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Author Figueiro, M.G.; Rea, M.S. url  doi
openurl 
  Title The effects of red and blue lights on circadian variations in cortisol, alpha amylase, and melatonin Type Journal Article
  Year 2010 Publication International Journal of Endocrinology Abbreviated Journal Int J Endocrinol  
  Volume 2010 Issue Pages 829351  
  Keywords blue light; red light; circadian rhythm; cortisol; alpha amylase; melatonin; photobiology; suprachiasmatic nuclei; endocrinology  
  Abstract The primary purpose of the present study was to expand our understanding of the impact of light exposures on the endocrine and autonomic systems as measured by acute cortisol, alpha amylase, and melatonin responses. We utilized exposures from narrowband long-wavelength (red) and from narrow-band short-wavelength (blue) lights to more precisely understand the role of the suprachiasmatic nuclei (SCN) in these responses. In a within-subjects experimental design, twelve subjects periodically received one-hour corneal exposures of 40 lux from the blue or from the red lights while continuously awake for 27 hours. Results showed-that, as expected, only the blue light reduced nocturnal melatonin. In contrast, both blue and red lights affected cortisol levels and, although less clear, alpha amylase levels as well. The present data bring into question whether the nonvisual pathway mediating nocturnal melatonin suppression is the same as that mediating other responses to light exhibited by the endocrine and the autonomic nervous systems.  
  Address Lighting Research Center, Rensselaer Polytechnic Institute, 21 Union Street, 3rd Floor, Troy, New York, NY 12180, USA  
  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 1687-8337 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:20652045; PMCID:PMC2905913 Approved no  
  Call Number IDA @ john @ Serial 291  
Permanent link to this record
 

 
Author Figueiro, M.G.; Bierman, A.; Plitnick, B.; Rea, M.S. url  doi
openurl 
  Title Preliminary evidence that both blue and red light can induce alertness at night Type Journal Article
  Year 2009 Publication BMC Neuroscience Abbreviated Journal BMC Neurosci  
  Volume 10 Issue Pages 105  
  Keywords Adult; Alpha Rhythm; Analysis of Variance; Beta Rhythm; Circadian Rhythm/*physiology; Cornea/physiology; Dose-Response Relationship, Radiation; Electrocardiography; Female; Humans; *Light; Male; Melatonin/secretion; Middle Aged; *Photic Stimulation; Psychomotor Performance; Radioimmunoassay; Salivary Glands/secretion; Wakefulness/*physiology; physiology of vision; blue light; red light  
  Abstract BACKGROUND: A variety of studies have demonstrated that retinal light exposure can increase alertness at night. It is now well accepted that the circadian system is maximally sensitive to short-wavelength (blue) light and is quite insensitive to long-wavelength (red) light. Retinal exposures to blue light at night have been recently shown to impact alertness, implicating participation by the circadian system. The present experiment was conducted to look at the impact of both blue and red light at two different levels on nocturnal alertness. Visually effective but moderate levels of red light are ineffective for stimulating the circadian system. If it were shown that a moderate level of red light impacts alertness, it would have had to occur via a pathway other than through the circadian system. METHODS: Fourteen subjects participated in a within-subject two-night study, where each participant was exposed to four experimental lighting conditions. Each night each subject was presented a high (40 lx at the cornea) and a low (10 lx at the cornea) diffuse light exposure condition of the same spectrum (blue, lambda(max) = 470 nm, or red, lambda(max) = 630 nm). The presentation order of the light levels was counterbalanced across sessions for a given subject; light spectra were counterbalanced across subjects within sessions. Prior to each lighting condition, subjects remained in the dark (< 1 lx at the cornea) for 60 minutes. Electroencephalogram (EEG) measurements, electrocardiogram (ECG), psychomotor vigilance tests (PVT), self-reports of sleepiness, and saliva samples for melatonin assays were collected at the end of each dark and light periods. RESULTS: Exposures to red and to blue light resulted in increased beta and reduced alpha power relative to preceding dark conditions. Exposures to high, but not low, levels of red and of blue light significantly increased heart rate relative to the dark condition. Performance and sleepiness ratings were not strongly affected by the lighting conditions. Only the higher level of blue light resulted in a reduction in melatonin levels relative to the other lighting conditions. CONCLUSION: These results support previous findings that alertness may be mediated by the circadian system, but it does not seem to be the only light-sensitive pathway that can affect alertness at night.  
  Address Lighting Research Center, Rensselaer Polytechnic Institute, Troy, NY, USA. figuem@rpi.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 1471-2202 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19712442; PMCID:PMC2744917 Approved no  
  Call Number IDA @ john @ Serial 285  
Permanent link to this record
 

 
Author Filipski, E.; Li, X.M.; Levi, F. url  doi
openurl 
  Title Disruption of circadian coordination and malignant growth Type Journal Article
  Year 2006 Publication Cancer Causes & Control : CCC Abbreviated Journal Cancer Causes Control  
  Volume 17 Issue 4 Pages 509-514  
  Keywords Human Health; Animals; Biological Clocks; Body Temperature; Cell Cycle Proteins; Cell Line, Tumor; Chronobiology Disorders/*complications/physiopathology; Circadian Rhythm; Corticosterone/blood; DNA-Binding Proteins/metabolism; Jet Lag Syndrome/complications/physiopathology; Lymphocyte Count; Mice; Neoplasm Transplantation; Nuclear Proteins/metabolism; Nuclear Receptor Subfamily 1, Group D, Member 1; Osteosarcoma/*pathology/physiopathology; Pancreatic Neoplasms/*pathology/physiopathology; Period Circadian Proteins; Receptors, Cytoplasmic and Nuclear/metabolism; Suprachiasmatic Nucleus/physiopathology; Transcription Factors/metabolism  
  Abstract Altered circadian rhythms predicted for poor survival in patients with metastatic colorectal or breast cancer. An increased incidence of cancers has been reported in flying attendants and in women working predominantly at night. To explore the contribution of circadian structure to tumor growth we ablated the 24-h rest-activity cycle and markedly altered the rhythms in body temperature, serum corticosterone and lymphocyte count in mice by complete stereotaxic destruction of the suprachiasmatic nuclei (SCN) or by subjecting the mice to experimental chronic jet-lag. Such disruption of circadian coordination significantly accelerated malignant growth in two transplantable tumor models, Glasgow osteosarcoma and Pancreatic adenocarcinoma. The mRNA expression of clock genes per2 and reverb-alpha in controls displayed significant circadian rhythms in the liver (Cosinor, p=0.006 and p=0.003, respectively) and in the tumor (p=0.04 and p<0.001, respectively). Both rhythms were suppressed in the liver and in the tumor of jet lagged mice. This functional disturbance of molecular clock resulted in down regulation of p53 and overexpression of c-Myc, two effects which may favor cancer growth. CONCLUSIONS: These results indicate that circadian system could play an important role in malignant growth control. This should be taken into consideration in cancer prevention and therapy.  
  Address INSERM E 354 Cancer Chronotherapeutics, Hopital Paul Brousse, Villejuif, France. filipski@vjf.inserm.fr  
  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:16596304 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 748  
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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 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  
Permanent link to this record
 

 
Author Fonken, L.K.; Nelson, R.J. url  doi
openurl 
  Title Dim light at night increases depressive-like responses in male C3H/HeNHsd mice Type Journal Article
  Year 2013 Publication Behavioural Brain Research Abbreviated Journal Behav Brain Res  
  Volume 243 Issue Pages 74-78  
  Keywords Affect/physiology; Anhedonia/physiology; Animals; Behavior, Animal/*physiology; Circadian Rhythm/*physiology; Depression/*etiology/physiopathology; Hippocampus/*metabolism/pathology; Light/*adverse effects; Male; Mice; Mice, Inbred C3H; Neuropsychological Tests; Photoperiod  
  Abstract Daily patterns of light exposure have become increasingly variable since the widespread adoption of electrical lighting during the 20th century. Seasonal fluctuations in light exposure, shift-work, and transmeridian travel are all associated with alterations in mood. These studies implicate fluctuations in environmental lighting in the development of depressive disorders. Here we argue that exposure to light at night (LAN) may be causally linked to depression. Male C3H/HeNHsd mice, which produce nocturnal melatonin, were housed in either a standard light/dark (LD) cycle or exposed to nightly dim (5 lux) LAN (dLAN). After four weeks in lighting conditions mice underwent behavioral testing and hippocampal tissue was collected at the termination of the study for qPCR. Here were report that mice exposed to dLAN increase depressive-like responses in both a sucrose anhedonia and forced swim test. In contrast to findings in diurnal grass rats, dLAN mice perform comparably to mice housed under dark nights in a hippocampus-dependent learning and memory task. TNFalpha and IL1beta gene expression do not differ between groups, demonstrating that changes in these pro-inflammatory cytokines do not mediate dLAN induced depressive-like responses in mice. BDNF expression is reduced in the hippocampus of mice exposed to dLAN. These results indicate that low levels of LAN can alter mood in mice. This study along with previous work implicates LAN as a potential factor contributing to depression. Further understanding of the mechanisms through which LAN contributes to changes in mood is important for characterizing and treating depressive disorders.  
  Address Department of Neuroscience, Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.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 0166-4328 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:23291153 Approved no  
  Call Number IDA @ john @ Serial 95  
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