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Anti-sliding short piles, a novel technique for slope stabilization, have been applied in engineering practices. Nonetheless, a mature structural calculation theory for these piles is still lacking. In this paper, the study presents an internal force solution model for anti-sliding short piles using the finite difference method. By extending the Euler–Bernoulli beam theory and defining boundary conditions, this study develops a set of finite difference equations for computing the structural forces of anti-sliding short piles. Furthermore, this study conducted laboratory model tests on soil landslide cases reinforced with anti-sliding short piles. By comparing the internal forces and deformations of these piles, the test validates the proposed calculation model for anti-sliding short piles. The results suggest that treating the load-bearing and embedded sections as a unified entity during the calculation process, instead of applying continuity conditions separately at the sliding surface as performed in traditional methods, simplifies the complex solving procedure. Moreover, under identical loading conditions, the displacement, bending moment, and shear force data obtained through the finite difference method closely coincide with the measurements from the model tests, confirming the reliability of the anti-sliding short pile calculation model. Additionally, this study demonstrates that reducing the spacing between nodes along the entire anti-sliding short pile, i.e., decreasing the value of the differential segment length 'h', results in more precise computational outcomes. This research offers valuable insights and references for sustainable solutions in the realm of geological disaster prevention and control. [ABSTRACT FROM AUTHOR]

Mutations in the EXT1 gene are responsible for human hereditary multiple exostosis type 1. The Drosophila EXT1 homologue, tout-velu, regulates Hedgehog diffusion and signaling, which play an important role in tissue patterning during both invertebrate and vertebrate development. The EXT1 protein is also required for the biosynthesis of heparan sulfate glycosaminoglycans that bind Hedgehog. In this study we generated EXT1-deficient mice by gene targeting. EXT1 homozygous mutants fail to gastrulate and generally lack organized mesoderm and extraembryonic tissues, resulting in smaller embryos compared to normal littermates. RT-PCR analysis of markers for visceral endoderm and mesoderm development indicates the delayed and abnormal development of both of these tissues. Immunohistochemical staining revealed a visceral endoderm pattern of Indian hedgehog (Ihh) in wild-type E6.5 embryos. However, in both EXT1-deficient embryos and wild-type embryos treated with heparitinase I, Ihh failed to associate with the cells. The effect of the EXT1 deletion on heparan sulfate formation was tested by HPLC and cellular glycosyltransferase activity assays. Heparan sulfate synthesis was abolished in EXT1 -/- ES cells and decreased to less than 50% in +/- cell lines. These results indicate that EXT1 is essential for both gastrulation and heparan sulfate biosynthesis in early embryonic development. [C] 2000 Academic Press Key Words: EXT1; gene targeting; embryonic development; heparan sulfate biosynthesis.