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Author Stern, M.; Broja, M.; Sansone, R.; Grone, M.; Skene, S.S.; Liebmann, J.; Suschek, C.V.; Born, M.; Kelm, M.; Heiss, C.
Title Blue light exposure decreases systolic blood pressure, arterial stiffness, and improves endothelial function in humans Type Journal Article
Year 2018 Publication European Journal of Preventive Cardiology Abbreviated Journal (down) Eur J Prev Cardiol
Volume 25 Issue 17 Pages 1875-1883
Keywords Human Health; Blue light; blood pressure; endothelial function; forearm blood flow; pulse wave velocity
Abstract AIMS: Previous studies have shown that ultraviolet light can lead to the release of nitric oxide from the skin and decrease blood pressure. In contrast to visible light the local application of ultraviolet light bears a cancerogenic risk. Here, we investigated whether whole body exposure to visible blue light can also decrease blood pressure and increase endothelial function in healthy subjects. METHODS: In a randomised crossover study, 14 healthy male subjects were exposed on 2 days to monochromatic blue light or blue light with a filter foil (control light) over 30 minutes. We measured blood pressure (primary endpoint), heart rate, forearm vascular resistance, forearm blood flow, endothelial function (flow-mediated dilation), pulse wave velocity and plasma nitric oxide species, nitrite and nitroso compounds (secondary endpoints) during and up to 2 hours after exposure. RESULTS: Blue light exposure significantly decreased systolic blood pressure and increased heart rate as compared to control. In parallel, blue light significantly increased forearm blood flow, flow-mediated dilation, circulating nitric oxide species and nitroso compounds while it decreased forearm vascular resistance and pulse wave velocity. CONCLUSION: Whole body irradiation with visible blue light at real world doses improves blood pressure, endothelial function and arterial stiffness by nitric oxide released from photolabile intracutanous nitric oxide metabolites into circulating blood.
Address Department of Clinical and Experimental Medicine, Faculty of Health and Medical Sciences, University of Surrey, Stag Hill, Guildford GU2 7XH, UK. Email: c.heiss(at)
Corporate Author Thesis
Publisher SAGE Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 2047-4873 ISBN Medium
Area Expedition Conference
Notes PMID:30196723 Approved no
Call Number IDA @ john @ Serial 2157
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Author Taufique, S.K.T.; Prabhat, A.; Kumar, V.
Title Illuminated night alters hippocampal gene expressions and induces depressive-like responses in diurnal corvids Type Journal Article
Year 2018 Publication The European Journal of Neuroscience Abbreviated Journal (down) Eur J Neurosci
Volume in press Issue Pages in press
Keywords Animals
Abstract Artificial light at night induces circadian disruptions and causes cognitive impairment and mood disorders; yet very little is known about the neural and molecular correlates of these effects in diurnal animals. We manipulated the night environment and examined cellular and molecular changes in hippocampus, the brain region involved in cognition and mood, of Indian house crows (Corvus splendens) exposed to 12 h light (150 lux): 12 h darkness (0 lux). Diurnal corvids are an ideal model species with cognitive abilities at par with mammals. Dim light (6 lux) at night (dLAN) altered daily activity:rest pattern, reduced sleep and induced depressive-like responses (decreased eating and self-grooming, self-mutilation and reduced novel object exploration); return to an absolute dark night reversed these negative effects. dLAN suppressed nocturnal melatonin levels, however, diurnal corticosterone levels were unaffected. Concomitant reduction of immunoreactivity for DCX and BDNF suggested dLAN-induced suppression of hippocampal neurogenesis and compromised neuronal health. dLAN also negatively influenced hippocampal expression of genes associated with depressive-like responses (bdnf, il-1beta, tnfr1, nr4a2), but not of those associated with neuronal plasticity (egr1, creb, syngap, syn2, grin2a, grin2b), cellular oxidative stress (gst, sod3, cat1) and neuronal death (caspase2, caspase3, foxo3). Furthermore, we envisaged the role of BDNF and showed epigenetic modification of bdnf gene by decreased histone H3 acetylation and increased hdac4 expression under dLAN. These results demonstrate transcriptional and epigenetic bases of dLAN-induced negative effects in diurnal crows, and provide insights into the risks of exposure to illuminated nights to animals including humans in an urban setting. This article is protected by copyright. All rights reserved.
Address IndoUS Center for Biological Timing Department of Zoology, University of Delhi, Delhi, 110 007, India
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 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30218624 Approved no
Call Number GFZ @ kyba @ Serial 2010
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Author Leise, T.L.; Goldberg, A.; Michael, J.; Montoya, G.; Solow, S.; Molyneux, P.; Vetrivelan, R.; Harrington, M.E.
Title Recurring circadian disruption alters circadian clock sensitivity to resetting Type Journal Article
Year 2018 Publication The European Journal of Neuroscience Abbreviated Journal (down) Eur J Neurosci
Volume in press Issue Pages
Keywords Animals
Abstract A single phase advance of the light:dark (LD) cycle can temporarily disrupt synchrony of neural circadian rhythms within the suprachiasmatic nucleus (SCN) and between the SCN and peripheral tissues. Compounding this, modern life can involve repeated disruptive light conditions. To model chronic disruption to the circadian system, we exposed male mice to more than a month of a 20 h light cycle (LD10:10), which mice typically cannot entrain to. Control animals were housed under LD12:12. We measured locomotor activity and body temperature rhythms in vivo, and rhythms of PER2::LUC bioluminescence in SCN and peripheral tissues ex vivo. Unexpectedly, we discovered strong effects of the time of dissection on circadian phase of PER2::LUC bioluminescent rhythms, which varied across tissues. White adipose tissue was strongly reset by dissection, while thymus phase appeared independent of dissection timing. Prior light exposure impacted the SCN, resulting in strong resetting of SCN phase by dissection for mice housed under LD10:10, and weak phase shifts by time of dissection in SCN from control LD12:12 mice. These findings suggest that exposure to circadian disruption may desynchronize SCN neurons, increasing network sensitivity to perturbations. We propose that tissues with a weakened circadian network, such as the SCN under disruptive light conditions, or with little to no coupling, e.g., some peripheral tissues, will show increased resetting effects. In particular, exposure to light at inconsistent circadian times on a recurring weekly basis disrupts circadian rhythms and alters sensitivity of the SCN neural pacemaker to dissection time. This article is protected by copyright. All rights reserved.
Address Neuroscience Program, Smith College, Northampton, MA, 01063, USA
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 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30269396 Approved no
Call Number GFZ @ kyba @ Serial 2036
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Author Vetter, C.
Title Circadian disruption: What do we actually mean? Type Journal Article
Year 2018 Publication The European Journal of Neuroscience Abbreviated Journal (down) Eur J Neurosci
Volume in press Issue Pages in press
Keywords Human Health; Review
Abstract The circadian system regulates physiology and behavior. Acute challenges to the system, such as those experienced during travel across time zones, will eventually result in re-synchronization to the local environmental time cues, but this re-synchronization is oftentimes accompanied by adverse short-term consequences. When such challenges are experienced chronically, adaptation may not be achieved, as for example in the case of rotating night shift workers. The transient and chronic disturbance of the circadian system is most frequently referred to as “circadian disruption”, but many other terms have been proposed and used to refer to similar situations. It is now beyond doubt that the circadian system contributes to health and disease, emphasizing the need for clear terminology when describing challenges to the circadian system and their consequences. The goal of this review is to provide an overview of the terms used to describe disruption of the circadian system, discuss proposed quantifications of disruption in experimental and observational settings with a focus on human research, and highlight limitations and challenges of currently available tools. For circadian research to advance as a translational science, clear, operationalizable, and scalable quantifications of circadian disruption are key, as they will enable improved assessment and reproducibility of results, ideally ranging from mechanistic settings, including animal research, to large-scale randomized clinical trials. This article is protected by copyright. All rights reserved.
Address Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, USA
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 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30402904 Approved no
Call Number GFZ @ kyba @ Serial 2057
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Author Zerbini, G.; Kantermann, T.; Merrow, M.
Title Strategies to decrease social jetlag: Reducing evening blue light advances sleep and melatonin Type Journal Article
Year 2018 Publication The European Journal of Neuroscience Abbreviated Journal (down) Eur J Neurosci
Volume in press Issue Pages
Keywords Human Health
Abstract The timing of sleep is under the control of the circadian clock, which uses light to entrain to the external light-dark cycle. A combination of genetic, physiological and environmental factors produces individual differences in chronotype (entrained phase as manifest in sleep timing). A mismatch between circadian and societal (e.g., work) clocks leads to a condition called social jetlag, which is characterized by changing sleep times over work and free days and accumulation of sleep debt. Social jetlag, which is prevalent in late chronotypes, has been related to several health issues. One way to reduce social jetlag would be to advance the circadian clock via modifications of the light environment. We thus performed two intervention field studies to describe methods for decreasing social jetlag. One study decreased evening light exposure (via blue-light-blocking glasses) and the other used increased morning light (via the use of curtains). We measured behaviour as well as melatonin; the latter in order to validate that behaviour was consistent with this neuroendocrinological phase marker of the circadian clock. We found that a decrease in evening blue light exposure led to an advance in melatonin and sleep onset on workdays. Increased morning light exposure advanced neither melatonin secretion nor sleep timing. Neither protocol led to a significant change in social jetlag. Despite this, our findings show that controlling light exposure at home can be effective in advancing melatonin secretion and sleep, thereby helping late chronotypes to better cope with early social schedules.
Address Institute of Medical Psychology, LMU Munich, 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 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30506899 Approved no
Call Number GFZ @ kyba @ Serial 2138
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