In recent years, there has been rapid growth of Chinese rail transit networks. Many of these networks require elevated bridges. This results in a bridge-borne noise source, which occurs in addition to the main noise source (i.e., wheel-rail interactions). Bridge-borne noise is attracting increasing attention because of its low-frequency noise characteristics. This review paper first analyzes the space distribution, spectral characteristics, and sound pressure levels of noise radiated by all-concrete, steelconcrete composite, and all-steel bridges, mainly according to experimental studies. Second, this paper reviews existing theoretical prediction models of noise emanating from bridges: the semianalytical method, the Rayleigh integral method, the boundary element method, and statistical energy analysis. Several case studies are reviewed, and their results are discussed. Finally, according to the results of the current review, the main factors affecting bridgeborne noise are analyzed, several noise reduction measures are proposed for different types of bridges, and their effectiveness is demonstrated.
The alphaherpesvirus pseudorabies virus (PRV) is the causative agent of pseudorabies, responsible for severe economic losses to the swine industry worldwide. The interferon-inducible GTPase guanylate-binding protein 1 (GBP1) exhibits antiviral immunity. Our findings show that there is a robust upregulation in the expression of porcine GBP1 during PRV infection. GBP1 knockout promotes PRV infection, while GBP1 overexpression restricts it. Importantly, we found that GBP1 impeded the normal structure of actin filaments in a GTPase-dependent manner, preventing PRV virions from reaching the nucleus. We also discovered that viral US3 protein bound GBP1 to interfere with its GTPase activity. Finally, the interaction between US3 and GBP1 requires US3 serine/threonine kinase activity sites and the GTPase domain (aa 1 to 308) of GBP1. Taken together, this study offers fresh perspectives on how PRV manipulates the host’s antiviral immune system.
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