No abstract

Understanding the contact mechanics of rough tooth surfaces is critical in order to understand phenomena such as tooth surface flash temperature, tooth surface wear, and gear vibration. In this paper, the contact behavior between the meshing tooth surfaces of beveloid gear pairs with elliptical asperities is the focus. The contact area distribution function of the elliptical asperity was proposed for the point contact of curved surfaces by transforming the elastic contact problem between gear meshing surfaces into the contact between elastic curved surfaces with an arbitrary radius of curvature. In addition, a fractal contact mechanics model for the rough surface of a beveloid gear with elliptical asperities was established. The influence of tooth surface topography on the contact load and contact stiffness under different fractal parameters was investigated, and the results demonstrated that the real contact load and the contact stiffness of curved surfaces increase with the increase in the fractal dimension D and the contact coefficient λ. Conversely, the real contact load and normal contact stiffness decrease with the increase in the fractal roughness G and eccentricity e.

The tooth surfaces of beveloid gears have different topography features due to machining methods, manufacturing accuracies, and surface wear, which will affect the contact state of the tooth surface, thereby affecting time-varying mesh stiffness between mating gear pairs. Therefore, a slice grouping method was proposed in this paper on the basis of potential energy to calculate the total meshing stiffness of beveloid gears with the surface topography. The method in this paper was verified by finite element method (FEM). Compared with the calculation results of this paper, the relative error is 5.9%, which demonstrated the feasibility and accuracy of the method in this paper. Then, the influence of parameters such as pressure angle, helix angle, pitch angle, tooth width, fractal dimension, and fractal roughness on meshing stiffness was investigated, of which results show that pressure angle, pitch angle, tooth width, and fractal dimension have an incremental impact on the mean value of mesh stiffness. However, the fluctuating value of mesh stiffness has also increased as the pressure angle, tooth width, and pitch cone angle increase. Both the helix angle and the fractal roughness have a depressive impact on the total stiffness. But the difference is that, with the increase of the helix angle, the fluctuation of meshing stiffness has been decreased. Conversely, with the increase of the fractal roughness, the fluctuation of meshing stiffness has been increased.

Despite recent advances in our understanding of the physiological importance of SEL1L-HRD1 endoplasmic reticulum (ER)-associated protein degradation (ERAD) using cell type-specific knockout (KO) mouse models, its relevance and importance in ataxia pathogenesis remain unknown. Here we show that loss of SEL1L-HRD1 ERAD complex interaction or function in Purkinje cells leads to cerebellar ataxia. Both homozygous knock-in (KI) mice carrying SEL1L variant p.Ser658Pro (S658P) and mice with Purkinje cell-specific deletion of SEL1L exhibit early-onset cerebellar ataxia, although disease severity and progression differ between the models. Structure-function analyses reveal that SEL1L S658P variant impairs, not abolishes, ERAD function by attenuating the interaction between SEL1L and HRD1. Proteomic screen of potential endogenous substrates leads to the identification of Astrotactin 1 and 2, two integral membrane proteins involved in neuronal function and development, whose maturation and biogenesis in the ER depend on SEL1L-HRD1 ERAD activity. These data demonstrate the pathophysiological importance of SEL1L-HRD1 interaction and function in the pathogenesis of cerebellar ataxia.