Статті в журналах: "Sleep-wake cycle"

1

Martell, M. "Sleep-Wake Cycle." Acta Scientific Paediatrics 5, no. 3 (February 26, 2022): 25–26. http://dx.doi.org/10.31080/aspe.2022.05.0506.

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2

Claustrat, B., J. Brun, M. Geoffriau, G. Chazot, and M. J. Challarmel. "Melatonin, sleep-wake cycle and sleep." Biological Psychiatry 42, no. 1 (July 1997): 226S. http://dx.doi.org/10.1016/s0006-3223(97)87830-4.

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3

Murillo-Rodriguez, Eric, Oscar Arias-Carrion, Katya Sanguino-Rodriguez, Mauricio Gonzalez-Arias, and Reyes Haro. "Mechanisms of Sleep-Wake Cycle Modulation." CNS & Neurological Disorders - Drug Targets 8, no. 4 (August 1, 2009): 245–53. http://dx.doi.org/10.2174/187152709788921654.

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4

Shadan, Farhad F. "Sleep-wake cycle, aging and cancer." Journal of Applied Biomedicine 6, no. 3 (July 31, 2008): 131–38. http://dx.doi.org/10.32725/jab.2008.016.

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5

Louzada, Fernando, and Luiz Menna-Barreto. "Sleep–Wake Cycle in Rural Populations." Biological Rhythm Research 35, no. 1-2 (February 2004): 153–57. http://dx.doi.org/10.1080/09291010412331313304.

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6

Wexler, D. B., and M. C. Moore-Ede. "Circadian sleep-wake cycle organization in squirrel monkeys." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 248, no. 3 (March 1, 1985): R353—R362. http://dx.doi.org/10.1152/ajpregu.1985.248.3.r353.

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To investigate the relationship between circadian rhythms of body temperature and sleep-wake stages, four squirrel monkeys were prepared for unrestrained monitoring of temperature, locomotor activity, electroencephalogram, electroculogram, and electromyogram. Continuous records for each animal were made for several 12-h light-dark (LD) cycles and then after a few days in constant illumination (LL). All animals maintained consolidated sleep-wake cycles and had a longer circadian period (mean 24.7 h) in LL than in LD (mean 24.1 h). The increased period reflected greater time per circadian cycle spent awake in LL (mean 14.0 h) than in LD (mean 12.8 h). Total night NREM sleep was less in LL (mean 6.5 h) than in LD (mean 8.2 h). Sleep onset occurred at later phases in LL (187 +/- 6 degrees) than in LD (170 +/- 2 degrees). Because the circadian phase measure of NREM sleep was unchanged between LD and LL conditions, the difference in sleep onsets reflected balanced changes in NREM circadian waveforms. Wake-up phases were the same in both conditions (mean 342 degrees). In summary, during free run squirrel monkeys maintain a stable consolidated circadian sleep-wake cycle with a period greater than 24 h, but they exhibit only minimal internal phase restructuring.

7

Duclos, Catherine, Marie Dumont, Caroline Arbour, Jean Paquet, Hélène Blais, David K. Menon, Louis De Beaumont, Francis Bernard, and Nadia Gosselin. "Parallel recovery of consciousness and sleep in acute traumatic brain injury." Neurology 88, no. 3 (December 21, 2016): 268–75. http://dx.doi.org/10.1212/wnl.0000000000003508.

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Objective:To investigate whether the progressive recuperation of consciousness was associated with the reconsolidation of sleep and wake states in hospitalized patients with acute traumatic brain injury (TBI).Methods:This study comprised 30 hospitalized patients (age 29.1 ± 13.5 years) in the acute phase of moderate or severe TBI. Testing started 21.0 ± 13.7 days postinjury. Consciousness level and cognitive functioning were assessed daily with the Rancho Los Amigos scale of cognitive functioning (RLA). Sleep and wake cycle characteristics were estimated with continuous wrist actigraphy. Mixed model analyses were performed on 233 days with the RLA (fixed effect) and sleep-wake variables (random effects). Linear contrast analyses were performed in order to verify if consolidation of the sleep and wake states improved linearly with increasing RLA score.Results:Associations were found between scores on the consciousness/cognitive functioning scale and measures of sleep-wake cycle consolidation (p < 0.001), nighttime sleep duration (p = 0.018), and nighttime fragmentation index (p < 0.001). These associations showed strong linear relationships (p < 0.01 for all), revealing that consciousness and cognition improved in parallel with sleep-wake quality. Consolidated 24-hour sleep-wake cycle occurred when patients were able to give context-appropriate, goal-directed responses.Conclusions:Our results showed that when the brain has not sufficiently recovered a certain level of consciousness, it is also unable to generate a 24-hour sleep-wake cycle and consolidated nighttime sleep. This study contributes to elucidating the pathophysiology of severe sleep-wake cycle alterations in the acute phase of moderate to severe TBI.

8

Marita, P., and R. Acharya Pandey. "Prevalence of sleep – wake cycle disturbance among cancer patients of Bhaktapur cancer hospital, Nepal." Journal of Chitwan Medical College 6, no. 2 (February 20, 2017): 6–13. http://dx.doi.org/10.3126/jcmc.v6i2.16678.

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Cancer patients are at great risk for developing insomnia and disorders of the sleep-wake cycle. Insomnia is the most common sleep disturbance in this population and is most often secondary to physical and/or psychological factors related to cancer and/or cancer treatment. It is estimated that nearly 45% of cancer patients experience sleep disturbances; this is nearly three times the estimate of its occurrence in the general population. The purpose of the study is to determine the prevalence of sleep-wake cycle disturbance in patient receiving chemotherapy. A descriptive cross-sectional study was carried out in 2013. A total of 205 respondents, visiting Bhaktapur Cancer Hospital and who met criteria were purposively sampled and interviewed face to face. Insomnia Severity Index Scale was used to grade insomnia. Descriptive statistics such as frequency and percentage was used to describe demographic data. Chi-square test was done to find out the association between prevalence of sleep-wake cycle disturbance and selected variables. Among the total respondents (205), 70.7% had sleep-wake cycle disturbances. Majority (71.21%) of respondents had some form of clinically significant insomnia. The ages of the respondents ranged from 20 to 81 years with the mean age of 56.25 (SD ± 13.87). More than half i.e. 69.3% of the respondents were female. Patients being treated with Methotrexate were found to be more associated with the development of sleep-wake cycle disturbance. The significant association was found on drinking tea/coffee with the prevalence sleep-wake cycle disturbance. Sleep disorders are a common and often chronic problem for patients with cancer. Recently, such symptoms have attracted little attention. This might be the reasons for increased prevalence of sleep-wake cycle disturbance. It is recommended to take early and adequate intervention for the reduction of increased prevalence rate of sleep-wake cycle disturbance.

9

Dijk, Derk-Jan, and Steven W. Lockley. "Invited Review: Integration of human sleep-wake regulation and circadian rhythmicity." Journal of Applied Physiology 92, no. 2 (February 1, 2002): 852–62. http://dx.doi.org/10.1152/japplphysiol.00924.2001.

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The human sleep-wake cycle is generated by a circadian process, originating from the suprachiasmatic nuclei, in interaction with a separate oscillatory process: the sleep homeostat. The sleep-wake cycle is normally timed to occur at a specific phase relative to the external cycle of light-dark exposure. It is also timed at a specific phase relative to internal circadian rhythms, such as the pineal melatonin rhythm, the circadian sleep-wake propensity rhythm, and the rhythm of responsiveness of the circadian pacemaker to light. Variations in these internal and external phase relationships, such as those that occur in blindness, aging, morning and evening, and advanced and delayed sleep-phase syndrome, lead to sleep disruptions and complaints. Changes in ocular circadian photoreception, interindividual variation in the near-24-h intrinsic period of the circadian pacemaker, and sleep homeostasis can contribute to variations in external and internal phase. Recent findings on the physiological and molecular-genetic correlates of circadian sleep disorders suggest that the timing of the sleep-wake cycle and circadian rhythms is closely integrated but is, in part, regulated differentially.

10

Bochkarev, M. V., L. S. Korostovtseva, A. B. Tataraidze, A. V. Orlov, O. P. Rotar, R. O. Ragozin, Zh I. Molchanova, and Yu V. Sviryaev. "Sleep-wake cycle regularity and cardiometabolic indicators." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 121, no. 4 (2021): 57. http://dx.doi.org/10.17116/jnevro202112104157.

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11

Cantero, Jose L., Eva Hita-Yañez, Bernardo Moreno-Lopez, Federico Portillo, Alicia Rubio, and Jesus Avila. "Tau Protein Role in Sleep-Wake Cycle." Journal of Alzheimer's Disease 21, no. 2 (August 11, 2010): 411–21. http://dx.doi.org/10.3233/jad-2010-100285.

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12

Geladze, Tina S., Kote S. Dzamashvili, and Maya G. Djibladze. "Sleep-Wake Cycle in Cluster Headache Patients." Cephalalgia 11, no. 11_suppl (June 1991): 260–61. http://dx.doi.org/10.1177/0333102491011s11139.

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13

Buguet, A., J. Bert, P. Tapie, F. Tabaraud, F. Doua, J. Lonsdorfer, P. Bogui, and M. Dumas. "Sleep-Wake Cycle in Human African Trypanosomiasis." Journal of Clinical Neurophysiology 10, no. 2 (April 1993): 190–96. http://dx.doi.org/10.1097/00004691-199304000-00006.

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14

Wagner, Daniel R. "DISORDERS OF THE CIRCADIAN SLEEP–WAKE CYCLE." Neurologic Clinics 14, no. 3 (August 1996): 651–70. http://dx.doi.org/10.1016/s0733-8619(05)70278-4.

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15

Karlsson, K. Æ., J. C. Kreider, and M. S. Blumberg. "Hypothalamic contribution to sleep–wake cycle development." Neuroscience 123, no. 2 (January 2004): 575–82. http://dx.doi.org/10.1016/j.neuroscience.2003.09.025.

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16

Ono, Daisuke, and Akihiro Yamanaka. "Hypothalamic regulation of the sleep/wake cycle." Neuroscience Research 118 (May 2017): 74–81. http://dx.doi.org/10.1016/j.neures.2017.03.013.

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17

Lemmer, Björn. "The sleep–wake cycle and sleeping pills." Physiology & Behavior 90, no. 2-3 (February 2007): 285–93. http://dx.doi.org/10.1016/j.physbeh.2006.09.006.

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18

Beersma, Domien G. M., and Marijke C. M. Gordijn. "Circadian control of the sleep–wake cycle." Physiology & Behavior 90, no. 2-3 (February 2007): 190–95. http://dx.doi.org/10.1016/j.physbeh.2006.09.010.

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19

DiNuzzo, Mauro, and Maiken Nedergaard. "Brain energetics during the sleep–wake cycle." Current Opinion in Neurobiology 47 (December 2017): 65–72. http://dx.doi.org/10.1016/j.conb.2017.09.010.

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20

Portas, Chiara M., Karsten Krakow, Phillip Allen, Oliver Josephs, Jorge L. Armony, and Chris D. Frith. "Auditory Processing across the Sleep-Wake Cycle." Neuron 28, no. 3 (December 2000): 991–99. http://dx.doi.org/10.1016/s0896-6273(00)00169-0.

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21

Székely, Miklós. "Orexins, energy balance, temperature, sleep-wake cycle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (September 2006): R530—R532. http://dx.doi.org/10.1152/ajpregu.00179.2006.

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22

Wollman, M., and P. Lavie. "Hypernychthemeral Sleep-Wake Cycle: Some Hidden Regularities." Sleep 9, no. 2 (June 1986): 324–34. http://dx.doi.org/10.1093/sleep/9.2.324.

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23

Culebras, Antonio. "Update on Disorders of Sleep and the Sleep-Wake Cycle." Psychiatric Clinics of North America 15, no. 2 (June 1992): 467–86. http://dx.doi.org/10.1016/s0193-953x(18)30250-8.

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24

Kunz, Dieter, and Werner Martin Herrmann. "Sleep-wake cycle, sleep-related disturbances, and sleep disorders: A chronobiological approach." Comprehensive Psychiatry 41, no. 2 (March 2000): 104–15. http://dx.doi.org/10.1016/s0010-440x(00)80016-4.

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25

Holth, Jerrah K., Sarah K. Fritschi, Chanung Wang, Nigel P. Pedersen, John R. Cirrito, Thomas E. Mahan, Mary Beth Finn, et al. "The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans." Science 363, no. 6429 (January 24, 2019): 880–84. http://dx.doi.org/10.1126/science.aav2546.

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The sleep-wake cycle regulates interstitial fluid (ISF) and cerebrospinal fluid (CSF) levels of β-amyloid (Aβ) that accumulates in Alzheimer’s disease (AD). Furthermore, chronic sleep deprivation (SD) increases Aβ plaques. However, tau, not Aβ, accumulation appears to drive AD neurodegeneration. We tested whether ISF/CSF tau and tau seeding and spreading were influenced by the sleep-wake cycle and SD. Mouse ISF tau was increased ~90% during normal wakefulness versus sleep and ~100% during SD. Human CSF tau also increased more than 50% during SD. In a tau seeding-and-spreading model, chronic SD increased tau pathology spreading. Chemogenetically driven wakefulness in mice also significantly increased both ISF Aβ and tau. Thus, the sleep-wake cycle regulates ISF tau, and SD increases ISF and CSF tau as well as tau pathology spreading.

26

Hsu, Chung-Yao, Yao-Chung Chuang, Fang-Chia Chang, Hung-Yi Chuang, Terry Ting-Yu Chiou, and Chien-Te Lee. "Disrupted Sleep Homeostasis and Altered Expressions of Clock Genes in Rats with Chronic Lead Exposure." Toxics 9, no. 9 (September 10, 2021): 217. http://dx.doi.org/10.3390/toxics9090217.

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Sleep disturbance is one of the neurobehavioral complications of lead neurotoxicity. The present study evaluated the impacts of chronic lead exposure on alteration of the sleep–wake cycle in association with changes of clock gene expression in the hypothalamus. Sprague–Dawley rats with chronic lead exposure consumed drinking water that contained 250 ppm of lead acetate for five weeks. Electroencephalography and electromyography were recorded for scoring the architecture of the sleep–wake cycle in animals. At six Zeitgeber time (ZT) points (ZT2, ZT6, ZT10, ZT14, ZT18, and ZT22), three clock genes, including rPer1, rPer2, and rBmal1b, were analyzed. The rats with chronic lead exposure showed decreased slow wave sleep and increased wakefulness in the whole light period (ZT1 to ZT12) and the early dark period (ZT13 to ZT15) that was followed with a rebound of rapid-eye-movement sleep at the end of the dark period (ZT22 to ZT24). The disturbance of the sleep–wake cycle was associated with changes in clock gene expression that was characterized by the upregulation of rPer1 and rPer2 and the feedback repression of rBmal1b. We concluded that chronic lead exposure has a negative impact on the sleep–wake cycle in rats that predominantly disrupts sleep homeostasis. The disruption of sleep homeostasis was associated with a toxic effect of lead on the clock gene expression in the hypothalamus.

27

Gavrilov, Yuri V., Kristina Z. Derevtsova, and Elena A. Korneva. "Morphofunctional alterations of the hypothalamic neurons activity during sleep-wake cycle regulation disturbances after experimental traumatic brain injury." Medical academic journal 19, no. 3 (December 26, 2019): 47–56. http://dx.doi.org/10.17816/maj19347-56.

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Relevance. The study of sleep disorders mechanisms after traumatic brain injury is complicated and poorly understood. Traumatic damage to the structures that are responsible for the sleep-wake cycle regulation is a common cause of sleep disorders after traumatic brain injury. The number of hypothalamic neurotransmitter systems, which are involved in the sleep-wake cycle regulation, could change its functional activity after trauma that suggests their key role in the development of disturbances of this process. The aim of the study was to assess the morphological alterations of the hypothalamus neurons that is involved in the regulation of sleep and wakefulness after traumatic brain injury in an experiment. Methods. For a combined analysis of posttraumatic disturbances of the sleep-wake cycle and morphofunctional changes in the neurotransmitter systems which are involved in the regulation of the sleep-wake cycle, we used a polysomnography in rats during a month and then an immunohistochemical method for estimating the quantify the orexin A, melanin-concentrating hormone, histamine and tyrosine hydroxylase. Results. The number of histamine-containing cells in the tuberomammillary nuclei of the hypothalamus is obviously decreased after traumatic brain injury in animals. This alteration of the degree of immunoreactivity of histamine-containing cells after traumatic brain injury correlated with sleep duration changes in animals. The number of noradrenergic and orexinergic neurons was compare with control animal group. Conclusion. These results suggest that a change in the functional activity of histamine-containing neurons after traumatic brain injury may be the cause of post-traumatic sleep and wakefulness disorders. Our results may lead to a creating of a new approach for a therapy for posttraumatic sleep-wake disturbances.

28

Yamanaka, Yujiro, Satoko Hashimoto, Yusuke Tanahashi, Shin-ya Nishide, Sato Honma, and Ken-ichi Honma. "Physical exercise accelerates reentrainment of human sleep-wake cycle but not of plasma melatonin rhythm to 8-h phase-advanced sleep schedule." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 3 (March 2010): R681—R691. http://dx.doi.org/10.1152/ajpregu.00345.2009.

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Effects of timed physical exercise were examined on the reentrainment of sleep-wake cycle and circadian rhythms to an 8-h phase-advanced sleep schedule. Seventeen male adults spent 12 days in a temporal isolation facility with dim light conditions (<10 lux). The sleep schedule was phase-advanced by 8 h from their habitual sleep times for 4 days, which was followed by a free-run session for 6 days, during which the subjects were deprived of time cues. During the shift schedule, the exercise group ( n = 9) performed physical exercise with a bicycle ergometer in the early and middle waking period for 2 h each. The control group ( n = 8) sat on a chair at those times. Their sleep-wake cycles were monitored every day by polysomnography and/or weight sensor equipped with a bed. The circadian rhythm in plasma melatonin was measured on the baseline day before phase shift: on the 4th day of shift schedule and the 5th day of free-run. As a result, the sleep-onset on the first day of free-run in the exercise group was significantly phase-advanced from that in the control and from the baseline. On the other hand, the circadian melatonin rhythm was significantly phase-delayed in the both groups, showing internal desynchronization of the circadian rhythms. The sleep-wake cycle resynchronized to the melatonin rhythm by either phase-advance or phase-delay shifts in the free-run session. These findings indicate that the reentrainment of the sleep-wake cycle to a phase-advanced schedule occurs independent of the circadian pacemaker and is accelerated by timed physical exercise.

29

Gomes, Matheus Antonio, Fernanda Veruska Narciso, Marco Tulio de Mello, and Andrea Maculano Esteves. "Identifying electronic-sport athletes’ sleep-wake cycle characteristics." Chronobiology International 38, no. 7 (April 11, 2021): 1002–9. http://dx.doi.org/10.1080/07420528.2021.1903480.

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30

Semenova, N. V., I. M. Madaeva, and L. I. Kolesnikova. "Clock Gene, Melatonin, and the Sleep–Wake Cycle." Russian Journal of Genetics 57, no. 3 (March 2021): 251–57. http://dx.doi.org/10.1134/s1022795421030121.

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31

Sinha, Prabhat, Susmita Chowdhuri, and James A. Rowley. "Sleep-Wake Cycle Diagnosed by CPAP Compliance Study." Journal of Clinical Sleep Medicine 4, no. 1 (February 15, 2008): 70–72. http://dx.doi.org/10.5664/jcsm.27084.

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32

Demeli, Meriç, Sibel Bayrak, and Bilge Pehlivanoğlu. "Effects of Adenosine on the Sleep-Wake Cycle." Journal of Turkish Sleep Medicine 9, no. 3 (September 6, 2022): 190–98. http://dx.doi.org/10.4274/jtsm.galenos.2022.36349.

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33

Nakanishi-Minami, Tomoko, Ken Kishida, Tohru Funahashi, and Iichiro Shimomura. "Sleep-wake cycle irregularities in type 2 diabetics." Diabetology & Metabolic Syndrome 4, no. 1 (2012): 18. http://dx.doi.org/10.1186/1758-5996-4-18.

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34

Kunz, D. "C.09.02 Melatonin and the sleep-wake cycle." European Neuropsychopharmacology 18 (August 2008): S597. http://dx.doi.org/10.1016/s0924-977x(08)70926-x.

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35

Van Erum, Jan, Debby Van Dam, and Peter Paul De Deyn. "Alzheimer’s disease: Neurotransmitters of the sleep-wake cycle." Neuroscience & Biobehavioral Reviews 105 (October 2019): 72–80. http://dx.doi.org/10.1016/j.neubiorev.2019.07.019.

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36

Rempe, Michael J., Janet Best, and David Terman. "A mathematical model of the sleep/wake cycle." Journal of Mathematical Biology 60, no. 5 (June 26, 2009): 615–44. http://dx.doi.org/10.1007/s00285-009-0276-5.

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37

Barre, V., and A. Petter-Rousseaux. "Seasonal variations in sleep-wake cycle inMicrocebus murinus." Primates 29, no. 1 (January 1988): 53–64. http://dx.doi.org/10.1007/bf02380849.

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38

Sedgwick, P. M. "Disorders of the sleep-wake cycle in adults." Postgraduate Medical Journal 74, no. 869 (March 1, 1998): 134–38. http://dx.doi.org/10.1136/pgmj.74.869.134.

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39

Carpenter, Gail A. "Mathematical models of the Circadian sleep-wake cycle." Mathematical Biosciences 79, no. 2 (June 1986): 231–33. http://dx.doi.org/10.1016/0025-5564(86)90152-5.

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40

Guaraldi, Pietro, Giovanna Calandra‐Buonaura, Federica Provini, and Pietro Cortelli. "Role of Thalamus in Sleep–Wake Cycle Regulation." Annals of Neurology 85, no. 4 (March 11, 2019): 611. http://dx.doi.org/10.1002/ana.25449.

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41

Assadzadeh, S., and P. A. Robinson. "Necessity of the sleep–wake cycle for synaptic homeostasis: system-level analysis of plasticity in the corticothalamic system." Royal Society Open Science 5, no. 10 (October 2018): 171952. http://dx.doi.org/10.1098/rsos.171952.

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Neural field theory is used to study the system-level effects of plasticity in the corticothalamic system, where arousal states are represented parametrically by the connection strengths of the system, among other physiologically based parameters. It is found that the plasticity dynamics have no fixed points or closed cycles in the parameter space of the connection strengths, but parameter subregions exist where flows have opposite signs. Remarkably, these subregions coincide with previously identified regions that correspond to wake and slow-wave sleep, thus demonstrating state dependence of the sign of synaptic modification. We then show that a closed cycle in the parameter space is possible when the plasticity dynamics are driven by the ascending arousal system, which cycles the brain between sleep and wake to complete a closed loop that includes arcs through the opposite-flow subregions. Thus, it is concluded that both wake and sleep are necessary, and together are able to stabilize connection weights in the brain over the daily cycle, thereby providing quantitative realization of the synaptic homeostasis hypothesis.

42

Krystal, Andrew D., Ruth M. Benca, and Thomas S. Kilduff. "Understanding the Sleep-Wake Cycle: Sleep, Insomnia, and the Orexin System." Journal of Clinical Psychiatry 74, suppl 1 (September 2013): 3–20. http://dx.doi.org/10.4088/jcp.13011su1c.

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43

Pires daRocha, M. C., and M. M. F. De Martino. "013 THE SLEEP-WAKE CYCLE AMONG NURSES USING MEDICATIONS TO SLEEP." Sleep Medicine 10 (December 2009): S4. http://dx.doi.org/10.1016/s1389-9457(09)70015-2.

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44

Arias-Carrión, Oscar, Salvador Huitrón-Reséndiz, Gloria Arankowsky-Sandoval, and Eric Murillo-Rodríguez. "Biochemical modulation of the sleep-wake cycle: Endogenous sleep-inducing factors." Journal of Neuroscience Research 89, no. 8 (May 6, 2011): 1143–49. http://dx.doi.org/10.1002/jnr.22666.

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45

Hajak, G. "Chronobiological issues of sleep and circadian rhythms." European Psychiatry 26, S2 (March 2011): 2133. http://dx.doi.org/10.1016/s0924-9338(11)73836-6.

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Progress in unravelling the cellular and molecular basis of mammalian circadian regulation over the past decade has provided us with data that deteriorations in measurable circadian output parameters, such as sleep/wake deficits and dysregulation of circulating hormone levels, are common features of most central nervous system disorders.At the core of the mammalian circadian system is a complex of molecular oscillations within the hypothalamic suprachiasmatic nucleus. These oscillations are modifiable by afferent signals from the environment, and integrated signals are subsequently conveyed to remote central neural circuits where specific output rhythms are regulated. Usually our sleep/wake cycle, temperature and melatonin rhythms are internally synchronized with a stable phase relationship. When there is a desynchrony between the sleep/wake cycle and circadian rhythm, sleep disorders such as advanced and delayed sleep phase syndrome can arise as well as transient chronobiologic disturbances, for example from jet lag and shift work.Increasing evidence suggests that disrupted temporal organization of biological functions impairs behaviour, cognition, affect, and emotion. Furthermore, disruption of circadian clock genes impairs the sleep-wake cycle and social rhythms, which may be implicated in particular in mental disorders. An increasing number of journal publications point to a crucial role of circadian rhythm dysregulations in particular for affective disorders, which should e addressed specifically in modern psychiatry.

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De Martino, Milva Maria Figueiredo, Ana Cristina Basto Abreu, Manuel Fernando dos Santos Barbosa, and João Eduardo Marques Teixeira. "The relationship between shift work and sleep patterns in nurses." Ciência & Saúde Coletiva 18, no. 3 (March 2013): 763–68. http://dx.doi.org/10.1590/s1413-81232013000300022.

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The scope of this study was to evaluate the sleep/wake cycle in shift work nurses, as well as their sleep quality and chronotype. The sleep/wake cycle was evaluated by keeping a sleep diary for a total of 60 nurses with a mean age of 31.76 years. The Horne & Östberg Questionnaire (1976) for the chronotype and the Pittsburgh Sleep Quality Index (PSQI) for sleep quality were applied. The results revealed a predominance of indifferent chronotypes (65.0%), followed by moderately evening persons (18.3%), decidedly evening persons (8.3%), moderately morning persons (6.6%) and decidedly morning persons (1.8%). The sleep quality perception was analyzed by the visual analogical scale, showing a mean score of 5.85 points for nighttime sleep and 4.70 points for daytime sleep, which represented a statistically significant difference. The sleep/wake schedule was also statistically different when considering weekdays and weekends. The PSQI showed a mean of 7.0 points, characterizing poor sleep quality. The results showed poor sleep quality in shift work nurses, possibly due to the lack of sport and shift work habits.

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Kanarskii, Mikhail, Julia Nekrasova, Pranil Pradhan, Ilya Borisov, Olga Korepina, Ekaterina Kondratyeva, Angelina Nikitkina, and Marina Petrova. "The High-Dose of Exogenous Melatonin Did Not Alter the Sleep-Wake Cycle in Anoxic Brain Injury Patients." Sleep Medicine Research 13, no. 2 (September 30, 2022): 112–17. http://dx.doi.org/10.17241/smr.2022.01361.

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Disturbance in circadian rhythms and the sleep-wake cycle is typical for patients in the intensive care unit, which retards rehabilitation. To assess the effect of exogenous melatonin and simultaneous mitigation of intensive care unit environmental factors on sleep duration. We studied five patients with chronic disorder of consciousness caused by anoxic brain injury. In addition, we varied the level of melatonin secretion in blood plasma to assess melatonin’s bioavailability and elimination time. We evaluated the sleep-wake cycle using continuous videoelectroencephalogram monitoring with the addition of oculographic and myographic channels for 72 hours. All the patients received melatonin tablets on the second day, wore masks and ear plugs, and had no feeding and nursing manipulations at night on the second and third days. There was no significant difference in sleep time between the first, second, and third days. Future studies of the circadian rhythm should aim at gaining a deeper analysis of the characteristics of the sleep-wake cycle in patients with severe anoxic brain injury together with further research for possible ways to influence the circadian component of sleep.

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Sattari, N., K. Simon, and S. Mednick. "0110 Fluctuations Across the Menstrual Cycle in Cardiac Autonomic Activity During Sleep and Wake May Affect Memory Consolidation." Sleep 43, Supplement_1 (April 2020): A43—A44. http://dx.doi.org/10.1093/sleep/zsaa056.108.

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Abstract Introduction Prior studies have shown that benefits of sleep for memory consolidation may be influenced by menstrual phase. Menstrual phase also impact autonomic regulation during sleep, and autonomic activity has been recently shown to play a role in sleep-dependent memory consolidation. Methods We investigated the interaction of menstrual cycle and autonomic activity measured by heart rate-variability (HRV) on sleep-dependent memory consolidation among 18-healthy females. Using a within-subjects design, we investigated episodic memory improvement with a nap paradigm during two phases of women’s menstrual cycle: 1) perimenses: −5 to +5 days from menses-onset, and 2) non-perimenses: window outside of perimenses. Subjects completed the memory test before (Test1) and after (Test2) a 90-minute polysomnographically (PSG)-recorded nap. We recorded sleep and HRV during 5-minutes of wake, and during the nap. Next, we compared sleep, HRV (RMSSD and HFnu), and memory performance between the two menstrual phases. Results Sleep architecture did not differ between perimenses and non-perimenses. Women performed similarly on the memory task at Test 1 (all ps>.061), but at Test 2, non-perimenses showed better performance (p = 0.02). Autonomically, perimenses had higher parasympathetic activity during wake (RMSSD-p = 0.04) and REM-sleep (HFnu-p = 0.04), compared with non-perimenses. Using bivariate correlations, we found positive associations between wake-HFnu and memory improvement (p = .02) during perimenses. In contrast, non-perimenses’ memory improvement was negatively correlated with wake-RMSSD (p <.001). In perimenses, memory improvement was also positively associtated with REM-HFnu (p = .04). No associations were found between autonomic sleep activity and memory in non-perimenses phase. Conclusion Our findings indicate a role for autonomic activity in memory improvement in both sleep and wake that is modulated by the menstrual cycle. HRV measures of parasympathetic activity were higher during perimenses phase in wake and REM-sleep. Interestingly, the HRV measures showed opposing relations with memory improvement based on the phase of the menstrual cycle. In sum, women’s cardiac autonomic activity fluctuates by menstrual phase and it is possible that these fluctuations affect the magnitude and direction of sleep-related memory consolidation. Support Sattari et al., 2017; Genzel et al., 2012; de Zambotti et al., 2013; Whitehurst et al., 2016.

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Yamanaka, Yujiro, Satoko Hashimoto, Satoru Masubuchi, Akiyo Natsubori, Shin-ya Nishide, Sato Honma, and Ken-ichi Honma. "Differential regulation of circadian melatonin rhythm and sleep-wake cycle by bright lights and nonphotic time cues in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 5 (September 1, 2014): R546—R557. http://dx.doi.org/10.1152/ajpregu.00087.2014.

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Our previous study demonstrated that physical exercise under dim lights (<10 lux) accelerated reentrainment of the sleep-wake cycle but not the circadian melatonin rhythm to an 8-h phase-advanced sleep schedule, indicating differential effects of physical exercise on the human circadian system. The present study examined the effects of bright light (>5,000 lux) on exercise-induced acceleration of reentrainment because timed bright lights are known to reset the circadian pacemaker. Fifteen male subjects spent 12 days in temporal isolation. The sleep schedule was advanced from habitual sleep times by 8 h for 4 days, which was followed by a free-run session. In the shift session, bright lights were given during the waking time. Subjects in the exercise group performed 2-h bicycle running twice a day. Subjects in the control kept quiet. As a result, the sleep-wake cycle was fully entrained by the shift schedule in both groups. Bright light may strengthen the resetting potency of the shift schedule. By contrast, the circadian melatonin rhythm was phase-advanced by 6.9 h on average in the exercise group but only by 2.0 h in the control. Thus physical exercise prevented otherwise unavoidable internal desynchronization. Polysomnographical analyses revealed that deterioration of sleep quality by shift schedule was protected by physical exercise under bright lights. These findings indicate differential regulation of sleep-wake cycle and circadian melatonin rhythm by physical exercise in humans. The melatonin rhythm is regulated primarily by bright lights, whereas the sleep-wake cycle is by nonphotic time cues, such as physical exercise and shift schedule.

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Radić, Neda, Ivan Zaletel, Milan Lakočević, Milica Labudović-Borović, Miloš Bajčetić, Milan Ćirić, Jelena Kostić, Aleksandar Mirčić, and Nela Puškaš. "The role of orexin/hypocretin in regulating the sleep: Wake cycle." Medicinska istrazivanja 48, no. 1 (2014): 42–47. http://dx.doi.org/10.5937/medist1401042r.

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The neurons of the lateral hypothalamus that synthesize peptides hypocretin/orexin from a common precursor pre-pro-orexin/preprohypocretin are the key stabilizers of sleep-wake cycle. Regulation of sleep-wake cycle is achieved through a functional interaction between orexinergic neurons of the hypothalamus, monoaminergic/cholinergic neurons of the brainstem and GABAergic/galanin neurons of the ventrolateral preoptic nucleus. Orexins/hypocretins originating from the hypothalamus excite monoaminergic neurons. In contrast to this, excited monoaminergic neurons reciprocally inhibit orexinergic neurons. GABAergic neurons, which also include galanin, send inhibitory signals to monoaminergic and orexinergic neurons, while monoaminergic neurons send inhibitory signals to GABAergic neurons who are active during sleep. Such an organization, with mutual influences is of great importance for the stabilization of sleep-wake cycle. Studies have also shown that the loss of orexinergic neurons is directly related to narcolepsy, a form of hypersomnia which is characterized by the sudden intrusion of NREM and REM sleep phase to wakefulness and frequent transitions between state of sleep and wakefulness. Narcolepsy may be accompanied by cataplexy, which is manifested by the sudden weak-ness of muscle tone. Discovery of the connection between the loss of orexinergic signaling and human narcolepsy-cata-plexy has led to new diagnostic and therapeutic options in the treatment of this disease.

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