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Author (up) Brainard, G.C.; Sliney, D.; Hanifin, J.P.; Glickman, G.; Byrne, B.; Greeson, J.M.; Jasser, S.; Gerner, E.; Rollag, M.D. url  doi
openurl 
  Title Sensitivity of the human circadian system to short-wavelength (420-nm) light Type Journal Article
  Year 2008 Publication Journal of Biological Rhythms Abbreviated Journal J Biol Rhythms  
  Volume 23 Issue 5 Pages 379-386  
  Keywords Human Health; Adult; Circadian Rhythm/*radiation effects; Female; Humans; *Light; Male; Melatonin/metabolism; Models, Biological; Neurosecretory Systems; Photons; Pineal Gland/metabolism; Retinal Ganglion Cells/*metabolism; Vision, Ocular  
  Abstract The circadian and neurobehavioral effects of light are primarily mediated by a retinal ganglion cell photoreceptor in the mammalian eye containing the photopigment melanopsin. Nine action spectrum studies using rodents, monkeys, and humans for these responses indicate peak sensitivities in the blue region of the visible spectrum ranging from 459 to 484 nm, with some disagreement in short-wavelength sensitivity of the spectrum. The aim of this work was to quantify the sensitivity of human volunteers to monochromatic 420-nm light for plasma melatonin suppression. Adult female (n=14) and male (n=12) subjects participated in 2 studies, each employing a within-subjects design. In a fluence-response study, subjects (n=8) were tested with 8 light irradiances at 420 nm ranging over a 4-log unit photon density range of 10(10) to 10(14) photons/cm(2)/sec and 1 dark exposure control night. In the other study, subjects (n=18) completed an experiment comparing melatonin suppression with equal photon doses (1.21 x 10(13) photons/cm(2)/sec) of 420 nm and 460 nm monochromatic light and a dark exposure control night. The first study demonstrated a clear fluence-response relationship between 420-nm light and melatonin suppression (p<0.001) with a half-saturation constant of 2.74 x 10(11) photons/cm(2)/sec. The second study showed that 460-nm light is significantly stronger than 420-nm light for suppressing melatonin (p<0.04). Together, the results clarify the visible short-wavelength sensitivity of the human melatonin suppression action spectrum. This basic physiological finding may be useful for optimizing lighting for therapeutic and other applications.  
  Address Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. george.brainard@jefferson.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 0748-7304 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:18838601 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 724  
Permanent link to this record
 

 
Author (up) Bray, M.S.; Young, M.E. url  doi
openurl 
  Title Chronobiological Effects on Obesity Type Journal Article
  Year 2012 Publication Current Obesity Reports Abbreviated Journal Curr Obes Rep  
  Volume 1 Issue 1 Pages 9-15  
  Keywords Human Health; Chronobiological effects; Circadian; Gene; Molecular clock; Obesity; Rhythm; Shift work; Sleep; Transcription  
  Abstract The development of obesity is the consequence of a multitude of complex interactions between both genetic and environmental factors. It has been suggested that the dramatic increase in the prevalence of obesity over the past 30 years has been the result of environmental changes that have enabled the full realization of genetic susceptibility present in the population. Among the many environmental alterations that have occurred in our recent history is the ever-increasing dyssynchrony between natural cycles of light/dark and altered patterns of sleep/wake and eating behavior associated with our “24-hour” lifestyle. An extensive research literature has established clear links between increased risk for obesity and both sleep deprivation and shift work, and our understanding of the consequences of such dyssynchrony at the molecular level is beginning to emerge. Studies linking alterations in cellular circadian clocks to metabolic dysfunction point to the increasing importance of chronobiology in obesity etiology.  
  Address Departments of Epidemiology and Genetics, University of Alabama at Birmingham, Birmingham, AL  
  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 2162-4968 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23682347; PMCID:PMC3653336 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 510  
Permanent link to this record
 

 
Author (up) Bray, M.S.; Young, M.E. url  doi
openurl 
  Title Chronobiological Effects on Obesity Type Journal Article
  Year 2012 Publication Current Obesity Reports Abbreviated Journal Curr Obes Rep  
  Volume 1 Issue 1 Pages 9-15  
  Keywords Human Health; Chronobiological effects; Circadian; Gene; Molecular clock; Obesity; Rhythm; Shift work; Sleep; Transcription  
  Abstract The development of obesity is the consequence of a multitude of complex interactions between both genetic and environmental factors. It has been suggested that the dramatic increase in the prevalence of obesity over the past 30 years has been the result of environmental changes that have enabled the full realization of genetic susceptibility present in the population. Among the many environmental alterations that have occurred in our recent history is the ever-increasing dyssynchrony between natural cycles of light/dark and altered patterns of sleep/wake and eating behavior associated with our “24-hour” lifestyle. An extensive research literature has established clear links between increased risk for obesity and both sleep deprivation and shift work, and our understanding of the consequences of such dyssynchrony at the molecular level is beginning to emerge. Studies linking alterations in cellular circadian clocks to metabolic dysfunction point to the increasing importance of chronobiology in obesity etiology.  
  Address Departments of Epidemiology and Genetics, University of Alabama at Birmingham, Birmingham, AL  
  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 2162-4968 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23682347; PMCID:PMC3653336 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 725  
Permanent link to this record
 

 
Author (up) Buijs, F.N.; Leon-Mercado, L.; Guzman-Ruiz, M.; Guerrero-Vargas, N.N.; Romo-Nava, F.; Buijs, R.M. url  doi
openurl 
  Title The Circadian System: A Regulatory Feedback Network of Periphery and Brain Type Journal Article
  Year 2016 Publication Physiology (Bethesda, Md.) Abbreviated Journal Physiology (Bethesda)  
  Volume 31 Issue 3 Pages 170-181  
  Keywords Human health; circadian rhythm; suprachiasmatic nucleus; brain; clock genes; SCN; review; circadian desynchronization; shiftwork  
  Abstract Circadian rhythms are generated by the autonomous circadian clock, the suprachiasmatic nucleus (SCN), and clock genes that are present in all tissues. The SCN times these peripheral clocks, as well as behavioral and physiological processes. Recent studies show that frequent violations of conditions set by our biological clock, such as shift work, jet lag, sleep deprivation, or simply eating at the wrong time of the day, may have deleterious effects on health. This infringement, also known as circadian desynchronization, is associated with chronic diseases like diabetes, hypertension, cancer, and psychiatric disorders. In this review, we will evaluate evidence that these diseases stem from the need of the SCN for peripheral feedback to fine-tune its output and adjust physiological processes to the requirements of the moment. This feedback can vary from neuronal or hormonal signals from the liver to changes in blood pressure. Desynchronization renders the circadian network dysfunctional, resulting in a breakdown of many functions driven by the SCN, disrupting core clock rhythms in the periphery and disorganizing cellular processes that are normally driven by the synchrony between behavior and peripheral signals with neuronal and humoral output of the hypothalamus. Consequently, we propose that the loss of synchrony between the different elements of this circadian network as may occur during shiftwork and jet lag is the reason for the occurrence of health problems.  
  Address Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico, Ciudad Universitaria, Mexico; ruudbuijs(at)gmail.com  
  Corporate Author Thesis  
  Publisher American Physiological Society Place of Publication Editor  
  Language English Summary Language English Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1548-9221 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27053731 Approved no  
  Call Number IDA @ john @ Serial 1429  
Permanent link to this record
 

 
Author (up) Bullock, B.; McGlashan, E.M.; Burns, A.C.; Lu, B.S.; Cain, S.W. url  doi
openurl 
  Title Traits related to bipolar disorder are associated with an increased post-illumination pupil response Type Journal Article
  Year 2019 Publication Psychiatry Research Abbreviated Journal Psychiatry Res  
  Volume 278 Issue Pages 35-41  
  Keywords Human Health  
  Abstract Mood states in bipolar disorder appear to be closely linked to changes in sleep and circadian function. It has been suggested that hypersensitivity of the circadian system to light may be a trait vulnerability for bipolar disorder. Healthy persons with emotional-behavioural traits associated with bipolar disorder also appear to exhibit problems with circadian rhythms, which may be associated with individual differences in light sensitivity. This study investigated the melanopsin-driven post-illumination pupil response (PIPR) in relation to emotional-behavioural traits associated with bipolar disorder (measured with the General Behavior Inventory) in a non-clinical group (n=61). An increased PIPR was associated with increased bipolar disorder-related traits. Specifically, the hypomania scale of the General Behavior Inventory was associated with an increased post-blue PIPR. Further, both the full hypomania and shortened '7 Up' scales were significantly predicted by PIPR, after age, sex and depressive traits were controlled. These findings suggest that increased sensitivity to light may be a risk factor for mood problems in the general population, and support the idea that hypersensitivity to light is a trait vulnerability for, rather than symptom of, bipolar disorder.  
  Address School of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash University, Melbourne, VIC, Australia. Electronic address: sean.cain@monash.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 0165-1781 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31136914 Approved no  
  Call Number GFZ @ kyba @ Serial 2510  
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