toggle visibility Search & Display Options

Select All    Deselect All
 |   | 
Details
   print
  Records Links
Author Reiter, R.J.; Rosales-Corral, S.; Coto-Montes, A.; Antonio Boga, J.; Tan, D.X.; Davis, J.M.; Konturek, P.C.; Konturek, S.J.; Brzozowski, T. url  openurl
  Title The photoperiod, circadian regulation and chronodisruption: the requisite interplay between the suprachiasmatic nuclei and the pineal and gut melatonin. Type Journal Article
  Year 2011 Publication Journal of Physiology and Pharmacology Abbreviated Journal  
  Volume 62 Issue Pages 269-274  
  Keywords Human Health; biological clock; chronodisruption; circadian rhythm; gastrointestinal melatonin; peptic ulcer; pineal gland; suprachiasmatic nucleus  
  Abstract Biological rhythms are essential for optimal health (1, 2). Throughout the course of human evolution, hominids were exposed to regularly alternating periods of light and dark during every 24-hour period. This evolutionary period, which for humans may have lasted for three million or more years, allowed species to take advantage of the light:dark cycle to adjust their physiology and to synchronize it with the prevailing light:dark environment. To take advantage of this information, vertebrates, including hominids, evolved a group of neurons to monitor the photoperiodic environment and to adjust organismal, organ and cellular function accordingly.

This paired group of light-responsive neurons is located in the mediobasal preoptic area at the diencephalic-telencephalic junction just anterior to the hypothalamus. Since these neurons lie immediately above the decussating axons of the optic nerve, i.e., the optic chiasma, they are named the suprachiasmatic nuclei (SCN) (3, 4). The SCN orchestrate all known circadian rhythms in vertebrates and are referred to as the master biological clock or the central rhythm generator.
 
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication (up) Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 522  
Permanent link to this record
 

 
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 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 (up) 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 Salgado-Delgado, R.; Tapia Osorio, A.; Saderi, N.; Escobar, C. url  doi
openurl 
  Title Disruption of circadian rhythms: a crucial factor in the etiology of depression Type Journal Article
  Year 2011 Publication Depression Research and Treatment Abbreviated Journal Depress Res Treat  
  Volume 2011 Issue Pages 839743  
  Keywords Human Health  
  Abstract Circadian factors might play a crucial role in the etiology of depression. It has been demonstrated that the disruption of circadian rhythms by lighting conditions and lifestyle predisposes individuals to a wide range of mood disorders, including impulsivity, mania and depression. Also, associated with depression, there is the impairment of circadian rhythmicity of behavioral, endocrine, and metabolic functions. Inspite of this close relationship between both processes, the complex relationship between the biological clock and the incidence of depressive symptoms is far from being understood. The efficiency and the timing of treatments based on chronotherapy (e.g., light treatment, sleep deprivation, and scheduled medication) indicate that the circadian system is an essential target in the therapy of depression. The aim of the present review is to analyze the biological and clinical data that link depression with the disruption of circadian rhythms, emphasizing the contribution of circadian desynchrony. Therefore, we examine the conditions that may lead to circadian disruption of physiology and behavior as described in depressive states, and, according to this approach, we discuss therapeutic strategies aimed at treating the circadian system and depression.  
  Address Departamento de Biologia Celular y Fisiologia, Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico, 04306 Mexico, DF, Mexico  
  Corporate Author Thesis  
  Publisher Place of Publication (up) Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2090-1321 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:21845223; PMCID:PMC3154570 Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 524  
Permanent link to this record
 

 
Author Chepesiuk, R. url  openurl
  Title Missing the Dark: Health Effects of Light Pollution Type Journal Article
  Year 2009 Publication Environmental Health Perspectives Abbreviated Journal  
  Volume 117 Issue 1 Pages A20-A27  
  Keywords Human Health  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication (up) Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 526  
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 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 (up) 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
Select All    Deselect All
 |   | 
Details
   print

Save Citations:
Export Records: