No abstract

Distributed parameter systems (DPSs) constitute an important class of systems that include many industrial processes modeled by partial differential equations (PDEs). Model predictive control (MPC) techniques for DPSs have been relatively scarce because of the relative difficulty of solving PDEs. Conventional MPC approaches for DPSs have usually been developed on the basis of approximate lumped models. The resulting controllers can exhibit poor performance characteristics or require substantial on-line computation to ensure adequate performance. This paper presents a novel MPC scheme for output control of distributed parameter systems that is based on the method of characteristics. It is shown via simulation that the proposed approach can yield a high-performance controller with a comparatively small computational load.

The chronic progressive decline in lung function observed in idiopathic pulmonary fibrosis (IPF) appears to result from persistent nonresolving injury to the epithelium, impaired restitution of the epithelial barrier in the lung, and enhanced fibroblast activation. Thus, understanding these key mechanisms and pathways modulating both is essential to greater understanding of IPF pathogenesis. We examined the association of VEGF with the IPF disease state and preclinical models in vivo and in vitro. Tissue and circulating levels of VEGF were significantly reduced in patients with IPF, particularly in those with a rapidly progressive phenotype, compared with healthy controls. Lung-specific overexpression of VEGF significantly protected mice following intratracheal bleomycin challenge, with a decrease in fibrosis and bleomycin-induced cell death observed in the VEGF transgenic mice. In vitro, apoptotic endothelial cell–derived mediators enhanced epithelial cell injury and reduced epithelial wound closure. This process was rescued by VEGF pretreatment of the endothelial cells via a mechanism involving thrombospondin-1 (TSP1). Taken together, these data indicate beneficial roles for VEGF during lung fibrosis via modulating epithelial homeostasis through a previously unrecognized mechanism involving the endothelium.