Vibration Analysis for Fault Detection of Wind Turbine Drivetrains-A Comprehensive Investigation.

Vibration analysis is an effective tool for the condition monitoring and fault diagnosis of wind turbine drivetrains. It enables the defect location of mechanical subassemblies and health indicator construction for remaining useful life prediction, which is beneficial to reducing the operation and maintenance costs of wind farms. This paper analyzes the structure features of different drivetrains of mainstream wind turbines and introduces a vibration data acquisition system. Almost all the research on the vibration-based diagnosis algorithm for wind turbines in the past decade is reviewed, with its effects being discussed. Several challenging tasks and their solutions in the vibration-based fault detection of wind turbine drivetrains are proposed from the perspective of practicality for wind turbines, including the fault detection of planetary subassemblies in multistage wind turbine gearboxes, fault feature extraction under nonstationary conditions, fault information enhancement techniques and health indicator construction. Numerous naturally damaged cases representing the real operational features of industrial wind turbines are given, with a discussion of the failure mechanism of defective parts in wind turbine drivetrains as well.

Downregulation of miR-146b-5p via iodine involvement repressed papillary thyroid carcinoma cell proliferation.

miR-146b-5p is overexpressed in papillary thyroid carcinoma (PTC) and is thought to be a related diagnostic marker. Previous studies have indicated the effects of iodine on oncogenic activation. However, the effect of iodine on the proliferation of PTC cells and the associated underlying mechanisms remain unclear. We found that miR-146b-5p was downregulated and smad4 was upregulated in patients exposed to high iodine concentration by in situ hybridisation (ISH) and immunohistochemical (IHC). NaI (10-3 M) treatment downregulated miR-146b-5p and upregulated Smad4 in PTC cell lines. Luciferase assay was used to confirm that Smad4 is a target of miR-146b-5p. Furthermore, MTT assay and cell cycle analysis indicated that 10-3 M NaI suppressed cell proliferation and caused G0/G1 phase arrest. Real-time PCR and Western blotting demonstrated that 10-3 M NaI increased p21, p27, and p57 levels and reduced cyclin D1 levels in PTC cells. Our findings suggest that 10-3 M NaI increases Smad4 levels through repression of miR-146b-5p expression, curbing the proliferation in PTC.