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Purpose: Given the potential role of light and its wavelength on ocular growth, this study investigated the effect of short-term exposure to red, cyan and blue light on ocular biometry in humans., Methods: Forty-four young adults and 20 children, comprising emmetropes and myopes, underwent 2-h sessions of cyan (507 nm), red (638 nm) and broadband white light on three separate days via light-emitting glasses. Additionally, young adults were exposed to blue light (454 nm) on an additional day. Axial length (AL) and choroidal thickness (CT) were measured in the right eye before the light exposure (0 min), after 60 and 120 min of exposure and 30 min after light offset using an optical biometer and optical coherence tomographer, respectively., Results: Compared to broadband light, exposure to red light resulted in a significant increase in AL (mean difference between white and red light at 120 min, +0.007 mm [0.002]), but no significant change in CT, while cyan light caused a significant AL reduction (-0.010 mm [0.003]) and choroidal thickening (+0.008 mm [0.002]) in young adults (p < 0.05). Blue light caused a significant decrease of -0.007 mm (0.002) in young adult eyes at 60 min (p < 0.05). In children, cyan light led to a significant reduction in AL (-0.016 mm [0.004]) and strong sustained choroidal thickening (+0.014 mm [0.004]) compared to broadband light at 120 min (p < 0.05). The effects of cyan light on AL and CT were found to be stronger in myopic young adults and emmetropic children. The opposing effects of red and cyan light on ocular biometry were similar between the two age groups (p > 0.05)., Conclusions: Exposure to cyan light resulted in AL reduction and choroidal thickening in both young adults and children. Further research is needed to determine the application of these results in developing interventions for myopia control., (© 2024 The Author(s). Ophthalmic and Physiological Optics published by John Wiley & Sons Ltd on behalf of College of Optometrists.)

Visible light serves as a crucial medium for vision formation.;however, prolonged or excessive exposure to light is recognized as a significant etiological factor contributing to retinal degenerative diseases. The retina, with its unique structure and adaptability, relies on the homeostasis of cellular functions to maintain visual health. Under normal conditions, the retina can mount adaptive responses to various insults, including light-induced damage. Unfortunately, exposure to intense and excessive light triggers a cascade of pathological alterations in retinal photoreceptor cells, pigment epithelial cells, ganglion cells, and glial cells. These alterations encompass disruption of intracellular REDOX and Ca²⁺ homeostasis, pyroptosis, endoplasmic reticulum stress, autophagy, and the release of inflammatory cytokines, culminating in irreversible retinal damage. We first delineate the mechanisms of retinal light damage through 4 main avenues: mitochondria function, endoplasmic reticulum stress, cell autophagy, and inflammation. Subsequently, we discuss protective strategies against retinal light damage, aiming to guide research toward the prevention and treatment of light-induced retinal conditions., Competing Interests: Declaration of Competing Interest All authors disclosed no relevant relationships., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: The development of the zebrafish visual system is significantly influenced by exposure to monochromatic light, yet investigations into its effects during juvenile stages are lacking. This study evaluated the impacts of varying intensities and durations of red and blue monochromatic light on the visual system and dopamine pathways in juvenile zebrafish., Methods: Juvenile zebrafish were exposed to red (650 nm) and blue (440 nm, 460 nm) monochromatic lights over four days at intensities ranging from 500 to 10,000 lx, for durations of 6, 10, and 14 h daily. A control group was maintained under standard laboratory conditions. Post-exposure assessments included the optokinetic response (OKR), retinal structural analysis, ocular dopamine levels, and the expression of genes related to dopamine pathways (Th, Dat, and Mao)., Results: (1) OKR enhancement was observed with increased 440 nm light intensity, while 460 nm and 650 nm light exposures showed initial improvements followed by declines at higher intensities. (2) Retinal thinning in the outer nuclear layer was observed under the most intense (10,000 lx for 14 h) light conditions in the 440 nm and 650 nm groups, while the 460 nm group remained unaffected. (3) Dopamine levels increased with higher intensities in the 440 nm group, whereas the 460 nm group exhibited initial increases followed by decreases. The 650 nm group displayed similar trends but were statistically insignificant compared to the control group. (4) Th expression increased with light intensity in the 440 nm group. Dat showed a rising and then declining pattern, and Mao expression significantly decreased. The 460 nm group exhibited similar patterns for Th and Dat to the behavioral observations, but an inverse pattern for Mao. The 650 nm group presented significant fluctuations in Th and Dat expressions, with pronounced variations in Mao., Conclusions: Specific red and blue monochromatic light conditions promote visual system development in juvenile zebrafish. However, exceeding these optimal conditions may impair visual function, highlighting the critical role of dopamine pathway in modulating light-induced effects on the visual system., (© 2024. The Author(s).)

This study aims to investigate the effect of the selective MT2 receptor agonist, IIK7, on corneal autophagy and apoptosis, aiming to reduce corneal epithelial damage and inflammation from blue light exposure in mice. Eight-week-old C57BL/6 mice were divided into BL-exposed (BL) and BL-exposed with IIK7 treatment (BL + IIK7 group). Mice underwent blue light exposure (410 nm, 100 J) twice daily with assessments at baseline and on days 3, 7, and 14. Corneal samples were analyzed for MT2 receptor expression, autophagy markers (LC3-II and p62), and apoptosis indicators (BAX expression and TUNEL assay). Then, mice were assigned to normal control, BL, and BL + IIK7. Ocular surface parameters, including corneal fluorescein staining scores, tear volume, and tear film break-up time, were evaluated on days 7 and 14. On day 14, reactive oxygen species (ROS) levels and CD4 + IFN-γ + T cells percentages were measured. The BL group exhibited higher LC3-II and p62 expression, while the BL + IIK7 group showed reduced expression ( p < 0.05). The TUNEL assay showed reduced apoptosis in the BL + IIK7 group compared to the BL group. ROS levels were lower in the BL + IIK7 group. The BL + IIK7 group showed improved ocular surface parameters, including decreased corneal fluorescein staining and increased tear volume. The percentages of CD4 + IFN-γ + T cells indicated reduced inflammatory responses in the BL + IIK7 group. The MT2 receptor agonist IIK7 regulates corneal autophagy and apoptosis, reducing corneal epithelial damage and inflammation from blue light exposure.

During the wound healing process, the activation of signal transducer and activator of transcription 3 (STAT3) is considered crucial for the migration and proliferation of epithelial cells, as well as for establishing the inflammatory environment. However, an excessive STAT3 activation aggravates scar formation. Here we show that 450 nm blue light and 630 nm red light can differentially regulate the phosphorylation of STAT3 (p-STAT3) and its downstream cytokines in keratinocytes. Further mechanistic studies reveal that red light promotes wound healing by activating the PI3 kinase p110 beta (PI3Kβ)/STAT3 signaling axis, while blue light inhibits p-STAT3 at the wound site by modulating cytochrome c-P450 (CYT-P450) activity and reactive oxygen species (ROS) generation. In a mouse scar model, skin wound healing can be significantly accelerated with red light followed by blue light to reduce scar formation. In summary, our study presents a potential strategy for regulating epithelial cell p-STAT3 through visible light to address skin scarring issues and elucidates the underlying mechanisms., (© 2024. The Author(s).)

Short-wavelength blue light is ubiquitous in daily life and has a lasting destructive influence. Its potential harm to biological health is significant. This study used Drosophila as a model organism to investigate the protective effects of kaempferol, a flavonoid, against the toxicity of blue light. It also examined its physiological effects on Drosophila under blue light irradiation. In this experiment, fruit flies were fed with three different concentrations of kaempferol solutions (0.1, 0.01, and 0.001 mol/L) dissolved in food. The survival rate and physiological indexes of Drosophila were investigated under blue light irradiation of 2500 lux. The results showed that 0.1 mol/L kaempferol increased the activity of male flies during the day and significantly extended the male survival time under blue light irradiation. However, the study found that kaempferol did not significantly prolong the survival time of Drosophila in the oxidative stress experiment, and no significant difference was observed in the feeding experiment. In summary, our research found that kaempferol, at the concentration of 0.1 mol/L, has a protective effect on Drosophila under blue light irradiation, potentially achieved through alterations in circadian rhythm., (© 2024 Wiley Periodicals LLC.)

Purpose: The mechanisms underlying a myopia control strategy using scattering lenses are unclear. Therefore, this study investigates the short-term effects of scatter lenses on central and peripheral choroidal thickness and axial length, which serve as a biomarker in myopia progression research., Methods: In total, 23 participants underwent a 60-minute lens wear phase each to five lens conditions: medium peripheral scattering, high peripheral scattering, medium full-field scattering, high full-field scattering and control (clear lens). Central and peripheral choroidal thickness, foveal axial length, and central visual acuity were measured before and after each lens wear condition., Results: Peripheral choroidal thickening was found after the lens wear phase of the medium peripheral scattering condition (+3.91 ± 5.37 µm, P = 0.04), revealing a significant difference to the control lens condition (P = 0.004), most pronounced in the superior peripheral retina (+1.95 ± 10.74 µm, P = 0.02). In the central retina, significant choroidal thickening was only found in the nasal part after exposure to medium full-field scattering (+3.91 ± 11.72 µm) compared to the control condition (P = 0.001). High peripheral and full-field scattering conditions did not significantly affect central or peripheral choroidal thickness. Visual acuity was significantly reduced in the full-field scattering conditions compared to control and peripheral scattering lenses, with no improvement after 60-minute lens wear. Axial length did not differ significantly after 60-minute exposure to any scattering lens condition or when compared to the control lens., Conclusions: The results indicate a local retinal contrast detection mechanism signals the choroid to thicken peripherally after adaptation to medium peripheral scattering but not high peripheral scattering or full-field scattering at all, while central thickening was only significant nasally after exposure to medium full-field scattering. This emphasizes the importance of the peripheral retina and the level of contrast reduction in the context of myopia research., Translational Relevance: This finding gives insight into the mechanism behind the myopia control strategy inducing peripheral scattering.

A star-filled sky has long been a source of awe and inspiration, and its loss adversely affects human, nonhuman, and environmental health. In one generation, this majestic nighttime overstory has been lost due to national and international overuse of light-emitting diodes lighting. This article canvasses ill health effects of excessive light at night. Blue wavelengths of light are damaging to many forms of life, and glare from unshielded light compromises road safety and infiltrates bedrooms, suppressing melatonin production, undermining sleep quality and duration, and exacerbating susceptibility to many kinds of illness., (Copyright 2024 American Medical Association. All Rights Reserved.)

Light-emitting diode (LED) is commonly used in lighting and digital devices in modern life, which delivers higher levels of blue light than other light sources. Previous work indicated that exposure to blue lights increases serum oxidative stress and affects hepatic functions in animals. However, the detailed hepatic pathogenesis caused by blue lights remains largely elusive. This study investigated the characteristics of hepatic injuries caused by LED light exposure in a mouse model. C57BL/6 mice were exposed the LED lights at 1000 lux, 12 h per day for 45 days or at 4500 lux, 1 h per day for 7 days. The mice were aged 8 weeks or 36 weeks in both genders and maintained under a 12 h light/dark cycle without alteration of diet pattern. Liver tissue sections were obtained for hematoxylin and eosin (H&E) and immunohistochemical staining. The mice with 1000 lux exposure displayed severe liver injuries, including inflammation, ballooning, and pyknosis, which were found to a lesser extent in the 4500 lux mice, and aging aggravated the hepatic injuries. The hepatocellular ballooning was found more severe in the males than the females. In contrast, the females expressed the F4/80 and TNF-α inflammatory markers more evidently. Taken together, LED light exposure may have detrimental effects on liver health, particularly in vulnerable groups such as the elderly and the females with excessive exposure to LED lights, even if they maintain a normal diet and regular light/dark cycles. The potential risk should be considered by both the clinicians and the public., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Han-Hsin Chang reports financial support was provided by National Science and Technology Council. Han-Hsin Chang reports a relationship with National Science and Technology Council that includes: travel reimbursement. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Inc.)

Artificial light at night (ALAN) is a common form of light pollution worldwide, and the intensity, timing, duration, and wavelength of light exposure can affect biological rhythms, which can lead to metabolic, reproductive, and immune dysfunctions and consequently, host-pathogen interactions. Insect vector-borne diseases are a global problem that needs to be addressed, and ALAN plays an important role in disease transmission by affecting the habits and physiological functions of vector organisms. In this work, we describe the mechanisms by which ALAN affects host physiology and biochemistry, host-parasite interactions, and vector-borne viruses and propose preventive measures for related infectious diseases to minimize the effects of artificial light on vector-borne diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interests., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Multiple mutations in the Rhodopsin gene cause sector retinitis pigmentosa in humans and a corresponding light-exacerbated retinal degeneration (RD) in animal models. Previously we have shown that T4K rhodopsin requires photoactivation to exert its toxic effect. Here we further investigated the mechanisms involved in rod cell death caused by T4K rhodopsin in mixed male and female Xenopus laevis In this model, RD was prevented by rearing animals in constant darkness but surprisingly also in constant light. RD was maximized by light cycles containing at least 1 h of darkness and 20 min of light exposure, light intensities >750 lux, and by a sudden light onset. Under conditions of frequent light cycling, RD occurred rapidly and synchronously, with massive shedding of ROS fragments into the RPE initiated within hours and subsequent death and phagocytosis of rod cell bodies. RD was minimized by reduced light levels, pretreatment with constant light, and gradual light onset. RD was prevented by genetic ablation of the retinal isomerohydrolase RPE65 and exacerbated by ablation of phototransduction components GNAT1, SAG, and GRK1. Our results indicate that photoactivated T4K rhodopsin is toxic, that cell death requires synchronized photoactivation of T4K rhodopsin, and that toxicity is mitigated by interaction with other rod outer segment proteins regardless of whether they participate in activation or shutoff of phototransduction. In contrast, RD caused by P23H rhodopsin does not require photoactivation of the mutant protein, as it was exacerbated by RPE65 ablation, suggesting that these phenotypically similar disorders may require different treatment strategies., Competing Interests: The authors declare no competing financial interests., (Copyright © 2024 the authors.)

Purpose: The retinal pigment epithelium (RPE) is a monolayer of epithelial cells essential for photoreceptor function and viability. Quail Coturnix japonica is a convenient experimental animal model for the study of age and pathological retina processes to an accelerated time regime. The three main types of pigment granules present in the RPE are melanin-containing melanosomes, lipofuscin-containing lipofuscin granules, and mixed melanolipofuscin granules containing both melanin and lipofuscin. The purpose of this work was to study the process of melanolipofuscinogenesis during aging and under light exposure., Methods: We examined melanolipofuscin granules in "macular" areas, the area of the retina containing oxycarotenoids, as a function of the macula in humans, of the quail retina by transmission electron microscopy in young, middle-aged, and old birds, and in middle-aged birds irradiated with blue LED light (450 nm, 4 J/cm2)., Results: It has been shown that during photo-oxidative stress caused by the action of blue light on the quail eye, active fusion of melanosomes and lipofuscin granules occurs with formation of various types, including giant, mixed melanolipofuscin-like granules. Increased accumulation of melanolipofuscin-like granules was also observed in non-irradiated old birds., Conclusions: It is assumed that the decrease in the number of melanosomes in the RPE during aging and photo-oxidative stress is associated with their fusion with lipofuscin granules and subsequent degradation of melanin by reactive oxygen species formed in melanolipofuscin-like granules. The disappearance of melanin deprives the RPE cells of light-filtering and antioxidant protection, and significantly increases the risk of their oxidative stress.

The widespread and pervasive use of artificial light at night (ALAN) in our modern 24-hour society has emerged as a substantial disruptor of natural circadian rhythms, potentially leading to a rise in unhealthy lifestyle-related behaviors (e.g., poor sleep; shift work). This phenomenon has been associated with an increased risk of type 2 diabetes mellitus (T2DM), which is a pressing global public health concern. However, to date, reviews summarizing associations between ALAN and T2DM have primarily focused on the limited characteristics of exposure (e.g., intensity) to ALAN. This literature review extends beyond prior reviews by consolidating recent studies from 2000 to 2024 regarding associations between both indoor and outdoor ALAN exposure and the incidence or prevalence of T2DM. We also described potential biological mechanisms through which ALAN modulates glucose metabolism. Furthermore, we outlined knowledge gaps and investigated how various ALAN characteristics beyond only light intensity (including light type, timing, duration, wavelength, and individual sensitivity) influence T2DM risk. Recognizing the detrimental impact of ALAN on sleep health and the behavioral correlates of physical activity and dietary patterns, we additionally summarized studies investigating the potential mediating role of each component in the relationship between ALAN and glucose metabolism. Lastly, we proposed implications of chronotherapies and chrononutrition for diabetes management in the context of ALAN exposure.

Purpose: Recent studies have investigated if the sodium fluorescein-guided (SFg) improves the extent of resection of BMs when compared to standard white light (sWL). Therefore, we aimed to assess the comparative efficacy and safety of SFg and sWL for resection of BMs., Methods: We searched Medline, Embase, and Cochrane Library databases following Cochrane and PRISMA guidelines for studies reporting comparative data of SFg and WL resection of BMs. We pooled odds ratios (OR) with 95% confidence intervals under random effects and applied I² statistics and leave-one-out sensitivity analysis to assess heterogeneity. I² > 40% was considered significant for heterogeneity., Results: Five studies involving 816 patients were included, of whom 390 underwent BMs resection with SFg and 426 with sWL, and ages ranging between 26 and 86.2 years old. Analysis revealed a statistically significant higher likelihood of complete resection in the SFg group when compared to the sWL group (OR = 2.15, 95%CI: 1.18-3.92, p = 0.01; I² = 47%). Sensitivity analysis revealed a consistent result in all five scenarios, with low heterogeneity in two of the five scenarios. Three studies reported significant improvement in OS in the SFg group, and the qualitative assessment of complications and procedure-related mortality did not provide sufficient information for conclusions., Conclusion: This systematic review and meta-analysis identified a higher likelihood of complete resection in the SFg group when compared to the standard sWL group. This study is the first to directly compare the impact of SFg and sWL on resection outcomes for BMs., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Photoclick reactions combine the advantages offered by light-driven processes, that is, non-invasive and high spatiotemporal control, with classical click chemistry and have found applications ranging from surface functionalization, polymer conjugation, photocrosslinking, protein labelling and bioimaging. Despite these advances, most photoclick reactions typically require near-ultraviolet (UV) and mid-UV light to proceed. UV light can trigger undesirable responses, including cellular apoptosis, and therefore, visible and near-infrared light-induced photoclick reaction systems are highly desirable. Shifting to a longer wavelength can also reduce degradation of the photoclick reagents and products. Several strategies have been used to induce a bathochromic shift in the wavelength of irradiation-initiating photoclick reactions. For instance, the extension of the conjugated π-system, triplet-triplet energy transfer, multi-photon excitation, upconversion technology, photocatalytic and photoinitiation approaches, and designs involving photocages have all been used to achieve this goal. Current design strategies, recent advances and the outlook for long wavelength-driven photoclick reactions are presented., (© 2024. Springer Nature Limited.)

Light wavelengths that induce meat discoloration and the photoreceptors in the meat were studied. We investigated the effects of the light wavelength on the oxidation rate of myoglobin (Mb) by exposing Mb extracts or model solutions containing Mb to light at specific wavelengths with a bandwidth of 5 nm using a fluorescence spectrophotometer. The wavelengths examined comprised 385, 415, 445, 460, 490, 525, 555, 580, 605, 630,660, and 750 nm. In the Mb extracts, Mb oxidation was induced through exposure to the light at 445 and 580-605 nm; Mb was insensitive to light at 445 nm. Mitochondria, containing cytochrome a and cytochrome a3 with absorption peaks at 448 and 600 nm, and riboflavin with fluorescence at 450 nm were studied as 445 nm receptors. Mitochondria significantly oxidized Mb via cytochrome c oxidation through complex IV activity; however, no 445 nm-specific photo sensitivity effects were observed. In contrast, riboflavin increased the Mb oxidation rate induced via exposure to the light at 450 nm in a concentration-dependent manner (minimum concentration: 38.4 μg L -1 ). While native mitochondria did not show 445 nm-specific photosensitivity effects on Mb, supernatants of heated mitochondria conferred 445 nm-wavelength sensitivity to Mb. Riboflavin concentration in this supernatant was 182 ± 60 μg L -1 . The Mb photosensitivity spectrum with 473 μg L -1 riboflavin had two peaks at 445 nm and 580 nm, which were similar to those of Mb extract. These results suggest that mitochondrial damage affects the meat discoloration through the release of cytochrome c and riboflavin., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Exposure to light at night (LAN) has been associated with multiple adverse health outcomes. However, evidence is limited regarding the impacts of LAN exposure on human inflammation., Objectives: To examine the association between real-ambient bedroom LAN exposure with systemic inflammation and circadian rhythm of inflammatory markers., Methods: Using data from a prospective cohort study of Chinese young adults. At baseline, bedroom LAN exposure was measured with a portable illuminance meter; fasting blood sample for high-sensitivity C-reactive protein (hs-CRP) assay was collected. At 3-year follow-up, 20 healthy young adults (10 LAN avg < 5 lx, 10 LAN avg ≥ 5 lx) were recruited from the same cohort; time-series venous blood samples were sampled every 4 h over a 24 h-cycle for the detection of 8 inflammatory markers. Circadian rhythm of inflammatory markers was assessed using cosinor analysis., Results: At baseline, the average age of the 276 participants was 18.7 years, and 33.3 % were male. Higher levels of bedroom LAN exposure were significantly associated with increased hs-CRP levels. The association between bedroom LAN exposure and systemic inflammation was only significant in the inactive group (MVPA < 2 h/d) but not in the physically active group (MVPA ≥ 2 h/d). In addition, exposure to higher levels of nighttime light (LAN avg ≥ 5 lx) disrupted circadian rhythms (including rhythmic expression, circadian amplitude and circadian phase) of some inflammatory cytokines and inflammatory balance indicators., Conclusion: Exposure to bedroom nighttime light increases systemic inflammation and disrupts circadian rhythm of inflammatory markers. Keep bedroom darkness at night may represent important strategies for the prevention of chronic inflammation. Additionally, for people living a community with higher nighttime light pollution, regular physical activity may be a viable option to counteract the negative impacts of LAN exposure on chronic inflammation., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper, (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Lycium ruthenicum Murray (LR) is a medicine and edible plant in Northwest China, and L. ruthenicum Murray anthocyanins (LRA) are green antioxidants with various pharmacological activities, such as antioxidant and anti-inflammatory activities. However, the protective effect and mechanism of LRA against retinal damage induced by blue light exposure are poorly understood. This study explored the protective effects and potential mechanisms of LRA on retinal damage induced by blue light exposure in vitro and in vivo. The results showed that LRA could ameliorate oxidative stress injury by activating the antioxidant stress nuclear factor-related factor 2 pathway, promoting the expression of phase II detoxification enzymes (HO-1, NQO1) and endogenous antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), and reducing reactive oxygen species and malondialdehyde levels. Additionally, LRA could inhibit inflammatory response by decreasing the expression of blue light exposure-induced nuclear factor-κB (NF-κB) pathway-related proteins (NF-κB and p-IκBα), as well as interleukin (IL)-6, tumor necrosis factor-α, IL-1β pro-inflammatory factors and pro-inflammatory chemokine VEGF, and increasing the expression of anti-inflammatory factor IL-10. Furthermore, LRA could ameliorate oxidative stress-induced apoptosis by upregulating Bcl-2 and downregulating Bax and Caspase-3 protein expression. All these results indicate that LRA can be used as an antioxidant dietary supplement for the treatment or prevention of retinal diseases., (© 2024 Institute of Food Technologists.)

Migraine is a complex disorder characterized by episodes of moderate-to-severe, often unilateral headaches and generally accompanied by nausea, vomiting, and increased sensitivity to light (photophobia), sound (phonophobia), and smell (hyperosmia). Photophobia is considered the most bothersome symptom of migraine attacks. Although the underlying mechanism remains unclear, the intrinsically photosensitive retinal ganglion cells (ipRGCs) are considered to be involved in photophobia associated with migraine. In this study, we investigated the association between the sensitivity of ipRGCs and migraines and cortical spreading depression (CSD), which may trigger migraine attacks. The pupillary responses closely associated with the function of ipRGCs in patients with migraine who were irradiated with lights were evaluated. Blue (486 nm) light irradiation elicited a response from ipRGCs; however, red light (560 nm) had no such effect. Melanopsin, a photosensitive protein, phototransduces in ipRGCs following blue light stimulation. Hypersensitivity of ipRGCs was observed in patients with migraine. CSD was more easily induced with blue light than with incandescent light using a mouse CSD model. Moreover, CSD was suppressed, even in the presence of blue light, after injecting opsinamide, a melanopsin inhibitor. The hypersensitivity of ipRGCs in patients with migraine may induce CSD, resulting in migraine attacks.

Light serves as a crucial external zeitgeber for maintaining and restoring physiological homeostasis in most organisms. Disrupting of light rhythms often leads to abnormal immune function, characterized by excessive inflammatory responses. However, the underlying regulatory mechanisms behind this phenomenon remain unclear. To address this concern, we use in vivo imaging to establish inflammation models in zebrafish, allowing us to investigate the effects and underlying mechanisms of light disruption on neutrophil recruitment. Our findings reveal that under sustained light conditions (LL), neutrophil recruitment in response to caudal fin injury and otic vesicle inflammation is significantly increased. This is accompanied by elevated levels of histone (H3K18) lactylation and reactive oxygen species (ROS) content. Through ChIP-sequencing and ChIP‒qPCR analysis, we discover that H3K18 lactylation regulates the transcriptional activation of the duox gene, leading to ROS production. In turn, ROS further promote H3K18 lactylation, forming a positive feedback loop. This loop, driven by H3K18 lactylation-ROS, ultimately results in the over recruitment of neutrophils to inflammatory sites in LL conditions. Collectively, our study provides evidence of a mutual loop between histone lactylation and ROS, exacerbating neutrophil recruitment in light disorder conditions, emphasizing the significance of maintaining a proper light-dark cycle to optimize immune function., (© 2024. The Author(s).)

Age-related macular degeneration (AMD) is one of the leading causes of blindness. AMD is currently incurable; the best solution is to prevent its occurrence. To develop drugs for AMD, it is crucial to have a model system that mimics the symptoms and mechanisms in patients. It is most important to develop safer and more effective anti-AMD drug. In this study, the dose of A2E and the intensity of blue light were evaluated to establish an appropriate atrophic in vitro model of AMD and anti-AMD effect and therapeutic mechanism of Codonopsis lanceolata. The experimental groups included a control group an AMD group treated with A2E and blue light, a lutein group treated with 25 μM lutein after AMD induction, and three groups treated with different doses of C. lanceolata (10, 20, and 50 μg/mL) after AMD induction. Intrinsic apoptotic pathway (Bcl-2 family), anti-oxidative system (Keap1/Nrf2/HO-1 antioxidant response element), and anti-carbonyl effect (4-hydroxynonenal [4-HNE]) were evaluated using immunofluorescence, MTT, TUNEL, FACS, and western blotting analyses. A2E accumulation in the cytoplasm of ARPE-19 cells depending on the dose of A2E. Cell viability of ARPE-19 cells according to the dose of A2E and/or blue light intensity. The population of apoptotic or necrotic cells increased based on the A2E dose and blue light intensity. Codonopsis lanceolata dose-dependently prevented cell death which was induced by A2E and blue light. The antiapoptotic effect of that was caused by activating Keap1/Nrf2/HO-1 pathway, suppressing 4-HNE, and modulating Bcl-2 family proteins like increase of antiapoptotic proteins such as Bcl-2 and Bcl-XL and decrease of proapoptotic protein such as Bim. Based on these findings, 30 μM A2E and 20 mW/cm 2 blue light on adult retinal pigment epithelium-19 cells was an appropriate condition for AMD model and C. lanceolata shows promise as an anti-AMD agent., (© 2024. The Author(s).)

Circadian rhythms are endogenous biological cycles that regulate physiology and behavior and are set to precisely 24-h by light exposure. Light at night (LAN) dysregulates physiology and function including immune response; a critical component that contributes to stroke pathophysiological progression of neuronal injury and may impair recovery from injury. The goal of this study is to explore the effects of dim LAN (dLAN) in a murine model of ischemic stroke to assess how nighttime lighting from hospital settings can affect stroke outcome. Further, this study sought to identify mechanisms underlying pathophysiological changes to immune response after circadian disruption. Male and female adult Swiss Webster (CFW) mice were subjected to transient or permanent focal cerebral ischemia, then were subsequently placed into either dark night conditions (LD) or one night of dLAN (5 lx). 24 h post-stroke, sensorimotor impairments and infarct sizes were quantified. A single night of dLAN following MCAO increased infarct size and sensorimotor deficits across both sexes and reduced survival in males after 24 h. Flow cytometry was performed to assess microglial phenotypes after MCAO, and revealed that dLAN altered the percentage of microglia that express pro-inflammatory markers (MHC II+ and IL-6) and microglia that express CD206 and IL-10 that likely contributed to poor ischemic outcomes. Following these results, microglia were reduced in the brain using Plexxikon 5622 (PLX 5622) a CSFR1 inhibitor, then the mice received an MCAO and were exposed to LD or dLAN conditions for 24 h. Microglial depletion by PLX5622 resulted in infarct sizes that were comparable between lighting conditions. This study provides supporting evidence that environmental lighting exacerbates ischemic injury and post-stroke mortality by a biological mechanism that exposure to dLAN causes a fundamental shift of activated microglial phenotypes from beneficial to detrimental at an early time point after stroke, resulting in irreversible neuronal death., Competing Interests: Declaration of competing interest None., (Copyright © 2023. Published by Elsevier Inc.)

Natural experiments provide remarkable opportunities to test the large-scale effects of human activities. Widespread energy blackouts offer such an 'experiment' to test the impacts of artificial light at night (ALAN) on wildlife. We use the situation in South Africa, where regular scheduled blackouts are being implemented, to highlight this opportunity., Competing Interests: Declaration of interests No interests are declared., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Circular RNAs (circRNAs) are implicated in retinal pathophysiology; however, their expression profiles and functions in photoreceptor apoptosis are largely unknown. We explored circRNA-expression profiles and circUvrag (host gene: Uvrag, ultraviolet radiation resistance associated gene) function in light-induced photoreceptor apoptosis., Methods: Sprague-Dawley rats and 661 W photoreceptor cells were exposed to blue light to establish light-induced photoreceptor degeneration. Differentially expressed circRNAs were identified using microarrays. Potential functions of dysregulated circRNAs were analysed using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. CircUvrag expression and localization were evaluated using quantitative RT-PCR and fluorescence in situ hybridization, respectively. CircUvrag overexpression and knockdown were induced using a plasmid and a small interfering RNA, respectively, and retinal function and structure were assessed using scotopic electroretinography, haematoxylin-eosin staining, and TUNEL staining. Microglial migration was assessed using IBA1 immunostaining. The apoptosis ratio of photoreceptor cells in vitro was detected using flow cytometry., Results: We identified 764 differentially expressed circRNAs, which were potentially related with the development of retinal structures, including neurons, dendrites, and synapses, and might participate in nervous-system pathophysiology. Light exposure enriched circUvrag in the cytoplasm of photoreceptors in the outer nuclear layer (ONL). CircUvrag knockdown decreased photoreceptor apoptosis and microglial migration to the ONL after light exposure, preserving ONL thickness and a-wave amplitude. In vitro, circUvrag knockdown inhibited photoreceptor apoptosis, although circUvrag overexpression slightly promoted photoreceptor apoptosis., Conclusions: CircUvrag knockdown attenuated light-induced photoreceptor apoptosis, and might be a potential target in retinal degeneration., (© 2024 Royal Australian and New Zealand College of Ophthalmologists.)

Photobiomodulation (PBM) therapy uses light of different wavelengths to treat various retinal degeneration diseases, but the potential damage to the retina caused by long-term light irradiation is still unclear. This study were designed to detect the difference between long- and short-wavelength light (650-nm red light and 450-nm blue light, 2.55 mW/cm 2 , reference intensity in PBM)-induced injury. In addition, a comparative study was conducted to investigate the differences in retinal light damage induced by different irradiation protocols (short periods of repeated irradiation and a long period of constant irradiation). Furthermore, the protective role of PARP-1 inhibition on the molecular mechanism of blue light-induced injury was confirmed by a gene knockdown technique or a specific inhibitor through in vitro and in vivo experiments. The results showed that the susceptibility to retinal damage caused by irradiation with long- and short-wavelength light is different. Shorter wavelength lights, such as blue light, induce more severe retinal damage, while the retina exhibits better resistance to longer wavelength lights, such as red light. In addition, repeated irradiation for short periods induces less retinal damage than constant exposure over a long period. PARP-1 plays a critical role in the molecular mechanism of blue light-induced damage in photoreceptors and retina, and inhibiting PARP-1 can significantly protect the retina against blue light damage. This study lays an experimental foundation for assessing the safety of phototherapy products and for developing target drugs to protect the retina from light damage., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Purpose: To determine whether visible light is needed to elicit axial eye shortening by exposure to long wavelength light., Methods: Incoherent narrow-band red (620 ± 10 nm) or near-infrared (NIR, 875 ± 30 nm) light was generated by an array of light-emitting diodes (LEDs) and projected monocularly in 17 myopic and 13 non-myopic subjects for 10 min. The fellow eye was occluded. Light sources were positioned 50 cm from the eye in a dark room. Axial length (AL) was measured before and after the exposure using low-coherence interferometry., Results: Non-myopic subjects responded to red light with significant eye shortening, while NIR light induced minor axial elongation (-13.3 ± 17.3 μm vs. +6.5 ± 11.6 μm, respectively, p = 0.005). Only 41% of the myopic subjects responded to red light exposure with a decrease in AL and changes were therefore, on average, not significantly different from those observed with NIR light (+0.2 ± 12.1 μm vs. +1.1 ± 11.2 μm, respectively, p = 0.83). Interestingly, there was a significant correlation between refractive error and induced changes in AL after exposure to NIR light in myopic eyes (r(15) = -0.52, p = 0.03) and induced changes in AL after exposure to red light in non-myopic eyes (r(11) = 0.62, p = 0.02), with more induced axial elongation with increasing refractive error., Conclusions: Incoherent narrow-band red light at 620 nm induced axial shortening in 77% of non-myopic and 41% of myopic eyes. NIR light did not induce any significant changes in AL in either refractive group, suggesting that the beneficial effect of red laser light therapy on myopia progression requires visible stimulation and not simply thermal energy., (© 2024 The Authors. Ophthalmic and Physiological Optics published by John Wiley & Sons Ltd on behalf of College of Optometrists.)

Light pollution is a potential risk for intestinal health in humans and animals. The gut microbiota is associated with the development of intestinal inflammation induced by extended exposure to light, but the underlying mechanism is not yet clear. The results of this study showed that extended exposure to light (18L:6D) damaged intestinal morphology, downregulated the expression of tight junction proteins, and upregulated the expression of the NLRP3 inflammasome and the concentration of pro-inflammatory cytokines. In addition, extended exposure to light significantly decreased the abundance of Lactobacillus, Butyricicoccus , and Sellimonas and increased the abundance of Bifidobacterium , unclassified Oscillospirales , Family&#95;XIII&#95;UCG-001 , norank&#95;f&#95;&#95;norank&#95;o&#95;&#95;Clostridia&#95;vadinBB60&#95;group , and Defluviitaleaceae&#95;UCG-01 . Spearman correlation analysis indicated that gut microbiota dysbiosis positively correlated with the activation of the NLRP3 inflammasome. The above results indicated that extended exposure to light induced intestinal injury by NLRP3 inflammasome activation and gut microbiota dysbiosis. Antibiotic depletion intestinal microbiota treatment and cecal microbiota transplantation (CMT) from the 12L:12D group to 18L:6D group indicated that the gut microbiota alleviated intestinal inflammatory injury induced by extended exposure to light via inhibiting the activation of the NLRP3 inflammasome. In conclusion, our findings indicated that the gut microbiota can alleviate intestinal inflammation induced by extended exposure to light via inhibiting the activation of the NLRP3 inflammasome.

The debate surrounding the benefits versus harms of blue light have become a topic of interest recently due to increased exposure. Blue light therapy has been utilized with some success in a variety of dermatologic conditions. However, potential harms have also been documented. Currently, there is no evidence to suggest a necessity for blue light photoprotection, but there are products available with proven efficacy for those desiring protection. J Drugs Dermatol. 2024;23(6):472-476.&nbsp; &nbsp;&nbsp; doi:10.36849/JDD.7665.

Background: Evidence suggests that variation in light exposure strongly influences the dynamic of inflammation, coagulation, and the immune system. Multiple injuries induce systemic inflammation that can lead to end-organ injury. Here, we hypothesize that alterations in light exposure influence posttrauma inflammation, coagulopathy, and end-organ injury., Methods: C57BL/6 mice underwent a validated multiple-injury and hemorrhage model performed following 72 hours of exposure to red (617 nm, 1,700 lux), blue (321 nm, 1,700 lux), and fluorescent white light (300 lux) (n = 6-8/group). The animals were sacrificed at 6 hours posttrauma. Plasma samples were evaluated and compared for proinflammatory cytokine expression levels, coagulation parameters, markers of liver and renal injury, and histological changes (Carstairs staining). One-way analysis of variance statistical tests were applied to compare study groups., Results: Preexposure to long-wavelength red light significantly reduced the inflammatory response at 6 hours after multiple injuries compared with blue and ambient light, as evidenced by decreased levels of interleukin 6, monocyte chemoattractant protein-1 (both p < 0.001), liver injury markers (alanine transaminase, p < 0.05), and kidney injury markers (cystatin C, p < 0.01). In addition, Carstairs staining of organ tissues revealed milder histological changes in the red light-exposed group, indicating reduced end-organ damage. Furthermore, prothrombin time was significantly lower ( p < 0.001), and fibrinogen levels were better maintained ( p < 0.01) in the red light-exposed mice compared with those exposed to blue and ambient light., Conclusion: Prophylactic light exposure can be optimized to reduce systemic inflammation and coagulopathy and minimize acute organ injury following multiple injuries. Understanding the mechanisms by which light exposure attenuates inflammation may provide a novel strategy to reducing trauma-related morbidity., (Copyright © 2023 American Association for the Surgery of Trauma.)

Purpose: A complication of using silicone oil as an intraocular endotamponade is its adhesion to intraocular lenses (IOLs). Forward light scattering is a measure to quantify the optical disturbance caused by adherent oil droplets. We tested the straylight caused by silicone oil adhesion to different IOLs and examined whether an approved cleaning solution, F4H5, reverses the induced straylight., Design: An experimental study., Methods: Two hydrophobic acrylic IOL models and 1 hydrophilic model with a hydrophobic surface (n = 8 per model: 24 lenses) had straylight measured before contact with silicone oils, providing a baseline for subsequent testing: 12 lenses with lighter-than-water silicone oil (Siluron 2000) and 12 with heavier-than-water oil (Densiron 68). The final measurement was performed after cleansing with F4H5 when we used scanning electron and light microscopy to detect surface changes., Results: Straylight was majorly increased in IOLs with adherent silicone oil (baseline vs adherent oil median 3.1 [2.1, 3.9] and 39.7 [22.7, 87.8] deg 2 /sr, respectively; P < .001). No difference was seen between heavier- and lighter-than-water silicone oils. Between IOL types, induced straylight varied significantly, with 1 hydrophobic model reaching the highest average straylight. F4H5 significantly reduced straylight values in all IOL types (median 9.4 [5.4, 13.8] deg 2 /sr). The microscopy revealed surface changes on the IOLs even after cleaning., Conclusions: Silicone oil adhesion to IOLs can induce amounts of straylight known to cause severe optical disturbance. F4H5 cleansing solution reversed straylight values to only slightly increased values. We found no difference in straylight formation between the lighter- and heavier-than-water silicone oils., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)

Purpose: Considering the putative role of light in myopia, and variations in socioeconomic, lifestyle, educational and environmental factors across ethnicities, we objectively investigated light exposure patterns in Indian school children., Methods: The light exposure profile of 143 school children (9-15 years, 50 myopes) recorded using a validated wearable light tracker for six continuous days was analysed. Additional data for non-school days were available for 87 children (26 myopes). The illuminance exposure levels, time spent outdoors and epoch (number of times participant is exposed to a predefined range of lux level per day) were compared between myopes and non-myopes across different light conditions: ≥1000, ≥3000, ≥5000 and ≥10 000 lux. For school days, light exposure profiles during (1) before school, school and after school hours; and (2) class, break and transition (when a student travels to and from school) time were analysed., Results: The overall median (IQR) daily illuminance exposure level, time spent outdoors and epochs at outdoors (≥1000 lux) were 807 (507-1079) lux/day, 46 (30-64) min/day and 9 (6-12) times/day, respectively. The daily illuminance exposure on non-school days was significantly higher in non-myopes than myopes (6369 (4508-9112) vs 5623 (2616-6929) lux/day, p=0.04). During transition time (school days), non-myopes had significantly higher illuminance exposure (910 (388-1479) vs 550 (263-1098) lux/day, p=0.04), spent more time outdoors (25 (10-43) vs 14 (4-29) min/day, p=0.01) and had higher outdoor epochs (6 (4-11) vs 5 (2-8) times/day, p=0.01) than myopes., Conclusions: A small but significant difference in illuminance exposure, time spent outdoors and epoch was noted between myopes and non-myopes during transition time, which may have implications in myopia control., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Although blue light can damage the skin to a certain extent, the pathogenesis of its damage remains still unclear. The available evidence suggests that oxidative stress may be the main cause of its damage. Lycium barbarum polysaccharide (LBP) has antioxidative effects in a variety of cells. In this paper, we investigated the protective role of LBP and its mechanism of action related to mitophagy in blue-light-damaged skin cells. The findings indicated that in HaCaT cells and mouse skin, LBP pretreatment was effective in reducing blue-light-induced apoptosis and ameliorating the elevated level of cellular autophagy/mitophagy caused by excessive blue light exposure. The markers reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) were used to assess oxidative stress. LBP could effectively inhibit blue-light-induced oxidative stress. It was also found that blue light exposure caused mitochondrial dysfunction in HaCaT cells, including increased intracellular calcium ion levels and decreased mitochondrial membrane potential. LBP pretreatment significantly relieved mitochondrial dysfunction in HaCaT cells. These findings imply that LBP pretreatment protects skin cells from damage induced by blue light irradiation and that mitophagy may be a significant factor in skin photodamage., (© 2023 American Society for Photobiology.)

Inherited retinal dystrophies (IRDs) are progressive diseases leading to vision loss. Mutation in the eyes shut homolog (EYS) gene is one of the most frequent causes of IRD. However, the mechanism of photoreceptor cell degeneration by mutant EYS has not been fully elucidated. Here, we generated retinal organoids from induced pluripotent stem cells (iPSCs) derived from patients with EYS-associated retinal dystrophy (EYS-RD). In photoreceptor cells of RD organoids, both EYS and G protein-coupled receptor kinase 7 (GRK7), one of the proteins handling phototoxicity, were not in the outer segment, where they are physiologically present. Furthermore, photoreceptor cells in RD organoids were vulnerable to light stimuli, and especially to blue light. Mislocalization of GRK7, which was also observed in eys-knockout zebrafish, was reversed by delivering control EYS into photoreceptor cells of RD organoids. These findings suggest that avoiding phototoxicity would be a potential therapeutic approach for EYS-RD.

Currently, more and more importance is being attached to the interaction of brain neurons with astrocytes in order to study the pathogenesis, and in the future, to develop methods for the prevention, early diagnosis and treatment of neurodegenerative diseases of the brain. In this review article, the authors attempt to demonstrate the role of astrocytes, disturbances in circadian rhythms, sleep-wake patterns, and light pollution in the development of Alzheimer's disease. Based on the analysis of literature data, possible mechanisms of synchronization and desynchronization of these processes are presented.

Introduction: There have recently been several clinical studies suggesting that brief periods of exposure to red light (repeated low-level red light, 'RLRL') may produce a dramatic anti-myopia effect, calling for further investigations into its therapeutic parameters. Unfortunately, many experimental species used in refractive studies develop myopia in response to this wavelength. Tree shrews are the only animal model other than rhesus monkeys that consistently exhibit hyperopic responses to ambient red light. Here, tree shrews were used to study the influence of the spectral purity, duty cycle and intensity of red light on its anti-myopic effect., Methods: Juvenile tree shrews (Tupaia belangeri) were raised from 24 to 35 days after eye opening under ambient lighting that was: standard white colony fluorescent light; pure narrow band red light of either 600, 50-100 or 5 lux; red light that was diluted with 10% white light (by lux) or 50% white and 2 s of pure red light that alternated with 2 s of pure white light (50% duty cycle). Refractive measures were taken with a NIDEK ARK-700 autorefractor and axial dimensions with a LenStar LS-900 Axial Biometer., Results: The pro-hyperopia effect of ambient red light was greatly reduced by even small amounts of concurrent white light 'contamination', but remained robust if 2-s periods of pure white light alternated with 2 s of red. Finally, the hyperopic effect of red light was maintained at reduced luminance levels in the 50-100 lux range and only failed at 5 lux., Conclusions: These results have implications for understanding the mechanisms by which ambient red light affects refractive development, and possibly also for clinical therapies using RLRL. Nevertheless, it remains to be determined if the mechanism of the current clinical RLRL therapy is the same as that operating on tree shrews in ambient red light., (© 2023 The Authors. Ophthalmic and Physiological Optics published by John Wiley & Sons Ltd on behalf of College of Optometrists.)

Light at night (LAN) induced cognitive impairment associated with oxidative stress in mice has been reported. Lycium barbarum polysaccharide (LBP) exhibits anti-tumor, anti-oxidant and neuroprotective effects, yet the neuroprotective effect on light-induced neuron damage still unclear. Here, mice exposed to LAN displayed cognitive impairment and depressive like behavior, which was reversed by LBP treatment. Meanwhile, LBP alleviated light-induced higher apoptosis and mitochondrial damage in HT-22 cells. Also, LBP prevented the decreased of mitochondrial membrane permeabilization (MMP) level in light-treated cells. Additionally, LBP demonstrated its antioxidant potential by reducing ROS production and malondialdehyde (MDA) level, while simultaneously enhancing the levels of superoxide dismutase (SOD) and glutathione peroxidases (GSH-Px) in both light-treated mice and HT-22 cells. Furthermore, the mRNA and protein expression of Nrf2 (NF-E2-related factor 2), heme oxygenease-1 (HO-1), and NAD(P)H quinone oxidoreductase (NQO1) were decreased in both light-treated mice and cells. Additionally, LBP treatment reversed light-induced the inhibition of Nrf2/HO-1 signaling pathway in both mice and cells. Moreover, Nrf2 antagonist ML385 significantly eliminated the neuroprotection of LBP on cell apoptosis, oxidative stress and mitochondrial damage in light-treated cells. These results indicate that LBP can rescue light-induced neurotoxicity in mice and HT-22 cells by activating the Nrf2/HO-1 signaling pathway., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Background: Erythropoietic protoporphyria and X-linked protoporphyria are inborn errors of heme biosynthesis that cause elevated circulating levels of metal-free protoporphyrin and phototoxicity. Both disorders are characterized by excruciating phototoxic attacks after exposure to visible light. Dersimelagon is a new, orally administered, selective melanocortin 1 receptor agonist that increases levels of skin eumelanin., Methods: We conducted a randomized, placebo-controlled, phase 2 trial to investigate the efficacy and safety of dersimelagon with respect to the time to onset and the severity of symptoms associated with sunlight exposure in patients with erythropoietic protoporphyria or X-linked protoporphyria. Patients 18 to 75 years of age were randomly assigned in a 1:1:1 ratio to receive placebo or dersimelagon at a dose of 100 or 300 mg once daily for 16 weeks. The primary end point was the change from baseline to week 16 in the time to the first prodromal symptom associated with sunlight exposure. Patients recorded daily sunlight exposure and symptom data in an electronic diary. Quality of life and safety were also assessed., Results: Of the 102 patients (93 with erythropoietic protoporphyria and 9 with X-linked protoporphyria) who underwent randomization, 90% completed the treatment period. The mean daily time to the first prodromal symptom associated with sunlight exposure increased significantly with dersimelagon: the least-squares mean difference from placebo in the change from baseline to week 16 was 53.8 minutes in the 100-mg dersimelagon group (P = 0.008) and 62.5 minutes in the 300-mg dersimelagon group (P = 0.003). The results also suggest that quality of life improved in patients receiving dersimelagon as compared with placebo. The most common adverse events that occurred or worsened during treatment were nausea, freckles, headache, and skin hyperpigmentation., Conclusions: At both doses evaluated, dersimelagon significantly increased the duration of symptom-free sunlight exposure in patients with erythropoietic protoporphyria or X-linked protoporphyria. (Funded by Mitsubishi Tanabe Pharma; Endeavor ClinicalTrials.gov number, NCT03520036.)., (Copyright © 2023 Massachusetts Medical Society.)

Blue light emitted by smartphones and tablets at night increases the risk of depression. Pu-erh tea has been reported to reduce the risk of depression by regulating tryptophan metabolism, but its underlying protective mechanism on depression induced by blue light at night (BLAN) remains unclear. In this work, two groups of C57BL6/J mice were given water or 0.25% (w/v) Pu-erh tea for 120 days, followed by a 45-day BLAN treatment (400 lux blue light between 21:00 and 23:00) to simulate blue light emitted from electronic equipment. Our results indicated that BLAN induced depression-like behaviors and gut microbiota disorders in healthy mice. Pu-erh tea intake significantly reshaped the gut microbiome (especially Bifidobacterium ) and regulated the metabolism of short-chain fatty acids (SCFAs) which protected the integrity of the intestinal barrier. This improvement further reduced blood-brain barrier (BBB) damage and alleviated neuroinflammation by inhibiting MyD88/NF-κB pathways which finally regulated neurotransmitters such as brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT). Collectively, 0.25% (w/v) Pu-erh tea has the potential to prevent BLAN-induced depression-like behaviors by reshaping the gut microbiota and increasing the generation of SCFAs via the gut-brain axis.

Background: Exposure to light at night (LAN) is a potent disruptor of the circadian system. Whether LAN exposure exerts a sex- or age-specific influence on obesity needs investigation., Objectives: To estimate the sex- and age-specific associations of exposure to outdoor LAN and obesity based on a national and cross-sectional survey., Methods: The study included a nationally representative sample of 98,658 adults aged ≥ 18 years who had lived in their current residence for ≥ 6 months from 162 study sites across mainland China in 2010. Outdoor LAN exposure was estimated from satellite imaging data. General obesity was defined as body-mass index (BMI) ≥ 28 kg/m 2 and central obesity was defined as waist circumference ≥ 90 cm in men and ≥ 85 cm in women. Linear and logistic regression models were used to examine the associations between LAN exposure and prevalent obesity in sex and age categories., Results: A monotonically increasing association of outdoor LAN with BMI, waist circumference was observed in all sex and age categories, except for adults aged 18-39 years. Significant associations of LAN exposure with prevalent obesity were observed in each sex and age category, especially in men and older people. Per 1-quintile increase in LAN was associated with 14% increased odds of general obesity in men (odds ratio, OR=1.14, 95% confidence interval, CI=1.07-1.23) and 24% in adults aged ≥ 60 years (OR=1.24, 95% CI=1.14-1.35). Per 1-quintile increase in LAN was associated with 19% increased odds of central obesity in men (OR=1.19, 95% CI=1.11-1.26) and 26% in adults aged ≥ 60 years (OR=1.26, 95% CI=1.17-1.35)., Conclusions: Increased chronic outdoor LAN exposure was associated with increased prevalence of obesity in sex- and age- specific Chinese populations. Public health policies on reducing light pollution at night might be considered in obesity prevention., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Zhang, Zheng, Xin, Zhao, Li, Wang, Xu, Lu, Wang, Lin, Wang, Ning, Bi, Chen and Xu.)

Context: Despite the absence of light within the body, the application of microscopy during stages of in vitro embryo production has led to the discovery of light irradiation effects on embryo preimplantation development., Aims: To determine the optimal light irradiation wavelengths at various embryo stages for improving the preimplantation development of mouse embryos and the quality (total cell number) of blastocysts., Method: All in vitro procedures of zygote or 2-cell embryo manipulation, embryo monitoring, and culture medium exchange were conducted under visible (390-750nm), blue (445-500nm), green (500-575nm), yellow (575-585nm), or red (620-750nm) light irradiation wavelength., Key Results: We found that blue, green, and yellow light irradiation during in vitro blastocyst production from zygotes significantly improved blastocyst production and quality, compared to visible and red light irradiation. However, 2-cell embryos exposed to yellow light during in vitro blastocyst production produced significantly more high-quality blastocysts than did 2-cell embryos exposed to visible, blue, green, or red light. After exposure to blue and green - but not yellow - light during in vitro zygote manipulation, yellow light irradiation during embryo monitoring and culture medium exchange triggered significant retardation of preimplantation development., Conclusion: These results demonstrate that yellow light irradiation during in vitro blastocyst production, regardless of embryo stage, improves preimplantation development of mouse embryos., Implications: The present study will contribute to produce greater high-quality blastocysts and reduce experimental errors generated by light exposure during mouse embryo-related studies.

Background: Oxidative stress can induce age-related diseases. Age-related retinal diseases, such as age-related macular degeneration (AMD), are difficult to cure owing to their complicated mechanisms. Although anti-neovascular therapeutics are used to treat wet AMD, vision cannot always be completely restored, and disease progression cannot always be inhibited. Therefore, determining a method to prevent or slow retinal damage is important. This study aimed to investigate the protective effect of a chrysanthemum water extract rich in flavone on the oxidatively stressed retina of mice., Methods: Light damage was induced to establish oxidative stress mouse models. For in vitro experiments, ARPE-19 cells were cultured and divided into four groups: control, light-damaged, and low- and high-dose chrysanthemum extract. No treatment was administered in the control group. The light-damaged and low- and high-dose chrysanthemum extract groups were exposed to a similar white light level. The chrysanthemum extract was added at a low dose of 0.4 mg/mL or a high dose of 1.0 mg/mL before cell exposure to 2500-lx white light. Reactive oxygen species (ROS) level and cellular viability were measured using MTT and immunofluorescence staining. For in vivo experiments, C57BL/6 J mice were divided into the same four groups. Low- (0.23 g/kg/day) and high-dose (0.38 g/kg/day) chrysanthemum extracts were continuously intragastrically administered for 8 weeks before mouse exposure to 10,000-lx white light. Retinal function was evaluated using electroretinography. In vivo optical coherence tomography and in vitro haematoxylin and eosin staining were performed to observe the pathological retinal changes in each group after light damage. Fluorescein fundus angiography of the arteriovenous vessel was performed, and the findings were analysed using the AngioTool software. TUNEL immunofluorescence staining was used to assess isolated retinal apoptosis., Results: In vitro, increased ROS production and decreased ARPE-19 cell viability were found in the light-damaged group. Improved ARPE-19 cell viability and reduced ROS levels were observed in the chrysanthemum extract treatment groups. In vivo, dysfunctional retinas and abnormal retinal structures were found in the light-damaged group, as well as increased apoptosis in the retinal ganglion cells (RGCs) and inner and outer nuclear layers. The apoptosis rate in the same layers was lower in the chrysanthemum extract treatment groups than in the light-damaged group. The production of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), increased in the treatment groups. NF-κB in the nucleus and TNF-α were more highly expressed in the light-damaged group than in the low- and high-dose chrysanthemum extract groups., Conclusions: Light damage-induced retinal oxidative stress can lead to ROS accumulation in the retinal tissues. Herein, RGC and photoreceptor layer apoptosis was triggered, and NF-κB in the nucleus and TNF-α were highly expressed in the light-damaged group. Preventive chrysanthemum extract administration decreased ROS production by increasing SOD, CAT, and GSH-Px activities and reversing the negative changes, demonstrating a potential protective effect on the retina., (© 2022. The Author(s).)

The state of red blood cells (RBCs) and their functional possibilities depend on the structural organization of the membranes. Cell morphology and membrane nanostructure are compositionally and functionally related to the cytoskeleton network. In this work, the influence of agents (hemin, endogenous oxidation during storage of packed RBCs, ultraviolet (UV) radiation, temperature, and potential of hydrogen (pH) changes) on the relationships between cytoskeleton destruction, membrane nanostructure, and RBC morphology was observed by atomic force microscope. It was shown that the influence of factors of a physical and biochemical nature causes structural rearrangements in RBCs at all levels of organization, forming a unified mechanism of disturbances in relationships "cytoskeleton-membrane nanosurface-cell morphology". Filament ruptures and, consequently, large cytoskeleton pores appeared. The pores caused membrane topological defects in the form of separate grain domains. Increasing loading doses led to an increase in the number of large cytoskeleton pores and defects and their fusion at the membrane nanosurfaces. This caused the changes in RBC morphology. Our results can be used in molecular cell biology, membrane biophysics, and in fundamental and practical medicine.

While blue LED (b-LED) light is increasingly being studied for its cytotoxic activity towards bacteria in therapy of skin-related infections, its effects on eukaryotic cells plasticity are less well characterized. Moreover, since different protocols are often used, comparing the effect of b-LED towards both microorganisms and epithelial surfaces may be difficult. The aim of this study was to analyze, in the same experimental setting, both the bactericidal activity and the effects on human keratinocytes. Exposure to b-LED induced an intense cytocidal activity against Gram-positive (i.e, Staphylococcus aureus ) and Gram-negative (i.e., Pseudomonas aeruginosa ) bacteria associated with catheter-related infections. Treatment with b-LED of a human keratinocyte cell line induced a transient cell cycle arrest. At the molecular level, exposure to b-LED induced a transient downregulation of Cyclin D1 and an upregulation of p21, but not signs of apoptosis. Interestingly, a transient induction of phosphor-histone γ-H2Ax, which is associated with genotoxic damages, was observed. At the same time, keratinocytes underwent a transient epithelial to mesenchymal transition (EMT)-like phenotype, characterized by E-cadherin downregulation and SNAIL/SLUG induction. As a functional readout of EMT induction, a scratch assay was performed. Surprisingly, b-LED treatment provoked a delay in the scratch closure. In conclusion, we demonstrated that b-LED microbicidal activity is associated with complex responses in keratinocytes that certainly deserve further analysis.