2,278 research outputs found

    Unsteady Aerodynamic Interaction Between Rotor and Ground Obstacle

    Get PDF
    The mutual aerodynamic interaction between rotor wake and surrounding obstacles is complex, and generates high compensatory workload for pilots, degradation of the handling qualities and performance, and unsteady force on the structure of the obstacles. The interaction also affects the minimum distance between rotorcrafts and obstacles to operate safely. A vortex-based approach is then employed to investigate the complex aerodynamic interaction between rotors and ground obstacle, and identify the distance where the interaction ends, and this is also the objective of the GARTEUR AG22 working group activities. In this approach, the aerodynamic loads of the rotor blades are described through a panel method, and the unsteady behaviour of the rotor wake is modelled using a vortex particle method. The effects of the ground plane and obstacle are accounted for via a viscous boundary model. The method is then applied to a “Large” and a “Wee” rotor near the ground and obstacle, and compared with the earlier experiments carried out at the University of Glasgow. The results show that the predicted rotor induced inflow and flow field compare reasonably well with the experiments. Furthermore, at certain conditions the tip vortices are pushed up and re-injected into the rotor wake due to the effect of the obstacle resulting in a recirculation. Moreover, contrary to without the obstacle case, the peak and thickness of the radial outwash near the obstacle is smaller due to the barrier effect of the obstacle, and an up-wash is observed. Additionally, as the rotor closes to the obstacle, the rotor slipstreams impinge directly on the obstacle, and the up-wash near the obstacle is faster, indicating a stronger interaction between the rotor wake and the obstacle. Also, contrary to the case without the obstacle, the fluctuations of the rotor thrust, rolling and pitching moments are obviously strengthened. When the distance between the rotor and the obstacle is larger than 3R, the effect of the obstacle is small

    Vortex approach for downwash and outwash of tandem rotors in ground effect

    Get PDF
    A vortex-based approach is employed to predict the downwash and outwash of a tandem rotor in ground effect and provide an understanding of its wake. The aerodynamic loads of the blades are represented through a panel method, and the behavior of the wake is captured by a viscous vortex particle method. The viscous effects of the ground are accounted for by a viscous boundary model satisfying the no-slip and nonpenetration boundary conditions. The method is first validated for an isolated full-scale Lynx tail rotor and a 172-mm-diameter-scale rotor in ground effect. The results show that the predicted trajectories of the tip vortices and the radial velocity profiles compare favorably with experiments and published computational fluid dynamics results. The results for model CH-47D are then compared with experiments for the downwash and outwash of the tandem rotor. As opposed to the isolated single rotor, a radial outward expansion in the overlapping area is observed, and the peak and the corresponding vertical distance of the velocity maximum of the radial outwash flow for the tandem rotor are larger. Moreover, the rotational direction of the tandem rotor leads to a wake with several vortical interactions resulting in different outwashes on the port and starboard sides

    Isoglycyrrhizin protects mouse lungs against acute respiratory distress syndrome via regulation of AMPK/Nrf2/ARE pathway

    Get PDF
    Purpose: To study the effect of isoglycyrrhizin on LPS-mediated acute respiratory distress syndrome (ARDS) in a mouse model, as well as the associated mechanism of action.Methods: Ninety (90) wild-type C57BL/6 male mice were randomly assigned to 3 groups, viz, control, ARDS and isoglycyrrhizin groups. Pathological lesions in mice lungs were determined using H&E staining. The mRNA and protein expressions of inducible nitric oxide synthase (iNOS), heme oxygenase (HO-1), cyclooxygenase-2 (COX-2), AMP- dependent protein kinase (AMPK), serine/threonine proteinkinase (Akt), glycogen synthase kinase 3 (GSK3), nucleotide-binding domain-like receptor protein 3 (NLRP3), and Nrf2 were assayed using quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunoblotting, respectively.Results: The levels of mRNA and protein expressions of INO) and COX-2 were significantly upregulated in ARDS, when compared to control, but were markedly down-regulated by isoglycyrrhizin (p < 0.05). Similarly, exposure of ARDS mice to isoglycyrrhizin led to upregulations of mRNA and proteinlevels of Nrf2, NQO1, HO-1, GCLM, GCLC, p-GSK3, GSK3, p-AMPK, AMPK, p-Akt and AKT (p < 0.05). Moreover, isoglycyrrhizin significantly downregulated p-IκB and Nucl-p65 with respect to protein and mRNA levels, but upregulated IκBα expression. Histopathological examination revealed that pretreatment of ARDS mice with isoglycyrrhizin significantly reduced the number of infiltrating inflammatory cells, edema and ARDS score (p < 0.05).Conclusion: Isoglycyrrhizin protects mouse lungs against ARDS via regulation of AMPK/Nrf2/ARE pathway. Thus, this compound has potential for use in the treatment of ARDS

    Nuclear proteome response to cell wall removal in rice (Oryza sativa)

    Get PDF
    Plant cells are routinely exposed to various pathogens and environmental stresses that cause cell wall perturbations. Little is known of the mechanisms that plant cells use to sense these disturbances and transduce corresponding signals to regulate cellular responses to maintain cell wall integrity. Previous studies in rice have shown that removal of the cell wall leads to substantial chromatin reorganization and histone modification changes concomitant with cell wall re-synthesis. But the genes and proteins that regulate these cellular responses are still largely unknown. Here we present an examination of the nuclear proteome differential expression in response to removal of the cell wall in rice suspension cells using multiple nuclear proteome extraction methods. A total of 382 nuclear proteins were identified with two or more peptides, including 26 transcription factors. Upon removal of the cell wall, 142 nuclear proteins were up regulated and 112 were down regulated. The differentially expressed proteins included transcription factors, histones, histone domain containing proteins, and histone modification enzymes. Gene ontology analysis of the differentially expressed proteins indicates that chromatin & nucleosome assembly, protein-DNA complex assembly, and DNA packaging are tightly associated with cell wall removal. Our results indicate that removal of the cell wall imposes a tremendous challenge to the cells. Consequently, plant cells respond to the removal of the cell wall in the nucleus at every level of the regulatory hierarchy.This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at [email protected]

    Collaborative simulation method with spatiotemporal synchronization process control

    Get PDF
    When designing a complex mechatronics system, such as high speed trains, it is relatively difficult to effectively simulate the entire system’s dynamic behaviors because it involves multi-disciplinary subsystems. Currently, a most practical approach for multi-disciplinary simulation is interface based coupling simulation method, but it faces a twofold challenge: spatial and time unsynchronizations among multi-directional coupling simulation of subsystems. A new collaborative simulation method with spatiotemporal synchronization process control is proposed for coupling simulating a given complex mechatronics system across multiple subsystems on different platforms. The method consists of 1) a coupler-based coupling mechanisms to define the interfacing and interaction mechanisms among subsystems, and 2) a simulation process control algorithm to realize the coupling simulation in a spatiotemporal synchronized manner. The test results from a case study show that the proposed method 1) can certainly be used to simulate the sub-systems interactions under different simulation conditions in an engineering system, and 2) effectively supports multi-directional coupling simulation among multi-disciplinary subsystems. This method has been successfully applied in China high speed train design and development processes, demonstrating that it can be applied in a wide range of engineering systems design and simulation with improved efficiency and effectiveness

    Cardiac-derived CTRP9 protects against myocardial ischemia/reperfusion injury via calreticulin-dependent inhibition of apoptosis.

    Get PDF
    Cardiokines play an essential role in maintaining normal cardiac functions and responding to acute myocardial injury. Studies have demonstrated the heart itself is a significant source of C1q/TNF-related protein 9 (CTRP9). However, the biological role of cardiac-derived CTRP9 remains unclear. We hypothesize cardiac-derived CTRP9 responds to acute myocardial ischemia/reperfusion (MI/R) injury as a cardiokine. We explored the role of cardiac-derived CTRP9 in MI/R injury via genetic manipulation and a CTRP9-knockout (CTRP9-KO) animal model. Inhibition of cardiac CTRP9 exacerbated, whereas its overexpression ameliorated, left ventricular dysfunction and myocardial apoptosis. Endothelial CTRP9 expression was unchanged while cardiomyocyte CTRP9 levels decreased after simulated ischemia/`reperfusion (SI/R) in vitro. Cardiomyocyte CTRP9 overexpression inhibited SI/R-induced apoptosis, an effect abrogated by CTRP9 antibody. Mechanistically, cardiac-derived CTRP9 activated anti-apoptotic signaling pathways and inhibited endoplasmic reticulum (ER) stress-related apoptosis in MI/R injury. Notably, CTRP9 interacted with the ER molecular chaperone calreticulin (CRT) located on the cell surface and in the cytoplasm of cardiomyocytes. The CTRP9-CRT interaction activated the protein kinase A-cAMP response element binding protein (PKA-CREB) signaling pathway, blocked by functional neutralization of the autocrine CTRP9. Inhibition of either CRT or PKA blunted cardiac-derived CTRP9\u27s anti-apoptotic actions against MI/R injury. We further confirmed these findings in CTRP9-KO rats. Together, these results demonstrate that autocrine CTRP9 of cardiomyocyte origin protects against MI/R injury via CRT association, activation of the PKA-CREB pathway, ultimately inhibiting cardiomyocyte apoptosis

    The effect of transforming growth factor-β1 on nasopharyngeal carcinoma cells: insensitive to cell growth but functional to TGF-β/Smad pathway

    Get PDF
    <p>Abstract</p> <p>Objectives</p> <p>This study explored the response of nasopharyngeal carcinoma cells to TGF-β1-induced growth suppression and investigated the roles of the TGF-β/Smad signaling pathway in nasopharyngeal carcinoma cells.</p> <p>Methods</p> <p>The cells of nasopharyngeal carcinoma cell line CNE2 were treated with TGF-β1. The growth responses of CNE2 cells were analyzed by MTT assay. The mRNA expression and protein subcellular localization of the TGF-β/Smad signaling components in the CNE2 were determined by real time RT-PCR and immunocytochemical analysis.</p> <p>Results</p> <p>We found that the growth of CNE2 cells was not suppressed by TGF-β1. The signaling proteins TβRII, Smad 7 were expressed normally, while Smad2, Smad3, and Smad4 increased significantly at the mRNA level. TGF-β type II receptor and Smad7 had no change compared to the normal nasopharyngeal epithelial cells. In addition, Smad2 was phosphorylated to pSmad2, and the activated pSmad2 translocated into the nucleus from the cytoplasm, while the inhibitory Smad-Smad7 translocated from the nucleus to the cytoplasm after TGF-β1 stimulation.</p> <p>Conclusion</p> <p>The results suggested that CNE2 cells are not sensitive to growth suppression by TGF-β1, but the TGF-β/Smad signaling transduction is functional. Further work is needed to address a more detailed spectrum of the TGF-β/Smad signaling pathway in CNE2 cells.</p
    corecore