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Author Shinobu Yasuo, Ayaka Iwamoto, Sang-il Lee, Shotaro Ochiai, Rina Hitachi, Satomi Shibata, Nobuo Uotsu, Chie Tarumizu, Sayuri Matsuoka, Mitsuhiro Furuse, Shigekazu Higuchi
Title L-Serine Enhances Light-Induced Circadian Phase Resetting in Mice and Humans Type Journal Article
Year 2017 Publication Journal of Nutrition Abbreviated Journal
Volume 147 Issue 12 Pages 2347-2355
Keywords (up) Animals; Human Health
Abstract Background: The circadian clock is modulated by the timing of ingestion or food composition, but the effects of specific nutrients are poorly understood.

Objective: We aimed to identify the amino acids that modulate the circadian clock and reset the light-induced circadian phase in mice and humans.

Methods: Male CBA/N mice were orally administered 1 of 20 L-amino acids, and the circadian and light-induced phase shifts of wheel-running activity were analyzed. Antagonists of several neurotransmitter pathways were injected before L-serine administration, and light-induced phase shifts were analyzed. In addition, the effect of L-serine on the light-induced phase advance was investigated in healthy male students (mean ± SD age 22.2 ± 1.8 y) by using dim-light melatonin onset (DLMO) determined by saliva samples as an index of the circadian phase.

Results: L-Serine administration enhanced light-induced phase shifts in mice (1.86-fold; P < 0.05). Both L-serine and its metabolite D-serine, a coagonist of N-methyl-D-aspartic acid (NMDA) receptors, exerted this effect, but D-serine concentrations in the hypothalamus did not increase after L-serine administration. The effect of L-serine was blocked by picrotoxin, an antagonist of &#947;-aminobutyric acid A receptors, but not by MK801, an antagonist of NMDA receptors. L-Serine administration altered the long-term expression patterns of clock genes in the suprachiasmatic nuclei. After advancing the light-dark cycle by 6 h, L-serine administration slightly accelerated re-entrainment to the shifted cycle. In humans, L-serine ingestion before bedtime induced significantly larger phase advances of DLMO after bright-light exposure during the morning (means ± SEMs—L-serine: 25.9 ± 6.6 min; placebo: 12.1 ± 7.0 min; P < 0.05).

Conclusion: These results suggest that L-serine enhances light-induced phase resetting in mice and humans, and it may be useful for treating circadian disturbances.
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Call Number LoNNe @ kyba @ Serial 1784
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Author Kronauer, R.E.; St Hilaire, M.A.; Rahman, S.A.; Czeisler, C.A.; Klerman, E.B.
Title An Exploration of the Temporal Dynamics of Circadian Resetting Responses to Short- and Long-Duration Light Exposures: Cross-Species Consistencies and Differences Type Journal Article
Year 2019 Publication Journal of Biological Rhythms Abbreviated Journal J Biol Rhythms
Volume 34 Issue 5 Pages 497-514
Keywords (up) Animals; Human Health
Abstract Light is the most effective environmental stimulus for shifting the mammalian circadian pacemaker. Numerous studies have been conducted across multiple species to delineate wavelength, intensity, duration, and timing contributions to the response of the circadian pacemaker to light. Recent studies have revealed a surprising sensitivity of the human circadian pacemaker to short pulses of light. Such responses have challenged photon counting-based theories of the temporal dynamics of the mammalian circadian system to both short- and long-duration light stimuli. Here, we collate published light exposure data from multiple species, including gerbil, hamster, mouse, and human, to investigate these temporal dynamics and explore how the circadian system integrates light information at both short- and long-duration time scales to produce phase shifts. Based on our investigation of these data sets, we propose 3 new interpretations: (1) intensity and duration are independent factors of total phase shift magnitude, (2) the possibility of a linear/log temporal function of light duration that is universal for all intensities for durations less than approximately 12 min, and (3) a potential universal minimum light duration of ~0.7 sec that describes a “dead zone” of light stimulus. We show that these properties appear to be consistent across mammalian species. These interpretations, if confirmed by further experiments, have important practical implications in terms of understanding the underlying physiology and for the design of lighting regimens to reset the mammalian circadian pacemaker.
Address Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, Massachusetts
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Language English Summary Language Original Title
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ISSN 0748-7304 ISBN Medium
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Notes PMID:31368391 Approved no
Call Number GFZ @ kyba @ Serial 2600
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Author Kernbach, M.E.; Newhouse, D.J.; Miller, J.M.; Hall, R.J.; Gibbons, J.; Oberstaller, J.; Selechnik, D.; Jiang, R.H.Y.; Unnasch, T.R.; Balakrishnan, C.N.; Martin, L.B.
Title Light pollution increases West Nile virus competence of a ubiquitous passerine reservoir species Type Journal Article
Year 2019 Publication Proceedings. Biological Sciences Abbreviated Journal Proc Biol Sci
Volume 286 Issue 1907 Pages 20191051
Keywords (up) Animals; Human Health; anthropogenic; ecoimmunology; host competence; light pollution; reservoir host
Abstract Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow (Passer domesticus), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas.
Address Center for Global Health Infectious Disease Research, University of South Florida, Tampa, FL 33620, USA
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ISSN 0962-8452 ISBN Medium
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Notes PMID:31337318; PMCID:PMC6661335 Approved no
Call Number GFZ @ kyba @ Serial 2611
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Author Xiang, S.; Dauchy, R.T.; Hoffman, A.E.; Pointer, D.; Frasch, T.; Blask, D.E.; Hill, S.M.
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
Series Editor Series Title Abbreviated Series Title
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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.
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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