Evolution of Wave Characteristics during Wind-Wave Generation

The generation of ocean surface waves by wind is a classic fluid mechanics problem whose theoretical study dates back to 1957, when the two seminal papers by Phillips and Miles were published in the incipient Journal of Fluid Mechanics. Comprehensively understanding the mechanism of wind-wave generation is of crucial importance to many naval applications. Here, we present the recent developments of our work on this profound and long-standing problem. We perform a wave phase-resolved direct numerical simulation (DNS) of the turbulent airflow over an initially calm water surface that responds dynamically to the wind forcing. Our simulation reveals the evolution of the surface wave statistics over the entire wind-wave generation process. As the wave fluctuations grow with time under the turbulent wind forcing, the temporal growth behavior of the surface elevation variance transitions from linear growth to exponential growth. Moreover, surface waves exhibit nonlinearity at the late stage of simulation when the wave amplitude is significant enough to alter the airflow field. Based on this rich DNS dataset, we systematically study the underlying mechanism and report several advances in the theoretical analysis of this problem.Comment: 34th Symposium on Naval Hydrodynamics, Washington, DC, USA, 26 June - 1 July 202

Reconstruction of three-dimensional turbulent flow structures using surface measurements for free-surface flows based on a convolutional neural network

A model based on a convolutional neural network (CNN) is designed to reconstruct the three-dimensional turbulent flows beneath a free surface using surface measurements, including the surface elevation and surface velocity. Trained on datasets obtained from the direct numerical simulation (DNS) of turbulent open-channel flows with a deformable free surface, the proposed model can accurately reconstruct the near-surface flow field and capture the characteristic large-scale flow structures away from the surface. The reconstruction performance of the model, measured by metrics such as the normalised mean squared reconstruction errors and scale-specific errors, is considerably better than that of the traditional linear stochastic estimation (LSE) method. We further analyse the saliency maps of the CNN model and the kernels of the LSE model and obtain insights into how the two models utilise surface features to reconstruct subsurface flows. The importance of different surface variables is analysed based on the saliency map of the CNN, which reveals knowledge about the surface-subsurface relations. The CNN is also shown to have a good generalization capability with respect to the Froude number if a model trained for a flow with a high Froude number is applied to predict flows with lower Froude numbers. The results presented in this work indicate that the CNN is effective regarding the detection of subsurface flow structures and by interpreting the surface-subsurface relations underlying the reconstruction model, the CNN can be a promising tool for assisting with the physical understanding of free-surface turbulence

PINK1 protects against oxidative stress by phosphorylating mitochondrial chaperone TRAP1.

Mutations in the PTEN induced putative kinase 1 (PINK1) gene cause an autosomal recessive form of Parkinson disease (PD). So far, no substrates of PINK1 have been reported, and the mechanism by which PINK1 mutations lead to neurodegeneration is unknown. Here we report the identification of TNF receptor-associated protein 1 (TRAP1), a mitochondrial molecular chaperone also known as heat shock protein 75 (Hsp75), as a cellular substrate for PINK1 kinase. PINK1 binds and colocalizes with TRAP1 in the mitochondria and phosphorylates TRAP1 both in vitro and in vivo. We show that PINK1 protects against oxidative-stress-induced cell death by suppressing cytochrome c release from mitochondria, and this protective action of PINK1 depends on its kinase activity to phosphorylate TRAP1. Moreover, we find that the ability of PINK1 to promote TRAP1 phosphorylation and cell survival is impaired by PD-linked PINK1 G309D, L347P, and W437X mutations. Our findings suggest a novel pathway by which PINK1 phosphorylates downstream effector TRAP1 to prevent oxidative-stress-induced apoptosis and implicate the dysregulation of this mitochondrial pathway in PD pathogenesis

catena-Poly[cadmium-μ-[1,3-bis­(imidazol-1-yl)propane]-di-μ-chlorido]

The title complex, [CdCl2(C9H12N4)]n, is characterized by the formation of a zigzag chain structure parallel to [001]. In the chain, the Cd2+ cation is coordinated by four bridging Cl− ligands in equatorial positions and two N atoms from symmetry-related and likewise bridging 1,3-bis­(imidazol-1-yl)propane ligands in axial positions, forming a distorted CdCl4N2 octa­hedron