Detection of Rail Defects Using NDT Methods.

The rapid development of high-speed and heavy-haul railways caused rapid rail defects and sudden failure. This requires more advanced rail inspection, i.e., real-time accurate identification and evaluation for rail defects. However, existing applications cannot meet future demand. In this paper, different types of rail defects are introduced. Afterwards, methods that have the potential to achieve rapid accurate detection and evaluation of rail defects are summarized, including ultrasonic testing, electromagnetic testing, visual testing, and some integrated methods in the field. Finally, advice on rail inspection is given, such as synchronously utilizing the ultrasonic testing, magnetic flux leakage, and visual testing for multi-part detection. Specifically, synchronously using the magnetic flux leakage and visual testing technologies can detect and evaluate surface and subsurface defects, and UT is used to detect internal defects in the rail. This will obtain full rail information, to prevent sudden failure, then ensure train ride safety.

A Review of NDT Methods for Wheel Burn Detection on Rails.

Wheel burn can affect the wheel-rail contact state and ride quality. With long-term operation, it can cause rail head spalling or transverse cracking, which will lead to rail breakage. By analyzing the relevant literature on wheel burn, this paper reviews the characteristics, mechanism of formation, crack extension, and NDT methods of wheel burn. The results are as follows: Thermal-induced, plastic-deformation-induced, and thermomechanical-induced mechanisms have been proposed by researchers; among them, the thermomechanical-induced wheel burn mechanism is more probable and convincing. Initially, the wheel burns appear as an elliptical or strip-shaped white etching layer with or without deformation on the running surface of the rails. In the latter stages of development, this may cause cracks, spalling, etc. Magnetic Flux Leakage Testing, Magnetic Barkhausen Noise Testing, Eddy Current Testing, Acoustic Emission Testing, and Infrared Thermography Testing can identify the white etching layer, and surface and near-surface cracks. Automatic Visual Testing can detect the white etching layer, surface cracks, spalling, and indentation, but cannot detect the depth of rail defects. Axle Box Acceleration Measurement can be used to detect severe wheel burn with deformation.

HnRNPK/miR-223/FBXW7 feedback cascade promotes pancreatic cancer cell growth and invasion.

Several studies have identified miR-223 critically involved in various types of cancer, including pancreatic ductal adenocarcinoma (PDAC). However, its action and regulatory mechanisms in PDAC remains largely unclear. In this study, we found that the expression levels of miR-223 were increased in clinical samples with PDAC (81.6%). The upregulation of miR-223 increases the proliferation, migration, and invasive abilities of PDAC cells in vitro and in vivo. Mechanistically, miR-223 directly targeted FBXW7 and overexpression of FBXW7 reverted miR-223- induced drastic proliferation in PDAC cells. Interestingly, miR-223 promoter was found to form a coprecipitable complex with hnRNPK, and siRNA knockdown of hnRNPK in PDAC cells reduced the levels of miR-223. These results show that hnRNPK is a cellular protein that binds and affects the accumulation of miR-223 in PDAC. Furthermore, FBXW7 interacts with hnRNPK and promotes its degradation, which requires phosphorylation of hnRNPK at threonine 1695 by GSK3. Consistently, we observed an inverse expression pattern between FBXW7 and miR-223, whereas a positive expression pattern between miR-223 and hnRNPK was found in human PDAC tissues. These data unveiled an important new miR-223/FBXW7/HnRNPK feedback cascade in human PDAC.

MiR-371-5p facilitates pancreatic cancer cell proliferation and decreases patient survival.

BACKGROUND: microRNAs (miRNAs) play a critical role in tumorigenesis, either as a tumor suppressor or as an oncogenic miRNA, depending on different tumor types. To date, scientists have obtained a substantial amount of knowledge with regard to miRNAs in pancreatic cancer. However, the expression and function of miR-371-5p in pancreatic cancer has not been clearly elucidated. The aim of this study was to investigate the roles of miR-371-5p in pancreatic cancer and its association with the survival of patients with pancreatic cancer. METHODS: The expression of miR-371-5p was examined in pancreatic duct adenocarcinoma (PDAC) and their adjacent normal pancreatic tissues (ANPT) or in pancreatic cancer cell lines by qRT-PCR. The association of miR-371-5p expression with overall survival was determined. The proliferation and apoptosis of SW-1990 and Panc-1 cells, transfected with miR-371-5p mimics or inhibitor, were assessed using MTT assay and flow cytometry, respectively. The tumorigenicity was evaluated via mice xenograft experiments. miR-371-5p promoter interactions were analyzed by chromatin immunoprecipitation assays (ChIP). Protein expression was analyzed by Western blot. RESULTS: The expression level of miR-371-5p was dramatically upregulated in clinical PDAC tissues compared with ANPT. Patients with high miR-371-5p expression had a significantly shorter survival than those with low miR-371-5p expression. The in vitro and in vivo assays showed that overexpression of miR-371-5p resulted in cell proliferation and increased tumor growth, which was associated with inhibitor of growth 1 (ING1) downregulation. Interestingly, we also found that ING1, in turn, inhibited expression of miR-371-5p in the promoter region. CONCLUSIONS: our study demonstrates a novel ING1-miR-371-5p regulatory feedback loop, which may have a critical role in PDAC. Thus miR-371-5p can prove to be a novel prognostic factor and therapeutic target for pancreatic cancer treatment.