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Author Yasuniwa, Y.; Izumi, H.; Wang, K.-Y.; Shimajiri, S.; Sasaguri, Y.; Kawai, K.; Kasai, H.; Shimada, T.; Miyake, K.; Kashiwagi, E.; Hirano, G.; Kidani, A.; Akiyama, M.; Han, B.; Wu, Y.; Ieiri, I.; Higuchi, S.; Kohno, K. url  doi
openurl 
  Title Circadian disruption accelerates tumor growth and angio/stromagenesis through a Wnt signaling pathway Type Journal Article
  Year 2010 Publication PloS one Abbreviated Journal PLoS One  
  Volume 5 Issue 12 Pages e15330  
  Keywords Animals; *Circadian Rhythm; Disease Progression; *Gene Expression Regulation, Neoplastic; HeLa Cells; Humans; Male; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Neoplasms/*pathology; *Neovascularization, Pathologic; Nerve Tissue Proteins/metabolism; Skin/metabolism; Vascular Endothelial Growth Factor A/metabolism; Wnt Proteins/*metabolism; Oncogenesis  
  Abstract Epidemiologic studies show a high incidence of cancer in shift workers, suggesting a possible relationship between circadian rhythms and tumorigenesis. However, the precise molecular mechanism played by circadian rhythms in tumor progression is not known. To identify the possible mechanisms underlying tumor progression related to circadian rhythms, we set up nude mouse xenograft models. HeLa cells were injected in nude mice and nude mice were moved to two different cases, one case is exposed to a 24-hour light cycle (L/L), the other is a more “normal” 12-hour light/dark cycle (L/D). We found a significant increase in tumor volume in the L/L group compared with the L/D group. In addition, tumor microvessels and stroma were strongly increased in L/L mice. Although there was a hypervascularization in L/L tumors, there was no associated increase in the production of vascular endothelial cell growth factor (VEGF). DNA microarray analysis showed enhanced expression of WNT10A, and our subsequent study revealed that WNT10A stimulates the growth of both microvascular endothelial cells and fibroblasts in tumors from light-stressed mice, along with marked increases in angio/stromagenesis. Only the tumor stroma stained positive for WNT10A and WNT10A is also highly expressed in keloid dermal fibroblasts but not in normal dermal fibroblasts indicated that WNT10A may be a novel angio/stromagenic growth factor. These findings suggest that circadian disruption induces the progression of malignant tumors via a Wnt signaling pathway.  
  Address Department of Molecular Biology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan  
  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 1932-6203 ISBN Medium  
  Area (up) Expedition Conference  
  Notes PMID:21203463; PMCID:PMC3009728 Approved no  
  Call Number IDA @ john @ Serial 162  
Permanent link to this record
 

 
Author Meng, Y.; He, Z.; Yin, J.; Zhang, Y.; Zhang, T. url  doi
openurl 
  Title Quantitative calculation of human melatonin suppression induced by inappropriate light at night Type Journal Article
  Year 2011 Publication Medical & Biological Engineering & Computing Abbreviated Journal Med Biol Eng Comput  
  Volume 49 Issue 9 Pages 1083-1088  
  Keywords Algorithms; Circadian Rhythm/physiology/*radiation effects; Humans; *Lighting; Melatonin/*secretion; *Models, Biological; Retinal Cone Photoreceptor Cells/physiology/radiation effects; Retinal Ganglion Cells/physiology/radiation effects; Retinal Rod Photoreceptor Cells/physiology/radiation effects  
  Abstract Melatonin (C(1)(3)H(1)(6)N(2)O(2)) has a wide range of functions in the body. When is inappropriately exposed to light at night, human circadian rhythm will be interfered and then melatonin secretion will become abnormal. For nearly three decades great progresses have been achieved in analytic action spectra and melatonin suppression by various light conditions. However, so far few articles focused on the quantitative calculation of melatonin suppression induced by light. In this article, an algorithm is established, in which all the contributions of rods, cones, and intrinsically photosensitive retinal ganglion cells are considered. Calculation results accords with the experimental data in references very well, which indicate the validity of this algorithm. This algorithm can also interpret the rule of melatonin suppression varying with light correlated color temperature very well.  
  Address Photonics Research Center, School of Physics, Nankai University, Tianjin 300071, China  
  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 0140-0118 ISBN Medium  
  Area (up) Expedition Conference  
  Notes PMID:21717231 Approved no  
  Call Number IDA @ john @ Serial 236  
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Author LeGates, T.A.; Altimus, C.M.; Wang, H.; Lee, H.-K.; Yang, S.; Zhao, H.; Kirkwood, A.; Weber, E.T.; Hattar, S. url  doi
openurl 
  Title Aberrant light directly impairs mood and learning through melanopsin-expressing neurons Type Journal Article
  Year 2012 Publication Nature Abbreviated Journal Nature  
  Volume 491 Issue 7425 Pages 594-598  
  Keywords Affect/drug effects/physiology/*radiation effects; Animals; Antidepressive Agents/pharmacology; Body Temperature Regulation/physiology/radiation effects; Circadian Rhythm/physiology; Cognition/drug effects/physiology/radiation effects; Corticosterone/metabolism; Depression/etiology/physiopathology; Desipramine/pharmacology; Fluoxetine/pharmacology; Learning/drug effects/physiology/*radiation effects; *Light; Long-Term Potentiation/drug effects; Male; Memory/physiology/radiation effects; Mice; Photoperiod; Retinal Ganglion Cells/drug effects/*metabolism/*radiation effects; *Rod Opsins/analysis; Sleep/physiology; Wakefulness/physiology  
  Abstract The daily solar cycle allows organisms to synchronize their circadian rhythms and sleep-wake cycles to the correct temporal niche. Changes in day-length, shift-work, and transmeridian travel lead to mood alterations and cognitive function deficits. Sleep deprivation and circadian disruption underlie mood and cognitive disorders associated with irregular light schedules. Whether irregular light schedules directly affect mood and cognitive functions in the context of normal sleep and circadian rhythms remains unclear. Here we show, using an aberrant light cycle that neither changes the amount and architecture of sleep nor causes changes in the circadian timing system, that light directly regulates mood-related behaviours and cognitive functions in mice. Animals exposed to the aberrant light cycle maintain daily corticosterone rhythms, but the overall levels of corticosterone are increased. Despite normal circadian and sleep structures, these animals show increased depression-like behaviours and impaired hippocampal long-term potentiation and learning. Administration of the antidepressant drugs fluoxetine or desipramine restores learning in mice exposed to the aberrant light cycle, suggesting that the mood deficit precedes the learning impairments. To determine the retinal circuits underlying this impairment of mood and learning, we examined the behavioural consequences of this light cycle in animals that lack intrinsically photosensitive retinal ganglion cells. In these animals, the aberrant light cycle does not impair mood and learning, despite the presence of the conventional retinal ganglion cells and the ability of these animals to detect light for image formation. These findings demonstrate the ability of light to influence cognitive and mood functions directly through intrinsically photosensitive retinal ganglion cells.  
  Address Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, 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 0028-0836 ISBN Medium  
  Area (up) Expedition Conference  
  Notes PMID:23151476; PMCID:PMC3549331 Approved no  
  Call Number IDA @ john @ Serial 238  
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Author Gooley, J.J.; Rajaratnam, S.M.W.; Brainard, G.C.; Kronauer, R.E.; Czeisler, C.A.; Lockley, S.W. url  doi
openurl 
  Title Spectral responses of the human circadian system depend on the irradiance and duration of exposure to light Type Journal Article
  Year 2010 Publication Science Translational Medicine Abbreviated Journal Sci Transl Med  
  Volume 2 Issue 31 Pages 31ra33  
  Keywords Adolescent; Adult; Circadian Rhythm/physiology/*radiation effects; Dose-Response Relationship, Radiation; Humans; Light; Melatonin/secretion; Photoperiod; Phototherapy; Retina/physiology/radiation effects; Retinal Cone Photoreceptor Cells/physiology/radiation effects; Retinal Ganglion Cells/physiology/radiation effects; Rod Opsins/physiology; Young Adult; blue light; light at night; melatonin; melanopsin; light therapy  
  Abstract In humans, modulation of circadian rhythms by light is thought to be mediated primarily by melanopsin-containing retinal ganglion cells, not rods or cones. Melanopsin cells are intrinsically blue light-sensitive but also receive input from visual photoreceptors. We therefore tested in humans whether cone photoreceptors contribute to the regulation of circadian and neuroendocrine light responses. Dose-response curves for melatonin suppression and circadian phase resetting were constructed in subjects exposed to blue (460 nm) or green (555 nm) light near the onset of nocturnal melatonin secretion. At the beginning of the intervention, 555-nm light was equally effective as 460-nm light at suppressing melatonin, suggesting a significant contribution from the three-cone visual system (lambda(max) = 555 nm). During the light exposure, however, the spectral sensitivity to 555-nm light decayed exponentially relative to 460-nm light. For phase-resetting responses, the effects of exposure to low-irradiance 555-nm light were too large relative to 460-nm light to be explained solely by the activation of melanopsin. Our findings suggest that cone photoreceptors contribute substantially to nonvisual responses at the beginning of a light exposure and at low irradiances, whereas melanopsin appears to be the primary circadian photopigment in response to long-duration light exposure and at high irradiances. These results suggest that light therapy for sleep disorders and other indications might be optimized by stimulating both photoreceptor systems.  
  Address Division of Sleep Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115, 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 1946-6234 ISBN Medium  
  Area (up) Expedition Conference  
  Notes PMID:20463367 Approved no  
  Call Number IDA @ john @ Serial 294  
Permanent link to this record
 

 
Author Miler, M.; Sosic-Jurjevic, B.; Nestorovic, N.; Ristic, N.; Medigovic, I.; Savin, S.; Milosevic, V. url  doi
openurl 
  Title Morphological and functional changes in pituitary-thyroid axis following prolonged exposure of female rats to constant light Type Journal Article
  Year 2014 Publication Journal of Morphology Abbreviated Journal J Morphol  
  Volume 275 Issue 10 Pages 1161-1172  
  Keywords TSH cells; constant light; immunohistochemistry; pituitary; rat; thyroid; light exposure  
  Abstract Light regulates numerous physiological functions and synchronizes them with the environment, in part by adjusting secretion of different hormones. We hypothesized that constant light (CL) would disturb pituitary-thyroid axis. Our aim was to determine morphological and functional changes in this endocrine system in such extreme conditions and, based on the obtained results, to propose the underlying mechanism(s). Starting from the thirtieth postnatal day, female Wistar rats were exposed to CL (600 lx) for the following 95 days. The controls were maintained under the regular laboratory lighting conditions. After decapitation, pituitaries and thyroids were prepared for further histomorphometric, immunohistochemical, and immunofluorescence examinations. Concentration of thyroid stimulating hormone (TSH), total T4 and T3 (TH) were determined. Thyroid tissue of light-treated rats was characterized by microfollicular structure. We detected no change in total thyroid volume, localization and accumulation of thyroglobulin, thyroid peroxidase, and sodium-iodide symporter in the follicular epithelium of CL rats. The volume of follicular epithelium and activation index were increased, while volume of the colloid and serum levels of TH decreased. In the pituitary, the relative intensity of TSH beta-immunofluorescence signal within the cytoplasm of thyrotrophs increased, but their average cell volume and the relative volume density decreased. Serum TSH was unaltered. We conclude that exposure of female rats to CL induced alterations in pituitary-thyroid axis. Thyroid tissue was characterized by microfollicular structure. Serum TH levels were reduced without accompanying increase in serum TSH. We hypothesize that increased secretion and clearance of TH together with unchanged or even decreased hormonal synthesis, resulted in decreased serum TH levels in CL group. We assume this decrease consequently led to increased synthesis and/or accumulation of pituitary TSH. However, decreased average TSH cell volume and relative volume density, together with unchanged serum TSH, point to additional, negative regulation of thyrotrophs. J. Morphol., 2014. (c) 2014 Wiley Periodicals, Inc.  
  Address Department of Cytology, Institute for Biological Research “Sinisa Stankovic,” University of Belgrade, Belgrade, Serbia  
  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 0022-2887 ISBN Medium  
  Area (up) Expedition Conference  
  Notes PMID:24797691 Approved no  
  Call Number IDA @ john @ Serial 304  
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