Search

This study proposes AVARA, an innovative adaptive Voronoi diagram algorithm explicitly designed for residential areas containing adjacent polygons. AVARA addresses the complex task of balancing computational efficiency and boundary position accuracy in existing Voronoi algorithms based on occurrence element discretization and difficulties constructing Voronoi diagrams for topologically adjacent polygonal objects. AVARA leverages interpolation strategies established on the classification result of neighbor pairs using co-edge relationships of residential area centroids. Additionally, AVARA incorporates graphical Boolean operations and node merging. The experiments used residential area datasets at 1:50,000, 1:10,000, and 1:2,000 map scales. The results showed that AVARA outperformed the Voronoi diagram algorithms based on intervisible points (VBIVP) and the equal-interval dense point method (VBEDP). AVARA achieved the highest accuracy rate in constructing Voronoi diagrams, with a 50% improvement. It also exhibited superior local position accuracy, demonstrating significant time performance improvements of 349.12% and 90.7% using datasets at map scales of 1:50,000 and 1:10,000, respectively. In the experiment using a dataset at a map scale of 1:2,000, AVARA consumed slightly less time than VBEDP with a 0.6 m interval. These findings highlight the significant overall advantage of AVARA. Additionally, the effectiveness of the algorithm was further validated using a large-scale building dataset.

ABSTRACTMarfan syndrome (MFS) is an autosomal dominant connective tissue disorder caused by mutation in fibrillin-1 (FBN1). However, the molecular mechanism underlying MFS remains poorly understood. The study aimed to explore how the L-type calcium channel (CaV1.2) modulates disease progression of MFS and to identify a potential effective target for attenuating MFS. KEGG enrichment analysis showed that the calcium signaling pathway gene set was significantly enriched. We demonstrated that FBN1 deficiency exhibited inhibition on both the expression of Cav1.2 and proliferation of vascular smooth muscle cells (VSMCs). Then, we examined whether FBN1 mediates Cav1.2 via regulating TGF-β1. Higher levels of TGF-β1 were observed in the serum and aortic tissues from patients with MFS. TGF-β1 modulated Cav1.2 expression in a concentration-dependent manner. We evaluated the role of Cav1.2 in MFS by small interfering RNA and Cav1.2 agonist Bay K8644. The effect of Cav1.2 on cell proliferation was dependent on c-Fos activity. These results demonstrated FBN1 deficiency decreased the expression levels of Cav1.2 via regulation of TGF-β1, and downregulation of Cav1.2 inhibited cell proliferation of human aortic smooth muscle cells (HASMCs) in MFS patients. These findings suggest that Cav1.2 may be an appealing therapeutic target for MFS.