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Journal articles on the topic 'Circadian'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 July 2024

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1

Pereira, Danyella Silva, Sergio Tufik, and Mario Pedrazzoli. "Moléculas que marcam o tempo: implicações para os fenótipos circadianos." Revista Brasileira de Psiquiatria 31, no. 1 (March 2009): 63–71. http://dx.doi.org/10.1590/s1516-44462009000100015.

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OBJETIVO: Revisar resumidamente a literatura dos últimos 36 anos de pesquisa em cronobiologia molecular a fim de informar aos profissionais de saúde os avanços obtidos nesta área e os potenciais para aplicação na clínica médica. MÉTODO: Buscas na literatura foram realizadas utilizando as bases de dados PubMed e Scopus usando como palavras-chave "clock genes, circadian rhythms, diurnal preference, delayed sleep phase syndrome, advanced sleep phase syndrome, photoperiod and mood disorder". DISCUSSÃO: Atualmente, o mecanismo molecular da regulação da ritmicidade circadiana é compreendido em grande detalhe. Muitos estudos publicados mostram associações de polimorfismos nos genes relógio com transtornos do ritmo circadiano e com transtornos do humor. CONCLUSÕES: De maneira geral, o progresso obtido na área de cronobiologia molecular traz um melhor entendimento da regulação do sistema de temporização biológico. O desenvolvimento de estudos nesta área tem o potencial de ser aplicável ao tratamento dos transtornos dos ritmos circadianos e certos transtornos do humor, além de prevenir riscos à saúde causados por viagens intercontinentais (Jet Lag) e por trabalhos noturnos e por turnos.

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2

Zepeda Ríos, Paola Alexandra, and María Olga Quintana Zavala. "Disincronía circadiana y su efecto sobre parámetros de síndrome metabólico en trabajadores: revisión integradora de la literatura." Enfermería Global 20, no. 2 (April 1, 2021): 592–613. http://dx.doi.org/10.6018/eglobal.426881.

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Introducción: La pérdida del ritmo circadiano causado por desórdenes del sueño es considerada un factor de riesgo importante para desarrollar enfermedades metabólicas como hiperglicemia y resistencia a la insulina. Objetivo: Analizar la literatura existente referente a estudios sobre disincronía circadiana en trabajadores y su influencia sobre parámetros antropométricos de síndrome metabólico de los mismos.Método: Se realizó una búsqueda en las bases de datos electrónicas EBSCO, Thompson Reuters, PubMed y Scopus, los términos de búsqueda seleccionados fueron: trabajo por turnos, melatonina, cortisol, síndrome metabólico, trabajo nocturno y ritmo circadiano, en los idiomas español e inglés, publicados de enero del 2015 a diciembre de 2018. La extracción se llevó a cabo utilizando un formulario prediseñado. Resultados: La búsqueda en las bases de datos arrojó 5,953 artículos, posterior a la indagación y depuración de los mismos aplicando los criterios de elegibilidad, se obtuvieron 13 artículos los cuales se organizaron en dos dimensiones para su análisis, estas se denominaron a) trabajo en turnos y factores de riesgo metabólico y b) trabajo en turnos y ciclo circadiano. Conclusiones: Es consistente la relación entre el trabajo nocturno o rotatorio, con diversas alteraciones metabólicas. Introduction: the loss of the circadian rhythm caused by sleep disorders is considered an important risk factor for developing metabolic diseases such as hyperglycemia and insulin resistance.Aim: to analyze the existing information regarding studies on circadian dyssynchrony in workers and its influence on anthropometric parameters of their metabolic syndrome.Method: The literature review was carried out by searching the EBSCO, Thompson Reuters, PubMed and Scopus electronic databases, the selected search terms were: shift work, melatonin, cortisol, metabolic syndrome, night work and circadian rhythm in the Spanish and English languages published from January 2015 to December 2018. The extraction was carried out using a predesigned form. Results: The search in the databases yielded 5,953 articles, after the investigation and purification of the same ones applying the eligibility criteria, 13 articles were obtained which were organized in two dimensions for their analysis, these were called a) work in shifts and metabolic risk factors and b) shift work and the circadian cycle.Conclusions: The relationship between night or rotating work with various metabolic disorders is consistent.

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3

Bernardi, Fabiana, Ana Beatriz Cauduro Harb, Rosa Maria Levandovski, and Maria Paz Loayza Hidalgo. "Transtornos alimentares e padrão circadiano alimentar: uma revisão." Revista de Psiquiatria do Rio Grande do Sul 31, no. 3 (December 2009): 170–76. http://dx.doi.org/10.1590/s0101-81082009000300006.

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Este artigo tem como objetivo revisar aspectos relacionados a transtornos alimentares e suas relações com as alterações no ritmo circadiano. Realizou-se uma busca sistematizada das informações nas bases de dados PubMed usando os seguintes descritores: eating disorders, circadian rhythm, night eating syndrome, binge eating disorder e sleep patterns. Os transtornos alimentares, como a síndrome do comer noturno e o transtorno da compulsão alimentar periódica, têm sido considerados e relacionados a um atraso no ritmo circadiano da ingestão alimentar e saciedade prejudicada. Os ritmos circadianos são aqueles que apresentam um período de 24 h, como, por exemplo, o ciclo sono-vigília, temperatura corporal, atividade e comportamento alimentar. Distúrbios provocados pelas alterações nos horários de sono/vigília influenciam o apetite, a saciedade e, consequentemente, a ingestão alimentar, o que parece favorecer o aumento desses transtornos. Percebe-se que o comportamento alimentar pode ser influenciado por ritmos circadianos. Porém, mais estudos e o maior conhecimento sobre a ritmicidade alimentar podem contribuir com o melhor entendimento do comportamento alimentar atual, atuando na prevenção e/ou tratamento de transtornos alimentares.

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Mishra, Shital Kumar, Zhaomin Zhong, and Han Wang. "Hundreds of LncRNAs Display Circadian Rhythmicity in Zebrafish Larvae." Cells 10, no. 11 (November 15, 2021): 3173. http://dx.doi.org/10.3390/cells10113173.

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Long noncoding RNAs (lncRNAs) have been shown to play crucial roles in various life processes, including circadian rhythms. Although next generation sequencing technologies have facilitated faster profiling of lncRNAs, the resulting datasets require sophisticated computational analyses. In particular, the regulatory roles of lncRNAs in circadian clocks are far from being completely understood. In this study, we conducted RNA-seq-based transcriptome analysis of zebrafish larvae under both constant darkness (DD) and constant light (LL) conditions in a circadian manner, employing state-of-the-art computational approaches to identify approximately 3220 lncRNAs from zebrafish larvae, and then uncovered 269 and 309 lncRNAs displaying circadian rhythmicity under DD and LL conditions, respectively, with 30 of them are coexpressed under both DD and LL conditions. Subsequently, GO, COG, and KEGG pathway enrichment analyses of all these circadianly expressed lncRNAs suggested their potential involvement in numerous biological processes. Comparison of these circadianly expressed zebrafish larval lncRNAs, with rhythmically expressed lncRNAs in the zebrafish pineal gland and zebrafish testis, revealed that nine (DD) and twelve (LL) larval lncRNAs are coexpressed in the zebrafish pineal gland and testis, respectively. Intriguingly, among peptides encoded by these coexpressing circadianly expressed lncRNAs, three peptides (DD) and one peptide (LL) were found to have the known domains from the Protein Data Bank. Further, the conservation analysis of these circadianly expressed zebrafish larval lncRNAs with human and mouse genomes uncovered one lncRNA and four lncRNAs shared by all three species under DD and LL conditions, respectively. We also investigated the conserved lncRNA-encoded peptides and found one peptide under DD condition conserved in these three species and computationally predicted its 3D structure and functions. Our study reveals that hundreds of lncRNAs from zebrafish larvae exhibit circadian rhythmicity and should help set the stage for their further functional studies.

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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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Powell, Weston, Lindsay Clark, Maria White, Lucille Rich, Camille Gates, Elizabeth Vanderwall, and Jason Debley. "0006 Circadian Cyclic Gene Expression in Human Airway Epithelial Cells in Asthma and Viral Infections." SLEEP 47, Supplement_1 (April 20, 2024): A3. http://dx.doi.org/10.1093/sleep/zsae067.0006.

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Abstract Introduction Cellular circadian rhythms regulate gene expression and innate immune pathways related to airway diseases in animal models of disease. However, circadian regulation of gene expression remains uninvestigated in human airway epithelial cells. Primary human airway epithelial cells can be grown at an air-liquid interface as an ex vivo organotypic model to characterize molecular circadian rhythms in the human airway. Using cells from healthy and donors with disease, we hypothesized that circadian cyclic gene expression would be altered in asthma and would display altered viral responses. Methods Cells were synchronized with temperature cycled incubators and RNA isolated every 4 hours over a 48 hour period for RNA-sequencing from primary human airway epithelial cells from healthy and asthmatic children. CompareRhythms in R was used to identify differential rhythmicity using the cosinor method. EnrichR pathway analysis for Reactome, Panther, GO molecular functions, and GO biological processes was used to identify relevant biological pathways with altered circadian rhythmic expression. Human rhinovirus 16 was applied to the apical surface at a multiplicity of infection of 0.5 and RNA isolated 96 hours later for genome copy number assessment with PCR. Results Circadain clock genes were rhythmic in airway epithelial cells from health and donors with asthma with preserved phase relationships indicating an intact core circadian clock. Analysis of circadian cyclic gene expression identified 4% of genes with circadian cyclic gene expression following temperature synchronization. Approximately 100 genes demonstrated altered circadian rhythmicity in airway epithelial cells from donors with asthma. Circadian rhythm and nuclear receptors had common rhythmicity in healthy and asthma. IL-17 signalling, cytokine receptor, and neutrophil chemotaxis pathways had altered circadian rhythmicity in asthma. Infection at time zero (end of temperature cycling) was associated with a two-fold lower viral replication than infection 12 hours later in healthy airway epithelial cells. Conclusion The core circadian clock genes maintain rhythmicity in healthy and asthma airway epithelia. Circadian regulation in immune and cytokine signaling pathways is altered in asthma. Support (if any) Sleep Research Society Foundation Career Development Award (WTP), ATS ASPIRE (WTP), Parker B Francis Fellowship (WTP), NIH R01AI163160 (JSD); NIH K24AI150991 (JSD)

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7

Menaker, M. "CIRCADIAN RHYTHMS: Circadian Photoreception." Science 299, no. 5604 (January 10, 2003): 213–14. http://dx.doi.org/10.1126/science.1081112.

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Harb, Ana Beatriz Cauduro, Wolnei Caumo, Priscila Raupp, and Maria Paz Loayza Hidalgo. "Síndrome do comer noturno: aspectos conceituais, epidemiológicos, diagnósticos e terapêuticos." Revista de Nutrição 23, no. 1 (February 2010): 127–36. http://dx.doi.org/10.1590/s1415-52732010000100014.

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O comportamento e o padrão alimentar são complexos, envolvendo aspectos metabólicos, fisiológicos e ambientais, e apresentando ritmicidade circadiana, herdada e espécie específica, sendo a humana essencialmente diurna. Este estudo tem como objetivo descrever a Síndrome do Comer Noturno, caracterizada por um atraso circadiano do padrão alimentar, mediado por alterações neuroendócrinas ao estresse. Procedeu-se à revisão da bibliografia existente, a partir do exame de artigos publicados pela literatura internacional nas bases de dados dos sites Pubmed, Lilacs, Sirus, referentes ao período de 1955 até as últimas publicações em 2007. Realizou-se um levantamento bibliográfico usando os seguintes descritores: night eating syndrome, sleep, circadian rhythm, appetite, nocturnal eating. Foram localizados 74 artigos e destes foram selecionados 26, cujo tema central era a Síndrome do Comer Noturno. Apesar dos estudos realizados, ainda existe longo percurso a ser percorrido para compreender a gênese da Síndrome do Comer Noturno e as relações intrínsecas desta com outros processos fisiopatogênicos. Tendo em conta que esta síndrome está vinculada ao controle da fome e da saciedade e à dessincronização entre o ritmo alimentar e o ritmo sono/vigília, a compreensão do seu processo gênico poderá demonstrar o impacto da dessincronização dos ritmos circadianos da alimentação no processo saúde-doença, e auxiliar a compreensão de fatores implicados no índice crescente de obesidade da sociedade moderna.

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Cenek, Lisa, Liubou Klindziuk, Cindy Lopez, Eleanor McCartney, Blanca Martin Burgos, Selma Tir, Mary E. Harrington, and Tanya L. Leise. "CIRCADA: Shiny Apps for Exploration of Experimental and Synthetic Circadian Time Series with an Educational Emphasis." Journal of Biological Rhythms 35, no. 2 (January 28, 2020): 214–22. http://dx.doi.org/10.1177/0748730419900866.

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Circadian rhythms are daily oscillations in physiology and behavior that can be assessed by recording body temperature, locomotor activity, or bioluminescent reporters, among other measures. These different types of data can vary greatly in waveform, noise characteristics, typical sampling rate, and length of recording. We developed 2 Shiny apps for exploration of these data, enabling visualization and analysis of circadian parameters such as period and phase. Methods include the discrete wavelet transform, sine fitting, the Lomb-Scargle periodogram, autocorrelation, and maximum entropy spectral analysis, giving a sense of how well each method works on each type of data. The apps also provide educational overviews and guidance for these methods, supporting the training of those new to this type of analysis. CIRCADA-E (Circadian App for Data Analysis–Experimental Time Series) allows users to explore a large curated experimental data set with mouse body temperature, locomotor activity, and PER2::LUC rhythms recorded from multiple tissues. CIRCADA-S (Circadian App for Data Analysis–Synthetic Time Series) generates and analyzes time series with user-specified parameters, thereby demonstrating how the accuracy of period and phase estimation depends on the type and level of noise, sampling rate, length of recording, and method. We demonstrate the potential uses of the apps through 2 in silico case studies.

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Bertolucci, Cristiano, Nicola Cavallari, Ilaria Colognesi, Jacopo Aguzzi, Zheng Chen, Pierpaolo Caruso, Augusto Foá, Gianluca Tosini, Francesco Bernardi, and Mirko Pinotti. "Evidence for an Overlapping Role of CLOCK and NPAS2 Transcription Factors in Liver Circadian Oscillators." Molecular and Cellular Biology 28, no. 9 (March 3, 2008): 3070–75. http://dx.doi.org/10.1128/mcb.01931-07.

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ABSTRACT The mechanisms underlying the circadian control of gene expression in peripheral tissues and influencing many biological pathways are poorly defined. Factor VII (FVII), the protease triggering blood coagulation, represents a valuable model to address this issue in liver since its plasma levels oscillate in a circadian manner and its promoter contains E-boxes, which are putative DNA-binding sites for CLOCK-BMAL1 and NPAS2-BMAL1 heterodimers and hallmarks of circadian regulation. The peaks of FVII mRNA levels in livers of wild-type mice preceded those in plasma, indicating a transcriptional regulation, and were abolished in Clock −/−; Npas2 −/− mice, thus demonstrating a role for CLOCK and NPAS2 circadian transcription factors. The investigation of Npas2 −/− and Clock Δ19/Δ19 mice, which express functionally defective heterodimers, revealed robust rhythms of FVII expression in both animal models, suggesting a redundant role for NPAS2 and CLOCK. The molecular bases of these observations were established through reporter gene assays. FVII transactivation activities of the NPAS2-BMAL1 and CLOCK-BMAL1 heterodimers were (i) comparable (a fourfold increase), (ii) dampened by the negative circadian regulators PER2 and CRY1, and (iii) abolished upon E-box mutagenesis. Our data provide the first evidence in peripheral oscillators for an overlapping role of CLOCK and NPAS2 in the regulation of circadianly controlled genes.

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11

Stupfel, M., V. Gourlet, A. Perramon, P. Merat, G. Putet, and L. Court. "Comparison of ultradian and circadian oscillations of carbon dioxide production by various endotherms." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 1 (January 1, 1995): R253—R265. http://dx.doi.org/10.1152/ajpregu.1995.268.1.r253.

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Carbon dioxide emission (VCO2) was computed every 20 min from continuous CO2 concentration recordings taken during 3-30 consecutive days, in strictly controlled environmental conditions, in 54 OF1 mice, 99 Japanese quail, 66 Sprague-Dawley rats, 50 Hartley guinea pigs, 7 chicks, for 7-15 days on 2 Cynomolgus monkeys, and for 24 h on 7 premature infants. This VCO2 shows circadian and ultradian oscillations that were analyzed for frequencies and amplitudes in light-dark 12-h alternation (LD 12:12), continuous light (LL), and continuous dark (DD). Circadians were not always identified or were often masked in LL or DD (mostly in guinea pigs, quail, and rats), while ultradians (tau > or = 40 min) were found in all species, at every time, and in all light regimens. Analysis of variance and chi 2 show significant (P < 0.001) interspecies differences for ultradian (1.07 < tau < 1.40 h) intervals and for circadian and ultradian VCO2 amplitudes. Relationships between ultradian and circadian VCO2 oscillations differ according to the species, ultradians appearing as an entity characteristic for each endotherm species.

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Froehlich, Allan C., Chen-Hui Chen, William J. Belden, Cornelia Madeti, Till Roenneberg, Martha Merrow, Jennifer J. Loros, and Jay C. Dunlap. "Genetic and Molecular Characterization of a Cryptochrome from the Filamentous Fungus Neurospora crassa." Eukaryotic Cell 9, no. 5 (March 19, 2010): 738–50. http://dx.doi.org/10.1128/ec.00380-09.

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ABSTRACT In plants and animals, cryptochromes function as either photoreceptors or circadian clock components. We have examined the cryptochrome from the filamentous fungus Neurospora crassa and demonstrate that Neurospora cry encodes a DASH-type cryptochrome that appears capable of binding flavin adenine dinucleotide (FAD) and methenyltetrahydrofolate (MTHF). The cry transcript and CRY protein levels are strongly induced by blue light in a wc-1-dependent manner, and cry transcript is circadianly regulated, with a peak abundance opposite in phase to frq. Neither deletion nor overexpression of cry appears to perturb the free-running circadian clock. However, cry disruption knockout mutants show a small phase delay under circadian entrainment. Using electrophoretic mobility shift assays (EMSA), we show that CRY is capable of binding single- and double-stranded DNA (ssDNA and dsDNA, respectively) and ssRNA and dsRNA. Whole-genome microarray experiments failed to identify substantive transcriptional regulatory activity of cry under our laboratory conditions.

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Yamanaka, Yujiro. "Chronobiology: Human circadian pacemaker and circadian rhythms." Japanese Journal of Physical Fitness and Sports Medicine 69, no. 4 (August 1, 2020): 343–50. http://dx.doi.org/10.7600/jspfsm.69.343.

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Milhiet, Vanessa, Bruno Etain, Carole Boudebesse, and Frank Bellivier. "Circadian biomarkers, circadian genes and bipolar disorders." Journal of Physiology-Paris 105, no. 4-6 (December 2011): 183–89. http://dx.doi.org/10.1016/j.jphysparis.2011.07.002.

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Love, Jessica, Jacqueline Lane, Richa Saxena, Frank Scheer, and Gregory Bormes. "0026 Novel home-based circadian phase assessment tool to enhance accessible quality care of circadian rhythm disorders- Circadia Study." SLEEP 46, Supplement_1 (May 1, 2023): A11—A12. http://dx.doi.org/10.1093/sleep/zsad077.0026.

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Abstract Introduction Circadian rhythm sleep-wake disorders (CRSWDs), shifted timing of physiology with the external environments. CRSWDs, often undiagnosed, can increase risk of cardiometabolic and psychiatric disorders, and may have substantial financial and social impacts. Dim light melatonin onset assay (DLMO), the current gold-standard diagnostic test for CRSWDs is expensive/difficult. We aim to develop a more accessible melatonin assessment. Methods Our DLMO assay kit is low-cost, home-based and self-administered. It contains all necessary components for a home-based DLMO assay, including 18 time-stamped saliva samples, a Philips Actiwatch, and a lux meter. We tested the feasibility of the kit across two DLMO assessments, one-week apart, in CRSWDs patients (N=5) and controls (N=5). We concurrently assessed sleep with wrist actigraphy and sleep diary over four weeks through a self-guided study website. Results We enrolled participants with delayed (n=4) and advanced (n=1) sleep disorder and 5 control participants (mean 38.2 y.o., SD 11.66 y.o.; biological sex: 9 female, 1 male (control)). Participants were 100% compliant completing questionnaires and sleep logging with little intervention and no in-person guidance. 5/10 participants completed 100% of sleep diary days. Average duration of study involvement, from consent to study completion, was 42.4 days. Participants successfully set up their collection space and collected saliva samples, remaining compliant to objectively-measured study protocols: 86.67% of samples were taken under sufficiently low light, and 82% were taken within five minutes of scheduled collection. We obtained and averaged two DLMO times for 7/10 participants (delayed sleep phase disorder (DPSD): 12:05 AM, controls: 9:56 PM). DLMO times were on average 3:18 hours earlier than self-reported sleep times. Conclusion Our pilot study, with both CRSWDs patients (N=5) and controls (N=5), found the at-home kits feasible and reproducible (5/6 participants had their DLMO times within an hour of each other). Using the kit, we confirmed their previous DSPD diagnoses and correctly classified controls through melatonin samples. We used objective measures (Actigraph) to verify the testing procedure was followed. These procedures will be tested on a larger scale in the Circadia Study (circadiastudy.org), set to launch in February 2023. Support (if any) This work was supported by the National Institutes of Health [DHHS] (grant number 1R35GM146839-01).

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Love, J., G. Bormes, R. Saxena, F. Scheer, and J. Lane. "Enhancing accessible quality care of circadian rhythm disorders through a novel home-based circadian phase assessment tool - circadia study." Sleep Medicine 115 (February 2024): 54–55. http://dx.doi.org/10.1016/j.sleep.2023.11.186.

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17

Jensen, Lasse Dahl, Charlotte Gyllenhaal, and Keith Block. "Circadian angiogenesis." Biomolecular Concepts 5, no. 3 (June 1, 2014): 245–56. http://dx.doi.org/10.1515/bmc-2014-0009.

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AbstractDaily rhythms of light/darkness, activity/rest and feeding/fasting are important in human physiology and their disruption (for example by frequent changes between day and night shifts) increases the risk of disease. Many of the diseases found to be associated with such disrupted circadian lifestyles, including cancer, cardiovascular diseases, metabolic disorders and neurological diseases, depend on pathological de-regulation of angiogenesis, suggesting that disrupting the circadian clock will impair the physiological regulation of angiogenesis leading to development and progression of these diseases. Today there is little known regarding circadian regulation of pathological angiogenesis but there is some evidence that supports both direct and indirect regulation of angiogenic factors by the cellular circadian clock machinery, as well as by circulating circadian factors, important for coordinating circadian rhythms in the organism. Through highlighting recent advances both in pre-clinical and clinical research on various diseases including cancer, cardiovascular disorders and obesity, we will here present an overview of the available knowledge on the importance of circadian regulation of angiogenesis and discuss how the circadian clock may provide alternative targets for pro- or anti-angiogenic therapy in the future.

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18

Dubey, Sneha. "Circadian Rhythm." International Journal of Nursing Education and Research 7, no. 1 (2019): 112. http://dx.doi.org/10.5958/2454-2660.2019.00022.x.

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19

Turek, Fred W. "Circadian Rhythms." Hormone Research in Paediatrics 49, no. 3-4 (1998): 109–13. http://dx.doi.org/10.1159/000023155.

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SAMPLES, JULIE F., MARY LOU VAN COTT, CHARLENE LONG, IMOGENE M. KING, and ANGELA KERSENBROCK. "Circadian Rhythms." Nursing Research 34, no. 6 (November 1985): 377???379. http://dx.doi.org/10.1097/00006199-198511000-00021.

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21

Grant, A. C., and E. P. Roter. "Circadian sneezing." Neurology 44, no. 3, Part 1 (March 1, 1994): 369. http://dx.doi.org/10.1212/wnl.44.3_part_1.369.

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22

Benitez, Margarita, and Markus Vogl. "Circadian Capital." Leonardo 43, no. 1 (February 2010): 10. http://dx.doi.org/10.1162/leon.2010.43.1.10.

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Granada, Adrián E., Trinitat Cambras, Antoni Díez-Noguera, and Hanspeter Herzel. "Circadian desynchronization." Interface Focus 1, no. 1 (November 17, 2010): 153–66. http://dx.doi.org/10.1098/rsfs.2010.0002.

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The suprachiasmatic nucleus (SCN) coordinates via multiple outputs physiological and behavioural circadian rhythms. The SCN is composed of a heterogeneous network of coupled oscillators that entrain to the daily light–dark cycles. Outside the physiological entrainment range, rich locomotor patterns of desynchronized rhythms are observed. Previous studies interpreted these results as the output of different SCN neural subpopulations. We find, however, that even a single periodically driven oscillator can induce such complex desynchronized locomotor patterns. Using signal analysis, we show how the observed patterns can be consistently clustered into two generic oscillatory interaction groups: modulation and superposition. In seven of 17 rats undergoing forced desynchronization, we find a theoretically predicted third spectral component. Combining signal analysis with the theory of coupled oscillators, we provide a framework for the study of circadian desynchronization.

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Hines, P. J. "Circadian Rhythms." Science Signaling 7, no. 319 (April 1, 2014): ec87-ec87. http://dx.doi.org/10.1126/scisignal.2005313.

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Riddihough, G. "Circadian Oscillations." Science Signaling 2, no. 69 (May 5, 2009): ec157-ec157. http://dx.doi.org/10.1126/scisignal.269ec157.

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26

Eichner, E. Randy. "Circadian Rhythms." Physician and Sportsmedicine 22, no. 10 (October 1994): 82–93. http://dx.doi.org/10.1080/00913847.1994.11710504.

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Schwartz, W. J. "Circadian Clockwork." Science 261, no. 5122 (August 6, 1993): 772–73. http://dx.doi.org/10.1126/science.261.5122.772.

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Lakin-Thomas, Patricia L. "Circadian rhythms." Trends in Genetics 16, no. 3 (March 2000): 135–42. http://dx.doi.org/10.1016/s0168-9525(99)01945-9.

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Persson, Pontus B., and Anja Bondke Persson. "Circadian rhythms." Acta Physiologica 225, no. 1 (December 4, 2018): e13220. http://dx.doi.org/10.1111/apha.13220.

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Hastings, Michael H. "Circadian clocks." Current Biology 7, no. 11 (November 1997): R670—R672. http://dx.doi.org/10.1016/s0960-9822(06)00350-2.

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Merrow, Martha, and Till Roenneberg. "Circadian Clocks." Cell 106, no. 2 (July 2001): 141–43. http://dx.doi.org/10.1016/s0092-8674(01)00443-3.

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Allada, Ravi. "Circadian Clocks." Cell 112, no. 3 (February 2003): 284–86. http://dx.doi.org/10.1016/s0092-8674(03)00076-x.

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Merrow, Martha. "Circadian rhythms." FEBS Letters 585, no. 10 (April 28, 2011): 1383. http://dx.doi.org/10.1016/j.febslet.2011.04.055.

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Vaze, Koustubh M., and Vijay Kumar Sharma. "Circadian rhythms." Resonance 18, no. 7 (July 2013): 662–72. http://dx.doi.org/10.1007/s12045-013-0085-4.

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Nikhil, K. L., and Vijay Kumar Sharma. "Circadian rhythms." Resonance 18, no. 9 (September 2013): 832–44. http://dx.doi.org/10.1007/s12045-013-0107-2.

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Vaze, Koustubh M., and Vijay Kumar Sharma. "Circadian rhythms." Resonance 18, no. 11 (November 2013): 1032–50. http://dx.doi.org/10.1007/s12045-013-0129-9.

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Vaze, Koustubh M., K. L. Nikhil, and Vijay Kumar Sharma. "Circadian rhythms." Resonance 19, no. 2 (February 2014): 175–89. http://dx.doi.org/10.1007/s12045-014-0020-3.

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Aronson, B. "Circadian rhythms." Brain Research Reviews 18, no. 3 (December 1993): 315–33. http://dx.doi.org/10.1016/0165-0173(93)90015-r.

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McFadden, E. R. "Circadian rhythms." American Journal of Medicine 85, no. 1 (July 1988): 2–5. http://dx.doi.org/10.1016/0002-9343(88)90230-6.

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McConnell, John. "Circadian clocks." Lancet 342, no. 8873 (September 1993): 736. http://dx.doi.org/10.1016/0140-6736(93)91725-2.

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Joo, Eun Yeon. "Circadian Neurobiology." Journal of Korean Sleep Research Society 3, no. 1 (June 30, 2006): 1–5. http://dx.doi.org/10.13078/jksrs.06001.

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Monk, Timothy H. "Circadian Rhythm." Clinics in Geriatric Medicine 5, no. 2 (May 1989): 331–46. http://dx.doi.org/10.1016/s0749-0690(18)30682-7.

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Abbott, Sabra M., and Phyllis C. Zee. "Circadian Rhythms." Neurologic Clinics 37, no. 3 (August 2019): 601–13. http://dx.doi.org/10.1016/j.ncl.2019.04.004.

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Rea, Mark S. "Circadian photonics." Nature Photonics 5, no. 5 (May 2011): 271–72. http://dx.doi.org/10.1038/nphoton.2011.71.

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&NA;. "CIRCADIAN PHYSIOLOGY." Shock 16, no. 4 (October 2001): 327. http://dx.doi.org/10.1097/00024382-200116040-00017.

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Ferrarelli, L. K. "Circadian Learning." Science Signaling 6, no. 278 (June 4, 2013): ec127-ec127. http://dx.doi.org/10.1126/scisignal.2004392.

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Devlin, Paul F., and Steve A. Kay. "Circadian Photoperception." Annual Review of Physiology 63, no. 1 (March 2001): 677–94. http://dx.doi.org/10.1146/annurev.physiol.63.1.677.

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Thompson, Chris. "Circadian Rhythms." British Journal of Psychiatry 146, no. 5 (May 1985): 557–58. http://dx.doi.org/10.1192/bjp.146.5.557.

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Niemitz, Emily. "Circadian genomics." Nature Genetics 44, no. 12 (November 28, 2012): 1293. http://dx.doi.org/10.1038/ng.2487.

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Muñoz, Estela, Michelle Brewer, and Ruben Baler. "Circadian Transcription." Journal of Biological Chemistry 277, no. 39 (July 18, 2002): 36009–17. http://dx.doi.org/10.1074/jbc.m203909200.

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