjects had significantly poorer memory for the task. The NREMA group showed a slight, but not significant deficit. It was concluded that Stage 2 sleep, rather than REM sleep was the important stage of sleep for efficient memory processing of the pursuit rotor task. PMID:10607127

  9. Sleep EEG and nocturnal secretion of testosterone and cortisol in patients with major endogenous depression during acute phase and after remission.

    PubMed

    Steiger, A; von Bardeleben, U; Wiedemann, K; Holsboer, F

    1991-01-01

    Sleep EEG and the nocturnal secretion of cortisol and testosterone in 12 male patients (mean age 46.4 +/- 11.26 years) with major endogenous depression were investigated concomitantly during acute depression, before treatment and after recovery and drug cessation. Testosterone concentration increased after remission, while cortisol secretion decreased. Sleep EEG disturbances remained unchanged in remitted patients. The data suggest that a blunted testosterone and an elevated cortisol secretion are state markers of acute depression, which normalize independently from sleep structure. An interaction between the hypothalamic-pituitary-gonadal axis and the limbic-hypothalamic-pituitary-adrenocortical axis appears likely.

  10. Morning pentraxin3 levels reflect obstructive sleep apnea–related acute inflammation

    PubMed Central

    Kobukai, Yusuke; Koyama, Takashi; Ito, Hiroshi

    2014-01-01

    This study investigated morning levels of pentraxin3 (PTX3) as a sensitive biomarker for acute inflammation in patients with obstructive sleep apnea (OSA). A total of 61 consecutive patients with OSA were divided into two groups: non-to-mild (n = 20) and moderate-to-severe (n = 41) OSA based on their apnea-hypopnea index (AHI) score. Those patients with moderate-to-severe OSA were further divided into continuous positive airway pressure (CPAP) treated (n = 21) and non-CPAP-treated (n = 20) groups. Morning and evening serum PTX3 and high-sensitivity (hs) C-reactive protein (CRP) levels were measured before and after 3 mo of CPAP therapy. The baseline hs-CRP and PTX3 levels were higher in patients with moderate-to-severe OSA than in those with non-to-mild OSA. Moreover, the serum PTX3 levels, but not the hs-CRP levels, were significantly higher after than before sleep in the moderate-to-severe OSA group (morning PTX3, 1.96 ± 0.52; evening PTX3, 1.71 ± 0.44 ng/ml). OSA severity as judged using the AHI was significantly correlated with serum PTX3 levels but not hs-CRP levels. The highest level of correlation was found between the AHI and morning PTX3 levels (r = 0.563, P < 0.001). CPAP therapy reduced evening and morning serum hs-CRP and PTX3 levels in patients with moderate-to-severe OSA; however, the reduction in PTX3 levels in the morning was greater than that in the evening (morning −29.8 ± 16.7% vs. evening −12.6 ± 26.8%, P = 0.029). Improvement in the AHI score following CPAP therapy was strongly correlated with reduced morning PTX3 levels(r = 0.727, P < 0.001). Based on these results, morning PTX3 levels reflect OSA-related acute inflammation and are a useful marker for improvement in OSA following CPAP therapy. PMID:25237185

  11. The Acute Effects of Alcohol on Sleep Architecture in Late Adolescence

    PubMed Central

    Chan, Julia K. M.; Trinder, John; Andrewes, Holly E.; Colrain, Ian M.; Nicholas, Christian L.

    2013-01-01

    Background Alcohol consumption is prevalent in late adolescence, however little is known about its effect on sleep in this group. In mature adults, alcohol decreases sleep onset latency (SOL) and sleep efficiency (SE) and increases wake after sleep onset (WASO). It also increases slow wave sleep (SWS) and decreases REM sleep in the first half of the night, with the inverse occurring in the second half. Alcohol’s effect on sleep during late adolescence is of interest given that this age group shows both dramatic increases in alcohol consumption, and significant developmental changes in the central nervous system. This study examined the effect of alcohol on sleep architecture in women and men aged 18–21 years and whether previously reported sleep architecture effects may have been as an artificial result of changes to sleep cycle length. Methods 24 (12 female) healthy 18–21 year old light social drinkers (19.1±1.0yrs) underwent two conditions: pre-sleep alcohol (Target BAC 0.10%) and placebo administered under controlled conditions, followed by standard polysomnography. Results In the alcohol condition, mean breath alcohol concentration (BAC) at lights out was 0.084 ±0.016%. Time in bed, total sleep time and sleep onset latency (all p>.05) did not differ between conditions. However, there was less REM (p=.011) and more stage 2 sleep (p=.035) in the alcohol condition. Further, alcohol increased SWS (p=.02) and decreased REM sleep (p<.001) in the first half of the night and disrupted sleep in the second half, with increased WASO (interaction: p=.034), and decreased SE (p=.04) and SWS (p=.01) and no REM sleep rebound in the second half of the night (p=.262). Additionally, alcohol had no effect on sleep cycle length (p=.598). Conclusions The results were broadly consistent with the adult literature with the novel extension that half night sleep architecture effects could not be attributed to changes in sleep cycle length. However, alcohol did not reduce SOL, or

  12. REM sleep loss associated changes in orexin-A levels in discrete brain areas in rats.

    PubMed

    Mehta, Rachna; Khanday, Mudasir Ahmad; Mallick, Birendra Nath

    2015-03-17

    Rapid eye movement sleep (REMS) serves house-keeping function of the brain and its loss affects several pathophysiological processes. Relative levels of neurotransmitters including orexin A (Orx-A) in various parts of the brain in health and diseases are among the key factors for modulation of behaviors, including REMS. The level of neurotransmitter in an area in the brain directly depends on number of projecting neurons and their firing rates. The locus coeruleus (LC), the site of REM-OFF neurons, receives densest, while the pedunculo-pontine area (PPT), the site of REM-ON neurons receives lesser projections from the Orx-ergic neurons. Further, the Orx-ergic neurons are active during waking and silent during REMS and NREMS. Therefore, the level of Orx-A in discrete regions of the brain is likely to be different during normal and altered states, which in turn is likely to be responsible for altered behaviors in health and diseases, including in relation to REMS. Therefore, in the present study, we estimated Orx-A level in LC, cortex, posterior hypothalamus (PH), hippocampus, and PPT after 96 h REMSD, in post-deprivation recovered rats and in control rats. This is the first report of estimation of Orx-A in different brain regions after prolonged REMSD. It was observed that after REMSD the Orx-A level increased significantly in LC, cortex and PH which returned to normal level after recovery; however, the level did not change in the hippocampus and PPT. The Orx-A induced modulation of REMS could be secondary to increased waking.

  13. 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

  14. 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

  15. 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

  16. Sleep loss and circadian disruption in shift work: health burden and management.

    PubMed

    Rajaratnam, Shantha M W; Howard, Mark E; Grunstein, Ronald R

    2013-10-21

    About 1.5 million Australians are shift workers. Shift work is associated with adverse health, safety and performance outcomes. Circadian rhythm misalignment, inadequate and poor-quality sleep, and sleep disorders such as sleep apnoea, insomnia and shift work disorder (excessive sleepiness and/or insomnia temporally associated with the work schedule) contribute to these associations. Falling asleep at work at least once a week occurs in 32%-36% of shift workers. Risk of occupational accidents is at least 60% higher for non-day shift workers. Shift workers also have higher rates of cardiometabolic diseases and mood disturbances. Road and workplace accidents related to excessive sleepiness, to which shift work is a significant contributor, are estimated to cost $71-$93 billion per annum in the United States. There is growing evidence that understanding the interindividual variability in sleep-wake responses to shift work will help detect and manage workers vulnerable to the health consequences of shift work. A range of approaches can be used to enhance alertness in shift workers, including screening and treating sleep disorders, melatonin treatment to promote sleep during the daytime, and avoidance of inappropriate use of sedatives and wakefulness-promoters such as modafinil and caffeine. Short naps, which minimise sleep inertia, are generally effective. Shifting the circadian pacemaker with appropriately timed melatonin and/or bright light may be used to facilitate adjustment to a shift work schedule in some situations, such as a long sequence of night work. It is important to manage the health risk of shift workers by minimising vascular risk factors through dietary and other lifestyle approaches.

  17. Acute bilateral vision loss in emergency department: A case report.

    PubMed

    Tanrikulu, Ceren Sen; Hocagil, Hilal; Kaya, Ural; Hocagil, Abdullah Cuneyt

    2016-03-01

    Stroke occurs due to the interruption of blood flow to the brain and it is divided into ischemic and hemorrhagic. In the ischemic strokes, while the most commonly affected vessel is median cerebral artery (MCA), it is particularly affected bilateral posterior cerebral artery (PCA) is very rare condition. In this study, a case of sudden loss of vision and bilateral occipital infarct associated with bilateral vertebral system pathology and methylene tetrahydrofolate reductase (MTHFR) gene mutation were reported. A 62-year-old man was admitted with sudden loss of vision complaint starting 10 h before applying to emergency department. The patient was oriented and cooperative. On neurological examination, there was complete loss of vision in the right eye and only a response to light in the left eye. On the brain computerized tomography (CT), ischemic lesions were observed in the bilateral occipital areas and on magnetic resonance imaging (MRI), there were foci showing diffusion limitation in cortico-subcortical areas of bilateral parieto-occipital region. On the detailed examination at the clinic, MTHFR (a1298c) gene mutation was detected. Bilateral occipital infarction is rare and its diagnosis can be difficult because of its atypical symptoms. Therefore, occipital infarction should be suspected when the only sign is isolated vision loss in patients with risk factor for thromboembolism in their history and detailed visual-neurological examination of these patients should be performed. PMID:27239639

  18. Sleep restores loss of generalized but not rote learning of synthetic speech.

    PubMed

    Fenn, Kimberly M; Margoliash, Daniel; Nusbaum, Howard C

    2013-09-01

    Sleep-dependent consolidation has been demonstrated for declarative and procedural memory but few theories of consolidation distinguish between rote and generalized learning, suggesting similar consolidation should occur for both. However, studies using rote and generalized learning have suggested different patterns of consolidation may occur, although different tasks have been used across studies. Here we directly compared consolidation of rote and generalized learning using a single speech identification task. Training on a large set of novel stimuli resulted in substantial generalized learning, and sleep restored performance that had degraded after 12 waking hours. Training on a small set of repeated stimuli primarily resulted in rote learning and performance also degraded after 12 waking hours but was not restored by sleep. Moreover performance was significantly worse 24-h after rote training. Our results suggest a functional dissociation between the mechanisms of consolidation for rote and generalized learning which has broad implications for memory models.

  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. 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.

  2. 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

  3. 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

  4. 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.…

  5. Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation.

    PubMed

    Zhong, Xu; Hilton, H John; Gates, Gregory J; Jelic, Sanja; Stern, Yaakov; Bartels, Matthew N; Demeersman, Ronald E; Basner, Robert C

    2005-06-01

    Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.

  6. Impact of acute sleep restriction on cortisol and leptin levels in young women.

    PubMed

    Omisade, Antonina; Buxton, Orfeu M; Rusak, Benjamin

    2010-04-19

    Sleep restriction alters hormone patterns and appetite in men, but less is known about effects on women. We assessed effects of overnight sleep restriction on cortisol and leptin levels and on appetite in young women. Participants' baseline sleep duration and eating habits were monitored for a week before the study. Salivary cortisol and leptin were sampled from fifteen healthy women (aged 18-25) during two consecutive days: first after a 10h overnight sleep opportunity (Baseline day) and then after a night including only 3h sleep (Post sleep-restriction day). Participants also completed appetite questionnaires on both days. Sleep restriction significantly reduced morning cortisol levels (p=0.02), elevated morning leptin levels (p=0.04), elevated afternoon/evening cortisol area under the curve values (p=0.008), and slowed the decline in cortisol concentration during the day (p=0.04). Hunger and craving scores did not differ significantly between days. A single night of restricted sleep affected cortisol rhythms and morning leptin levels in young women.

  7. Acute Sensorineural Hearing Loss After Abuse of an Inhaled, Crushed Oxymorphone Extended-Release Tablet.

    PubMed

    MacDonald, Lisa E; Onsrud, Jennifer E; Mullins-Hodgin, Rita

    2015-07-01

    Oxymorphone, a semisynthetic μ-opioid receptor agonist, is the major active metabolite of oxycodone. It is a highly potent narcotic analgesic due to its high lipid solubility, which allows it to readily cross the blood-brain barrier and enter the central nervous system. It is available as both an immediate-release and extended-release (ER) formulation. Oxymorphone can be abused by injection or inhalation of crushed tablets; thus, in 2011, the manufacturer of ER oxymorphone reformulated the drug with crush-resistant technology to deter its misuse and abuse. We describe the case of a previously healthy, 24-year-old male who experienced reproducible acute subjective bilateral temporary hearing loss that occurred after inhalation of oxymorphone. He presented to the emergency department complaining of acute bilateral hearing loss after he reported snorting a crushed oxymorphone ER 30-mg tablet. Emergency department evaluation revealed obvious bilateral hearing loss as well as coincidental aspiration pneumonia. The patient's medical history revealed that he had experienced a similar episode of hearing loss after a previous episode of oxymorphone inhalation. His hearing loss began to improve 3 hours after presentation to the emergency department and was completely resolved by the following day. Use of the Naranjo adverse drug reaction probability scale revealed oxymorphone to be a probable cause of this patient's acute hearing loss (score of 6). The mechanism of action of opioid-associated hearing loss (OAHL) is not completely understood, but it is thought to be due to disturbances within the cochlea, such as cochlear ischemia. To our knowledge, this is only the second published case report of acute reversible hearing loss following oxymorphone inhalation and the first published case report of reproducible OAHL. Since opioid misuse continues to be prevalent despite attempts at reformulations to make the drugs crush resistant, a high degree of clinical suspicion is needed

  8. Loss of appetite in acutely ill medical inpatients: physiological response or therapeutic target?

    PubMed

    Schütz, Philipp; Bally, Martina; Stanga, Zeno; Keller, Ulrich

    2014-01-01

    Loss of appetite and ensuing weight loss is a key feature of severe illnesses. Protein-energy malnutrition (PEM) contributes significantly to the adverse outcome of these conditions. Pharmacological interventions to target appetite stimulation have little efficacy but considerable side effects. Therefore nutritional therapy appears to be the logical step to combat inadequate nutrition. However, clinical trial data demonstrating benefits are sparse and there is no current established standard algorithm for use of nutritional support in malnourished, acutely ill medical inpatients. Recent high-quality evidence from critical care demonstrating harmful effects when parenteral nutritional support is used indiscriminately has led to speculation that loss of appetite in the acute phase of illness is indeed an adaptive, protective response that improves cell recycling (autophagy) and detoxification. Outside critical care, there is an important gap in high quality clinical trial data shedding further light on these important issues. The selection, timing, and doses of nutrition should be evaluated as carefully as with any other therapeutic intervention, with the aim of maximising efficacy and minimising adverse effects and costs. In light of the current controversy, a reappraisal of how nutritional support should be used in acutely ill medical inpatients outside critical care is urgently required. The aim of this review is to discuss current pathophysiological concepts of PEM and to review the current evidence for the efficacy of nutritional support regarding patient outcomes when used in an acutely ill medical patient population outside critical care. PMID:24782139

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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

  14. 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.

  15. 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.

  16. Precocious loss of physiological sleep in a case of Creutzfeldt Jakob disease: a serial polygraphic study.

    PubMed

    Terzano, M G; Parrino, L; Pietrini, V; Mancia, D; Spaggiari, M C; Rossi, G; Tagliavini, F

    1995-12-01

    Creutzfeldt-Jakob disease (CJD) is a prion-related subacute encephalopathy producing widespread neuronal degeneration and spongiform pathological changes, especially in the neocortex. Progressive dementia, motor signs and electroencephalographic (EEG) alterations characterize the full stage of the disease. A series of eight 24-hour polygraphic recordings were carried out in the last 3 months of life of a 68-year-old female patient affected by CJD that was confirmed neuropathologically. Genetic classification demonstrated this patient to have a sporadic form of the disease. The polygraphic recordings demonstrated three types of EEG findings, as follows: 1) sustained pseudoperiodic discharges (SPD), characterized by long-lasting diffuse sequences of slow sharp waves or di- or triphasic slow waves recurring at 0.5- to 1.5-second intervals; 2) discontinuous pseudoperiodic discharges (DPD), consisting of runs of pseudoperiodic discharges (PD)(phase A) cyclically replaced at about 1-minute intervals with semi-rhythmic theta-delta activities (phase B); 3) non-rapid eye movement (NREM) sleep-like pattern, with dominant 0.5- to 4-Hz activities, less rhythmic than the EEG of phase B. Only these three EEG patterns occurred spontaneously during the repeated polygraphic sessions. The NREM sleep-like pattern was found only in the first recording, whereas the following polygraphic sessions were occupied exclusively by SPD or by a DPD pattern. SPD was associated with either a relatively high level of vigilance (along the first three recordings) or a state of alert-appearing silent immobility (following the fourth recording). During DPD, the patient was unable to accomplish any voluntary movement and fluctuated between levels of greater arousal (phase A) and lesser arousal (phase B). Just as in stage 2 coma, the fluctuations between phases A and B of DPD were synchronous with phasic modifications of muscle activity and neurovegetative functions. In particular, reinforcement of

  17. Carbohydrate-Binding Non-Peptidic Pradimicins for the Treatment of Acute Sleeping Sickness in Murine Models

    PubMed Central

    Castillo-Acosta, Víctor M.; Ruiz-Pérez, Luis M.; Reichardt, Niels C.; Igarashi, Yasuhiro; Liekens, Sandra; Balzarini, Jan

    2016-01-01

    Current treatments available for African sleeping sickness or human African trypanosomiasis (HAT) are limited, with poor efficacy and unacceptable safety profiles. Here, we report a new approach to address treatment of this disease based on the use of compounds that bind to parasite surface glycans leading to rapid killing of trypanosomes. Pradimicin and its derivatives are non-peptidic carbohydrate-binding agents that adhere to the carbohydrate moiety of the parasite surface glycoproteins inducing parasite lysis in vitro. Notably, pradimicin S has good pharmaceutical properties and enables cure of an acute form of the disease in mice. By inducing resistance in vitro we have established that the composition of the sugars attached to the variant surface glycoproteins are critical to the mode of action of pradimicins and play an important role in infectivity. The compounds identified represent a novel approach to develop drugs to treat HAT. PMID:27662652

  18. 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

  19. Obesity and obstructive sleep apnea--clinical significance of weight loss.

    PubMed

    Tuomilehto, Henri; Seppä, Juha; Uusitupa, Matti

    2013-10-01

    Obesity is a major health burden that contributes to increased morbidity and mortality. Obesity is also the most important risk factor for obstructive sleep apnea (OSA); at least 70% of patients are obese. OSA as such, has been linked with increased cardiovascular morbidity and mortality, and OSA patients often display metabolic syndrome. The exact underlying mechanisms behind these associations are complex and not fully understood. In obese individuals, weight reduction and increased physical activity form cornerstones for the prevention and treatment of metabolic syndrome, and recent controlled intervention trials strongly suggest that weight reduction together with a healthy diet and increased physical activity may correct or at least improve the symptoms of OSA. However, regardless of promising results in terms of symptoms of OSA and the undoubted metabolic benefits of changing lifestyles, weight reduction as a treatment of OSA is still underrated by many clinicians. Based on the current knowledge, clinicians should revise their previous attitudes, including suspicions about weight reduction as an effective treatment for OSA patients. Nevertheless, we also need large well-controlled trials on the effects of different weight reduction programs among OSA patients to determine the overall efficacy of different treatment modalities and their long-term success.

  20. The body weight loss during acute exposure to high-altitude hypoxia in sea level residents.

    PubMed

    Ge, Ri-Li; Wood, Helen; Yang, Hui-Huang; Liu, Yi-Ning; Wang, Xiu-Juan; Babb, Tony

    2010-12-25

    Weight loss is frequently observed after acute exposure to high altitude. However, the magnitude and rate of weight loss during acute exposure to high altitude has not been clarified in a controlled prospective study. The present study was performed to evaluate weight loss at high altitude. A group of 120 male subjects [aged (32±6) years] who worked on the construction of the Golmud-Lhasa Railway at Kunlun Mountain (altitude of 4 678 m) served as volunteer subjects for this study. Eighty-five workers normally resided at sea level (sea level group) and 35 normally resided at an altitude of 2 200 m (moderate altitude group). Body weight, body mass index (BMI), and waist circumference were measured in all subjects after a 7-day stay at Golmud (altitude of 2 800 m, baseline measurements). Measurements were repeated after 33-day working on Kunlun Mountain. In order to examine the daily rate of weight loss at high altitude, body weight was measured in 20 subjects from the sea level group (sea level subset group) each morning before breakfast for 33 d at Kunlun Mountain. According to guidelines established by the Lake Louise acute mountain sickness (AMS) consensus report, each subject completed an AMS self-report questionnaire two days after arriving at Kunlun Mountain. After 33-day stay at an altitude of 4 678 m, the average weight loss for the sea level group was 10.4% (range 6.5% to 29%), while the average for the moderate altitude group was 2.2% (-2% to 9.1%). The degree of weight loss (Δ weight loss) after a 33-day stay at an altitude of 4 678 m was significantly correlated with baseline body weight in the sea level group (r=0.677, P<0.01), while the correlation was absent in the moderate altitude group (r=0.296, P>0.05). In the sea level subset group, a significant weight loss was observed within 20 d, but the weight remained stable thereafter. AMS-score at high altitude was significantly higher in the sea level group (4.69±2.48) than that in the moderate

  1. 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

  2. The effect of acute sleep deprivation and fatigue in cardiovascular perfusion students: a mixed methods study.

    PubMed

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

    2012-09-01

    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 high-fidelity 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 period

  3. 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

  4. The effect of acute sleep deprivation and fatigue in cardiovascular perfusion students: a mixed methods study.

    PubMed

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

    2012-09-01

    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 high-fidelity 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 period

  5. The acute effects of light on murine sleep during the dark phase: importance of melanopsin for maintenance of light-induced sleep

    PubMed Central

    Muindi, Fanuel; Zeitzer, Jamie M.; Colas, Damien; Heller, H. Craig

    2016-01-01

    Light exerts a direct effect on sleep and wakefulness in nocturnal and diurnal animals, with a light pulse during the dark phase suppressing locomotor activity and promoting sleep in the former. In the present study, we investigated this direct effect of light on various sleep parameters by exposing mice to a broad range of illuminances (0.2–200 μW/cm2; equivalent to 1–1000 lux) for 1 h during the dark phase (zeitgeber time 13–14). Fitting the data with a three-parameter log model indicated that ~0.1 μW/cm2 can generate half the sleep response observed at 200 μW/cm2. We observed decreases in total sleep time during the 1 h following the end of the light pulse. Light reduced the latency to sleep from ~30 min in darkness (baseline) to ~10 min at the highest intensity, although this effect was invariant across the light intensities used. We then assessed the role of melanopsin during the rapid transition from wakefulness to sleep at the onset of a light pulse and the maintenance of sleep with a 6-h 20 μW/cm2 light pulse. Even though the melanopsin knockout mice had robust induction of sleep (~35 min) during the first hour of the pulse, it was not maintained. Total sleep decreased by almost 65% by the third hour in comparison with the first hour of the pulse in mice lacking melanopsin, whereas only an 8% decrease was observed in wild-type mice. Collectively, our findings highlight the selective effects of light on murine sleep, and suggest that melanopsin-based photoreception is primarily involved in sustaining light-induced sleep. PMID:23510299

  6. A single night of sleep curtailment increases plasma acylcarnitines: Novel insights in the relationship between sleep and insulin resistance.

    PubMed

    van den Berg, Rosa; Mook-Kanamori, Dennis O; Donga, Esther; van Dijk, Marieke; van Dijk, J Gert; Lammers, Gert-Jan; van Kralingen, Klaas W; Prehn, Cornelia; Adamski, Jerzy; Romijn, Johannes A; van Dijk, Ko Willems; Corssmit, Eleonora P M; Rensen, Patrick C N; Biermasz, Nienke R

    2016-01-01

    We have previously shown that acute sleep curtailment induces insulin resistance, both in healthy individuals as well as in patients with type 1 diabetes, suggesting a causal role for sleep disturbances in pathogenesis of insulin resistance, independent of endogenous insulin production. However, the underlying mechanisms remain unclear. This study aimed to explore the metabolic pathways affected by sleep loss using targeted metabolomics in human fasting plasma samples. Healthy individuals (n = 9) and patients with type 1 diabetes (n = 7) were studied after a single night of short sleep (4 h) versus normal sleep (8 h) in a cross-over design. Strikingly, one night of short sleep specifically increased the plasma levels of acylcarnitines, essential intermediates in mitochondrial fatty acid oxidation (FAO). Specifically, short sleep increased plasma levels of tetradecenoyl-l-carnitine (C14:1) (+32%, p = 2.67*10(-4)), octadecanoyl-l-carnitine (C18:1) (+22%, p = 1.92*10(-4)) and octadecadienyl-l-carnitine (C18:2) (+27%, p = 1.32*10(-4)). Since increased plasma acylcarnitine levels could be a sign of disturbed FAO, it is possible that sleep curtailment acutely induces inefficient mitochondrial function. Our observations provide a basis for further research into the role of acylcarnitines as a potential mechanistic pathway by which sleep deprivation - even short term - causes adverse metabolic effects, such as insulin resistance.

  7. 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

  8. 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

  9. 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

  10. 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

  11. The development of insomnia or the plasticity of good sleep? A preliminary study of acute changes in sleep and insomnia resulting from an analogue trauma.

    PubMed

    Richardson, Cele; Gradisar, Michael; Pulford, Amanda

    2015-01-01

    The present preliminary study aimed to shed light on the mechanisms underlying the development of insomnia. An analogue stressor (i.e., trauma video) was used to prevent presleep cognitive de-arousal. Subsequent changes in nocturnal sleep and sleep-related attentional processing were examined. Thirty-four participants were randomly assigned to either a cognitive arousal (trauma video; age: M = 22.9, SD = 4.3, 6 male, 11 female) or control (pleasant video; age: M = 23.8, SD = 5.8, 7 male, 10 female) condition. Although no significant differences were found for presleep cognitive de-arousal (p = .39), the cognitive arousal group experienced a significant worsening in sleep latency (p = .048, partial η(2) = .12) and an increase in sleep-related attentional bias (p = .032, d = 0.51) following the manipulation. However, changes in sleep and attentional bias were not maintained. Vulnerability to stress did not significantly account for any change in attentional bias, arousal, or sleep. These findings challenge current conceptualizations of the development of insomnia, yet also supporting the notion that good sleep is a default state that protects individuals from sleep disturbance.

  12. 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

  13. 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

  14. Acute sleep deprivation increases the rate and efficiency of cocaine self-administration, but not the perceived value of cocaine reward in rats.

    PubMed

    Puhl, Matthew D; Fang, Jidong; Grigson, Patricia Sue

    2009-12-01

    Relapse to drug seeking and drug taking is elicited by exposure to stress, drug-associated cues, or drugs of abuse themselves. According to the clinical literature, relapse also can be elicited in humans by sleep deprivation. Even so, the effect of sleep deprivation on drug-seeking and drug-taking behaviors has received relatively little attention in the laboratory (i.e., currently, no animal model exists) and the underlying circuitry remains unexplored. In the present study, 42 naïve male Sprague-Dawley rats were trained to self-administer cocaine and were then divided, on the basis of their behavior, into low (n=20) and high (n=22) drug-taking groups. Self-administration behavior was extinguished, and the effect of acute sleep deprivation (0, 4, or 8h) on drug-induced reinstatement and on progressive ratio responding (i.e., on the motivation to work for drug) was investigated. The results showed that, relative to low drug-takers, high drug-takers took more drug in acquisition, made more infusion attempts during drug-induced reinstatement, worked harder for drug, and exhibited greater goal-directed behavior. Acute sleep deprivation had little impact on high drug-takers beyond increasing the rate of infusions self-administered during progressive ratio (PR) testing. Conversely, in low drug-takers, acute sleep deprivation completely abolished cocaine-induced reinstatement during extinction testing. During PR testing, however, sleep deprivation increased the speed with which low drug-taking rats initiated responding for drug, increased the rate of infusions, and increased goal-directed behavior. It did not, however, increase the perceived value of the cocaine reward (i.e., neither sleep-deprived low drug-takers nor high drug-takers exhibited a higher break point for cocaine than their non-deprived counterparts). These data are the first to demonstrate a direct link between sleep deprivation and responding for cocaine, particularly in subjects that would otherwise

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

    PubMed

    Mowatt, Lizette; Foster, Tecah

    2013-08-20

    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.

  16. 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

  17. 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

  18. 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

  19. Genetic Dissociation of Daily Sleep and Sleep Following Thermogenetic Sleep Deprivation in Drosophila

    PubMed Central

    Dubowy, Christine; Moravcevic, Katarina; Yue, Zhifeng; Wan, Joy Y.; Van Dongen, Hans P.A.; Sehgal, Amita

    2016-01-01

    Study Objectives: Sleep rebound—the increase in sleep that follows sleep deprivation—is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila. Methods: To develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits. Results: We identified two lines that consistently exhibit a blunted increase in the

  20. 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

  1. Acute heat shock leads to cortical domain internalization and polarity loss in the C. elegans embryo.

    PubMed

    Singh, Deepika; Odedra, Devang; Lehmann, Christina; Pohl, Christian

    2016-04-01

    Many developmental processes are inherently robust due to network organization of the participating factors and functional redundancy. The heterogeneity of the factors involved and their connectivity puts these processes at risk of abrupt system collapse under stress. The polarization of the one-cell C. elegans embryo constitutes such an inherently robust process with functional redundancy. However, how polarization is affected by acute stress has not been thoroughly investigated. Here, we report that heat shock (34°C, 1 h) triggers a highly reproducible loss of the anterior and collapse of the posterior polarity domains. Temperature-dependent loss of cortical non-muscle myosin II drastically reduces cortical tension and leads to internalization of large plasma membrane domains including the membrane-associated polarity factor PAR-2. After internalization, plasma membrane vesicles and associated factors cluster around centrosomes and are thereby withdrawn from the polarization process. Transient formation of the posterior polarity domain suggests that microtubule-induced self-organization of this domain is not compromised after heat shock. Hence, our data uncover that the polarization system undergoes a temperature-dependent collapse under acute stress.

  2. [Acute low tone sensorineural hearing loss caused by inner ear barotrauma].

    PubMed

    Abe, T; Sasamori, S; Oikawa, T; Aigami, T; Endo, Y; Matsuki, C

    1989-09-01

    Three cases of inner ear barotrauma with subjective symptoms and hearing impairment which were similar to the low tone sudden deafness were reported. Case 1 was a 34-year-old man who developed a hearing loss in the next morning of taking an airplane and recovered four days after. Case 2 was a 42-year-old man who developed a hearing loss 2 days after flying in an airplane and hearing loss have recurred 4 times in his right ear for 3 months. Eight months after recovery of previous recurrent attack, a hearing loss occurred in his left ear without flying and recurred twice for 3 weeks. Case 3 was a 25-year-old woman who developed a hearing loss in the right ear after 24 meter depth scuba diving and recurred 4 times for 40 days. Those three patients complained of no vertigo at any attacks and were treated conservatively. From previous reports and the onset and the course of hearing disturbance, acute low tone sensorineural hearing loss in case 1 and case 2 was thought to be caused by circulatory disturbance of the inner ear and in case 3 thought to be caused by inner ear window rupture. But, endolymphatic hydrops was also needed to be take into account in those three cases as a common possible cause. Inner ear barotrauma and so called labyrinthine window rupture were considered to be one of the diseases needed to differentiate from low tone sudden deafness without reference to mono-attack type or recurrent type.

  3. 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.

  4. 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

  5. Acute effects of oxygen administration on transmural pulmonary artery pressure in obstructive sleep apnea.

    PubMed

    Marrone, O; Bellia, V; Pieri, D; Salvaggio, A; Bonsignore, G

    1992-04-01

    In order to investigate the role of hypoxia on the cyclic oscillation of transmural pulmonary artery pressure (PAP) in obstructive sleep apnea, oxygen was administered during one half of the night to six patients affected by obstructive sleep apnea syndrome during a nocturnal polysomnographic study. In each patient, transmural PAP measurements were performed on 15 randomly selected apneas recorded while breathing room air, and on 15 during O2 administration. During O2 administration in all patients, apneas were associated with a higher oxyhemoglobin saturation (SaO2), a smaller SaO2 swing, and a higher transcutaneous PCO2. The mean highest level of transmural PAP in the apneic episodes, commonly reached at their end, was significantly lower than while breathing room air in only two patients; however, due to a decrease in the mean lowest PAP level (at the beginning of apneas), the extent of the PAP increase within apneas did not differ between air and O2 breathing; these patients showed the smallest increase in transcutaneous PCO2 in our sample. End-apneic transmural PAP during O2 administration was significantly higher in one subject (for systolic values) and was not significantly different in the remaining three subjects. The extent of the increase in transmural PAP within apneas was greater in one patient; it was smaller in another one, but only for the diastolic values; and it did not differ significantly with respect to the value observed while breathing room air in all of the other subjects. The results suggest that hypoxia in obstructive apneas, at least in some patients, may lead to a steady increase in PAP, detectable both at the beginning and at the end of the episodes; conversely, the increase in PAP within apneas does not seem to be influenced by the simultaneous decrease in SaO2. PMID:1555416

  6. Neurobiological consequences of sleep deprivation.

    PubMed

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

    2013-05-01

    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.

  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. 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

  9. Acute vision loss and choroidal filling delay in the absence of giant-cell arteritis

    PubMed Central

    Bei, Ling; Lee, Iris; Lee, Michael S; Van Stavern, Greg P; McClelland, Collin M

    2016-01-01

    Giant-cell arteritis (GCA) is a visually devastating disease that often progresses to severe bilateral vision loss if untreated. Diagnosis of GCA is made challenging by the protean nature of the disease and the lack of a simple test that is both highly sensitive and specific. Choroidal filling delay on fluorescein angiography (FA) has been touted as a highly characteristic feature of GCA-related vision loss, although knowledge of both the sensitivity and specificity of this finding remains unproven. We report our experience of delayed choroidal filling on FA in a series of seven patients referred to an academic neuro-ophthalmology practice due to concern for GCA. Despite the FA findings, our examination, diagnostic testing, and long-term follow-up excluded the diagnosis of GCA in all cases, suggesting that choroidal perfusion abnormalities may occur in the absence of GCA. When evaluating a patient for acute vision loss, the astute clinician must remain cognizant of the limitations of FA in the diagnosis of GCA.

  10. 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

  11. Acute vision loss and choroidal filling delay in the absence of giant-cell arteritis

    PubMed Central

    Bei, Ling; Lee, Iris; Lee, Michael S; Van Stavern, Greg P; McClelland, Collin M

    2016-01-01

    Giant-cell arteritis (GCA) is a visually devastating disease that often progresses to severe bilateral vision loss if untreated. Diagnosis of GCA is made challenging by the protean nature of the disease and the lack of a simple test that is both highly sensitive and specific. Choroidal filling delay on fluorescein angiography (FA) has been touted as a highly characteristic feature of GCA-related vision loss, although knowledge of both the sensitivity and specificity of this finding remains unproven. We report our experience of delayed choroidal filling on FA in a series of seven patients referred to an academic neuro-ophthalmology practice due to concern for GCA. Despite the FA findings, our examination, diagnostic testing, and long-term follow-up excluded the diagnosis of GCA in all cases, suggesting that choroidal perfusion abnormalities may occur in the absence of GCA. When evaluating a patient for acute vision loss, the astute clinician must remain cognizant of the limitations of FA in the diagnosis of GCA. PMID:27695279

  12. 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.

  13. 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

  14. 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.

  15. 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

  16. 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.

  17. 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

  18. Increased loss and decreased synthesis of hepatic glutathione after acute ethanol administration. Turnover studies.

    PubMed Central

    Speisky, H; MacDonald, A; Giles, G; Orrego, H; Israel, Y

    1985-01-01

    The effect of acute ethanol administration on rates of synthesis and utilization of hepatic glutathione (GSH) was studied in rats after a pulse of [35S]cysteine. A 35% decrease in hepatic GSH content 5h after administration of 4 g of ethanol/kg body wt. was accompanied by a 33% increase in the rate of GSH utilization. The decrease occurred without increases in hepatic oxidized glutathione (GSSG) or in the GSH/GSSG ratio. The rate of non-enzymic condensation of GSH with acetaldehyde could account for only 6% of the rate of hepatic GSH disappearance. The increased loss of [35S]GSH induced by ethanol was not accompanied by an increased turnover; rather, a 30% inhibition of GSH synthesis balanced the increased rate of loss, leaving the turnover rate unchanged. The rate of acetaldehyde condensation with cysteine in vitro occurred at about one-third of the rate of GSH loss in ethanol-treated animals. However, ethanol induced only a minor decrease in liver cysteine content, which did not precede, but followed, the decrease in GSH. The characteristics of 2-methylthiazolidine-4-carboxylic acid, the condensation product between acetaldehyde and cysteine, were studied and methodologies were developed to determine its presence in tissues. It was not found in the liver of ethanol-treated animals. Ethanol administration led to a marked increase (47%) in plasma GSH in the post-hepatic inferior vena cava, but not in its pre-hepatic segment. Data suggest that an increased loss of GSH from the liver constitutes an important mechanism for the decrease in GSH induced by ethanol. In addition, an inhibition of GSH synthesis is observed. PMID:3977847

  19. Factors affecting loss of tympanic membrane mobility in acute otitis media model of chinchilla.

    PubMed

    Guan, Xiying; Chen, Yongzheng; Gan, Rong Z

    2014-03-01

    Recently we reported that middle ear pressure (MEP), middle ear effusion (MEE), and ossicular changes each contribute to the loss of tympanic membrane (TM) mobility in a guinea pig model of acute otitis media (AOM) induced by Streptococcus pneumoniae (Guan and Gan, 2013). However, it is not clear how those factors vary along the course of the disease and whether those effects are reproducible in different species. In this study, a chinchilla AOM model was produced by transbullar injection of Haemophilus influenzae. Mobility of the TM at the umbo was measured by laser vibrometry in two treatment groups: 4 days (4D) and 8 days (8D) post inoculation. These time points represent relatively early and later phases of AOM. In each group, the vibration of the umbo was measured at three experimental stages: unopened, pressure-released, and effusion-removed ears. The effects of MEP and MEE and middle ear structural changes were quantified in each group by comparing the TM mobility at one stage with that of the previous stage. Our findings show that the factors affecting TM mobility do change with the disease time course. The MEP was the dominant contributor to reduction of TM mobility in 4D AOM ears, but showed little effect in 8D ears when MEE filled the tympanic cavity. MEE was the primary factor affecting TM mobility loss in 8D ears, but affected the 4D ears only at high frequencies. After the release of MEP and removal of MEE, residual loss of TM mobility was seen mainly at low frequencies in both 4D and 8D ears, and was associated with middle ear structural changes. Our findings establish that the factors contributing to TM mobility loss in the chinchilla ear were similar to those we reported previously for the guinea pig ears with AOM. Outcomes did not appear to differ between the two major bacterial species causing AOM in these animal models.

  20. 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

  1. Effect of edaravone on acute brainstem-cerebellar infarction with vertigo and sudden hearing loss.

    PubMed

    Inoue, Yuta; Yabe, Takao; Okada, Kazunari; Nakamura, Yuka

    2014-06-01

    We report 2 cases with acute brainstem and brainstem-cerebellar infarction showed improvement of their signs and symptoms after administration of edaravone. Case 1, a 74-year-old woman who experienced sudden vertigo, also had dysarthria and left hemiplegia. Magnetic resonance imaging (MRI) showed an abnormal region in the right ventrolateral medulla oblongata. The patient's vertigo and hemiplegia improved completely after treatment. Case 2, a 50-year-old man who experienced sudden vertigo and sensorineural hearing loss (SNHL), developed dysarthria after admission. MRI revealed acute infarction in the right cerebellar hemisphere. Magnetic resonance angiography revealed dissection of the basilar artery and occlusion of the right anterior inferior cerebellar artery. The patient's vertigo and hearing remarkably improved. We have described 2 patients whose early symptoms were vertigo and sudden SNHL, but who were later shown to have ischemic lesions of the central nervous system. Edaravone is neuroprotective drug with free radical-scavenging actions. Free radicals in the ear are responsible for ischemic damage. Edaravone, a free radical scavenger, may be useful in the treatment of vertigo and SNHL.

  2. Acute effect of rheopheresis on peripheral endothelial dysfunction in patients suffering from sudden hearing loss.

    PubMed

    Balletshofer, Bernd M; Stock, Jan; Rittig, Kilian; Lehn-Stefan, Angela; Braun, Norbert; Burkart, Frank; Plontke, Stefan; Klingel, Reinhard; Häring, Hans-Ulrich

    2005-10-01

    Single low density lipoprotein (LDL) fibrinogen apheresis has shown beneficial effects in the treatment of patients with sudden sensorineural hearing loss (SSHL). Pathophysiologically, a microcirculatory disorder of the inner ear, probably caused by disturbed endothelial function, is discussed as a final common pathway of a variety of SSHL etiologies. Thus, we carried out a prospective pilot study on the efficacy of Rheopheresis on vascular function in these patients, embedded into an ongoing randomized controlled multicenter trial investigating the efficacy of Rheopheresis for the treatment of SSHL. Potential modulation of systemic endothelial dysfunction by Rheopheresis was examined by measuring flow-associated vasodilatation of the brachial artery (according to the criteria of the American College of Cardiology) in a small group of patients suffering from SSHL (N=6, 5m/1f, mean age 56+/-11 years) within the last 3 days. At baseline, five of the six patients with acute hearing loss showed endothelial dysfunction as evidenced by diminished flow-mediated vasodilatation (FMD<5%). After a single Rheopheresis treatment, flow-mediated vasodilatation improved significantly (from 3.9+/-3.6% to 7.2+/-2.4%, P=0.05, mean+/-SD, two-sided paired T-test). This was paralleled by a reduction in fibrinogen (364+/-216 mg/dL to 142+/-96 mg/dL, P=0.03), total cholesterol (228+/-23 to 98+/-10, P<0.0001) and LDL cholesterol levels (153+/-8 mg/dL to 83+/-23 mg/dL, P<0.01). Based on this case series we conclude that single Rheopheresis treatment might have an acute beneficial effect on endothelial dysfunction in patients suffering from SSHL.

  3. Acute Effects of Self-Selected Regimen of Rapid Body Mass Loss in Combat Sports Athletes

    PubMed Central

    Timpmann, Saima; Ööpik, Vahur; Pääsuke, Mati; Medijainen, Luule; Ereline, Jaan

    2008-01-01

    The purpose of the study was to assess the acute effects of the self-selected regimen of rapid body mass loss (RBML) on muscle performance and metabolic response to exercise in combat sports athletes. Seventeen male athletes (20.8 ± 1.0 years; mean ± SD) reduced their body mass by 5.1 ± 1.1% within 3 days. The RBML was achieved by a gradual reduction of energy and fluid intake and mild sauna procedures. A battery of tests was performed before (Test 1) and immediately after (Test 2) RBML. The test battery included the measurement of the peak torque of knee extensors for three different speeds, assessment of total work (Wtot) performed during a 3-min intermittent intensity knee extension exercise and measurements of blood metabolites (ammonia, lactate, glucose and urea). Absolute peak torque was lower in Test 2 compared with Test 1 at angular velocities of 1.57 rad·s-1 (218.6 ± 40.9 vs. 234.4 ± 42.2 N·m; p = 0.013) and 3.14 rad·s-1 (100.3 ± 27.8 vs. 111.7 ± 26.2 N·m; p = 0.008). The peak torque in relation to body mass remained unchanged for any speed. Absolute Wtot was lower in Test 2 compared with Test 1 (6359 ± 2326 vs. 7452 ± 3080 J; p = 0.003) as well as Wtot in relation to body mass (89.1 ± 29.9 vs. 98.6 ± 36.4 J·kg-1; p = 0.034), respectively. As a result of RBML, plasma urea concentration increased from 4.9 to 5.9 mmol·l-1 (p = 0.003). The concentration of ammonia in a post-test sample in Test 2 tended to be higher in comparison with Test 1 (80.9 ± 29.1 vs. 67.6 ± 26.5 mmol·l-1; p = 0.082). The plasma lactate and glucose responses to exercise were similar in Test 1 and Test 2. We conclude that the self-selected regimen of RBML impairs muscle performance in 3-min intermittent intensity exercise and induces an increase in blood urea concentration in experienced male combat sports athletes. Key pointsPrevious studies have revealed a negative effect of rapid body mass loss on performance. However, there are some performance characteristics

  4. Acute changes in sleep duration on eating behaviors and appetite-regulating hormones in overweight/obese adults

    PubMed Central

    Hart, Chantelle N.; Carskadon, Mary A.; Demos, Kathryn E.; Van Reen, Eliza; Sharkey, Katherine M.; Raynor, Hollie A.; Considine, Robert V.; Jones, Richard N.; Wing, Rena R.

    2015-01-01

    There is considerable interest in the role of sleep in weight regulation, yet few studies have examined this relationship in overweight/obese (OW/OB) adults. Using a within-subject, counterbalanced design, 12 OW/OB women were studied in lab with two nights of short (5 hours time in bed [TIB]) and two nights of long (9 hours TIB) sleep. Hunger, consumption at a buffet, and fasting hormone levels were obtained. Significant polysomnographic differences occurred between conditions in total sleep time and sleep architecture (p's < .001). Percent energy from protein at the buffet increased following short sleep. No differences were observed for total energy intake or measured hormones. Further research is needed to determine how lengthening sleep impacts weight regulation in OW/OB adults. PMID:25105727

  5. Acute Myeloid Leukemia Relapse Presenting as Complete Monocular Vision Loss due to Optic Nerve Involvement

    PubMed Central

    2016-01-01

    Acute myeloid leukemia (AML) involvement of the central nervous system is relatively rare, and detection of leptomeningeal disease typically occurs only after a patient presents with neurological symptoms. The case herein describes a 48-year-old man with relapsed/refractory AML of the mixed lineage leukemia rearrangement subtype, who presents with monocular vision loss due to leukemic eye infiltration. MRI revealed right optic nerve sheath enhancement and restricted diffusion concerning for nerve ischemia and infarct from hypercellularity. Cerebrospinal fluid (CSF) analysis showed a total WBC count of 81/mcl with 96% AML blasts. The onset and progression of visual loss were in concordance with rise in peripheral blood blast count. A low threshold for diagnosis of CSF involvement should be maintained in patients with hyperleukocytosis and high-risk cytogenetics so that prompt treatment with whole brain radiation and intrathecal chemotherapy can be delivered. This case suggests that the eye, as an immunoprivileged site, may serve as a sanctuary from which leukemic cells can resurge and contribute to relapsed disease in patients with high-risk cytogenetics. PMID:27668104

  6. Acute Myeloid Leukemia Relapse Presenting as Complete Monocular Vision Loss due to Optic Nerve Involvement

    PubMed Central

    2016-01-01

    Acute myeloid leukemia (AML) involvement of the central nervous system is relatively rare, and detection of leptomeningeal disease typically occurs only after a patient presents with neurological symptoms. The case herein describes a 48-year-old man with relapsed/refractory AML of the mixed lineage leukemia rearrangement subtype, who presents with monocular vision loss due to leukemic eye infiltration. MRI revealed right optic nerve sheath enhancement and restricted diffusion concerning for nerve ischemia and infarct from hypercellularity. Cerebrospinal fluid (CSF) analysis showed a total WBC count of 81/mcl with 96% AML blasts. The onset and progression of visual loss were in concordance with rise in peripheral blood blast count. A low threshold for diagnosis of CSF involvement should be maintained in patients with hyperleukocytosis and high-risk cytogenetics so that prompt treatment with whole brain radiation and intrathecal chemotherapy can be delivered. This case suggests that the eye, as an immunoprivileged site, may serve as a sanctuary from which leukemic cells can resurge and contribute to relapsed disease in patients with high-risk cytogenetics.

  7. Mechanisms of tympanic membrane and incus mobility loss in acute otitis media model of guinea pig.

    PubMed

    Guan, Xiying; Gan, Rong Z

    2013-06-01

    Acute otitis media (AOM) is a rapid infection of middle ear due to bacterial or viral invasion. The infection commonly leads to negative pressure and purulent effusion in the middle ear. To identify how these changes affect tympanic membrane (TM) mobility or sound transmission through the middle ear, we hypothesize that pressure, effusion, and structural changes of the middle ear are the main mechanisms of conductive hearing loss in AOM. To test the hypothesis, a guinea pig AOM model was created by injection of Streptococcus pneumoniae. Three days post inoculation, vibration of the TM at umbo in response to input sound in the ear canal was measured at three experimental stages: intact, pressure-released, and effusion-drained AOM ears. The vibration of the incus tip was also measured after the effusion was removed. Results demonstrate that displacement of the TM increased mainly at low frequencies when pressure was released. As the effusion was removed, the TM mobility increased further but did not reach the level of the normal ear at low frequencies. This was caused by middle ear structural changes or adhesions on ossicles in AOM. The structural changes also affected movement of the incus at low and high frequencies. The results provide new evidence for understanding the mechanism of conductive hearing loss in AOM. PMID:23483330

  8. A case of cerebral venous thrombosis presenting as acute reversible visual loss: a rarely reported association.

    PubMed

    Ray, Sayantan; Khanra, Dibbendhu; Sonthalia, Nikhil; Saha, Manjari; Talukdar, Arunansu

    2013-07-01

    Cerebral venous sinus thrombosis (CVST) is not an uncommon cause of stroke but very often unrecognized at initial presentation due to lack of clinical suspicion and thus frequently left untreated. CVST is a potentially serious condition which manifests with diverse clinical manifestations, from isolated headache to focal neurological signs and even coma. CVST usually takes place either an inherited thrombophilia or any acquired hyperviscosity state and thus prompting anticoagulation was regimen as is the cornerstone of successful treatment. We describe a 47-year-old woman who presented with recurrent bouts of vomiting in the post-operative period and later developed cortical blindness and asymmetric limb weakness. Magnetic resonance imaging (MRI) showed hyperintensity involving bilateral parieto-occipital corticomedullary junction. MR venography showed signal void in the superior sagittal sinus. She was diagnosed as CVST and achieved complete recovery with anticoagulation therapy. Bilateral occipital infarction as a consequence of cerebral venous thrombosis is a rare cause of visual loss. Thrombosis in the superior sagittal sinus was related to her cortical blindness and weakness. This case illustrates that cerebral venous thrombosis should be considered in cases of occipital vascular lesions leading to acute painless loss of vision prompting anticoagulation therapy which can improve the outcome significantly. Dehydration could be considered as a risk factor for development of CVST in appropriate situations. PMID:25206031

  9. Acute Myeloid Leukemia Relapse Presenting as Complete Monocular Vision Loss due to Optic Nerve Involvement.

    PubMed

    Patel, Shyam A

    2016-01-01

    Acute myeloid leukemia (AML) involvement of the central nervous system is relatively rare, and detection of leptomeningeal disease typically occurs only after a patient presents with neurological symptoms. The case herein describes a 48-year-old man with relapsed/refractory AML of the mixed lineage leukemia rearrangement subtype, who presents with monocular vision loss due to leukemic eye infiltration. MRI revealed right optic nerve sheath enhancement and restricted diffusion concerning for nerve ischemia and infarct from hypercellularity. Cerebrospinal fluid (CSF) analysis showed a total WBC count of 81/mcl with 96% AML blasts. The onset and progression of visual loss were in concordance with rise in peripheral blood blast count. A low threshold for diagnosis of CSF involvement should be maintained in patients with hyperleukocytosis and high-risk cytogenetics so that prompt treatment with whole brain radiation and intrathecal chemotherapy can be delivered. This case suggests that the eye, as an immunoprivileged site, may serve as a sanctuary from which leukemic cells can resurge and contribute to relapsed disease in patients with high-risk cytogenetics. PMID:27668104

  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

    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

  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 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

  12. 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.

  13. Thermogenic effect of an acute ingestion of a weight loss supplement

    PubMed Central

    Hoffman, Jay R; Kang, Jie; Ratamess, Nicholas A; Rashti, Stefanie L; Tranchina, Christopher P; Faigenbaum, Avery D

    2009-01-01

    Background The purpose of this study was to examine the acute effects of a weight loss supplement on resting oxygen uptake (VO2), respiratory quotient (RQ), caloric expenditure (kcal), heart rate (HR), and blood pressure (BP) in healthy and physically active individuals. Methods Ten subjects (5 male, 5 female; 20.2 ± 1.2 y; 172.2 ± 8.9 cm; 71.5 ± 17.2 kg; 17.3 ± 2.6% body fat) underwent two testing sessions administered in a randomized and double-blind fashion. During each session, subjects reported to the Human Performance Laboratory after at least 3-h post-absorptive state and were provided either 3 capsules of the weight loss supplement (SUP), commercially marketed as Meltdown® or 3 capsules of a placebo (P). Subjects then rested in a semi-recumbent position for three hours. VO2 and HR were determined every 5 min during the first 30 min and every 10 min during the next 150 min. BP was determined every 15 min during the first 30 min and every 30 min thereafter. The profile of mood states was assessed every 30 min. Results Area under the curve analysis revealed a significant 28.9% difference in VO2 between SUP and P for the three hour study period. In addition, a significant difference in energy expenditure was also seen between SUP (1.28 ± 0.33 kcal·min-1) and P (1.00 ± 0.32 kcal·min-1). A trend (p = 0.06) towards a greater utilization of stored fat as an energy source was also demonstrated (0.78 ± 0.23 kcal·min-1 and 0.50 ± 0.38 kcal·min-1 in P and SUP, respectively). Significant elevations in HR were seen during hours two and three of the study, and significantly higher average systolic BP was observed between SUP (118.0 ± 7.3 mmHg) and P (111.4 ± 8.2 mmHg). No significant differences were seen in diastolic blood pressure at any time point. Significant increases in tension and confusion were seen in SUP. Conclusion Results indicate a significant increase in energy expenditure in young, healthy individuals following an acute ingestion of a weight

  14. 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

  15. 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

  16. 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

  17. 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.

  18. Loss of n-6 fatty acid induced pediatric obesity protects against acute murine colitis

    PubMed Central

    Nagy-Szakal, Dorottya; Mir, Sabina A. V.; Harris, R. Alan; Dowd, Scot E.; Yamada, Takeshi; Lacorazza, H. Daniel; Tatevian, Nina; Smith, C. Wayne; de Zoeten, Edwin F.; Klein, John; Kellermayer, Richard

    2015-01-01

    Dietary influences may affect microbiome composition and host immune responses, thereby modulating propensity toward inflammatory bowel diseases (IBDs): Crohn disease (CD) and ulcerative colitis (UC). Dietary n-6 fatty acids have been associated with UC in prospective studies. However, the critical developmental period when (n-6) consumption may induce UC is not known. We examined the effects of transiently increased n-6 consumption during pediatric development on subsequent dextran-sulfate-sodium (DSS)-induced acute murine colitis. The animals transiently became obese then rapidly lost this phenotype. Interestingly, mice were protected against DSS colitis 40 days after n-6 consumption. The transient high n-6-induced protection against colitis was fat type- and dietary reversal-dependent and could be transferred to germ-free mice by fecal microbiota transplantation. We also detected decreased numbers of chemokine receptor (Cxcr)5+ CD4+ T cells in the mesenteric lymph nodes (MLNs) of transiently n-6-fed mice. Further experiments revealed that anti-chemokine ligand (Cxcl)13 (the ligand of Cxcr5) antibody treatment decreased DSS colitis severity, implicating the importance of the Cxcr5-Cxcl13 pathway in mammalian colitis. Consecutively, we found elevated CXCL13 concentrations (CD: 1.8-fold, P = 0.0077; UC: 1.9-fold, P = 0.056) in the serum of untreated pediatric IBD patients. The human serologic observations supported the translational relevance of our findings.—Nagy-Szakal, D., Mir, S. A. V., Harris, R. A., Dowd, S. E., Yamada, T., Lacorazza, H. D., Tatevian, N., Smith, C. W., de Zoeten, E. F., Klein, J., Kellermayer, R. Loss of n-6 fatty acid induced pediatric obesity protects against acute murine colitis. PMID:25903104

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

    PubMed Central

    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

  20. 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

  1. Association of loss of heterozygosity with cytogenetic abnormalities in acute myeloid leukemia and myelodysplastic syndrome.

    PubMed

    Pinheiro, R F; Serio, F M; Silva, M R R; Briones, M R S; Chauffaille, M L L F

    2008-07-01

    Deletions on chromosomes 5 and 7 are frequently seen in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). It is assumed that these deletions indicate loss of tumor suppressor genes on these chromosomes and until these tumor suppressor genes are identified, the functional consequences of these deletions and the molecular basis of these myeloid disorders cannot be completely understood. We evaluated loss of heterozygosity (LOH) in 44 patients (18 MDS and 26 AML, diagnosed according to WHO classification criteria) at diagnosis, using a four-microsatellite marker panel: an intragenic marker on the 7th intron of gene IRF-1 of the 5q31.1 region and three markers located inside the 7q31.1 region and correlated the LOH with karyotype abnormalities. The microsatellites chosen corresponded to chromosome regions frequently deleted in MDS/AML. The samples with Q (peak area) less than or equal to 0.50 were indicative of LOH. The percent of informative samples (i.e., heterozygous) for the intragenic microsatellite in gene IRF-1 and in loci D7S486, D7S515 and D7S522 were 66.6, 73.7, 75.5, and 48.8%, respectively. Cytogenetic abnormalities by G-banding were found in 36% (16/44) of the patients (2 of 18 MDS and 14 of 26 AML patients). We found a significantly positive association of the occurrence of LOH with abnormal karyotype (P < 0.05; chi-square test) and there were cases with LOH but the karyotype was normal (by G-banding). These data indicate that LOH in different microsatellite markers is possibly an event previous to chromosomal abnormalities in these myeloid neoplasias.

  2. 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

  3. 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 ...

  4. 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

  5. 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

  6. GABAergic inhibition of histaminergic neurons regulates active waking but not the sleep-wake switch or propofol-induced loss of consciousness.

    PubMed

    Zecharia, Anna Y; Yu, Xiao; Götz, Thomas; Ye, Zhiwen; Carr, David R; Wulff, Peer; Bettler, Bernhard; Vyssotski, Alexei L; Brickley, Stephen G; Franks, Nicholas P; Wisden, William

    2012-09-19

    The activity of histaminergic neurons in the tuberomammillary nucleus (TMN) of the hypothalamus correlates with an animal's behavioral state and maintains arousal. We examined how GABAergic inputs onto histaminergic neurons regulate this behavior. A prominent hypothesis, the "flip-flop" model, predicts that increased and sustained GABAergic drive onto these cells promotes sleep. Similarly, because of the histaminergic neurons' key hub-like place in the arousal circuitry, it has also been suggested that anesthetics such as propofol induce loss of consciousness by acting primarily at histaminergic neurons. We tested both these hypotheses in mice by genetically removing ionotropic GABA(A) or metabotropic GABA(B) receptors from histidine decarboxylase-expressing neurons. At the cellular level, histaminergic neurons deficient in synaptic GABA(A) receptors were significantly more excitable and were insensitive to the anesthetic propofol. At the behavioral level, EEG profiles were recorded in nontethered mice over 24 h. Surprisingly, GABAergic transmission onto histaminergic neurons had no effect in regulating the natural sleep-wake cycle and, in the case of GABA(A) receptors, for propofol-induced loss of righting reflex. The latter finding makes it unlikely that the histaminergic TMN has a central role in anesthesia. GABA(B) receptors on histaminergic neurons were dispensable for all behaviors examined. Synaptic inhibition of histaminergic cells by GABA(A) receptors, however, was essential for habituation to a novel environment.

  7. [Normal and disordered sleep].

    PubMed

    Arnulf, I

    2007-07-01

    Normal sleep is a complex and reversible state of brain functioning, including reduced inputs and outputs, blunted reflexes, and metabolic and cognitive changes. Evidence supports a role for sleep in the consolidation of an array of learning and memory tasks. Sleep deprivation and fragmentation result in executive dysfunction, increased appetite/weight and cellular stress. Sleep is a vital, complex but plastic function that can be modulated depending on individual heritage and motivation. The major role of sleep in attention and memory raises about concern the reduction in sleep duration recently pointed in teenagers and young adults. Sleep disorders are numerous and various. Their mechanism is not always identified, but may result from a central dysfunction in sleep-wake (e.g. narcolepsy) or circadian (e.g. advanced sleep phase syndrome) systems, from the sleep-related loss of compensation of reflexes normally effective during wakefulness (breathing is the most vulnerable function during sleep), or from other diseases preventing sleep (e.g. psychiatric insomnia, restless legs syndrome). PMID:17652992

  8. 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.

  9. Postural responses without versus with acute external cervical spine fixation: a comparative study in healthy subjects and patients with acute unilateral vestibular loss.

    PubMed

    Bohne, Silvia; Heine, Sabrina; Volk, G Fabian; Stadler, Joachim; Guntinas-Lichius, Orlando

    2013-01-01

    Using a diagnostic prospective cohort single center study design, the influence of a cervical collar on standing balance during dynamic postural perturbations in healthy adults and patients with acute unilateral vestibular dysfunction was measured in 31 healthy subjects and 27 patients with acute unilateral vestibular loss. The main outcome measures were completed standard protocols on the Sensory Organization Test (SOT) and Motor Control Test (MCT) of the NeuroCom Equitest(®) computerized posturography platform measured without and with acute cervical fixation, respectively. Paired t test showed no significant difference during the six conditions of neither the SOT scores nor analyzing the SOT strategies or during the MCT between the non-fixed and fixed neck in healthy subjects and in the patients (all p > 0.05). Older healthy subjects showed decreased SOT scores but equal MCT results. The age effect was more dominant in the patients when wearing the collar. Gender had no influence whether in healthy individuals nor in patients. In almost all conditions of the SOT but only in some MCT subtests patients had significantly lower scores than healthy subjects without collar and with collar (all p < 0.05). In conclusion, the SOT but only some subtest of the MCT could clearly distinguish between healthy adults and patient with acute unilateral vestibular loss. Equilibrium scores did not change significantly when the cervical spine was fixed with a collar. Acute fixation of the neck with a collar seems not to affect standing balance, even not when vestibular, visual and/or somatosensory input are also reduced. PMID:22237759

  10. 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

  11. The negative impact of being underweight and weight loss on survival of children with acute lymphoblastic leukemia.

    PubMed

    den Hoed, Marissa A H; Pluijm, Saskia M F; de Groot-Kruseman, Hester A; te Winkel, Mariël L; Fiocco, Martha; van den Akker, Erica L T; Hoogerbrugge, Peter; van den Berg, Henk; Leeuw, Jan A; Bruin, Marrie C A; Bresters, Dorine; Veerman, Anjo J P; Pieters, Rob; van den Heuvel-Eibrink, Marry M

    2015-01-01

    Body mass index and change in body mass index during treatment may influence treatment outcome of pediatric patients with acute lymphoblastic leukemia. However, previous studies in pediatric acute lymphoblastic leukemia reported contradictory results. We prospectively collected data on body composition from a cohort of newly diagnosed Dutch pediatric patients with acute lymphoblastic leukemia (n=762, age 2-17 years). Patients were treated from 1997-2004 and the median follow-up was 9 years (range, 0-10). Body mass index at diagnosis was expressed as age- and gender-matched standard deviation scores and on the basis of these scores the patients were categorized as being underweight, of normal weight or overweight. Multivariate analyses showed that patients who were underweight (8%) had a higher risk of relapse [hazard ratio: 1.88, 95% confidence interval (1.13-3.13)], but similar overall survival and event-free survival as patients who had a normal weight or who were overweight. Patients with loss of body mass index during the first 32 weeks of treatment had a similar risk of relapse and event-free survival, but decreased overall survival [hazard ratio: 2.10, 95% confidence interval (1.14-3.87)] compared to patients without a loss of body mass index. In addition, dual X-ray absorptiometry scans were performed in a nested, single-center cohort. Data from these scans revealed that a loss of body mass consisted mainly of a loss of lean body mass, while there was a gain in the percentage of fat. In conclusion, being underweight at diagnosis is a risk factor for relapse, and a decrease in body mass index early during treatment is associated with decreased survival. In addition, loss of body mass during treatment seems to consist mainly of a loss of lean body mass. This study was approved by the Medical Ethical Committee in 1996 (trial number NTR460/SNWLK-ALL-9).

  12. Sensorineural hearing loss: a complication of acute otitis media in adults.

    PubMed

    Park, Joo Hyun; Park, Sung Joon; Kim, Young Ho; Park, Min-Hyun

    2014-07-01

    We aim to evaluate the incidence and clinical manifestations of sensorineural hearing loss (SNHL) in adult patients with acute otitis media (AOM). Seventy-five patients (age > 18 years; 83 ears) diagnosed with AOM between January 2008 and March 2011 at our clinic were enroled and retrospectively reviewed. We detected audiometrically confirmed SNHL during the course of AOM in eight patients. The clinical course, treatment, and audiometric final outcome of each case were reviewed. SNHL was associated with AOM in 8 out of 83 ears (9.3%). The mean age of patients was 57.5 years, and the mean follow-up period was 21.1 months (range 0.6-46.3 months). The most common symptom was tinnitus. Mean bone conduction hearing threshold was 39.5 dB in pure tone audiometry. All patients showed high-frequency HL, and three showed pan-frequency HL. All patients were treated with oral antibiotics at the initial visit. Seven ears were treated with a combination of oral steroids. Myringotomy was also performed. Seven of eight patients showed improvement; however, 8 kHz thresholds were not improved. This suggested that the inflammation spread through the round window. The mean duration of recovery was 18.6 days. SNHL associated with AOM in adult patients occurs during the early phases of the disease course. High-frequency hearing was commonly affected and was well treated with oral antibiotics, myringotomy, and steroid therapy. Audiometry can be helpful for treating adult patients with AOM. Active treatment, including myringotomy, should be performed during the early phase, if SNHL is suspected. PMID:23990061

  13. 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…

  14. 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 - ...

  15. 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 ...

  16. Neurocognitive Consequences of Sleep Deprivation

    PubMed Central

    Goel, Namni; Rao, Hengyi; Durmer, Jeffrey S.; Dinges, David F.

    2012-01-01

    Sleep deprivation is associated with considerable social, financial, and health-related costs, in large measure because it produces impaired cognitive performance due to increasing sleep propensity and instability of waking neurobehavioral functions. Cognitive functions particularly affected by sleep loss include psychomotor and cognitive speed, vigilant and executive attention, working memory, and higher cognitive abilities. Chronic sleep-restriction experiments—which model the kind of sleep loss experienced by many individuals with sleep fragmentation and premature sleep curtailment due to disorders and lifestyle—demonstrate that cognitive deficits accumulate to severe levels over time without full awareness by the affected individual. Functional neuroimaging has revealed that frequent and progressively longer cognitive lapses, which are a hallmark of sleep deprivation, involve distributed changes in brain regions including frontal and parietal control areas, secondary sensory processing areas, and thalamic areas. There are robust differences among individuals in the degree of their cognitive vulnerability to sleep loss that may involve differences in prefrontal and parietal cortices, and that may have a basis in genes regulating sleep homeostasis and circadian rhythms. Thus, cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss. PMID:19742409

  17. 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

  18. 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

  19. 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

  20. 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

  1. 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

  2. Estimating individual optimal sleep duration and potential sleep debt

    PubMed Central

    Kitamura, Shingo; Katayose, Yasuko; Nakazaki, Kyoko; Motomura, Yuki; Oba, Kentaro; Katsunuma, Ruri; Terasawa, Yuri; Enomoto, Minori; Moriguchi, Yoshiya; Hida, Akiko; Mishima, Kazuo

    2016-01-01

    In this study, we hypothesized that dynamics of sleep time obtained over consecutive days of extended sleep in a laboratory reflect an individual’s optimal sleep duration (OSD) and that the difference between OSD and habitual sleep duration (HSD) at home represents potential sleep debt (PSD). We found that OSD varies among individuals and PSD showed stronger correlation with subjective/objective sleepiness than actual sleep time, interacting with individual’s vulnerability of sleep loss. Furthermore, only 1 h of PSD takes four days to recover to their optimal level. Recovery from PSD was also associated with the improvement in glycometabolism, thyrotropic activity and hypothalamic-pituitary-adrenocortical axis. Additionally, the increase (rebound) in total sleep time from HSD at the first extended sleep would be a simple indicator of PSD. These findings confirmed self-evaluating the degree of sleep debt at home as a useful clinical marker. To establish appropriate sleep habits, it is necessary to evaluate OSD, vulnerability to sleep loss, and sleep homeostasis characteristics on an individual basis. PMID:27775095

  3. 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.

  4. 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

  5. Cardiovascular physiology and sleep.

    PubMed

    Murali, Narayana S; Svatikova, Anna; Somers, Virend K

    2003-05-01

    effects of sleep could be objectively differentiated from the effects of rest and recumbency. Furthermore, the specific effects of sleep onset and termination, and the effects of different sleep stages, could be assessed. Technological advances, with consequently enhanced and relatively non-invasive approaches to cardiovascular regulation, have greatly broadened our understanding of the effects of sleep stage on cardiovascular function. Continuous monitoring of simultaneous measures of polysomnographic and cardiovascular variables enables characterization of the effects of dynamic changes and rapid transitions in sleep stage, such as arousals. The capacity for measuring acute and immediate changes in autonomic, EEG and hemodynamic responses to sleep and arousal on a continuous basis has played an important role in enabling us to understand the interplay between changes in EEG and changes in the more peripheral measurements of neural and circulatory variables, such as sympathetic nerve traffic, heart rate (HR) and blood pressure (BP). Measurements of heart rate variability (HRV) (8-10), baroreflex sensitivity (BRS) (11-16), and intraneural measurement of sympathetic nerve traffic to muscle (MSNA) (17-22) and skin (SSNA) (23-24) have further advanced our understanding of mechanisms linking sleep and cardiovascular physiology.

  6. 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

  7. 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.

  8. 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

  9. Sleep duration, sleep quality and body weight: parallel developments.

    PubMed

    Gonnissen, Hanne K J; Adam, Tanja C; Hursel, Rick; Rutters, Femke; Verhoef, Sanne P M; Westerterp-Plantenga, Margriet S

    2013-09-10

    The increase in obesity, including childhood obesity, has developed over the same time period as the progressive decrease in self-reported sleep duration. Since epidemiological studies showed an inverse relationship between short or disturbed sleep and obesity, the question arose, how sleep duration and sleep quality are associated with the development of obesity. In this review, the current literature on these topics has been evaluated. During puberty, changes in body mass index (BMI) are inversely correlated to changes in sleep duration. During adulthood, this relationship remains and at the same time unfavorable metabolic and neuro-endocrinological changes develop, that promote a positive energy balance, coinciding with sleep disturbance. Furthermore, during excessive weight loss BMI and fat mass decrease, in parallel, and related with an increase in sleep duration. In order to shed light on the association between sleep duration, sleep quality and obesity, until now it only has been shown that diet-induced body-weight loss and successive body-weight maintenance contribute to sleep improvement. It remains to be demonstrated whether body-weight management and body composition improve during an intervention concomitantly with spontaneous sleep improvement compared with the same intervention without spontaneous sleep improvement.

  10. 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

  11. 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.

  12. Recognising sleep apnoea

    PubMed Central

    How, Choon How; Hsu, Pon Poh; Tan, Kah Leong Alvin

    2015-01-01

    Most people spend a third of their lives sleeping, and thus, sleep has a major impact on all of us. As sleep is a function and not a structure, it is challenging to treat and prevent its complications. Sleep apnoea is one such complication, with serious and potentially life-threatening consequences. Local studies estimate that about 15% of Singapore’s population is afflicted with sleep apnoea. The resulting sleep fragmentation may result in poor quality of sleep, leading to daytime sleepiness. Sleep apnoea may also be the underlying cause of high blood pressure, memory loss, poor concentration and work performance, motor vehicle accidents, and marital problems. Evaluation involves a sleep study, followed by patient education, and an individualised step-wise management approach should be explored. Many patients will require follow-up for a long period of time, as management options may not offer a permanent cure; other contributory causes may arise at different phases of their lives, compounded by genetic and hormonal issues, ethnicity and the modern hazards of a fast-paced society. PMID:25820844

  13. Recognising sleep apnoea.

    PubMed

    How, C H; Hsu, P P; Tan, K L

    2015-03-01

    Most people spend a third of their lives sleeping, and thus, sleep has a major impact on all of us. As sleep is a function and not a structure, it is challenging to treat and prevent its complications. Sleep apnoea is one such complication, with serious and potentially life-threatening consequences. Local studies estimate that about 15% of Singapore's population is afflicted with sleep apnoea. The resulting sleep fragmentation may result in poor quality of sleep, leading to daytime sleepiness. Sleep apnoea may also be the underlying cause of high blood pressure, memory loss, poor concentration and work performance, motor vehicle accidents, and marital problems. Evaluation involves a sleep study, followed by patient education, and an individualised step-wise management approach should be explored. Many patients will require follow-up for a long period of time, as management options may not offer a permanent cure; other contributory causes may arise at different phases of their lives, compounded by genetic and hormonal issues, ethnicity and the modern hazards of a fast-paced society.

  14. Acute neurological visual loss in young adults: causes, diagnosis and management.

    PubMed

    Sawaya, R; El Ayoubi, N; Hamam, R

    2015-12-01

    Visual loss in the young adult can be caused by demyelinating diseases, inflammatory and autoimmune processes, infections, ischaemic events, and compressive lesions of the optic nerve. Diagnosis of the aetiologies of visual loss is reached by combining data from radiological studies, electrophysiological tests, and blood and cerebrospinal fluid analysis. Treatment is primarily aimed at decreasing the insult on the optic nerve and eventually controlling the primary disorder. The literature discusses separately the different aetiologies of visual loss. We present a review of the clinical characteristics of visual loss in the young adult, the different diagnostic measures, and the latest therapeutic strategies. The aim of this work is to summarise this entity in a practical way to guide clinicians in the diagnosis and management of this disorder. PMID:26504248

  15. The effects of acute stress exposure on striatal activity during Pavlovian conditioning with monetary gains and losses.

    PubMed

    Lewis, Andrea H; Porcelli, Anthony J; Delgado, Mauricio R

    2014-01-01

    Pavlovian conditioning involves the association of an inherently neutral stimulus with an appetitive or aversive outcome, such that the neutral stimulus itself acquires reinforcing properties. Across species, this type of learning has been shown to involve subcortical brain regions such as the striatum and the amygdala. It is less clear, however, how the neural circuitry involved in the acquisition of Pavlovian contingencies in humans, particularly in the striatum, is affected by acute stress. In the current study, we investigate the effect of acute stress exposure on Pavlovian conditioning using monetary reinforcers. Participants underwent a partial reinforcement conditioning procedure in which neutral stimuli were paired with high and low magnitude monetary gains and losses. A between-subjects design was used, such that half of the participants were exposed to cold stress while the remaining participants were exposed to a no stress control procedure. Cortisol measurements and subjective ratings were used as measures of stress. We observed an interaction between stress, valence, and magnitude in the ventral striatum, with the peak in the putamen. More specifically, the stress group exhibited an increased sensitivity to magnitude in the gain domain. This effect was driven by those participants who experienced a larger increase in circulating cortisol levels in response to the stress manipulation. Taken together, these results suggest that acute stress can lead to individual differences in circulating cortisol levels which influence the striatum during Pavlovian conditioning with monetary reinforcers.

  16. The effects of acute stress exposure on striatal activity during Pavlovian conditioning with monetary gains and losses

    PubMed Central

    Lewis, Andrea H.; Porcelli, Anthony J.; Delgado, Mauricio R.

    2014-01-01

    Pavlovian conditioning involves the association of an inherently neutral stimulus with an appetitive or aversive outcome, such that the neutral stimulus itself acquires reinforcing properties. Across species, this type of learning has been shown to involve subcortical brain regions such as the striatum and the amygdala. It is less clear, however, how the neural circuitry involved in the acquisition of Pavlovian contingencies in humans, particularly in the striatum, is affected by acute stress. In the current study, we investigate the effect of acute stress exposure on Pavlovian conditioning using monetary reinforcers. Participants underwent a partial reinforcement conditioning procedure in which neutral stimuli were paired with high and low magnitude monetary gains and losses. A between-subjects design was used, such that half of the participants were exposed to cold stress while the remaining participants were exposed to a no stress control procedure. Cortisol measurements and subjective ratings were used as measures of stress. We observed an interaction between stress, valence, and magnitude in the ventral striatum, with the peak in the putamen. More specifically, the stress group exhibited an increased sensitivity to magnitude in the gain domain. This effect was driven by those participants who experienced a larger increase in circulating cortisol levels in response to the stress manipulation. Taken together, these results suggest that acute stress can lead to individual differences in circulating cortisol levels which influence the striatum during Pavlovian conditioning with monetary reinforcers. PMID:24904331

  17. Lack of Sleep May Stretch Your Waistline

    MedlinePlus

    ... risks in today's society in which chronic sleep loss is becoming more common. More research is needed to investigate the importance of long-term, partial sleep deprivation as a risk factor for obesity and whether ...

  18. 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. ...

  19. 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 ...

  20. Links between the innate immune system and sleep.

    PubMed

    Majde, Jeannine A; Krueger, James M

    2005-12-01

    Sleep is a fundamental physiologic process with unknown functions. It is divided into 2 distinct states: non-rapid-eye-movement sleep and rapid-eye-movement sleep. After acute infection with nonneurotropic agents, there are stereotypic changes in non-rapid-eye-movement sleep, particularly increased time spent in slow-wave sleep, and often a reduction of time spent in rapid-eye-movement sleep. It is now recognized that both infection-associated sleep and spontaneous sleep are regulated, in part, by immune mediators called cytokines. This review provides brief tutorials on the elements of the innate immune system that detect infection, how sleep is characterized in the laboratory, issues regarding the interpretation of sleep effects on immune function, the interaction of sleep with circadian rhythms and stress, and some of the microbial products, cytokines, and neuropeptides associated with sleep regulation. We also summarize our current understanding of the role of sleep in host defense and asthma exacerbation.

  1. Metal and pharmaceutical mixtures: is ion loss the mechanism underlying acute toxicity and widespread additive toxicity in zebrafish?

    PubMed

    Alsop, Derek; Wood, Chris M

    2013-09-15

    The acute toxicities and mechanisms of action of a variety of environmental contaminants were examined using zebrafish larvae (Danio rerio; 4-8 days post fertilization). Toxic interactions were observed between metals. For example, the addition of a sublethal level of nickel (15% of the LC50, one third of the LC01) to all copper treatments decreased the copper 96 h LC50 by 58%, while sublethal copper exposure (6% of the copper LC50, 13% of the LC01) decreased the cadmium 96 h LC50 by 47%. Two predictive models were assessed, the concentration addition (CA) model, which assumes similar mechanisms of action, and the independent action (IA) model, which assumes different mechanisms of action. Quantitative comparisons indicated the CA model performed better than the IA model; the latter tended to underestimate combined toxicity to a greater extent. The effects of mixtures with nickel or ammonia were typically additive, while mixtures with copper or cadmium were typically greater than additive. Larvae exposed to cadmium, copper or nickel experienced whole body ion loss. Decreases were greatest for Na(+) followed by K(+) (as high as 19% and 9%, respectively, in 24h). Additive toxicity between copper and other pharmaceutical compounds such as fluoxetine (Prozac™), β-naphthoflavone, estrogen and 17α-ethinylestradiol were also observed. Similar to metals, acutely toxic concentrations of fluoxetine, β-naphthoflavone and ammonia all decreased whole body Na(+) and K(+). Overall, whole body Na(+) loss showed the greatest correlation with mortality across a variety of toxicants. We theorize that a disruption of ion homeostasis may be a common mechanism underlying the acute additive toxicity of many contaminants in fish.

  2. [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

  3. [Acute hearing loss in the orchestral musician : Noise trauma or idiopathic sudden deafness?].

    PubMed

    Brusis, T

    2011-07-01

    During an orchestral performance musicians are exposed to high noise levels, which may exceed the intensity which could evoke hearing impairment after many years of exposure. From experience the degree of hearing loss in musicians is in general less than would be expected from the levels of exposure. The likelihood that an orchestral musician would develop a noise-induced hearing loss is much lower than for an industrial worker in a noise-intense factory. On the other hand it has to be considered that it is imperative for musicians to have non-impaired hearing to practise their profession. In some cases a sudden onset of hearing loss is traced to the noise stress of a loud performance. In such cases, the high noise levels predominantly produced by brass instruments or drums were assumed to be the cause. This publication presents five cases of expert opinions, where previous expert opinions had assumed noise or a blast trauma as the cause for the hearing loss. By careful analysis, a noise or a blast trauma was not regarded as probable in any of the cases. Interestingly, three of the five musicians had a normal contralateral hearing. In one case normal bilateral hearing was observed without the typical c(5) notch although the musician had been subject to noise stress in an orchestra for years.

  4. 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...

  5. 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 ...

  6. Sleep, memory, and learning.

    PubMed

    Blissitt, P A

    2001-08-01

    The relationship of sleep to memory and learning is complex. Sleep affects memory, and memory must be present for learning to occur. A number of studies have been conducted to increase our understanding of their relationship. In addition to the numerous scientific investigations of each concept separately, sleep, memory, and learning have been studied together to determine (a) the effect of sleep on memory and learning, (b) the effect of sleep deprivation in general on memory and learning, (c) the effect of rapid eye movement (REM) sleep deprivation on memory and learning, (d) the effect of memory and learning on REM sleep, and (e) the effect of non-REM sleep loss on memory and learning. Neuroanatomic correlates have been pursued as well with most attention to the hippocampus. Despite considerable efforts to date, many of the studies reveal contradictory or inconclusive findings. Much remains unknown, and additional work is needed. Implications for nursing include those that have a direct effect on the patient, the nurse, and nursing science.

  7. 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

  8. 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.

  9. 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

  10. Persistent penile prolapse associated with acute blood loss and acepromazine maleate administration in a horse.

    PubMed

    Nie, G J; Pope, K C

    1997-09-01

    Prolonged penile prolapse in horses has been reported in association with administration of phenothiazine tranquilizers, trauma, neuropathies, severe general debilitation or exhaustion, starvation, rabies, herpes myeloencephalitis, equine infectious anemia, and purpura hemorrhagica. A 5-year-old gelding was admitted for treatment of prolonged penile prolapse of 12 days' duration that developed after acepromazine maleate was administered to allow examination of a laceration that had resulted in severe blood loss. The horse was sedated, and the penis was replaced in the preputial cavity by use of a combination of massage and bandaging. Treatment was successful, and recovery was complete.

  11. 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

  12. Cetacean sleep: an unusual form of mammalian sleep.

    PubMed

    Lyamin, Oleg I; Manger, Paul R; Ridgway, Sam H; Mukhametov, Lev M; Siegel, Jerome M

    2008-10-01

    Our knowledge of the form of lateralized sleep behavior, known as unihemispheric slow wave sleep (USWS), seen in all members of the order Cetacea examined to date, is described. We trace the discovery of this phenotypically unusual form of mammalian sleep and highlight specific aspects that are different from sleep in terrestrial mammals. We find that for cetaceans sleep is characterized by USWS, a negligible amount or complete absence of rapid eye movement (REM) sleep, and a varying degree of movement during sleep associated with body size, and an asymmetrical eye state. We then compare the anatomy of the mammalian somnogenic system with what is known in cetaceans, highlighting areas where additional knowledge is needed to understand cetacean sleep. Three suggested functions of USWS (facilitation of movement, more efficient sensory processing and control of breathing) are discussed. Lastly, the possible selection pressures leading to this form of sleep are examined, leading us to the suggestion that the selection pressure necessitating the evolution of cetacean sleep was most likely the need to offset heat loss to the water from birth and throughout life. Aspects such as sentinel functions and breathing are likely to be proximate evolutionary phenomenon of this form of sleep.

  13. Fatigue and mood correlates of sleep length in three age-social groups: School children, students, and employees.

    PubMed

    Oginska, Halszka; Pokorski, Janusz

    2006-01-01

    The aim of the study was to trace the consequences of insufficient sleep, in terms of chronic sleep reduction rather than acute sleep deprivation, on fatigue, mood, cognitive performance self-estimations, and daytime sleepiness in different age-social groups. The age group of the subjects reflects their social situation and their working time organization: adolescents (n = 191) obeyed the strict school schedules with starting times often before 08:00 h; university students (n = 115) had more flexible timetables; young employees (n = 126) were engaged in regular morning schedules or irregular daytime hours or day and night shifts. A questionnaire study determined the declared need of sleep, self-reported sleep length, chronic fatigue (using a scale comprised of eight fatigue symptoms and four mood and three cognitive items), and daytime sleepiness (Epworth Sleepiness Scale). The declared need for sleep decreased in subsequent age groups from 9 h 23 min in school children to 8 h 22 min in university students and to 7 h 37 min in young employees. Consequently, the discrepancy between preferred and real sleep length (sleep deficit) was the largest in adolescents: 106 min. Females showed a greater need of sleep than males (p = .025) and significantly more fatigue, mood, and cognitive problems; they also exhibited higher level of daytime sleepiness (p < .000). The sleep index (reported sleep length related to requirements) correlated significantly with all health issues in women (p < .000), while only with fatigue symptoms in men (p = .013). Actual sleep length was unrelated to mood and fatigue issues; the declared individual need of sleep and sleep index showed significant associations, especially in the group of adolescents. The most frequent complaints of adolescents included tiredness on awakening (46%), nervousness, and general weakness; university students reported excessive drowsiness (50%), tension, and nervousness; employees suffered mostly from negative moods

  14. 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

  15. Impact of predischarge nocturnal pulse oximetry (sleep-disordered breathing) on postdischarge clinical outcomes in hospitalized patients with left ventricular systolic dysfunction after acute decompensated heart failure.

    PubMed

    Ohmura, Takayasu; Iwama, Yoshitaka; Kasai, Takatoshi; Kato, Takao; Suda, Shoko; Takagi, Atsutoshi; Daida, Hiroyuki

    2014-02-15

    Stratifying patients at a high risk for readmission and mortality before their discharge after acute decompensated heart failure (ADHF) is important. Although sleep-disordered breathing (SDB) is prevalent in patients with chronic heart failure, only few studies have investigated the impact of SDB on hospitalized patients with left ventricular (LV) systolic dysfunction after ADHF. Thus, we assessed the prevalence of SDB using nocturnal pulse oximetry and the relation between SDB and clinical events in this patient group. One hundred consecutive patients with LV systolic dysfunction who were hospitalized for ADHF were enrolled in the study. Predischarge nocturnal oximetry was performed to determine if they had SDB (defined as an oxygen desaturation index of ≥5 events/hour with ≥4% decrease in saturation level). Data on death and readmission for ADHF were collected. Forty-one patients had SDB. Complete outcome data were collected in the mean follow-up period of 14.2 months during which 33 events occurred. On multivariate Cox proportional hazards regression analysis, the presence of SDB was a significant independent predictor of postdischarge readmission and mortality (hazard ratio 2.93, p = 0.006). In conclusion, SDB, as determined by predischarge nocturnal oximetry, is prevalent and is an independent predictor of the combined end point of readmission and mortality in hospitalized patients with LV systolic dysfunction after ADHF.

  16. 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

  17. 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.

  18. Exploring the Lived Experience of Difficult Sleep and Good Sleep Among Psychiatric Inpatients.

    PubMed

    Zust, Barbara Lois; Gruenberg, Marjorie E; Sendelbach, Susan Ellen

    2016-01-01

    The purpose of this qualitative study was to explore psychiatric inpatients' reflections on their experiences with sleep throughout their lives. Fourteen patients in an acute care behavioral health unit agreed to participate in this study. Participants met individually with a researcher to reflect on times in their lives when they experienced good sleep; times when they had difficulty sleeping; and times when difficult sleep was resolved. The major findings of the study indicated that feeling alone with life problems triggered difficult sleep; while feelings of belonging and purpose were associated with good sleep.

  19. Acute pancreatitis in aging animals: Loss of pancreatitis-associated protein protection?

    PubMed Central

    Fu, Sophia; Stanek, Albert; Mueller, Cathy M; Brown, Nefertti A; Huan, Chongmin; Bluth, Martin H; Zenilman, Michael E

    2012-01-01

    AIM: To investigate the effect of age on severity of acute pancreatitis (AP) using biochemical markers, histology and expression of the protective pancreatitis-associated proteins (PAPs). METHODS: AP was induced via intraductal injection of 4% sodium taurocholate in young and old rats. Sera and pancreata were assayed at 24 h for the parameters listed above; we also employed a novel molecular technique to assess bacterial infiltration using polymerase chain reaction to measure bacterial genomic ribosomal RNA. RESULTS: At 24 h after induction of AP, the pancreata of older animals had less edema (mean ± SE histologic score of young vs old: 3.11 ± 0.16 vs 2.50 ± -0.11, P < 0.05), decreased local inflammatory response (histologic score of stromal infiltrate: 3.11 ± 0.27 vs 2.00 ± 0.17, P < 0.05) and increased bacterial infiltration (174% ± 52% increase from sham vs 377% ± 4%, P < 0.05). A decreased expression of PAP1 and PAP2 was demonstrated by Western blotting analysis and immunohistochemical staining. There were no differences in serum amylase and lipase activity, or tissue myeloperoxidase or monocyte chemotactic protein-1 levels. However, in the most-aged group, serum C-reactive protein levels were higher (young vs old: 0.249 ± 0.04 mg/dL vs 2.45 ± 0.68 mg/dL, P < 0.05). CONCLUSION: In older animals, there is depressed PAP expression related to a blunted inflammatory response in AP which is associated with worsened bacterial infiltration and higher C-reactive protein level; this may explain the more aggressive clinical course. PMID:22807607

  20. [Sleep health education for elderly people].

    PubMed

    Miyazaki, Soichiro; Nishiyama, Akiko

    2015-06-01

    Successful aging is characterized by minimal age-associated loss of the physiological functions of sleep and circadian clock. Sleep health education is necessary to have normal, quality nighttime sleep and full daytime alertness. Elderly people show changes of sleep parameters, accompanied by increased napping. Many studies have reported that daytime sleepiness or napping in elderly people could have potentially serious effects such as dementia and life-style related diseases. The main topics of sleep health education for elderly people are as follows: Right knowledge of sleep mechanism, understanding the bad influence of excessive napping, the effects of light on the circadian rhythm and negative effects of caffeine, alcohol and television.

  1. 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

  2. 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.

  3. 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.

  4. 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

  5. Inducing jet lag in the laboratory: patterns of adjustment to an acute shift in routine.

    PubMed

    Monk, T H; Moline, M L; Graeber, R C

    1988-08-01

    Eight middle-aged males were studied in a temporal isolation experimental lasting 15 d. After 5 d and nights of entrainment to his own habitual routine, each subject experienced an acute, unheralded 6-h phase advance in routine, accomplished by truncating his sixth sleep episode. For the remaining 10 d of the study, subjects were held to a routine 6-h phase advanced to the original. Significant symptoms of jet lag appeared in mood, performance efficiency, sleep, and circadian temperature rhythms. When plotted as a function to "days post-shift," some variables (temperature phase, percent rapid eye movement sleep) showed a fairly monotonic recovery to baseline levels. However, other variables (actual sleep duration, percent slow wave sleep, motivation loss, subjective sleepiness) showed a zig-zag recovery pattern, suggesting the interaction of two competing processes, and reinforcing the need for greater sophistication in the development of jet lag coping strategies.

  6. 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

  7. 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

  8. 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 ...

  9. 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 ...

  10. 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 ...

  11. 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 ...

  12. Adverse effects of sleep deprivation in the ICU.

    PubMed

    Salas, Rachel E; Gamaldo, Charlene E

    2008-07-01

    The hospital is not conducive to sleep. Patients in the ICU are particularly susceptible to sleep disruption secondary to environmental and medical issues. Despite the frequency of sleep disruption in the ICU, the quality of critically ill patients' sleep is often overlooked. This article discusses the following issues essential to understanding the factors associated with sleep loss in the ICU: (1) core elements to consider from the baseline sleep history, (2) impact of the ICU environment on the ICU patient's sleep pattern, and (3) overall systematic impact of sleep deprivation on the ICU patient.

  13. Sleep allostasis in chronic sleep restriction: the role of the norepinephrine system

    PubMed Central

    Kim, Youngsoo; Chen, Lichao; McCarley, Robert W.; Strecker, Robert E.

    2013-01-01

    Sleep responses to chronic sleep restriction may be very different from those observed after acute total sleep deprivation. Specifically, when sleep restriction is repeated for several consecutive days, animals express attenuated compensatory increases in sleep time and intensity during daily sleep opportunities. The neurobiological mechanisms underlying these adaptive, or more specifically, allostatic, changes in sleep homeostasis are unknown. Several lines of evidence indicate that norepinephrine may play a key role in modulating arousal states and NREM EEG delta power, which is widely recognized as a marker for sleep intensity. Therefore, we investigated time course changes in brain adrenergic receptor mRNA levels in response to chronic sleep restriction using a rat model. Here, we observed that significantly altered mRNA levels of the α1- adrenergic receptor in the basal forebrain as well as α2- and β1-adrenergic receptor in the anterior cingulate cortex only on the first sleep restriction day. On the other hand, the frontal cortex α1-, α2-, and β1- adrenergic receptor mRNA levels were reduced throughout the period of sleep restriction. Combined with our earlier findings on EEG that sleep time and intensity significantly increased only on the first sleep restriction days, these results suggest that alterations in the brain norepinephrine system in the basal forebrain and cingulate cortex may mediate allostatic changes in sleep time and intensity observed during chronic sleep restriction. PMID:23916734

  14. 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 ...

  15. 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

  16. The cognitive cost of sleep lost

    PubMed Central

    McCoy, John G.; Strecker, Robert E.

    2013-01-01

    A substantial body of literature supports the intuitive notion that a good night’s sleep can facilitate human cognitive performance the next day. Deficits in attention, learning & memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances. PMID:21875679

  17. The cognitive cost of sleep lost.

    PubMed

    McCoy, John G; Strecker, Robert E

    2011-11-01

    A substantial body of literature supports the intuitive notion that a good night's sleep can facilitate human cognitive performance the next day. Deficits in attention, learning & memory, emotional reactivity, and higher-order cognitive processes, such as executive function and decision making, have all been documented following sleep disruption in humans. Thus, whilst numerous clinical and experimental studies link human sleep disturbance to cognitive deficits, attempts to develop valid and reliable rodent models of these phenomena are fewer, and relatively more recent. This review focuses primarily on the cognitive impairments produced by sleep disruption in rodent models of several human patterns of sleep loss/sleep disturbance. Though not an exclusive list, this review will focus on four specific types of sleep disturbance: total sleep deprivation, experimental sleep fragmentation, selective REM sleep deprivation, and chronic sleep restriction. The use of rodent models can provide greater opportunities to understand the neurobiological changes underlying sleep loss induced cognitive impairments. Thus, this review concludes with a description of recent neurobiological findings concerning the neuroplastic changes and putative brain mechanisms that may underlie the cognitive deficits produced by sleep disturbances.

  18. Changes in mechanisms proposed to mediate fat loss following an acute bout of high-intensity interval and endurance exercise.

    PubMed

    Williams, Cameron B; Zelt, Jason G E; Castellani, Laura N; Little, Jonathan P; Jung, Mary E; Wright, David C; Tschakovsky, Michael E; Gurd, Brendon J

    2013-12-01

    The purpose of this study was to investigate the acute effects of endurance exercise (END; 65% V̇O2peak for 60 min) and high-intensity interval exercise (HIE; four 30 s Wingates separated by 4.5 min of active rest) on cardiorespiratory, hormonal, and subjective appetite measures that may account for the previously reported superior fat loss with low volume HIE compared with END. Recreationally active males (n = 18) completed END, HIE, and control (CON) protocols. On each test day, cardiorespiratory measures including oxygen uptake (V̇O2), respiratory exchange ratio (RER), and heart rate were recorded and blood samples were obtained at baseline (BSL), 60 min after exercise, and 180 min after exercise (equivalent times for CON). Subjective measures of appetite (hunger, fullness, nausea, and prospective consumption) were assessed using visual analogue scales, administered at BSL, 0, 60, 120, and 180 min after exercise. No significant differences in excess postexercise oxygen consumption (EPOC) were observed between conditions. RER was significantly (P < 0.05) depressed in HIE compared with CON at 60 min after exercise, yet estimates of total fat oxidation over CON were not different between HIE and END. No differences in plasma adiponectin concentrations between protocols or time points were present. Epinephrine and norepinephrine were significantly (P < 0.05) elevated immediately after exercise in HIE compared with CON. Several subjective measures of appetite were significantly (P < 0.05) depressed immediately following HIE. Our data indicate that increases in EPOC or fat oxidation following HIE appear unlikely to contribute to the reported superior fat loss compared with END.

  19. The study for loss of bcl-xs expression as a prognostic factor in acute myeloid leukemia.

    PubMed

    Yamaguchi, Hiroki; Inokuchi, Koiti; Dan, Kazuo

    2002-12-01

    We reported here abnormal expression profile of the bcl-x gene is associated with the recurrence in acute myelogenous leukemia (AML).The bcl-x gene product exists in two forms, bcl-xl and bcl-xs. The bcl-xl, similar to bcl-2, inhibits apoptosis, whereas bcl-xs counters the effects of bcl-2 and bcl-xl. Mononuclear cells of bone marrow cells were obtained from 50 patients with recurrent AML at diagnosis prior to treatment and during relapse. We investigated the expression of the two isoforms of the bcl-x gene, bcl-xl and bcl-xs. The bcl-xl transcript was detected in all patients at both stages, but the bcl-xs transcript was not detected in six cases at both stages and in seven other cases at relapse (bcl-xs (-) group, n=13). The duration of relapse-free survival (RFS) and overall survival (OS) of the bcl-xs (-) group were significantly shorter than those of the bcl-xs (+) group (RFS: P=0.04; OS: P=0.02). Subsequently, mutation of the bcl-x gene was investigated. No mutation of the bcl-x gene was detected in all patients of both stages. Some refractory leukemic cells which escape chemotherapy-induced apoptosis due to loss of the bcl-xs transcript may continue to proliferate, resulting in the relapse of chemotherapy-resistant leukemia. The examination of the expression status of the bcl-x gene could facilitate the prediction of chemotherapy resistance and the prognosis of patients with refractory AML. The future large study will confirm the present data about loss of bcl-xs gene expression as prognostic factor.

  20. 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

  1. Sleep in the intensive care unit.

    PubMed

    Beltrami, Flávia Gabe; Nguyen, Xuân-Lan; Pichereau, Claire; Maury, Eric; Fleury, Bernard; Fagondes, Simone

    2015-01-01

    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

  2. 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

  3. 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.

  4. 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

  5. DNA hydroxymethylation profiling reveals that WT1 mutations result in loss of TET2 function in acute myeloid leukemia

    PubMed Central

    Rampal, Raajit; Alkalin, Altuna; Madzo, Jozef; Vasanthakumar, Aparna; Pronier, Elodie; Patel, Jay; Li, Yushan; Ahn, Jihae; Abdel-Wahab, Omar; Shih, Alan; Lu, Chao; Ward, Patrick S.; Tsai, Jennifer J.; Hricik, Todd; Tosello, Valeria; Tallman, Jacob E.; Zhao, Xinyang; Daniels, Danette; Dai, Qing; Ciminio, Luisa; Aifantis, Iannis; He, Chuan; Fuks, Francois; Tallman, Martin S.; Ferrando, Adolfo; Nimer, Stephen; Paietta, Elisabeth; Thompson, Craig B.; Licht, Jonathan D.; Mason, Chris; Godley, Lucy A.; Melnick, Ari; Figueroa, Maria E.; Levine, Ross L.

    2014-01-01

    Summary Somatic mutations in IDH1/2 and TET2 result in impaired TET2 mediated conversion of 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC). The observation that WT1 inactivating mutations anti-correlate with TET2/IDH1/2 mutations in AML led us to hypothesize that WT1 mutations may impact TET2 function. WT1 mutant acute myeloid leukemia (AML) patients have reduced 5-hmC levels similar to TET2/IDH1/2-mutant AML. These mutations are characterized by convergent, site-specific alterations in DNA hydroxymethylation, which drive differential gene expression more than alterations in DNA promoter methylation. WT1 overexpression increases global levels of 5-hmC, and WT1 silencing reduced 5-hmC levels. WT1 physically interacts with TET2 and TET3, and WT1 loss of function results in a similar hematopoietic differentiation phenotype as observed with TET2 deficiency. These data provide a novel role for WT1 in regulating DNA hydroxymethylation and suggest that TET2 IDH1/2, and WT1 mutations define a novel AML subtype defined by dysregulated DNA hydroxymethylation. PMID:25482556

  6. 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

  7. Tissue-Specific B-Cell Dysfunction and Generalized Memory B-Cell Loss during Acute SIV Infection

    PubMed Central

    Peruchon, Sandrine; Chaoul, Nada; Burelout, Chantal; Delache, Benoit; Brochard, Patricia; Laurent, Pascale; Cognasse, Fabrice; Prévot, Sophie; Garraud, Olivier; Le Grand, Roger; Richard, Yolande

    2009-01-01

    Background Primary HIV-infected patients display severe and irreversible damage to different blood B-cell subsets which is not restored by highly efficient anti-retroviral therapy (HAART). Because longitudinal investigations of primary HIV-infection is limited by the availability of lymphoid organs, we studied the tissue-specific B-cell dysfunctions in acutely simian immunodeficiency virus (SIV) mac251-infected Cynomolgus macaques. Methods and Findings Experiments were performed on three groups of macaques infected for 14, 21 or 28 days and on three groups of animals treated with HAART for two-weeks either initiated at 4 h, 7 or 14 days post-infection (p.i.). We have simultaneously compared changes in B-cell phenotypes and functions and tissue organization of B-cell areas in various lymphoid organs. We showed that SIV induced a steady decline in SIgG-expressing memory (SIgD−CD27+) B-cells in spleen and lymph nodes during the first 4 weeks of infection, concomitant to selective homing/sequestration of B-cells to the small intestine and spleen. SIV non-specific Ig production was transiently increased before D14p.i., whereas SIV-specific Ig production was only detectable after D14p.i., coinciding with the presence of CD8+ T-cells and IgG-expressing plasma cells within germinal centres. Transient B-cell apoptosis on D14p.i. and commitment to terminal differentiation contributed to memory B-cell loss. HAART abrogated B-cell apoptosis, homing to the small intestine and SIV-specific Ig production but had minimal effect on early Ig production, increased B-cell proportions in spleen and loss of memory B-cells. Therefore, virus–B-cell interactions and SIV-induced inflammatory cytokines may differently contribute to early B-cell dysfunction and impaired SIV/HIV-specific antibody response. Conclusions These data establish tissue-specific impairments in B-cell trafficking and functions and a generalized and steady memory B-cell loss in secondary lymphoid organs

  8. 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

  9. 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

  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. 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

  12. Sleep insufficiency, sleep health problems and performance in high school students.

    PubMed

    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.

  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-related eating disorder as a cause of obstructive sleep apnea.

    PubMed

    Eveloff, S E; Millman, R P

    1993-08-01

    A patient with obesity resulting from sleep-related eating disorder demonstrated signs and symptoms of obstructive sleep apnea (OSA). Incarceration restricted access to food during the night, leading to weight loss and clinical improvement. Release from prison allowed recurrence of unrestricted sleep-eating, recurrent obesity, and documented OSA. Successful treatment of sleep-related eating disorder can result in improvement in coexisting OSA.

  15. [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

  16. Sleep disorders in morbid obesity.

    PubMed

    Akinnusi, Morohunfolu E; Saliba, Ranime; Porhomayon, Jahan; El-Solh, Ali A

    2012-04-01

    The increasing prevalence of obesity has lead to an increase in the prevalence of sleep disordered breathing in the general population. The disproportionate structural characteristics of the pharyngeal airway and the diminished neural regulation of the pharyngeal dilating muscles during sleep predispose the obese patients to pharyngeal airway collapsibility. A subgroup of obese apneic patients is unable to compensate for the added load of obesity on the respiratory system, with resultant daytime hypercapnia. Weight loss using dietary modification and life style changes is the safest approach to reducing the severity of sleep apnea, but its efficacy is limited on the long run. Although it has inherent risks, bariatric surgery provides the most immediate result in alleviating sleep apnea. Obesity has been linked also to narcolepsy. The loss of neuropeptides co-localized in hypocretin neurons is suggested as the potential mechanism. Poor sleep quality, which leads to overall sleep loss and excessive daytime sleepiness has also become a frequent complaint in this population. Identifying abnormal nocturnal eating is critically important for patient care. Both sleep related eating disorder and night eating syndrome are treatable and represent potentially reversible forms of obesity.

  17. A dynamic deep sleep stage in Drosophila

    PubMed Central

    van Alphen, Bart; Yap, Melvyn H.W.; Kirszenblat, Leonie; Kottler, Benjamin; van Swinderen, Bruno

    2013-01-01

    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 use 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 minutes 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 (cAMP) 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 (FMRP), increases sleep intensity during the day. Our results show that sleep is not homogenous in insects, and suggest that waking behavior and associated synaptic plasticity mechanisms determine the timing and intensity of deep sleep stages in Drosophila. PMID:23595750

  18. Changing your sleep habits

    MedlinePlus

    Insomnia - sleep habits; Sleep disorder - sleep habits; Problems falling asleep; Sleep hygiene ... Philadelphia, PA: Elsevier; 2017:chap 86. Vaughn BV. Disorders of sleep. In: Goldman L, Schafer AI, eds. Goldman's Cecil ...

  19. 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 ( ...

  20. 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.

  1. 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

  2. Effects of mirtazapine on sleep polygraphic variables in major depression.

    PubMed

    Schittecatte, Michel; Dumont, Françoise; Machowski, Robert; Cornil, Catherine; Lavergne, Francis; Wilmotte, Jean

    2002-01-01

    Mirtazapine, a noradrenergic and specific serotonergic antidepressant(NaSSA), was administered on a flexible schedule in a sample of 17 drug-free patients meeting DSM-IV criteria for a major depressive episode. Sleep polygraphic recordings were performed before and during acute and chronic treatment. Severity of depression and subjective assessment of changes within different aspects of sleep were also evaluated. During the acute administration (first 2 days), mirtazapine significantly increased total sleep time, sleep efficiency, stage II, stage rapid eye movement and slow-wave sleep percentages, and decreased sleep latency and stage awake percentage. These effects persisted after 5 weeks of treatment. Subjectively, mirtazapine induced an improvement of sleep. This open, noncontrolled study suggests that mirtazapine ameliorates the sleep disturbances encountered in depressed patients both objectively and subjectively. PMID:12566938

  3. 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

  4. 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

  5. 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.

  6. Performance, ability to stay awake, and tendency to fall asleep during the night after a diurnal sleep with temazepam or placebo.

    PubMed

    Porcù, S; Bellatreccia, A; Ferrara, M; Casagrande, M

    1997-07-01

    Sleep loss and increased sleepiness on the job are among the most prevalent problems encountered by people involved in night shift work, especially in cases of abrupt shift of the wake-sleep cycle. In such conditions, detrimental effects on performance are well documented. In these situations, to avoid decrements of performance at night, one possibility is to use hypnotics for improving the quality and quantity of daytime sleep. In this study, we evaluated the effects of 20 mg of temazepam on daytime sleep, the subsequent levels of nocturnal alertness/sleepiness, and performance in a laboratory simulation of acute night shift. For evaluating alertness, sleepiness, and performance we used, respectively, the maintenance of wakefulness test (MWT), the multiple sleep latency test (MSLT), and two pencil and paper tests: digit symbol substitution test (DSST) and deux barrages test (DBT). All tests were administered four times at 2-hour intervals during the nighttime after daytime sleep. Results showed that the ability to maintain wakefulness (MWT) and to perform some visuo-attentive tasks were substantially maintained during the night. On the other hand, sleep tendency (MSLT) linearly increased during the night. Temazepam resulted in being an effective diurnal hypnotic, increasing total sleep time with no residual detrimental effects on sleepiness and performance and with an increase in the ability to stay awake.

  7. 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

  8. 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

  9. [The importance of sleep in the mental health].

    PubMed

    Hashizume, Yuji

    2014-02-01

    Japanese average sleeping time is decreasing year by year. The National Sleep Foundation of United States of America released that Japan reports the least amount of sleep. Japanese reports sleeping about 30 to 40 minutes less on workdays than those in the other countries surveyed, averaging 6 hours 22 minutes of sleep. There are many reports that insomnia has been suggested to cause depression and other mental disorders. And epidemiological evidence supports a link between sleep loss and obesity. Obesity is one of risk factors of obstructive sleep apnea syndrome which causes cognitive dysfunction, mood disorders and so on. Sleep loss and sleep insufficiency can cause mental disorders and be impaired cognitive function and performance.

  10. Sleep Tight.

    ERIC Educational Resources Information Center

    Black, Susan

    2000-01-01

    At the same time their biological systems program them for later sleep and waking times, adolescents' schedules and lifestyles keep them from getting a healthy amount of sleep. Although a few schools have altered their schedules, most are confounded by costs and contractual complications. Minnesota schools are leaders. (MLH)

  11. 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

  12. Effects of dialysis modality on blood loss, bleeding complications and transfusion requirements in critically ill patients with dialysis-dependent acute renal failure.

    PubMed

    Pschowski, R; Briegel, S; Von Haehling, S; Doehner, W; Bender, T O; Pape, U F; Hasper, D; Jörress, A; Schefold, J C

    2015-11-01

    Blood loss and bleeding complications may often be observed in critically ill patients on renal replacement therapies (RRT). Here we investigate procedural (i.e. RRT-related) and non-procedural blood loss as well as transfusion requirements in regard to the chosen mode of dialysis (i.e. intermittent haemodialysis [IHD] versus continuous veno-venous haemofiltration [CVVH]). Two hundred and fifty-two patients (122 CVVH, 159 male; aged 61.5±13.9 years) with dialysis-dependent acute renal failure were analysed in a sub-analysis of the prospective randomised controlled clinical trial-CONVINT-comparing IHD and CVVH. Bleeding complications including severity of bleeding and RRT-related blood loss were assessed. We observed that 3.6% of patients died related to severe bleeding episodes (between group P=0.94). Major all-cause bleeding complications were observed in 23% IHD versus 26% of CVVH group patients (P=0.95). Under CVVH, the rate of RRT-related blood loss events (57.4% versus 30.4%, P=0.01) and mean total blood volume lost was increased (222.3±291.9 versus 112.5±222.7 ml per patient, P <0.001). Overall, transfusion rates did not differ between the study groups. In patients with sepsis, transfusion rates of all blood products were significantly higher when compared to cardiogenic shock (all P <0.01) or other conditions. In conclusion, procedural and non-procedural blood loss may often be observed in critically ill patients on RRT. In CVVH-treated patients, procedural blood loss was increased but overall transfusion rates remained unchanged. Our data show that IHD and CVVH may be regarded as equivalent approaches in critically ill patients with dialysis-dependent acute renal failure in this regard.

  13. Ancestral sleep.

    PubMed

    de la Iglesia, Horacio O; Moreno, Claudia; Lowden, Arne; Louzada, Fernando; Marqueze, Elaine; Levandovski, Rosa; Pilz, Luisa K; Valeggia, Claudia; Fernandez-Duque, Eduardo; Golombek, Diego A; Czeisler, Charles A; Skene, Debra J; Duffy, Jeanne F; Roenneberg, Till

    2016-04-01

    While we do not yet understand all the functions of sleep, its critical role for normal physiology and behaviour is evident. Its amount and temporal pattern depend on species and condition. Humans sleep about a third of the day with the longest, consolidated episode during the night. The change in lifestyle from hunter-gatherers via agricultural communities to densely populated industrialized centres has certainly affected sleep, and a major concern in the medical community is the impact of insufficient sleep on health [1,2]. One of the causal mechanisms leading to insufficient sleep is altered exposure to the natural light-dark cycle. This includes the wide availability of electric light, attenuated exposure to daylight within buildings, and evening use of light-emitting devices, all of which decrease the strength of natural light-dark signals that entrain circadian systems [3].

  14. Ancestral sleep.

    PubMed

    de la Iglesia, Horacio O; Moreno, Claudia; Lowden, Arne; Louzada, Fernando; Marqueze, Elaine; Levandovski, Rosa; Pilz, Luisa K; Valeggia, Claudia; Fernandez-Duque, Eduardo; Golombek, Diego A; Czeisler, Charles A; Skene, Debra J; Duffy, Jeanne F; Roenneberg, Till

    2016-04-01

    While we do not yet understand all the functions of sleep, its critical role for normal physiology and behaviour is evident. Its amount and temporal pattern depend on species and condition. Humans sleep about a third of the day with the longest, consolidated episode during the night. The change in lifestyle from hunter-gatherers via agricultural communities to densely populated industrialized centres has certainly affected sleep, and a major concern in the medical community is the impact of insufficient sleep on health [1,2]. One of the causal mechanisms leading to insufficient sleep is altered exposure to the natural light-dark cycle. This includes the wide availability of electric light, attenuated exposure to daylight within buildings, and evening use of light-emitting devices, all of which decrease the strength of natural light-dark signals that entrain circadian systems [3]. PMID:27046809

  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. Sleep extension normalizes ERP of waking auditory sensory gating in healthy habitually short sleeping individuals.

    PubMed

    Gumenyuk, Valentina; Korzyukov, Oleg; Roth, Thomas; Bowyer, Susan M; Drake, Christopher L

    2013-01-01

    Chronic sleep loss has been associated with increased daytime sleepiness, as well as impairments in memory and attentional processes. In the present study, we evaluated the neuronal changes of a pre-attentive process of wake auditory sensory gating, measured by brain event-related potential (ERP)--P50 in eight normal sleepers (NS) (habitual total sleep time (TST) 7 h 32 m) vs. eight chronic short sleeping individuals (SS) (habitual TST ≤6 h). To evaluate the effect of sleep extension on sensory gating, the extended sleep condition was performed in chronic short sleeping individuals. Thus, one week of time in bed (6 h 11 m) corresponding to habitual short sleep (hSS), and one week of extended time (∼ 8 h 25 m) in bed corresponding to extended sleep (eSS), were counterbalanced in the SS group. The gating ERP assessment was performed on the last day after each sleep condition week (normal sleep and habitual short and extended sleep), and was separated by one week with habitual total sleep time and monitored by a sleep diary. We found that amplitude of gating was lower in SS group compared to that in NS group (0.3 µV vs. 1.2 µV, at Cz electrode respectively). The results of the group × laterality interaction showed that the reduction of gating amplitude in the SS group was due to lower amplitude over the left hemisphere and central-midline sites relative to that in the NS group. After sleep extension the amplitude of gating increased in chronic short sleeping individuals relative to their habitual short sleep condition. The sleep condition × frontality interaction analysis confirmed that sleep extension significantly increased the amplitude of gating over frontal and central brain areas compared to parietal brain areas.

  17. Sleep extension normalizes ERP of waking auditory sensory gating in healthy habitually short sleeping individuals.

    PubMed

    Gumenyuk, Valentina; Korzyukov, Oleg; Roth, Thomas; Bowyer, Susan M; Drake, Christopher L

    2013-01-01

    Chronic sleep loss has been associated with increased daytime sleepiness, as well as impairments in memory and attentional processes. In the present study, we evaluated the neuronal changes of a pre-attentive process of wake auditory sensory gating, measured by brain event-related potential (ERP)--P50 in eight normal sleepers (NS) (habitual total sleep time (TST) 7 h 32 m) vs. eight chronic short sleeping individuals (SS) (habitual TST ≤6 h). To evaluate the effect of sleep extension on sensory gating, the extended sleep condition was performed in chronic short sleeping individuals. Thus, one week of time in bed (6 h 11 m) corresponding to habitual short sleep (hSS), and one week of extended time (∼ 8 h 25 m) in bed corresponding to extended sleep (eSS), were counterbalanced in the SS group. The gating ERP assessment was performed on the last day after each sleep condition week (normal sleep and habitual short and extended sleep), and was separated by one week with habitual total sleep time and monitored by a sleep diary. We found that amplitude of gating was lower in SS group compared to that in NS group (0.3 µV vs. 1.2 µV, at Cz electrode respectively). The results of the group × laterality interaction showed that the reduction of gating amplitude in the SS group was due to lower amplitude over the left hemisphere and central-midline sites relative to that in the NS group. After sleep extension the amplitude of gating increased in chronic short sleeping individuals relative to their habitual short sleep condition. The sleep condition × frontality interaction analysis confirmed that sleep extension significantly increased the amplitude of gating over frontal and central brain areas compared to parietal brain areas. PMID:23520548

  18. Medicines for sleep

    MedlinePlus

    Benzodiazepines; Sedatives; Hypnotics; Sleeping pills; Insomnia - medicines; Sleep disorder - medicines ... the-counter (OTC) sleeping pills contain antihistamines. These medicines are commonly used to treat allergies. While these ...

  19. 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

  20. [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

  1. 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 ...

  2. 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 ...

  3. 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 ...

  4. 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 ...

  5. 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 ...

  6. 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 ...

  7. 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…

  8. [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

  9. 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.

  10. 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

  11. 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

  12. Sleep in Othello

    PubMed Central

    Dimsdale, Joel E.

    2009-01-01

    Some of our best descriptions of sleep disorders come from literature. While Shakespeare is well known for his references to insomnia and sleep walking, his works also demonstrate a keen awareness of many other sleep disorders. This paper examines sleep themes in Shakespeare's play Othello. The play indicates Shakespeare's astute eye for sleep deprivation, sexual parasomnias, and effects of stress and drugs on sleep. Citation: Dimsdale JE. Sleep in Othello. J Clin Sleep Med 2009;5(3):280-281. PMID:19960651

  13. Increased Sleep Depth in Developing Neural Networks: New Insights from Sleep Restriction in Children

    PubMed Central

    Kurth, Salome; Dean, Douglas C.; Achermann, Peter; O’Muircheartaigh, Jonathan; Huber, Reto; Deoni, Sean C. L.; LeBourgeois, Monique K.

    2016-01-01

    Brain networks respond to sleep deprivation or restriction with increased sleep depth, which is quantified as slow-wave activity (SWA) in the sleep electroencephalogram (EEG). When adults are sleep deprived, this homeostatic response is most pronounced over prefrontal brain regions. However, it is unknown how children’s developing brain networks respond to acute sleep restriction, and whether this response is linked to myelination, an ongoing process in childhood that is critical for brain development and cortical integration. We implemented a bedtime delay protocol in 5- to 12-year-old children to obtain partial sleep restriction (1-night; 50% of their habitual sleep). High-density sleep EEG was assessed during habitual and restricted sleep and brain myelin content was obtained using mcDESPOT magnetic resonance imaging. The effect of sleep restriction was analyzed using statistical non-parametric mapping with supra-threshold cluster analysis. We observed a localized homeostatic SWA response following sleep restriction in a specific parieto-occipital region. The restricted/habitual SWA ratio was negatively associated with myelin water fraction in the optic radiation, a developing fiber bundle. This relationship occurred bilaterally over parieto-temporal areas and was adjacent to, but did not overlap with the parieto-occipital region showing the most pronounced homeostatic SWA response. These results provide evidence for increased sleep need in posterior neural networks in children. Sleep need in parieto-temporal areas is related to myelin content, yet it remains speculative whether age-related myelin growth drives the fading of the posterior homeostatic SWA response during the transition to adulthood. Whether chronic insufficient sleep in the sensitive period of early life alters the anatomical generators of deep sleep slow-waves is an important unanswered question. PMID:27708567

  14. 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

  15. Acute antidepressant response to sleep deprivation combined with light therapy is influenced by the catechol-O-methyltransferase Val(108/158)Met polymorphism.

    PubMed

    Benedetti, Francesco; Barbini, Barbara; Bernasconi, Alessandro; Fulgosi, Mara Cigala; Dallaspezia, Sara; Gavinelli, Chiara; Locatelli, Clara; Lorenzi, Cristina; Pirovano, Adele; Radaelli, Daniele; Smeraldi, Enrico; Colombo, Cristina

    2010-02-01

    Catechol-O-methyltransferase (COMT) inactivates norepinephrine and dopamine via methyl conjugation, and a G-A transition in the COMT gene (rs4680) influences the enzyme activity. It is a current area of debate whether rs4680 can influence antidepressant response in major depressive disorder, and whether this influence extends to bipolar depression. Chronotherapeutic interventions, such as sleep deprivation and light therapy, are multi-target in nature and are effective in bipolar depression. Here we studied the effect of rs4680 on response to sleep deprivation combined with light therapy (36 h awake followed by a night of undisturbed sleep, with 10,000 lx light administered for 30 min during the night awake and upon awakening) in 87 bipolar depressed inpatients. Patients who were homozygotic for the Val/Val variant showed a significantly less efficient antidepressant effect after the night awake than those who were heterozygotic and homozygotic for the Met variant. This effect of rs4680 is similar to its observed influence on response to serotonergic and noradrenergic drug treatments in major depressive disorder. This is the first study reporting an influence of rs4680 on antidepressant response in bipolar depression. This finding supports the hypothesis of a major role for catecholamines in the mechanism of action of chronotherapeutics, and for rs4680 in modulating this effect.

  16. The effect of acute fluid consumption following exercise-induced fluid loss on hydration status, percent body fat, and minimum wrestling weight in wrestlers.

    PubMed

    Cutrufello, Paul T; Dixon, Curt B

    2014-07-01

    Acute fluid consumption (approximately 1 L) has been shown to reduce urine specific gravity (Usg) among subjects after an overnight fast, yet it is unknown if Usg may be reduced among subjects who have experienced exercise-induced fluid loss. The purpose of this study was to examine the effect of acute fluid consumption on Usg, body mass, percent body fat (%BF), and minimum wrestling weight (MWW) following an exercise-induced fluid loss protocol. National Collegiate Athletic Association coaches' perceptions of the weight certification program (WCP) were also evaluated. Twelve men wrestlers (19.8 ± 1.14 years) were tested prepractice (PRE), postpractice (POST), and 1 hour after consuming 1 L of water (PFC). Percent body fat was measured by skinfolds (SF), air displacement plethysmography (ADP), and multifrequency and leg-to-leg bioelectrical impedance analysis to calculate MWW. Urine specific gravity measurements significantly increased above PRE (1.013 ± 0.006) at the POST (1.019 ± 0.007; p = 0.017) and PFC (1.022 ± 0.008; p = 0.025) assessments; however, POST and PFC were not significantly different (p = 0.978) from one another. The %BF values were similar (p > 0.05) at each assessment point when using SF and ADP. When compared with PRE, MWW significantly reduced at the POST assessment when using SF (67.2 ± 8.4 vs. 65.7 ± 8.2 kg; p < 0.001) and ADP (66.6 ± 9.1 vs. 64.8 ± 9.0 kg; p = 0.001), reflecting the reduction in body mass observed after exercise. Forty-seven National Collegiate Athletic Association coaches completed the questionnaire and 2 central themes emerged: (a) concerns with the 1.5% weight loss plan and (b) wrestlers using strategies in an attempt to circumvent the WCP. Exercise-induced fluid loss followed by acute fluid consumption equal to 1 L was ineffective in reducing Usg.

  17. 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.

  18. [Acute hearing loss from scuba-diving holidays: diagnosis and treatment of barotrauma of the inner ear].

    PubMed

    Brocks, C; Wollenberg, B; Graefe, H

    2009-03-01

    A 35-year-old diver noticed hearing loss and tinnitus after his diving holiday. He presented to the Lübeck clinical practice for divers, and we found vascular injections on the eardrum. Audiometry showed a high-degree hearing loss of 40-60 dB. Under the assumption of a perilymphatic fistula, we performed a tympanoscopy with covering of the oval and round windows. Bone-conduction hearing improved immediately postoperatively to 25 dB. A postoperative rheological infusion treatment was given. After 6 months the diver was assessed fit to dive with almost normal inner ear function.

  19. 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

  20. Lentiviral infection, immune response peptides and sleep.

    PubMed

    Darko, D F; Mitler, M M; Henriksen, S J

    1995-01-01

    The aberrant sleep documented in subjects with human immunodeficiency virus (HIV) infection is uniquely important because of the contribution this poor quality sleep makes to the fatigue, disability, and eventual unemployment that befalls these patients. Especially given this importance in clinical care, the research on the prominent sleep changes described in HIV infection remains modest in quantity. The chronic asymptomatic stage of HIV infection is associated with the most intriguing and singular sleep structure changes. Especially robust is the increase in slow wave sleep, particularly in latter portions of the sleep period. This finding is rare in other primary or secondary sleep disorders. The sleep structure alterations are among the most replicable of several pathophysiological sequelae in the brain associated with early HIV infection. It is unlikely that these sleep architecture changes are psychosocial in etiology, and they occur before medical pathology is evident. They are not associated with stress, anxiety, or depression. Evidence is accumulating to support a role for the somnogenic immune peptides tumor necrosis factor (TNF)alpha and interleukin (IL-1 beta) in the sleep changes and fatigue commonly seen in HIV infection. These peptides are elevated in the blood of HIV-infected individuals, and are somnogenic in clinical use and animal models. The peripheral production of these peptides may also have a role in the regulation of normal sleep physiology. The lentivirus family contains both HIV and the feline immunodeficiency virus (FIV). The use of the FIV model of HIV infection may provide a way to further investigate the mechanism of a neurotropic, neurotoxic virus initiating the immune acute phase response and affecting sleep. Neurotropic lentivirus infection is a microbiological probe facilitating neuroimmune investigation. PMID:7795894

  1. 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.

  2. 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

  3. 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

  4. Herpes Simplex Virus/Sleeping Beauty Vector-Based Embryonic Gene Transfer Using the HSB5 Mutant: Loss of Apparent Transposition Hyperactivity In Vivo

    PubMed Central

    de Silva, Suresh; Mastrangelo, Michael A.; Lotta, Louis T.; Burris, Clark A.; Izsvák, Zsuzsanna; Ivics, Zoltán

    2010-01-01

    Abstract 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

  5. 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.

  6. Loss of neuromuscular control related to motion in the acutely ACL-injured knee: an experimental study.

    PubMed

    Bonsfills, N; Gómez-Barrena, E; Raygoza, J J; Núñez, A

    2008-10-01

    Ligamentomuscular and muscular stretch reflexes are known to contribute to knee joint stability. After anterior cruciate ligament (ACL) injury, a more intense and adjusted muscular response is required to maintain joint stability, but this neuromuscular control of the knee has not been clearly proved. The aim of the study is to record electromyography (EMG) signal and muscular fibre length variations in quadriceps and hamstrings of the knee with and without ACL, and to analyze and integrate the ligament strain and the muscular reaction to forced anterior tibial translation (ATT). In 17 knees from 12 cats, EMG electrodes and ultrasonomicrometry crystals were inserted into four main periarticular muscles, with strain gauges on periarticular ligament insertions. Their output signal was compared before and after ACL surgical section in series of ATT (at 90 degrees and 30 degrees knee flexion), and also during knee flexion and extension. Linear regression analysis was performed between the EMG signal and muscular fibre length variations, and between the EMG signal and the strain on ligament insertions, in the search of this reflex neuromuscular response. In the ACL deficient knees, the studied muscles showed a poor adjustment to motion of EMG firing, inversely to controls. The muscle stretch reflexes showed poorer correlation with post-peak EMG activity than the ligaments. ATT control depended mainly on hamstrings activity in control knees, whereas in unstable knees, quadriceps activity was associated with more tibial translation. Acute ACL-deficient knees showed poor neuromuscular control with weak ligamentomuscular reflexes and no muscular stretch reflexes, suggesting the ineffectiveness of acute muscular reaction to provide early mechanical knee stabilization after injury.

  7. 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

  8. 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

  9. 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

  10. Phencyclidine-induced loss of asymmetric spine synapses in rodent prefrontal cortex is reversed by acute and chronic treatment with olanzapine.

    PubMed

    Elsworth, John D; Morrow, Bret A; Hajszan, Tibor; Leranth, Csaba; Roth, Robert H

    2011-09-01

    Enduring cognitive deficits exist in schizophrenic patients, long-term abusers of phencyclidine (PCP), as well as in animal PCP models of schizophrenia. It has been suggested that cognitive performance and memory processes are coupled with remodeling of pyramidal dendritic spine synapses in prefrontal cortex (PFC), and that reduced spine density and number of spine synapses in the medial PFC of PCP-treated rats may potentially underlie, at least partially, the cognitive dysfunction previously observed in this animal model. The present data show that the decrease in number of asymmetric (excitatory) spine synapses in layer II/III of PFC, previously noted at 1-week post PCP treatment also occurs, to a lesser degree, in layer V. The decrease in the number of spine synapses in layer II/III was sustained and persisted for at least 4 weeks, paralleling the observed cognitive deficits. Both acute and chronic treatment with the atypical antipsychotic drug, olanzapine, starting at 1 week after PCP treatment at doses that restore cognitive function, reversed the asymmetric spine synapse loss in PFC of PCP-treated rats. Olanzapine had no significant effect on spine synapse number in saline-treated controls. These studies demonstrate that the effect of PCP on asymmetric spine synapse number in PFC lasts at least 4 weeks in this model. This spine synapse loss in PFC is reversed by acute treatment with olanzapine, and this reversal is maintained by chronic oral treatment, paralleling the time course of the restoration of the dopamine deficit, and normalization of cognitive function produced by olanzapine.

  11. Obesity and upper airway control during sleep

    PubMed Central

    Patil, Susheel P.; Squier, Samuel; Schneider, Hartmut; Kirkness, Jason P.; Smith, Philip L.

    2010-01-01

    Mechanisms linking obesity with upper airway dysfunction in obstructive sleep apnea are reviewed. Obstructive sleep apnea is due to alterations in upper airway anatomy and neuromuscular control. Upper airway structural alterations in obesity are related to adipose deposition around the pharynx, which can increase its collapsibility or critical pressure (Pcrit). In addition, obesity and, particularly, central adiposity lead to reductions in resting lung volume, resulting in loss of caudal traction on upper airway structures and para