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This paper gives a method of quantifying small visual differences between 3D mesh models with conforming topology, based on the theory of strain fields. Strain field is a geometric quantity in elasticity which is used to describe the deformation of elastomer. In this paper we consider the 3D models as objects with elasticity. The further demonstrations are provided: the first is intended to give the reader a visual impression of how our measure works in practice; and the second is to give readers a visual impression of how our measure works in evaluating filter algorithms. Our experiments show that our difference estimates are well correlated with human perception of differences. This work has applications in the evaluation of 3D mesh watermarking, 3D mesh compression reconstruction, and 3D mesh filtering.

No abstract

This paper gives a method of quantifying (small) visual differences between 3D mesh models with conforming topology, based on the theory of strain fields. Our experiments show that our difference estimates are well correlated with human perception of differences. This work has applications in the evaluation of 3D mesh watermarking, 3D mesh compression reconstruction, and 3D mesh filtering.

The inhibitory effect of long intergenic non-coding RNA 00320 (LINC00320) in glioma cell proliferation has been proposed in a recent study. However, the mechanisms by which LINC00320 regulate aquaporin 9 (AQP9) in glioma require further exploration. Hence, this study aims to investigate effects of LINC00320 on tumorigenicity of glioma cells and angiogenesis of microvascular endothelial cells (MVECs). Expression of LINC00320 and AQP9 in glioma tissues and cells was measured by reverse transcription–quantitative polymerase chain reaction and Western blot analysis. The relationship among LINC00320, nuclear factor κB subunit 1 (NFKB1) and AQP9 was examined by RNA immunoprecipitation, dual-luciferase reporter gene, and chromatin immunoprecipitation assays. The participation of LINC00320 and AQP9 in glioma cell proliferation and MVEC angiogenesis was analyzed using gain- and loss-of-function approaches. Finally, a nude mouse orthotopic xenograft model of glioma was established to investigate the effects of LINC00320 and AQP9 on glioma growth in vivo. LINC00320 was under-expressed and AQP9 was over-expressed in glioma tissues. Further mechanistic investigation showed that LINC00320 downregulated AQP9 by inhibiting the recruitment of NFKB1 to the promoter region of AQP9. LINC00320 overexpression or AQP9 silencing inhibited the proliferation of glioma cells and angiogenesis of MVECs. Also, upregulation of LINC00320 restrained tumor growth and angiogenesis in xenograft mice by downregulating AQP9. Taken together, LINC00320 acts as a tumor suppressor in glioma, thus presenting a novel therapeutic target.