Search

This paper presents and validates an analytical formulation, denoted as Performance Prediction Equations (PPEs), that relates the seismic response engineering demand parameter (EDP) of buildings to earthquake parameters such as magnitude, epicentral distance, and type of faulting. PPEs are conceptually novel and can be readily included in any hazard calculation program to directly estimate EDP hazard curves. The PPEs presented herein are based on the linearization of response spectrum analysis (RSA) formulation for estimation of the seismic response of multi-degree-of-freedom (MDOF) models for planar structural systems. Equations for mean and variance are provided for floor displacement, interstory drift ratio, and normalized base shear. The input parameters needed to apply the proposed PPEs are the modal properties of the structural system and the selection of an existing ground motion model (GMM). The proposed PPEs are validated against simulated results using a set of planar building models and the Campbell-Bozorgnia 2014GMM. The comparison confirms that the proposed PPEs provide an accurate estimate of the statistics of the said EDPs.

The accumulation of T cells in the synovial membrane is the crucial step in the pathophysiology of the inflammatory processes characterizing juvenile idiopathic arthritis (JIA). In this study, we evaluated the expression and the pathogenetic role in oligoarticular JIA of a CXC chemokine involved in the directional migration of activated T cells, i.e. IFNγ-inducible protein 10 (CXCL10) and its receptor, CXCR3. Immunochemistry with an antihuman CXCL10 showed that synovial macrophages, epithelial cells, and endothelial cells bear the chemokine. By flow cytometry and immunochemistry, it has been shown that CXCR3 is expressed at high density by virtually all T lymphocytes isolated from synovial fluid (SF) and infiltrating the synovial membrane. Particularly strongly stained CXCR3+ T cells can be observed close to the luminal space and in the perivascular area. Furthermore, densitometric analysis has revealed that the mRNA levels for CXCR3 are significantly higher in JIA patients than in controls. T cells purified from SF exhibit a definite migratory capability in response to CXCL10. Furthermore, SF exerts significant chemotactic activity on the CXCR3+ T-cell line, and this activity is inhibited by the addition of an anti-CXCL10 neutralizing antibody. Taken together, these data suggest that CXCR3/CXCL10 interactions are involved in the pathophysiology of JIA-associated inflammatory processes, regulating both the activation of T cells and their recruitment into the inflamed synovium.