Parallel chemistry acceleration algorithm with ISAT table-size control in the application of gaseous detonation

In order to improve the computational efficiency of a parallel ISAT (in situ adaptive tabulation)-based chemistry acceleration algorithm in the computations of transient, chemically reacting flows, a control strategy is proposed to maintain the sizes of the data tables in the ISAT computations. The table-size control strategy is then combined with a parallel algorithm to simulate two-dimensional gaseous detonation wave propagation. In the computation of 2H2 + O2 detonation, two sets of tests are conducted to identify the size control strategy. In the first set, the maximum total table size (Mtot) summed over all sub-zones is fixed, while the maximum size of the table on each sub-zone (Msin) is varied. In the second set, a fixed Msin is used for all the tables on the sub-zones while Mtot is varied. A maximum speedup ratio of 4.29 is found in the former tests, while 5.52 is found in the latter. Two parameters, σf and p, are proposed to analyze the load balance and synchronization among table operations in the parallel ISAT computations in the above tests. It is found that both load balance and synchronization have clear influences on the speedup ratio. A parameter pM is defined, and a strategy to choose the optimal maximum table sizes (both Mtot and Msin) based on pM is proposed and is verified to be universal in the computations of both 2H2 + O2 detonation and C2H4 + 3O2 detonation. Finally, the parallel acceleration algorithm enhanced with table-size control is shown to be highly accurate for the detonations in both fuels

Functional Wnt Signaling Is Increased in Idiopathic Pulmonary Fibrosis

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease, characterized by distorted lung architecture and loss of respiratory function. Alveolar epithelial cell injury and hyperplasia, enhanced extracellular matrix deposition, and (myo)fibroblast activation are features of IPF. Wnt/beta-catenin signaling has been shown to determine epithelial cell fate during development. As aberrant reactivation of developmental signaling pathways has been suggested to contribute to IPF pathogenesis, we hypothesized that Wnt/beta-catenin signaling is activated in epithelial cells in IPF. Thus, we quantified and localized the expression and activity of the Wnt/beta-catenin pathway in IPF. METHODOLOGY/PRINCIPAL FINDINGS: The expression of Wnt1, 3a, 7b, and 10b, the Wnt receptors Fzd1-4, Lrp5-6, as well as the intracellular signal transducers Gsk-3beta, beta-catenin, Tcf1, 3, 4, and Lef1 was analyzed in IPF and transplant donor lungs by quantitative real-time (q)RT-PCR. Wnt1, 7b and 10b, Fzd2 and 3, beta-catenin, and Lef1 expression was significantly increased in IPF. Immunohistochemical analysis localized Wnt1, Wnt3a, beta-catenin, and Gsk-3beta expression largely to alveolar and bronchial epithelium. This was confirmed by qRT-PCR of primary alveolar epithelial type II (ATII) cells, demonstrating a significant increase of Wnt signaling in ATII cells derived from IPF patients. In addition, Western blot analysis of phospho-Gsk-3beta, phospho-Lrp6, and beta-catenin, and qRT-PCR of the Wnt target genes cyclin D1, Mmp 7, or Fibronectin 1 demonstrated increased functional Wnt/beta-catenin signaling in IPF compared with controls. Functional in vitro studies further revealed that Wnt ligands induced lung epithelial cell proliferation and (myo)fibroblast activation and collagen synthesis. CONCLUSIONS/SIGNIFICANCE: Our study demonstrates that the Wnt/beta-catenin pathway is expressed and operative in adult lung epithelium. Increased Wnt/beta-catenin signaling may be involved in epithelial cell injury and hyperplasia, as well as impaired epithelial-mesenchymal cross-talk in IPF. Thus, modification of Wnt signaling may represent a therapeutic option in IPF