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• Novel CRB vibration model considering contact stiffness and natural frequency characteristics. • The outer raceway spalling fault with varying sizes is simulated in this paper, considering spalling defect extents and load distribution. • This paper showed that the effects of contact stiffness variation on natural frequency characteristics by the statistical distribution of fault feature signals. The modeling of early spalling defects in cylindrical roller bearings (CRB) is a challenging problem in fault diagnosis. Due to the absence of prominent "drop-in" excitation, accurately describing the signal characteristics of the early failure mechanism model for CRBs becomes difficult. In this paper, the failure of cylindrical roller bearings due to spalling caused by fatigue is a frequent occurrence. The previous defect models have been centered on sharp-edge impact between the roller and spalling defects. However, they have not provided an adequate depiction of the variation in contact stiffness caused by roller-fault interaction. In this paper, a novel CRB vibration model that takes into account contact stiffness and natural frequency characteristics is proposed. The model considers both the load redistribution and contact stiffness variation caused by spalling defects. This new model provides a spring-damper system based on contact stiffness between the roller and raceway, enabling an estimation of the CRB system's natural frequency characteristics. The outer raceway spalling fault with varying sizes is simulated in this paper, taking into account spalling defect extents and load distribution. The vibration response of the fault signal model is investigated. The simulation results show that the load and contact stiffness will change as the roller passes through the defect zone. Furthermore, the statistical distribution of fault feature signals demonstrates the effects of contact stiffness variation on natural frequency characteristics. The experiments given in this paper have verified the simulation results of the proposed signal model. [ABSTRACT FROM AUTHOR]

Progesterone has been recognized as essential for the establishment and maintenance of pregnancy, and is typically known as an immunosuppressive agent. However, its effects on mediating Brucella infection-induced inflammation have not been evaluated. Here we demonstrated that Brucella abortus infection inhibits progesterone levels in the pregnant mouse by suppressing the production of progesterone by placenta. Progesterone treatment significantly reduced the secretion of inflammatory cytokines in serum, macrophages, and trophoblasts of B. abortus-infected mice, leading to decreased placentitis and enhancing the pup viability. Mechanistically, this decreased inflammatory response results from inhibition of NF-kB activation by progesterone. Moreover, progesterone treatment suppresses B. abortus growth within trophoblasts associated with an inability of bacteria to escape the late endosome compartment in vitro. Collectively, our data illustrate that progesterone treatment might be useful therapeutically in protection against placentitis or abortion caused by B. abortus infection. [ABSTRACT FROM AUTHOR]

• A host circular RNA, circRNA_0050463, is up-regulated in influenza A virus (IAV)-infected lung epithelial (A549) cells. • CircRNA_0050463 knockdown suppresses IAV replication in A549 cells. • CircRNA_0050463 acts as an endogenous sponge of miR-33b-5p. • CircRNA_0050463 facilitates IAV replication via miR-33b-5p/EEF1A1 axis. Circular RNAs (circRNAs), a new class of widely expressed endogenous regulatory RNAs, are characterized by a covalently closed loop structure without a 5' cap or 3' tail. Increasing numbers of studies have shown that circRNAs play important roles in diverse physiological and pathological processes, including the dynamic interactions between viruses and hosts. However, their multifaceted roles in cellular responses to influenza A virus (IAV) infection remain largely unknown. Here, we analyzed the expression of circ_0050463, which is predominantly localized in cytoplasm, in response to IAV infection. Knockdown of circ_0050463 with siRNA in A549 cells inhibited IAV replication. In addition, the activation of nuclear factor κB (NF-κB) was involved in IAV-induced circ_0050463 expression, as revealed by assay using a NF-Kb inhibitor (Bay 11-7082). By performing biotin-labeled RNA pull-down and luciferase reporter assay, we demonstrated that circ_0050463 functioned as an endogenous microRNA-33b-5p sponge to sequester and inhibit miR-33b-5p activity, resulting in increased eukaryotic translation elongation factor 1 alpha 1 (EEF1A1) expression with subsequent facilitation of IAV replication. Taken together, the results of our study indicate that the circ_0050463 promotes IAV replication via miR-33b-5p/EEF1A1 axis, thus providing evidence for the host circRNAs utilized by viruses to support their replication. [ABSTRACT FROM AUTHOR]