A Survey on Federated Learning Poisoning Attacks and Defenses

As one kind of distributed machine learning technique, federated learning enables multiple clients to build a model across decentralized data collaboratively without explicitly aggregating the data. Due to its ability to break data silos, federated learning has received increasing attention in many fields, including finance, healthcare, and education. However, the invisibility of clients' training data and the local training process result in some security issues. Recently, many works have been proposed to research the security attacks and defenses in federated learning, but there has been no special survey on poisoning attacks on federated learning and the corresponding defenses. In this paper, we investigate the most advanced schemes of federated learning poisoning attacks and defenses and point out the future directions in these areas

Effects of Geometry Design Parameters on the Static Strength and Dynamics for Spiral Bevel Gear

Considering the geometry design parameters, a quasi-static mesh model of spiral bevel gears was established and the mesh characteristics were computed. Considering the time-varying effects of mesh points, mesh force, line-of-action vector, mesh stiffness, transmission error, friction force direction, and friction coefficient, a nonlinear lumped parameter dynamic model was developed for the spiral bevel gear pair. Based on the mesh model and the nonlinear dynamic model, the effects of main geometry parameters on the contact and bending strength were analyzed. Also, the effects on the dynamic mesh force and dynamic transmission error were investigated. Results show that higher value for the pressure angle, root fillet radius, and the ratio of tooth thickness tend to improve the contact and bending strength and to reduce the risk of tooth fracture. Improved gears have a better vibration performance in the targeted frequency range. Finally, bench tests for both types of spiral bevel gears were performed. Results show that the main failure mode is the tooth fracture and the life was increased a lot for the spiral bevel gears with improved geometry parameters compared to the original design

Propagation Modeling of Passive Worms in P2P Networks

Abstract-Recent years, researchers have recognized the damage resulting from P2P worms, and some works on P2P worms have been done. However, compared with the study of active worm propagation, passive worm propagation has been less highlighted. Passive worms propagate slowly in Internet, but P2P system can be a potential vehicle to fast the propagation of passive worms. In this paper, we address the issue by analyzing the passive worm propagation models in P2P networks and passive worm propagation is modeled in the mean-field method. The fact that the theory values are in consistence with the simulation values shows that these models proposed are valid and can be used to analyze and predict P2P worm propagation patterns

Di-n-butyl phthalate stress hampers compost multifunctionality by reducing microbial biomass, diversity and network complexity

Phthalates are common pollutants in agriculture. Here, the influence of di-n-butyl phthalate (DBP) on multifunctionality of composting was assessed. Results indicated that DBP stress (100 mg/kg) hampered multifunctionality from the thermophilic phase onwards and resulted in a 6.5 % reduction of all assessed functions. DBP stress also significantly reduced microbial biomass (P &lt; 0.05), altered microbial composition (P &lt; 0.05), and decreased network complexity (P &lt; 0.01). Multifunctionality was found to be strongly correlated (P &lt; 0.001) with microbial biomass, diversity, and network complexity. In addition, keystone taxa responsive to DBP were identified as Streptomyces, Thermoactinomyces, Mycothermus, and Lutispora. These taxa were significantly (P &lt; 0.001) affected by DBP stress, and a correlation between them and multifunctionality was shown. This study contributes to a better understanding of the negative implications of phthalates during composting processes, which is of great significance to the development of new treatment strategies for agricultural waste.</p

PinX1-Promoted Autophagy Inhibits Cell Proliferation and Induces Cell Apoptosis by Inhibiting the NF-κB/p65 Signaling Pathway in Nasopharyngeal Carcinoma

Background: The role of Pin2 telomeric repeat factor 1-interacting telomerase inhibitor 1 (PinX1) in tumorigenesis and development has been extensively studied. As we previously demonstrated, PinX1 plays an important role in modulating epithelial-mesenchymal transition (EMT), stemness, cell proliferation, and apoptosis in nasopharyngeal carcinoma (NPC). However, the relationship between PinX1, autophagy, and cell function in NPC remains unclear. This study aimed to investigate the mechanisms by which PinX1 regulates autophagy in NPC, and to explore its biological role and clinical significance in disease progression. Methods: The proliferative capacity of NPC cells was assessed by MTT and xenograft tumorigenicity assays. Autophagic flux was monitored using a tandem monomeric DAPI–FITC–LC3 reporter assay. The rates of apoptosis and the cell cycle in NPC cells were analyzed using flow cytometry. The activation of autophagy and the signaling status of the AKT/mTOR and NF-κB/p65 pathways were evaluated by Western blot analysis. Results: In addition to promoting autophagy and apoptosis, PinX1 overexpression suppressed proliferation, migration, invasion, and decelerated cell-cycle progression in NPC cells. These effects were reversed by inhibiting autophagy with 3-methyladenine. Mechanistic investigations clarified that PinX1 overexpression significantly reduced the expression of p-AKT, p-mTOR, p65, and p-p65. Chloroquine treatment in PinX1-overexpressing cells did not significantly alter p-AKT and p-mTOR levels, whereas 3-MA treatment in PinX1-overexpressing cells resulted in increased p65 and p-p65 expression, relative to untreated PinX1-overexpressing cells. Conclusions: It appears that PinX1 promotes autophagy by inhibiting the AKT/mTOR signaling pathway, which then inhibits NF-κB/p65 pathways, and consequently inhibiting cell proliferation and causing cell apoptosis in NPC cells