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Author Reddy, A.B.; O'Neill, J.S. url  doi
openurl 
  Title Healthy clocks, healthy body, healthy mind Type Journal Article
  Year 2010 Publication Trends in Cell Biology Abbreviated Journal Trends Cell Biol  
  Volume 20 Issue 1 Pages 36-44  
  Keywords Aging; Animals; Cell Cycle; *Circadian Rhythm; Humans; Neoplasms/genetics/metabolism; Signal Transduction  
  Abstract Circadian rhythms permeate mammalian biology. They are manifested in the temporal organisation of behavioural, physiological, cellular and neuronal processes. Whereas it has been shown recently that these approximately 24-hour cycles are intrinsic to the cell and persist in vitro, internal synchrony in mammals is largely governed by the hypothalamic suprachiasmatic nuclei that facilitate anticipation of, and adaptation to, the solar cycle. Our timekeeping mechanism is deeply embedded in cell function and is modelled as a network of transcriptional and/or post-translational feedback loops. Concurrent with this, we are beginning to understand how this ancient timekeeper interacts with myriad cell systems, including signal transduction cascades and the cell cycle, and thus impacts on disease. An exemplary area where this knowledge is rapidly expanding and contributing to novel therapies is cancer, where the Period genes have been identified as tumour suppressors. In more complex disorders, where aetiology remains controversial, interactions with the clockwork are only now starting to be appreciated.  
  Address Department of Clinical Neurosciences, University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Cambridge CB2 OQQ, UK. abr20@cam.ac.uk  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor (up) Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0962-8924 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19926479; PMCID:PMC2808409 Approved no  
  Call Number IDA @ john @ Serial 133  
Permanent link to this record
 

 
Author Kantermann, T.; Roenneberg, T. url  doi
openurl 
  Title Is light-at-night a health risk factor or a health risk predictor? Type Journal Article
  Year 2009 Publication Chronobiology International Abbreviated Journal Chronobiol Int  
  Volume 26 Issue 6 Pages 1069-1074  
  Keywords *Chronobiology Disorders; Circadian Rhythm; Environmental Exposure; Humans; *Light; Neoplasms; Risk Factors  
  Abstract In 2007, the IARC (WHO) has classified “shift-work that involves circadian disruption” as potentially carcinogenic. Ample evidence leaves no doubt that shift-work is detrimental for health, but the mechanisms behind this effect are not well understood. The hormone melatonin is often considered to be a causal link between night shift and tumor development. The underlying “light-at-night” (LAN) hypothesis is based on the following chain of arguments: melatonin is a hormone produced under the control of the circadian clock at night, and its synthesis can be suppressed by light; as an indolamine, it potentially acts as a scavenger of oxygen radicals, which in turn can damage DNA, which in turn can cause cancer. Although there is no experimental evidence that LAN is at the basis of increased cancer rates in shiftworkers, the scenario “light at night can cause cancer” influences research, medicine, the lighting industry and (via the media) also the general public, well beyond shiftwork. It is even suggested that baby-lights, TVs, computers, streetlights, moonlight, emergency lights, or any so-called “light pollution” by urban developments cause cancer via the mechanisms proposed by the LAN hypothesis. Our commentary addresses the growing concern surrounding light pollution. We revisit the arguments of the LAN theory and put them into perspective regarding circadian physiology, physical likelihood (e.g., what intensities reach the retina), and potential risks, specifically in non-shiftworkers.  
  Address Institute for Medical Psychology, University of Munich LMU, Munich, Germany  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor (up) Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0742-0528 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19731106 Approved no  
  Call Number IDA @ john @ Serial 134  
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Author Kavcic, P.; Rojc, B.; Dolenc-Groselj, L.; Claustrat, B.; Fujs, K.; Poljak, M. url  doi
openurl 
  Title The impact of sleep deprivation and nighttime light exposure on clock gene expression in humans Type Journal Article
  Year 2011 Publication Croatian Medical Journal Abbreviated Journal Croat Med J  
  Volume 52 Issue 5 Pages 594-603  
  Keywords genomics; epigenetics; hPer2; hBmal1; clock genes; gene expression; biology; human health  
  Abstract Aim

To examine the effect of acute sleep deprivation under light conditions on the expression of two key clock genes, hPer2 and hBmal1, in peripheral blood mononuclear cells (PBMC) and on plasma melatonin and cortisol levels.

Methods

Blood samples were drawn from 6 healthy individuals at 4-hour intervals for three consecutive nights, including a night of total sleep deprivation (second night). The study was conducted in April-June 2006 at the University Medical Centre Ljubljana.

Results

We found a significant diurnal variation in hPer2 and hBmal1 expression levels under baseline (P < 0.001, F = 19.7, df = 30 for hPer2 and P < 0.001, F = 17.6, df = 30 for hBmal1) and sleep-deprived conditions (P < 0.001, F = 9.2, df = 30 for hPer2 and P < 0.001, F = 13.2, df = 30 for hBmal1). Statistical analysis with the single cosinor method revealed circadian variation of hPer2 under baseline and of hBmal1 under baseline and sleep-deprived conditions. The peak expression of hPer2 was at 13:55 ± 1:15 hours under baseline conditions and of hBmal1 at 16:08 ± 1:18 hours under baseline and at 17:13 ± 1:35 hours under sleep-deprived conditions. Individual cosinor analysis of hPer2 revealed a loss of circadian rhythm in 3 participants and a phase shift in 2 participants under sleep-deprived conditions. The plasma melatonin and cortisol rhythms confirmed a conventional alignment of the central circadian pacemaker to the habitual sleep/wake schedule.

Conclusion

Our results suggest that 40-hour acute sleep deprivation under light conditions may affect the expression of hPer2 in PBMCs.
 
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  Series Editor (up) Series Title Abbreviated Series Title  
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  ISSN 0353-9504 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number IDA @ john @ Serial 135  
Permanent link to this record
 

 
Author Wood, B.; Rea, M.S.; Plitnick, B.; Figueiro, M.G. url  doi
openurl 
  Title Light level and duration of exposure determine the impact of self-luminous tablets on melatonin suppression Type Journal Article
  Year 2013 Publication Applied Ergonomics Abbreviated Journal Appl Ergon  
  Volume 44 Issue 2 Pages 237-240  
  Keywords Adolescent; *Computers, Handheld; Female; Humans; Light/*adverse effects; Male; Melatonin/*biosynthesis; Photoperiod; Saliva/*metabolism; Sleep/radiation effects; Time Factors; Young Adult; melatonin  
  Abstract Exposure to light from self-luminous displays may be linked to increased risk for sleep disorders because these devices emit optical radiation at short wavelengths, close to the peak sensitivity of melatonin suppression. Thirteen participants experienced three experimental conditions in a within-subjects design to investigate the impact of self-luminous tablet displays on nocturnal melatonin suppression: 1) tablets-only set to the highest brightness, 2) tablets viewed through clear-lens goggles equipped with blue light-emitting diodes that provided 40 lux of 470-nm light at the cornea, and 3) tablets viewed through orange-tinted glasses (dark control; optical radiation <525 nm approximately 0). Melatonin suppressions after 1-h and 2-h exposures to tablets viewed with the blue light were significantly greater than zero. Suppression levels after 1-h exposure to the tablets-only were not statistically different than zero; however, this difference reached significance after 2 h. Based on these results, display manufacturers can determine how their products will affect melatonin levels and use model predictions to tune the spectral power distribution of self-luminous devices to increase or to decrease stimulation to the circadian system.  
  Address Lighting Research Center, Rensselaer Polytechnic Institute, 21 Union Street, Troy, NY 12180, USA. woodb5@rpi.edu  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor (up) Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0003-6870 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22850476 Approved no  
  Call Number IDA @ john @ Serial 136  
Permanent link to this record
 

 
Author Reiter, R.; Tan, D.; SanchezBarcelo, E.; Mediavilla, M.; Gitto, E.; Korkmaz, A. url  doi
openurl 
  Title Circadian mechanisms in the regulation of melatonin synthesis: disruption with light at night and the pathophysiological consequences Type Journal Article
  Year 2011 Publication Journal of Experimental and Integrative Medicine Abbreviated Journal J Exp Integr Med  
  Volume 1 Issue 1 Pages 13  
  Keywords Human Health  
  Abstract In the past two decades, the results of a number of epidemiological studies have uncovered an association between excessive light exposure at night and the prevalence of cancer. Whereas the evidence supporting this link is strongest between nighttime light and female breast and male prostate cancer, the frequency of other tumor types may also be elevated. Individuals who have the highest reported increase in cancer are chronic night shift workers and flight attendants who routinely fly across numerous time zones.

There are at least two obvious physiological consequences of nighttime light exposure, i.e., a reduction in circulating melatonin levels and disruption of the circadian system (chronodisruption). Both these perturbations in experimental animals aggravate tumor growth. Melatonin has a long investigative history in terms of its ability to stymie the growth of many tumor types. Likewise, in the last decade chronodisruption has been unequivocally linked to a variety of abnormal metabolic conditions including excessive tumor growth.

This brief review summarizes the processes by which light after darkness onset impedes melatonin production and disturbs circadian rhythms. The survey also reviews the evidence associating the ostensible danger of excessive nighttime light pollution to cancer risk. If an elevated tumor frequency is definitively proven to be a consequence of light at night and/or chronodisruption, it seems likely that cancer will not be the exclusive pathophysiological change associated with the rampant light pollution characteristic of modern societies.
 
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  Series Editor (up) Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1309-4572 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number IDA @ john @ Serial 137  
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