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

Mallika, M. C. Vasantha, and Ajay Jayakumar Nair. "Effect of Sleep-Wake Cycles on Academic Performances and Behavioural Changes among Undergraduate Medical Students." Healthline 15, no. 1 (March 31, 2024): 86–90. http://dx.doi.org/10.51957/healthline5772023.

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Introduction: Sleep wake cycles form major part in the life of every student, starting from the school ages itself. This cycle has a major relationship in ensuring the proper functioning and day to day activities of the individual in all walks of life. Objectives: To assess the quality of sleep wake cycle among undergraduate medical students and to find out the association of sleep wake cycle with academic performances and behavioural changes among undergraduate medical students Results: In a cross sectional study among 300 participants, 35.3 % of the participants had good sleep-wake cycle. There was a positive association between sleep-wake cycles and academic performances. (χ2 value 5.24 with p value <0.05). Age, gender, residence, socioeconomic status and year of study showed statistically significant association with behavioural patterns (p value <0.05) Conclusion: Good quality of sleep wake cycle was present among one third of participants. There was a positive association between sleep-wake cycles and academic performance, but no significant association between behavioral patterns and sleep-wake cycles.

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3

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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4

Kniazkina, Marina, and Vyacheslav Dyachuk. "Does EGFR Signaling Mediate Orexin System Activity in Sleep Initiation?" International Journal of Molecular Sciences 24, no. 11 (May 30, 2023): 9505. http://dx.doi.org/10.3390/ijms24119505.

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Sleep–wake cycle disorders are an important symptom of many neurological diseases, including Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis. Circadian rhythms and sleep–wake cycles play a key role in maintaining the health of organisms. To date, these processes are still poorly understood and, therefore, need more detailed elucidation. The sleep process has been extensively studied in vertebrates, such as mammals and, to a lesser extent, in invertebrates. A complex, multi-step interaction of homeostatic processes and neurotransmitters provides the sleep–wake cycle. Many other regulatory molecules are also involved in the cycle regulation, but their functions remain largely unclear. One of these signaling systems is epidermal growth factor receptor (EGFR), which regulates the activity of neurons in the modulation of the sleep–wake cycle in vertebrates. We have evaluated the possible role of the EGFR signaling pathway in the molecular regulation of sleep. Understanding the molecular mechanisms that underlie sleep–wake regulation will provide critical insight into the fundamental regulatory functions of the brain. New findings of sleep-regulatory pathways may provide new drug targets and approaches for the treatment of sleep-related diseases.

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5

Putilov, Arcady A. "Can the Brain’s Thermostatic Mechanism Generate Sleep-Wake and NREM-REM Sleep Cycles? A Nested Doll Model of Sleep-Regulating Processes." Clocks & Sleep 6, no. 1 (February 19, 2024): 97–113. http://dx.doi.org/10.3390/clockssleep6010008.

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Evidence is gradually accumulating in support of the hypothesis that a process of thermostatic brain cooling and warming underlies sleep cycles, i.e., the alternations between non-rapid-eye-movement and rapid-eye-movement sleep throughout the sleep phase of the sleep-wake cycle. A mathematical thermostat model predicts an exponential shape of fluctuations in temperature above and below the desired temperature setpoint. If the thermostatic process underlies sleep cycles, can this model explain the mechanisms governing the sleep cyclicities in humans? The proposed nested doll model incorporates Process s generating sleep cycles into Process S generating sleep-wake cycles of the two-process model of sleep-wake regulation. Process s produces ultradian fluctuations around the setpoint, while Process S turns this setpoint up and down in accord with the durations of the preceding wake phase and the following sleep phase of the sleep-wake cycle, respectively. Predictions of the model were obtained in an in silico study and confirmed by simulations of oscillations of spectral electroencephalographic indexes of sleep regulation obtained from night sleep and multiple napping attempts. Only simple—inverse exponential and exponential—functions from the thermostatic model were used for predictions and simulations of rather complex and varying shapes of sleep cycles during an all-night sleep episode. To further test the proposed model, experiments on mammal species with monophasic sleep are required. If supported, this model can provide a valuable framework for understanding the involvement of sleep-wake regulatory processes in the mechanism of thermostatic brain cooling/warming.

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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.

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7

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.

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8

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.

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9

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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10

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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11

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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12

Westmark, Pamela R., Timothy J. Swietlik, Ethan Runde, Brian Corsiga, Rachel Nissan, Brynne Boeck, Ricky Granger, et al. "Adult Inception of Ketogenic Diet Therapy Increases Sleep during the Dark Cycle in C57BL/6J Wild Type and Fragile X Mice." International Journal of Molecular Sciences 25, no. 12 (June 18, 2024): 6679. http://dx.doi.org/10.3390/ijms25126679.

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Sleep problems are a significant phenotype in children with fragile X syndrome. Our prior work assessed sleep–wake cycles in Fmr1KO male mice and wild type (WT) littermate controls in response to ketogenic diet therapy where mice were treated from weaning (postnatal day 18) through study completion (5–6 months of age). A potentially confounding issue with commencing treatment during an active period of growth is the significant reduction in weight gain in response to the ketogenic diet. The aim here was to employ sleep electroencephalography (EEG) to assess sleep–wake cycles in mice in response to the Fmr1 genotype and a ketogenic diet, with treatment starting at postnatal day 95. EEG results were compared with prior sleep outcomes to determine if the later intervention was efficacious, as well as with published rest-activity patterns to determine if actigraphy is a viable surrogate for sleep EEG. The data replicated findings that Fmr1KO mice exhibit sleep–wake patterns similar to wild type littermates during the dark cycle when maintained on a control purified-ingredient diet but revealed a genotype-specific difference during hours 4–6 of the light cycle of the increased wake (decreased sleep and NREM) state in Fmr1KO mice. Treatment with a high-fat, low-carbohydrate ketogenic diet increased the percentage of NREM sleep in both wild type and Fmr1KO mice during the dark cycle. Differences in sleep microstructure (length of wake bouts) supported the altered sleep states in response to ketogenic diet. Commencing ketogenic diet treatment in adulthood resulted in a 15% (WT) and 8.6% (Fmr1KO) decrease in body weight after 28 days of treatment, but not the severe reduction in body weight associated with starting treatment at weaning. We conclude that the lack of evidence for improved sleep during the light cycle (mouse sleep time) in Fmr1KO mice in response to ketogenic diet therapy in two studies suggests that ketogenic diet may not be beneficial in treating sleep problems associated with fragile X and that actigraphy is not a reliable surrogate for sleep EEG in mice.

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13

Westmark, Pamela R., Aaron K. Gholston, Timothy J. Swietlik, Rama K. Maganti, and Cara J. Westmark. "Ketogenic Diet Affects Sleep Architecture in C57BL/6J Wild Type and Fragile X Mice." International Journal of Molecular Sciences 24, no. 19 (September 22, 2023): 14460. http://dx.doi.org/10.3390/ijms241914460.

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Nearly half of children with fragile X syndrome experience sleep problems including trouble falling asleep and frequent nighttime awakenings. The goals here were to assess sleep–wake cycles in mice in response to Fmr1 genotype and a dietary intervention that reduces hyperactivity. Electroencephalography (EEG) results were compared with published rest–activity patterns to determine if actigraphy is a viable surrogate for sleep EEG. Specifically, sleep–wake patterns in adult wild type and Fmr1KO littermate mice were recorded after EEG electrode implantation and the recordings manually scored for vigilance states. The data indicated that Fmr1KO mice exhibited sleep–wake patterns similar to wild type littermates when maintained on a control purified ingredient diet. Treatment with a high-fat, low-carbohydrate ketogenic diet increased the percentage of non-rapid eye movement (NREM) sleep in both wild type and Fmr1KO mice during the dark cycle, which corresponded to decreased activity levels. Treatment with a ketogenic diet flattened diurnal sleep periodicity in both wild type and Fmr1KO mice. Differences in several sleep microstructure outcomes (number and length of sleep and wake bouts) supported the altered sleep states in response to a ketogenic diet and were correlated with altered rest–activity cycles. While actigraphy may be a less expensive, reduced labor surrogate for sleep EEG during the dark cycle, daytime resting in mice did not correlate with EEG sleep states.

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14

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.

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15

Martoni, Monica, Marco Fabbri, Annalisa Grandi, Luisa Sist, and Lara Colombo. "Self-Care Practices as a Mediator between Workaholism and Sleep–Wake Problems during COVID-19." Sustainability 15, no. 16 (August 20, 2023): 12603. http://dx.doi.org/10.3390/su151612603.

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Self-care practices are considered an important resource for workers’ psychophysical well-being. These resources were especially relevant during the COVID-19 outbreak, during which both workaholism and sleep–wake problems were documented. Our study aimed to examine whether workaholism could predict sleep–wake quality through the mediating effects of self-care practices. A convenient sample of 405 Italian workers (71.1% females; mean age = 42.58 ± 10.68 years) completed the Self-Care Practices Scale, Mini-Sleep Questionnaire, and Working Excessively and Working Compulsively Scale during the first lockdown in Italy in 2020. The main results showed that workaholism directly affected sleep–wake quality, suggesting that high levels of workaholism increased the likelihood of sleep–wake problems being reported. At the same time, people with high levels of workaholism reported scarce use of self-care practices and, in turn, lower sleep–wake quality. Our findings confirm the importance of monitoring the quality of life at work to protect workers’ sleep–wake cycle quality and investing in self-care. Both individual and organizational efforts can help break the vicious cycle of workaholism and sleep–wake disorders.

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16

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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17

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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18

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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19

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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20

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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21

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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22

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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23

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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24

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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25

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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26

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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27

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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28

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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29

Xu, Jiayang. "Analysis of the role of clock genes in the sleep-wake cycle and other biological processes." Theoretical and Natural Science 23, no. 1 (December 20, 2023): 235–41. http://dx.doi.org/10.54254/2753-8818/23/20231067.

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Clock genes, forming the crux of the body's circadian system, underpin the molecular basis of circadian rhythms. These rhythms, following approximately 24-hour cycles, regulate an array of biological processes, enabling organisms to adjust to environmental shifts. The sleep-wake cycle, a fundamental manifestation of this, alongside crucial brain functions and basic physiological processes, demonstrates significant links to circadian rhythms. This paper explores the interplay between clock genes and the sleep-wake cycle, illustrating that these genes modulate the cycle by managing associated hormones and neurotransmitters. Conversely, disruptions to the sleep-wake cycle influence the expressions of clock genes. Furthermore, the bidirectional relationships between these genes and other processes are also examined. Clock genes exert direct or indirect influence on vital life processes, which in turn modulate clock gene expression in various ways. Ultimately, the paper concludes with an in-depth understanding of the underlying mechanisms and identifies potential avenues for future research. These insights significantly contribute to the knowledge of the genetic basis of circadian rhythms and their potential clinical implications.

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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.

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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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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.

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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.

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34

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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35

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.

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36

García-García, Fabio, Mario Eduardo Acosta-Hernández, Luis Beltrán-Parrazal, and Juan Carlos Rodríguez-Alba. "The Role of Neuroglobin in the Sleep-Wake Cycle." Sleep Science 16, no. 03 (September 2023): e362-e367. http://dx.doi.org/10.1055/s-0043-1772806.

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AbstractNeuroglobin (Ngb) is a protein expressed in the central and peripherical nervous systems of the vertebrate. The Ngb has different functions in neurons, including regulating O2 homeostasis, oxidative stress, and as a neuroprotector after ischemia/hypoxia events. The Ngb is a hemoprotein of the globin family, structurally like myoglobin and hemoglobin. Ngb has higher expression in the cortex, hypothalamus, thalamus, brainstem, and cerebellum in mammals. Interestingly, Ngb immunoreactivity oscillates according to the sleep-wake cycle and decreases after 24 hours of sleep deprivation, suggesting that sleep homeostasis regulates Ngb expression. In addition, Ngb expresses in brain areas related to REM sleep regulation. Therefore, in the present review, we discuss the potential role of the Ngb in the sleep-wake regulation of mammals.

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37

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.

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38

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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39

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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40

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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41

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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42

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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43

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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44

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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45

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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46

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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47

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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48

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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49

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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50

Melnikov, Alexey. "Agent-based modeling of the sleep-wake cycle." Artificial societies 18, no. 2 (2023): 0. http://dx.doi.org/10.18254/s207751800024523-4.

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This study presents a circadian rhythm model. Specificity of such model is in consideration of the dynamic of two hormones and a neuromediator. Such an approach was taken due to the fact that circadian rhythms dynamics are largely expressed by cyclic quantity alteration of adenosine, cortisole and melatonin throughout the day. External factors effects were explored and their influence was imitated in the model. External factors influence on hormone's dynamic was analysed. Decision making assistance algorithm of external factors usage in correcting quantities of adenosine,cortisole and melatonin, was developed.

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