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Bucket elevators are efficient machines to transport the granular materials in the vertical direction or along the inclined planes. Traditional bucket elevators have strong limitations in the discharging position and discharging mode. So it has important practical significance to design and develop a chain bucket elevator with multipoint discharge which can realize the horizontal and vertical simultaneous continuous transportation. The bucket is the load bearing component of the bucket elevators. This article presents the method of solving the maximum contour of the bucket, which is the combination of analytic method and graphical method. The constraint conditions and the mathematical model of the interference analysis are obtained by the interference analysis at the inflection points, and the boundary contour of the bucket at the inflection points is obtained by solving the constraint equation with MATLAB. And the boundary contour of the bucket at the discharging position is obtained by the graphical method. Therefore, the maximum contour of the bucket is determined, which can ensure not only that there is no interference between the adjacent buckets in the whole process but also that the granular materials can be fully discharged and the maximum loading capacity of the buckets can be achieved.

The molecular mechanism underlying hyperuricemia-induced lipid metabolism disorders is not clear. The purpose of the current study was to investigate the mechanism of lipid disturbances in a hyperuricemia mice model. RNA-Seq showed that differentially expressed genes (DEGs) in the fatty acid synthesis signaling pathway were mainly enriched and CXCL-13 was significantly enriched in protein-protein interaction networks. Western blotting, Q-PCR, and immunofluorescence results further showed that hyperuricemia upregulated CXCL-13 and disturbed lipid metabolism in vivo and in vitro. Furthermore, CXCL-13 alone also promoted the accumulation of lipid droplets and upregulated the expression of FAS and SREBP1, blocking AMPK signaling and activating the PKC and P38 signaling pathways. Silencing CXCL-13 reversed uric-acid-induced lipid droplet accumulation, which further downregulated FAS and SREBP1 expression, inhibited the p38 and PKC signaling, and activated AMPK signaling. In conclusion, hyperuricemia induces lipid metabolism disorders via the CXCL-13 pathway, making CXCL-13 a key regulatory factor linking hyperuricemia and lipid metabolism disorders. These results may provide novel insights for the treatment of hyperuricemia. NEW & NOTEWORTHY The underlying molecular mechanism of hyperuricemia-induced lipid metabolism disorders is still unclear. The study aimed to investigate the mechanism of lipid disturbance in hyperuricemia mice model. To our knowledge, we proposed for the first time that CXCL-13 may be a key regulator of hyperuricemia and lipid metabolism disorders. These results may provide new insights for the clinical treatment of hyperuricemia. [ABSTRACT FROM AUTHOR]