Effect of welding parameters on microstructure and mechanical properties of AA7075-T6 friction stir welded joints

The effects of advancing speed and rotational speed on the microstructure and the mechanical properties of friction stir welded 7075-T6 aluminium alloy sheets were studied. The fatigue strength of sound joints was measured and compared to tensile testing results. Macrographs and microhardness maps were carried out to reveal the microstructure transformations. Fractographic observations were made to identify the failure mechanisms. The effects of welding parameters on the fatigue strength are discussed in terms of welding pitch\u2002k\u2002(mm/rev) and heat input (J/mm). At a high welding pitch, crack initiation at the root of the circular grooves left by the tool on the weld surface is the most detrimental failure mechanism. As the size and the depth of the grooves are related to the welding pitch, the fatigue strength increases when the welding pitch is reduced. However, when the heat input is excessive, the failure is caused by sub-surface defects produced after abnormal stirring and/or by softening of the heat-affected zone. Lateral lips on the weld surface edges also have an effect on the fatigue strength for intermediate welding pitch values.Peer reviewed: YesNRC publication: Ye

Effect of post weld treatments on the fatigue behavior of AA7075-T6 friction stir welded butt joints

Peer reviewed: YesNRC publication: Ye

Development of a fracture criterion for cold heading

Peer reviewed: YesNRC publication: N

The E3 ubiquitin ligase complex component COP1 regulates PEA3 group member stability and transcriptional activity

International audienceIn this study, we report that the PEA3 group members interact with the mammalian really interesting new gene (RING) E3 ubiquitin ligase constitutive photomorphogenetic 1 (COP1), which mediates ubiquitylation and subsequent proteasome degradation of the p53 and c-Jun transcription factors. This interaction is mediated by the central region of COP1 including the coiled-coil domain and two COP1-interacting consensus motifs localized in the well-conserved N-terminal transactivation domain of the PEA3 group members. At the transcriptional level, COP1 reduces the transcriptional activity of ERM and the two other PEA3 group proteins on Ets-responsive reporter genes; this effect being dependent on the RING domain of COP1 and the two COP1-interacting motifs of ERM. Reduced transcriptional activity was, however, not related to COP1-induced changes in ERM stability. In fact, increased ubiquitylation and subsequent proteasomemediated degradation of ERM is achieved only when COP1 is expressed with DET1, a key COP1 partner within the ubiquitylation complex. Conversely, we show that the depletion of COP1 or DET1 by small interference RNA (siRNA) in U2OS cells stabilizes endogenous ERM whereas only COP1 knockdown enhances expression of ICAM-1, a gene regulated by this transcription factor. These results indicate that COP1 is a complex regulator of ERM and the two other PEA3 group members

Modeling the cold heading of steel wire rod

NRC publication: N