Thermal stability changes the properties of the turbulent atmospheric boundary layer, and in turn affects the behaviour of wind-turbine wakes. To better understand the effects of thermal stability on the wind-turbine wake structure, wind-tunnel experiments were carried out with a simulated convective boundary layer (CBL) and a neutral boundary layer. The CBL was generated by cooling the airflow to 12-15 • C and heating up the test section floor to 73-75 • C. The freestream wind speed was set at about 2.5 m s −1 , resulting in a bulk Richardson number of −0.13. The wake of a horizontal-axis 3-blade wind-turbine model, whose height was within the lowest one third of the boundary layer, was studied using stereoscopic particle image velocimetry (S-PIV) and triple-wire (x-wire/cold-wire) anemometry. Data acquired with the SPIV were analyzed to characterize the highly three-dimensional turbulent flow in the near wake (0.2-3.2 rotor diameters) as well as to visualize the shedding of tip vortices. Profiles of the mean flow, turbulence intensity, and turbulent momentum and heat fluxes were measured with the triple-wire anemometer at downwind locations from 2-20 rotor diameters in the centre plane of the wake. In comparison with the wake of the same wind turbine in a neutral boundary layer, a smaller velocity deficit (about 15 % at the wake centre) is observed in the CBL, where an enhanced radial momentum transport leads to a more rapid momentum recovery, particularly in the lower part of the wake. The velocity deficit at the wake centre decays following a power law regardless of the thermal stability. While the peak turbulence intensity (and the maximum added turbulence) occurs at the top-tip height at a downwind distance of about three rotor diameters in both cases, the magnitude is about 20 % higher
Excessive proliferation and migration of fibroblasts contribute to pulmonary fibrosis in silicosis, and both epithelial cells and endothelial cells participate in the accumulation of fibroblasts via the epithelial–mesenchymal transition (EMT) and the endothelial–mesenchymal transition (EndMT), respectively. A mouse endothelial cell line (MML1) was exposed to silicon dioxide (SiO2, 50 μg/cm2), and immunofluorescence and western blot analyses were performed to evaluate levels of specific endothelial and mesenchymal markers and to elucidate the mechanisms by which SiO2 induces the EndMT. Functional changes were evaluated by analyzing cell migration and proliferation. The mRNA and circular RNA (circRNA) levels were measured using qPCR and fluorescent in situ hybridization (FISH). Lung tissue samples from both Tie2-GFP mice exposed to SiO2 and silicosis patients were applied to confirm the observations from in vitro experiments. Based on the results from the current study, SiO2 increased the expression of mesenchymal markers (type I collagen (COL1A1), type III collagen (COL3A1) and alpha smooth muscle actin (α-SMA/Acta2)) and decreased the expression of endothelial markers (vascular endothelial cadherin (VE-Cad/Cdh 5) and platelet endothelial cell adhesion molecule-1 (PECAM1)), indicating the occurrence of the EndMT in response to SiO2 exposure both in vivo and in vitro. SiO2 concomitantly increased circHECTD1 expression, which, in turn, inhibited HECTD1 protein expression. SiO2-induced increases in cell proliferation, migration, and changes in marker levels were restored by either a small interfering RNA (siRNA) targeting circHECTD1 or overexpression of HECTD1 via the CRISPR/Cas9 system, confirming the involvement of the circHECTD1/HECTD1 pathway in the EndMT. Moreover, tissue samples from SiO2-exposed mice and silicosis patients confirmed the EndMT and change in HECTD1 expression. Our findings reveal a potentially new function for the circHECTD1/HECTD1 pathway and suggest a possible mechanism of fibrosis in patients with pulmonary silicosis.
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