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The corrosion failure of steel is one of the key problems to shorten the service life of power facilities in some strong corrosive environments， such as marine and chemical plants.To address this problem， the proposition of substituting steel in power transmission and transformation equipment with high-strength 7xxx series aluminum alloys was introduced.Accelerated indoor simulation tests were conducted， using a 5%NaCl salt spray corrosion environment to emulate marine atmospheric conditions.A comparative analysis was performed on the mechanical property degradation and change law of surface corrosion morphology of Q345 steel for substation facilities and 7075 aluminum alloy after varying corrosion durations (7，21，42 d) by integrating tensile tests and microscopic structural observations.Further， employing corrosion weight loss methods and computer simulation techniques， the mechanical properties of the two materials under identical corrosion conditions and loads were comparatively studied.Results indicated that the mechanical properties of both materials tended to decline with the extension of salt spray corrosion time under 5%NaCl salt spray corrosion environment， moreover， the highest tensile strength attenuation rate of Q345 steel (24.58%) was 8 times that of 7075 aluminum alloy (3.00%).Both materials displayed a corrosion rate trend that initially increased and then decreased， with the average corrosion rate of Q345 steel [0.03 g/(m2·d)] being approximately 15 times that of the 7075 aluminum alloy [0.002 g/(m2·d)].At the same corrosion cycle， the corrosion pits in Q345 steel were larger and deeper than those in the 7075 aluminum alloy， resulting in a significantly higher degree of stress concentration caused by corrosion pits in Q345 steel under the same external load compared to 7075 aluminum alloy.Consequently， in theory，7075 aluminum alloy could replace Q345 steel as the base material for power facility components.

USRP (ultrasonic surface rolling processing) was used to change the surface layer of 6061 aluminum alloy, so as to realize the change of the second phase microstructure of 6061 aluminum alloy by USRP under different static pressure conditions to improve corrosion resistant, which was characterized by using scanning electron microscopy, laser confocal microscopy, scanning Kelvin probe force microscopy, etc. Based on the principle of microzone galvanic corrosion and considering the impedance of solution and oxide, the correlation law between the size of the second phase and the development of local corrosion was obtained. The effect of the size of the second phase on the development of local corrosion was verified by in-situ observation using laser confocal microscope. The results show that the initial self-corrosion current density of aluminum alloy in 3.5%(mass fraction) NaCl solution is only 1/15 of that of the untreated sample, the corrosion rate is reduced by 93.04%, when the surface layer is rolled with 0.10 MPa static pressure. The Mg2Si phase has no significant morphology change during the rolling process, and it has no significant effect on the corrosion performance before and after USRP. The AlFeSi phases with long strip continuous distribution are refined into micro- and nano-scale dispersion distributions under the action of USRP. The fully refined AlFeSi phase weakens the galvanic corrosion effect due to the reduction of the local anode/cathode area ratio of the corrosion microcell, which promotes the metastable pitting nucleation rate of the aluminum alloy matrix, but also cause the rapid dissolution of the aluminum alloy itself. When self-dissolution occurs or Al2O3 oxide film is formed in the inner wall of metastable corrosion hole, the electrochemical corrosion effect of AlFeSi relative to aluminum alloy matrix is greatly weakened, so as to improve the corrosion resistance of 6061 aluminum alloy as a whole.

In this study, the decomposition of a martensite/austenite (M/A) microconstituent in bainitic steels was analyzed using differential scanning calorimetry (DSC) data in conjunction with Kissinger's and Johnson–Mehl–Avrami–Kolmogorov (JMAK)'s formulas. In bainitic steel subjected to austempering heat treatment, the presence of an M/A microstructure adversely affects the mechanical properties. According to the kinetic equations derived, it is observed that after tempering the sample at 600 °C for 4000 s, the generation of each phase reaches its maximum. The SEM images taken before and after tempering reveal extensive decomposition of the M/A constituent in the microstructure. The proportion of the M/A microstructure decreased significantly from about 10% before tempering to less than 1% after. Additionally, the content of residual austenite also reduced nearly to zero. These observations are consistent with the predictions of the kinetic equations. [ABSTRACT FROM AUTHOR]

Soluble E‐cadherin (sE‐cad) is an 80 kDa fragment derived from E‐cadherin that is shed from the cell surface through proteolytic cleavage and is a biomarker in various cancers that promotes invasion and migration. Alveolar epithelial destruction, aberrant lung fibroblast migration and inflammation contribute to pulmonary fibrosis. Here, we hypothesized that E‐cadherin plays an important role in lung fibrosis. In this study, we found that E‐cadherin was markedly increased in the bronchoalveolar lavage fluid (BALF) and serum of mice with pulmonary fibrosis and that blocking sE‐cad with HECD‐1, a neutralizing antibody targeting the ectodomain of E‐cadherin, effectively inhibited myofibroblast accumulation and collagen deposition in the lungs after bleomycin (BLM) exposure. Moreover, transforming growth factor‐β (TGF‐β1) induced the shedding of sE‐cad from A549 cells, and treatment with HECD‐1 inhibited epithelial–mesenchymal transition (EMT) stimulated by TGF‐β1. Fc‐E‐cadherin (Fc‐Ecad), which is an exogenous form of sE‐cad, robustly promoted lung fibroblast migration. E‐cadherin participates in bleomycin (BLM)‐induced lung fibrosis by promoting EMT in the alveolar epithelium and fibroblast activation. E‐cadherin may be a novel therapeutic target for lung fibrosis. [ABSTRACT FROM AUTHOR]