Model X-ray:Detect Backdoored Models via Decision Boundary

Deep neural networks (DNNs) have revolutionized various industries, leading to the rise of Machine Learning as a Service (MLaaS). In this paradigm, well-trained models are typically deployed through APIs. However, DNNs are susceptible to backdoor attacks, which pose significant risks to their applications. This vulnerability necessitates a method for users to ascertain whether an API is compromised before usage. Although many backdoor detection methods have been developed, they often operate under the assumption that the defender has access to specific information such as details of the attack, soft predictions from the model API, and even the knowledge of the model parameters, limiting their practicality in MLaaS scenarios. To address it, in this paper, we begin by presenting an intriguing observation: the decision boundary of the backdoored model exhibits a greater degree of closeness than that of the clean model. Simultaneously, if only one single label is infected, a larger portion of the regions will be dominated by the attacked label. Building upon this observation, we propose Model X-ray, a novel backdoor detection approach for MLaaS through the analysis of decision boundaries. Model X-ray can not only identify whether the target API is infected by backdoor attacks but also determine the target attacked label under the all-to-one attack strategy. Importantly, it accomplishes this solely by the hard prediction of clean inputs, regardless of any assumptions about attacks and prior knowledge of the training details of the model. Extensive experiments demonstrated that Model X-ray can be effective for MLaaS across diverse backdoor attacks, datasets, and architectures

Research on how the digital economy has affected the improvement and modernization of the industrial structure in the Beijing-Tianjin-Hebei area

Due to the Internet's rapid technological advancement, the level of digital economy development has become a crucial metric for assessing the quality of economic development as well as a significant driver for the improvement and modernization of industrial structure. It is crucial to examine and research the effects of the digital economy's growth on the modernization and optimization of the industrial structure in Beijing, Tianjin, and Hebei from the standpoint of cooperative development. Based on collecting and organizing relevant literature, this essay explains and evaluates Beijing, Tianjin, and Hebei's current state of industrial structure modernization and the growth of the digital economy, and conducts an econometric analysis to conclude that the level of digital economy development and industrial structure upgrading in Beijing, Tianjin and Hebei is improving. Next, the degree of government intervention, the amount of direct investment by foreign businessmen and the level of innovation in technology are introduced as control variables to construct a regression model, and it is discovered that the upgrading of the industrial structure in Beijing, Tianjin, and Hebei is significantly benefited by the digital economy.</jats:p

GSDMD Mediates LPS-Induced Septic Myocardial Dysfunction by Regulating ROS-dependent NLRP3 Inflammasome Activation

Myocardial dysfunction is a serious consequence of sepsis and contributes to high mortality. Currently, the molecular mechanism of myocardial dysfunction induced by sepsis remains unclear. In the present study, we investigated the role of gasdermin D (GSDMD) in cardiac dysfunction in septic mice and the underlying mechanism. C57BL/6 wild-type (WT) mice and age-matched Gsdmd-knockout (Gsdmd-/-) mice were intraperitoneally injected with lipopolysaccharide (LPS) (10 mg/kg) to mimic sepsis. The results showed that GSDMD-NT, the functional fragment of GSDMD, was upregulated in the heart tissue of septic WT mice induced by LPS, which was accompanied by decreased cardiac function and myocardial injury, as shown by decreased ejection fraction (EF) and fractional shortening (FS) and increased cardiac troponin I (cTnI), creatine kinase isoenzymes MB (CK-MB), and lactate dehydrogenase (LDH). Gsdmd-/- mice exhibited protection against LPS-induced myocardial dysfunction and had a higher survival rate. Gsdmd deficiency attenuated LPS-induced myocardial injury and cell death. Gsdmd deficiency prevented LPS-induced the increase of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in serum, as well as IL-1β and TNF-α mRNA levels in myocardium. In addition, LPS-mediated inflammatory cell infiltration into the myocardium was ameliorated and activation of NF-κB signaling pathway and the NOD-like receptor protein 3 (NLPR3) inflammasome were suppressed in Gsdmd-/- mice. Further research showed that in the myocardium of LPS-induced septic mice, GSDMD-NT enrichment in mitochondria led to mitochondrial dysfunction and reactive oxygen species (ROS) overproduction, which further regulated the activation of the NLRP3 inflammasome. In summary, our data suggest that GSDMD plays a vital role in the pathophysiology of LPS-induced myocardial dysfunction and may be a crucial target for the prevention and treatment of sepsis-induced myocardial dysfunction.</jats:p

Rapid ILs-polishing Processes Toward Flexible Nanostructured Paper with Dually High Transparency and Haze

AbstractBiodegradable highly nanostructured paper has received great interest in past years due to its excellent optical properties which facilitate its wide applications in green flexible electronics and devices. However, energy and/or time-consuming procedure during the process of fabricating most nanostructured transparent paper are presently the main obstacle to their scalable production. In this work, we demonstrated a novel nanostructured paper with dually high transparency (∼91%) and high haze (∼89%) that was directly fabricated from original paper with rapid ILs-polishing processes. The whole fabricating time only requires 10 min. Compared to the previously reported nanopaper made of the isolated cellulose nanofibers by pure mechanical and/or chemical approaches, this work presented herein is devoted to use green ILs to polish directly the micrometer-sized fibrous paper into the nanostructured paper. This new method brings a rapid fabrication of transparent nanostructured paper while also retaining dual intriguing properties both in optical transmittance and haze. This work is capable of fabricating next-generation flexible and highly transparent and haze paper by a high-speed roll-to-roll manufacturing process with a much lower cost.</jats:p

Table1_GSDMD Mediates LPS-Induced Septic Myocardial Dysfunction by Regulating ROS-dependent NLRP3 Inflammasome Activation.xlsx

Myocardial dysfunction is a serious consequence of sepsis and contributes to high mortality. Currently, the molecular mechanism of myocardial dysfunction induced by sepsis remains unclear. In the present study, we investigated the role of gasdermin D (GSDMD) in cardiac dysfunction in septic mice and the underlying mechanism. C57BL/6 wild-type (WT) mice and age-matched Gsdmd-knockout (Gsdmd-/-) mice were intraperitoneally injected with lipopolysaccharide (LPS) (10 mg/kg) to mimic sepsis. The results showed that GSDMD-NT, the functional fragment of GSDMD, was upregulated in the heart tissue of septic WT mice induced by LPS, which was accompanied by decreased cardiac function and myocardial injury, as shown by decreased ejection fraction (EF) and fractional shortening (FS) and increased cardiac troponin I (cTnI), creatine kinase isoenzymes MB (CK-MB), and lactate dehydrogenase (LDH). Gsdmd-/- mice exhibited protection against LPS-induced myocardial dysfunction and had a higher survival rate. Gsdmd deficiency attenuated LPS-induced myocardial injury and cell death. Gsdmd deficiency prevented LPS-induced the increase of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in serum, as well as IL-1β and TNF-α mRNA levels in myocardium. In addition, LPS-mediated inflammatory cell infiltration into the myocardium was ameliorated and activation of NF-κB signaling pathway and the NOD-like receptor protein 3 (NLPR3) inflammasome were suppressed in Gsdmd-/- mice. Further research showed that in the myocardium of LPS-induced septic mice, GSDMD-NT enrichment in mitochondria led to mitochondrial dysfunction and reactive oxygen species (ROS) overproduction, which further regulated the activation of the NLRP3 inflammasome. In summary, our data suggest that GSDMD plays a vital role in the pathophysiology of LPS-induced myocardial dysfunction and may be a crucial target for the prevention and treatment of sepsis-induced myocardial dysfunction.</p