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Simon Archer

Bio: Simon Archer is an academic researcher from University of Surrey. The author has contributed to research in topics: Circadian rhythm & PER3. The author has an hindex of 53, co-authored 139 publications receiving 9832 citations. Previous affiliations of Simon Archer include Spanish National Research Council & University of Bristol.


Papers
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Journal ArticleDOI
TL;DR: This review of the psychometric properties and validity of CT measures as well as individual, environmental and genetic factors that influence the circadian typology provides a state of the art discussion to allow professionals to integrate chronobiological aspects of human behavior into their daily practice.
Abstract: The interest in the systematic study of the circadian typology (CT) is relatively recent and has developed rapidly in the two last decades. All the existing data suggest that this individual difference affects our biological and psychological functioning, not only in health, but also in disease. In the present study, we review the current literature concerning the psychometric properties and validity of CT measures as well as individual, environmental and genetic factors that influence the CT. We present a brief overview of the biological markers that are used to define differences between CT groups (sleep-wake cycle, body temperature, cortisol and melatonin), and we assess the implications for CT and adjustment to shiftwork and jet lag. We also review the differences between CT in terms of cognitive abilities, personality traits and the incidence of psychiatric disorders. When necessary, we have emphasized the methodological limitations that exist today and suggested some future avenues of work in order to overcome these. This is a new field of interest to professionals in many different areas (research, labor, academic and clinical), and this review provides a state of the art discussion to allow professionals to integrate chronobiological aspects of human behavior into their daily practice.

936 citations

Journal ArticleDOI
15 Jun 2003-Sleep
TL;DR: The length of the Per3 repeat region identifies a potential genetic marker for extreme diurnal preference and was strongly associated with the delayed sleep phase syndrome patients, 75% of whom were homozygous.
Abstract: Study objectives To investigate the link between extreme diurnal preference, delayed sleep phase syndrome, and a length polymorphism in Per3. Design Subjects were genotyped using polymerase chain reaction. Patients or participants Subjects with defined diurnal preference as determined by the Horne-Ostberg questionnaire and patients with delayed sleep phase syndrome. Measurements and results The Per3 polymorphism correlated significantly with extreme diurnal preference, the longer allele associating with morningness and the shorter allele with eveningness. The shorter allele was strongly associated with the delayed sleep phase syndrome patients, 75% of whom were homozygous. Conclusion The length of the Per3 repeat region identifies a potential genetic marker for extreme diurnal preference.

624 citations

01 Jan 2003
TL;DR: In this paper, the authors investigated the link between extreme diurnal preference, delayed sleep phase syndrome, and a length polymorphism in Per3 and found that the longer allele associated with morningness and the shorter allele with eveningness.
Abstract: STUDY OBJECTIVES To investigate the link between extreme diurnal preference, delayed sleep phase syndrome, and a length polymorphism in Per3. DESIGN Subjects were genotyped using polymerase chain reaction. PATIENTS OR PARTICIPANTS Subjects with defined diurnal preference as determined by the Horne-Ostberg questionnaire and patients with delayed sleep phase syndrome. MEASUREMENTS AND RESULTS The Per3 polymorphism correlated significantly with extreme diurnal preference, the longer allele associating with morningness and the shorter allele with eveningness. The shorter allele was strongly associated with the delayed sleep phase syndrome patients, 75% of whom were homozygous. CONCLUSION The length of the Per3 repeat region identifies a potential genetic marker for extreme diurnal preference.

602 citations

Journal ArticleDOI
TL;DR: The data show that this polymorphism in PER3 predicts individual differences in the sleep-loss-induced decrement in performance and that this differential susceptibility may be mediated by its effects on sleep homeostasis.

484 citations

Journal ArticleDOI
TL;DR: It is shown that one wk of insufficient sleep alters gene expression in human blood cells, reduces the amplitude of circadian rhythms in gene expression, and intensifies the effects of subsequent acute total sleep loss on gene expression.
Abstract: Insufficient sleep and circadian rhythm disruption are associated with negative health outcomes, including obesity, cardiovascular disease, and cognitive impairment, but the mechanisms involved remain largely unexplored. Twenty-six participants were exposed to 1 wk of insufficient sleep (sleep-restriction condition 5.70 h, SEM = 0.03 sleep per 24 h) and 1 wk of sufficient sleep (control condition 8.50 h sleep, SEM = 0.11). Immediately following each condition, 10 whole-blood RNA samples were collected from each participant, while controlling for the effects of light, activity, and food, during a period of total sleep deprivation. Transcriptome analysis revealed that 711 genes were up- or down-regulated by insufficient sleep. Insufficient sleep also reduced the number of genes with a circadian expression profile from 1,855 to 1,481, reduced the circadian amplitude of these genes, and led to an increase in the number of genes that responded to subsequent total sleep deprivation from 122 to 856. Genes affected by insufficient sleep were associated with circadian rhythms (PER1, PER2, PER3, CRY2, CLOCK, NR1D1, NR1D2, RORA, DEC1, CSNK1E), sleep homeostasis (IL6, STAT3, KCNV2, CAMK2D), oxidative stress (PRDX2, PRDX5), and metabolism (SLC2A3, SLC2A5, GHRL, ABCA1). Biological processes affected included chromatin modification, gene-expression regulation, macromolecular metabolism, and inflammatory, immune and stress responses. Thus, insufficient sleep affects the human blood transcriptome, disrupts its circadian regulation, and intensifies the effects of acute total sleep deprivation. The identified biological processes may be involved with the negative effects of sleep loss on health, and highlight the interrelatedness of sleep homeostasis, circadian rhythmicity, and metabolism.

459 citations


Cited by
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Journal ArticleDOI
TL;DR: This review aims to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings.
Abstract: Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

1,964 citations

Journal ArticleDOI
TL;DR: Cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss.
Abstract: Deficits in daytime performance due to sleep loss are experienced universally and associated with a significant social, financial, and human cost. Microsleeps, sleep attacks, and lapses in cognition increase with sleep loss as a function of state instability. Sleep deprivation studies repeatedly show a variable (negative) impact on mood, cognitive performance, and motor function due to an increasing sleep propensity and destabilization of the wake state. Specific neurocognitive domains including executive attention, working memory, and divergent higher cognitive functions are particularly vulnerable to sleep loss. In humans, functional metabolic and neurophysiological studies demonstrate that neural systems involved in executive function (i.e., prefrontal cortex) are more susceptible to sleep deprivation in some individuals than others. Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness. Sleep deprivation associated with disease-related sleep fragmentation (i.e., sleep apnea and restless legs syndrome) also results in neurocognitive performance decrements similar to those seen in sleep restriction studies. Performance deficits associated with sleep disorders are often viewed as a simple function of disease severity; however, recent experiments suggest that individual vulnerability to sleep loss may play a more critical role than previously thought.

1,864 citations

Journal ArticleDOI
TL;DR: Sensory systems, signals, signaling behavior, and habitat choice are evolutionarily coupled and should coevolve in predictable directions, determined by environmental biophysics, neurobiology, and the genetics of the suites of traits.
Abstract: There is a bewildering diversity of signals, sensory systems, and signaling behavior. A consideration of how these traits affect each other's evolution explains some of this diversity. Natural selection favors signals, receptors, and signaling behavior that maximize the received signals relative to background noise and minimize signal degradation. Properties of sensory systems bias the direction of evolution of the signals that they receive. For example, females may prefer males whose signals they can perceive more easily, and this will lead to the spread of more easily perceived male traits. Environmental conditions during signal transmission and detection also affect signal perception. Specific environmental conditions will bias the evolutionary direction of behavior, which affects the time and place of signaling as well as microhabitat preferences. Increased specialization of microhabitats and signaling behavior may lead to biased evolution of the sensory systems to work more efficiently. Thus, sensory...

1,717 citations

Journal ArticleDOI
TL;DR: The general mechanisms of the circadian clockwork are reviewed, recent findings that elucidate tissue-specific expression patterns of the clock genes are described and the importance of circadian regulation in peripheral tissues for an organism's overall well-being is addressed.
Abstract: Mammals synchronize their circadian activity primarily to the cycles of light and darkness in the environment. This is achieved by ocular photoreception relaying signals to the suprachiasmatic nucleus (SCN) in the hypothalamus. Signals from the SCN cause the synchronization of independent circadian clocks throughout the body to appropriate phases. Signals that can entrain these peripheral clocks include humoral signals, metabolic factors, and body temperature. At the level of individual tissues, thousands of genes are brought to unique phases through the actions of a local transcription/translation-based feedback oscillator and systemic cues. In this molecular clock, the proteins CLOCK and BMAL1 cause the transcription of genes which ultimately feedback and inhibit CLOCK and BMAL1 transcriptional activity. Finally, there are also other molecular circadian oscillators which can act independently of the transcription-based clock in all species which have been tested.

1,550 citations

Book
01 Jan 2004
TL;DR: Learning style instruments are widely used but not enough is known about their reliability and validity and their impact on pedagogy in post-16 learning as mentioned in this paper, and the implications of learning styles for teaching and learning.
Abstract: Learning style instruments are widely used but not enough is known about their reliability and validity and their impact on pedagogy in post-16 learning. This report documents work from a project commissioned by the Learning and Skills Development Agency (LSDA) to carry out an extensive review of research on post-16 learning styles, to evaluate the main models of learning styles, and to discuss the implications of learning styles for post-16 teaching and learning. The following research questions were addressed: What models of learning styles are influential and potentially influential? What empirical evidence is there to support the claims made for these models? What are the broad implications for pedagogy of these models? What empirical evidence is there that models of learning styles have an impact on students’ learning? The project identified the range of models that are available and influential or potentially influential in research and practice, located these models within identifiable ‘families’ of ideas about learning styles, evaluated the theories, claims and applications of these models, with a particular focus on evaluating the authors’ claims for reliability and validity, evaluated the claims made for the pedagogical implications of the selected models of learning styles, identified what gaps there are in current knowledge and what future research is needed in this area, and made recommendations and drew conclusions about the research field as a whole. In conclusion, the implications for pedagogy are drawn out and recommendations and conclusions are offered for practitioners, policymakers and the research community. The report concludes that it matters fundamentally which model is chosen. A second report (indexed at TD/TNC 79.72) discusses the appeal of learning styles as well as offering an overview of ways in which political and institutional contexts in the learning and skills sector affect the ways that learning styles might be put into practice.

1,394 citations