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Author Xiang, S.; Dauchy, R.T.; Hoffman, A.E.; Pointer, D.; Frasch, T.; Blask, D.E.; Hill, S.M. url  doi
openurl 
  Title Epigenetic inhibition of the tumor suppressor ARHI by light at night-induced circadian melatonin disruption mediates STAT3-driven paclitaxel resistance in breast cancer Type Journal Article
  Year 2019 Publication Journal of Pineal Research Abbreviated Journal J Pineal Res  
  Volume 67 Issue 2 Pages e12586  
  Keywords (up) Animals; Human Health; Circadian Rhythm; Cancer; tumor suppression  
  Abstract Disruption of circadian time structure and suppression of circadian nocturnal melatonin (MLT) production by exposure to dim light at night (dLAN), as occurs with night shift work and/or disturbed sleep-wake cycles, is associated with a significantly increased risk of breast cancer and resistance to tamoxifen and doxorubicin. Melatonin inhibition of human breast cancer chemo-resistance involves mechanisms including suppression of tumor metabolism and inhibition of kinases and transcription factors which are often activated in drug-resistant breast cancer. Signal Transducer and Activator of Transcription 3 (STAT3), frequently overexpressed and activated in Paclitaxel (PTX)-resistant breast cancer, promotes the expression of DNA methyltransferase one (DNMT1) to epigenetically suppresses the transcription of tumor suppressor Aplasia Ras homolog one (ARHI) which can sequester STAT3 in the cytoplasm to block PTX-resistance. We demonstrate that breast tumor xenografts in rats exposed to dLAN and circadian MLT disrupted express elevated levels of phosphorylated and acetylated STAT3, increased DNMT1, but reduced Sirtuin 1 (SIRT1) and ARHI. Furthermore, MLT and/or SIRT1 administration blocked/reversed Interleukin 6 (IL-6)-induced acetylation of STAT3 and its methylation of ARH1 to increase ARH1 mRNA expression in MCF-7 breast cancer cells. Finally, analyses of the I-SPY 1 trial demonstrates that elevated MT1 receptor expression is significantly correlated with pathologic complete response following neo-adjuvant therapy in breast cancer patients. This is the first study to demonstrate circadian disruption of MLT by dLAN driving intrinsic resistance to PTX via epigenetic mechanisms increasing STAT3 expression and that MLT administration can reestablish sensitivity of breast tumors to PTX and drive tumor regression.  
  Address Tulane Circadian Cancer Biology Group, New Orleans, Louisiana  
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  Language English Summary Language Original Title  
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  Series Volume Series Issue Edition  
  ISSN 0742-3098 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31077613 Approved no  
  Call Number GFZ @ kyba @ Serial 2383  
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Author Nicholls, S. K., Casiraghi, L. P., Wang. W., Weber, E. T., & Harrington, M. E. url  openurl
  Title Evidence for Internal Desynchrony Caused by Circadian Clock Resetting Type Journal Article
  Year 2019 Publication Yale Journal of Biology and Medicine Abbreviated Journal  
  Volume 92 Issue 2 Pages 259-270  
  Keywords (up) Animals; Human Health; Review  
  Abstract Circadian disruption has been linked to markers for poor health outcomes in humans and animal models. What is it about circadian disruption that is problematic? One hypothesis is that phase resetting of the circadian system, which occurs in response to changes in environmental timing cues, leads to internal desynchrony within the organism. Internal desynchrony is understood as acute changes in phase relationships between biological rhythms from different cell groups, tissues, or organs within the body. Do we have strong evidence for internal desynchrony associated with or caused by circadian clock resetting? Here we review the literature, highlighting several key studies from measures of gene expression in laboratory rodents. We conclude that current evidence offers strong support for the premise that some protocols for light-induced resetting are associated with internal desynchrony. It is important to continue research to test whether internal desynchrony is necessary and/or sufficient for negative health impact of circadian disruption.  
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  Notes Approved no  
  Call Number IDA @ intern @ Serial 2631  
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Author Walker, W.H. 2nd; Borniger, J.C.; Gaudier-Diaz, M.M.; Hecmarie Melendez-Fernandez, O.; Pascoe, J.L.; Courtney DeVries, A.; Nelson, R.J. url  doi
openurl 
  Title Acute exposure to low-level light at night is sufficient to induce neurological changes and depressive-like behavior Type Journal Article
  Year 2019 Publication Molecular Psychiatry Abbreviated Journal Mol Psychiatry  
  Volume Issue Pages s41380  
  Keywords (up) Animals; mouse models; mood disorders; Human Health  
  Abstract The advent and wide-spread adoption of electric lighting over the past century has profoundly affected the circadian organization of physiology and behavior for many individuals in industrialized nations; electric lighting in homes, work environments, and public areas have extended daytime activities into the evening, thus, increasing night-time exposure to light. Although initially assumed to be innocuous, chronic exposure to light at night (LAN) is now associated with increased incidence of cancer, metabolic disorders, and affective problems in humans. However, little is known about potential acute effects of LAN. To determine whether acute exposure to low-level LAN alters brain function, adult male, and female mice were housed in either light days and dark nights (LD; 14 h of 150 lux:10 h of 0 lux) or light days and low level light at night (LAN; 14 h of 150 lux:10 h of 5 lux). Mice exposed to LAN on three consecutive nights increased depressive-like responses compared to mice housed in dark nights. In addition, female mice exposed to LAN increased central tendency in the open field. LAN was associated with reduced hippocampal vascular endothelial growth factor-A (VEGF-A) in both male and female mice, as well as increased VEGFR1 and interleukin-1beta mRNA expression in females, and reduced brain derived neurotrophic factor mRNA in males. Further, LAN significantly altered circadian rhythms (activity and temperature) and circadian gene expression in female and male mice, respectively. Altogether, this study demonstrates that acute exposure to LAN alters brain physiology and can be detrimental to well-being in otherwise healthy individuals.  
  Address Department of Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, 26506, USA  
  Corporate Author Thesis  
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  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1359-4184 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31138889; PMCID:PMC6881534 Approved no  
  Call Number GFZ @ kyba @ Serial 2768  
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Author Walker, W.H. 2nd; Melendez-Fernandez, O.H.; Nelson, R.J. url  doi
openurl 
  Title Prior exposure to dim light at night impairs dermal wound healing in female C57BL/6 mice Type Journal Article
  Year 2019 Publication Archives of Dermatological Research Abbreviated Journal Arch Dermatol Res  
  Volume 311 Issue 7 Pages 573-576  
  Keywords (up) Animals; mouse models; Skin; Human Health  
  Abstract Artificial light at night (LAN) is a pervasive phenomenon in today's society, and the detrimental consequences of LAN exposure are becoming apparent. LAN is associated with the increased incidence of metabolic disorders, cancers, mood alterations, and immune dysfunction in mammals. Consequently, we examined the effects of dim LAN (DLAN) on wound healing. Female C57BL/6 mice were housed for 3 weeks in DLAN or LD conditions prior to wounding. Following wounding, mice were maintained in either their previous light conditions or switched to the opposite lighting conditions for 3 weeks. DLAN prior to wounding impaired healing; specifically, mice in DLAN/DLAN had significantly larger wounds on day 8. Additionally, mice in DLAN/LD had significantly larger wounds on days 5, 7, 8, and 9, and increased average time to closure. These data demonstrate a potential harmful effect of DLAN on wound healing that should be considered and may represent a target for therapeutic intervention.  
  Address Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, 26506, 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 0340-3696 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31144020 Approved no  
  Call Number GFZ @ kyba @ Serial 2515  
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Author Kyba, C.C.M.; Aronson, K.J. url  doi
openurl 
  Title Assessing Exposure to Outdoor Lighting and Health Risks Type Journal Article
  Year 2015 Publication Epidemiology Abbreviated Journal Epidemiology  
  Volume 26 Issue 4 Pages e50  
  Keywords (up) Commentary, Human Health  
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  Series Volume Series Issue Edition  
  ISSN 1044-3983 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number LoNNe @ christopher.kyba @ Serial 1164  
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