Object detection systems are widely used in various fields such as autonomous vehicles and facial recognition. In particular, object detection using deep learning networks enables real-time processing in low-performance edge devices, and can maintain high detection rates. However, edge devices that operate far from administrators are vulnerable to various physical attacks by malicious adversaries. In this paper, we implement a function for detecting traffic signs by using three versions of You Only Look Once (YOLO) and Faster-RCNN, which can be adopted by edge devices of autonomous vehicles. Then, assuming the role of a malicious attacker, we executed adversarial patch attacks with Adv-Patch and Dpatch. As a result of experimenting with misdetection of traffic stop signs using Adv-Patch and Dpatch, we confirmed the attacks can succeed with a high probability. To defeat these attacks, we propose an image reconstruction method using an autoencoder and the Structural Similarity Index Measure (SSIM). We confirm that the proposed method can sufficiently defend against an attack, attaining an AP above 91.46% even when two adversarial attacks are launched.

Recently, deep neural networks (DNNs) have been widely used in various fields such as autonomous vehicles and smart homes. Since these DNNs can be directly implemented on edge devices, they offer advantages such as real-time processing in low-power and low-bandwidth environments. However, deployment of DNNs in embedded systems, including edge devices, exposes them to threats such as fault injection attacks. In this paper, we introduce two methods to induce misclassifications by using clock and voltage glitch-based fault attacks in devices where DNN models are executed. As a result of experiments on a microcontroller implemented with a DNN for image classification, we show that glitch injection attacks can lead with high probability to serious misclassifications. Furthermore, we propose a countermeasure to glitch attacks on the softmax function, and confirm that this method is effective in preventing misclassifications.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising chemotherapeutic agent because of its selective apoptotic action on cancer cells. However, resistance to TRAIL-induced apoptosis remains a challenge in many cancers. The gintonin-enriched Panax ginseng extract fraction (GEF) has diverse pharmacological benefits. We explored the combined efficacy of GEF and TRAIL in inducing apoptosis in human renal cell carcinoma (RCC) cells. The effect of GEF treatment on viability, clonogenic potential, wound healing, and TRAIL-induced apoptotic signaling of RCC cells was studied in vitro. Our investigation revealed that GEF pre-treatment sensitized RCC cells to TRAIL-induced apoptosis, as evidenced by DNA fragmentation and cell proliferation, colony formation, and migration inhibition. This sensitization was linked to the upregulation of death receptors 4 and 5 and alterations in apoptotic protein expression; notably, decreased expression of Mu-2-related death-inducing gene, a novel anti-apoptotic protein. Our findings underscore the necessity of caspase activation for GEF/TRAIL-induced apoptosis using the pan-caspase inhibitor Z-VAD-FMK. It demonstrates that GEF sensitizes human RCC cells to TRAIL-induced apoptosis by upregulating DR4/5 and modulating apoptotic protein expression. These findings suggest a promising strategy for overcoming TRAIL resistance in cancer therapy and highlight the potential of GEF as a valuable adjunct to TRAIL-based treatments.