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This study presents a comprehensive method for detecting debonding defects in concrete-filled steel tube (CFST) structures using wave propagation analysis with externally attached piezoelectric ceramic sensors. Experimental tests and numerical simulations were conducted to evaluate the sensitivity and accuracy of two measurement techniques—the flat and oblique measurement methods—in detecting debonding defects of varying lengths and heights. The results demonstrate that the flat measurement method excels in detecting debonding height, while the oblique method is more effective for detecting debonding length. A normalized judgment index (DI) was introduced to quantify the correlation between debonding characteristics and the detected signal amplitude, revealing the significant influence of sensor spacing on detection accuracy. Furthermore, a mathematical model based on wavelet packet energy analysis was developed to establish a linear relationship between wavelet packet energy and debonding size. This model offers a scientific foundation for the quantitative detection of debonding defects and provides a new approach to the health monitoring of CFST structures. The integrated use of both measurement techniques enhances detection precision, enabling both qualitative and quantitative defect analysis, which can significantly guide the maintenance and repair of CFST structures. [ABSTRACT FROM AUTHOR]

The aim of the study was to demonstrate how transthyretin (TTR) could affect long non-coding RNA (lncRNA) of maternally expressed gene 3 (MEG3) and play important roles in diabetic retinopathy (DR). A DR model in C57BL/6 mice was established after intraperitoneal injection of streptozotocin (STZ). After intravitreal injection with TTR pAAV vector, MEG3 short hairpin RNA (shRNA), scrambled shRNA, or MEG3, retinal imaging, retinal trypsin digestion, and fundus vascular permeability tests were performed. Cell counting kit-8 (CCK8), transwell, and Matrigel assays were employed to detect the proliferation and migration of human retinal microvascular endothelial cells (hRECs). The binding between long non-coding RNA of maternally expressed gene 3 (lncRNA-MEG3) and microRNA-223-3p (miR-223-3p) was observed by using luciferase reporter assays, while co-immunoprecipitation (co-IP) was employed to confirm the interaction between TTR and the target. In the DR mice model, retinal vascular leakage and angiogenesis were repressed by overexpressing TTR. In vitro, the added TTR promoted the level of lncRNA-MEG3 by interacting with poly (A) binding protein cytoplasmic 1 (PABPC1), and then repressed proliferation and angiogenesis of hRECs. In vivo, silencing or overexpressing lncRNA-MEG3 significantly affected retinal vascular phenotypes. Additionally, the interaction between lncRNA-MEG3 and miR-223-3p was confirmed, and silencing of miR-223-3p revealed similar effects on hRECs as overexpression of lncRNA-MEG3. In summary, in the DR environment, TTR might affect the lncRNA MEG3/miR-223-3p axis by the direct binding with PABPC1, and finally repress retinal vessel proliferation. [ABSTRACT FROM AUTHOR]