Study on In-Service Inspection of Nuclear Fuel Assembly Failure Using Ultrasonic Plate Wave.

As protection for nuclear power plants is quite necessary, the nuclear fuel is sealed in zirconium alloy thin wall cladding. During service, fuel rods might be damaged caused by wall-thickness thinning, cladding corrosion and cracking, etc. This will cause the coolant to enter into the fuel rod, which may lead to the failure of the fuel assembly. However, current diagnostic methods have limitations due to the special structure of the fuel assembly and the underwater and radioactive environment. In this paper, a novel inspection method is proposed to recognize the failure of a fuel rod. The fuel rod failure can be detected based on the presence or absence of coolant inside the fuel rod by using an ultrasonic plate wave. The inspection model and process algorithm are proposed for in-service inspection. The relationship between signal and scanning position is established and analyzed. Both ultrasound field simulation and experiment have been carried out for validation. The corresponding results illustrate that the failed nuclear fuel rod of the whole fuel assembly (including the internal rods) can be effectively detected without the influence of the near-field region by using the proposed method.

[Degradation of AO7 with Magnetic Fe3O4-CuO Heterogeneous Catalyzed Sodium Percarbonate System].

Magnetically recyclable Fe3O4-CuO was synthesized by a one-step hydrothermal method and characterized by scanning electron microscopy coupled with energy dispersive spectrometer (SEM-EDS) and X-ray diffraction (XRD). The degradation of azo dye acid orange 7 (AO7) by percarbonate (SPC) activated with Fe3O4-CuO was studied. The effects of Fe3O4-CuO catalyst loading, SPC concentration, pH value, and common chloride ions on AO7 degradation in the Fe3O4-CuO/SPC system were evaluated. The main reaction mechanism of AO7 degradation was analyzed. The results show that Fe3O4-CuO could effectively activate SPC to degrade AO7 and the reaction was accelerated with the increase of Fe3O4-CuO dosage. The increase of SPC dosage was favorable for the degradation of AO7, but excessive SPC dosage inhibited the degradation of AO7. Common ions (e.g., Cl-) in dye wastewater could promote the degradation of AO7, and the degradation rate increased with increasing concentration of Cl-. The reaction mainly occurred on the surface of the catalyst, and·OH was identified as the main active species for the degradation of AO7. The catalyst Fe3O4-CuO showed excellent stability owing to the high catalytic activity remaining after 4 cycles of repeated use. The Fe3O4-CuO/SPC system achieved a high mineralization rate in the process of decolorization of AO7.

Chemokine- and adhesion-dependent survival of neutrophils after transmigration through cytokine-stimulated endothelium.

We examined the fate of neutrophils following transmigration through an endothelial monolayer cultured on "Transwell" membrane filters. Treatment of human umbilical vein endothelial cells (HUVEC) with increasing doses of tumor necrosis factor-alpha increased the efficiency of transmigration and markedly reduced apoptosis among the transmigrated neutrophils in a dose-dependent manner. Apoptosis was also inhibited after transmigration of neutrophils through HUVEC stimulated with interleukin (IL)-1beta but not so effectively after chemotaxis through unstimulated HUVEC driven by IL-8 added below the filter. Inhibition of beta2-integrin binding after transmigration or coating the lower chamber with a nonadhesive polymer (polyhydroxyl-ethyl-methacrylate) abrogated neutrophil survival. Although integrin engagement during migration itself was not essential to inhibit apoptosis, activation of neutrophils through CXC chemokine receptors was necessary. Quite brief exposure to the HUVEC (30-120 min) was effective in reducing subsequent apoptosis, although if coincubation with the HUVEC were prolonged, neutrophil apoptosis was reduced further. Neutralization of granulocyte macrophage-colony stimulating factor inhibited this additional effect. Thus, a complex interplay between migration- and activation-dependent signals and adhesive interaction in tissue may combine to effectively prolong the survival of neutrophils recruited during inflammation.

The role of heterodimerization between VEGFR-1 and VEGFR-2 in the regulation of endothelial cell homeostasis.

VEGF-A activity is tightly regulated by ligand and receptor availability. Here we investigate the physiological function of heterodimers between VEGF receptor-1 (VEGFR-1; Flt-1) and VEGFR-2 (KDR; Flk-1) (VEGFR(1-2)) in endothelial cells with a synthetic ligand that binds specifically to VEGFR(1-2). The dimeric ligand comprises one VEGFR-2-specific monomer (VEGF-E) and a VEGFR-1-specific monomer (PlGF-1). Here we show that VEGFR(1-2) activation mediates VEGFR phosphorylation, endothelial cell migration, sustained in vitro tube formation and vasorelaxation via the nitric oxide pathway. VEGFR(1-2) activation does not mediate proliferation or elicit endothelial tissue factor production, confirming that these functions are controlled by VEGFR-2 homodimers. We further demonstrate that activation of VEGFR(1-2) inhibits VEGF-A-induced prostacyclin release, phosphorylation of ERK1/2 MAP kinase and mobilization of intracellular calcium from primary endothelial cells. These findings indicate that VEGFR-1 subunits modulate VEGF activity predominantly by forming heterodimer receptors with VEGFR-2 subunits and such heterodimers regulate endothelial cell homeostasis.