Zhuan Li

Abstract Compared to human vision, conventional machine vision composed of an image sensor and processor suffers from high latency and large power consumption due to physically separated image sensing and processing. A neuromorphic vision system with brain-inspired visual perception provides a promising solution to the problem. Here we propose and demonstrate a prototype neuromorphic vision system by networking a retinomorphic sensor with a memristive crossbar. We fabricate the retinomorphic sensor by using WSe2/h-BN/Al2O3 van der Waals heterostructures with gate-tunable photoresponses, to closely mimic the human retinal capabilities in simultaneously sensing and processing images. We then network the sensor with a large-scale Pt/Ta/HfO2/Ta one-transistor-one-resistor (1T1R) memristive crossbar, which plays a similar role to the visual cortex in the human brain. The realized neuromorphic vision system allows for fast letter recognition and object tracking, indicating the capabilities of image sensing, processing and recognition in the full analog regime. Our work suggests that such a neuromorphic vision system may open up unprecedented opportunities in future visual perception applications.

BACKGROUND: Doxorubicin (DOX)-induced cardiotoxicity (DIC) is a major impediment to its clinical application. It is indispensable to explore alternative treatment molecules or drugs for mitigating DIC. WGX50, an organic extract derived from Zanthoxylum bungeanum Maxim, has anti-inflammatory and antioxidant biological activity, however, its function and mechanism in DIC remain unclear. METHODS: , MDA, and GPX4 were measured using ELISA, RT-qPCR, and western blot assays. The morphology of mitochondria was investigated with a transmission electron microscope. The levels of mitochondrial membrane potential, mitochondrial ROS, and lipid ROS were detected using JC-1, MitoSOX™, and C11-BODIPY 581/591 probes. RESULTS: Our findings demonstrate that WGX50 protects DOX-induced cardiotoxicity via restraining mitochondrial ROS and ferroptosis. In vivo, WGX50 effectively relieves doxorubicin-induced cardiac dysfunction, cardiac injury, fibrosis, mitochondrial damage, and redox imbalance. In vitro, WGX50 preserves mitochondrial function by reducing the level of mitochondrial membrane potential and increasing mitochondrial ATP production. Furthermore, WGX50 reduces iron accumulation and mitochondrial ROS, increases GPX4 expression, and regulates lipid metabolism to inhibit DOX-induced ferroptosis. CONCLUSION: Taken together, WGX50 protects DOX-induced cardiotoxicity via mitochondrial ROS and the ferroptosis pathway, which provides novel insights for WGX50 as a promising drug candidate for cardioprotection.