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Author (up) Arendt, J.; Middleton, B. url  doi
openurl 
  Title Human seasonal and circadian studies in Antarctica (Halley, 75 degrees S) Type Journal Article
  Year 2018 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol  
  Volume 258 Issue Pages 250-258  
  Keywords Human Activities; Acclimatization/*physiology; Actigraphy; Adult; Antarctic Regions; Behavior/*physiology; Circadian Rhythm/*physiology; Darkness; Female; Heart Rate/physiology; Humans; Libido; Light; Male; Melatonin/blood; Photoperiod; *Seasons; Sleep/physiology; Young Adult; *Antarctica; *Circadian; *Light; *Melatonin; *Seasonal  
  Abstract Living for extended periods in Antarctica exposes base personnel to extremes of daylength (photoperiod) and temperature. At the British Antarctic Survey base of Halley, 75 degrees S, the sun does not rise for 110 d in the winter and does not set for 100 d in summer. Photoperiod is the major time cue governing the timing of seasonal events such as reproduction in many species. The neuroendocrine signal providing photoperiodic information to body physiology is the duration of melatonin secretion which reflects the length of the night: longer in the short days of winter and shorter in summer. Light of sufficient intensity and spectral composition serves to suppress production of melatonin and to set the circadian timing and the duration of the rhythm. In humans early observations suggested that bright (>2000 lux) white light was needed to suppress melatonin completely. Shortly thereafter winter depression (Seasonal Affective Disorder or SAD) was described, and its successful treatment by an artificial summer photoperiod of bright white light, sufficient to shorten melatonin production. At Halley dim artificial light intensity during winter was measured, until 2003, at a maximum of approximately 500 lux in winter. Thus a strong seasonal and circadian time cue was absent. It seemed likely that winter depression would be common in the extended period of winter darkness and could be treated with an artificial summer photoperiod. These observations, and predictions, inspired a long series of studies regarding human seasonal and circadian status, and the effects of light treatment, in a small overwintering, isolated community, living in the same conditions for many months at Halley. We found little evidence of SAD, or change in duration of melatonin production with season. However the timing of the melatonin rhythm itself, and/or that of its metabolite 6-sulphatoxymelatonin (aMT6s), was used as a primary marker of seasonal, circadian and treatment changes. A substantial phase delay of melatonin in winter was advanced to summer phase by a two pulse 'skeleton' bright white light treatment. Subsequently a single morning pulse of bright white light was effective with regard to circadian phase and improved daytime performance. The circadian delay evidenced by melatonin was accompanied by delayed sleep (logs and actigraphy): poor sleep is a common complaint in Polar regions. Appropriate extra artificial light, both standard white, and blue enriched, present throughout the day, effectively countered delay in sleep timing and the aMT6s rhythm. The most important factor appeared to be the maximum light experienced. Another manifestation of the winter was a decline in self-rated libido (men only on base at this time). Women on the base showed lower aspects of physical and mental health compared to men. Free-running rhythms were seen in some subjects following night shift, but were rarely found at other times, probably because this base has strongly scheduled activity and leisure time. Complete circadian adaptation during a week of night shift, also seen in a similar situation on North Sea oil rigs, led to problems readapting back to day shift in winter, compared to summer. Here again timed light treatment was used to address the problem. Sleep, alertness and waking performance are critically dependent on optimum circadian phase. Circadian desynchrony is associated with increased risk of major disease in shift workers. These studies provide some groundwork for countering/avoiding circadian desynchrony in rather extreme conditions.  
  Address Biochemistry and Physiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, UK. Electronic address: b.middleton@surrey.ac.uk  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0016-6480 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28526480 Approved no  
  Call Number IDA @ john @ Serial 2248  
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Author (up) Barclay, J.L.; Husse, J.; Bode, B.; Naujokat, N.; Meyer-Kovac, J.; Schmid, S.M.; Lehnert, H.; Oster, H. url  doi
openurl 
  Title Circadian desynchrony promotes metabolic disruption in a mouse model of shiftwork Type Journal Article
  Year 2012 Publication PloS one Abbreviated Journal PLoS One  
  Volume 7 Issue 5 Pages e37150  
  Keywords Animals; Biological Clocks/*physiology; Circadian Rhythm/*physiology; Disease Models, Animal; Eating/genetics; Gene Expression Regulation; Liver/metabolism; Male; Mice; Sleep Disorders, Circadian Rhythm/*metabolism/physiopathology; Suprachiasmatic Nucleus/*metabolism; Transcriptome  
  Abstract Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers.  
  Address Max Planck Institute of Biophysical Chemistry, Gottingen, Germany  
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  ISSN 1932-6203 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22629359; PMCID:PMC3357388 Approved no  
  Call Number IDA @ john @ Serial 94  
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Author (up) Bauer, S.E.; Wagner, S.E.; Burch, J.; Bayakly, R.; Vena, J.E. url  doi
openurl 
  Title A case-referent study: light at night and breast cancer risk in Georgia Type Journal Article
  Year 2013 Publication International Journal of Health Geographics Abbreviated Journal Int J Health Geogr  
  Volume 12 Issue Pages 23  
  Keywords Human Health; Aged; Aged, 80 and over; Breast Neoplasms/*diagnosis/*epidemiology; Case-Control Studies; Circadian Rhythm/*physiology; Female; Georgia/epidemiology; Humans; Lighting/*adverse effects; Lung Neoplasms/diagnosis/epidemiology; Middle Aged; Registries; Risk Factors  
  Abstract BACKGROUND: Literature has identified detrimental health effects from the indiscriminate use of artificial nighttime light. We examined the co-distribution of light at night (LAN) and breast cancer (BC) incidence in Georgia, with the goal to contribute to the accumulating evidence that exposure to LAN increases risk of BC. METHODS: Using Georgia Comprehensive Cancer Registry data (2000-2007), we conducted a case-referent study among 34,053 BC cases and 14,458 lung cancer referents. Individuals with lung cancer were used as referents to control for other cancer risk factors that may be associated with elevated LAN, such as air pollution, and since this cancer type was not previously associated with LAN or circadian rhythm disruption. DMSP-OLS Nighttime Light Time Series satellite images (1992-2007) were used to estimate LAN levels; low (0-20 watts per sterradian cm(2)), medium (21-41 watts per sterradian cm(2)), high (>41 watts per sterradian cm(2)). LAN levels were extracted for each year of exposure prior to case/referent diagnosis in ArcGIS. RESULTS: Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression models controlling for individual-level year of diagnosis, race, age at diagnosis, tumor grade, stage; and population-level determinants including metropolitan statistical area (MSA) status, births per 1,000 women aged 15-50, percentage of female smokers, MSA population mobility, and percentage of population over 16 in the labor force. We found that overall BC incidence was associated with high LAN exposure (OR = 1.12, 95% CI [1.04, 1.20]). When stratified by race, LAN exposure was associated with increased BC risk among whites (OR = 1.13, 95% CI [1.05, 1.22]), but not among blacks (OR = 1.02, 95% CI [0.82, 1.28]). CONCLUSIONS: Our results suggest positive associations between LAN and BC incidence, especially among whites. The consistency of our findings with previous studies suggests that there could be fundamental biological links between exposure to artificial LAN and increased BC incidence, although additional research using exposure metrics at the individual level is required to confirm or refute these findings.  
  Address Department of Epidemiology and Biostatistics, College of Public Health, University of Georgia, Athens, GA, USA. secbauer@ufl.edu  
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  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1476-072X ISBN Medium  
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  Notes PMID:23594790; PMCID:PMC3651306 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 718  
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Author (up) Bedrosian, T.A.; Vaughn, C.A.; Galan, A.; Daye, G.; Weil, Z.M.; Nelson, R.J. url  doi
openurl 
  Title Nocturnal light exposure impairs affective responses in a wavelength-dependent manner Type Journal Article
  Year 2013 Publication The Journal of Neuroscience : the Official Journal of the Society for Neuroscience Abbreviated Journal J Neurosci  
  Volume 33 Issue 32 Pages 13081-13087  
  Keywords Analysis of Variance; Animals; Circadian Rhythm/*physiology; Cricetinae; Dose-Response Relationship, Radiation; Female; Food Deprivation/physiology; Food Preferences/physiology/radiation effects; Fourier Analysis; Gene Expression Regulation/radiation effects; Hippocampus/pathology/radiation effects; Immobility Response, Tonic/radiation effects; Light/*adverse effects; Mood Disorders/*etiology/pathology; Motor Activity/physiology/radiation effects; Phodopus; Proto-Oncogene Proteins c-fos/metabolism; Social Behavior; Suprachiasmatic Nucleus/metabolism; Time Factors  
  Abstract Life on earth is entrained to a 24 h solar cycle that synchronizes circadian rhythms in physiology and behavior; light is the most potent entraining cue. In mammals, light is detected by (1) rods and cones, which mediate visual function, and (2) intrinsically photosensitive retinal ganglion cells (ipRGCs), which primarily project to the suprachiasmatic nucleus (SCN) in the hypothalamus to regulate circadian rhythms. Recent evidence, however, demonstrates that ipRGCs also project to limbic brain regions, suggesting that, through this pathway, light may have a role in cognition and mood. Therefore, it follows that unnatural exposure to light may have negative consequences for mood or behavior. Modern environmental lighting conditions have led to excessive exposure to light at night (LAN), and particularly to blue wavelength lights. We hypothesized that nocturnal light exposure (i.e., dim LAN) would induce depressive responses and alter neuronal structure in hamsters (Phodopus sungorus). If this effect is mediated by ipRGCs, which have reduced sensitivity to red wavelength light, then we predicted that red LAN would have limited effects on brain and behavior compared with shorter wavelengths. Additionally, red LAN would not induce c-Fos activation in the SCN. Our results demonstrate that exposure to LAN influences behavior and neuronal plasticity and that this effect is likely mediated by ipRGCs. Modern sources of LAN that contain blue wavelengths may be particularly disruptive to the circadian system, potentially contributing to altered mood regulation.  
  Address Department of Neuroscience, Ohio State University Wexner Medical Center, Columbus, Ohio 43210, USA. Bedrosian.2@osu.edu  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0270-6474 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23926261 Approved no  
  Call Number IDA @ john @ Serial 27  
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Author (up) Blask, D.E.; Brainard, G.C.; Dauchy, R.T.; Hanifin, J.P.; Davidson, L.K.; Krause, J.A.; Sauer, L.A.; Rivera-Bermudez, M.A.; Dubocovich, M.L.; Jasser, S.A.; Lynch, D.T.; Rollag, M.D.; Zalatan, F. url  doi
openurl 
  Title Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats Type Journal Article
  Year 2005 Publication Cancer Research Abbreviated Journal Cancer Res  
  Volume 65 Issue 23 Pages 11174-11184  
  Keywords Human Health; Animals; Breast Neoplasms/*blood/genetics/pathology; Cell Growth Processes/physiology; Circadian Rhythm/*physiology; Female; Humans; Light; Liver Neoplasms, Experimental/metabolism; Male; Melatonin/blood/*deficiency; Premenopause/blood; RNA, Messenger/biosynthesis/genetics; Rats; Rats, Nude; Receptors, Melatonin/biosynthesis/genetics; Transplantation, Heterologous  
  Abstract The increased breast cancer risk in female night shift workers has been postulated to result from the suppression of pineal melatonin production by exposure to light at night. Exposure of rats bearing rat hepatomas or human breast cancer xenografts to increasing intensities of white fluorescent light during each 12-hour dark phase (0-345 microW/cm2) resulted in a dose-dependent suppression of nocturnal melatonin blood levels and a stimulation of tumor growth and linoleic acid uptake/metabolism to the mitogenic molecule 13-hydroxyoctadecadienoic acid. Venous blood samples were collected from healthy, premenopausal female volunteers during either the daytime, nighttime, or nighttime following 90 minutes of ocular bright, white fluorescent light exposure at 580 microW/cm2 (i.e., 2,800 lx). Compared with tumors perfused with daytime-collected melatonin-deficient blood, human breast cancer xenografts and rat hepatomas perfused in situ, with nocturnal, physiologically melatonin-rich blood collected during the night, exhibited markedly suppressed proliferative activity and linoleic acid uptake/metabolism. Tumors perfused with melatonin-deficient blood collected following ocular exposure to light at night exhibited the daytime pattern of high tumor proliferative activity. These results are the first to show that the tumor growth response to exposure to light during darkness is intensity dependent and that the human nocturnal, circadian melatonin signal not only inhibits human breast cancer growth but that this effect is extinguished by short-term ocular exposure to bright, white light at night. These mechanistic studies are the first to provide a rational biological explanation for the increased breast cancer risk in female night shift workers.  
  Address Laboratory of Chrono-Neuroendocrine Oncology, Bassett Research Institute, The Mary Imogene Bassett Hospital, Cooperstown, New York 13326, USA. david.blask@bassett.org  
  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 0008-5472 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:16322268 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 721  
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