The effect of quenching and defects size on the HCF behaviour of Boron steel
Abstract This work investigates the effect of natural and artificial surface defects and quenching on the fatigue strength of a Boron steel (22MnB5). A vast experimental campaign has been undertaken to study the high cycle fatigue behaviour and more specifically the fatigue damage mechanisms observed in quenched and untreated materials, under different loading conditions and with differents artificial defects sizes (from 25 μm to 370 μm radius). In order to test the sheet metal in shear an original test apparatus is used. The critical defect size is determined to be 100 ± 50 μm. This critical size does not appear to depend on the loading type or the microstructure of the material (i.e. ferritic–perlitic or martensitic). However, for large defects, the quenched material is more sensitive to the defect size than the untreated material. For a defect size range of 100–300 μm the slope of the Kitagawa–Takahashi diagram is approximately −1/3 and −1/6 for the quenched and untreated materials respectively. A probabilistic approach that leads naturally to a probabilistic Kitagawa type diagram is developed. This methodology can be used to explain the relationship between the influence of the heat treatment and the defect size on the fatigue behaviour of this steel.
Fatigue strength and fracture mechanism of steel modified by super-rapid induction heating and quenching
Abstract Four kinds of surface hardened-specimens (ordinary structural steel with carbon content of 0.45% C) having hardened thicknesses of 0.7–1.8 mm were prepared using a ‘super-rapid induction heating (SRIH) system’. Rotation bending fatigue tests were performed with special focus on the effect of a hardened thickness on fatigue properties. Measurement of residual stress and observation of the fracture surface were also carried out to investigate the fracture mechanism of the specimen with a shallow hardened layer. It was found that there is not much improvement of fatigue strength at 10 7 cycles for specimens with shallow hardened layers in spite of having a high compressive residual stress of about 1000 MPa. This is because the fatigue crack originating from inside the hardened layer leads to the final fracture of the specimen (internal fracture mode). Improvement of fatigue strength has been achieved on the specimen with thick hardened layers, such as those about 1.8 mm thick. In this case, fatigue cracks originate from inclusions located in hardened layers, which leads to final fracture (hardened-layer fracture mode).
Primary Breast Cancer Tumours Contain High Amounts of IgA1 Immunoglobulin: An Immunohistochemical Analysis of a Possible Carrier of the Tumour-Associated Tn Antigen
The Tn antigen (GalNAc alpha-O-Ser/Thr) as defined by the binding of the lectin, helix pomatia agglutinin (HPA) or anti-Tn monoclonal antibodies, is known to be exposed in a majority of cancers, and it has also been shown to correlate positively with the metastatic capacity in breast carcinoma. The short O-glycan that forms the antigen is carried by a number of different proteins. One potential carrier of the Tn antigen is immunoglobulin A1 (IgA1), which we surprisingly found in tumour cells of the invasive parts of primary breast carcinoma. Conventional immunohistochemical analysis of paraffin-embedded sections from primary breast cancers showed IgA1 to be present in the cytoplasm and plasma membrane of 35 out of 36 individual primary tumours. The immunohistochemical staining of HPA and anti-Tn antibody (GOD3-2C4) did to some extent overlap with the presence of IgA1 in the tumours, but differences were seen in the percentage of stained cells and in the staining pattern in the different breast cancers analysed. Anti-Tn antibody and HPA were also shown to specifically bind to a number of possible constellations of the Tn antigen in the hinge region of IgA1. Both reagents could also detect the presence of Tn positive IgA in serum. On average 51% of the tumour cells in the individual breast cancer tumour sections showed staining for IgA1. The overall amount of staining in the invasive part of the tumour with the anti Tn antibody was 67%, and 93% with HPA. The intra-expression or uptake of IgA1 in breast cancer makes it a new potential carrier of the tumour associated and immunogenic Tn antigen.