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Author Bray, M.S.; Young, M.E.
Title Chronobiological Effects on Obesity Type (up) 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
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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
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Author Chamorro, E.; Bonnin-Arias, C.; Perez-Carrasco, M.J.; Munoz de Luna, J.; Vazquez, D.; Sanchez-Ramos, C.
Title Effects of light-emitting diode radiations on human retinal pigment epithelial cells in vitro Type (up) Journal Article
Year 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
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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
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Author Dickerman, B.; Liu, J.
Title Does current scientific evidence support a link between light at night and breast cancer among female night-shift nurses? Review of evidence and implications for occupational and environmental health nurses Type (up) Journal Article
Year 2012 Publication Workplace Health & Safety Abbreviated Journal Workplace Health Saf
Volume 60 Issue 6 Pages 273-81; quiz 282
Keywords Human Health; Breast Neoplasms/*epidemiology/nursing; Chronobiology Disorders/*epidemiology/nursing; Education, Nursing, Continuing; Environmental Health; Evidence-Based Nursing; Female; Humans; Light; Night Care/*statistics & numerical data; *Occupational Health Nursing; Risk Factors; *Work Schedule Tolerance
Abstract Breast cancer is increasingly prevalent in industrialized regions of the world, and exposure to light at night (LAN) has been proposed as a potential risk factor. Epidemiological observations have documented an increased breast cancer risk among female night-shift workers, and strong experimental evidence for this relationship has also been found in rodent models. Indirect support for the LAN hypothesis comes from studies involving blind women, sleep duration, bedroom light levels, and community nighttime light levels. This article reviews the literature, discusses possible mechanisms of action, and provides recommendations for occupational health nursing research, practice, and education. Research is needed to further explore the relationship between exposure to LAN and breast cancer risk and elucidate the mechanisms underlying this relationship before interventions can be designed for prevention and mitigation of breast cancer.
Address MultiCare Good Samaritan Hospital, Puyallup, WA, USA. barbra.dickerman@gmail.com
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 2165-0799 ISBN Medium
Area Expedition Conference
Notes PMID:22658734 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 512
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Author Lahti, T.; Merikanto, I.; Partonen, T.
Title Circadian clock disruptions and the risk of cancer Type (up) Journal Article
Year 2012 Publication Annals of Medicine Abbreviated Journal Ann Med
Volume 44 Issue 8 Pages 847-853
Keywords Human Health; Cell Division; Chronobiology Disorders/*complications/genetics/*physiopathology; Circadian Clocks/*genetics; Humans; Neoplasms/*etiology; Work Schedule Tolerance/physiology
Abstract Disrupted circadian rhythms may lead to failures in the control of the cell division cycle and the subsequent malignant cell growth. In order to understand the pathogenesis of cancer more in detail, it is crucial to identify those mechanisms of action which contribute to the loss of control of the cell division cycle. This mini-review focuses on the recent findings concerning the links between the human circadian clock and cancer. Clinical implications concern not only feasible methods for the assessment of the circadian time of an individual or for the determination of the best time for administration of a drug of treatment, but also in the future genetic tests for screening and for planning treatment.
Address Department of Mental Health and Substance Abuse Services, National Institute for Health and Welfare, Helsinki, Finland
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 0785-3890 ISBN Medium
Area Expedition Conference
Notes PMID:23072403 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 513
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Author Savvidis, C.; Koutsilieris, M.
Title Circadian rhythm disruption in cancer biology Type (up) Journal Article
Year 2012 Publication Molecular Medicine (Cambridge, Mass.) Abbreviated Journal Mol Med
Volume 18 Issue Pages 1249-1260
Keywords Human Health; Animals; CLOCK Proteins/genetics/metabolism; Circadian Clocks/genetics; *Circadian Rhythm/genetics; Environment; Humans; Melatonin/metabolism; Neoplasms/genetics/pathology/*physiopathology/therapy
Abstract Circadian rhythms show universally a 24-h oscillation pattern in metabolic, physiological and behavioral functions of almost all species. This pattern is due to a fundamental adaptation to the rotation of Earth around its own axis. Molecular mechanisms of generation of circadian rhythms organize a biochemical network in suprachiasmatic nucleus and peripheral tissues, building cell autonomous clock pacemakers. Rhythmicity is observed in transcriptional expression of a wide range of clock-controlled genes that regulate a variety of normal cell functions, such as cell division and proliferation. Desynchrony of this rhythmicity seems to be implicated in several pathologic conditions, including tumorigenesis and progression of cancer. In 2007, the International Agency for Research on Cancer (IARC) categorized “shiftwork that involves circadian disruption [as] probably carcinogenic to humans” (Group 2A in the IARC classification system of carcinogenic potency of an agentagent) (Painting, Firefighting, and Shiftwork; IARC; 2007). This review discusses the potential relation between disruptions of normal circadian rhythms with genetic driving machinery of cancer. Elucidation of the role of clockwork disruption, such as exposure to light at night and sleep disruption, in cancer biology could be important in developing new targeted anticancer therapies, optimizing individualized chronotherapy and modifying lighting environment in workplaces or homes.
Address Department of Endocrinology and Metabolism, Hippocration General Hospital, Athens, Greece. csavvidis@med.uoa.gr
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Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1076-1551 ISBN Medium
Area Expedition Conference
Notes PMID:22811066; PMCID:PMC3521792 Approved no
Call Number LoNNe @ christopher.kyba @ Serial 514
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