This network analysis indicates that a range of interventions can significantly reduce myopia progression when compared with single vision spectacle lenses or placebo. In terms of refraction, atropine, pirenzepine, and progressive addition spectacle lenses were effective. In terms of axial length, atropine, orthokeratology, peripheral defocus modifying contact lenses, pirenzepine, and progressive addition spectacle lenses were effective. The most effective interventions were pharmacologic, that is, muscarinic antagonists such as atropine and pirenzepine. Certain specially designed contact lenses, including orthokeratology and peripheral defocus modifying contact lenses, had moderate effects, whereas specially designed spectacle lenses showed minimal effect.

Owing to their low-cost production, simple fabrication, and high energy conversion efficiency, dye-sensitized solar cells (DSSCs) have attracted much attention since Oregan and Grätzels seminal report in 1991. [1] A typical DSSC device consists of a dye-adsorbed TiO 2 photoanode, counter electrode, and iodide electrolyte. The counter (cathode) electrode plays a key role in regulating the DSSC device performance by catalyzing the reduction of the iodide-triiodide redox species used as a mediator to regenerate the sensitizer after electron injection. The ideal counter electrode material should possess a low sheet resistance, high reduction catalytic activity, good chemical stability, and low production costs. Because of its excellent electrocatalytic activity for the iodine reduction, high conductivity, and good chemical stability, platinum has been widely used as a counter electrode in DSSCs. However, the high costs of Pt and its limited reserves in nature have been a major concern for the energy community. Recently, much effort has been made to reduce or replace Pt-based electrodes in DSSCs. [2][3][4][5][6][7][8][9][10][11] In particular, carbon black, [5] carbon nanoparticles, [6] carbon nanotubes, [7,8] and graphene nanosheets [3,[9][10][11] have been studied as the counter electrode in DSSCs. However, their electrical conductivities and reduction catalytic activities still cannot match up to those of platinum.To improve the device performance for DSSCs with a carbon-based counter electrode, it is important to balance its electrical conductivity and the electrocatalytic activity. [10][11][12] Since the electrocatalytic activity of graphene for the triiodide reduction often increases with increasing number of defect sites (e.g., oxygen-containing functional groups in reduced graphene oxide), [10] a perfect graphene sheet may have a low charge-transfer resistance (R ct ), but a limited number of active sites for catalyzing the triiodide reduction. Unlike chemical functionalization of graphene to introduce electrocatalytic active sites by damaging the conjugated structure in the graphitic basal plan with a concomitant decrease in the electrical conductivity, doping the carbon network with heteroatoms (e.g., N, B, and P) can introduce electrocatalytic active sites with a minimized change of the conjugation length. [13] Furthermore, heteroatom doping has also been demonstrated to enhance the electrical conductivity and surface hydrophilicity to facilitate charge-transfer and electrolyte-electrode interactions, respectively, and even impart electrocatalytic activities. [13,14] Indeed, our recent articles, along with articles of others, on nitrogen doping of carbon nanotubes and graphene [13][14][15][16][17][18] have clearly shown that nitrogen-doped carbon nanomaterials can act as metal-free electrodes to show even higher electrocatalytic activities, better long-term operation stability, and more tolerance to crossover/poisoning effects relative to a platinum electrode used for oxygen reduction in fuel cells. [17,18]...

Worldwide, myopia is the leading cause of visual impairment. It results from inappropriate extension of the ocular axis and concomitant declines in scleral strength and thickness caused by extracellular matrix (ECM) remodeling. However, the identities of the initiators and signaling pathways that induce scleral ECM remodeling in myopia are unknown. Here, we used single-cell RNA-sequencing to identify pathways activated in the sclera during myopia development. We found that the hypoxia-signaling, the eIF2-signaling, and mTOR-signaling pathways were activated in murine myopic sclera. Consistent with the role of hypoxic pathways in mouse model of myopia, nearly one third of human myopia risk genes from the genome-wide association study and linkage analyses interact with genes in the hypoxia-inducible factor-1α (HIF-1α)-signaling pathway. Furthermore, experimental myopia selectively induced HIF-1α up-regulation in the myopic sclera of both mice and guinea pigs. Additionally, hypoxia exposure (5% O) promoted myofibroblast transdifferentiation with down-regulation of type I collagen in human scleral fibroblasts. Importantly, the antihypoxia drugs salidroside and formononetin down-regulated HIF-1α expression as well as the phosphorylation levels of eIF2α and mTOR, slowing experimental myopia progression without affecting normal ocular growth in guinea pigs. Furthermore, eIF2α phosphorylation inhibition suppressed experimental myopia, whereas mTOR phosphorylation induced myopia in normal mice. Collectively, these findings defined an essential role of hypoxia in scleral ECM remodeling and myopia development, suggesting a therapeutic approach to control myopia by ameliorating hypoxia.