2. Mechanics of Slides / 13 2.1 Types of Failure Surfaces / 13 2.2 Plane Failure Surfaces / 14 2.3 Cylindrical Failure Surfaces / 16 2.4 Total Stress Versus Effective Stress / 17 2.5 Guidelines for Stability Analysis / 21 2.6 Factors of Safety / 23 3. Shear Strength / 26 3.1 Subsurface Investigations / 26 3.2 Field Tests / 26 3.3 Laboratory Tests / 29 3.4 Typical Ranges and Correlations / 35 vii viii CONTENTS 4. Phreatic Surfaces / 40 4.1 Flow Nets / 40 4.2 Earth Dams Without Filter Drains / 41 4.3 Earth Dams With Filter Drains / 45 4.4 Pore Pressure Ratio / 48 5. Remedial Measures for Correcting Slides / 52 5.1 Field Investigations / 52 5.2 Preliminary Planning / 55 5.3 Corrective Methods / 58 PART II SIMPLIFIED METHODS OF STABILITY ANALYSIS 6. Simplified Methods for Plane Failure / 71 6.1 Infinite Slopes / 71 6.2 Triangular Cross Section / 73 6.3 Trapezoidal Cross Section / 74 6.4 Illustrative Examples / 76 7. Simplified Methods for Cylindrical Failure / 79 7.1 Existing Stability Charts / 79 7.2 Triangular Fills on Rock Slopes / 91 7.3 Trapezoidal Fills on Rock Slopes / 95 7.4 Triangular Fills on Soil Slopes / 98 7.5 Effective Stress Analysis of Homogeneous Dams / 103 7.6 Effective Stress Analysis of Nonhomogeneous Dams / 107 7.7 Total Stress Analysis of Slopes / 118 7.8 Summary of Methods / 122 PART III. COMPUTERIZED METHODS OF STABILITY ANALYSIS

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Background/Aims: This study aimed to investigate the mechanism by which microRNA-206 (miR-206) affects the proliferation, apoptosis, migration and invasion of osteosarcoma (OS) cells by targeting ANXA2 via the AKT signaling pathway. Methods: A total of 132 OS tissues and 120 osteochondroma tissues were examined in this study. The targeting relationship between miR-206 and ANXA2 was verified with a dual-luciferase reporter assay. The miR-206 expression and ANXA2, AKT, PARP, FASN, Survivin, Bax, Mcl-1 and Bcl-1 mRNA and protein expression in the above two groups were examined by qRT-PCR and western blotting. The cultured OS cells were divided into 6 groups: a blank group, negative control (NC) group, miR-206 mimic group, miR-206 inhibitor group, si-ANXA2 group and miR-206 inhibitor + si-ANXA2 group. Cell cycle and apoptosis were assessed by flow cytometry, cell migration was examined with a wound-healing assay, and cell invasion was assessed with a Transwell assay. Pearson correlation analysis was used to determine the correlation between ANXA2 mRNA expression and miR-206 expression in OS. Results: OS tissues exhibited increased mRNA and protein expression of ANXA2, AKT, PARP, FASN, Survivin, Mcl-1 and Bcl-2; decreased miR-206 expression; and decreased Bax mRNA and protein expression. ANXA2 mRNA expression was strongly negatively correlated with miR-206 expression in OS. ANXA2 was found to be a miR-206 target gene. In the miR-206 mimic group and the si-ANXA2 group, the mRNA and protein expression of ANXA2, AKT, PARP, FASN, Survivin, Mcl-1 and Bcl-1 decreased markedly, cell proliferation was inhibited, apoptosis was promoted, higher cell growth in G1 phase and decreased growth in S phase was detected, and decreased cell migration and invasion were observed compared with those in the blank group. Conclusion: The current results demonstrate that miR-206 overexpression inhibits OS cell proliferation, migration and invasion and promotes apoptosis through targeting ANXA2 by blocking the AKT signaling pathway.

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Circular RNAs (circRNAs) were discovered in the 1970s, but they have drawn increasing attention in recent years. Currently, we know that circRNAs are not “wrongly spliced” during transcription but play important roles in the initiation and development of various diseases, including cancers. Recently, a growing number of studies have suggested that cancer stem cells (CSCs) may contribute to the origination and maintenance of cancers. This review briefly introduces the major functions of circRNAs, including interacting with other noncoding RNAs, competing with pre-mRNA splicing, binding with proteins to form a scaffold, promoting protein nuclear translocation and even translating proteins in a cap-independent manner. Furthermore, we describe the regulatory mechanism of circRNAs in CSC phenotypes and discuss the potential clinical applications of circRNAs in CSC-targeted therapy, including functioning as new biomarkers, acting as vaccines and breaking the therapeutic resistance of CSCs. Finally, we discuss the major limitations and challenges in the field, which will be beneficial for the future clinical use of circRNAs.