Enabling Fast and Universal Audio Adversarial Attack Using Generative Model

Recently, the vulnerability of DNN-based audio systems to adversarial attacks has obtained the increasing attention. However, the existing audio adversarial attacks allow the adversary to possess the entire user's audio input as well as granting sufficient time budget to generate the adversarial perturbations. These idealized assumptions, however, makes the existing audio adversarial attacks mostly impossible to be launched in a timely fashion in practice (e.g., playing unnoticeable adversarial perturbations along with user's streaming input). To overcome these limitations, in this paper we propose fast audio adversarial perturbation generator (FAPG), which uses generative model to generate adversarial perturbations for the audio input in a single forward pass, thereby drastically improving the perturbation generation speed. Built on the top of FAPG, we further propose universal audio adversarial perturbation generator (UAPG), a scheme crafting universal adversarial perturbation that can be imposed on arbitrary benign audio input to cause misclassification. Extensive experiments show that our proposed FAPG can achieve up to 167X speedup over the state-of-the-art audio adversarial attack methods. Also our proposed UAPG can generate universal adversarial perturbation that achieves much better attack performance than the state-of-the-art solutions.Comment: Publish on AAAI2

Exploring the shared molecular mechanism of microvascular and macrovascular complications in diabetes: Seeking the hub of circulatory system injury

BackgroundMicrovascular complications, such as diabetic retinopathy (DR) and diabetic nephropathy (DN), and macrovascular complications, referring to atherosclerosis (AS), are the main complications of diabetes. Blindness or fatal microvascular diseases are considered to be identified earlier than fatal macrovascular complications. Exploring the intrinsic relationship between microvascular and macrovascular complications and the hub of pathogenesis is of vital importance for prolonging the life span of patients with diabetes and improving the quality of life.Materials and methodsThe expression profiles of GSE28829, GSE30529, GSE146615 and GSE134998 were downloaded from the Gene Expression Omnibus database, which contained 29 atherosclerotic plaque samples, including 16 AS samples and 13 normal controls; 22 renal glomeruli and tubules samples from diabetes nephropathy including 12 DN samples and 10 normal controls; 73 lymphoblastoid cell line samples, including 52 DR samples and 21 normal controls. The microarray datasets were consolidated and DEGs were acquired and further analyzed by bioinformatics techniques including GSEA analysis, GO-KEGG functional clustering by R (version 4.0.5), PPI analysis by Cytoscape (version 3.8.2) and String database, miRNA analysis by Diana database, and hub genes analysis by Metascape database. The drug sensitivity of characteristic DEGs was analyzed.ResultA total of 3709, 4185 and 8086 DEGs were recognized in AS, DN, DR, respectively, with 1820, 1666, 888 upregulated and 1889, 2519, 7198 downregulated. GO and KEGG pathway analyses of DEGs and GSEA analysis of common differential genes demonstrated that these significant sites focused primarily on inflammation-oxidative stress and immune regulation pathways. PPI networks show the connection and regulation on top-250 significant sites of AS, DN, DR. MiRNA analysis explored the non-coding RNA upstream regulation network and significant pathway in AS, DN, DR. The joint analysis of multiple diseases shows the common influenced pathways of AS, DN, DR and explored the interaction between top-1000 DEGs at the same time.ConclusionIn the microvascular and macrovascular complications of diabetes, immune-mediated inflammatory response, chronic inflammation caused by endothelial cell activation and oxidative stress are the three links linking atherosclerosis, diabetes retinopathy and diabetes nephropathy together. Our study has clarified the intrinsic relationship and common tissue damage mechanism of microcirculation and circulatory system complications in diabetes, and explored the mechanism center of these two vascular complications. It has far-reaching clinical and social value for reducing the incidence of fatal events and early controlling the progress of disabling and fatal circulatory complications in diabetes