Lift Augmentation at Subsonic Speeds by Lateral Jets for a Hypersonic Aircraft

This paper presents a numerical investigation on the lift augmentation at subsonic speeds by using lateral jets for a hypersonic aircraft equipped with a waverider-type lifting body, which consists of three main parts. The jet slots were arranged along the side edges of the lifting body to study the effect of lateral blowing on the lift augmentation at a freestream Mach number of 0.3. The numerical results based on solving the Reynolds-averaged Navier–Stokes equation indicate that a well-designed lateral blowing can produce a significant lift rise. Then, further work was carried out to investigate the effects of jet parameters, including the jet location, the blowing strength and the blowing direction on lift augmentation, and to provide insights into the associated flow physics. It was found that blowing on the middle and rear parts of the lifting body achieves the maximum lift augmentation among the chosen configurations. Additionally, it was confirmed that the lift augmentation increases as the jet momentum increases, and blowing in the direction of θjet = −45°, which means the jet blows slightly towards the lower surface of the lifting body, produces a larger lift rise than other directions. The lift augmentation can be explained by the fact that a well-designed lateral blowing can amplify the effectiveness of the vortices shedding from the side edges of the lifting body, resulting in an increase in the vortex lift

Tetrandrine Ameliorates Airway Remodeling of Chronic Asthma by Interfering TGF-β1/Nrf-2/HO-1 Signaling Pathway-Mediated Oxidative Stress

Background. Imbalanced oxidative stress and antioxidant defense are involved in airway remodeling in asthma. It has been demonstrated that Tetrandrine has a potent role in antioxidant defense in rheumatoid arthritis and hypertension. However, the correlation between Tetrandrine and oxidative stress in asthma is utterly blurry. This study aimed to investigate the role of Tetrandrine on oxidative stress-mediated airway remolding. Materials and Methods. Chronic asthma was established by ovalbumin (OVA) administration in male Wistar rats. Histopathology was determined by HE staining. Immunofluorescence was employed to detect the expression of α-SMA and Nrf-2. Level of oxidative stress and matrix metalloproteinases were examined by ELISA kits. Cell viability and cell cycle of primary airway smooth muscle cells (ASMCs) were evaluated by CCK8 and flow cytometry, respectively. Signal molecules were detected using western blot. Results. Tetrandrine effectively impairs OVA-induced airway inflammatory and airway remodeling by inhibiting the expression of CysLT1 and CysLTR1. The increase of oxidative stress and subsequent enhancement of MMP9 and TGF-β1 expression were rescued by the administration of Tetrandrine in the rat model of asthma. In in vitro experiments, Tetrandrine markedly suppressed TGF-β1-evoked cell viability and cell cycle promotion of ASMCs in a dose-dependent manner. Furthermore, Tetrandrine promoted Nrf-2 nuclear transcription and activated its downstream HO-1 in vivo and in vitro. Conclusion. Tetrandrine attenuates airway inflammatory and airway remodeling in rat model of asthma and TGF-β1-induced cell proliferation of ASMCs by regulating oxidative stress in primary ASMCs, suggesting that Tetrandrine possibly is an effective candidate therapy for asthma

The Mechanism by Which Luteolin Disrupts the Cytoplasmic Membrane of Methicillin-Resistant <i>Staphylococcus aureus</i>

Methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) is one of the most versatile human pathogens. Luteolin (LUT) has anti-MRSA activity by disrupting the MRSA cytoplasmic membrane. However, the mechanism by which luteolin disrupts the membrane remains unclear. Here, we performed differential scanning calorimetry (DSC) and all-atomic molecular dynamics (AA-MD) simulations to investigate the interactions and effects of LUT on model membranes composed of phosphatidylcholine (PC) and phosphatidylglycerol (PG). We detected the transition thermodynamic parameters of dipalmitoylphosphatidylcholine (DPPC) liposomes, dipalmitoylphosphatidylglycerol (DPPG) liposomes, and liposomes composed of both DPPC and DPPG at different LUT concentrations and showed that LUT molecules were located between polar heads and the hydrophobic region of DPPC/DPPG. In the MD trajectories, LUT molecules ranging from 5 to 50 had different effects on the membranes thickness, fluidity and ordered property of lipids, and lateral pressure of lipid bilayers composed of dioleoylphosphatidylcholine (DOPC) and dioleoylphosphatidylglycerol (DOPG). Also, most LUT molecules were distributed in the region between the phosphorus atoms and C9 atoms of DOPC and DOPG. On the basis of the combination of these results, we conclude that the distinct effects of LUT on lipid bilayers composed of PCs and PGs may elucidate the mechanism by which LUT disrupts the cytoplasmic membrane of MRSA