Publications (8)28.59 Total impact
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Article: Computational fluid dynamics and experimental study of lock-in phenomenon in vortex-induced motions of a cell-truss spar
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ABSTRACT: Spar platforms could be subject to vortex-induced-motions (VIM) in certain current conditions. Lockin is a phenomenon which occurs in a range of reduced velocities in VIM. In this paper, a new concept of spar platform called cell-truss spar is studied using both computational fluid dynamics (CFD) and model test to investigate the VIM of the spar under different reduced velocities. The unique configuration of the cell-truss spar is carefully considered, and the unsteady flow around the spar is calculated and visualized in CFD simulations. A physical model with a scale ratio of 1:100 of the cell-truss spar is fabricated, and model tests are carried out in the current-generating ocean engineering basin. Many important parameters in VIM of the cell-truss spar are obtained, the occurrence of lock-in phenomenon is successfully simulated, and the mechanism and rules of lock-in are analyzed.Journal of Shanghai Jiaotong University (Science) 04/2012; 14(6):757-762. -
Article: Hepcidin destabilizes atherosclerotic plaque via overactivating macrophages after erythrophagocytosis.
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ABSTRACT: To explore a direct and causal relationship between vascular hepcidin and atherosclerotic plaque stability. Accelerated atherosclerotic lesions were established by perivascular collar placement in apolipoprotein E-deficient (ApoE(-/-)) mice. Adenoviral overexpression of hepcidin in the carotid artery during plaque formation enhanced intraplaque macrophage infiltration and suppressed the contents of collagen and vascular smooth muscle cells, whereas hepcidin shRNA treatment exerts opposite effects. The overexpression or knockdown of hepcidin did not affect plaque lipid deposition but increased or decreased oxidized low-density lipoprotein (ox-LDL) levels within intraplaque macrophages. In cultured macrophages, ox-LDL not only increased reactive oxygen species formation, inflammatory cytokine production, and apoptosis but also upregulated hepcidin expression. However, hepcidin did not exaggerate the ox-LDL-induced activation of macrophages until an onset of erythrophagocytosis. Whereas hepcidin was critical for the upregulation of L-ferritin and H-ferritin in both ox-LDL-treated erythrophagocytosed macrophages and atherosclerotic plaques, the adding of iron chelators suppressed the intracellular lipid accumulation, reactive oxygen species formation, inflammatory cytokine expression, and apoptosis in erythrophagocytosed macrophages. Hepcidin promotes plaque destabilization partly by exaggerating inflammatory cytokine release, intracellular lipid accumulation, oxidative stress, and apoptosis in the macrophages with iron retention.Arteriosclerosis Thrombosis and Vascular Biology 03/2012; 32(5):1158-66. · 6.37 Impact Factor -
Article: CRP enhances soluble LOX-1 release from macrophages by activating TNF-α converting enzyme.
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ABSTRACT: Circulating levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) play an important role in the development and progression of atherosclerosis. We hypothesized that the inflammatory marker C-reactive protein (CRP) might stimulate sLOX-1 release by activating tumor necrosis factor-α converting enzyme (TACE). Macrophages differentiated from THP-1 cells were stimulated with TNF-α and further treated with CRP in the absence or presence of specific inhibitors or small interfering RNA (siRNA). Our results showed that CRP increased sLOX-1 release from activated macrophages in a dose-dependent manner and that these effects were regulated by Fc γ receptor II (FcγRII)-mediated p47(phox) phosphorylation, reactive oxygen species (ROS) production, and TACE activation. CRP also enhanced sLOX-1 release from macrophages derived from peripheral blood mononuclear cells (PBMC) of patients with acute coronary syndrome (ACS). Pretreatment with antibody against FcγRII or with CD32 siRNA, p47(phox) siRNA, apocynin, N-acetylcysteine, tumor necrosis factor-α protease inhibitor 1 (TAPI-1) or TACE siRNA attenuated sLOX-1 release induced by CRP. CRP also elevated serum sLOX-1 levels in a rabbit model of atherosclerosis. Thus, CRP might stimulate sLOX-1 release, and the underlying mechanisms possibly involved FcγRII-mediated p47(phox) phosphorylation, ROS production, and TACE activation.The Journal of Lipid Research 03/2011; 52(5):923-33. · 5.56 Impact Factor -
Article: Atorvastatin suppresses LPS-induced rapid upregulation of Toll-like receptor 4 and its signaling pathway in endothelial cells.
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ABSTRACT: In the present study, we tested our hypothesis that atorvastatin exerts its anti-inflammation effect via suppressing LPS-induced rapid upregulation of Toll-like receptor 4 (TLR4) mRNA and its downstream p38, ERK, and NF-κB signaling pathways in human umbilical-vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs). TLR4 mRNA expression and its downstream kinase activities induced by LPS alone or atorvastatin + LPS in endothelial cells were quantified using quantitative real-time PCR and enzyme-linked immunosorbent assay. Preincubation of LPS-stimulated endothelial cells with TLR4 siRNA was conducted to identify the target of the anti-inflammatory effects of atorvastatin. Atorvastatin incubation resulted in the reduction of LPS-induced TLR4 mRNA expression, ERK1/2 and P38 MAPK phosphorylation, and NF-κB binding activity. Pretreatment with MEK/ERK1/2 inhibitor PD98059 attenuated atorvastatin + LPS-induced NF-κB activity but had no effect on P38 MAPK phosphorylation. In contrast, pretreatment with P38 MAPK inhibitor SB203580 resulted in upregulation of atorvastatin + LPS-induced ERK1/2 phosphorylation but had no significant effects on NF-κB activity. On the other hand, blocking NF-κB with SN50 produced no effects on atorvastatin + LPS-induced ERK1/2 and P38 MAPK phosphorylation. Moreover, TLR4 gene silencing produced the same effects as the atorvastatin treatment. In conclusion, atorvastatin downregulated TLR4 mRNA expression by two distinct signaling pathways. First, atorvastatin stabilized Iκ-Bα, which directly inhibited NF-κB activation. Second, atorvastatin inactivated ERK phosphorylation, which indirectly inhibited NF-κB activation. Suppression of p38 MAPK by atorvastatin upregulates ERK but exerts no effect on NF-κB.AJP Heart and Circulatory Physiology 02/2011; 300(5):H1743-52. · 3.71 Impact Factor -
Article: Anxiolytic effect of music exposure on BDNFMet/Met transgenic mice.
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ABSTRACT: Brain-derived neurotrophic factor (BDNF) has been reported to play important roles in the modulation of anxiety, mood stabilizers, and pathophysiology of affective disorders. Recently, a single nucleotide polymorphism (SNP) in the BDNF gene (Val66Met) has been found to be associated with depression and anxiety disorders. The humanized BDNF(Met/Met) knock-in transgenic mice exhibited increased anxiety-related behaviors that were unresponsive to serotonin reuptake inhibitors, fluoxetine. Music is known to be able to elicit emotional changes, including anxiolytic effects. In this study, we found that music treatment could significantly decrease anxiety state in BDNF(Met/Met) mice, but not in BDNF(+/)(-), mice compared with white noise exposure in open field and elevated plus maze test. Moreover, in contrast to white noise exposure, BDNF expression levels in the prefrontal cortex (PFC), amygdala and hippocampus were significantly increased in music-exposed adult BDNF(Met/Met) mice. However, music treatment could not upregulate BDNF levels in the PFC, amygdala, and hippocampus in BDNF(+/)(-) mice, which suggests the essential role of BDNF in the anxiolytic effect of music. Together, our results imply that music may provide an effective therapeutic intervention for anxiety disorders in humans with this genetic BDNF(Met) variant.Brain research 08/2010; 1347:71-9. · 2.46 Impact Factor -
Article: Combinatorial interference of toll‐like receptor 2 and 4 synergistically stabilizes atherosclerotic plaque in apolipoprotein E‐knockout mice
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ABSTRACT: To test the hypothesis that combinatorial interference of toll-like receptor 2 (TLR2) and TLR4 is superior to isolated interference of TLR2 or TLR4 in stabilizing atherosclerotic plaques, lentiviruses carrying small interfering RNA of TLR2 or TLR4 were constructed and proved efficacious for knocking down mRNA and protein expression of TLR2 or TLR4 significantly in vitro. One hundred and fifty apolipoprotein E−/− mice fed a high-fat diet were divided into the control, mock, TLR2i, TLR4i and TLR2 + 4i subgroups and a constrictive collar was placed around carotid artery of these mice to induce plaque formation. TLR2i and TLR4i viral suspension was transfected into carotid plaques, respectively, in TLR2i and TLR4i subgroups, or in combination in TLR2 + 4i subgroup. Four weeks after lentivirus transfection, mRNA and protein expression of TLR2 or TLR4 was attenuated markedly in carotid plaques, leading to reduced local inflammatory cytokine expression and plaque content of lipid and macrophages, increased plaque content of collagen and lowered plaque vulnerability index. Factorial ANOVA analysis revealed that there was a synergistic effect between TLR4i and TLR2i in stabilizing plaques. In conclusion, combinatorial interference of TLR2 and TLR4 reduces local inflammation and stabilizes plaques more effectively than interference of TLR2 or TLR4 alone.Journal of Cellular and Molecular Medicine 02/2010; 15(3):602 - 611. · 4.13 Impact Factor -
Article: Cross talk among Smad, MAPK, and integrin signaling pathways enhances adventitial fibroblast functions activated by transforming growth factor-beta1 and inhibited by Gax.
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ABSTRACT: We investigated whether Smad, mitogen-activated protein kinase (MAPK), and integrin signaling pathways cross-talk to enhance adventitial fibroblast (AF) bioactivity, which was activated by transforming growth factor (TGF)-beta1 and inhibited by Gax. Cultured AFs were stimulated with Ad-Gax, TGF-beta1, and siRNA-Gax. Assays for AFs viabilities demonstrated that TGF-beta1 and siRNA-Gax enhanced AFs proliferative, migratory, and adherent abilities, whereas Gax counteracted TGF-beta1-activated actions. Flow cytometry revealed that TGF-beta1 and siRNA-Gax increased S phase cells; however, Gax decreased AFs in the S phase and increased those in the G0-G1 and apoptotic phases. RT-PCR, Western blotting, and immunocytochemistry showed that TGF-beta1 and siRNA-Gax upregulated the expression of cytokines in Smad, MAPK, and integrin signaling pathways, and downregulated that of p15, p16, and p21. Conversely, Gax induced downregulation of these cytokines and upregulation of p15, p16, and p21. Thus, these signaling pathways cross-talk to enhance AF bioactivity; Gax effectively counteracts TGF-beta1 effects, blocks the cross-talk of these pathways, inhibits AF functions, and increases AF apoptosis. Our findings indicate that cross-talk among Smad, MAPK, and integrin signaling pathways may account mainly for the mechanism of AF functions. Gax is a promising therapeutic gene for dissecting the signaling pathways controlling AF bioactivities.Arteriosclerosis Thrombosis and Vascular Biology 05/2008; 28(4):725-31. · 6.37 Impact Factor -
Article: Theoretical Research on Hydrodynamics of a Geometric Spar in Frequency- and Time-Domains
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ABSTRACT: Considering the coupling effects of the vessel and its riser and mooring system, hydrodynamic analyses of a geometric spar were performed both in frequency- and time-domains. Based on the boundary element method, the 3-D panel model of the geometric spar and the related free water surface model were established, and the first-order and second-order difference-frequency wave loads and other hydrodynamic coefficients were calculated. Frequency domain analysis of the motion Response Amplitude Operators (RAO) and Quadratic Transfer Functions (QTF) and time domain analysis of the response series and spectra in an extreme wave condition were conducted for the coupled system with the mooring lines and risers involved. These analyses were further validated by the physical model test results.Journal of Hydrodynamics, Ser. B.
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Institutions
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2010–2012
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Shandong University
- Key Laboratory for Cardiovascular Remodelling and Function Research
Jinan, Shandong Sheng, China
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