RESUMEN
Aiming at the problems of low efficiency and poor accuracy in the product surface defect detection. In this paper, an online surface defects detection method based on YOLOV3 is proposed. Firstly, using lightweight network MobileNetV2 to replace the original backbone as the feature extractor to improve network speed. Then, we propose an extended feature pyramid network (EFPN) to extend the detection layer for multi-size object detection and design a novel feature fusing module (FFM) embedded in the extend layer to super-resolve features and capture more regional details. In addition, we add an IoU loss function to solve the mismatch between classification and bounding box regression. The proposed method is used to train and test on the hot rolled steel open dataset NEU-DET, which contains six typical defects of a steel surface, namely rolled-in scale, patches, crazing, pitted surface, inclusion and scratches. The experimental results show that our method achieves a satisfactory balance between performance and consumption and reaches 86.96% mAP with a speed of 80.96 FPS, which is more accurate and faster than many other algorithms and can realize real-time and high-precision inspection of product surface defects.
RESUMEN
Many synaptic proteins form biological condensates via liquid-liquid phase separation (LLPS). Synaptopathy, a key feature of autism spectrum disorders (ASD), is likely relevant to the impaired phase separation and/or transition of ASD-linked synaptic proteins. Here, we report that LLPS and zinc-induced liquid-to-gel phase transition regulate the synaptic distribution and protein-protein interaction of cortactin-binding protein 2 (CTTNBP2), an ASD-linked protein. CTTNBP2 forms self-assembled condensates through its C-terminal intrinsically disordered region and facilitates SHANK3 co-condensation at dendritic spines. Zinc binds the N-terminal coiled-coil region of CTTNBP2, promoting higher-order assemblies. Consequently, it leads to reduce CTTNBP2 mobility and enhance the stability and synaptic retention of CTTNBP2 condensates. Moreover, ASD-linked mutations alter condensate formation and synaptic retention of CTTNBP2 and impair mouse social behaviors, which are all ameliorated by zinc supplementation. Our study suggests the relevance of condensate formation and zinc-induced phase transition to the synaptic distribution and function of ASD-linked proteins.