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Your search keyword '"Guo, Zhongzhou"' showing total 17 results
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17 results on '"Guo, Zhongzhou"'

5. Corrigendum to “Empagliflozin attenuates cardiac microvascular ischemia/reperfusion through activating the AMPKα1/ULK1/FUNDC1/mitophagy pathway” [Redox Biol. 52 (2022) 102288]

Author

Cai, Chen, primary, Guo, Zhongzhou, additional, Chang, Xing, additional, Li, Ziying, additional, Wu, Feng, additional, He, Jing, additional, Cao, Tiantian, additional, Wang, Kangrong, additional, Shi, Nengxian, additional, Zhou, Hao, additional, Toan, Sam, additional, Muid, David, additional, and Tan, Ying, additional

Published
2023
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7. Pgam5-mediated PHB2 dephosphorylation contributes to endotoxemia-induced myocardial dysfunction by inhibiting mitophagy and the mitochondrial unfolded protein response

Author

Cai, Chen, primary, Li, Ziying, additional, Zheng, Zemao, additional, Guo, Zhongzhou, additional, Li, Qian, additional, Deng, Shuxian, additional, Shi, Nengxian, additional, Ou, Qing, additional, Zhou, Hao, additional, Guo, Zhigang, additional, Chen, Zhongqing, additional, and Zhu, Hang, additional

Published
2023
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16. Validation of Gas-Kinetic Scheme Solver for the Compressible and Incompressible Flows Simulation

Author

Liu, Hualin, Guo, Zhongzhou, Chen, Weifang, Xu, Kun, Liu, Hualin, Guo, Zhongzhou, Chen, Weifang, and Xu, Kun

Abstract

Gas-kinetic scheme(GKS) is becoming more and more popular in computational fluid dynamics(CFD). From low-speed incompressible to hypersonic compressible flows and from inviscid to viscous and heat conducting flows, the GKS can always show good performance. By using a time dependent gas distribution function at the cell interfacewhich includes the particle free transport and particle collision terms, a GKSsolver can constructa flux evaluation process different from a Riemann solver. In a finite volume method (FVM), the GKS construct a gas evolution process from a piecewise discontinuous initial data. In the smooth flow region, the Navier-StokeS(NS)solution with correct Prandtl number can be recovered from the GKS model with a modification inthe heat flux.Inthecontinuum flow regime, the Chapman-Enskog expansion can be used to construct a NS solution based on the macroscopic variables(density, velocity, pressure). Thereforea continuous microscopic particle velocity space can be used for the construction of the gas distribution function. This paper includes some numerical examples to validate the current FVM GKS solver developed by the authors. The simulationscover from one-dimension to three-dimension and from incompressible to compressiblecases. © 2017, American Institute of Aeronautics and Astronautics Inc, AIAA. All rights reserved.

Published
2017

17. Abstract 15399: Sulfotransferase 2B1b Inhibits Reverse Cholesterol Transport and Promotes Cholesterol Accumulation and Inflammation in Lymphocytes From Acute Myocardial Infarction Patients With Low Low-Density Lipoprotein Cholesterol Levels

Author

Zhang, Yanan, Guo, Zhongzhou, Wu, Tongwei, Lang, Jiping, Dai, Qiuyue, and Guo, Zhigang

Abstract

Introduction:Presently, the main treatment of coronary artery disease(CAD) for reducing LDL-C by statins could reduce the incidence of major adverse cardiovascular events (MACEs) by 30%,a lot of residual risks remains. To clarify the mechanism, we studied some patients with acute myocardial infarction(AMI) but with low LDL-C levels.Hypothesis:The expression of sulfotransferase 2B1b(SULT2B1b) is elevated in lymphocytes of CAD patients and affects the function of lymphocytes through LXR.Methods:We isolated the lymphocytes in both AMI and non-CAD patients with low LDL-C levels. Western blotting and RT-qPCR was used to compare the expression of ABCA1, ABCG1, LXR-? and SULT2B1b, and [3H]-cholesterol was used to compare cholesterol efflux capacity of lymphocytes. The methylation status of the promoter regions of SULT2B1b in human lymphocytes was detected by bisulfite PCR. Cholesterol content was investigated using the free cholesterol marker filipin.Results:We isolated the lymphocytes and found that although there was no difference in plasma LDL-C levels, the cholesterol content was higher in AMI patient lymphocytes than in non-CAD patient,that means the decrease in intracellular cholesterol content was inconsistent with that in plasma.The [3H]-cholesterol efflux rate was lower, while the inflammatory factors TNF-? and IFN-? had higher mRNA levels in AMI patients. We also found that SULT2B1b expression was higher in AMI patientlymphocytes. Further research on Jurkat T lymphocytes confirmed that SULT2B1b knockdown could increase cholesterol efflux capacity and decrease the mRNA level of TNF-? and IFN-? by increasing LXR-?.We also found that the degree of CpG island methylation in the SULT2B1b promoter in AMI patients was downregulated.Conclusion:SULT2B1b upregulation because of the SULT2B1b promoter hypomethylation promotes cholesterol accumulation and inflammation through inhibiting LXR-? in lymphocytes of AMI patients with low LDL-C levels. Therefore, it is not enough to only reduce plasma cholesterol levels. Reducing intracellular cholesterol levels is also very important, therapeutic approaches to decrease SULT2B1b expression are potentially beneficial for preventing CAD by decreasing intracellular cholesterol.

Published
2019
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