Inverse Design of Broadband Dispersion Compensation Fiber Based on Deep Learning and Differential Evolution Algorithm

A Ge-doped dual-core dispersion compensation photonic crystal fiber (DC-DCPCF) is proposed. The small diameters of two layers’ air holes make DC-DCPCF form a dual-core structure, which is conducive to broadband dispersion compensation. Low Ge-doped silica as the only background material reduces the preparation difficulty and cost. It is inversely designed by using artificial neural network (ANN) combined with differential evolution algorithm (DE) to obtain target dispersion compensation. ANN replaces the finite element method to accomplish fast forward prediction of DC-DCPCF properties. DE solves the single solution problem of single or cascade network that makes it flexible and reproducible. The results demonstrate that the designed DC-DCPCF can not only compensate 45 and 25 times its length of Corning single-mode fiber 28 (SMF28) in S+C+L+U bands and E+S+C+L+U bands respectively, but also accurately compensate the residual dispersion with effective dispersion compensation being only +0.005∼+0.842ps/(nm·km) and −0.03∼+1.31ps/(nm·km), respectively. In addition, the kappa values of DCP-PCF are well matched with SMF28 in the broadband wavelength range. It takes only about 10 seconds to complete the inverse design of the target DC-DCPCF. It provides a design method for custom DC-DCPCF and an efficient inverse design solution for photonic automation in fiber optical communication systems

The Protective Role of Apelin in the Early Stages of Diabetic Retinopathy

Diabetic retinopathy (DR) is one of the most common and serious microvascular complications of diabetes. Although current treatments can control the progression of DR to a certain extent, there is no effective treatment for early DR. Apart from vascular endothelial growth factor, it has been noted that the apelin/APJ system contributes to the pathogenesis of DR. We used a high-fat diet/streptozotocin-induced type 2 diabetic mouse model. The mice were divided into a lentivirus control group (LV-EGFP), an apelin-overexpression group (LV-Apelin+), and an apelin-knockdown group (LV-Apelin−), all of which were administrated intravitreal injections. LV-Apelin+ ameliorated the loss of pericytes in DR mice, whereas LV-Apelin− aggravated the loss of pericytes. Similarly, LV-Apelin+ reduced the leakage of retinal vessels, whereas LV-Apelin− exacerbated it. The genes and signaling pathway related to cell adhesion molecules were downregulated, whereas the cell–cell tight junctions and anti-apoptotic genes were upregulated in response to apelin overexpression. However, the alterations of these same genes and signaling pathways were reversed in the case of apelin knockdown. Additionally, LV-Apelin+ increased ZO-1 and occludin levels, whereas LV-Apelin− decreased them. Our results suggest that apelin can reduce vascular leakage by protecting pericytes, which offers a promising new direction for the early treatment of DR