Effect of Irradiation on Corrosion Behavior of 316L Steel in Lead-Bismuth Eutectic with Different Oxygen Concentrations

In an accelerator-driven system (ADS), the beam window material of the spallation neutron target is heavily irradiated under severe conditions, in which the radiation damage and corrosion co-occur because of high-energy neutron and/or proton irradiation in the lead–bismuth flow. The materials used in ADSs must be compatible with the liquid metal (lead–bismuth eutectic (LBE)) to prevent issues such as liquid metal embrittlement (LME) and liquid metal corrosion (LMC). This study considers the LMC behavior after ion irradiation of 316L austenitic steel for self-ion irradiations followed by the corrosion tests in LBE with critical oxygen concentration. The 316L samples were irradiated by 10.5 MeV-Fe3+ ions at a temperature of 450 °C, up to 50 displacements per atom (dpa). After the corrosion test performed at 450 °C in LBE with low oxygen concentration, a surface of the nonirradiated area was not oxidized but appeared with locally corrosive morphology, Ni depletion, whereas an iron/chromium oxide layer fully covered the irradiated area. In the case of the corrosion surface with high oxygen concentration in LBE, the surface of the nonirradiated area was covered by an iron oxide layer only, whereas the irradiated area was covered by the duplex layers comprising iron and iron/chromium oxides. It is suggested that irradiation can enhance the oxide layer formation because of the enhancement of Fe and/or oxygen diffusion induced by the radiation defects in 316L steel

Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-b pathway

AbstractObjectivesWe sought to clarify that a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activator inhibits myocardial fibrosis and its resultant diastolic dysfunction in hypertensive heart disease, as well as to investigate whether inflammatory mediators through the nuclear factor (NF)-kappa-B pathway are involved in the effects.BackgroundPatients with hypertensive heart disease often have diastolic heart failure without systolic dysfunction. Meanwhile, it has been well established in atherosclerosis that PPAR-alpha activation negatively regulates early inflammation. In hypertensive hearts, however, it is still unclear whether PPAR-alpha activation inhibits inflammation and fibrosis.MethodsTwenty-one rats were randomly separated into the following three groups: deoxycorticosterone acetate (DOCA)-salt hypertensive rats treated with a PPAR-alpha activator, fenofibrate (80 mg/kg/day for 5 weeks); DOCA-salt rats treated with vehicle only; and uni-nephrectomized rats as normotensive controls.ResultsFenofibrate significantly inhibited the elevation of left ventricular end-diastolic pressure and the reduction of the magnitude of the negative maximum rate of left ventricular pressure rise and decline, corrected by left ventricular pressure (−dP/dtmax/P), which are indicators of diastolic dysfunction. Next, fenofibrate prevented myocardial fibrosis and reduced the hydroxyproline content and procollagen I and III messenger ribonucleic acid expression. Finally, inflammatory gene expression associated with NF-kappa-B (interleukin-6, cyclooxygenase-2, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1), which is upregulated in DOCA-salt rats, was significantly suppressed by fenofibrate. Activation of NF-kappa-B and expression of I-kappa-B-alpha in DOCA-salt rats were normalized by fenofibrate.ConclusionsA PPAR-alpha activator reduced myocardial fibrosis and prevented the development of diastolic dysfunction in DOCA-salt rats. The effects of a PPAR-alpha activator may be mediated partly by prevention of inflammatory mediators through the NF-kappa-B pathway. These results suggest that treatment with PPAR-alpha activators will improve diastolic dysfunction in hypertensive heart disease