Journal articles: 'Circadian timing'

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Philippe, Jacques, and Charna Dibner. "Thyroid Circadian Timing." Journal of Biological Rhythms 30, no. 2 (November 19, 2014): 76–83. http://dx.doi.org/10.1177/0748730414557634.

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Petersen, Christian C., and Ralph E. Mistlberger. "Interval Timing Is Preserved Despite Circadian Desynchrony in Rats: Constant Light and Heavy Water Studies." Journal of Biological Rhythms 32, no. 4 (June 26, 2017): 295–308. http://dx.doi.org/10.1177/0748730417716231.

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The mechanisms that enable mammals to time events that recur at 24-h intervals (circadian timing) and at arbitrary intervals in the seconds-to-minutes range (interval timing) are thought to be distinct at the computational and neurobiological levels. Recent evidence that disruption of circadian rhythmicity by constant light (LL) abolishes interval timing in mice challenges this assumption and suggests a critical role for circadian clocks in short interval timing. We sought to confirm and extend this finding by examining interval timing in rats in which circadian rhythmicity was disrupted by long-term exposure to LL or by chronic intake of 25% D2O. Adult, male Sprague-Dawley rats were housed in a light-dark (LD) cycle or in LL until free-running circadian rhythmicity was markedly disrupted or abolished. The rats were then trained and tested on 15- and 30-sec peak-interval procedures, with water restriction used to motivate task performance. Interval timing was found to be unimpaired in LL rats, but a weak circadian activity rhythm was apparently rescued by the training procedure, possibly due to binge feeding that occurred during the 15-min water access period that followed training each day. A second group of rats in LL were therefore restricted to 6 daily meals scheduled at 4-h intervals. Despite a complete absence of circadian rhythmicity in this group, interval timing was again unaffected. To eliminate all possible temporal cues, we tested a third group of rats in LL by using a pseudo-randomized schedule. Again, interval timing remained accurate. Finally, rats tested in LD received 25% D2O in place of drinking water. This markedly lengthened the circadian period and caused a failure of LD entrainment but did not disrupt interval timing. These results indicate that interval timing in rats is resistant to disruption by manipulations of circadian timekeeping previously shown to impair interval timing in mice.

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Kessler, Katharina, and Olga Pivovarova-Ramich. "Meal Timing, Aging, and Metabolic Health." International Journal of Molecular Sciences 20, no. 8 (April 18, 2019): 1911. http://dx.doi.org/10.3390/ijms20081911.

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A growing body of evidence suggests that meal timing is an important factor for metabolic regulation and that the circadian clock tightly interacts with metabolic functions. The proper functioning of the circadian clock is critical for maintaining metabolic health. Therefore, chrononutrition, a novel discipline which investigates the relation between circadian rhythms, nutrition, and metabolism, has attracted increasing attention in recent years. Circadian rhythms are strongly affected by obesity, type 2 diabetes, and other dietary-induced metabolic diseases. With increasing age, the circadian system also undergoes significant changes which contribute to the dysregulation of metabolic rhythms. Metabolic diseases are a major health concern, particularly in light of a growing aging population, and effective approaches for their prevention and treatment are urgently needed. Recently, animal studies have impressively shown beneficial effects of several dietary patterns (e.g., caloric restriction or time-restricted feeding) on circadian rhythms and metabolic outcomes upon nutritional challenges. Whether these dietary patterns show the same beneficial effects in humans is, however, less well studied. As indicated by recent studies, dietary approaches might represent a promising, attractive, and easy-to-adapt strategy for the prevention and therapy of circadian and metabolic disturbances in humans of different age.

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van Oosterhout, WPJ, EJW van Someren, GG Schoonman, MA Louter, GJ Lammers, MD Ferrari, and GM Terwindt. "Chronotypes and circadian timing in migraine." Cephalalgia 38, no. 4 (March 20, 2017): 617–25. http://dx.doi.org/10.1177/0333102417698953.

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Background It has been suggested that migraine attacks strike according to circadian patterns and that this might be related to individual chronotype. Here we evaluated and correlated individual chronotypes, stability of the circadian rhythm, and circadian attack timing in a large and well-characterised migraine population. Methods In 2875 migraine patients and 200 non-headache controls we assessed differences in: (i) distribution of chronotypes (Münich Chronotype Questionnaire); (ii) the circadian rhythm’s amplitude and stability (Circadian Type Inventory); and (iii) circadian timing of migraine attacks. Data were analysed using multinomial and linear regression models adjusted for age, gender, sleep quality and depression. Results Migraineurs more often showed an early chronotype compared with controls (48.9% versus 38.6%; adjusted odds ratio [OR] = 2.42; 95% confidence interval [CI] = 1.58–3.69; p < 0.001); as well as a late chronotypes (37.7% versus 38.1%; adjusted OR = 1.69; 95% CI = 1.10–2.61; p = 0.016). Migraineurs, particularly those with high attack frequency, were more tired after changes in circadian rhythm (i.e. more languid; p < 0.001) and coped less well with being active at unusual hours (i.e. more rigid; p < 0.001) than controls. Of 2389 migraineurs, 961 (40.2%) reported early morning attack onset. Conclusion Migraine patients are less prone to be of a normal chronotype than controls. They are more languid and more rigid when changes in circadian rhythm occur. Most migraine attacks begin in the early morning. These data suggest that chronobiological mechanisms play a role in migraine pathophysiology.

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Hisler, G., S. Pedersen, D. Clark, S. Rothenberger, and B. Hasler. "0216 Is There a Daily Rhythm in Alcohol Craving and Does It Vary by Circadian Timing?" Sleep 43, Supplement_1 (April 2020): A84. http://dx.doi.org/10.1093/sleep/zsaa056.214.

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Abstract Introduction People with later circadian timing tend to consume more alcohol, potentially due to altered rhythms in when and how much they crave alcohol throughout the day. However, whether circadian factors play a role in alcohol craving has received scant attention. Here, we investigated if the daily rhythm of alcohol craving varied by circadian timing in two independent studies of late adolescent and young adult drinkers. Methods In Study 1, 32 participants (18–22 years of age; 61% female; 69% White) completed momentary reports of alcohol craving five times a day for 14 days. Participants wore wrist actigraphs and completed two in-lab assessments of dim light melatonin onset (DLMO). Average actigraphically-assessed midpoint of sleep on weekends and average DLMO were used as indicators of circadian timing. In Study 2, 231 participants (21–35 years of age; 28% female; 71% White) completed momentary reports of alcohol craving six times a day for 10 days. Average midpoint of self-reported time-in-bed on weekends was used to estimate circadian timing. Results Multilevel cosinor analysis revealed a 24-hour daily rhythm in alcohol craving which was moderated by circadian timing in both studies (p’s<0.05). In both Study 1 and 2, people with later circadian timing had a later timed peak of craving. In Study 1, but not Study 2, later circadian timing predicted a blunted amplitude in craving. Conclusion Findings support a daily rhythm in craving that varies by individual differences in circadian timing. Because craving is an important predictor of future alcohol use, the findings implicate circadian factors as a useful area to advance alcohol research and potentially improve interventions. Support R21AA023209; R01DA044143; K01AA021135; ABMRF/The Foundation for Alcohol Research.

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Hrushesky, W. "Circadian timing of cancer chemotherapy." Science 228, no. 4695 (April 5, 1985): 73–75. http://dx.doi.org/10.1126/science.3883493.

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Lévi, Francis. "Circadian timing for cancer treatments." Toxicology Letters 189 (September 2009): S115. http://dx.doi.org/10.1016/j.toxlet.2009.06.871.

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Saper, Clifford B. "The central circadian timing system." Current Opinion in Neurobiology 23, no. 5 (October 2013): 747–51. http://dx.doi.org/10.1016/j.conb.2013.04.004.

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Ditty, J. L., S. B. Williams, and S. S. Golden. "A Cyanobacterial Circadian Timing Mechanism." Annual Review of Genetics 37, no. 1 (December 2003): 513–43. http://dx.doi.org/10.1146/annurev.genet.37.110801.142716.

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Lévi, Francis, Alper Okyar, Sandrine Dulong, Pasquale F. Innominato, and Jean Clairambault. "Circadian Timing in Cancer Treatments." Annual Review of Pharmacology and Toxicology 50, no. 1 (February 2010): 377–421. http://dx.doi.org/10.1146/annurev.pharmtox.48.113006.094626.

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Wolff, Christopher A., and Karyn A. Esser. "Exercise timing and circadian rhythms." Current Opinion in Physiology 10 (August 2019): 64–69. http://dx.doi.org/10.1016/j.cophys.2019.04.020.

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Swaminathan, Krithika, Elizabeth B. Klerman, and Andrew J. K. Phillips. "Are Individual Differences in Sleep and Circadian Timing Amplified by Use of Artificial Light Sources?" Journal of Biological Rhythms 32, no. 2 (April 2017): 165–76. http://dx.doi.org/10.1177/0748730417699310.

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Within the human population, there is large interindividual variability in the timing of sleep and circadian rhythms. This variability has been attributed to individual differences in sleep physiology, circadian physiology, and/or light exposure. Recent experimental evidence suggests that the latter is necessary to evoke large interindividual differences in sleep and circadian timing. We used a validated model of human sleep and circadian physiology to test the hypothesis that intrinsic differences in sleep and circadian timing are amplified by self-selected use of artificial light sources. We tested the model under 2 conditions motivated by an experimental study (Wright et al., 2013): (1) a “natural” light cycle, and (2) a “realistic” light cycle that included attenuation of light due to living indoors when natural light levels are high and use of electric light when natural light levels are low. Within these conditions, we determined the relationship between intrinsic circadian period (within the range of 23.7-24.6 h) and timing of sleep onset, sleep offset, and circadian rhythms. In addition, we simulated a work week, with fixed wake time for 5 days and free sleep times on weekends. Under both conditions, a longer intrinsic period resulted in later sleep and circadian timing. Compared to the natural condition, the realistic condition evoked more than double the variation in sleep timing across the physiological range of intrinsic circadian periods. Model predictions closely matched data from the experimental study. We found that if the intrinsic circadian period was long (>24.2 h) under the realistic condition, there was significant mismatch in sleep timing between weekdays and weekends, which is known as social jetlag. These findings indicate that individual tendencies to have very delayed schedules can be greatly amplified by self-selected modifications to the natural light/dark cycle. This has important implications for therapeutic treatment of advanced or delayed sleep phase disorders.

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Duffy, Jeanne F., Jamie M. Zeitzer, David W. Rimmer, Elizabeth B. Klerman, Derk-Jan Dijk, and Charles A. Czeisler. "Peak of circadian melatonin rhythm occurs later within the sleep of older subjects." American Journal of Physiology-Endocrinology and Metabolism 282, no. 2 (February 1, 2002): E297—E303. http://dx.doi.org/10.1152/ajpendo.00268.2001.

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We investigated the relationship between sleep timing and the timing of the circadian rhythm of plasma melatonin secretion in a group of healthy young and older subjects without sleep complaints. The timing of sleep and the phase of the circadian melatonin rhythm were earlier in the older subjects. The relationship between the plasma melatonin rhythm and the timing of sleep was such that the older subjects were sleeping and waking earlier relative to their nightly melatonin secretory episode. Consequently, the older subjects were waking at a time when they had higher relative melatonin levels, in contrast with younger subjects, whose melatonin levels were relatively lower by wake time. Our findings indicate that aging is associated not only with an advance of sleep timing and the timing of circadian rhythms but also with a change in the internal phase relationship between the sleep-wake cycle and the output of the circadian pacemaker. In healthy older subjects, the relative timing of the melatonin rhythm with respect to sleep may not play a causal role in sleep disruption.

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Mori, Tetsuya, and Carl Hirschie Johnson. "Independence of Circadian Timing from Cell Division in Cyanobacteria." Journal of Bacteriology 183, no. 8 (April 15, 2001): 2439–44. http://dx.doi.org/10.1128/jb.183.8.2439-2444.2001.

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ABSTRACT In the cyanobacterium Synechococcus elongatus, cell division is regulated by a circadian clock. Deletion of the circadian clock gene, kaiC, abolishes rhythms of gene expression and cell division timing. Overexpression of the ftsZ gene halted cell division but not growth, causing cells to grow as filaments without dividing. The nondividing filamentous cells still exhibited robust circadian rhythms of gene expression. This result indicates that the circadian timing system is independent of rhythmic cell division and, together with other results, suggests that the cyanobacterial circadian system is stable and well sustained under a wide range of intracellular conditions.

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Hurley, Jennifer M. "Cytoplasmic traffic jams affect circadian timing." Science Translational Medicine 12, no. 569 (November 11, 2020): eabf4681. http://dx.doi.org/10.1126/scitranslmed.abf4681.

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Mendlewicz, Julien. "Disruption of the Circadian Timing Systems." CNS Drugs 23, Supplement 2 (September 2009): 15–26. http://dx.doi.org/10.2165/11318630-000000000-00000.

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Golden, Susan S., and Shannon R. Canales. "Cyanobacterial circadian clocks — timing is everything." Nature Reviews Microbiology 1, no. 3 (December 2003): 191–99. http://dx.doi.org/10.1038/nrmicro774.

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Reppert, Steven M., and David R. Weaver. "Coordination of circadian timing in mammals." Nature 418, no. 6901 (August 2002): 935–41. http://dx.doi.org/10.1038/nature00965.

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Drouyer, Elise, Ouria Dkhissi-Benyahya, Christophe Chiquet, Elizabeth WoldeMussie, Guadalupe Ruiz, Larry A. Wheeler, Philippe Denis, and Howard M. Cooper. "Glaucoma Alters the Circadian Timing System." PLoS ONE 3, no. 12 (December 12, 2008): e3931. http://dx.doi.org/10.1371/journal.pone.0003931.

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Beaulé, Christian, Barry Robinson, Elaine Waddington Lamont, and Shimon Amir. "Melanopsin in the Circadian Timing System." Journal of Molecular Neuroscience 21, no. 1 (2003): 73–90. http://dx.doi.org/10.1385/jmn:21:1:73.

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Lopez-Minguez, J., P. Gómez-Abellán, and M. Garaulet. "Circadian rhythms, food timing and obesity." Proceedings of the Nutrition Society 75, no. 4 (June 24, 2016): 501–11. http://dx.doi.org/10.1017/s0029665116000628.

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It is known that our physiology changes throughout the day and that several physiological hormones display circadian rhythmicity. The alteration of this normal pattern is called chronodisruption (CD). In recent years, it has been demonstrated that CD is related to obesity. Although several factors may be causing CD, one important aspect to consider is the failure in our internal clock. Indeed, studies performed in mutant animals have demonstrated that mutations in clock genes are related to obesity. In human subjects, mutations are rare (<1 % of the population). Nevertheless, it is rather common to have genetic variations in one SNP, which underlie differences in our vulnerability to disease. Several SNP in clock genes are related to obesity and weight loss. Taking into account that genetics is behind CD, as has already been demonstrated in twins’ models, the question is: Are we predestinated? We will see along these lines that nutrigenetics and epigenetics answer: ‘No, we are not predestinated’. Through nutrigenetics we know that our behaviours may interact with our genes and may decrease the deleterious effect of one specific risk variant. From epigenetics the message is even more positive: it is demonstrated that by changing our behaviours we can change our genome. Herein, we propose modifying ‘what, how, and when we eat’ as an effective tool to decrease our genetic risk, and as a consequence to diminish CD and decrease obesity. This is a novel and very promising area in obesity prevention and treatment.

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VAN SOMEREN, Eus JW. "Thermosensitivity of the circadian timing system." Sleep and Biological Rhythms 1, no. 1 (February 2003): 55–64. http://dx.doi.org/10.1046/j.1446-9235.2003.00002.x.

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Simon, Stacey L., Laura McWhirter, Cecilia Diniz Behn, Kate M. Bubar, Jill L. Kaar, Laura Pyle, Haseeb Rahat, et al. "Morning Circadian Misalignment Is Associated With Insulin Resistance in Girls With Obesity and Polycystic Ovarian Syndrome." Journal of Clinical Endocrinology & Metabolism 104, no. 8 (March 19, 2019): 3525–34. http://dx.doi.org/10.1210/jc.2018-02385.

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Abstract Context To our knowledge, circadian rhythms have not been examined in girls with polycystic ovarian syndrome (PCOS), despite the typical delayed circadian timing of adolescence, which is an emerging link between circadian health and insulin sensitivity (SI), and decreased SI in PCOS. Objective To examine differences in the circadian melatonin rhythm between obese adolescent girls with PCOS and control subjects, and evaluate relationships between circadian variables and SI. Design Cross-sectional study. Participants Obese adolescent girls with PCOS (n = 59) or without PCOS (n = 33). Outcome Measures Estimated sleep duration and timing from home actigraphy monitoring, in-laboratory hourly sampled dim-light, salivary-melatonin and fasting hormone analysis. Results All participants obtained insufficient sleep. Girls with PCOS had later clock-hour of melatonin offset, later melatonin offset relative to sleep timing, and longer duration of melatonin secretion than control subjects. A later melatonin offset after wake time (i.e., morning wakefulness occurring during the biological night) was associated with higher serum free testosterone levels and worse SI regardless of group. Analyses remained significant after controlling for daytime sleepiness and sleep-disordered breathing. Conclusion Circadian misalignment in girls with PCOS is characterized by later melatonin offset relative to clock time and sleep timing. Morning circadian misalignment was associated with metabolic dysregulation in girls with PCOS and obesity. Clinical care of girls with PCOS and obesity would benefit from assessment of sleep and circadian health. Additional research is needed to understand mechanisms underlying the relationship between morning circadian misalignment and SI in this population.

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Hut, R. A., and D. G. M. Beersma. "Evolution of time-keeping mechanisms: early emergence and adaptation to photoperiod." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1574 (July 27, 2011): 2141–54. http://dx.doi.org/10.1098/rstb.2010.0409.

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Virtually all species have developed cellular oscillations and mechanisms that synchronize these cellular oscillations to environmental cycles. Such environmental cycles in biotic (e.g. food availability and predation risk) or abiotic (e.g. temperature and light) factors may occur on a daily, annual or tidal time scale. Internal timing mechanisms may facilitate behavioural or physiological adaptation to such changes in environmental conditions. These timing mechanisms commonly involve an internal molecular oscillator (a ‘clock’) that is synchronized (‘entrained’) to the environmental cycle by receptor mechanisms responding to relevant environmental signals (‘ Zeitgeber ’, i.e. German for time-giver). To understand the evolution of such timing mechanisms, we have to understand the mechanisms leading to selective advantage. Although major advances have been made in our understanding of the physiological and molecular mechanisms driving internal cycles ( proximate questions), studies identifying mechanisms of natural selection on clock systems ( ultimate questions) are rather limited. Here, we discuss the selective advantage of a circadian system and how its adaptation to day length variation may have a functional role in optimizing seasonal timing. We discuss various cases where selective advantages of circadian timing mechanisms have been shown and cases where temporarily loss of circadian timing may cause selective advantage. We suggest an explanation for why a circadian timing system has emerged in primitive life forms like cyanobacteria and we evaluate a possible molecular mechanism that enabled these bacteria to adapt to seasonal variation in day length. We further discuss how the role of the circadian system in photoperiodic time measurement may explain differential selection pressures on circadian period when species are exposed to changing climatic conditions (e.g. global warming) or when they expand their geographical range to different latitudes or altitudes.

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Taleb, Z., K. Stokes, H. Wang, S. M. Collins, W. I. Khan, and P. Karpowicz. "A4 THE CIRCADIAN TIMING OF INFLAMMATORY BOWEL DISEASE." Journal of the Canadian Association of Gastroenterology 4, Supplement_1 (March 1, 2021): 4–5. http://dx.doi.org/10.1093/jcag/gwab002.003.

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Abstract Background The circadian clock is a highly conserved molecular pacemaker found in nearly every cell of the body. It consists of the genes BMAL1 and CLOCK that positively regulate CRY and PER, their negative regulators, resulting in a transcription/translation feedback loop that has a 24 hour cycle. This core clock mechanism drives the rhythmic expression of over 40% of the genome in a tissue-specific manner and therefore imposes 24 hour rhythms on many physiological processes. Shift work, which causes disruptions to the natural 24 hour physiological rhythms, has been shown to lead to an increased incidence of inflammatory bowel disease (IBD). Aims This study aims to characterize daily rhythms in inflammation and regeneration of the colon upon induction of acute colitis. We also aim to investigate the intestinal epithelial-specific effects of circadian clock disruption on overall disease progression. We hypothesize that the absence of a functional circadian clock eliminates proliferation rhythms of intestinal epithelial cells and disrupts the rhythms of inflammatory cytokines, thereby increasing the pathogenesis of IBD. Methods We tested the role of the clock in IBD using BMAL1+/+ (wild type) and BMAL1-/- (null mutant) mice. We also investigated the effects of the circadian clock specific to intestinal epithelial tissue using Vil+/+;BMAL1flox/flox (control) and VilCre/+;BMAL1flox/flox (conditional intestinal epithelial mutant) mice. Dextran Sulfate Sodium (DSS) was applied to induce acute colitis. Results We observed significantly decreased survival of BMAL1 circadian clock mutant mice when given colitis. A histology analysis indicates increased lesioning and overall inflammation in BMAL1-/- colon tissue. Disease activity and cytokine analyses reveal time-dependent severity in inflammatory response that is worse in BMAL1-/- mice. To test the circadian rhythms in intestinal regeneration of mice with IBD, we performed a 24 hour analysis comparing epithelial cell proliferation and cell death in colon tissue. We observed rhythmic expression of phosphor-histone H3 (a mitosis marker) in wild type mice which is eliminated in the BMAL1-/- lacking a circadian clock. Cell death which was measured by caspase 3 did not exhibit any differences between genotypes. Based on these results, we conclude that the loss of clock function leads to impaired regeneration during IBD, in part due to decreased and arrhythmic cell proliferation. Preliminary results in our VilCre/+;BMAL1flox/flox conditional intestinal epithelial mutant mice indicate that some of these effects may be epithelial-specific. Conclusions Our results support a critical role of the circadian clock in inflammatory bowel disease development. These data highlight that the circadian clock affects the regenerative abilities of intestinal epithelial cells. Funding Agencies CIHRChron’s and Colitis Canada, Ontario, University of Windsor

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Scully, Christopher G., Abdoulaye Karaboué, Wei-Min Liu, Joseph Meyer, Pasquale F. Innominato, Ki H. Chon, Alexander M. Gorbach, and Francis Lévi. "Skin surface temperature rhythms as potential circadian biomarkers for personalized chronotherapeutics in cancer patients." Interface Focus 1, no. 1 (December 2010): 48–60. http://dx.doi.org/10.1098/rsfs.2010.0012.

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Chronotherapeutics involve the administration of treatments according to circadian rhythms. Circadian timing of anti-cancer medications has been shown to improve treatment tolerability up to fivefold and double efficacy in experimental and clinical studies. However, the physiological and the molecular components of the circadian timing system (CTS), as well as gender, critically affect the success of a standardized chronotherapeutic schedule. In addition, a wrongly timed therapy or an excessive drug dose disrupts the CTS. Therefore, a non-invasive approach to accurately detect and monitor circadian rhythms is needed for a dynamic assessment of the CTS in order to personalize chronomodulated drug delivery schedule in cancer patients. Since core body temperature is a robust circadian biomarker, we recorded temperature at multiple locations on the skin of the upper chest and back of controls and cancer patients continuously. Variability in the circadian phase existed among patch locations in individual subjects over the course of 2–6 days, demonstrating the need to monitor multiple skin temperature locations to determine the precise circadian phase. Additionally, we observed that locations identified by infrared imaging as relatively cool had the largest 24 h temperature variations. Disruptions in skin temperature rhythms during treatment were found, pointing to the need to continually assess circadian timing and personalize chronotherapeutic schedules.

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Stone, J., S. Cain, and A. Phillips. "O024 Modifying light environments according to individual circadian light sensitivity." SLEEP Advances 3, Supplement_1 (October 1, 2022): A9. http://dx.doi.org/10.1093/sleepadvances/zpac029.023.

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Abstract Introduction Large inter-individual differences exist in how sensitive the circadian system is to light. Circadian light sensitivity can be affected by medications, such as antidepressants, and varies as a function of age and some mood disorders. Using a computational model, we investigated how differences in an individual’s light sensitivity can be offset by changes in their light environment to maintain stable circadian timing. Methods A previously validated computational model was used to simulate sleep and circadian timing under realistic assumptions about light and sleep schedules in day workers across two weeks. The model predicted circadian phase (dim light melatonin onset) and sleep onset/offset times for each day. Simulations were repeated varying two parameters: (i) light sensitivity, representing changes in the dose-response curve to light, and (ii) evening illuminance, representing home lighting levels after sunset. Results Higher light sensitivity and higher evening illuminance levels resulted in systematically later predicted sleep and circadian timing. The effects of increasing light sensitivity could be offset by reducing the level of evening illuminance, with this relationship holding over a wide range of light sensitivity values. Low light sensitivity combined with high evening illuminance produced a non-entrained (non-24) phenotype; decreasing evening illuminance from this state resulted in stable entrainment. Discussion We are only beginning to understand the influence of medications and health conditions on circadian light sensitivity. Our results show how modifications to evening light levels can be used to offset impacts of variable light sensitivity on sleep and circadian timing.

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Clark, Gretchen T., Yanlei Yu, Cooper A. Urban, Guo Fu, Chunyu Wang, Fuming Zhang, Robert J. Linhardt, and Jennifer M. Hurley. "Circadian control of heparan sulfate levels times phagocytosis of amyloid beta aggregates." PLOS Genetics 18, no. 2 (February 10, 2022): e1009994. http://dx.doi.org/10.1371/journal.pgen.1009994.

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Alzheimer’s Disease (AD) is a neuroinflammatory disease characterized partly by the inability to clear, and subsequent build-up, of amyloid-beta (Aβ). AD has a bi-directional relationship with circadian disruption (CD) with sleep disturbances starting years before disease onset. However, the molecular mechanism underlying the relationship of CD and AD has not been elucidated. Myeloid-based phagocytosis, a key component in the metabolism of Aβ, is circadianly-regulated, presenting a potential link between CD and AD. In this work, we revealed that the phagocytosis of Aβ42 undergoes a daily circadian oscillation. We found the circadian timing of global heparan sulfate proteoglycan (HSPG) biosynthesis was the molecular timer for the clock-controlled phagocytosis of Aβ and that both HSPG binding and aggregation may play a role in this oscillation. These data highlight that circadian regulation in immune cells may play a role in the intricate relationship between the circadian clock and AD.

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Gibbs, J. E., S. Beesley, J. Plumb, D. Singh, S. Farrow, D. W. Ray, and A. S. I. Loudon. "Circadian Timing in the Lung; A Specific Role for Bronchiolar Epithelial Cells." Endocrinology 150, no. 1 (September 11, 2008): 268–76. http://dx.doi.org/10.1210/en.2008-0638.

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In addition to the core circadian oscillator, located within the suprachiasmatic nucleus, numerous peripheral tissues possess self-sustaining circadian timers. In vivo these are entrained and temporally synchronized by signals conveyed from the core oscillator. In the present study, we examine circadian timing in the lung, determine the cellular localization of core clock proteins in both mouse and human lung tissue, and establish the effects of glucocorticoids (widely used in the treatment of asthma) on the pulmonary clock. Using organotypic lung slices prepared from transgenic mPER2::Luc mice, luciferase levels, which report PER2 expression, were measured over a number of days. We demonstrate a robust circadian rhythm in the mouse lung that is responsive to glucocorticoids. Immunohistochemical techniques were used to localize specific expression of core clock proteins, and the glucocorticoid receptor, to the epithelial cells lining the bronchioles in both mouse and human lung. In the mouse, these were established to be Clara cells. Murine Clara cells retained circadian rhythmicity when grown as a pure population in culture. Furthermore, selective ablation of Clara cells resulted in the loss of circadian rhythm in lung slices, demonstrating the importance of this cell type in maintaining overall pulmonary circadian rhythmicity. In summary, we demonstrate that Clara cells are critical for maintaining coherent circadian oscillations in lung tissue. Their coexpression of the glucocorticoid receptor and core clock components establishes them as a likely interface between humoral suprachiasmatic nucleus output and circadian lung physiology. There is a glucocorticoid-sensitive circadian clock within the lung. The bronchial epithelial Clara cells play a critical role in pulmonary circadian timing.

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Sen, Aritro, and Michael T. Sellix. "The Circadian Timing System and Environmental Circadian Disruption: From Follicles to Fertility." Endocrinology 157, no. 9 (August 8, 2016): 3366–73. http://dx.doi.org/10.1210/en.2016-1450.

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The internal or circadian timing system is deeply integrated in female reproductive physiology. Considerable details of rheostatic timing function in the neuroendocrine control of pituitary hormone secretion, adenohypophyseal hormone gene expression and secretion, gonadal steroid hormone biosynthesis and secretion, ovulation, implantation, and parturition have been reported. The molecular clock, an autonomous feedback loop oscillator of interacting transcriptional regulators, dictates the timing and amplitude of gene expression in each tissue of the female hypothalamic-pituitary-gonadal (HPG) axis. Although multiple targets of the molecular clock have been identified, many associated with critical physiological functions in the HPG axis, the full extent of clock-driven gene expression and physiology in this critical system remains unknown. Environmental circadian disruption (ECD), the disturbance of temporal relationships within and between internal clocks (brain and periphery), and external timing cues (eg, light, nutrients, social cues) due to rotating/night shift work or transmeridian travel have been linked to reproductive dysfunction and subfertility. Moreover, ECD resulting from exposure to endocrine disrupting chemicals, environmental toxins, and/or irregular hormone levels during sexual development can also reduce fertility. Thus, perturbations that disturb clock function at the molecular, cellular or systemic level correlate with significant declines in female reproductive function. Here we briefly review the evidence for molecular clock function in each tissue of the female HPG axis (GnRH neuron, pituitary, uterus, oviduct, and ovary), describe the human epidemiological and animal data supporting the negative effects of ECD on fertility, and explore the potential for novel chronotherapeutics in women's health and fertility.

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Murakami, D. M., B. A. Horwitz, and C. A. Fuller. "Circadian rhythms of temperature and activity in obese and lean Zucker rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 5 (November 1, 1995): R1038—R1043. http://dx.doi.org/10.1152/ajpregu.1995.269.5.r1038.

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The circadian timing system is important in the regulation of feeding and metabolism, both of which are aberrant in the obese Zucker rat. This study tested the hypothesis that these abnormalities involve a deficit in circadian regulation by examining the circadian rhythms of body temperature and activity in lean and obese Zucker rats exposed to normal light-dark cycles, constant light, and constant dark. Significant deficits in both daily mean and circadian amplitude of temperature and activity were found in obese Zucker female rats relative to lean controls in all lighting conditions. However, the circadian period of obese Zucker rats did not exhibit differences relative to lean controls in either of the constant lighting conditions. These results indicate that although the circadian regulation of temperature and activity in obese Zucker female rats is in fact depressed, obese rats do exhibit normal entrainment and pacemaker functions in the circadian timing system. The results suggest a deficit in the process that generates the amplitude of the circadian rhythm.

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Pinato, Luciana, Caio Sergio Galina Spilla, Regina Pekelmann Markus, and Sanseray da Silveira Cruz-Machado. "Dysregulation of Circadian Rhythms in Autism Spectrum Disorders." Current Pharmaceutical Design 25, no. 41 (January 8, 2020): 4379–93. http://dx.doi.org/10.2174/1381612825666191102170450.

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Background: The alterations in neurological and neuroendocrine functions observed in the autism spectrum disorder (ASD) involves environmentally dependent dysregulation of neurodevelopment, in interaction with multiple coding gene defects. Disturbed sleep-wake patterns, as well as abnormal melatonin and glucocorticoid secretion, show the relevance of an underlying impairment of the circadian timing system to the behavioral phenotype of ASD. Thus, understanding the mechanisms involved in the circadian dysregulation in ASD could help to identify early biomarkers to improve the diagnosis and therapeutics as well as providing a significant impact on the lifelong prognosis. Objective: In this review, we discuss the organization of the circadian timing system and explore the connection between neuroanatomic, molecular, and neuroendocrine responses of ASD and its clinical manifestations. Here we propose interconnections between circadian dysregulation, inflammatory baseline and behavioral changes in ASD. Taking into account, the high relevancy of melatonin in orchestrating both circadian timing and the maintenance of physiological immune quiescence, we raise the hypothesis that melatonin or analogs should be considered as a pharmacological approach to suppress inflammation and circadian misalignment in ASD patients. Strategy: This review provides a comprehensive update on the state-of-art of studies related to inflammatory states and ASD with a special focus on the relationship with melatonin and clock genes. The hypothesis raised above was analyzed according to the published data. Conclusion: Current evidence supports the existence of associations between ASD to circadian dysregulation, behavior problems, increased inflammatory levels of cytokines, sleep disorders, as well as reduced circadian neuroendocrine responses. Indeed, major effects may be related to a low melatonin rhythm. We propose that maintaining the proper rhythm of the circadian timing system may be helpful to improve the health and to cope with several behavioral changes observed in ASD subjects.

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Buxton, Orfeu M., Mireille L'Hermite-Balériaux, Fred W. Turek, and Eve van Cauter. "Daytime naps in darkness phase shift the human circadian rhythms of melatonin and thyrotropin secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 2 (February 1, 2000): R373—R382. http://dx.doi.org/10.1152/ajpregu.2000.278.2.r373.

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To systematically determine the effects of daytime exposure to sleep in darkness on human circadian phase, four groups of subjects participated in 4-day studies involving either no nap (control), a morning nap (0900–1500), an afternoon nap (1400–2000), or an evening nap (1900–0100) in darkness. Except during the scheduled sleep/dark periods, subjects remained awake under constant conditions, i.e., constant dim light exposure (36 lx), recumbence, and caloric intake. Blood samples were collected at 20-min intervals for 64 h to determine the onsets of nocturnal melatonin and thyrotropin secretion as markers of circadian phase before and after stimulus exposure. Sleep was polygraphically recorded. Exposure to sleep and darkness in the morning resulted in phase delays, whereas exposure in the evening resulted in phase advances relative to controls. Afternoon naps did not change circadian phase. These findings indicate that human circadian phase is dependent on the timing of darkness and/or sleep exposure and that strategies to treat circadian misalignment should consider not only the timing and intensity of light, but also the timing of darkness and/or sleep.

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Zhou, Meiyu, Jianghui Chen, Rongfeng Huang, Haoran Xin, Xiaogen Ma, Lihua Li, Fang Deng, Zhihui Zhang, and Min-Dian Li. "Circadian signatures of anterior hypothalamus in time-restricted feeding." F1000Research 11 (September 22, 2022): 1087. http://dx.doi.org/10.12688/f1000research.125368.1.

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Background: Meal timing resets circadian clocks in peripheral tissues, such as the liver, in seven days without affecting the phase of the central clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Anterior hypothalamus plays an essential role in energy metabolism, circadian rhythm, and stress response. However, it remains to be elucidated whether and how anterior hypothalamus adapts its circadian rhythms to meal timing. Methods: Here, we applied transcriptomics to profile rhythmic transcripts in the anterior hypothalamus of nocturnal female mice subjected to day- (DRF) or night (NRF)-time restricted feeding for seven days. Results: This global profiling identified 128 and 3,518 rhythmic transcripts in DRF and NRF, respectively. NRF entrained diurnal rhythms among 990 biological processes, including ‘Electron transport chain’ and ‘Hippo signaling’ that reached peak time in the late sleep and late active phase, respectively. By contrast, DRF entrained only 20 rhythmic pathways, including ‘Cellular amino acid catabolic process’, all of which were restricted to the late active phase. The rhythmic transcripts found in both DRF and NRF tissues were largely resistant to phase entrainment by meal timing, which were matched to the action of the circadian clock. Remarkably, DRF for 36 days partially reversed the circadian clock compared to NRF. Conclusions: Collectively, our work generates a useful dataset to explore anterior hypothalamic circadian biology and sheds light on potential rhythmic processes influenced by meal timing in the brain (www.circametdb.org.cn).

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Arredondo-Amador, María, Carolina Zambrano, Agné Kulyté, Juán Luján, Kun Hu, Fermín Sánchez de Medina, Frank A. J. L. Scheer, et al. "Circadian Rhythms in Hormone-sensitive Lipase in Human Adipose Tissue: Relationship to Meal Timing and Fasting Duration." Journal of Clinical Endocrinology & Metabolism 105, no. 12 (July 29, 2020): e4407-e4416. http://dx.doi.org/10.1210/clinem/dgaa492.

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Abstract Background Fat mobilization in adipose tissue (AT) has a specific timing. However, circadian rhythms in the activity of the major enzyme responsible for fat mobilization, hormone-sensitive lipase (HSL), have not been demonstrated in humans. Objective To analyze in a cross-sectional study whether there is an endogenous circadian rhythm in HSL activity in human AT ex vivo and whether rhythm characteristics are related to food timing or fasting duration. Methods Abdominal AT biopsies were obtained from 18 severely obese participants (age: 46 ± 11 years; body mass index 42 ± 6 kg/m2) who underwent laparoscopic gastric bypass. Twenty-four-hour rhythms of HSL activity and LIPE (HSL transcript in humans) expression in subcutaneous AT were analyzed together with habitual food timing and night fasting duration. Results HSL activity exhibited a circadian rhythm (P = .023) and reached the maximum value at circadian time 16 (CT) that corresponded to around midnight (relative local clock time. Similarly, LIPE displayed a circadian rhythm with acrophase also at night (P = .0002). Participants with longer night fasting duration >11.20 hours displayed almost double the amplitude (1.91 times) in HSL activity rhythm than those with short duration (P = .013); while habitual early diners (before 21:52 hours) had 1.60 times higher amplitude than late diners (P = .035). Conclusions Our results demonstrate circadian rhythms in HSL activity and may lead to a better understanding of the intricate relationships between food timing, fasting duration and body fat regulation.

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Singh, Manjul, and Paloma Mas. "A Functional Connection between the Circadian Clock and Hormonal Timing in Arabidopsis." Genes 9, no. 12 (November 23, 2018): 567. http://dx.doi.org/10.3390/genes9120567.

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The rotation of the Earth entails changes in environmental conditions that pervasively influence an organism’s physiology and metabolism. An internal cellular mechanism known as the circadian clock acts as an internal timekeeper that is able to perceive the changes in environmental cues to generate 24-h rhythms in synchronization with daily and seasonal fluctuations. In plants, the circadian clock function is particularly important and regulates nearly every aspect of plant growth and development as well as proper responses to stresses. The circadian clock does not function in isolation but rather interconnects with an intricate network of different pathways, including those of phytohormones. Here, we describe the interplay of the circadian clock with a subset of hormones in Arabidopsis. The molecular components directly connecting the circadian and hormone pathways are described, highlighting the biological significance of such connections in the control of growth, development, fitness, and survival. We focus on the overlapping as well as contrasting circadian and hormonal functions that together provide a glimpse on how the Arabidopsis circadian system regulates hormone function in response to endogenous and exogenous cues. Examples of feedback regulation from hormone signaling to the clock are also discussed.

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Hastings, Michael H., Elizabeth S. Maywood, and Marco Brancaccio. "The Mammalian Circadian Timing System and the Suprachiasmatic Nucleus as Its Pacemaker." Biology 8, no. 1 (March 11, 2019): 13. http://dx.doi.org/10.3390/biology8010013.

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The past twenty years have witnessed the most remarkable breakthroughs in our understanding of the molecular and cellular mechanisms that underpin circadian (approximately one day) time-keeping. Across model organisms in diverse taxa: cyanobacteria (Synechococcus), fungi (Neurospora), higher plants (Arabidopsis), insects (Drosophila) and mammals (mouse and humans), a common mechanistic motif of delayed negative feedback has emerged as the Deus ex machina for the cellular definition of ca. 24 h cycles. This review will consider, briefly, comparative circadian clock biology and will then focus on the mammalian circadian system, considering its molecular genetic basis, the properties of the suprachiasmatic nucleus (SCN) as the principal circadian clock in mammals and its role in synchronising a distributed peripheral circadian clock network. Finally, it will consider new directions in analysing the cell-autonomous and circuit-level SCN clockwork and will highlight the surprising discovery of a central role for SCN astrocytes as well as SCN neurons in controlling circadian behaviour.

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Innominato, Pasquale F., Véronique P. Roche, Oxana G. Palesh, Ayhan Ulusakarya, David Spiegel, and Francis A. Lévi. "The circadian timing system in clinical oncology." Annals of Medicine 46, no. 4 (June 2014): 191–207. http://dx.doi.org/10.3109/07853890.2014.916990.

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MOORE, ROBERT Y., and J. PATRICK CARD. "Neuropeptide Y in the Circadian Timing System." Annals of the New York Academy of Sciences 611, no. 1 Central and P (November 1990): 247–57. http://dx.doi.org/10.1111/j.1749-6632.1990.tb48936.x.

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Roizen, Jeffrey, Christina E. Luedke, Erik D. Herzog, and Louis J. Muglia. "Oxytocin in the Circadian Timing of Birth." PLoS ONE 2, no. 9 (September 26, 2007): e922. http://dx.doi.org/10.1371/journal.pone.0000922.

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Wehrens, Sophie M. T., Skevoulla Christou, Cheryl Isherwood, Benita Middleton, Michelle A. Gibbs, Simon N. Archer, Debra J. Skene, and Jonathan D. Johnston. "Meal Timing Regulates the Human Circadian System." Current Biology 27, no. 12 (June 2017): 1768–75. http://dx.doi.org/10.1016/j.cub.2017.04.059.

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Cordes, Sara, and C. R. Gallistel. "Intact interval timing in circadian CLOCK mutants." Brain Research 1227 (August 2008): 120–27. http://dx.doi.org/10.1016/j.brainres.2008.06.043.

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Kobayashi, Minoru, Hideto To, Akihiko Tokue, Akio Fujimura, and Eiji Kobayashi. "CISPLATIN-INDUCED VOMITING DEPENDS ON CIRCADIAN TIMING." Chronobiology International 18, no. 5 (January 2001): 851–63. http://dx.doi.org/10.1081/cbi-100107520.

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Dunbar, Sandra B., Lisa Marchette, and Evelyn Salerno. "Circadian rhythms and timing of digoxin administration." Journal of Cardiovascular Nursing 2, no. 4 (August 1988): 1–11. http://dx.doi.org/10.1097/00005082-198808000-00002.

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Agostino, Patricia V., Micaela do Nascimento, Ivana L. Bussi, Manuel C. Eguía, and Diego A. Golombek. "Circadian modulation of interval timing in mice." Brain Research 1370 (January 2011): 154–63. http://dx.doi.org/10.1016/j.brainres.2010.11.029.

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Emery, Patrick, and Michael Francis. "Circadian Rhythms: Timing the Sense of Smell." Current Biology 18, no. 13 (July 2008): R569—R571. http://dx.doi.org/10.1016/j.cub.2008.05.011.

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Slomski, Anita. "Circadian Timing of Medications Affects CVD Outcomes." JAMA 322, no. 24 (December 24, 2019): 2375. http://dx.doi.org/10.1001/jama.2019.20565.

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Hut, Roelof A., Silvia Paolucci, Roi Dor, Charalambos P. Kyriacou, and Serge Daan. "Latitudinal clines: an evolutionary view on biological rhythms ,." Proceedings of the Royal Society B: Biological Sciences 280, no. 1765 (August 22, 2013): 20130433. http://dx.doi.org/10.1098/rspb.2013.0433.

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Properties of the circadian and annual timing systems are expected to vary systematically with latitude on the basis of different annual light and temperature patterns at higher latitudes, creating specific selection pressures. We review literature with respect to latitudinal clines in circadian phenotypes as well as in polymorphisms of circadian clock genes and their possible association with annual timing. The use of latitudinal (and altitudinal) clines in identifying selective forces acting on biological rhythms is discussed, and we evaluate how these studies can reveal novel molecular and physiological components of these rhythms.

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Loewke, Adrienne C., Alex Garrett, Athreya Steiger, Nathan Fisher, H. Craig Heller, Damien Colas, and Norman F. Ruby. "Loss of Circadian Timing Disrupts Theta Episodes during Object Exploration." Clocks & Sleep 2, no. 4 (December 1, 2020): 523–35. http://dx.doi.org/10.3390/clockssleep2040038.

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This study examined whether theta oscillations were compromised by the type of circadian disruption that impairs hippocampal-dependent memory processes. In prior studies on Siberian hamsters, we developed a one-time light treatment that eliminated circadian timing in the central pacemaker, the suprachiasmatic nucleus (SCN). These arrhythmic animals had impaired hippocampal-dependent memory whereas animals made arrhythmic with SCN lesions did not. The current study examined whether theta oscillations are compromised by the same light treatment that produced memory impairments in these animals. We found that both methods of inducing circadian-arrhythmia shortened theta episodes in the EEG by nearly 50%. SCN-lesioned animals, however, exhibited a 3-fold increase in the number of theta episodes and more than doubled the total time that theta dominated the EEG compared to SCN-intact circadian-arrhythmic animals. Video tracking showed that changes in theta were paralleled by similar changes in exploration behavior. These results suggest that the circadian-arrhythmic SCN interferes with hippocampal memory encoding by fragmenting theta oscillations. SCN-lesioned animals can, however, compensate for the shortened theta episodes by increasing their frequency. Implications for rhythm coherence and theta sequence models of memory formation are discussed.

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Mascaro, L., S. Rajaratnam, J. Leota, D. Hoffman, S. Drummond, and E. Facer-Childs. "O067 The role of biological sex in the relationship between circadian alignment and well-being in elite athletes." SLEEP Advances 3, Supplement_1 (October 1, 2022): A28—A29. http://dx.doi.org/10.1093/sleepadvances/zpac029.066.

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Abstract Introduction Circadian rhythms govern physiological timing and influence sleep, well-being, and performance. Desynchrony between circadian timing and behaviours (circadian misalignment) can compromise daily functioning. We investigated sex differences in sleep and circadian timing, and their relationship with sleep and mental health outcomes in elite athletes. Methods Participants were 87 elite Australian Rules Football (AFL) athletes (43% female; M-age =23.8±4.0 years). Data were collected prior to the start of the 2021 and 2022 AFL seasons (n= 54 participating in a repeat assessment). Circadian phase was assessed via salivary DLMO (collected hourly from 5hrs pre- to 1h post-habitual bedtime). A questionnaire battery, and two weeks of actigraphy were also completed. Results Female athletes had a significantly later circadian phase (DLMO; 20:42 vs 20:13) and midsleep time (03:24 vs 02:58), and worse self-reported athlete psychological strain (APSQ), daytime sleepiness, and insomnia, relative to male athletes. There was no sex difference in phase angle (interval between sleep onset and DLMO times; M = 2.5hrs ± 49 mins). DLMO time did not predict sleep efficiency, sleep latency, insomnia, sleepiness, or APSQ. Phase angle predicted APSQ for female athletes only, via a quadratic trend (p=.001): psychological strain was worse among female athletes with shorter and longer phase angles. Discussion Our results suggest female athletes have a later circadian phase, which is not associated with adverse outcomes except for higher psychological strain for those with greater circadian misalignment. Sports practitioners may require specific attention for circadian alignment in female athletes who are at particular risk when misaligned.

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Journal articles on the topic 'Circadian timing'

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