| Records |
Author  |
Femia, N.; Fortunato, M.; Vitelli, M. |
| Title |
Light-to-Light: PV-Fed LED Lighting Systems |
Type |
Journal Article |
| Year |
2013 |
Publication |
IEEE Transactions on Power Electronics |
Abbreviated Journal |
IEEE Trans. Power Electron. |
| Volume |
28 |
Issue |
8 |
Pages |
4063-4073 |
| Keywords |
light-to-light systems; outdoor lighting; lighting technology; LED; LED lighting; photovoltaics; PV |
| Abstract |
This paper discusses the principle of operation, dynamic modeling, and control design for light-to-light (LtL) systems, whose aim is to directly convert the sun irradiation into artificial light. The system discussed in this paper is composed by a photovoltaic (PV) panel, an LED array, a dc-dc converter dedicated to the maximum power point tracking of the PV panel and a dc-dc converter dedicated to drive the LEDs array. A system controller is also included, whose goal is to ensure the matching between the maximum available PV power and the LED power by means of a low-frequency LEDs dimming. An experimental design example is discussed to illustrate the functionalities of the LtL system. |
| Address |
Dipt. di Ing. Elettron. e Ing. Inf., Univ. of Salerno, Salerno, Italy |
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0885-8993 |
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IDA @ john @ |
Serial |
331 |
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| Author |
Figueiro, M.G.; Wood, B.; Plitnick, B.; Rea, M.S. |
| Title |
The impact of watching television on evening melatonin levels: Impact of watching television on evening melatonin |
Type |
Journal Article |
| Year |
2013 |
Publication |
Journal of the Society for Information Display |
Abbreviated Journal |
Jnl Soc Info Display |
| Volume |
21 |
Issue |
10 |
Pages |
417-421 |
| Keywords |
Human Health; television; correlated color temperature; sleep; melatonin levels; blue light; circadian disruption |
| Abstract |
Self-luminous electronic devices emit optical radiation at short wavelengths, close to the peak sensitivity of melatonin suppression. The present paper investigated if light from a 178-cm (70 in.) television suppressed melatonin. Results showed that light from televisions does not impact melatonin levels in the evening. |
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| ISSN |
1071-0922 |
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no |
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LoNNe @ christopher.kyba @ |
Serial |
498 |
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| Author |
Fonken, L.K.; Aubrecht, T.G.; Melendez-Fernandez, O.H.; Weil, Z.M.; Nelson, R.J. |
| Title |
Dim light at night disrupts molecular circadian rhythms and increases body weight |
Type |
Journal Article |
| Year |
2013 |
Publication |
Journal of Biological Rhythms |
Abbreviated Journal |
J Biol Rhythms |
| Volume |
28 |
Issue |
4 |
Pages |
262-271 |
| Keywords |
Animals; Blood Glucose/metabolism; Body Weight/*physiology; CLOCK Proteins/biosynthesis/genetics; Circadian Rhythm/*physiology; Corticosterone/metabolism; Feeding Behavior/physiology; Immunohistochemistry; Light; *Lighting; Male; Mice; Motor Activity; Polymerase Chain Reaction; Suprachiasmatic Nucleus/metabolism/physiology; clock genes; feeding rhythm; light pollution; obesity |
| Abstract |
With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption. |
| Address |
Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.edu |
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English |
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0748-7304 |
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| Notes |
PMID:23929553; PMCID:PMC4033305 |
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no |
| Call Number |
IDA @ john @ |
Serial |
28 |
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| Author |
Fonken, L.K.; Lieberman, R.A.; Weil, Z.M.; Nelson, R.J. |
| Title |
Dim light at night exaggerates weight gain and inflammation associated with a high-fat diet in male mice |
Type |
Journal Article |
| Year |
2013 |
Publication |
Endocrinology |
Abbreviated Journal |
Endocrinology |
| Volume |
154 |
Issue |
10 |
Pages |
3817-3825 |
| Keywords |
Adipose Tissue, White/*immunology/metabolism/pathology; Animals; Antigens, CD11b/biosynthesis/genetics/metabolism; Appetite Regulation/*radiation effects; Arcuate Nucleus/*immunology/metabolism/pathology; Behavior, Animal/radiation effects; Circadian Rhythm; Cytokines/biosynthesis/genetics/metabolism; Diet, High-Fat/*adverse effects; Feeding Behavior/radiation effects; Gene Expression Regulation; Glucose Intolerance/etiology/immunology/metabolism/pathology; I-kappa B Kinase/biosynthesis/genetics/metabolism; Insulin Resistance; Lighting/*adverse effects; Male; Mice; Microglia/immunology/metabolism/pathology; Nerve Tissue Proteins/biosynthesis/genetics/metabolism; Obesity/*etiology/immunology/metabolism/pathology; Random Allocation; *Weight Gain |
| Abstract |
Elevated nighttime light exposure is associated with symptoms of metabolic syndrome. In industrialized societies, high-fat diet (HFD) and exposure to light at night (LAN) often cooccur and may contribute to the increasing obesity epidemic. Thus, we hypothesized that dim LAN (dLAN) would provoke additional and sustained body mass gain in mice on a HFD. Male mice were housed in either a standard light/dark cycle or dLAN and fed either chow or HFD. Exposure to dLAN and HFD increase weight gain, reduce glucose tolerance, and alter insulin secretion as compared with light/dark cycle and chow, respectively. The effects of dLAN and HFD appear additive, because mice exposed to dLAN that were fed HFD display the greatest increases in body mass. Exposure to both dLAN and HFD also change the timing of food intake and increase TNFalpha and MAC1 gene expression in white adipose tissue after 4 experimental weeks. Changes in MAC1 gene expression occur more rapidly due to HFD as compared with dLAN; after 5 days of experimental conditions, mice fed HFD already increase MAC1 gene expression in white adipose tissue. HFD also elevates microglia activation in the arcuate nucleus of the hypothalamus and hypothalamic TNFalpha, IL-6, and Ikbkb gene expression. Microglia activation is increased by dLAN, but only among chow-fed mice and dLAN does not affect inflammatory gene expression. These results suggest that dLAN exaggerates weight gain and peripheral inflammation associated with HFD. |
| Address |
Department of Neuroscience, Wexner Medical Center, The Ohio State University, 636 Biomedical Research Tower, 460 West 12th Avenue, Columbus, Ohio 43210. fonken.1@osu.edu |
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English |
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0013-7227 |
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| Notes |
PMID:23861373 |
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no |
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IDA @ john @ |
Serial |
93 |
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| Author |
Fonken, L.K.; Nelson, R.J. |
| Title |
Dim light at night increases depressive-like responses in male C3H/HeNHsd mice |
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Journal Article |
| Year |
2013 |
Publication |
Behavioural Brain Research |
Abbreviated Journal |
Behav Brain Res |
| Volume |
243 |
Issue |
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Pages |
74-78 |
| Keywords |
Affect/physiology; Anhedonia/physiology; Animals; Behavior, Animal/*physiology; Circadian Rhythm/*physiology; Depression/*etiology/physiopathology; Hippocampus/*metabolism/pathology; Light/*adverse effects; Male; Mice; Mice, Inbred C3H; Neuropsychological Tests; Photoperiod |
| Abstract |
Daily patterns of light exposure have become increasingly variable since the widespread adoption of electrical lighting during the 20th century. Seasonal fluctuations in light exposure, shift-work, and transmeridian travel are all associated with alterations in mood. These studies implicate fluctuations in environmental lighting in the development of depressive disorders. Here we argue that exposure to light at night (LAN) may be causally linked to depression. Male C3H/HeNHsd mice, which produce nocturnal melatonin, were housed in either a standard light/dark (LD) cycle or exposed to nightly dim (5 lux) LAN (dLAN). After four weeks in lighting conditions mice underwent behavioral testing and hippocampal tissue was collected at the termination of the study for qPCR. Here were report that mice exposed to dLAN increase depressive-like responses in both a sucrose anhedonia and forced swim test. In contrast to findings in diurnal grass rats, dLAN mice perform comparably to mice housed under dark nights in a hippocampus-dependent learning and memory task. TNFalpha and IL1beta gene expression do not differ between groups, demonstrating that changes in these pro-inflammatory cytokines do not mediate dLAN induced depressive-like responses in mice. BDNF expression is reduced in the hippocampus of mice exposed to dLAN. These results indicate that low levels of LAN can alter mood in mice. This study along with previous work implicates LAN as a potential factor contributing to depression. Further understanding of the mechanisms through which LAN contributes to changes in mood is important for characterizing and treating depressive disorders. |
| Address |
Department of Neuroscience, Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.edu |
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English |
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0166-4328 |
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| Notes |
PMID:23291153 |
Approved |
no |
| Call Number |
IDA @ john @ |
Serial |
95 |
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