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Tension-compression and tension-tension fatigue tests were conducted on a high-strength steel and a titanium alloy in the very-high-cycle fatigue (VHCF) regime. A shared interior crack initiation mechanism for high strength steel and titanium alloy was proposed based on the common nanograins and facet formation, i.e., (i) cleavage of local brittle microstructure; (ii) gradual growth of originated cracks (facets), and the coalescence of adjacent facets, facets disappear and nanograins form for the cyclic pressing in the cases of tension-compression fatigue and (iii) coalesced crack forming a main crack. The experimental results indicate that the stress ratio magnitude has a substantial effect on the fatigue strength, which decreases with the increasing of stress ratio. The tendency of the S-N curves from low cycle fatigue to VHCF regime is similar for the high-strength steel and the titanium alloy with different stress ratios. It is shown that the relationship of fatigue strength, fatigue life, inclusion size and stress ratio in the VHCF of high-strength steel and Ti-6Al-4V are correlated by the Sun model. The predicted results are in good agreement with the experimental data.

Due to the improvement of the wear property, rolling contact fatigue including shattered rim and shelling are the main failure causes of the high-speed railway wheels. In this paper, shattered rim and shelling occurred on the service wheels of the China Railway High-speed (CRH) trains were systematically investigated. The recorded data of the last ten years CRH operation indicated that all shattered rims and shelling were detected with serving >106 km (corresponding to the fatigue life 107–109 cycles) which is very-high-cycle fatigue (VHCF). The crack initiation region of shattered rim located at the depth of 10–25 mm from the tread, while that of shelling located at the depth

The shattered rim on railway wheels is increasingly concerned in recent years. Based on the failure analysis, the mechanism of shattered rim was revealed. The contact stress distribution of wheel/rail with inclusions in the wheel was analyzed by ABAQUS. Then the stress field was imported into FRANC3D to simulate the crack propagation. It is found that the simulation results were in good agreement with those obtained experimentally from the actual shattered rim, which proves the availability of the simulation. Meanwhile, the influence of the size and location of the inclusions on the fatigue life of the wheel was evaluated. Based on the crack propagation curves obtained by simulation, the rolling contact fatigue damage tolerance analysis and remaining fatigue life assessment method of wheels were proposed.

The effects of inclusion size and stress ratio (R) on the very-high-cycle fatigue (VHCF) behavior of pearlitic steel were experimentally assessed. The S–N curve under rotating bending loading exhibited a horizontal asymptote shape and a clear fatigue limit. In contrast, the S–N curve under ultrasonic axial loading exhibited a continuously descending shape, and the fatigue limit disappeared at a fatigue life of 107 cycles. The fine granular area (FGA) within nanograins formed in the crack initiation region only for the samples subjected to VHCF at R = −1. All instances of interior crack initiation were caused by the MnS inclusions.

The left atrium (LA) is a dynamic apparatus that modulates left ventricular (LV) filling and cardiovascular performance with its reservoir, conduit, and booster pump functions. We used two dimensional speckle tracking echocardiography (2DSTE)-based strain and strain rate imaging to evaluate LA

Delta-catenin was first identified because of its interaction with presenilin-1, and its aberrant expression has been reported in various human tumors and in patients with Cri-du-Chat syndrome, a form of mental retardation. However, the mechanism whereby delta-catenin is regulated in cells has not been fully elucidated. We investigated the possibility that glycogen-synthase kinase-3 (GSK-3) phosphorylates delta-catenin and thus affects its stability. Initially, we found that the level of delta-catenin was greater and the half-life of delta-catenin was longer in GSK-3beta(-/-) fibroblasts than those in GSK-3beta(+/+) fibroblasts. Furthermore, four different approaches designed to specifically inhibit GSK-3 activity, i.e. GSK-3-specific chemical inhibitors, Wnt-3a conditioned media, small interfering RNAs, and GSK-3alpha and -3beta kinase dead constructs, consistently showed that the levels of endogenous delta-catenin in CWR22Rv-1 prostate carcinoma cells and primary cortical neurons were increased by inhibiting GSK-3 activity. In addition, it was found that both GSK-3alpha and -3beta interact with and phosphorylate delta-catenin. The phosphorylation of DeltaC207-delta-catenin (lacking 207 C-terminal residues) and T1078A delta-catenin by GSK-3 was noticeably reduced compared with that of wild type delta-catenin, and the data from liquid chromatography-tandem mass spectrometry analyses suggest that the Thr(1078) residue of delta-catenin is one of the GSK-3 phosphorylation sites. Treatment with MG132 or ALLN, specific inhibitors of proteosome-dependent proteolysis, increased delta-catenin levels and caused an accumulation of ubiquitinated delta-catenin. It was also found that GSK-3 triggers the ubiquitination of delta-catenin. These results suggest that GSK-3 interacts with and phosphorylates delta-catenin and thereby negatively affects its stability by enabling its ubiquitination/proteosome-mediated proteolysis.

Mycotoxins are commonly encountered natural products, and are capable of poisoning animals or humans that inhale mold particles from mycotoxin-contaminated foods. Ochratoxin A (OTA) is produced by Aspergillu ochracus and Penicillium verrucosum, and is often found in cereals and agricultural products. Although previous studies have focused on the potent nephrotoxicity and renal carcinogenicity of OTA, more recent studies suggest that it accumulates in the brain and causes oxidative stress and DNA damage in various brain regions and neuronal populations. In the present study, we undertook to investigate the potential harm caused by environmental exposure to OTA in terms of its effects on neuronal cell viability and proteome profiles. OTA was found to significantly reduce the viabilities of human neuroblastoma SH-SY5Y and mouse hippocampal HT22 cells, as assessed by lactic dehydrogenase release into culture media. Generation of reactive oxygen species was detected in OTA-treated SH-SY5Y and HT22 cells, however, caspase activation and increase in p53 phosphorylation were only detected in HT22 cells, and the expressions of several proteins were found to be significantly altered after treating HT22 cells with OTA. Valosin containing protein, prolyl 4-hydroxylase, Atp5b protein, nucleophosmin 1, eukaryotic translation elongation factor 1 delta isoform, ornithine aminotransferase, prohibitin, and peroxiredoxin 6, which have been suggested to be implicated in the pathogenesis of neurodegenerative disorders, were up-regulated. Our findings suggest that coordinated regulations of molecular networks are involved in the OTA-induced cytotoxicity and that proteome response can be an indicative for neurodegeneration.