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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 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 (up)  
  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 0028-0836 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23698508 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 503  
Permanent link to this record
 

 
Author Kempenaers, B.; Borgstrom, P.; Loes, P.; Schlicht, E.; Valcu, M. url  doi
openurl 
  Title Artificial night lighting affects dawn song, extra-pair siring success, and lay date in songbirds Type Journal Article
  Year 2010 Publication Current Biology : CB Abbreviated Journal Curr Biol  
  Volume 20 Issue 19 Pages 1735-1739  
  Keywords Animals; Environmental Pollution; Female; Light; *Lighting; Male; *Reproduction; Sexual Behavior, Animal/*physiology; Songbirds/*physiology; Time Factors; *Vocalization, Animal  
  Abstract (up) Associated with a continued global increase in urbanization, anthropogenic light pollution is an important problem. However, our understanding of the ecological consequences of light pollution is limited. We investigated effects of artificial night lighting on dawn song in five common forest-breeding songbirds. In four species, males near street lights started singing significantly earlier at dawn than males elsewhere in the forest, and this effect was stronger in naturally earlier-singing species. We compared reproductive behavior of blue tits breeding in edge territories with and without street lights to that of blue tits breeding in central territories over a 7 year period. Under the influence of street lights, females started egg laying on average 1.5 days earlier. Males occupying edge territories with street lights were twice as successful in obtaining extra-pair mates than their close neighbors or than males occupying central forest territories. Artificial night lighting affected both age classes but had a stronger effect on yearling males. Our findings indicate that light pollution has substantial effects on the timing of reproductive behavior and on individual mating patterns. It may have important evolutionary consequences by changing the information embedded in previously reliable quality-indicator traits.  
  Address Department of Behavioural Ecology and Evolutionary Genetics, Max Planck Institute for Ornithology, Eberhard-Gwinner-Strasse, 82319 Seewiesen, Germany. b.kempenaers@orn.mpg.de  
  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 0960-9822 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20850324 Approved no  
  Call Number IDA @ john @ Serial 51  
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Author Arendt, J. url  doi
openurl 
  Title Biological rhythms during residence in polar regions Type Journal Article
  Year 2012 Publication Chronobiology International Abbreviated Journal Chronobiol Int  
  Volume 29 Issue 4 Pages 379-394  
  Keywords *Acclimatization; Activities of Daily Living; Affect; Antarctic Regions; Arctic Regions; *Biological Clocks; *Circadian Rhythm; *Cold Climate; *Cold Temperature; Energy Metabolism; Feeding Behavior; Humans; Melatonin/metabolism; Personnel Staffing and Scheduling; *Photoperiod; Seasonal Affective Disorder/physiopathology/prevention & control/psychology; *Seasons; Sleep; Sleep Disorders, Circadian Rhythm/etiology/physiopathology/*prevention & control/psychology; Time Factors; Workload; Workplace  
  Abstract (up) At Arctic and Antarctic latitudes, personnel are deprived of natural sunlight in winter and have continuous daylight in summer: light of sufficient intensity and suitable spectral composition is the main factor that maintains the 24-h period of human circadian rhythms. Thus, the status of the circadian system is of interest. Moreover, the relatively controlled artificial light conditions in winter are conducive to experimentation with different types of light treatment. The hormone melatonin and/or its metabolite 6-sulfatoxymelatonin (aMT6s) provide probably the best index of circadian (and seasonal) timing. A frequent observation has been a delay of the circadian system in winter. A skeleton photoperiod (2 x 1-h, bright white light, morning and evening) can restore summer timing. A single 1-h pulse of light in the morning may be sufficient. A few people desynchronize from the 24-h day (free-run) and show their intrinsic circadian period, usually >24 h. With regard to general health in polar regions, intermittent reports describe abnormalities in various physiological processes from the point of view of daily and seasonal rhythms, but positive health outcomes are also published. True winter depression (SAD) appears to be rare, although subsyndromal SAD is reported. Probably of most concern are the numerous reports of sleep problems. These have prompted investigations of the underlying mechanisms and treatment interventions. A delay of the circadian system with “normal” working hours implies sleep is attempted at a suboptimal phase. Decrements in sleep efficiency, latency, duration, and quality are also seen in winter. Increasing the intensity of ambient light exposure throughout the day advanced circadian phase and was associated with benefits for sleep: blue-enriched light was slightly more effective than standard white light. Effects on performance remain to be fully investigated. At 75 degrees S, base personnel adapt the circadian system to night work within a week, in contrast to temperate zones where complete adaptation rarely occurs. A similar situation occurs on high-latitude North Sea oil installations, especially when working 18:00-06:00 h. Lack of conflicting light exposure (and “social obligations”) is the probable explanation. Many have problems returning to day work, showing circadian desynchrony. Timed light treatment again has helped to restore normal phase/sleep in a small number of people. Postprandial response to meals is compromised during periods of desynchrony with evidence of insulin resistance and elevated triglycerides, risk factors for heart disease. Only small numbers of subjects have been studied intensively in polar regions; however, these observations suggest that suboptimal light conditions are deleterious to health. They apply equally to people living in temperate zones with insufficient light exposure.  
  Address Centre for Chronobiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, UK. arendtjo@gmail.com  
  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 0742-0528 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22497433; PMCID:PMC3793275 Approved no  
  Call Number IDA @ john @ Serial 143  
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 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 (up) 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  
  Publisher Place of Publication Editor  
  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  
Permanent link to this record
 

 
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 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 (up) 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  
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