Chlorophyll (Chl) a fluorescence parameters and rapid light curves of soybean [Glycine max (L.) Merrill] were measured by pulse amplitude modulation fluorometry. Measurements were taken during different stages of soybean growth under field conditions with 20% enhancement in ultraviolet-B (UV-B) radiation. Results showed that supplemental UV-B radiation decreased Chl contents by 5.5% (P=0.048), 8.7% (P=0.046), and 10.5% (P=0.005) in seedling, in branching-flowering, and in pod-setting stages, respectively. In the branching-flowering and pod-setting stages, maximum quantum yield of photosystem (PS) II photochemistry (Fv/Fm) decreased by 6.1% (P=0.001) and 3.0% (P=0.009), respectively. Supplemental UV-B radiation significantly decreased the effective quantum yield (Y). The photosynthetic capacity at light saturation (Pm) also decreased in both the seedling and branching-flowering stages by 28.9% (P=0.007) and 15.5% (P=0.041), respectively. However, Y and Pm showed no significant difference in the trefoil and pod-setting stages with and without the UV treatment. The light saturation parameter (E k) decreased by 21.1% (P=0.000) and 23.2% (P=0.029) in the trefoil and seedling stages, respectively. Moreover, the initial slope (α) decreased by 21.1% (P=0.001) in the branching-flowering stage. Nonphotochemical quenching (NPQ) in the seedling stage and photochemical quenching coefficient (qp) in the
branching-flowering stage decreased significantly under UV-B treatments. The results of the present study suggest that supplemental UV-B radiation adversely affected Chl content and electron transport activity in PSII and consequently decreased the photosynthetic efficiency of soybean plants., Z. Hu ... [et al.]., and Obsahuje bibliografii
Endothelial cells (ECs) are primary targets of glucose-induced tissue damage. As a result of hyperglycemia, endothelin-1 (ET-1) is upregulated in organs affected by chronic diabetic complications. The objective of the present study was to identify novel transcriptional mechanisms that influence ET-1 regulation in diabetes. We carried out the investigation in microvascular ECs using multiple approaches. ECs were incubated with 5 mM glucose (NG) or 25 mM glucose (HG) and analyses for DNA methylation, histone methylation, or long non-coding RNA- mediated regulation of ET-1 mRNA were then performed. DNA methylation array analyses demonstrated the presence of hypomethylation in the proximal promoter and 5’ UTR/first exon regions of EDN1 following HG culture. Further, globally blocking DNA methylation or histone methylation significantly increased ET-1 mRNA expressions in both NG and HG-treated HRECs. While, knocking down the pathogenetic lncRNAs ANRIL, MALAT1, and ZFAS1 subsequently prevented the glucose-induced upregulation of ET-1 transcripts. Based on our past and present findings, we present a novel paradigm that reveals a complex web of epigenetic mechanisms regulating glucose-induced transcription of ET-1. Improving our understanding of such processes may lead to better targeted therapies., S. Biswas, B. Feng, A. Thomas, S. Chen, E. Aref-Eshghi, B. Sadikovic, S. Chakrabarti., and Seznam literatury