toggle visibility Search & Display Options

Select All    Deselect All
 |   | 
Details
   print
  Records Links
Author Reiter, R.J.; Tan, D.-X.; Korkmaz, A.; Ma, S. url  doi
openurl 
  Title Obesity and metabolic syndrome: association with chronodisruption, sleep deprivation, and melatonin suppression Type Journal Article
  Year 2012 Publication Annals of Medicine Abbreviated Journal Ann Med  
  Volume 44 Issue 6 Pages 564-577  
  Keywords (up) Human Health; Adolescent; Adult; Animals; Child; Chronobiology Disorders/*epidemiology; Comorbidity; Disease Models, Animal; Humans; Light/adverse effects; Melatonin/*deficiency/physiology; Metabolic Syndrome X/*epidemiology; Mice; Obesity/*epidemiology; Rats; Sleep Deprivation/*epidemiology  
  Abstract Obesity has become an epidemic in industrialized and developing countries. In 30 years, unless serious changes are made, a majority of adults and many children will be classified as overweight or obese. Whereas fatness alone endangers physiological performance of even simple tasks, the associated co-morbidity of obesity including metabolic syndrome in all its manifestations is a far more critical problem. If the current trend continues as predicted, health care systems may be incapable of handling the myriad of obesity-related diseases. The financial costs, including those due to medical procedures, absenteeism from work, and reduced economic productivity, will jeopardize the financial well-being of industries. The current review summarizes the potential contributions of three processes that may be contributing to humans becoming progressively more overweight: circadian or chronodisruption, sleep deficiency, and melatonin suppression. Based on the information provided in this survey, life-style factors (independent of the availability of abundant calorie-rich foods) may aggravate weight gain. Both epidemiological and experimental data support associations between disrupted physiological rhythms, a reduction in adequate sleep, and light-at-night-induced suppression of an essential endogenously produced molecule, melatonin. The implication is that if these problems were corrected with life-style changes, body-weight could possibly be more easily controlled.  
  Address Department of Cellular and Structural Biology, UT Health Science Center, San Antonio, Texas, USA. reiter@uthscsa.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 0785-3890 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21668294 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 523  
Permanent link to this record
 

 
Author Eisenstein, M. url  doi
openurl 
  Title Chronobiology: stepping out of time Type Journal Article
  Year 2013 Publication Nature Abbreviated Journal Nature  
  Volume 497 Issue 7450 Pages S10-2  
  Keywords (up) Human Health; Animals; Benzofurans/therapeutic use; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/genetics/*physiology; Cyclopropanes/therapeutic use; Efficiency/physiology; Humans; Melatonin/agonists/metabolism; Obesity/metabolism; Sleep/genetics/*physiology; Suprachiasmatic Nucleus/metabolism  
  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 0028-0836 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23698500 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 500  
Permanent link to this record
 

 
Author Blask, D.E.; Brainard, G.C.; Dauchy, R.T.; Hanifin, J.P.; Davidson, L.K.; Krause, J.A.; Sauer, L.A.; Rivera-Bermudez, M.A.; Dubocovich, M.L.; Jasser, S.A.; Lynch, D.T.; Rollag, M.D.; Zalatan, F. url  doi
openurl 
  Title Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats Type Journal Article
  Year 2005 Publication Cancer Research Abbreviated Journal Cancer Res  
  Volume 65 Issue 23 Pages 11174-11184  
  Keywords (up) Human Health; Animals; Breast Neoplasms/*blood/genetics/pathology; Cell Growth Processes/physiology; Circadian Rhythm/*physiology; Female; Humans; Light; Liver Neoplasms, Experimental/metabolism; Male; Melatonin/blood/*deficiency; Premenopause/blood; RNA, Messenger/biosynthesis/genetics; Rats; Rats, Nude; Receptors, Melatonin/biosynthesis/genetics; Transplantation, Heterologous  
  Abstract The increased breast cancer risk in female night shift workers has been postulated to result from the suppression of pineal melatonin production by exposure to light at night. Exposure of rats bearing rat hepatomas or human breast cancer xenografts to increasing intensities of white fluorescent light during each 12-hour dark phase (0-345 microW/cm2) resulted in a dose-dependent suppression of nocturnal melatonin blood levels and a stimulation of tumor growth and linoleic acid uptake/metabolism to the mitogenic molecule 13-hydroxyoctadecadienoic acid. Venous blood samples were collected from healthy, premenopausal female volunteers during either the daytime, nighttime, or nighttime following 90 minutes of ocular bright, white fluorescent light exposure at 580 microW/cm2 (i.e., 2,800 lx). Compared with tumors perfused with daytime-collected melatonin-deficient blood, human breast cancer xenografts and rat hepatomas perfused in situ, with nocturnal, physiologically melatonin-rich blood collected during the night, exhibited markedly suppressed proliferative activity and linoleic acid uptake/metabolism. Tumors perfused with melatonin-deficient blood collected following ocular exposure to light at night exhibited the daytime pattern of high tumor proliferative activity. These results are the first to show that the tumor growth response to exposure to light during darkness is intensity dependent and that the human nocturnal, circadian melatonin signal not only inhibits human breast cancer growth but that this effect is extinguished by short-term ocular exposure to bright, white light at night. These mechanistic studies are the first to provide a rational biological explanation for the increased breast cancer risk in female night shift workers.  
  Address Laboratory of Chrono-Neuroendocrine Oncology, Bassett Research Institute, The Mary Imogene Bassett Hospital, Cooperstown, New York 13326, USA. david.blask@bassett.org  
  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 0008-5472 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:16322268 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 721  
Permanent link to this record
 

 
Author Chamorro, E.; Bonnin-Arias, C.; Perez-Carrasco, M.J.; Munoz de Luna, J.; Vazquez, D.; Sanchez-Ramos, C. url  doi
openurl 
  Title Effects of light-emitting diode radiations on human retinal pigment epithelial cells in vitro Type Journal Article
  Year 2013 Publication Photochemistry and Photobiology Abbreviated Journal Photochem Photobiol  
  Volume 89 Issue 2 Pages 468-473  
  Keywords (up) 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  
  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 0031-8655 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:22989198 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 511  
Permanent link to this record
 

 
Author Smolensky, M.H.; Sackett-Lundeen, L.L.; Portaluppi, F. url  doi
openurl 
  Title Nocturnal light pollution and underexposure to daytime sunlight: Complementary mechanisms of circadian disruption and related diseases Type Journal Article
  Year 2015 Publication Chronobiology International Abbreviated Journal Chronobiol Int  
  Volume Issue Pages 1-20  
  Keywords (up) Human Health; Artificial light at night; cancer; circadian time structure; development and disruption; melatonin; sleep/wake cycle disturbance; sunlight; vitamin D; vitamin D deficiency; circadian time structure; circadian rhythm; desynchrony  
  Abstract Routine exposure to artificial light at night (ALAN) in work, home, and community settings is linked with increased risk of breast and prostate cancer (BC, PC) in normally sighted women and men, the hypothesized biological rhythm mechanisms being frequent nocturnal melatonin synthesis suppression, circadian time structure (CTS) desynchronization, and sleep/wake cycle disruption with sleep deprivation. ALAN-induced perturbation of the CTS melatonin synchronizer signal is communicated maternally at the very onset of life and after birth via breast or artificial formula feedings. Nighttime use of personal computers, mobile phones, electronic tablets, televisions, and the like – now epidemic in adolescents and adults and highly prevalent in pre-school and school-aged children – is a new source of ALAN. However, ALAN exposure occurs concomitantly with almost complete absence of daytime sunlight, whose blue-violet (446-484 nm lambda) spectrum synchronizes the CTS and whose UV-B (290-315 nm lambda) spectrum stimulates vitamin D synthesis. Under natural conditions and clear skies, day/night and annual cycles of UV-B irradiation drive corresponding periodicities in vitamin D synthesis and numerous bioprocesses regulated by active metabolites augment and strengthen the biological time structure. Vitamin D insufficiency and deficiency are widespread in children and adults in developed and developing countries as a consequence of inadequate sunlight exposure. Past epidemiologic studies have focused either on exposure to too little daytime UV-B or too much ALAN, respectively, on vitamin D deficiency/insufficiency or melatonin suppression in relation to risk of cancer and other, e.g., psychiatric, hypertensive, cardiac, and vascular, so-called, diseases of civilization. The observed elevated incidence of medical conditions the two are alleged to influence through many complementary bioprocesses of cells, tissues, and organs led us to examine effects of the totality of the artificial light environment in which humans reside today. Never have chronobiologic or epidemiologic investigations comprehensively researched the potentially deleterious consequences of the combination of suppressed vitamin D plus melatonin synthesis due to life in today's man-made artificial light environment, which in our opinion is long overdue.  
  Address c Hypertension Center, S. Anna University Hospital, University of Ferrara , Ferrara , Italy  
  Corporate Author Thesis  
  Publisher Taylor & Francis Place of Publication Editor  
  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:26374931 Approved no  
  Call Number IDA @ john @ Serial 1271  
Permanent link to this record
Select All    Deselect All
 |   | 
Details
   print

Save Citations:
Export Records: