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Author Filipski, E.; Subramanian, P.; Carriere, J.; Guettier, C.; Barbason, H.; Levi, F. url  doi
openurl 
  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 (up) 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 0027-5107 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19833225 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 747  
Permanent link to this record
 

 
Author Kovac, J.; Husse, J.; Oster, H. url  doi
openurl 
  Title A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock Type Journal Article
  Year 2009 Publication Molecules and Cells Abbreviated Journal Mol Cells  
  Volume 28 Issue 2 Pages 75-80  
  Keywords (up) Human Health; Animals; Biological Clocks/*physiology; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/*physiology; Energy Metabolism/*physiology; Gene Expression Regulation; Homeostasis; Humans; Period Circadian Proteins/genetics/metabolism; Time Factors  
  Abstract The cyclic environmental conditions brought about by the 24 h rotation of the earth have allowed the evolution of endogenous circadian clocks that control the temporal alignment of behaviour and physiology, including the uptake and processing of nutrients. Both metabolic and circadian regulatory systems are built upon a complex feedback network connecting centres of the central nervous system and different peripheral tissues. Emerging evidence suggests that circadian clock function is closely linked to metabolic homeostasis and that rhythm disruption can contribute to the development of metabolic disease. At the same time, metabolic processes feed back into the circadian clock, affecting clock gene expression and timing of behaviour. In this review, we summarize the experimental evidence for this bimodal interaction, with a focus on the molecular mechanisms mediating this exchange, and outline the implications for clock-based and metabolic diseases.  
  Address Circadian Rhythms Group, Max Planck Institute of Biophysical Chemistry, 37077, Gottingen, Germany  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1016-8478 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19714310 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 772  
Permanent link to this record
 

 
Author Stevens, R.G. url  doi
openurl 
  Title Light-at-night, circadian disruption and breast cancer: assessment of existing evidence Type Journal Article
  Year 2009 Publication International Journal of Epidemiology Abbreviated Journal Int J Epidemiol  
  Volume 38 Issue 4 Pages 963-970  
  Keywords (up) Human Health; Animals; Blindness/complications/epidemiology; Breast Neoplasms/epidemiology/*etiology/metabolism; Chronobiology Disorders/*complications/epidemiology/metabolism; Circadian Rhythm/physiology; Disease Models, Animal; Female; Humans; Light Signal Transduction/physiology; Lighting/adverse effects; Melatonin/biosynthesis; Sleep/physiology; Time Factors; *Work Schedule Tolerance  
  Abstract BACKGROUND: Breast cancer incidence is increasing globally for largely unknown reasons. The possibility that a portion of the breast cancer burden might be explained by the introduction and increasing use of electricity to light the night was suggested >20 years ago. METHODS: The theory is based on nocturnal light-induced disruption of circadian rhythms, notably reduction of melatonin synthesis. It has formed the basis for a series of predictions including that non-day shift work would increase risk, blind women would be at lower risk, long sleep duration would lower risk and community nighttime light level would co-distribute with breast cancer incidence on the population level. RESULTS: Accumulation of epidemiological evidence has accelerated in recent years, reflected in an International Agency for Research on Cancer (IARC) classification of shift work as a probable human carcinogen (2A). There is also a strong rodent model in support of the light-at-night (LAN) idea. CONCLUSION: If a consensus eventually emerges that LAN does increase risk, then the mechanisms for the effect are important to elucidate for intervention and mitigation. The basic understanding of phototransduction for the circadian system, and of the molecular genetics of circadian rhythm generation are both advancing rapidly, and will provide for the development of lighting technologies at home and at work that minimize circadian disruption, while maintaining visual efficiency and aesthetics. In the interim, there are strategies now available to reduce the potential for circadian disruption, which include extending the daily dark period, appreciate nocturnal awakening in the dark, using dim red light for nighttime necessities, and unless recommended by a physician, not taking melatonin tablets.  
  Address Department of Community Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-6325, USA. bugs@uchc.edu  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0300-5771 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19380369; PMCID:PMC2734067 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 527  
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Author Owens, B. url  doi
openurl 
  Title Obesity: heavy sleepers Type Journal Article
  Year 2013 Publication Nature Abbreviated Journal Nature  
  Volume 497 Issue 7450 Pages S8-9  
  Keywords (up) 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  
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  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:23698508 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 503  
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Author Zukauskas, A.; Vaicekauskas, R.; Vitta, P. url  doi
openurl 
  Title Optimization of solid-state lamps for photobiologically friendly mesopic lighting Type Journal Article
  Year 2012 Publication Applied Optics Abbreviated Journal Appl Opt  
  Volume 51 Issue 35 Pages 8423-8432  
  Keywords (up) Lighting Systems; Circadian Rhythm; Color; Equipment Design; Humans; Light; *Lighting; Melatonin/metabolism; Photobiology/*methods; Semiconductors; Time Factors; Vision, Ocular  
  Abstract The circadian and visual-performance-based mesopic systems of photometry were applied for the optimization of the spectral power distributions (SPDs) of the solid-state sources of light for low-illuminance lighting applications. At mesopic adaptation luminances typical of outdoor lighting (0.1-2 cd/m(2)), the optimal SPDs were obtained through the minimization of the mesopic circadian action factor, which is the ratio of the circadian efficacy of radiation to mesopic luminous efficacy of radiation. For correlated color temperatures below ~3000 K, the optimized dichromatic light-emitting diodes (LEDs) are shown to pose a lower circadian hazard than high-pressure sodium lamps and common warm white LEDs; also they are potentially more efficacious and have acceptable color rendition properties under mesopic conditions.  
  Address Institute of Applied Research, Vilnius University, Sauletekio al. 9-III, Vilnius LT-10222, Lithuania. arturas.zukauskas@ff.vu.lt  
  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 0003-6935 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23262538 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 448  
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