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Author Aubé, M.; Roby, J.; Kocifaj, M. url  doi
openurl 
  Title Evaluating potential spectral impacts of various artificial lights on melatonin suppression, photosynthesis, and star visibility Type Journal Article
  Year 2013 Publication PloS one Abbreviated Journal PLoS One  
  Volume 8 Issue 7 Pages (down) e67798  
  Keywords Humans; *Light; Lighting/methods; Melatonin/*metabolism; Photosynthesis/*radiation effects; Plant Development/radiation effects; blue light; circadian disruption  
  Abstract Artificial light at night can be harmful to the environment, and interferes with fauna and flora, star visibility, and human health. To estimate the relative impact of a lighting device, its radiant power, angular photometry and detailed spectral power distribution have to be considered. In this paper we focus on the spectral power distribution. While specific spectral characteristics can be considered harmful during the night, they can be considered advantageous during the day. As an example, while blue-rich Metal Halide lamps can be problematic for human health, star visibility and vegetation photosynthesis during the night, they can be highly appropriate during the day for plant growth and light therapy. In this paper we propose three new indices to characterize lamp spectra. These indices have been designed to allow a quick estimation of the potential impact of a lamp spectrum on melatonin suppression, photosynthesis, and star visibility. We used these new indices to compare various lighting technologies objectively. We also considered the transformation of such indices according to the propagation of light into the atmosphere as a function of distance to the observer. Among other results, we found that low pressure sodium, phosphor-converted amber light emitting diodes (LED) and LED 2700 K lamps filtered with the new Ledtech's Equilib filter showed a lower or equivalent potential impact on melatonin suppression and star visibility in comparison to high pressure sodium lamps. Low pressure sodium, LED 5000 K-filtered and LED 2700 K-filtered lamps had a lower impact on photosynthesis than did high pressure sodium lamps. Finally, we propose these indices as new standards for the lighting industry to be used in characterizing their lighting technologies. We hope that their use will favor the design of new environmentally and health-friendly lighting technologies.  
  Address Departement de physique, Cegep de Sherbrooke, Sherbrooke, Quebec, Canada. martin.aube@cegepsherbrooke.qc.ca  
  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 1932-6203 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23861808; PMCID:PMC3702543 Approved no  
  Call Number IDA @ john @ Serial 282  
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Author 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 (down) 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  
  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 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 Yasuniwa, Y.; Izumi, H.; Wang, K.-Y.; Shimajiri, S.; Sasaguri, Y.; Kawai, K.; Kasai, H.; Shimada, T.; Miyake, K.; Kashiwagi, E.; Hirano, G.; Kidani, A.; Akiyama, M.; Han, B.; Wu, Y.; Ieiri, I.; Higuchi, S.; Kohno, K. url  doi
openurl 
  Title Circadian disruption accelerates tumor growth and angio/stromagenesis through a Wnt signaling pathway Type Journal Article
  Year 2010 Publication PloS one Abbreviated Journal PLoS One  
  Volume 5 Issue 12 Pages (down) e15330  
  Keywords Animals; *Circadian Rhythm; Disease Progression; *Gene Expression Regulation, Neoplastic; HeLa Cells; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Neoplasms/*pathology; *Neovascularization, Pathologic; Nerve Tissue Proteins/metabolism; Skin/metabolism; Vascular Endothelial Growth Factor A/metabolism; Wnt Proteins/*metabolism; Oncogenesis  
  Abstract Epidemiologic studies show a high incidence of cancer in shift workers, suggesting a possible relationship between circadian rhythms and tumorigenesis. However, the precise molecular mechanism played by circadian rhythms in tumor progression is not known. To identify the possible mechanisms underlying tumor progression related to circadian rhythms, we set up nude mouse xenograft models. HeLa cells were injected in nude mice and nude mice were moved to two different cases, one case is exposed to a 24-hour light cycle (L/L), the other is a more “normal” 12-hour light/dark cycle (L/D). We found a significant increase in tumor volume in the L/L group compared with the L/D group. In addition, tumor microvessels and stroma were strongly increased in L/L mice. Although there was a hypervascularization in L/L tumors, there was no associated increase in the production of vascular endothelial cell growth factor (VEGF). DNA microarray analysis showed enhanced expression of WNT10A, and our subsequent study revealed that WNT10A stimulates the growth of both microvascular endothelial cells and fibroblasts in tumors from light-stressed mice, along with marked increases in angio/stromagenesis. Only the tumor stroma stained positive for WNT10A and WNT10A is also highly expressed in keloid dermal fibroblasts but not in normal dermal fibroblasts indicated that WNT10A may be a novel angio/stromagenic growth factor. These findings suggest that circadian disruption induces the progression of malignant tumors via a Wnt signaling pathway.  
  Address Department of Molecular Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 1932-6203 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21203463; PMCID:PMC3009728 Approved no  
  Call Number IDA @ john @ Serial 162  
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Author 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 (down) 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 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 (down) 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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