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Author Figueiro, M.G.; Bierman, A.; Plitnick, B.; Rea, M.S.
Title Preliminary evidence that both blue and red light can induce alertness at night Type Journal Article
Year 2009 Publication BMC Neuroscience Abbreviated Journal BMC Neurosci
Volume 10 Issue Pages 105
Keywords Adult; Alpha Rhythm; Analysis of Variance; Beta Rhythm; Circadian Rhythm/*physiology; Cornea/physiology; Dose-Response Relationship, Radiation; Electrocardiography; Female; Humans; *Light; Male; Melatonin/secretion; Middle Aged; *Photic Stimulation; Psychomotor Performance; Radioimmunoassay; Salivary Glands/secretion; Wakefulness/*physiology; physiology of vision; blue light; red light
Abstract BACKGROUND: A variety of studies have demonstrated that retinal light exposure can increase alertness at night. It is now well accepted that the circadian system is maximally sensitive to short-wavelength (blue) light and is quite insensitive to long-wavelength (red) light. Retinal exposures to blue light at night have been recently shown to impact alertness, implicating participation by the circadian system. The present experiment was conducted to look at the impact of both blue and red light at two different levels on nocturnal alertness. Visually effective but moderate levels of red light are ineffective for stimulating the circadian system. If it were shown that a moderate level of red light impacts alertness, it would have had to occur via a pathway other than through the circadian system. METHODS: Fourteen subjects participated in a within-subject two-night study, where each participant was exposed to four experimental lighting conditions. Each night each subject was presented a high (40 lx at the cornea) and a low (10 lx at the cornea) diffuse light exposure condition of the same spectrum (blue, lambda(max) = 470 nm, or red, lambda(max) = 630 nm). The presentation order of the light levels was counterbalanced across sessions for a given subject; light spectra were counterbalanced across subjects within sessions. Prior to each lighting condition, subjects remained in the dark (< 1 lx at the cornea) for 60 minutes. Electroencephalogram (EEG) measurements, electrocardiogram (ECG), psychomotor vigilance tests (PVT), self-reports of sleepiness, and saliva samples for melatonin assays were collected at the end of each dark and light periods. RESULTS: Exposures to red and to blue light resulted in increased beta and reduced alpha power relative to preceding dark conditions. Exposures to high, but not low, levels of red and of blue light significantly increased heart rate relative to the dark condition. Performance and sleepiness ratings were not strongly affected by the lighting conditions. Only the higher level of blue light resulted in a reduction in melatonin levels relative to the other lighting conditions. CONCLUSION: These results support previous findings that alertness may be mediated by the circadian system, but it does not seem to be the only light-sensitive pathway that can affect alertness at night.
Address Lighting Research Center, Rensselaer Polytechnic Institute, Troy, NY, USA. figuem@rpi.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 1471-2202 ISBN Medium
Area Expedition Conference (up)
Notes PMID:19712442; PMCID:PMC2744917 Approved no
Call Number IDA @ john @ Serial 285
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Author Reddy, A.B.; O'Neill, J.S.
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 Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0962-8924 ISBN Medium
Area Expedition Conference (up)
Notes PMID:19926479; PMCID:PMC2808409 Approved no
Call Number IDA @ john @ Serial 133
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Author Kantermann, T.; Roenneberg, T.
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 Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0742-0528 ISBN Medium
Area Expedition Conference (up)
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.
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.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0353-9504 ISBN Medium
Area Expedition Conference (up)
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.
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 Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0003-6870 ISBN Medium
Area Expedition Conference (up)
Notes PMID:22850476 Approved no
Call Number IDA @ john @ Serial 136
Permanent link to this record