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Author Kalousová, L.; Xiao, B.; Burgard, S.A.
Title Material hardship and sleep: results from the Michigan Recession and Recovery Study Type Journal Article
Year 2019 Publication Sleep Health Abbreviated Journal Sleep Health
Volume 5 Issue 2 Pages 113-127
Keywords Human Health; Remote Sensing; Sleep; sleep inequality; Society; sleep outcomes
Abstract Objective

Sleep is unequally distributed in the US population. People with low socioeconomic status report worse quality and shorter sleep than people with high socioeconomic status. Past research hypothesized that a potential reason for this link could be exposure to material hardship. This study examines the associations between several material hardships and sleep outcomes.

Methods

We use population-representative cross-sectional data (n = 730) from the Michigan Recession and Recovery Study collected in 2013 and examine the associations between 6 indicators of material hardship (employment instability, financial problems, housing instability, food insecurity, forgone medical care, and the total number of material hardships reported) and 3 sleep outcomes (short sleep, sleep problems, and nonrestorative sleep). We build multivariable logistic regression models controlling for respondents’ characteristics and light pollution near their residence.

Results

In unadjusted models, all material hardships were associated with negative sleep outcomes. In adjusted models, forgone medical care was a statistically significant predictor of nonrestorative sleep (average marginal effect 0.16), as was employment instability (average marginal effect 0.12). The probability of sleep problems and nonrestorative sleep increased with a greater number of hardships overall (average marginal effects of .02 and .05, respectively). We found marginally statistically significant positive associations between food insecurity and short sleep and sleep problems.

Conclusions

This study finds that, except when considering foregone medical care, employment instability, and total count of material hardships, associations between material hardship and negative sleep outcomes are not statistically significant after adjusting for a robust set of sociodemographic and health characteristics.
Address (down) Nuffield College, 1 New Rd, Oxford, OX1 1NF, United Kingdom; lucie.kalousova(at)nuffield.ox.ac.uk
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 2352-7218 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number GFZ @ kyba @ Serial 2180
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Author Schirmer, A.E.; Gallemore, C.; Liu, T.; Magle, S.; DiNello, E.; Ahmed, H.; Gilday, T.
Title Mapping behaviorally relevant light pollution levels to improve urban habitat planning Type Journal Article
Year 2019 Publication Scientific Reports Abbreviated Journal Sci Rep
Volume 9 Issue 1 Pages 1-13
Keywords Animals; Remote Sensing; Society; remote sensing; cities; Urban planning; urban wildlife; urban ecology
Abstract Artificial nighttime lights have important behavioral and ecological effects on wildlife. Combining laboratory and field techniques, we identified behaviorally relevant levels of nighttime light and mapped the extent of these light levels across the city of Chicago. We began by applying a Gaussian finite mixture model to 998 sampled illumination levels around Chicago to identify clusters of light levels. A simplified sample of these levels was replicated in the laboratory to identify light levels at which C57BL/6J mice exhibited altered circadian activity patterns. We then used camera trap and high-altitude photographic data to compare our field and laboratory observations, finding activity pattern changes in the field consistent with laboratory observations. Using these results, we mapped areas across Chicago exposed to estimated illumination levels above the value associated with statistically significant behavioral changes. Based on this measure, we found that as much as 36% of the greenspace in the city is in areas illuminated at levels greater than or equal to those at which we observe behavioral differences in the field and in the laboratory. Our findings provide evidence that artificial lighting patterns may influence wildlife behavior at a broad scale throughout urban areas, and should be considered in urban habitat planning.
Address (down) Northeastern Illinois University, Dept. of Biology, 5500 St. Louis Ave., Chicago, IL, 60625, USA; a-schirmer(at) neiu.edu)
Corporate Author Thesis
Publisher Nature Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 2045-2322 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 2615
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Author Nickla, D.L.
Title Ocular diurnal rhythms and eye growth regulation: where we are 50 years after Lauber Type Journal Article
Year 2013 Publication Experimental eye Research Abbreviated Journal Exp Eye Res
Volume 114 Issue Pages 25-34
Keywords Vision; Human Health; Review
Abstract Many ocular processes show diurnal oscillations that optimize retinal function under the different conditions of ambient illumination encountered over the course of the 24 h light/dark cycle. Abolishing the diurnal cues by the use of constant darkness or constant light results in excessive ocular elongation, corneal flattening, and attendant refractive errors. A prevailing hypothesis is that the absence of the Zeitgeber of light and dark alters ocular circadian rhythms in some manner, and results in an inability of the eye to regulate its growth in order to achieve emmetropia, the matching of the front optics to eye length. Another visual manipulation that results in the eye growth system going into a “default” mode of excessive growth is form deprivation, in which a translucent diffuser deprives the eye of visual transients (spatial or temporal) while not significantly reducing light levels; these eyes rapidly elongate and become myopic. It has been hypothesized that form deprivation might constitute a type of “constant condition” whereby the absence of visual transients drives the eye into a similar default mode as that in response to constant light or dark. Interest in the potential influence of light cycles and ambient lighting in human myopia development has been spurred by a recent study showing a positive association between the amount of time that children spent outdoors and a reduced prevalence of myopia. The growing eyes of chickens and monkeys show a diurnal rhythm in axial length: Eyes elongate more during the day than during the night. There is also a rhythm in choroidal thickness that is in approximate anti-phase to the rhythm in eye length. The phases are altered in eyes growing too fast, in response to form deprivation or negative lenses, or too slowly, in response to myopic defocus, suggesting an influence of phase on the emmetropization system. Other potential rhythmic influences include dopamine and melatonin, which form a reciprocal feedback loop, and signal “day” and “night” respectively. Retinal dopamine is reduced during the day in form deprived myopic eyes, and dopamine D2 agonists inhibit ocular growth in animal models. Rhythms in intraocular pressure as well, may influence eye growth, perhaps as a mechanical stimulus triggering changes in scleral extracellular matrix synthesis. Finally, evidence shows varying influences of environmental lighting parameters on the emmetropization system, such as high intensity light being protective against myopia in chickens. This review will cover the evidence for the possible influence of these various factors on ocular growth. The recognition that ocular rhythms may play a role in emmetropization is a first step toward understanding how they may be manipulated in treatment therapies to prevent myopia in humans.
Address (down) New England College of Optometry, Department of Biosciences, 424 Beacon Street, Boston, MA 02115, USA. nicklad@neco.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 0014-4835 ISBN Medium
Area Expedition Conference
Notes PMID:23298452; PMCID:PMC3742730 Approved no
Call Number GFZ @ kyba @ Serial 1987
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Author Leise, T.L.; Goldberg, A.; Michael, J.; Montoya, G.; Solow, S.; Molyneux, P.; Vetrivelan, R.; Harrington, M.E.
Title Recurring circadian disruption alters circadian clock sensitivity to resetting Type Journal Article
Year 2018 Publication The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci
Volume in press Issue Pages
Keywords Animals
Abstract A single phase advance of the light:dark (LD) cycle can temporarily disrupt synchrony of neural circadian rhythms within the suprachiasmatic nucleus (SCN) and between the SCN and peripheral tissues. Compounding this, modern life can involve repeated disruptive light conditions. To model chronic disruption to the circadian system, we exposed male mice to more than a month of a 20 h light cycle (LD10:10), which mice typically cannot entrain to. Control animals were housed under LD12:12. We measured locomotor activity and body temperature rhythms in vivo, and rhythms of PER2::LUC bioluminescence in SCN and peripheral tissues ex vivo. Unexpectedly, we discovered strong effects of the time of dissection on circadian phase of PER2::LUC bioluminescent rhythms, which varied across tissues. White adipose tissue was strongly reset by dissection, while thymus phase appeared independent of dissection timing. Prior light exposure impacted the SCN, resulting in strong resetting of SCN phase by dissection for mice housed under LD10:10, and weak phase shifts by time of dissection in SCN from control LD12:12 mice. These findings suggest that exposure to circadian disruption may desynchronize SCN neurons, increasing network sensitivity to perturbations. We propose that tissues with a weakened circadian network, such as the SCN under disruptive light conditions, or with little to no coupling, e.g., some peripheral tissues, will show increased resetting effects. In particular, exposure to light at inconsistent circadian times on a recurring weekly basis disrupts circadian rhythms and alters sensitivity of the SCN neural pacemaker to dissection time. This article is protected by copyright. All rights reserved.
Address (down) Neuroscience Program, Smith College, Northampton, MA, 01063, 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 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30269396 Approved no
Call Number GFZ @ kyba @ Serial 2036
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Author Sharma, A.; Goyal, R.
Title Long-term exposure to constant light induces dementia, oxidative stress and promotes aggregation of sub-pathological Abeta42 in Wistar rats Type Journal Article
Year 2020 Publication Pharmacology, Biochemistry, and Behavior Abbreviated Journal Pharmacol Biochem Behav
Volume in press Issue Pages 172892
Keywords Animals; Amyloid beta; Behavior, fluoxetine, rifampicin; Oxidative stress
Abstract Constant exposure to light is prevalent in modern society where light noise, shift work, and jet lag is common. Constant light exposure disrupts circadian rhythm, induces stress and thus influences memory performance. We subjected adult male Wistar rats to a two-month exposure to constant light (LL), constant dark or normal light-dark cycles. Significant cognitive impairment and oxidative stress were observed in LL rats without a significant elevation in soluble Abeta1-42 levels. Next, we examined whether long-term exposure to constant light may accelerate dementia in a sub-pathological Abeta model of rats. Normal control rats received ACSF, AD rats received 440pmol, and sub-pathological Abeta rats (Abeta(s)) received 220pmol of human Abeta42 peptide in a single unilateral ICV administration. Sub-pathological Abeta rats exposed to constant light (LL+Abeta(s)) show significant memory deficits and oxidative damage, although not significantly different from LL rats. Additionally, constant light promoted aggregation of exogenous Abeta42 in LL+Abeta(s) rats shown by the presence of congophilic plaques. Furthermore, chronic fluoxetine treatment (5mg/kg/day) rescued rats from the behavioral deficits, oxidative damage and amyloid aggregation. Whereas, rifampicin treatment (20mg/kg/day) did not reverse the behavioral deficits or oxidative stress but rescued rats from amyloid plaque formation. It was concluded that constant light for two months induces behavioral deficits, oxidative stress, and accelerates aggregation of sub-pathological concentrations of human-Abeta42 peptides in Wistar rats, which is reversed by daily fluoxetine administration.
Address (down) Neuropharmacology Laboratory, School of Pharmaceutical Sciences, Shoolini University, Solan 173 212, Himachal Pradesh, India. Electronic address: rohitgoyal@shooliniuniversity.com
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 0091-3057 ISBN Medium
Area Expedition Conference
Notes PMID:32142744 Approved no
Call Number GFZ @ kyba @ Serial 2841
Permanent link to this record