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Author Chamorro, E.; Bonnin-Arias, C.; Perez-Carrasco, M.J.; Munoz de Luna, J.; Vazquez, D.; Sanchez-Ramos, C. url  doi
openurl 
  Title Effects of light-emitting diode radiations on human retinal pigment epithelial cells in vitro Type Journal Article
  Year (down) 2013 Publication Photochemistry and Photobiology Abbreviated Journal Photochem Photobiol  
  Volume 89 Issue 2 Pages 468-473  
  Keywords Human Health; Apoptosis/*radiation effects; Biological Markers/metabolism; Caspases/metabolism; Cell Survival/radiation effects; DNA Damage; Epithelial Cells/cytology/metabolism/*radiation effects; Histones/metabolism; Humans; Light; Membrane Potential, Mitochondrial/*radiation effects; Mitochondria/*radiation effects; Photoperiod; Primary Cell Culture; Reactive Oxygen Species/metabolism; Retinal Pigment Epithelium/cytology/metabolism/*radiation effects  
  Abstract Human visual system is exposed to high levels of natural and artificial lights of different spectra and intensities along lifetime. Light-emitting diodes (LEDs) are the basic lighting components in screens of PCs, phones and TV sets; hence it is so important to know the implications of LED radiations on the human visual system. The aim of this study was to investigate the effect of LEDs radiations on human retinal pigment epithelial cells (HRPEpiC). They were exposed to three light-darkness (12 h/12 h) cycles, using blue-468 nm, green-525 nm, red-616 nm and white light. Cellular viability of HRPEpiC was evaluated by labeling all nuclei with DAPI; Production of reactive oxygen species (ROS) was determined by H2DCFDA staining; mitochondrial membrane potential was quantified by TMRM staining; DNA damage was determined by H2AX histone activation, and apoptosis was evaluated by caspases-3,-7 activation. It is shown that LED radiations decrease 75-99% cellular viability, and increase 66-89% cellular apoptosis. They also increase ROS production and DNA damage. Fluorescence intensity of apoptosis was 3.7% in nonirradiated cells and 88.8%, 86.1%, 83.9% and 65.5% in cells exposed to white, blue, green or red light, respectively. This study indicates three light-darkness (12 h/12 h) cycles of exposure to LED lighting affect in vitro HRPEpiC.  
  Address Neuro-Computing and Neuro-Robotics Research Group, Universidad Complutense de Madrid, Madrid, Spain. eva.chamorro@opt.ucm.es  
  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 0031-8655 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22989198 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 511  
Permanent link to this record
 

 
Author LeGates, T.A.; Altimus, C.M.; Wang, H.; Lee, H.-K.; Yang, S.; Zhao, H.; Kirkwood, A.; Weber, E.T.; Hattar, S. url  doi
openurl 
  Title Aberrant light directly impairs mood and learning through melanopsin-expressing neurons Type Journal Article
  Year (down) 2012 Publication Nature Abbreviated Journal Nature  
  Volume 491 Issue 7425 Pages 594-598  
  Keywords Affect/drug effects/physiology/*radiation effects; Animals; Antidepressive Agents/pharmacology; Body Temperature Regulation/physiology/radiation effects; Circadian Rhythm/physiology; Cognition/drug effects/physiology/radiation effects; Corticosterone/metabolism; Depression/etiology/physiopathology; Desipramine/pharmacology; Fluoxetine/pharmacology; Learning/drug effects/physiology/*radiation effects; *Light; Long-Term Potentiation/drug effects; Male; Memory/physiology/radiation effects; Mice; Photoperiod; Retinal Ganglion Cells/drug effects/*metabolism/*radiation effects; *Rod Opsins/analysis; Sleep/physiology; Wakefulness/physiology  
  Abstract The daily solar cycle allows organisms to synchronize their circadian rhythms and sleep-wake cycles to the correct temporal niche. Changes in day-length, shift-work, and transmeridian travel lead to mood alterations and cognitive function deficits. Sleep deprivation and circadian disruption underlie mood and cognitive disorders associated with irregular light schedules. Whether irregular light schedules directly affect mood and cognitive functions in the context of normal sleep and circadian rhythms remains unclear. Here we show, using an aberrant light cycle that neither changes the amount and architecture of sleep nor causes changes in the circadian timing system, that light directly regulates mood-related behaviours and cognitive functions in mice. Animals exposed to the aberrant light cycle maintain daily corticosterone rhythms, but the overall levels of corticosterone are increased. Despite normal circadian and sleep structures, these animals show increased depression-like behaviours and impaired hippocampal long-term potentiation and learning. Administration of the antidepressant drugs fluoxetine or desipramine restores learning in mice exposed to the aberrant light cycle, suggesting that the mood deficit precedes the learning impairments. To determine the retinal circuits underlying this impairment of mood and learning, we examined the behavioural consequences of this light cycle in animals that lack intrinsically photosensitive retinal ganglion cells. In these animals, the aberrant light cycle does not impair mood and learning, despite the presence of the conventional retinal ganglion cells and the ability of these animals to detect light for image formation. These findings demonstrate the ability of light to influence cognitive and mood functions directly through intrinsically photosensitive retinal ganglion cells.  
  Address Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, 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 0028-0836 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23151476; PMCID:PMC3549331 Approved no  
  Call Number IDA @ john @ Serial 238  
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Author Sporl, F.; Korge, S.; Jurchott, K.; Wunderskirchner, M.; Schellenberg, K.; Heins, S.; Specht, A.; Stoll, C.; Klemz, R.; Maier, B.; Wenck, H.; Schrader, A.; Kunz, D.; Blatt, T.; Kramer, A. url  doi
openurl 
  Title Kruppel-like factor 9 is a circadian transcription factor in human epidermis that controls proliferation of keratinocytes Type Journal Article
  Year (down) 2012 Publication Proceedings of the National Academy of Sciences of the United States of America Abbreviated Journal Proc Natl Acad Sci U S A  
  Volume 109 Issue 27 Pages 10903-10908  
  Keywords Human Health; Anti-Inflammatory Agents/pharmacology; Biological Clocks/genetics/physiology; Cell Differentiation/physiology; Cell Proliferation/drug effects; Cells, Cultured; Circadian Rhythm/genetics/*physiology; Epidermis/cytology/*physiology; Genome-Wide Association Study; Homeostasis/physiology; Humans; Hydrocortisone/pharmacology; Keratinocytes/cytology/drug effects/*physiology; Kruppel-Like Transcription Factors/*genetics/*metabolism; Luciferases/genetics; Skin Neoplasms/genetics/physiopathology  
  Abstract Circadian clocks govern a wide range of cellular and physiological functions in various organisms. Recent evidence suggests distinct functions of local clocks in peripheral mammalian tissues such as immune responses and cell cycle control. However, studying circadian action in peripheral tissues has been limited so far to mouse models, leaving the implication for human systems widely elusive. In particular, circadian rhythms in human skin, which is naturally exposed to strong daytime-dependent changes in the environment, have not been investigated to date on a molecular level. Here, we present a comprehensive analysis of circadian gene expression in human epidermis. Whole-genome microarray analysis of suction-blister epidermis obtained throughout the day revealed a functional circadian clock in epidermal keratinocytes with hundreds of transcripts regulated in a daytime-dependent manner. Among those, we identified a circadian transcription factor, Kruppel-like factor 9 (Klf9), that is substantially up-regulated in a cortisol and differentiation-state-dependent manner. Gain- and loss-of-function experiments showed strong antiproliferative effects of Klf9. Putative Klf9 target genes include proliferation/differentiation markers that also show circadian expression in vivo, suggesting that Klf9 affects keratinocyte proliferation/differentiation by controlling the expression of target genes in a daytime-dependent manner.  
  Address Research and Development, Beiersdorf AG, 20245 Hamburg, 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 0027-8424 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22711835; PMCID:PMC3390879 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 814  
Permanent link to this record
 

 
Author Meng, Y.; He, Z.; Yin, J.; Zhang, Y.; Zhang, T. url  doi
openurl 
  Title Quantitative calculation of human melatonin suppression induced by inappropriate light at night Type Journal Article
  Year (down) 2011 Publication Medical & Biological Engineering & Computing Abbreviated Journal Med Biol Eng Comput  
  Volume 49 Issue 9 Pages 1083-1088  
  Keywords Algorithms; Circadian Rhythm/physiology/*radiation effects; Humans; *Lighting; Melatonin/*secretion; *Models, Biological; Retinal Cone Photoreceptor Cells/physiology/radiation effects; Retinal Ganglion Cells/physiology/radiation effects; Retinal Rod Photoreceptor Cells/physiology/radiation effects  
  Abstract Melatonin (C(1)(3)H(1)(6)N(2)O(2)) has a wide range of functions in the body. When is inappropriately exposed to light at night, human circadian rhythm will be interfered and then melatonin secretion will become abnormal. For nearly three decades great progresses have been achieved in analytic action spectra and melatonin suppression by various light conditions. However, so far few articles focused on the quantitative calculation of melatonin suppression induced by light. In this article, an algorithm is established, in which all the contributions of rods, cones, and intrinsically photosensitive retinal ganglion cells are considered. Calculation results accords with the experimental data in references very well, which indicate the validity of this algorithm. This algorithm can also interpret the rule of melatonin suppression varying with light correlated color temperature very well.  
  Address Photonics Research Center, School of Physics, Nankai University, Tianjin 300071, China  
  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 0140-0118 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21717231 Approved no  
  Call Number IDA @ john @ Serial 236  
Permanent link to this record
 

 
Author Sherman, H.; Gutman, R.; Chapnik, N.; Meylan, J.; le Coutre, J.; Froy, O. url  doi
openurl 
  Title Caffeine alters circadian rhythms and expression of disease and metabolic markers Type Journal Article
  Year (down) 2011 Publication The International Journal of Biochemistry & Cell Biology Abbreviated Journal Int J Biochem Cell Biol  
  Volume 43 Issue 5 Pages 829-838  
  Keywords Human Health; Animals; Biological Markers/blood/metabolism; Body Weight/drug effects/physiology; Caffeine/*pharmacology; Caloric Restriction; Circadian Rhythm/*drug effects/genetics/physiology; *Disease/genetics; Eating/drug effects/physiology; Gene Expression Regulation/*drug effects/genetics; HEK293 Cells; Humans; Inflammation/metabolism; Male; Mice; Mice, Inbred C57BL; Motor Activity/drug effects/physiology  
  Abstract The circadian clock regulates many aspects of physiology, energy metabolism, and sleep. Restricted feeding (RF), a regimen that restricts the duration of food availability entrains the circadian clock. Caffeine has been shown to affect both metabolism and sleep. However, its effect on clock gene and clock-controlled gene expression has not been studied. Here, we tested the effect of caffeine on circadian rhythms and the expression of disease and metabolic markers in the serum, liver, and jejunum of mice supplemented with caffeine under ad libitum (AL) feeding or RF for 16 weeks. Caffeine significantly affected circadian oscillation and the daily levels of disease and metabolic markers. Under AL, caffeine reduced the average daily mRNA levels of certain disease and inflammatory markers, such as liver alpha fetoprotein (Afp), C-reactive protein (Crp), jejunum alanine aminotransferase (Alt), growth arrest and DNA damage 45beta (Gadd45beta), Interleukin 1alpha (Il-1alpha), Il-1beta mRNA and serum plasminogen activator inhibitor 1 (PAI-1). Under RF, caffeine reduced the average daily levels of Alt, Gadd45beta, Il-1alpha and Il-1beta mRNA in the jejunum, but not in the liver. In addition, caffeine supplementation led to decreased expression of catabolic factors under RF. In conclusion, caffeine affects circadian gene expression and metabolism possibly leading to beneficial effects mainly under AL feeding.  
  Address Institute of Biochemistry, Food Science and Nutrition, Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot 76100, Israel  
  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 1357-2725 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21352949 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 810  
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