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Author (up) 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  
  Publisher Place of Publication Editor  
  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 (up) Filipski, E.; Subramanian, P.; Carriere, J.; Guettier, C.; Barbason, H.; Levi, F. url  doi
openurl 
  Title Circadian disruption accelerates liver carcinogenesis in mice Type Journal Article
  Year 2009 Publication Mutation Research Abbreviated Journal Mutat Res  
  Volume 680 Issue 1-2 Pages 95-105  
  Keywords Human Health; Animals; Alanine Transaminase/blood; Animals; Aspartate Aminotransferases/blood; Bile Duct Neoplasms/chemically induced/pathology; Bile Ducts, Intrahepatic/drug effects/pathology; Body Weight/drug effects; Carcinogens/administration & dosage/*toxicity; Carcinoma, Hepatocellular/chemically induced/pathology; Cholangiocarcinoma/chemically induced/pathology; Circadian Rhythm/*drug effects; Diethylnitrosamine/administration & dosage/*toxicity; Dose-Response Relationship, Drug; Injections, Intraperitoneal; Liver/drug effects/pathology; Liver Neoplasms/blood/*chemically induced/pathology; Male; Mice; Neoplasms, Multiple Primary/chemically induced/pathology; Sarcoma/chemically induced/pathology; Time Factors  
  Abstract BACKGROUND: The circadian timing system rhythmically controls behavior, physiology, cellular proliferation and xenobiotic metabolism over the 24-h period. The suprachiasmatic nuclei in the hypothalamus coordinate the molecular clocks in most mammalian cells through an array of circadian physiological rhythms including rest-activity, body temperature, feeding patterns and hormonal secretions. As a result, shift work that involves circadian disruption is probably carcinogenic in humans. In experimental models, chronic jet-lag (CJL) suppresses rest-activity and body temperature rhythms and accelerates growth of two transplantable tumors in mice. CJL also suppresses or significantly alters the expression rhythms of clock genes in liver and tumors. Circadian clock disruption from CJL downregulates p53 and upregulates c-Myc, thus favoring cellular proliferation. Here, we investigate the role of CJL as a tumor promoter in mice exposed to the hepatic carcinogen, diethylnitrosamine (DEN). METHODS: In experiment 1 (Exp 1), the dose-dependent carcinogenicity of chronic intraperitoneal (i.p.) administration of DEN was explored in mice. In Exp 2, mice received DEN at 10 mg/kg/day (cumulative dose: 243 mg/kg), then were randomized to remain in a photoperiodic regimen where 12 h of light alternates with 12 h of darkness (LD 12:12) or to be submitted to CJL (8-h advance of light onset every 2 days). Rest-activity and body temperature were monitored. Serum liver enzymes were determined repeatedly. Mice were sacrificed and examined for neoplastic lesions at 10 months. RESULTS: In Exp 1, DEN produced liver cancers in all the mice receiving 10 mg/kg/day. In Exp 2, mice on CJL had increased mean plasma levels of aspartate aminotransferase and more liver tumors as compared to LD mice at approximately 10 months (p = 0.005 and 0.028, respectively). The mean diameter of the largest liver tumor was twice as large in CJL vs LD mice (8.5 vs 4.4 mm, p = 0.027). In LD, a single histologic tumor type per liver was observed. In CJL, up to four different types were associated in the same liver (hepatocellular- or cholangio-carcinomas, sarcomas or mixed tumors). DEN itself markedly disrupted the circadian rhythms in rest-activity and body temperature in all the mice. DEN-induced disruption was prolonged for >or= 3 months by CJL exposure. CONCLUSIONS: The association of circadian disruption with chronic DEN exposure suggests that circadian clocks actively control the mechanisms of liver carcinogenesis in mice. Persistent circadian coordination may further be critical for slowing down and/or reverting cancer development after carcinogen exposure.  
  Address INSERM, U776 Rythmes Biologiques et Cancers, Hopital Paul Brousse, Villejuif F-94807, France  
  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 0027-5107 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19833225 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 747  
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Author (up) Gooley, J.J.; Chamberlain, K.; Smith, K.A.; Khalsa, S.B.S.; Rajaratnam, S.M.W.; Van Reen, E.; Zeitzer, J.M.; Czeisler, C.A.; Lockley, S.W. url  doi
openurl 
  Title Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans Type Journal Article
  Year 2011 Publication The Journal of Clinical Endocrinology and Metabolism Abbreviated Journal J Clin Endocrinol Metab  
  Volume 96 Issue 3 Pages E463-72  
  Keywords Adolescent; Adult; Female; Humans; *Light; *Lighting; Male; Melatonin/*blood; Sleep/physiology; Time Factors; Young Adult  
  Abstract CONTEXT: Millions of individuals habitually expose themselves to room light in the hours before bedtime, yet the effects of this behavior on melatonin signaling are not well recognized. OBJECTIVE: We tested the hypothesis that exposure to room light in the late evening suppresses the onset of melatonin synthesis and shortens the duration of melatonin production. DESIGN: In a retrospective analysis, we compared daily melatonin profiles in individuals living in room light (<200 lux) vs. dim light (<3 lux). PATIENTS: Healthy volunteers (n = 116, 18-30 yr) were recruited from the general population to participate in one of two studies. SETTING: Participants lived in a General Clinical Research Center for at least five consecutive days. INTERVENTION: Individuals were exposed to room light or dim light in the 8 h preceding bedtime. OUTCOME MEASURES: Melatonin duration, onset and offset, suppression, and phase angle of entrainment were determined. RESULTS: Compared with dim light, exposure to room light before bedtime suppressed melatonin, resulting in a later melatonin onset in 99.0% of individuals and shortening melatonin duration by about 90 min. Also, exposure to room light during the usual hours of sleep suppressed melatonin by greater than 50% in most (85%) trials. CONCLUSIONS: These findings indicate that room light exerts a profound suppressive effect on melatonin levels and shortens the body's internal representation of night duration. Hence, chronically exposing oneself to electrical lighting in the late evening disrupts melatonin signaling and could therefore potentially impact sleep, thermoregulation, blood pressure, and glucose homeostasis.  
  Address Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, 221 Longwood Avenue, Boston, Massachusetts 02115, USA. gmsjjg@nus.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 0021-972X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21193540; PMCID:PMC3047226 Approved no  
  Call Number IDA @ john @ Serial 139  
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Author (up) Kempenaers, B.; Borgstrom, P.; Loes, P.; Schlicht, E.; Valcu, M. url  doi
openurl 
  Title Artificial night lighting affects dawn song, extra-pair siring success, and lay date in songbirds Type Journal Article
  Year 2010 Publication Current Biology : CB Abbreviated Journal Curr Biol  
  Volume 20 Issue 19 Pages 1735-1739  
  Keywords Animals; Environmental Pollution; Female; Light; *Lighting; Male; *Reproduction; Sexual Behavior, Animal/*physiology; Songbirds/*physiology; Time Factors; *Vocalization, Animal  
  Abstract Associated with a continued global increase in urbanization, anthropogenic light pollution is an important problem. However, our understanding of the ecological consequences of light pollution is limited. We investigated effects of artificial night lighting on dawn song in five common forest-breeding songbirds. In four species, males near street lights started singing significantly earlier at dawn than males elsewhere in the forest, and this effect was stronger in naturally earlier-singing species. We compared reproductive behavior of blue tits breeding in edge territories with and without street lights to that of blue tits breeding in central territories over a 7 year period. Under the influence of street lights, females started egg laying on average 1.5 days earlier. Males occupying edge territories with street lights were twice as successful in obtaining extra-pair mates than their close neighbors or than males occupying central forest territories. Artificial night lighting affected both age classes but had a stronger effect on yearling males. Our findings indicate that light pollution has substantial effects on the timing of reproductive behavior and on individual mating patterns. It may have important evolutionary consequences by changing the information embedded in previously reliable quality-indicator traits.  
  Address Department of Behavioural Ecology and Evolutionary Genetics, Max Planck Institute for Ornithology, Eberhard-Gwinner-Strasse, 82319 Seewiesen, Germany. b.kempenaers@orn.mpg.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 0960-9822 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20850324 Approved no  
  Call Number IDA @ john @ Serial 51  
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Author (up) 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  
  Publisher Place of Publication Editor  
  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 PMID:19714310 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 772  
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