Experimental and numerical study of a 10MW TLP wind turbine in waves and wind

This paper presents tests on a 1:60 version of the DTU 10MW wind turbine mounted on a tension leg platform and their numerical reproduction. Both the experimental setup and the numerical model are Froude-scaled, and the dynamic response of the floating wind turbine to wind and waves is compared in terms of motion in the six degrees of freedom, nacelle acceleration and mooring line tension. The numerical model is implemented in the aero-elastic code Flex5, featuring the unsteady BEM method and the Morison equation for the modelling of aerodynamics and hydrodynamics, respectively. It was calibrated with the tests by matching key system features, namely the steady thrust curve and the decay tests in water. The calibrated model is used to reproduce the wind-wave climates in the laboratory, including regular and irregular waves, with and without wind. The model predictions are compared to the measured data, and a good agreement is found for surge and heave, while some discrepancies are observed for pitch, nacelle acceleration and line tension. The addition of wind generally improves the agreement with test results. The aerodynamic damping is identified in both tests and simulations. Finally, the sources of the discrepancies are discussed and some improvements in the numerical model are suggested in order to obtain a better agreement with the experiments

Genetic and hypoxic alterations of the microRNA-210-ISCU1/2 axis promote iron–sulfur deficiency and pulmonary hypertension

Iron–sulfur (Fe-S) clusters are essential for mitochondrial metabolism, but their regulation in pulmonary hypertension (PH) remains enigmatic. We demonstrate that alterations of the miR-210-ISCU1/2 axis cause Fe-S deficiencies in vivo and promote PH. In pulmonary vascular cells and particularly endothelium, hypoxic induction of miR-210 and repression of the miR-210 targets ISCU1/2 down-regulated Fe-S levels. In mouse and human vascular and endothelial tissue affected by PH, miR-210 was elevated accompanied by decreased ISCU1/2 and Fe-S integrity. In mice, miR-210 repressed ISCU1/2 and promoted PH. Mice deficient in miR-210, via genetic/pharmacologic means or via an endothelial-specific manner, displayed increased ISCU1/2 and were resistant to Fe-S-dependent pathophenotypes and PH. Similar to hypoxia or miR-210 overexpression, ISCU1/2 knockdown also promoted PH. Finally, cardiopulmonary exercise testing of a woman with homozygous ISCU mutations revealed exercise-induced pulmonary vascular dysfunction. Thus, driven by acquired (hypoxia) or genetic causes, the miR-210-ISCU1/2 regulatory axis is a pathogenic lynchpin causing Fe-S deficiency and PH. These findings carry broad translational implications for defining the metabolic origins of PH and potentially other metabolic diseases sharing similar underpinnings