Yue Li

Chinese Academy of Sciences, Peping, Beijing, China

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Publications (66)191.47 Total impact

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    ABSTRACT: Obstructive sleep apnea (OSA) is closely related to atrial fibrillation (AF). However, the roles and mechanisms of chronic OSA in atrial remodeling are still unclear. Canine model of chronic OSA was simulated by stopping the ventilator and closing the airway for 4 h per day and lasting for 12 weeks. AF inducibility and duration was increased while atrial effective refractory period (AERP) was shortened after chronic apnea. Meanwhile, upregulation of proteins encoding inward rectifier K(+) current (I K1), delayed rectifier K(+) current (I Kr and I Ks), acetylcholine activated K(+) current (I KACh), transient outward K(+) current (I to) and ultra-rapid delayed rectifier potassium current (I Kur) as well as downregulation of protein encoding L-type Ca(2+) current (I Ca,L) were found after chronic OSA. Besides abnormal electrical activity, chronic OSA induced apoptosis and interstitial fibrosis of atrial myocytes, which was partly mediated by caspase 9, phosphorylation of extracellular-regulated kinase 1/2, and α-smooth muscle actin. In addition, atrial sympathetic and parasympathetic hyperinnervation were found manifesting by enhanced growth-associated protein 43, tyrosine hydroxylase and elevated choline acetyltransferase. Moreover, protein expression of β1, β2, and M2 receptor were markedly increased by chronic OSA. In summary, we firstly demonstrated in canine model that chronic OSA could shorten AERP and lead to altered expression of important channel proteins, moreover, induce atrial structure remodeling by increased atrial apoptosis, fibrosis, and autonomic remodeling, eventually promoting the development of a substrate of AF. Our findings suggested that reversing atrial remodeling might be a potential therapeutic strategy for OSA-induced AF.
    Basic research in cardiology. 09/2014; 109(5):427.
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    ABSTRACT: Erythropoietin (EPO) and granulocyte colony-stimulating factor (G-CSF) are both potential novel therapeutics for use after myocardial infarction (MI). However, their underlying mechanisms remain unclear and the efficacy of monotherapy with EPO or G-CSF is also controversial. Therefore, we investigated the effects of combined treatment with EPO and G-CSF on neovascularization and cardiac function in post-infarction rats and explored the potential mechanisms. Four groups of rats were used: control (saline injection after MI, i.h.), EPO (a single dose of 5 000 IU/kg after MI, i.h.), G-CSF (a dose of 50 µg× kg(-1)× d(-1) for 5 days after MI, i.h.), and both EPO and G-CSF (EPO+G-CSF, using the same regiment as above). Cardiac function was assessed by echocardiography before and 1 day, 7 days, 14 days and 21 days after MI. CD34(+)/Flk-1(+) cells in the peripheral blood were evaluated by flow cytometry before and 3 days, 5 days and 7 days after MI. The infarct area and angiogenesis in the peri-infarct area were analyzed. The mRNA and protein expression of vascular endothelial growth factor (VEGF) and stromal-derived factor-1a (SDF-1α) in the peri-infarct area were detected by real-time quantitative RT-PCR and Western blotting. Compared with the control and monotherapy groups, the EPO+G-CSF group had significantly increased CD34(+)/Flk-1(+) endothelial progenitor cells (EPCs) in the peripheral blood (P < 0.05), up-regulated VEGF and SDF-1α levels in the peri-infarct region (P < 0.05), enhanced capillary density (P < 0.05), reduced infarct size (P < 0.05) and improved cardiac structure and function (P < 0.05). G-CSF alone did not dramatically increase EPCs in the peripheral blood, enhance capillary density in the peri-infarct area or reduce infarct size compared with the control group. Combined treatment with EPO and G-CSF increased EPCs mobilization, up-regulated VEGF and SDF-1α levels in the post-infarction microenvironment, subsequently enhanced neovascularization in the peri-infarct region and reduced infarct size. All factors contributed to its beneficial effects on cardiac function in post-infarction rats.
    Chinese medical journal 05/2014; 127(9):1677-83. · 0.90 Impact Factor
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    ABSTRACT: Balloon crossing failure after passing a guidewire usually leads to unsuccessful percutaneous recanalization of chronic total occlusions (CTOs). We sought to investigate a novel technique for solving this problem. Twenty-one patients with failed balloon crossing through CTOs after successful guidewire passing were treated with the "seesaw balloon-wire cutting" technique between July 2012 and May 2013. The main process of this technique was to insert two guidewires (guidewire A and guidewire B) into the distal true lumen of CTOs and then to advance two short and lowprofile balloons (balloon A and balloon B) over the two guidewires, respectively. Balloon A was first advanced over guidewire A as distally as possible, and then was inflated with high pressure (≥18 atm) to press guidewire B, producing a cutting power to crush the proximal fibrous cap of the CTO. Subsequently, balloon A was withdrawn slightly, and balloon B was advanced as distally as possible and then was inflated to press guidewire A, producing a similar cutting effect to crush the proximal fibrous cap on the other side. The two balloons were progressed alternatively until one of them was able to cross through the occluded segment. This new technique was successfully applied in 17 patients (81.0%), leading to procedural success of their CTOs. The technique failed in 4 patients (19.0%) due to heavy calcification. No complications occurred in all patients. The seesaw balloon-wire cutting technique is an effective and safe approach to facilitate balloon crossing during CTO interventions.
    The Journal of invasive cardiology 04/2014; 26(4):167-70. · 1.57 Impact Factor
  • International journal of cardiology 01/2014; · 6.18 Impact Factor
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    ABSTRACT: ANRIL has long been considered as the strongest candidate gene at the 9p21 locus, robustly associated with stroke and coronary artery disease. However, the underlying molecular mechanism remains unknown. The present study works to elucidate such a mechanism. Using expression quantitative loci analysis, we identified potential genes whose expression may be influenced by genetic variation in ANRIL. To verify the identified gene(s), knockdown and overexpression of ANRIL were evaluated in human umbilical vein endothelial cells and HepG2 cells. Ischemic stroke and coronary artery disease risk were then evaluated in the gene(s) demonstrated to be mediated by ANRIL in 3 populations of Chinese Han ancestry: 2 ischemic stroke populations consisting of the Central China cohort (903 cases and 873 controls) and the Northern China cohort (816 cases and 879 controls) and 1 coronary artery disease cohort consisting of 772 patients and 873 controls. Expression quantitative loci analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and overexpression of ANRIL increasing CARD8 expression. The minor T allele of a previously identified CARD8 variant (rs2043211) was found to be significantly associated with a protective effect of ischemic stroke under the recessive model in 2 independent stroke cohorts. No significant association was found between rs2043211 and coronary artery disease. CARD8 is a downstream target gene regulated by ANRIL. Single nucleotide polymorphism rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.
    Stroke 01/2014; · 6.16 Impact Factor
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    ABSTRACT: Early Ordovician (late Tremadocian to early Floian) reefs on the Yangtze Platform margin of the Hunghuayuan Formation at Zhangzhai section in southeastern Guizhou, South China show three types of reefs in two broad categories: microbial-dominated (stromatolite and lithistid sponge-Calathium-calcimicrobial) reefs and metazoan-dominated (lithistid sponge-Calathium) reefs. These reef types represent different communities controlled by varying environmental settings. Stromatolites tended to develop in the shallow subtidal zone, whereas unlaminated calcimicrobial mounds and metazoan-dominated reefs thrived at greater depths. This is the first report on metazoan-dominated reefs at the platform margin of the Hunghuayuan Formation.
    Gff -Uppsala- 01/2014; 136(1). · 1.38 Impact Factor
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    ABSTRACT: Reefs in the Late Ordovician are usually built up by metazoans, whereas in the Early and Middle Ordovician microbial reefs are dominating. In the Late Ordovician (Katian) Lianglitag Formation, at Bachu, Tarim, NW China, however, three distinct stages of thrombolithic microbial reefs are exposed. The lower and upper reef intervals are characterized by widespread microbial carbonates with almost constant thicknesses (biostromes). The middle reef interval exposes dome-like mounds, and shows a higher diversity of reef-building and reef-dwelling organisms. Calcareous algae such as Vermiporella are abundant, but also other components such as fragments of Halysis, brachiopods, molluscs, echinoderms, bryozoans, and trilobites have been found in the microbial reef units. The purpose of this study is to describe for the first time the composition and microfacies of the reefs in this remote area. Especially the question of whether or not these Late Ordovician reefs represent remnants of the Early/Middle Ordovician microbial-dominated reef type just lacking Calathium and lithistid sponge is addressed. The results indicate that the local conditions on the leeward side of the carbonate platform, where waters are less well agitated and thus less well oxygenated, and probably also characterized by temporarily elevated water temperatures hampering the growth of metazoan reefs, were responsible for the proliferation of the Late Ordovician microbial reefs in the Bachu area.
    Facies 01/2014; 60(2). · 1.77 Impact Factor
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    ABSTRACT: After the end-Ordovician mass extinction, reef recovery (size and biotic diversity) took several million years. On the Upper Yangtze Platform, South China Block, the initial reef reconstruction episode is recorded in limestone of middle Aeronian age in northern Guizhou Province. By late Aeronian, reefs were widespread on the Yangtze carbonate platform, today represented by patch reefs cropping out in a 10-km2 large area near Shuibatang, Tongzi County, where two stratigraphic intervals with reefs are recognized. Late Aeronian reefs constitute a complex and diverse reef community dominated by corals, and to a lesser extent stromatoporoids. They contain an accessory fauna of abundant bryozoans and crinoids and some brachiopods, trilobites, molluscs and calcimicrobes. These reefs correlate in time with similar reefs in Anticosti, Laurentia, palaeogeographically very distant from South China. Thus, there is good evidence that recovery and geographic expansion of reefs after the end-Ordovician extinction occur simultaneously in at least two continents.
    Gff -Uppsala- 01/2014; 136(1). · 1.38 Impact Factor
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    ABSTRACT: Background: The beta 3-adrenoceptor (β3-AR) is closely associated with energy metabolism. This study aimed to explore the role of β3-AR in energy remodeling in a rabbit model of pacing-induced atrial fibrillation (AF). Methods: Rabbits with a sham-operation or pacing-induced AF were used for this study, and the latter group was further divided into three subgroups: 1) the pacing group, 2) the β3-AR agonist (BRL37344)-treated group, and 3) the β3-AR antagonist (SR59230A)-treated group. Atrial electrogram morphology and surface ECG were used to monitor the induction of AF and atrial effective refractory period (AERP). RT-PCR and western blot (WB) were used to show alterations in β3-AR and metabolic-related protein. Results: RT-PCR and WB results showed that β3-AR was significantly upregulated in the pacing group, and that it corresponded with high AF inducibility and significantly decreased AERP200 and ATP production in this group. Inhibition of β3-AR decreased the AF induction rate, reversed AERP200 reduction, and restored ATP levels in the AF rabbits. Further activation of β3-AR using agonist BRL37344 exacerbated AF-induced metabolic disruption. Periodic acid Schiff (PAS) and Oil Red O staining showed β3-AR-dependent glycogen and lipid droplet accumulation in cardiac myocytes with AF. Glucose transporter-4 (GLUT-4) and CD36, key transporters of glucose and fatty acids, were downregulated in the pacing group. Expression of carnitine-palmitoyltransferase I (CPT-1), a key regulator in fatty acid metabolism, was also significantly downregulated in the pacing group. Reduced glucose transportation and fatty acid oxidation could be restored by inhibition of β3-AR. Furthermore, key regulators of metabolism, peroxisome proliferator-activated receptor-α (PPARα) and PPAR co-activator (PGC-1α) can be regulated by pharmacological intervention of the β3-AR. Conclusions: β3-AR is involved in metabolic protein remodeling in AF. PPARα/PGC-1α signaling pathway might be the relevant down-stream molecular machinery in response to AF-induced activation of β3-AR. β3-AR might be a novel target in AF treatment. © 2014 S. Karger AG, Basel.
    Cellular Physiology and Biochemistry 12/2013; 32(6):1631-1642. · 3.42 Impact Factor
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    ABSTRACT: The effects of interleukin-33 (IL-33) on the immune system have been clearly demonstrated; however, in cardiovascular diseases, especially in coronary artery disease (CAD), these effects have not yet been clarified. In this study, we investigate the genetic role of the IL-33-ST2L pathway in CAD. We performed three-stage case-control association analyses on a total of 4,521 individuals with CAD and 4,809 controls via tag SNPs in the genes encoding IL-33 and ST2L-IL-1RL1. One tag SNP in each gene was significantly associated with CAD (rs7025417(T) in IL33, padj = 1.19 × 10(-28), OR = 1.39, 95% CI: 1.31-1.47; rs11685424(G) in IL1RL1, padj = 6.93 × 10(-30), OR = 1.40, 95% CI: 1.32-1.48). Combining significant variants in two genes, the risk for CAD increased nearly 5-fold (padj = 8.90 × 10(-21), OR = 4.98, 95% CI: 3.56-6.97). Traditional risk factors for CAD were adjusted for the association studies by SPSS with logistic regression analysis. With the two variants above, both located within the gene promoter regions, reporter gene analysis indicated that the rs7025417 C>T and rs11685424 A>G changes resulted in altered regulation of IL33 and IL1RL1 gene expression, respectively (p < 0.005). Further studies revealed that the rs7025417 genotype was significantly associated with plasma IL-33 levels in the detectable subjects (n = 227, R(2) = 0.276, p = 1.77 × 10(-17)): the level of IL-33 protein increased with the number of rs7025417 risk (T) alleles. Based on genetic evidence in humans, the IL-33-ST2L pathway appears to have a causal role in the development of CAD, highlighting this pathway as a valuable target for the prevention and treatment of CAD.
    The American Journal of Human Genetics 09/2013; · 11.20 Impact Factor
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    ABSTRACT: A series of pyrrolo[1,2-a]pyrazinone compounds (5a–9f) were synthesized, and their cytotoxic activity against SKOV-3, A549, HeLa cells in vitro were evaluated by the MTT method. Some of the compounds showed potential antitumor activity against three tumor cell lines. Among them, compounds 9c and 9d showed the most potent cytotoxic activity. The preliminary mechanism of action was discussed.
    Chinese Chemical Letters 07/2013; 24(7):619–621. · 1.18 Impact Factor
  • International journal of cardiology 05/2013; · 6.18 Impact Factor
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    ABSTRACT: Atrial fibrillation (AF) is a highly prevalent arrhythmia with pronounced morbidity and mortality. Inward-rectifier K+ current (IK1) is believed to be an important regulator of reentrant-spiral dynamics and a major component of AF-related electrical remodeling. MicroRNA-26 (miR-26) is predicted to target the gene encoding KIR2.1, KCNJ2. We found that miR-26 was downregulated in atrial samples from AF animals and patients and this downregulation was accompanied by upregulation of IK1/KIR2.1 protein. miR-26 overexpression suppressed expression of KCNJ2/KIR2.1. In contrast, miR-26 knockdown, inhibition, or binding-site mutation enhanced KCNJ2/KIR2.1 expression, establishing KCNJ2 as a miR-26 target. Knockdown of endogenous miR-26 promoted AF in mice, whereas adenovirus-mediated expression of miR-26 reduced AF vulnerability. Kcnj2-specific miR-masks eliminated miR-26-mediated reductions in Kcnj2, abolishing miR-26's protective effects, while coinjection of a Kcnj2-specific miR-mimic prevented miR-26 knockdown-associated AF in mice. Nuclear factor of activated T cells (NFAT), a known actor in AF-associated remodeling, was found to negatively regulate miR-26 transcription. Our results demonstrate that miR-26 controls the expression of KCNJ2 and suggest that this downregulation may promote AF.
    The Journal of clinical investigation 04/2013; · 15.39 Impact Factor
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    ABSTRACT: Identifying the key factor mediating pathological cardiac hypertrophy is critically important for developing the strategy to protect against heart failure. Bone morphogenetic protein-4 (BMP4) is a mechanosensitive and proinflammatory gene. In this study, we investigated the role of BMP4 in cardiac hypertrophy, apoptosis, and fibrosis in experimentally pathological cardiac hypertrophy. The in vivo pathological cardiac hypertrophy models were induced by pressure-overload and angiotensin (Ang) II constant infusion in mice, and the in vitro model was induced by Ang II exposure to cultured cardiomyocytes. The expression of BMP4 increased in pressure overload, Ang II constant infusion-induced pathological cardiac hypertrophy, but not in swimming exercise-induced physiological cardiac hypertrophy in mice. BMP4 expression also increased in Ang II-induced cardiomyocyte hypertrophy in vitro. In turn, BMP4 induced cardiomyocyte hypertrophy, apoptosis, and cardiac fibrosis, and these pathological consequences were inhibited by the treatment with BMP4 inhibitors noggin and DMH1. Moreover, Ang II-induced cardiomyocyte hypertrophy was inhibited by BMP4 inhibitors. The underlying mechanism that BMP4-induced cardiomyocyte hypertrophy and apoptosis was through increasing NADPH oxidase 4 expression and reactive oxygen species-dependent pathways. Lentivirus-mediated overexpression of BMP4 recapitulated hypertrophy and apoptosis in cultured cardiomyocytes. BMP4 inhibitor DMH1 inhibited pressure overload-induced cardiac hypertrophy in mice in vivo. The plasma BMP4 level of heart failure patients was increased compared with that of subjects without heart failure. In summary, we conclude that BMP4 is a mediator and novel therapeutic target for pathological cardiac hypertrophy.
    Hypertension 12/2012; · 6.87 Impact Factor
  • International journal of cardiology 10/2012; · 6.18 Impact Factor
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    ABSTRACT: Accumulating evidence suggests that the adrenergic receptors (ARs) play an important role in cardiac diseases. The expression of β3-AR has been recently demonstrated in atria, however, its role in atrial structural remodeling of atrial fibrillation (AF) is unclear. Therefore, the present study was designed to investigate the role of β3-AR in atrial structural remodeling in AF and to clarify its possible mechanisms. Twenty-eight dogs were randomly divided into sham, pacing, β3-AR agonist (BRL37344) and β3-AR antagonist (L748337) groups. AF was induced by rapid atrial pacing at 600 beats per minute for 3 weeks and evaluated by determining the ultrastructure and function of atria. The expression of β3-AR and p38 mitogen-activated protein kinase (MAPK) was examined by western blot, immunohistochemistry and real-time RT-PCR. Additionally, the extent of oxidative stress was tested. We found the atrial enlargement and dysfunction in pacing group. Moreover, atrial interstitial fibrosis, apoptosis and oxidative stress were increased and the levels of β3-AR and phosphorylated p38 MAPK were increased after pacing. Activation of β3-AR exacerbated the pathologic changes and oxidative stress, which were effectively inhibited by L748337. We concluded that β3-AR was upregulated in paced atria, which contributed to oxidative stress and exacerbated atrial structural remodeling by regulating p38 MAPK. Our study provides novel insights into the pharmacological role of β3-AR in AF.
    Cellular Physiology and Biochemistry 07/2012; 30(2):372-81. · 3.42 Impact Factor
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    ABSTRACT: The purpose of the present study was to evaluate the effects of overexpression of microRNA-1 (miR-1) on cardiac contractile function and the potential molecular mechanisms. Transgenic (Tg) mice (C57BL/6) for cardiac-specific overexpression of miR-1 driven by the α-myosin heavy chain promoter were generated and identified by real-time reverse-transcription polymerase chain reaction with left ventricular samples. We found an age-dependent decrease in the heart function in Tg mice by pressure-volume loop analysis. Histological analysis and electron microscopy displayed short sarcomeres with the loss of the clear zone and H-zone as well as myofibril fragmentation and deliquescence in Tg mice. Further studies demonstrated miR-1 post-transcriptionally down-regulated the expression of calmodulin (CaM) and cardiac myosin light chain kinase (cMLCK) proteins by targeting the 3'UTRs of MYLK3, CALM1, and CALM2 genes, leading to decreased phosphorylations of myosin light chain 2v (MLC2v) and cardiac myosin binding protein-C (cMyBP-C). Knockdown of miR-1 by locked nucleic acid-modified anti-miR-1 antisense (LNA-antimiR-1) mitigated the adverse changes of cardiac function associated with overexpression of miR-1. miR-1 induces adverse structural remodelling to impair cardiac contractile function. Targeting cMLCK and CaM likely underlies the detrimental effects of miR-1 on structural components of muscles related to the contractile machinery. Our study provides the first evidence that miRNAs cause adverse structural remodelling of the heart.
    Cardiovascular research 06/2012; 95(3):385-93. · 5.81 Impact Factor
  • International journal of cardiology 03/2012; 155(3):497-8. · 6.18 Impact Factor
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    ABSTRACT: This study was designed to investigate the effects and mechanism of action of the traditional Chinese drug formula, qiliqiangxin (QLQX), on cardiac function in spontaneously hypertensive rats (SHRs). We evaluated the effects of oral high-dose (4 g/kg/day, n = 7) and low-dose (1 g/kg/day, n = 7) QLQX on cardiac function in SHRs aged between 8 compared to control, the 8-week-old Wistar-Kyoto (WKY) rats. Echocardiography was performed to evaluate cardiac function and hemodynamic parameters. Hematoxylin and eosin (HE) and Masson's trichrome staining were performed, and the expression of myocardial angiotensin (Ang)-converting enzyme, chymase, transforming growth factor (TGF)-β, and collagen-type I and III were evaluated with real-time reverse transcription-PCR. Myocardial chymase, Ang-converting enzyme (ACE), and Ang II activities were measured with radioimmunoassay (RIA) techniques. Cardiac mast cells were detected with toluidine blue staining. In SHRs, the number of chymase enzyme-positive mast cells increased in the left ventricle (LV) compared with WKY rats. QLQX significantly decreased mast cell density and cardiac chymase levels, and it improved ejection fraction values and cardiac systolic function compared with vehicle. Moreover, QLQX decreased left atrial diameters and improved the E/A ratio. QLQX suppressed collagen-type I and III and TGF-β mRNA levels, and Ang II activity, in a dose-dependent manner. Whereas no difference in ACE activity was found between SHRs, chymase expression and activity were significantly decreased with QLQX. These data suggest that QLQX improves both systolic and diastolic cardiac function in SHRs through downregulating the cardiac chymase signaling pathway and chymase-mediated Ang II production.
    American Journal of Hypertension 11/2011; 25(2):250-60. · 3.67 Impact Factor
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    ABSTRACT: Coronary artery disease (CAD) causes more than 700,000 deaths each year in China. Previous genome-wide association studies (GWAS) in populations of European ancestry identified several genetic loci for CAD, but no such study has yet been reported in the Chinese population. Here we report a three-stage GWAS in the Chinese Han population. We identified a new association between rs6903956 in a putative gene denoted as C6orf105 on chromosome 6p24.1 and CAD (P = 5.00 × 10⁻³, stage 2 validation; P = 3.00 × 10⁻³, P = 1.19 × 10⁻⁸ and P = 4.00 × 10⁻³ in three independent stage 3 replication populations; P = 4.87 × 10⁻¹², odds ratio = 1.51 in the combined population). The minor risk allele A of rs6903956 is associated with decreased C6orf105 mRNA expression. We report the first GWAS for CAD in the Chinese Han population and identify a SNP, rs6903956, in C6orf105 associated with susceptibility to CAD in this population.
    Nature Genetics 03/2011; 43(4):345-9. · 35.21 Impact Factor

Publication Stats

425 Citations
191.47 Total Impact Points


  • 2007–2014
    • Chinese Academy of Sciences
      • Nanjing Institute of Geology and Palaeontology
      Peping, Beijing, China
    • Northeast Institute of Geography and Agroecology
      • Nanjing Institute of Geology and Palaeontology
      Beijing, Beijing Shi, China
  • 2004–2014
    • Harbin Medical University
      • Department of Cardiology
      Charbin, Heilongjiang Sheng, China
  • 2013
    • Shenyang Pharmaceutical University
      Feng-t’ien, Liaoning, China
  • 2011
    • Huazhong University of Science and Technology
      • Key Laboratory of Molecular Biophysics of Ministry of Education
      Wu-han-shih, Hubei, China