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Girth welds are weak points in pipelines, and failures occur frequently. In a gas transmission pipeline, a girth weld experienced cracking, prompting a failure analysis using experimental methods and finite element analysis (FEA). Experimental results showed that X-ray non-destructive testing (NDT) revealed cracks, porosity, and lack of fusion in the girth weld. However, the hardness and microstructure of the material showed no abnormalities. During operation, the pipeline experienced an increase in soil cover and was subjected to ground subsidence and vehicle loads. Finite element analysis was conducted on the defective girth weld under different conditions, including varying soil cover depths, different levels of subsidence, and varying vehicle loads, to examine the pipeline's stress response. The results indicated that the combination of soil cover, subsidence, and vehicle loads led to pipeline failure, whereas none of these factors alone was sufficient to cause girth weld failure. To prevent such failures from occurring again, the following measures are recommended: strengthen on-site welding quality control of girth welds, conduct inspections for defects in girth welds of in-service pipelines, and promptly address any defects that exceed acceptable limits. [ABSTRACT FROM AUTHOR]

Three current paths are proposed, and theoretical analysis and laboratory tests are carried out to investigate the root causes of bearing failure in IGBT inverter-fed locomotives and EMUs. The three types of current paths that run through the drive unit bearings and axle box bearings used on EMUs and electric locomotives are classified as the primary side current path, the main traction system current path, and the current path between the vehicles of the EMU or electric locomotive and the vehicles it hauls. The research found that the EDM current path in the main traction system caused by common mode voltage is distinguished as the main cause resulting in the failure of the bogie motor bearings or the bearings of the load connected to the motor shaft. The cause of common mode voltage is analyzed, and the thresholds of current density and voltage without causing bearing damage are analyzed and presented. The lab tests carried out on the bearings on the main traction system's current path verified that the current path does exist. The proof to identify electric erosion, such as craters and washboards, and corresponding measures to prevent the failure of bogie bearings are proposed. Further research about the other two current paths is urgent and necessary. [ABSTRACT FROM AUTHOR]

Objectives: Epulis is considered to be a massive reactive lesion rather than a true neoplasia. AhR is thought to be associated with inflammation and development of neoplasms. Here, we aimed to observe the expression of AhR in fibrous epulis and explore its role and possible mechanism in the pathogenesis of epulis. Materials and Methods: Epulis and normal gingival tissues were collected, and AhR expression was detected at the mRNA and protein levels by quantitative polymerase chain reaction (qPCR) and immunohistochemistry, respectively. The expression levels of proinflammatory cytokines and apoptosis‐related factor genes in human periodontal ligament cells (hPDLCs) and human gingival fibroblasts (hGFs) transfected with AhR short interfering RNA (siRNA) or negative control siRNA, upon stimulation with lipopolysaccharide of Porphyromonas gingivalis (Pg‐LPS), were then examined. Finally, the expression levels of the proinflammatory cytokines and apoptosis‐related factor genes in the epulis tissues were observed by qPCR. Results: AhR expression in fibrous epulis was significantly increased at both the mRNA and protein levels. The expression of proinflammatory cytokines and apoptosis‐related factor genes in hPDLCs transfected with AhR siRNA was significantly decreased when stimulated with Pg‐LPS. The same trends were observed for hGFs. The opposite trend was detected in the epulis tissues. Conclusion: AhR may be a key factor in fibrous epulis pathogenesis that acts by regulating the expression of BCL2 family genes and inflammatory factor‐related genes. [ABSTRACT FROM AUTHOR]