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Ritonja, J.; McIsaac, M.A.; Sanders, E.; Kyba, C.C.M.; Grundy, A.; Cordina-Duverger, E.; Spinelli, J.J.; Aronson, K.J. |
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Title |
Outdoor light at night at residences and breast cancer risk in Canada |
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Journal Article |
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Year  |
2020 |
Publication |
European Journal of Epidemiology |
Abbreviated Journal |
Eur J Epidemiol |
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in press |
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Keywords |
Human Health; Breast cancer; Case-control study; Circadian disruption; Light at night; Night work; Women's health |
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Abstract |
Experimental and epidemiologic studies suggest that light at night (LAN) exposure disrupts circadian rhythm, and this disruption may increase breast cancer risk. We investigated the potential association between residential outdoor LAN and breast cancer risk. A population-based case-control study was conducted in Vancouver, British Columbia and Kingston, Ontario, Canada with incident breast cancer cases, and controls frequency matched by age in the same region. This analysis was restricted to 844 cases and 905 controls who provided lifetime residential histories. Using time-weighted average duration at each home 5-20 years prior to study entry, two measures of cumulative average outdoor LAN were calculated using two satellite data sources. Logistic regression was used to estimate the relationship between outdoor LAN and breast cancer risk, considering interactions for menopausal status and night shift work. We found no association between residential outdoor LAN and breast cancer for either measure of LAN [OR comparing highest vs. lowest tertile (DNB) = 0.95, 95% CI 0.70-1.27]. We also found no association when considering interactions for menopausal status and past/current night work status. These findings were robust to changes to years of residential data considered, residential mobility, and longer exposure windows. Our findings are consistent with studies reporting that outdoor LAN has a small effect or no effect on breast cancer risk. |
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Division of Cancer Care and Epidemiology, Cancer Research Institute, Queen's University, Kingston, ON, Canada. aronson@queensu.ca |
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0393-2990 |
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PMID:32026169 |
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Call Number |
GFZ @ kyba @ |
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2826 |
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Kyba, C.C.M.; Conrad, J.; Shatwell, T. |
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Title |
Lunar illuminated fraction is a poor proxy for moonlight exposure |
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Journal Article |
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Year |
2020 |
Publication |
Nature Ecology & Evolution |
Abbreviated Journal |
Nat Ecol Evol |
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4 |
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318-319 |
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Keywords |
Animals; Moonlight; Commentary |
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San-Jose et al. recently demonstrated that the colouration of barn owls impacts their hunting success under moonlit conditions, and therefore affects their reproductive success1. They found that near full-moon conditions, the youngest nestlings with white fathers were fed more and were likelier to survive than those with redder fathers. While the study is interesting, the percentage of the Moon that is illuminated (lunar illuminated fraction) is unfortunately a poor proxy for moonlight exposure. We suggest that lunar illluminated fraction should, in general, never be used in biological studies, as alternative variables such as horizontal illuminance better represent moonlight exposure, and therefore offer a greater chance of detecting the effects of moonlight. Here, we provide a brief explanation of how moonlight varies with season and time of night, and stress the need for greater collaboration between biologists and astronomers or physicists in such studies in the future. |
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Seenforschung, Helmholtz-Zentrum fur Umweltforschung-UFZ, Magdeburg, Germany |
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2397-334X |
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PMID:32015523 |
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GFZ @ kyba @ |
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2827 |
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Yue, F.; Xia, K.; Wei, L.; Xing, L.; Wu, S.; Shi, Y.; Man, L.S.; Shui, G.; Xiang, X.; Russell, R.; Zhang, D. |
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Title |
Effects of constant light exposure on sphingolipidomics and progression of NASH in high‐fat‐fed rats |
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Journal Article |
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Year |
2020 |
Publication |
Journal of Gastroenterology and Hepatology |
Abbreviated Journal |
J Gastroenterol Hepatol |
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in press |
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Animals; apoptosis; ceramide; light pollution; non-alcoholic fatty liver disease; sphingolipids |
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BACKGROUND AND AIM: Non-alcoholic fatty liver disease (NAFLD) is a growing public health concern worldwide. With the progression of urbanization, light pollution is becoming an inevitable risk factor for NAFLD. However, the role of light pollution on NAFLD is insufficiently understood, and the underlying mechanism remains unclear. The present study explored effects of constant light exposure on NAFLD and elucidated its related mechanisms. METHODS: Thirty-two male SD rats were divided into 4 groups (n=8 each): 1) rats on a normal diet exposed to standard light-dark cycle (ND-LD); 2) rats on a normal diet exposed to constant light (ND-LL); 3) rats on a high fat diet exposed to standard light-dark cycle (HFD-LD); 4) and rats on a high fat diet exposed to constant light (HFD-LL). After 12 weeks treatment, rats were sacrificed and pathophysiological assessments were performed. Targeted lipidomics was used to measure sphingolipids, including ceramides, glucosylceramides and lactosylceramides, sphingomyelins and sphingosine-1-phosphates in plasma and liver tissues. RESULTS: In normal chow rats, constant light exposure led to glucose abnormalities and dyslipidemia. In high-fat fed rats, constant light exposure exacerbated glucose abnormalities, dyslipidemia, insulin resistance, inflammation and aggravated steatohepatitis. Compared to HFD-LD rats, HFD-LL had decreased plasma sphingosine-1-phosphate and elevated liver concentrations of total ceramides and specific ceramide species (ceramide d18:0/24:0, ceramide d18:1/22:0, ceramide d18:1/24:0 and ceramide d18:1/24:1), and which were associated with increased hepatocyte apoptosis. CONCLUSIONS: Constant light exposure causes dysregulation of sphingolipids and promotes steatohepatitis in high-fat fed rats. |
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Department of Endocrinology, Xiangya Hospital, Central South University, Changsha, Hunan, China |
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0815-9319 |
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PMID:32027419 |
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GFZ @ kyba @ |
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2829 |
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Pan, Y.-R.; Song, J.-Y.; Fan, B.; Wang, Y.; Che, L.; Zhang, S.-M.; Chang, Y.-X.; He, C.; Li, G.-Y. |
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Title |
mTOR may interact with PARP-1 to regulate visible light-induced parthanatos in photoreceptors |
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Journal Article |
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Year |
2020 |
Publication |
Cell Communication and Signaling : CCS |
Abbreviated Journal |
Cell Commun Signal |
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18 |
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1 |
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27 |
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Keywords |
Health; Aif; Parp-1; Parthanatos; Retinal neuroprotection; Sirt1; mTOR |
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BACKGROUND: Excessive light exposure is a detrimental environmental factor that plays a critical role in the pathogenesis of retinal degeneration. However, the mechanism of light-induced death of retina/photoreceptor cells remains unclear. The mammalian/mechanistic target of rapamycin (mTOR) and Poly (ADP-ribose) polymerase-1 (PARP-1) have become the primary targets for treating many neurodegenerative disorders. The aim of this study was to elucidate the mechanisms underlying light-induced photoreceptor cell death and whether the neuroprotective effects of mTOR and PARP-1 inhibition against death are mediated through apoptosis-inducing factor (AIF). METHODS: Propidium iodide (PI)/Hoechst staining, lentiviral-mediated short hairpin RNA (shRNA), Western blot analysis, cellular fraction separation, plasmid transient transfection, laser confocal microscopy, a mice model, electroretinography (ERG), and hematoxylin-eosin (H & E) staining were employed to explore the mechanisms by which rapamycin/3-Aminobenzamide (3AB) exert neuroprotective effects of mTOR/PARP-1 inhibition in light-injured retinas. RESULTS: A parthanatos-like death mechanism was evaluated in light-injured 661 W cells that are an immortalized photoreceptor-like cell line that exhibit cellular and biochemical feature characteristics of cone photoreceptor cells. The death process featured over-activation of PARP-1 and AIF nuclear translocation. Either PARP-1 or AIF knockdown played a significantly protective role for light-damaged photoreceptors. More importantly, crosstalk was observed between mTOR and PARP-1 signaling and mTOR could have regulated parthanatos via the intermediate factor sirtuin 1 (SIRT1). The parthanatos-like injury was also verified in vivo, wherein either PARP-1 or mTOR inhibition provided significant neuroprotection against light-induced injury, which is evinced by both structural and functional retinal analysis. Overall, these results elucidate the mTOR-regulated parthanatos death mechanism in light-injured photoreceptors/retinas and may facilitate the development of novel neuroprotective therapies for retinal degeneration diseases. CONCLUSIONS: Our results demonstrate that inhibition of the mTOR/PARP-1 axis exerts protective effects on photoreceptors against visible-light-induced parthanatos. These protective effects are conducted by regulating the downstream factors of AIF, while mTOR possibly interacts with PARP-1 via SIRT1 to regulate parthanatos. Video Abstract Schematic diagram of mTOR interacting with PARP-1 to regulate visible light-induced parthanatos. Increased ROS caused by light exposure penetrates the nuclear membrane and causes nuclear DNA strand breaks. PARP-1 detects DNA breaks and synthesizes PAR polymers to initiate the DNA repair system that consumes a large amount of cellular NAD+. Over-production of PAR polymers prompts the release of AIF from the mitochondria and translocation to the nucleus, which leads to parthanatos. Activated mTOR may interact with PARP-1 via SIRT1 to regulate visible light-induced parthanatos. |
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Department of Ophthalmology, Second Hospital of JiLin University, No.218 Zi-Qiang St, ChangChun, 130041, China. liguangyu@aliyun.com |
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1478-811X |
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PMID:32066462 |
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Call Number |
GFZ @ kyba @ |
Serial |
2830 |
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Author |
Letzkus, L. |
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Title |
Red Light at Night: A Feasibility Study in Hospitalized Patients |
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Journal Article |
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Year |
2020 |
Publication |
MEDSURG Nursing |
Abbreviated Journal |
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29 |
Issue |
1 |
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38-42 |
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Keywords |
Human Health |
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Light can be a noxious stimulus during hospitalization. The study evaluated use of a red night-light intervention for hospitalized adults. The red light was found to be a feasible intervention and well received by participants. |
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GFZ @ kyba @ |
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2831 |
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