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Author Erren, T.C.; Pape, H.G.; Reiter, R.J.; Piekarski, C. url  doi
openurl 
  Title Chronodisruption and cancer Type Journal Article
  Year 2008 Publication Die Naturwissenschaften Abbreviated Journal Naturwissenschaften  
  Volume 95 Issue 5 Pages 367-382  
  Keywords Human Health; Animals; Chronobiology Phenomena/*physiology; *Circadian Rhythm; Humans; Incidence; Light; Mammals; Neoplasms/*epidemiology; Work Schedule Tolerance  
  Abstract Research into health effects of chronodisruption (CD), a relevant disturbance of the circadian organization of physiology, endocrinology, metabolism and behaviour, is evolving at a rapid pace. With regard to malignancies, our synthesis of key experiments indicates that CD can play a causal role for cancer growth and tumor progression in animals. Moreover, our meta-analyses of 30 epidemiological studies evince that flight personnel and shift workers exposed to chronodisruption may have increased breast and prostate cancer risks: summary relative risks (RRs) for investigations of flight personnel and of shift workers suggested a 70 and 40% increase in the risk of breast cancer, respectively, and excess relative risks of prostate cancer in nine studies in flight personnel (40%) and in two studies in male shift workers. There was a remarkable indication of homogeneity of results from the individual studies that contribute to the average statistics. However, in view of doubts about whether the differing assessments of CD can really be regarded as valid reflections of the same causative phenomenon and the lack of control of covariates in the majority of studies, it is premature to conclude that the risk observations reflect a real, rather than spurious, association with CD. The challenge for future epidemiological investigations of the biologically plausible links between chronodisruption and human cancers is to conduct studies which appreciate details of transmeridian travelling, of shift work and of covariates for the development of the diseases.  
  Address School of Medicine and Dentistry, University of Cologne, Cologne, Germany. tim.erren@uni-koeln.de  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0028-1042 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:18196215 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 744  
Permanent link to this record
 

 
Author Evans, J.A.; Carter, S.N.; Freeman, D.A.; Gorman, M.R. url  doi
openurl 
  Title Dim nighttime illumination alters photoperiodic responses of hamsters through the intergeniculate leaflet and other photic pathways Type Journal Article
  Year 2012 Publication Neuroscience Abbreviated Journal Neuroscience  
  Volume 202 Issue Pages 300-308  
  Keywords Animals; Biological Clocks/physiology; Circadian Rhythm/physiology; Cricetinae; Darkness; Data Interpretation, Statistical; Geniculate Bodies/*physiology; *Lighting; Male; Motor Activity/physiology; Phodopus; *Photoperiod; Visual Pathways/*physiology  
  Abstract In mammals, light entrains the central pacemaker within the suprachiasmatic nucleus (SCN) through both a direct neuronal projection from the retina and an indirect projection from the intergeniculate leaflet (IGL) of the thalamus. Although light comparable in intensity to moonlight is minimally effective at resetting the phase of the circadian clock, dimly lit and completely dark nights are nevertheless perceived differentially by the circadian system, even when nighttime illumination is below putative thresholds for phase resetting. Under a variety of experimental paradigms, dim nighttime illumination exerts effects that may be characterized as enhancing the plasticity of circadian entrainment. For example, relative to completely dark nights, dimly lit nights accelerate development of photoperiodic responses of Siberian hamsters transferred from summer to winter day lengths. Here we assess the neural pathways underlying this response by testing whether IGL lesions eliminate the effects of dim nighttime illumination under short day lengths. Consistent with previous work, dimly lit nights facilitated the expansion of activity duration under short day lengths. Ablation of the IGL, moreover, did not influence photoperiodic responses in animals held under completely dark nights. However, among animals that were provided dimly lit nights, IGL lesions prevented the short-day typical expansion of activity duration as well as the seasonally appropriate gonadal regression and reduction in body weight. Thus, the present data indicate that the IGL plays a central role in mediating the facilitative effects of dim nighttime illumination under short day lengths, but in the absence of the IGL, dim light at night influences photoperiodic responses through residual photic pathways.  
  Address Department of Psychology, University of California, San Diego, La Jolla, CA, USA. jevans@msm.edu  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0306-4522 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22155265; PMCID:PMC3578228 Approved no  
  Call Number IDA @ john @ Serial 87  
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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  
  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 0748-7304 ISBN Medium  
  Area Expedition Conference  
  Notes 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.  
  Address  
  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 0960-9822 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19243688 Approved no  
  Call Number IDA @ john @ Serial 152  
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Author Fernandez, F.; Lu, D.; Ha, P.; Costacurta, P.; Chavez, R.; Heller, H.C.; Ruby, N.F. url  doi
openurl 
  Title Circadian rhythm. Dysrhythmia in the suprachiasmatic nucleus inhibits memory processing Type Journal Article
  Year 2014 Publication Science (New York, N.Y.) Abbreviated Journal Science  
  Volume 346 Issue 6211 Pages 854-857  
  Keywords Animals; circadian rhythm; circadian disruption; memory; suprachiasmatic nucleus; Biological Clocks; dysrhythmia; Siberian hamster; Phodopus sungorus; sleep  
  Abstract Chronic circadian dysfunction impairs declarative memory in humans but has little effect in common rodent models of arrhythmia caused by clock gene knockouts or surgical ablation of the suprachiasmatic nucleus (SCN). An important problem overlooked in these translational models is that human dysrhythmia occurs while SCN circuitry is genetically and neurologically intact. Siberian hamsters (Phodopus sungorus) are particularly well suited for translational studies because they can be made arrhythmic by a one-time photic treatment that severely impairs spatial and recognition memory. We found that once animals are made arrhythmic, subsequent SCN ablation completely rescues memory processing. These data suggest that the inhibitory effects of a malfunctioning SCN on cognition require preservation of circuitry between the SCN and downstream targets that are lost when these connections are severed.  
  Address Biology Department, Stanford University, Stanford CA, USA. ruby@stanford.edu  
  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 0036-8075 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:25395537 Approved no  
  Call Number IDA @ john @ Serial 1069  
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