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1,582 results on '"Wang, Longfei"'

6. Flow Dynamics of a Dodecane Jet in Oxygen Crossflow at Supercritical Pressures

Author

Ding, Siyu, Li, Jiabin, Wang, Longfei, Ni, Chenxu, and Wang, Xingjian

Subjects
Physics - Fluid Dynamics
Abstract

In advanced aero-propulsion engines, kerosene is often injected into the combustor at supercritical pressures, where flow dynamics is distinct from the subcritical counterpart. Large-eddy simulation combined with real-fluid thermodynamics and transport theories of a N-dodecane jet in oxygen crossflow at supercritical pressures is presented. Liquid dodecane at 600 K is injected into a supercritical oxygen environment at 700 K at different supercritical pressures and jet-to-crossflow momentum flux ratios (J). Various vortical structures are discussed in detail. The results shown that, with the same jet-to-crossflow velocity ratio of 0.75, the upstream shear layer (USL) is absolutely unstable at 6.0 MPa (J = 7.1) and convectively unstable at 3.0 MPa (J = 13.2). This trend is consistent with the empirical criterion for the stability characteristics of a jet in crossflow at subcritical pressures (Jcr = 10). While decreasing J to 7.1 at 3.0 MPa, however, the dominant Strouhal number of the USL varies along the upstream jet trajectory, and the USL becomes convectively unstable. Such abnormal change in stability behavior can be attributed to the real-fluid effect induced by strong density stratification at pressure of 3.0 MPa, under which a point of inflection in the upstream mixing layer renders large density gradient and tends to stabilize the USL. The stability behavior with varying pressure and J is further corroborated by linear stability analysis. The analysis of spatial mixing deficiencies reveals that the mixing efficiency is enhanced at a higher jet-to-crossflow momentum flux ratio., Comment: 1. The citations "Cortelezzi & Karagozian 2001; Yang & Wang 2005" in Page2 were wrong, which are not "compressible". This would mislead the readers. 2. The Reynolds number announced in Page7 was wrong by an order of magnitude

Published
2023

19. Inverse Kinematics and Dexterous Workspace Formulation for 2-Segment Continuum Robots with Inextensible Segments

Author

Wang, Yifan, Wu, Zhonghao, Wang, Longfei, Feng, Bo, and Xu, Kai

Subjects
Computer Science - Robotics
Abstract

The inverse kinematics (IK) problem of continuum robots has been investigated in depth in the past decades. Under the constant-curvature bending assumption, closed-form IK solution has been obtained for continuum robots with variable segment lengths. Attempting to close the gap towards a complete solution, this paper presents an efficient solution for the IK problem of 2-segment continuum robots with one or two inextensible segments (a.k.a, constant segment lengths). Via representing the robot's shape as piecewise line segments, the configuration variables are separated from the IK formulation such that solving a one-variable nonlinear equation leads to the solution of the entire IK problem. Furthermore, an in-depth investigation of the boundaries of the dexterous workspace of the end effector caused by the configuration variables limits as well as the angular velocity singularities of the continuum robots was established. This dexterous workspace formulation, which is derived for the first time to the best of the authors' knowledge, is particularly useful to find the closest orientation to a target pose when the target orientation is out of the dexterous workspace. In the comparative simulation studies between the proposed method and the Jacobian-based IK method involving 500,000 cases, the proposed variable separation method solved 100% of the IK problems with much higher computational efficiency., Comment: Submitted to IEEE Robotics and Automation Letters

Published
2021

36. Static Voltage Stability Analysis of Receiving-End Power Grid of LCC-HVDC with the Connection of Non-synchronous Generation Sources

Author

Hua, Wen, Wang, Longfei, Ye, Lin, Zhou, Zhengyang, Zhang, Nan, Zhang, Zheren, Xu, Zheng, Angrisani, Leopoldo, Series Editor, Arteaga, Marco, Series Editor, Chakraborty, Samarjit, Series Editor, Chen, Jiming, Series Editor, Chen, Shanben, Series Editor, Chen, Tan Kay, Series Editor, Dillmann, Rüdiger, Series Editor, Duan, Haibin, Series Editor, Ferrari, Gianluigi, Series Editor, Ferre, Manuel, Series Editor, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Li, Yong, Series Editor, Liang, Qilian, Series Editor, Martín, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Oneto, Luca, Series Editor, Panigrahi, Bijaya Ketan, Series Editor, Pascucci, Federica, Series Editor, Qin, Yong, Series Editor, Seng, Gan Woon, Series Editor, Speidel, Joachim, Series Editor, Veiga, Germano, Series Editor, Wu, Haitao, Series Editor, Zamboni, Walter, Series Editor, Zhang, Junjie James, Series Editor, Zeng, Pingliang, editor, Zhang, Xiao-Ping, editor, Terzija, Vladimir, editor, Ding, Yi, editor, and Luo, Yunxia, editor

Published
2023
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38. Genetic aetiologies for childhood speech disorder: novel pathways co-expressed during brain development

Author

Kaspi, Antony, Hildebrand, Michael S., Jackson, Victoria E., Braden, Ruth, van Reyk, Olivia, Howell, Tegan, Debono, Simone, Lauretta, Mariana, Morison, Lottie, Coleman, Matthew J., Webster, Richard, Coman, David, Goel, Himanshu, Wallis, Mathew, Dabscheck, Gabriel, Downie, Lilian, Baker, Emma K., Parry-Fielder, Bronwyn, Ballard, Kirrie, Harrold, Eva, Ziegenfusz, Shaun, Bennett, Mark F., Robertson, Erandee, Wang, Longfei, Boys, Amber, Fisher, Simon E., Amor, David J., Scheffer, Ingrid E., Bahlo, Melanie, and Morgan, Angela T.

Published
2023
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46. Metabolic Syndrome Mediates ROS-miR-193b-NFYA–Dependent Downregulation of Soluble Guanylate Cyclase and Contributes to Exercise-Induced Pulmonary Hypertension in Heart Failure With Preserved Ejection Fraction

Author

Satoh, Taijyu, Wang, Longfei, Espinosa-Diez, Cristina, Wang, Bing, Hahn, Scott A, Noda, Kentaro, Rochon, Elizabeth R, Dent, Matthew R, Levine, Andrea R, Baust, Jeffrey J, Wyman, Samuel, Wu, Yijen L, Triantafyllou, Georgios A, Tang, Ying, Reynolds, Mike, Shiva, Sruti, St. Hilaire, Cynthia, Gomez, Delphine, Goncharov, Dmitry A, Goncharova, Elena A, Chan, Stephen Y, Straub, Adam C, Lai, Yen-Chun, McTiernan, Charles F, and Gladwin, Mark T

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Nutrition, Obesity, Diabetes, Cardiovascular, Heart Disease, Aetiology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, Animals, Animals, Genetically Modified, Biomarkers, CCAAT-Binding Factor, Disease Models, Animal, Disease Susceptibility, Exercise, Gene Expression Regulation, Heart Failure, Humans, Hypertension, Pulmonary, Metabolic Syndrome, MicroRNAs, Mitochondria, Heart, Myocytes, Smooth Muscle, Phenotype, Rats, Reactive Oxygen Species, Signal Transduction, Soluble Guanylyl Cyclase, Stress, Physiological, Stroke Volume, Ventricular Dysfunction, Right, MIRN193 microRNA, human, nitric oxide, nuclear factor Y, pulmonary hypertension, MIRN193 microRNA, human, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences, Sports science and exercise
Abstract

BackgroundMany patients with heart failure with preserved ejection fraction have metabolic syndrome and develop exercise-induced pulmonary hypertension (EIPH). Increases in pulmonary vascular resistance in patients with heart failure with preserved ejection fraction portend a poor prognosis; this phenotype is referred to as combined precapillary and postcapillary pulmonary hypertension (CpcPH). Therapeutic trials for EIPH and CpcPH have been disappointing, suggesting the need for strategies that target upstream mechanisms of disease. This work reports novel rat EIPH models and mechanisms of pulmonary vascular dysfunction centered around the transcriptional repression of the soluble guanylate cyclase (sGC) enzyme in pulmonary artery (PA) smooth muscle cells.MethodsWe used obese ZSF-1 leptin-receptor knockout rats (heart failure with preserved ejection fraction model), obese ZSF-1 rats treated with SU5416 to stimulate resting pulmonary hypertension (obese+sugen, CpcPH model), and lean ZSF-1 rats (controls). Right and left ventricular hemodynamics were evaluated using implanted catheters during treadmill exercise. PA function was evaluated with magnetic resonance imaging and myography. Overexpression of nuclear factor Y α subunit (NFYA), a transcriptional enhancer of sGC β1 subunit (sGCβ1), was performed by PA delivery of adeno-associated virus 6. Treatment groups received the SGLT2 inhibitor empagliflozin in drinking water. PA smooth muscle cells from rats and humans were cultured with palmitic acid, glucose, and insulin to induce metabolic stress.ResultsObese rats showed normal resting right ventricular systolic pressures, which significantly increased during exercise, modeling EIPH. Obese+sugen rats showed anatomic PA remodeling and developed elevated right ventricular systolic pressure at rest, which was exacerbated with exercise, modeling CpcPH. Myography and magnetic resonance imaging during dobutamine challenge revealed PA functional impairment of both obese groups. PAs of obese rats produced reactive oxygen species and decreased sGCβ1 expression. Mechanistically, cultured PA smooth muscle cells from obese rats and humans with diabetes or treated with palmitic acid, glucose, and insulin showed increased mitochondrial reactive oxygen species, which enhanced miR-193b-dependent RNA degradation of nuclear factor Y α subunit (NFYA), resulting in decreased sGCβ1-cGMP signaling. Forced NYFA expression by adeno-associated virus 6 delivery increased sGCβ1 levels and improved exercise pulmonary hypertension in obese+sugen rats. Treatment of obese+sugen rats with empagliflozin improved metabolic syndrome, reduced mitochondrial reactive oxygen species and miR-193b levels, restored NFYA/sGC activity, and prevented EIPH.ConclusionsIn heart failure with preserved ejection fraction and CpcPH models, metabolic syndrome contributes to pulmonary vascular dysfunction and EIPH through enhanced reactive oxygen species and miR-193b expression, which downregulates NFYA-dependent sGCβ1 expression. Adeno-associated virus-mediated NFYA overexpression and SGLT2 inhibition restore NFYA-sGCβ1-cGMP signaling and ameliorate EIPH.

Published
2021

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