Cluster-based feedback control of turbulent post-stall separated flows

We propose a novel model-free self-learning cluster-based control strategy for general nonlinear feedback flow control technique, benchmarked for high-fidelity simulations of post-stall separated flows over an airfoil. The present approach partitions the flow trajectories (force measurements) into clusters, which correspond to characteristic coarse-grained phases in a low-dimensional feature space. A feedback control law is then sought for each cluster state through iterative evaluation and downhill simplex search to minimize power consumption in flight. Unsupervised clustering of the flow trajectories for in-situ learning and optimization of coarse-grained control laws are implemented in an automated manner as key enablers. Re-routing the flow trajectories, the optimized control laws shift the cluster populations to the aerodynamically favorable states. Utilizing limited number of sensor measurements for both clustering and optimization, these feedback laws were determined in only $O(10)$ iterations. The objective of the present work is not necessarily to suppress flow separation but to minimize the desired cost function to achieve enhanced aerodynamic performance. The present control approach is applied to the control of two and three-dimensional separated flows over a NACA 0012 airfoil with large-eddy simulations at an angle of attack of $9^\circ$, Reynolds number $Re = 23,000$ and free-stream Mach number $M_\infty = 0.3$. The optimized control laws effectively minimize the flight power consumption enabling the flows to reach a low-drag state. The present work aims to address the challenges associated with adaptive feedback control design for turbulent separated flows at moderate Reynolds number.Comment: 32 pages, 18 figure

The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation.

Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation