Abstract A spiral case with its steel spiral case (SSC) being embedded in reinforced concrete under a pressurized condition is called a preloaded filling spiral case structure (PFSCS) in a hydropower plant. As a steel-concrete composite structure, a PFSCS is designed to work reliably. The non-uniform gap and contact nonlinearity between the SSC and the surrounding mass concrete have a great effect on the bearing mechanism of the composite structure. However, the description of the gap and contact nonlinearity in a PFSCS is a tough work. With the aim of efficiently describing the evolution process of the non-uniform gap and contact nonlinearity, we performed an experimental investigation and proposed a novel numerical simulation technique for structural finite element analyses (FEA) of PFSCSs. In the technique, the gap and contact nonlinearity as well as the construction process and operation process of a PFSCS are taken into account. A friction-contact model is used to simulate the sliding of the SSC against the concrete. A plasticity damage model is employed to describe the concrete. The development of the gap, contact status between the steel liner and the surrounding concrete, stresses of the steel liner and the steel bars, as well as the concrete cracking time and crack pattern, are presented in this work. The FEA results agree well with the experimental results. The agreement provides evidence that the applicability and competence of the proposed technique are valid and satisfactory.
ABSTRACT We previously revealed the involvement of extracellular regulated protein kinases 1/2 (ERK1/2) in interleukin-6 (IL-6) secretion induced by cyclic compressive force (CCF) in MLO-Y4 cells. In this study, we investigated the contributions of the p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways to IL-6 secretion by stimulating MLO-Y4 cells with CCF. At 80% confluence, different magnitudes (1000μstrain, 2000 μstrain and 4000 μstrain), frequencies (0.5 Hz, 1.0 Hz and 2.0 Hz) and durations (10 min, 30 min, 1 h, 3 h and 6 h) of CCF were loaded onto cells using a four-point bending system. Flow Cytometry (FCM) analysis was used to analyze cell mortality rates after CCF loading. p38 and p65 phosphorylation as well as IκBα degradation in MLO-Y4 cells were detected by Western blotting (WB). Changes in IL-6 secretion after inhibitor treatment were assessed by enzyme-linked immunosorbent assays (ELISAs). Cellular viability was over 90 percent after CCF. p38 and p65 phosphorylation increased under all conditions, whereas IκBα protein levels decreased. However, phosphorylation and degradation were not completely dependent on the loading magnitude, frequency or duration. Furthermore, p38 inhibition using the specific inhibitor SB203580 reduced both p38 phosphorylation and IL-6 secretion. Similarly, NF-κB inhibition using BAY 11-7082 decreased p65 phosphorylation and IL-6 secretion but increased the concentration of IκBα. These findings reveal significant roles for the p38 and NF-κB signaling pathways in IL-6 secretion induced by CCF in MLO-Y4 cells.