The Power of Far-Red Light at Night: Photomorphogenic, Physiological, and Yield Response in Pepper During Dynamic 24 Hour Lighting.

Supplemental light is needed during the winter months in high latitude regions to achieve the desired daily light integral (DLI) (photoperiod × intensity) for greenhouse pepper (Capsicum annuum) production. Peppers tend to have short internodes causing fruit stacking and higher labor time for plant maintenance when grown under supplemental light. Far-red light can increase internode length, and our previous study on tomatoes (Solanum lycopersicum) also discovered monochromatic blue light at night during continuous lighting (CL, 24 h) increased stem elongation. Furthermore, the use of low-intensity, long photoperiod lighting can reduce light fixture costs and overall electricity costs due to lower power prices during the night. Therefore, we investigated the use of blue and/or far-red light during the night period of CL to increase stem elongation. Three pepper cultivars with different internode lengths/growing characteristics ('Maureno,' 'Gina,' and 'Eurix') were used to investigate the effects on plant morphology in a short experiment, and one cultivar 'Maureno' was used in a long experiment to assess the impact on fruit yield. The five lighting treatments that were used are as follows: 16 h of white light during the day followed by either 8 h of darkness (16W - control), white light (24W), blue light only (16W + 8B), blue + far-red light (16W + 8BFR), or far-red light only (16W + 8FR). Calculated nighttime phytochrome photostationary state (PSS) was 0.833, 0.566, 0.315, and 0.186 for 24W, 16W + 8B, 16W + 8BFR, and 16W + 8FR respectively. All five treatments had the same DLI in photosynthetically active radiation (PAR) and far-red light. The 16W + 8BFR and 16W + 8FR treatments significantly increased internode length compared to 16W and 24W but neither was more impactful than the other. The 16W + 8B treatment also increased internode length but to a lesser extent than 16W + 8BFR and 16W + 8FR. This indicates that a nighttime PSS of 0.315 is sufficient to maximize stem elongation. Both 16W + 8B and 16W + 8BFR drove photosynthesis during the nighttime supporting a similar yield compared to 16W. Therefore, 16W + 8BFR is the most potential lighting strategy as it can lead to a greater reduction in the light fixture and electrical costs while maintaining yield and enhancing internode length.

Repair of UVB damage in mouse skin by adipose derived stem cells / 中华医学美学美容杂志

Objective:To explore the therapeutic effect of adipose-derived stem cells (ADSC) on long-wave UV damage in mouse skin in order to provide ideas for the treatment of skin photodamage.Methods:The inguinal and perirenal adipose tissues of C57BL/6 mice were extracted and processed to obtain mouse ADSCs, and the surface markers, adipogenic and osteogenic differentiation capabilities were identified. The mouse photoaging model was irradiated with the SS-03AB UV illuminator, the total UVB dose was 9.45 J/cm 2, and the total UVA dose was 94.5 J/cm 2. Experimental mice (72 in total) were divided into normal group, model group, DMEM (medium) group and ADSC group, each with 18 mice. In the normal group and model group, the materials were taken two weeks after the end of irradiation. After irradiation, the ADSC group was given a subcutaneous injection of 200 μl ADSC suspension, and the DMEM group was given 200 μl of serum-free medium for treatment, and the materials were taken for pathological staining after 2 weeks. The experimental data was processed by analysis of variance. This study was carried out from August 2018 to July 2019 in the First Affiliated Hospital of Zhengzhou University. Results:The extracted cells were identified as adipose-derived stem cells. HE staining showed that the inflammatory cell infiltration in the ADSC group was significantly reduced compared with the DMEM group ( t=20.649, P<0.001) and the normal group ( t=16.147, P<0.001), and the thickness of the dermis layer was significantly increased. Masson staining showed collagen fibers were arranged neatly and the density increased significantly after ADSC treatment. Conclusions:Subcutaneous injection of ADSC can reduce inflammation, promote collagen tissue proliferation, increase the thickness of the dermis, effectively resist inflammatory damage and collagen breakdown caused by UVB.

Protective Effect of Astaxanthin on Blue Light Light-Emitting Diode-Induced Retinal Cell Damage via Free Radical Scavenging and Activation of PI3K/Akt/Nrf2 Pathway in 661W Cell Model.

Light-emitting diodes (LEDs) are widely used and energy-efficient light sources in modern life that emit higher levels of short-wavelength blue light. Excessive blue light exposure may damage the photoreceptor cells in our eyes. Astaxanthin, a xanthophyll that is abundantly available in seafood, is a potent free radical scavenger and anti-inflammatory agent. We used a 661W photoreceptor cell line to investigate the protective effect of astaxanthin on blue light LED-induced retinal injury. The cells were treated with various concentrations of astaxanthin and then exposed to blue light LED. Our results showed that pretreatment with astaxanthin inhibited blue light LED-induced cell apoptosis and prevented cell death. Moreover, the protective effect was concentration dependent. Astaxanthin suppressed the production of reactive oxygen species and oxidative stress biomarkers and diminished mitochondrial damage induced by blue light exposure. Western blot analysis confirmed that astaxanthin activated the PI3K/Akt pathway, induced the nuclear translocation of Nrf2, and increased the expression of phase II antioxidant enzymes. The expression of antioxidant enzymes and the suppression of apoptosis-related proteins eventually protected the 661W cells against blue light LED-induced cell damage. Thus, our results demonstrated that astaxanthin exerted a dose-dependent protective effect on photoreceptor cells against damage mediated by blue light LED exposure.

Effects of the Emitted Light Spectrum of Liquid Crystal Displays on Light-Induced Retinal Photoreceptor Cell Damage.

Liquid crystal displays (LCDs) are used as screens in consumer electronics and are indispensable in the modern era of computing. LCDs utilize light-emitting diodes (LEDs) as backlight modules and emit high levels of blue light, which may cause retinal photoreceptor cell damage. However, traditional blue light filters may decrease the luminance of light and reduce visual quality. We adjusted the emitted light spectrum of LED backlight modules in LCDs and reduced the energy emission but maintained the luminance. The 661W photoreceptor cell line was used as the model system. We established a formula of the ocular energy exposure index (OEEI), which could be used as the indicator of LCD energy emission. Cell viability decreased and apoptosis increased significantly after exposure to LCDs with higher emitted energy. Cell damage occurred through the induction of oxidative stress and mitochondrial dysfunction. The molecular mechanisms included activation of the NF-κB pathway and upregulation of the expression of proteins associated with inflammation and apoptosis. The effect was correlated with OEEI intensity. We demonstrated that LCD exposure-induced photoreceptor damage was correlated with LCD energy emission. LCDs with lower energy emission may, therefore, serve as suitable screens to prevent light-induced retinal damage and protect consumers' eye health.

Histologic changes associated with talaporfin sodium-mediated photodynamic therapy in rat skin.

BACKGROUND AND OBJECTIVE: Alternative treatments are needed to achieve consistent and more complete port wine stain (PWS) removal, especially in darker skin types; photodynamic therapy (PDT) is a promising alternative treatment. To this end, we previously reported on Talaporfin Sodium (TS)-mediated PDT. It is essential to understand treatment tissue effects to design a protocol that will achieve selective vascular injury without ulceration and scarring. The objective of this work is to assess skin changes associated with TS-mediated PDT with clinically relevant treatment parameters. STUDY DESIGN/MATERIALS AND METHODS: We performed TS (0.75 mg/kg)-mediated PDT (664 nm) on Sprague Dawley rats. Radiant exposures were varied between 15 and 100 J/cm2 . We took skin biopsies from subjects at 9 hours following PDT. We assessed the degree and depth of vascular and surrounding tissue injury using histology and immunohistochemical staining. RESULTS: TS-mediated PDT at 0.75 mg/kg combined with 15 and 25 J/cm2 light doses resulted in vascular injury with minimal epidermal damage. At light dose of 50 J/cm2 , epidermal damage was noted with vascular injury. At light doses >50 J/cm2 , both vascular and surrounding tissue injury were observed in the forms of vasculitis, extravasated red blood cells, and coagulative necrosis. Extensive coagulative necrosis involving deeper adnexal structures was observed for 75 and 100 J/cm2 light doses. Observed depth of injury increased with increasing radiant exposure, although this relationship was not linear. CONCLUSION: TS-mediated PDT can cause selective vascular injury; however, at higher light doses, significant extra-vascular injury was observed. This information can be used to contribute to design of safe protocols to be used for treatment of cutaneous vascular lesions. Lasers Surg. Med. 49:767-772, 2017. © 2017 Wiley Periodicals, Inc.

A selective cannabinoid CB2 agonist attenuates damage and improves memory retention following stroke in mice.

AIMS: We have recently demonstrated that treatment with a cannabinoid CB2 agonist was protective in a mouse middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. The present study aimed to determine whether these protective effects of CB2 agonism would extend to a mouse photoinjury model of permanent ischemia and determine associated alterations in cognition and infarct size. MAIN METHODS: Mice received three injections of the CB2 selective agonist O-1966 or vehicle 1h prior to and 2 and 5days following induction of stroke. Infarct size was assessed at 1, 3, or 7days post-injury and learning and memory effects of injury and O-1966 treatment were assessed on days 6 and 7 using a novel object recognition task and an operant acquisition and retention procedure. KEY FINDINGS: O-1966 treated mice had significantly smaller infarct volumes compared with vehicle treated mice. Photoinjury was also associated with a significant memory impairment on day 7 post-injury, and this deficit was reversed with O-1966 treatment. Surprisingly, sham-operated mice receiving O-1966 treatment showed a significant learning deficit in both the recognition and operant tasks compared with vehicle treated sham mice. SIGNIFICANCE: We conclude that CB2 activation is protective against cognitive deficits and tissue damage following permanent ischemia, but may dysregulate glial or neuronal function of learning and memory circuits in the absence of injury and/or inflammation.