Time-Constrained Adversarial Defense in IoT Edge Devices through Kernel Tensor Decomposition and Multi-DNN Scheduling.

The development of deep learning technology has resulted in great contributions in many artificial intelligence services, but adversarial attack techniques on deep learning models are also becoming more diverse and sophisticated. IoT edge devices take cloud-independent on-device DNN (deep neural network) processing technology to exhibit a fast response time. However, if the computational complexity of the denoizer for adversarial noises is high, or if a single embedded GPU is shared by multiple DNN models, adversarial defense at the on-device level is bound to represent a long latency. To solve this problem, eDenoizer is proposed in this paper. First, it applies Tucker decomposition to reduce the computational amount required for convolutional kernel tensors in the denoizer. Second, eDenoizer effectively orchestrates both the denoizer and the model defended by the denoizer simultaneously. In addition, the priority of the CPU side can be projected onto the GPU which is completely priority-agnostic, so that the delay can be minimized when the denoizer and the defense target model are assigned a high priority. As a result of confirming through extensive experiments, the reduction of classification accuracy was very marginal, up to 1.78%, and the inference speed accompanied by adversarial defense was improved up to 51.72%.

Effect of Impurities Control on the Crystallization and Densification of Polymer-Derived SiC Fibers.

The polymer-derived SiC fibers are mainly used as reinforcing materials for ceramic matrix composites (CMCs) because of their excellent mechanical properties at high temperature. However, decomposition reactions such as release of SiO and CO gases and the formation of pores proceed above 1400 °C because of impurities introduced during the curing process. In this study, polycrystalline SiC fibers were fabricated by applying iodine-curing method and using controlled pyrolysis conditions to investigate crystallization and densification behavior. Oxygen and iodine impurities in amorphous SiC fibers were reduced without pores by diffusion and release to the fiber surface depending on the pyrolysis time. In addition, the reduction of the impurity content had a positive effect on the densification and crystallization of polymer-derived SiC fibers without a sintering aid above the sintering temperature. Consequently, dense Si-Al-C-O polycrystalline fibers containing ß-SiC crystal grains of 50~100 nm were easily fabricated through the blending method and controlled pyrolysis conditions.

Sofalcone, a gastroprotective drug, covalently binds to KEAP1 to activate Nrf2 resulting in anti-colitic activity.

Sofalcone is a synthetic chalcone being used as a gastric mucosa protective agent in Japan. Sofalcone contains a 1,3-diaryl-2-propen-1-one moiety, which is a common chemical scaffold in naturally occurring chalcones. The α,ß-unsaturated carbonyl group (Michael reaction acceptor) has electrophilic properties. We investigated the biochemical mechanisms by which sofalcone activated the cytoprotective and anti-inflammatory nuclear factor-erythroid 2 (NF-E2) p45-related factor 2 (Nrf2)-heme oxygenase (HO)-1 pathway. Furthermore, we investigated whether the activation of this pathway was involved in sofalcone -mediated protective effects in an experimental colitis model. Sofalcone induced HO-1 protein expression, which was dependent on increased nuclear accumulation of Nrf2 in human colon carcinoma cells. In addition, Sofalcone reacted with nucleophilic thiol compounds to form Michael adducts. A reduced form of sofalcone (SFCR) in which the Michael reaction acceptor was deactivated, did not exert biological or chemical activity. Biotin-tagged sofalcone bound to Kelch-like ECH-associated protein 1 (KEAP1), a cytosolic repressor of Nrf2. This binding was prevented by pretreatment with sofalcone and a thiol compound but not with SFCR. Furthermore, sofalcone treatment induced dissociation of the Nrf2-KEAP1 complex. Rectal administration of sofalcone alleviated colon damage and inflammation and increased colon nuclear accumulation of Nrf2 and HO-1 levels in a dinitrobenzene sulfonic acid-induced rat colitis model. The protective effects of sofalcone against colon damage and inflammation were significantly inhibited by co-administration of an HO-1 inhibitor. In conclusion, sofalcone activated the Nrf2-HO-1 pathway by covalently binding to KEAP1 via Michael addition, and may confer anti-colitic effects by inducing Nrf2 activation.

CCN5 knockout mice exhibit lipotoxic cardiomyopathy with mild obesity and diabetes.

Obesity is associated with various human disorders, such as type 2 diabetes, cardiovascular diseases, hypertension, and cancers. In this study, we observed that knockout (KO) of CCN5, which encodes a matricellular protein, caused mild obesity in mice. The CCN5 KO mice also exhibited mild diabetes characterized by high fasting glucose levels and impaired insulin and glucose tolerances. Cardiac hypertrophy, ectopic lipid accumulation, and impaired lipid metabolism in hearts were observed in the CCN5 KO mice, as determined using histology, quantitative RT-PCR, and western blotting. Fibrosis was significantly greater in hearts from the CCN5 KO mice both in interstitial and perivascular regions, which was accompanied by higher expression of pro-fibrotic and pro-inflammatory genes. Both systolic and diastolic functions were significantly impaired in hearts from the CCN5 KO mice, as assessed using echocardiography. Taken together, these results indicate that CCN5 KO leads to lipotoxic cardiomyopathy with mild obesity and diabetes in mice.