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Author Wright, K.P.J.; Hull, J.T.; Czeisler, C.A. url  doi
openurl 
  Title Relationship between alertness, performance, and body temperature in humans Type Journal Article
  Year 2002 Publication American Journal of Physiology. Regulatory, Integrative and Comparative Physiology Abbreviated Journal Am J Physiol Regul Integr Comp Physiol  
  Volume 283 Issue 6 Pages R1370-7  
  Keywords Human Health; Adult; Attention/*physiology; *Body Temperature; Circadian Rhythm/physiology; Cognition/*physiology; Female; Humans; Male; Memory/physiology; Reaction Time; Sleep/physiology; Time Factors; Wakefulness/physiology; NASA Discipline Regulatory Physiology; Non-NASA Center  
  Abstract Body temperature has been reported to influence human performance. Performance is reported to be better when body temperature is high/near its circadian peak and worse when body temperature is low/near its circadian minimum. We assessed whether this relationship between performance and body temperature reflects the regulation of both the internal biological timekeeping system and/or the influence of body temperature on performance independent of circadian phase. Fourteen subjects participated in a forced desynchrony protocol allowing assessment of the relationship between body temperature and performance while controlling for circadian phase and hours awake. Most neurobehavioral measures varied as a function of internal biological time and duration of wakefulness. A number of performance measures were better when body temperature was elevated, including working memory, subjective alertness, visual attention, and the slowest 10% of reaction times. These findings demonstrate that an increased body temperature, associated with and independent of internal biological time, is correlated with improved performance and alertness. These results support the hypothesis that body temperature modulates neurobehavioral function in humans.  
  Address Division of Sleep Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. kenneth.wright@colorado.edu  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0363-6119 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:12388468 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 835  
Permanent link to this record
 

 
Author Evans, J.A.; Elliott, J.A.; Gorman, M.R. url  doi
openurl 
  Title Circadian effects of light no brighter than moonlight Type Journal Article
  Year 2007 Publication Journal of Biological Rhythms Abbreviated Journal J Biol Rhythms  
  Volume 22 Issue 4 Pages 356-367  
  Keywords Animals; Biological Clocks/physiology/*radiation effects; *Circadian Rhythm; Cricetinae; Dose-Response Relationship, Radiation; Lighting/*methods; Male; Mesocricetus; Motor Activity; Oscillometry; Photic Stimulation/methods; *Photoperiod; Physical Conditioning, Animal; Time Factors  
  Abstract In mammals, light entrains endogenous circadian pacemakers by inducing daily phase shifts via a photoreceptor mechanism recently discovered in retinal ganglion cells. Light that is comparable in intensity to moonlight is generally ineffective at inducing phase shifts or suppressing melatonin secretion, which has prompted the view that circadian photic sensitivity has been titrated so that the central pacemaker is unaffected by natural nighttime illumination. However, the authors have shown in several different entrainment paradigms that completely dark nights are not functionally equivalent to dimly lit nights, even when nighttime illumination is below putative thresholds for the circadian visual system. The present studies extend these findings. Dim illumination is shown here to be neither a strong zeitgeber, consistent with published fluence response curves, nor a potentiator of other zeitgebers. Nevertheless, dim light markedly alters the behavior of the free-running circadian pacemaker. Syrian hamsters were released from entrained conditions into constant darkness or dim narrowband green illumination (~0.01 lx, 1.3 x 10(-9) W/cm(2), peak lambda = 560 nm). Relative to complete darkness, constant dim light lengthened the period by ~0.3 h and altered the waveform of circadian rhythmicity. Among animals transferred from long day lengths (14 L:10 D) into constant conditions, dim illumination increased the duration of the active phase (alpha) by ~3 h relative to complete darkness. Short day entrainment (8 L:16 D) produced initially long alpha that increased further under constant dim light but decreased under complete darkness. In contrast, dim light pulses 2 h or longer produced effects on circadian phase and melatonin secretion that were small in magnitude. Furthermore, the amplitude of phase resetting to bright light and nonphotic stimuli was similar against dimly lit and dark backgrounds, indicating that the former does not directly amplify circadian inputs. Dim illumination markedly alters circadian waveform through effects on alpha, suggesting that dim light influences the coupling between oscillators theorized to program the beginning and end of subjective night. Physiological mechanisms responsible for conveying dim light stimuli to the pacemaker and implications for chronotherapeutics warrant further study.  
  Address Department of Psychology, University of California, San Diego, La Jolla, CA 92093, usa. jaevans@ucsd.edu  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0748-7304 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:17660452 Approved no  
  Call Number IDA @ john @ Serial 31  
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Author Evans, J.A.; Elliott, J.A.; Gorman, M.R. url  doi
openurl 
  Title Dim nighttime illumination accelerates adjustment to timezone travel in an animal model Type Journal Article
  Year 2009 Publication Current Biology : CB Abbreviated Journal Curr Biol  
  Volume 19 Issue 4 Pages R156-7  
  Keywords *Adaptation, Physiological; Animals; Behavior, Animal/physiology; Biological Clocks/*physiology; Circadian Rhythm/*physiology; Cricetinae; Humans; *Lighting; Mesocricetus; Mice; Motor Activity/physiology; Phodopus; *Photoperiod; Time Factors  
  Abstract Jetlag reflects a mismatch between local and circadian time following rapid timezone travel [1]. Appropriately timed bright light can shift human circadian rhythms but recovery is slow (e.g., 1-2 days per timezone). Most symptoms subside after resynchronization, but chronic jetlag may have enduring negative effects [2], including even accelerated mortality in mice [3]. Melatonin, prescription drugs, and/or exercise may help shift the clock but, like bright light, require complex schedules of application [1]. Thus, there is a need for more efficient and practical treatments for addressing jetlag. In contrast to bright daytime lighting, nighttime conditions have received scant attention. By incorporating more naturalistic nighttime lighting comparable in intensity to dim moonlight, we demonstrate that recovery after simulated jetlag is accelerated when nights are dimly lit rather than completely dark.  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0960-9822 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:19243688 Approved no  
  Call Number IDA @ john @ Serial 152  
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Author Stevens, R.G. url  doi
openurl 
  Title Light-at-night, circadian disruption and breast cancer: assessment of existing evidence Type Journal Article
  Year 2009 Publication International Journal of Epidemiology Abbreviated Journal Int J Epidemiol  
  Volume 38 Issue 4 Pages 963-970  
  Keywords Human Health; Animals; Blindness/complications/epidemiology; Breast Neoplasms/epidemiology/*etiology/metabolism; Chronobiology Disorders/*complications/epidemiology/metabolism; Circadian Rhythm/physiology; Disease Models, Animal; Female; Humans; Light Signal Transduction/physiology; Lighting/adverse effects; Melatonin/biosynthesis; Sleep/physiology; Time Factors; *Work Schedule Tolerance  
  Abstract BACKGROUND: Breast cancer incidence is increasing globally for largely unknown reasons. The possibility that a portion of the breast cancer burden might be explained by the introduction and increasing use of electricity to light the night was suggested >20 years ago. METHODS: The theory is based on nocturnal light-induced disruption of circadian rhythms, notably reduction of melatonin synthesis. It has formed the basis for a series of predictions including that non-day shift work would increase risk, blind women would be at lower risk, long sleep duration would lower risk and community nighttime light level would co-distribute with breast cancer incidence on the population level. RESULTS: Accumulation of epidemiological evidence has accelerated in recent years, reflected in an International Agency for Research on Cancer (IARC) classification of shift work as a probable human carcinogen (2A). There is also a strong rodent model in support of the light-at-night (LAN) idea. CONCLUSION: If a consensus eventually emerges that LAN does increase risk, then the mechanisms for the effect are important to elucidate for intervention and mitigation. The basic understanding of phototransduction for the circadian system, and of the molecular genetics of circadian rhythm generation are both advancing rapidly, and will provide for the development of lighting technologies at home and at work that minimize circadian disruption, while maintaining visual efficiency and aesthetics. In the interim, there are strategies now available to reduce the potential for circadian disruption, which include extending the daily dark period, appreciate nocturnal awakening in the dark, using dim red light for nighttime necessities, and unless recommended by a physician, not taking melatonin tablets.  
  Address Department of Community Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-6325, USA. bugs@uchc.edu  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0300-5771 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:19380369; PMCID:PMC2734067 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 527  
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Author Kovac, J.; Husse, J.; Oster, H. url  doi
openurl 
  Title A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock Type Journal Article
  Year 2009 Publication Molecules and Cells Abbreviated Journal Mol Cells  
  Volume 28 Issue 2 Pages 75-80  
  Keywords Human Health; Animals; Biological Clocks/*physiology; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/*physiology; Energy Metabolism/*physiology; Gene Expression Regulation; Homeostasis; Humans; Period Circadian Proteins/genetics/metabolism; Time Factors  
  Abstract The cyclic environmental conditions brought about by the 24 h rotation of the earth have allowed the evolution of endogenous circadian clocks that control the temporal alignment of behaviour and physiology, including the uptake and processing of nutrients. Both metabolic and circadian regulatory systems are built upon a complex feedback network connecting centres of the central nervous system and different peripheral tissues. Emerging evidence suggests that circadian clock function is closely linked to metabolic homeostasis and that rhythm disruption can contribute to the development of metabolic disease. At the same time, metabolic processes feed back into the circadian clock, affecting clock gene expression and timing of behaviour. In this review, we summarize the experimental evidence for this bimodal interaction, with a focus on the molecular mechanisms mediating this exchange, and outline the implications for clock-based and metabolic diseases.  
  Address Circadian Rhythms Group, Max Planck Institute of Biophysical Chemistry, 37077, Gottingen, Germany  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1016-8478 ISBN Medium  
  Area Expedition Conference  
  Notes (up) PMID:19714310 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 772  
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