Double-shock control bump design optimization using hybridized evolutionary algorithms

This study investigates the application of two advanced optimization methods for solving active flow control (AFC) device shape design problem and compares their optimization efficiency in terms of computational cost and design quality. The first optimization method uses hierarchical asynchronous parallel multi-objective evolutionary algorithm and the second uses hybridized evolutionary algorithm with Nash-Game strategies (Hybrid-Game). Both optimization methods are based on a canonical evolution strategy and incorporate the concepts of parallel computing and asynchronous evaluation. One type of AFC device named shock control bump (SCB) is considered and applied to a natural laminar flow (NLF) aerofoil. The concept of SCB is used to decelerate supersonic flow on suction/pressure side of transonic aerofoil that leads to a delay of shock occurrence. Such active flow technique reduces total drag at transonic speeds which is of special interest to commercial aircraft. Numerical results show that the Hybrid-Game helps an EA to accelerate optimization process. From the practical point of view, applying a SCB on the suction and pressure sides significantly reduces transonic total drag and improves lift-to-drag (L/D) value when compared to the baseline design.

Optimal-stopping control for airborne collision avoidance and return-to-course flight

This paper considers an aircraft collision avoidance design problem that also incorporates design of the aircraft’s return-to-course flight. This control design problem is formulated as a non-linear optimal-stopping control problem; a formulation that does not require a prior knowledge of time taken to perform the avoidance and return-to-course manoeuvre. A dynamic programming solution to the avoidance and return-to-course problem is presented, before a Markov chain numerical approximation technique is described. Simulation results are presented that illustrate the proposed collision avoidance and return-to-course flight approach.

A new control-volume finite-element scheme for heterogeneous porous media : application to the drying of softwood

An improved mesoscopic model is presented for simulating the drying of porous media. The aim of this model is to account for two scales simultaneously: the scale of the whole product and the scale of the heterogeneities of the porous medium. The innovation of this method is the utilization of a new mass-conservative scheme based on the Control-Volume Finite-Element (CV-FE) method that partitions the moisture content field over the individual sub-control volumes surrounding each node within the mesh. Although the new formulation has potential for application across a wide range of transport processes in heterogeneous porous media, the focus here is on applying the model to the drying of small sections of softwood consisting of several growth rings. The results conclude that, when compared to a previously published scheme, only the new mass-conservative formulation correctly captures the true moisture content evolution in the earlywood and latewood components of the growth rings during drying.

Practical stability with respect to model mismatch of approximate discrete-time output feedback control

This paper establishes a practical stability result for discrete-time output feedback control involving mismatch between the exact system to be stabilised and the approximating system used to design the controller. The practical stability is in the sense of an asymptotic bound on the amount of error bias introduced by the model approximation, and is established using local consistency properties of the systems. Importantly, the practical stability established here does not require the approximating system to be of the same model type as the exact system. Examples are presented to illustrate the nature of our practical stability result.

Genetic and gene expression analyses of the polycystic ovary syndrome candidate gene fibrillin-3 and other fibrillin family members in human ovaries

Several studies have demonstrated an association between polycystic ovary syndrome (PCOS) and the dinucleotide repeat microsatellite marker D19S884, which is located in intron 55 of the fibrillin-3 (FBN3) gene. Fibrillins, including FBN1 and 2, interact with latent transforming growth factor (TGF)-β-binding proteins (LTBP) and thereby control the bioactivity of TGFβs. TGFβs stimulate fibroblast replication and collagen production. The PCOS ovarian phenotype includes increased stromal collagen and expansion of the ovarian cortex, features feasibly influenced by abnormal fibrillin expression. To examine a possible role of fibrillins in PCOS, particularly FBN3, we undertook tagging and functional single nucleotide polymorphism (SNP) analysis (32 SNPs including 10 that generate non-synonymous amino acid changes) using DNA from 173 PCOS patients and 194 controls. No SNP showed a significant association with PCOS and alleles of most SNPs showed almost identical population frequencies between PCOS and control subjects. No significant differences were observed for microsatellite D19S884. In human PCO stroma/cortex (n = 4) and non-PCO ovarian stroma (n = 9), follicles (n = 3) and corpora lutea (n = 3) and in human ovarian cancer cell lines (KGN, SKOV-3, OVCAR-3, OVCAR-5), FBN1 mRNA levels were approximately 100 times greater than FBN2 and 200–1000-fold greater than FBN3. Expression of LTBP-1 mRNA was 3-fold greater than LTBP-2. We conclude that FBN3 appears to have little involvement in PCOS but cannot rule out that other markers in the region of chromosome 19p13.2 are associated with PCOS or that FBN3 expression occurs in other organs and that this may be influencing the PCOS phenotype.

Brivanib alaninate, a dual inhibitor of vascular endothelial growth factor receptor and fibroblast growth factor receptor tyrosine kinases, induces growth inhibition in mouse models of human hepatocellular carcinoma

PURPOSE: Hreceptor (VEGFR) and FGF receptor (FGFR) signaling pathways. EXPERIMENTAL DESIGN: Six different s.c. patient-derived HCC xenografts were implanted into mice. Tumor growth was evaluated in mice treated with brivanib compared with control. The effects of brivanib on apoptosis and cell proliferation were evaluated by immunohistochemistry. The SK-HEP1 and HepG2 cells were used to investigate the effects of brivanib on the VEGFR-2 and FGFR-1 signaling pathways in vitro. Western blotting was used to determine changes in proteins in these xenografts and cell lines. RESULTS: Brivanib significantly suppressed tumor growth in five of six xenograft lines. Furthermore, brivanib-induced growth inhibition was associated with a decrease in phosphorylated VEGFR-2 at Tyr(1054/1059), increased apoptosis, reduced microvessel density, inhibition of cell proliferation, and down-regulation of cell cycle regulators. The levels of FGFR-1 and FGFR-2 expression in these xenograft lines were positively correlated with its sensitivity to brivanib-induced growth inhibition. In VEGF-stimulated and basic FGF stimulated SK-HEP1 cells, brivanib significantly inhibited VEGFR-2, FGFR-1, extracellular signal-regulated kinase 1/2, and Akt phosphorylation. CONCLUSION: This study provides a strong rationale for clinical investigation of brivanib in patients with HCC.