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Author Revell, V.L.; Molina, T.A.; Eastman, C.I.
Title Human phase response curve to intermittent blue light using a commercially available device Type Journal Article
Year 2012 Publication The Journal of Physiology Abbreviated Journal J Physiol
Volume 590 Issue Pt 19 Pages 4859-4868
Keywords Adolescent; Adult; Circadian Clocks/physiology/*radiation effects; Female; Humans; *Light; Male; Melatonin/analysis/physiology; Saliva/chemistry; Young Adult; blue light
Abstract Light shifts the timing of the circadian clock according to a phase response curve (PRC). To date, all human light PRCs have been to long durations of bright white light. However, melanopsin, the primary photopigment for the circadian system, is most sensitive to short wavelength blue light. Therefore, to optimise light treatment it is important to generate a blue light PRC.We used a small, commercially available blue LED light box, screen size 11.2 x 6.6 cm at approximately 50 cm, approximately 200 muW cm(-2), approximately 185 lux. Subjects participated in two 5 day laboratory sessions 1 week apart. Each session consisted of circadian phase assessments to obtain melatonin profiles before and after 3 days of free-running through an ultradian light-dark cycle (2.5 h wake in dim light, 1.5 h sleep in the dark), forced desynchrony protocol. During one session subjects received intermittent blue light (three 30 min pulses over 2 h) once a day for the 3 days of free-running, and in the other session (control) they remained in dim room light, counterbalanced. The time of blue light was varied among subjects to cover the entire 24 h day. For each individual, the phase shift to blue light was corrected for the free-run determined during the control session. The blue light PRC had a broad advance region starting in the morning and extending through the afternoon. The delay region started a few hours before bedtime and extended through the night. This is the first PRC to be constructed to blue light and to a stimulus that could be used in the real world.
Address University of Surrey, Guildford, Surrey GU2 7XH, 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 (up) 0022-3751 ISBN Medium
Area Expedition Conference
Notes PMID:22753544; PMCID:PMC3487041 Approved no
Call Number IDA @ john @ Serial 345
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Author Filipski, E.; Subramanian, P.; Carriere, J.; Guettier, C.; Barbason, H.; Levi, F.
Title Circadian disruption accelerates liver carcinogenesis in mice Type Journal Article
Year 2009 Publication Mutation Research Abbreviated Journal Mutat Res
Volume 680 Issue 1-2 Pages 95-105
Keywords Human Health; Animals; Alanine Transaminase/blood; Animals; Aspartate Aminotransferases/blood; Bile Duct Neoplasms/chemically induced/pathology; Bile Ducts, Intrahepatic/drug effects/pathology; Body Weight/drug effects; Carcinogens/administration & dosage/*toxicity; Carcinoma, Hepatocellular/chemically induced/pathology; Cholangiocarcinoma/chemically induced/pathology; Circadian Rhythm/*drug effects; Diethylnitrosamine/administration & dosage/*toxicity; Dose-Response Relationship, Drug; Injections, Intraperitoneal; Liver/drug effects/pathology; Liver Neoplasms/blood/*chemically induced/pathology; Male; Mice; Neoplasms, Multiple Primary/chemically induced/pathology; Sarcoma/chemically induced/pathology; Time Factors
Abstract BACKGROUND: The circadian timing system rhythmically controls behavior, physiology, cellular proliferation and xenobiotic metabolism over the 24-h period. The suprachiasmatic nuclei in the hypothalamus coordinate the molecular clocks in most mammalian cells through an array of circadian physiological rhythms including rest-activity, body temperature, feeding patterns and hormonal secretions. As a result, shift work that involves circadian disruption is probably carcinogenic in humans. In experimental models, chronic jet-lag (CJL) suppresses rest-activity and body temperature rhythms and accelerates growth of two transplantable tumors in mice. CJL also suppresses or significantly alters the expression rhythms of clock genes in liver and tumors. Circadian clock disruption from CJL downregulates p53 and upregulates c-Myc, thus favoring cellular proliferation. Here, we investigate the role of CJL as a tumor promoter in mice exposed to the hepatic carcinogen, diethylnitrosamine (DEN). METHODS: In experiment 1 (Exp 1), the dose-dependent carcinogenicity of chronic intraperitoneal (i.p.) administration of DEN was explored in mice. In Exp 2, mice received DEN at 10 mg/kg/day (cumulative dose: 243 mg/kg), then were randomized to remain in a photoperiodic regimen where 12 h of light alternates with 12 h of darkness (LD 12:12) or to be submitted to CJL (8-h advance of light onset every 2 days). Rest-activity and body temperature were monitored. Serum liver enzymes were determined repeatedly. Mice were sacrificed and examined for neoplastic lesions at 10 months. RESULTS: In Exp 1, DEN produced liver cancers in all the mice receiving 10 mg/kg/day. In Exp 2, mice on CJL had increased mean plasma levels of aspartate aminotransferase and more liver tumors as compared to LD mice at approximately 10 months (p = 0.005 and 0.028, respectively). The mean diameter of the largest liver tumor was twice as large in CJL vs LD mice (8.5 vs 4.4 mm, p = 0.027). In LD, a single histologic tumor type per liver was observed. In CJL, up to four different types were associated in the same liver (hepatocellular- or cholangio-carcinomas, sarcomas or mixed tumors). DEN itself markedly disrupted the circadian rhythms in rest-activity and body temperature in all the mice. DEN-induced disruption was prolonged for >or= 3 months by CJL exposure. CONCLUSIONS: The association of circadian disruption with chronic DEN exposure suggests that circadian clocks actively control the mechanisms of liver carcinogenesis in mice. Persistent circadian coordination may further be critical for slowing down and/or reverting cancer development after carcinogen exposure.
Address INSERM, U776 Rythmes Biologiques et Cancers, Hopital Paul Brousse, Villejuif F-94807, France
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 (up) 0027-5107 ISBN Medium
Area Expedition Conference
Notes PMID:19833225 Approved no
Call Number LoNNe @ kagoburian @ Serial 747
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Author Fonken, L.K.; Workman, J.L.; Walton, J.C.; Weil, Z.M.; Morris, J.S.; Haim, A.; Nelson, R.J.
Title Light at night increases body mass by shifting the time of food intake Type Journal Article
Year 2010 Publication Proceedings of the National Academy of Sciences of the United States of America Abbreviated Journal Proc Natl Acad Sci U S A
Volume 107 Issue 43 Pages 18664-18669
Keywords Animals; Body Mass Index; *Circadian Rhythm; Disease Models, Animal; Eating/*physiology/psychology/*radiation effects; Energy Intake; Feeding Behavior/physiology/psychology/radiation effects; Glucose Tolerance Test; Humans; Male; Metabolic Syndrome X/etiology; Mice; Motor Activity; Obesity/*etiology/pathology/physiopathology/psychology; *Photoperiod
Abstract The global increase in the prevalence of obesity and metabolic disorders coincides with the increase of exposure to light at night (LAN) and shift work. Circadian regulation of energy homeostasis is controlled by an endogenous biological clock that is synchronized by light information. To promote optimal adaptive functioning, the circadian clock prepares individuals for predictable events such as food availability and sleep, and disruption of clock function causes circadian and metabolic disturbances. To determine whether a causal relationship exists between nighttime light exposure and obesity, we examined the effects of LAN on body mass in male mice. Mice housed in either bright (LL) or dim (DM) LAN have significantly increased body mass and reduced glucose tolerance compared with mice in a standard (LD) light/dark cycle, despite equivalent levels of caloric intake and total daily activity output. Furthermore, the timing of food consumption by DM and LL mice differs from that in LD mice. Nocturnal rodents typically eat substantially more food at night; however, DM mice consume 55.5% of their food during the light phase, as compared with 36.5% in LD mice. Restricting food consumption to the active phase in DM mice prevents body mass gain. These results suggest that low levels of light at night disrupt the timing of food intake and other metabolic signals, leading to excess weight gain. These data are relevant to the coincidence between increasing use of light at night and obesity in humans.
Address Department of Neuroscience, Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.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 (up) 0027-8424 ISBN Medium
Area Expedition Conference
Notes PMID:20937863; PMCID:PMC2972983 Approved no
Call Number IDA @ john @ Serial 169
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Author LeGates, T.A.; Altimus, C.M.; Wang, H.; Lee, H.-K.; Yang, S.; Zhao, H.; Kirkwood, A.; Weber, E.T.; Hattar, S.
Title Aberrant light directly impairs mood and learning through melanopsin-expressing neurons Type Journal Article
Year 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 (up) 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 Owens, B.
Title Obesity: heavy sleepers Type Journal Article
Year 2013 Publication Nature Abbreviated Journal Nature
Volume 497 Issue 7450 Pages S8-9
Keywords Human Health; Animals; Body Mass Index; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/physiology; Energy Metabolism/*physiology; Ghrelin/metabolism; Humans; Insulin Resistance/physiology; Leptin/metabolism; Male; Mice; Obesity/*physiopathology; Satiety Response/physiology; Sleep/*physiology; Suprachiasmatic Nucleus/physiology; Time Factors; Weight Gain/physiology; Weight Loss/physiology
Abstract
Address
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 (up) 0028-0836 ISBN Medium
Area Expedition Conference
Notes PMID:23698508 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 503
Permanent link to this record