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Author Haus, E.L.; Smolensky, M.H. url  doi
openurl 
  Title Shift work and cancer risk: potential mechanistic roles of circadian disruption, light at night, and sleep deprivation Type Journal Article
  Year 2013 Publication Sleep Medicine Reviews Abbreviated Journal Sleep Med Rev  
  Volume 17 Issue 4 Pages 273-284  
  Keywords Cell Cycle/physiology; Circadian Rhythm/*physiology; Epigenesis, Genetic/physiology; Humans; Light; Melatonin/physiology; Neoplasms/*etiology; Risk Factors; Sleep Deprivation/*complications; Work Schedule Tolerance/*physiology; oncogenesis  
  Abstract Shift work that includes a nighttime rotation has become an unavoidable attribute of today's 24-h society. The related disruption of the human circadian time organization leads in the short-term to an array of jet-lag-like symptoms, and in the long-run it may contribute to weight gain/obesity, metabolic syndrome/type II diabetes, and cardiovascular disease. Epidemiologic studies also suggest increased cancer risk, especially for breast cancer, in night and rotating female shift workers. If confirmed in more controlled and detailed studies, the carcinogenic effect of night and shift work will constitute additional serious medical, economic, and social problems for a substantial proportion of the working population. Here, we examine the possible multiple and interconnected cancer-promoting mechanisms as a consequence of shift work, i.e., repeated disruption of the circadian system, pineal hormone melatonin suppression by exposure to light at night, sleep-deprivation-caused impairment of the immune system, plus metabolic changes favoring obesity and generation of proinflammatory reactive oxygen species.  
  Address Department of Laboratory Medicine & Pathology, University of Minnesota and Health Partners Medical Group, Regions Hospital, 640 Jackson Street, St. Paul, Minnesota 55101, USA. Erhard.X.Haus@HealthPartners.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 1087-0792 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23137527 Approved no  
  Call Number IDA @ john @ Serial 157  
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Author Jasser, S.A.; Blask, D.E.; Brainard, G.C. url  doi
openurl 
  Title Light during darkness and cancer: relationships in circadian photoreception and tumor biology Type Journal Article
  Year 2006 Publication Cancer Causes & Control : CCC Abbreviated Journal Cancer Causes Control  
  Volume 17 Issue 4 Pages 515-523  
  Keywords Human Health; Animals; *Circadian Rhythm; *Darkness; Humans; *Light; Light Signal Transduction; Melatonin/physiology/secretion; Neoplasms/etiology/pathology/*physiopathology; Suprachiasmatic Nucleus/physiology  
  Abstract The relationship between circadian phototransduction and circadian-regulated processes is poorly understood. Melatonin, commonly a circadian phase marker, may play a direct role in a myriad of physiologic processes. The circadian rhythm for pineal melatonin secretion is regulated by the hypothalamic suprachiasmatic nucleus (SCN). Its neural source of light input is a unique subset of intrinsically photosensitive retinal ganglion cells expressing melanopsin, the primary circadian photopigment in rodents and primates. Action spectra of melatonin suppression by light have shown that light in the 446-477 nm range, distinct from the visual system's peak sensitivity, is optimal for stimulating the human circadian system. Breast cancer is the oncological disease entity whose relationship to circadian rhythm fluctuations has perhaps been most extensively studied. Empirical data has increasingly supported the hypothesis that higher risk of breast cancer in industrialized countries is partly due to increased exposure to light at night. Studies of tumor biology implicate melatonin as a potential mediator of this effect. Yet, causality between lifestyle factors and circadian tumor biology remains elusive and likely reflects significant variability with physiologic context. Continued rigorous empirical inquiry into the physiology and clinical implications of these habitual, integrated aspects of life is highly warranted at this time.  
  Address Department of Neurology, Light Research Program, Thomas Jefferson University, 1025 Walnut Street, Suite 507, Philadelphia, PA 19107, USA. samar.jasser@jefferson.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 0957-5243 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:16596305 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 766  
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Author Ruger, M.; St Hilaire, M.A.; Brainard, G.C.; Khalsa, S.-B.S.; Kronauer, R.E.; Czeisler, C.A.; Lockley, S.W. url  doi
openurl 
  Title Human phase response curve to a single 6.5 h pulse of short-wavelength light Type Journal Article
  Year 2013 Publication The Journal of Physiology Abbreviated Journal J Physiol  
  Volume 591 Issue Pt 1 Pages 353-363  
  Keywords Adolescent; Adult; Body Temperature; Circadian Rhythm/*physiology; Female; Humans; *Light; Male; Melatonin/physiology; Young Adult; blue light; melatonin; photic response; whort-wavelength  
  Abstract The photic resetting response of the human circadian pacemaker depends on the timing of exposure, and the direction and magnitude of the resulting shift is described by a phase response curve (PRC). Previous PRCs in humans have utilized high-intensity polychromatic white light. Given that the circadian photoreception system is maximally sensitive to short-wavelength visible light, the aim of the current study was to construct a PRC to blue (480 nm) light and compare it to a 10,000 lux white light PRC constructed previously using a similar protocol. Eighteen young healthy participants (18-30 years) were studied for 9-10 days in a time-free environment. The protocol included three baseline days followed by a constant routine (CR) to assess initial circadian phase. Following this CR, participants were exposed to a 6.5 h 480 nm light exposure (11.8 muW cm(-2), 11.2 lux) following mydriasis via a modified Ganzfeld dome. A second CR was conducted following the light exposure to re-assess circadian phase. Phase shifts were calculated from the difference in dim light melatonin onset (DLMO) between CRs. Exposure to 6.5 h of 480 nm light resets the circadian pacemaker according to a conventional type 1 PRC with fitted maximum delays and advances of -2.6 h and 1.3 h, respectively. The 480 nm PRC induced approximately 75% of the response of the 10,000 lux white light PRC. These results may contribute to a re-evaluation of dosing guidelines for clinical light therapy and the use of light as a fatigue countermeasure.  
  Address Circadian Physiology Program, Division of Sleep Medicine, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA. mrueger@rics.bwh.harvard.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 0022-3751 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23090946; PMCID:PMC3630790 Approved no  
  Call Number IDA @ john @ Serial 239  
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