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International cooperation for renewable energy under the Belt and Road Initiative (BRI) plays a pivotal role in the transition to low-carbon energy in BRI developing countries. However, the rise in energy, debt, food, and geopolitical crises, along with the unique internal challenges found in different BRI developing countries, introduce multiple uncertainties to international renewable energy cooperation (IREC). Therefore, it is crucial to analyze the risks associated with IREC across different BRI countries by incorporating international cooperation theory. This study proposes an analytical framework comprising cooperation consensus–state capacity–institutional environment, which encompasses the willingness to cooperate, national capabilities, and international institutional considerations. An evaluation indicator system is constructed based on this framework. The study optimizes the indicator weights obtained from expert surveys using the analytic hierarchy process and the criteria importance through intercriteria correlation method. A quantitative assessment of IREC risks was conducted for 114 BRI countries from 2010 to 2020. The results indicate a gradual reduction in IREC risks between China and BRI countries. Regional risk assessments reveal that Southeast Asia exhibits the lowest average risk, while Africa not only records the highest average risk but also indicates substantial cooperation potential. Therefore, we recommend a comprehensive approach to risk mitigation. Such an approach would include gradually improving cooperation mechanisms, promoting both top-down and bottom-up cooperation, encouraging the involvement of multiple stakeholders, and prioritizing early-stage risk assessments and research. • A new analytical framework based on international cooperation theories. • A dynamic risk map for Belt and Road renewable energy cooperation. • The combination of AHP and CRITIC. • Tailored risk mitigation strategies for different regions. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (AMD) is a multifactor disease, which is primarily characterized by retinal pigment epithelium (RPE) cell loss. Since the retina is the most metabolically active tissue, RPE cells are exposed to consistent oxidative environment. So, oxidation-induced RPE cell death has long been considered a contributor to the onset of AMD. Here, we applied a retinal degeneration (RD) rat model induced by blue light-emitting diode (LED) and a cell model constructed by H 2 O 2 stimulus to mimic the prooxidant environment of the retina. We detected that the expression of miR-27a was upregulated and the expression of FOXO1 was downregulated in both models. So, we furtherly investigated the role of miR-27a-FOXO1 axis in RPE in protesting against oxidants. Lentivirus-mediated RNA was injected intravitreally into rats to modulate the miR-27a-FOXO1 axis. Retinal function and histopathological changes were evaluated by electroretinography (ERG) analysis and hematoxylin and eosin (H&E) staining, respectively. Massive photoreceptor and RPE cell death were examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The damage to the retina was aggravated in the FOXO1 gene-knockdown and miR-27a-overexpression groups after exposure to LED but was alleviated in the FOXO1 gene-overexpression or miR-27a-knockdown groups. Dual luciferase assay was used to detect the binding site of miR-27a and FOXO1. Upregulated miR-27a inhibited the expression of FOXO1 by directly binding to the FOXO1 mRNA 3'UTR and decreased the autophagy activity of ARPE-19 cells, resulting in the accumulation of reactive oxygen species (ROS) and decrease of cell viability. The results suggest that miR-27a is a negative regulator of FOXO1. Also, our data emphasize the prominent role of miR-27a/FOXO1 axis in modulating ROS accumulation and cell death in RPE cell model under oxidative stress and influencing the retinal function in the LED-induced RD rat model., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2021 Chengda Ren et al.)