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Airborne wind energy (AWE) technology aspires to provide increased options for wind energy harvesting at a lower cost than conventional turbines. As AWE technology is still in its infancy, there is relatively little published information concerning its aerodynamic details. In this study, we apply the FLOWUnsteady suite of aerodynamic analysis tools—including a vortex particle method for wakes and actuator line methods for rotors and wings—to the analysis of a fixed‐wing, on‐board generation, wind harvesting aircraft (or windcraft for short). Specifically, we explore variations in the rotation directions and vertical and horizontal (front to back) spacing of the rotors to understand the complex interactional aerodynamics of a multirotor windcraft design. Our results indicate that for the configurations presented herein, the rotor‐on‐rotor and wing‐on‐rotor interactions induce maximum total variations on cumulative rotor performance of less than 3% relative to baseline, with most configurations varying from baseline by 2% or less. In addition, rotor‐on‐wing interactions cause decreases in wing lift coefficient of up to roughly 7% (for the configurations simulated) relative to the isolated wing. Furthermore, through selecting specific rotor rotation directions, it is possible to prescribe a portion of the shape of the wing lift distribution. Further exploration, perhaps with the assistance of optimization techniques, may yield greater insights into this uncharted space of windcraft interactional aerodynamics. [ABSTRACT FROM AUTHOR]

Specific correlations among diffusion tensor imaging (DTI)-derived metrics and magnetic resonance spectroscopy (MRS) metabolite ratios in brains with glioblastoma are still not completely understood.

The vortex particle method (VPM) has gained popularity in recent years due to a growing need to predict complex aerodynamic interactions during the preliminary design of electric multirotor aircraft. However, VPM is known to be numerically unstable when vortical structures break down close to the turbulent regime. In recent work, the VPM has been reformulated as a large-eddy simulation (LES) in a scheme that is both meshless and numerically stable without increasing its computational cost. In this study, we build upon this meshless LES scheme to create a solver for interactional aerodynamics. Propeller blades are introduced through an actuator line model following well-established practices for LES. A novel, vorticity-based actuator surface model (ASM) is developed for wings, which is suitable for propeller-wing interactions when a wake impinges on the surface of a wing. This ASM imposes the no-flow-through condition at the airfoil centerline by calculating the circulation that meets this condition and by immersing the associated vorticity in the LES following a pressure-like distribution. Extensive validation of propeller-wing interactions is presented by simulating a tailplane with tip-mounted propellers and a blown wing with propellers mounted midspan. [ABSTRACT FROM AUTHOR]

Internalization from the cell membrane and endosomal trafficking of receptor tyrosine kinases (RTKs) are important regulators of signaling in normal cells that can frequently be disrupted in cancer. The adrenal tumor pheochromocytoma (PCC) can be caused by activating mutations of the rearranged during transfection (RET) receptor tyrosine kinase, or inactivation of TMEM127, a transmembrane tumor suppressor implicated in trafficking of endosomal cargos. However, the role of aberrant receptor trafficking in PCC is not well understood. Here, we show that loss of TMEM127 causes wildtype RET protein accumulation on the cell surface, where increased receptor density facilitates constitutive ligand-independent activity and downstream signaling, driving cell proliferation. Loss of TMEM127 altered normal cell membrane organization and recruitment and stabilization of membrane protein complexes, impaired assembly, and maturation of clathrin-coated pits, and reduced internalization and degradation of cell surface RET. In addition to RTKs, TMEM127 depletion also promoted surface accumulation of several other transmembrane proteins, suggesting it may cause global defects in surface protein activity and function. Together, our data identify TMEM127 as an important determinant of membrane organization including membrane protein diffusability and protein complex assembly and provide a novel paradigm for oncogenesis in PCC where altered membrane dynamics promotes cell surface accumulation and constitutive activity of growth factor receptors to drive aberrant signaling and promote transformation. [ABSTRACT FROM AUTHOR]

Aims: Biliary atresia (BA) is characterized by intrahepatic inflammation and rapid progression of liver fibrosis. Galectin‐3, a beta‐galactoside binding protein, is a key regulator of inflammation and fibrosis. The aim of this study was to characterize circulating and hepatic Galectin‐3 levels in children with BA. Methods: Plasma and liver samples were obtained from children with early BA at time of Kasai hepatoportoenterostomy, late BA at time of transplant, early and late other cholestatic liver diseases (CLD), and controls. Plasma Galectin‐3 was measured using standard enzyme‐linked immunoassay. Liver tissue was analyzed with multiplex immunohistochemistry and quantified using whole slide analysis. Statistical comparisons were made using nonparametric testing. Results: Plasma Galectin‐3 in late BA was significantly higher than in early BA (20.82 [12.45–30.46] vs. 11.30 [8.74–16.83] ng/mL, p = 0.0096). Galectin‐3 levels correlated with markers of disease severity and interleukin‐6. There were significantly more Galectin‐3+ M2 macrophages in late BA in comparison to late other CLD (162 [157–233] vs. 49 [33–59] cells/mm2, p = 0.03). The number of Galectin‐3+ M2 macrophages correlated with the number of activated hepatic stellate cells and bile duct proliferation. Conclusions: Plasma Galectin‐3 is higher in late BA at time of transplant in comparison to early BA at time of Kasai. The number of Galectin‐3 expressing M2 macrophages in late BA is elevated relative to late other CLD and was associated with other prognostic histological findings. Galectin‐3 targeted therapy may be beneficial in slowing disease progression to cirrhosis in children with BA. [ABSTRACT FROM AUTHOR]