Investigating Three-Dimensional and Rotational Effects on Wind Turbine Blades by Means of a Quasi-3D Navier-Stokes Solver

Three-dimensional and rotational viscous effects on wind turbine blades are investigated by means of a quasi-3D Navier-Stokes model. The governing equations of the model are derived from the 3-D primitive variable Navier-Stokes equations written in cylindrical coordinates in the rotating frame of reference. The latter are integrated along the radial direction and certain assumptions are made for the mean values of the radial derivatives. The validity of these assumptions is cross-checked through fully 3-D Navier-Stokes calculations. The resulting quasi-3D model suggests that three-dimensional and rotational effects be strongly related to the local chord by radii ratio and the twist angle. The equations of the model are numerically integrated by means of a pressure correction algorithm. Both laminar and turbulent flow simulations are performed. The former is used for identifying the physical mechanism associated with the 3-D and rotational effects, while the latter for establishing semiempirical correction laws for the load coefficients, based on 2-D airfoil data. Comparing calculated and measured power curves of a stall controlled wind turbine, it is shown that the suggested correction laws may improve significantly the accuracy of the predictions. [S0098-2202(00)02702-4]</jats:p

BI 5700, a Selective Chemical Inhibitor of IκB Kinase 2, Specifically Suppresses Epithelial-Mesenchymal Transition and Metastasis in Mouse Models of Tumor Progression

Increasing evidence suggests that processes termed epithelial-mesenchymal transitions (EMTs) play a key role in therapeutic resistance, tumor recurrence, and metastatic progression. NF-κB signaling has been previously identified as an important pathway in the regulation of EMT in a mouse model of tumor progression. However, it remains unclear whether there is a broad requirement for this pathway to govern EMT and what the relative contribution of IKK family members acting as upstream NF-κB activators is toward promoting EMT and metastasis. To address this question, we have used a novel, small-molecule inhibitor of IκB kinase 2 (IKK2/IKKβ), termed BI 5700. We investigated the role of IKK2 in a number of mouse models of EMT, including TGFβ-induced EMT in the mammary epithelial cell line EpRas, CT26 colon carcinoma cells, and 4T1 mammary carcinoma cells. The latter model was also used to evaluate in vivo activities of BI 5700.We found that BI 5700 inhibits IKK2 with an IC50 of 9 nM and was highly selective as compared to other IKK family members (IKK1, IKKε, and TBK1) and other kinases. BI 5700 effectively blocks NF-κB activity in EpRas cells and prevents TGFβ-induced EMT. In addition, BI 5700 reverts EMT in mesenchymal CT26 cells and prevents EMT in the 4T1 model. Oral application of BI 5700 significantly interferes with metastasis after mammary fat-pad injection of 4T1 cells, yielding fewer, smaller, and more differentiated metastases as compared to vehicle-treated control animals. We conclude that IKK2 is a key regulator of both the induction and maintenance of EMT in a panel of mouse tumor progression models and that the IKK2 inhibitor BI 5700 constitutes a promising candidate for the treatment of metastatic cancers