Towards robust data-driven reduced-order modelling for turbulent flows: application to vortex-induced vibrations.

This work presents a robust method that minimises the impact of user-selected parameter on the identification of generic models to study the coherent dynamics in turbulent flows. The objective is to gain insight into the flow dynamics from a data-driven reduced order model (ROM) that is developed from measurement data of the respective flow. For an efficient separation of the coherent dynamics, spectral proper orthogonal decomposition (SPOD) is used, projecting the flow field onto a low-dimensional subspace, so that the dominating dynamics can be represented with a minimal number of modes. A function library is defined using polynomial combinations of the temporal modal coefficients to describe the flow dynamics with a system of nonlinear ordinary differential equations. The most important library functions are identified in a two-stage cross-validation procedure (conservative and restrictive sparsification) and combined in the final model. In the first stage, the process uses a simple approximation of the derivative to match the model with the data. This stage delivers a reduced set of possible library function candidates for the model. In the second, more complex stage, the model of the entire flow is integrated over a short time and compared with the progression of the measured data. This restrictive stage allows a robust identification of nonlinearities and modal interactions in the data and their representation in the model. The method is demonstrated using data from particle image velocimetry (PIV) measurements of a circular cylinder undergoing vortex-induced vibration (VIV) at Re = 4000 . It delivers a reduced order model that reproduces the average dynamics of the flow and reveals the interaction of coexisting flow dynamics by the model structure.

Salt overload damages the glycocalyx sodium barrier of vascular endothelium.

Sodium overload stiffens vascular endothelial cells in vitro and promotes arterial hypertension in vivo. The hypothesis was tested that the endothelial glycocalyx (eGC), a mesh of anionic biopolymers covering the surface of the endothelium, participates in the stiffening process. By using a mechanical nanosensor, mounted on an atomic force microscope, height (∼400 nm) and stiffness (∼0.25 pN/nm) of the eGC on the luminal endothelial surface of split-open human umbilical arteries were quantified. In presence of aldosterone, the increase of extracellular sodium concentration from 135 to 150 mM over 5 days (sodium overload) led the eGC shrink by ∼50% and stiffening by ∼130%. Quantitative eGC analyses reveal that sodium overload caused a reduction of heparan sulphate residues by 68% which lead to destabilization and collapse of the eGC. Sodium overload transformed the endothelial cells from a sodium release into a sodium-absorbing state. Spironolactone, a specific aldosterone antagonist, prevented these changes. We conclude that the endothelial glycocalyx serves as an effective buffer barrier for sodium. Damaged eGC facilitates sodium entry into the endothelial cells. This could explain endothelial dysfunction and arterial hypertension observed in sodium abuse.