Hongyan Zhou

Sun Yat-Sen University, Shengcheng, Guangdong, China

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Publications (51)125.85 Total impact

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    ABSTRACT: Histone deacetylases (HDACs) regulate gene transcription by modifying the acetylation of histone and nonhistone proteins. Deregulated expression of HDACs has been implicated in tumorigenesis and angiogenesis. In this study, we examined the effect of suberoylanilide hydroxamic acid (SAHA), a potent inhibitor of HDACs, on inflammatory corneal angiogenesis. In a mouse model of alkali-induced corneal neovascularization (CNV), topical application of SAHA to the injured corneas attenuated CNV. In addition, in vivo treatment with SAHA downregulated the expression of the pro-angiogenic factors vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor beta 1 (TGFβ1), and epidermal growth factor (EGF), but upregulated the expression of the anti-angiogenic factors thrombospondin (TSP)-1, TSP-2, and ADAMTS-1 in the injured corneas. Furthermore, SAHA inhibited the expression of pro-angiogenic factors, migration, proliferation, and tube formation by human microvascular endothelial cells (HEMC-1) in vitro. These data indicate that SAHA has therapeutic potential for CNV.
    Canadian Journal of Physiology and Pharmacology 10/2014; 92(10):879-885. · 1.56 Impact Factor
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    ABSTRACT: Interleukin-28A (IL-28A), a member of type III interferons (IFN-λs), promotes antiviral, antitumor and immune responses. However, its ability to regulate autoimmune diseases is poorly understood. In this study, we examined the effect of IL-28A on retinal antigen-induced experimental autoimmune uveoretinitis (EAU), a mouse model of human T-cell-mediated autoimmune eye disease. We found that administration of IL-28A enhanced EAU scores and autoimmune response parameters including delayed-type hypersensitivity (DTH), Ag-specific T cell proliferation and the production of Ag-specific IL-17 and IFN-γ in the priming phase. The effect of IL-28A was abrogated by administration of a neutralizing antibody against IL-28A. Our results suggest that IL-28A is capable of exacerbating a T-cell-mediated autoimmune disease. Thus, targeting IL-28A may provide a new therapeutic approach to T cell-mediated autoimmune diseases such as uveitis.
    Cytokine 08/2014; · 2.52 Impact Factor
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    ABSTRACT: Interleukin-1β (IL-1β) is a potent proinflammatory cytokine that plays a critical role in initiating immunoinflammatory responses. In this study, we generated recombinant mouse IL-1β and anti-mouse IL-1β polyclonal antibodies to examine the effect of IL-1β on experimental autoimmune uveoretinitis (EAU), a mouse model for T cell-mediated eye autoimmune disease. Administration of mouse IL-1β by i.p. in the priming phase, but not in the effector phase, of immune response of EAU enhanced disease scores and its related immune responses including DTH, Ag-specific T cell proliferation and the production of IL-17 and IFN-γ. Furthermore, administration of anti-IL-1β antibody in the priming phase reduced EAU scores. These results suggest that IL-1β is an important mediator in the pathogenesis of autoimmune diseases such as uveitis.
    International immunopharmacology. 07/2014;
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    ABSTRACT: Histone deacetylases (HDACs) regulate gene transcription by modifying the acetylation level of histone and nonhistone proteins. In this study, we examined the effect of largazole, an inhibitor of class I HDACs, on inflammatory corneal angiogenesis. In a mouse model of alkali-induced corneal neovascularization (CNV), topical application of largazole to the injured corneas attenuated CNV. In addition, in vivo treatment with largazole down-regulated the expression of the pro-angiogenic factors VEGF, b-FGF, TGFβ1 and EGF but up-regulated the expression of the anti-angiogenic factors Thrombospondin-1 (Tsp-1), Tsp-2 and ADAMTS-1 in the injured corneas. Furthermore, largazole inhibited the expression of pro-angiogenic factors, migration, proliferation and tube formation by human microvascular endothelial cells (HEMC-1) in vitro. These data indicate that largazole has therapeutic potential for angiogenesis-associated diseases.
    European journal of pharmacology. 06/2014;
  • Ruijuan Zhao, Hongyan Zhou, Shao Bo Su
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    ABSTRACT: Interleukin-1β (IL-1β) belongs to IL-1 family and is a potent pro-inflammatory cytokine. It is known to be also involved in a variety of cellular activities, including cell proliferation, differentiation and apoptosis. In addition to its pathophysiologic role in host protection, IL-1β promotes the progression of a number of autoimmune diseases. Most of such diseases can be controlled by anti-IL-1β treatment. This review discusses the contribution of IL-1β to the course of autoimmune diseases, such as rheumatic diseases, uveitis, autoimmune thyroid diseases (AITD), insulin-dependent diabetes mellitus (IDDM), autoimmune inner ear disease (AIED), multiple sclerosis (MS), myocarditis, hepatitis and kidney diseases. The critical involvement of IL-1β in the pathogenesis of autoimmune diseases provides targets for developing therapeutic treatment.
    International immunopharmacology 09/2013; · 2.21 Impact Factor
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    Xiaomin Lin, Dan Fang, Hongyan Zhou, Shao Bo Su
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    ABSTRACT: Müller cells, the principal glial cells of the retina, play an important role in immune responses. Toll-like receptors (TLRs) are members of the pattern recognition receptor family and mediate innate and adaptive immune responses. In this study, we isolated, characterized Müller cells from mouse retina, and analyzed the expression of TLRs in these cells. We found that the mRNA of TLR2, TLR3, TLR4, and TLR5 was highly expressed by Müller cells. PAM3 and LPS, the agonists for TLR2 and TLR4, promoted Müller cells to produce the inflammatory cytokine Interleukine-6 and the chemokine MIP-2/CXCL2. These results suggest that Müller cells may be involved in innate and adaptive responses via TLR signaling in the eye. Our study should facilitate further study of the role of Müller cell in eye diseases and identification of the potential therapeutic targets.
    Neurological Sciences 12/2012; · 1.41 Impact Factor
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    ABSTRACT: PURPOSE: To investigate the changes of color vision and central visual field in a cohort of patients with Vogt-Koyanagi-Harada (VKH) syndrome. METHODS: Sixteen VKH patients (32 eyes) were enrolled in this study. All the patients were treated with immunosuppressive agents. The best visual acuity, visual field testing and color vision testing were available from the records in all these patients at different time points, i.e. before treatment and 1 month (±7 days), 3 months (±15 days), 6 months (±20 days) and 12 months (±30 days) after treatment. RESULTS: All patients showed active intraocular inflammation at their first visit. A decreased visual acuity, abnormality of color vision and abnormal visual field were observed at presentation. Visual acuity and color vision rapidly improved at 1 and 3 months and gradually improved thereafter. Visual field defects significantly improved at 6 months and gradually improved thereafter. However, visual field defects were still observed in 27.5% of the tested patients following a 12-month treatment. Color vision returned to the normal level only in about one-third of these patients at this time point. CONCLUSIONS: Visual function was severely impaired in VKH patients with active uveitis but rapidly improved following immunosuppressive therapy. Visual fields are much more severely affected by the disease than visual acuity and its improvement lagged behind that of visual acuity and color vision.
    Journal of ophthalmic inflammation and infection. 02/2012;
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    ABSTRACT: Cognitive impairments have been reported to be common in Parkinson's disease (PD) without dementia, which occur not only in the late stages of PD, but also in the early and middle stages. Until now, no reports on the profile of cognitive impairment in Chinese non-demented PD population have been published yet. Different ethnic groups should be assessed to improve evaluation of cognitive impairment in clinical practice. The aims of this study are to estimate the frequencies and profile of cognitive impairments and to explore the risk factors of cognitive impairments in Han Chinese non-demented PD patients at early and middle stages. Eighty non-demented PD patients in early and middle stages and 86 healthy controls were invited to participate in this study. Neuropsychological batteries testing executive function, visuospatial function, memory and attention were evaluated. Cognitive impairments were defined as impaired performance in at least one cognitive domain. Neuropsychological batteries detected 30 cases with executive dysfunction, 27 cases with memory impairment, eight cases with visuospatial dysfunction and seven cases with attention impairment. As many as 48 cases (60%) of PD patients presented cognitive impairment. Logistic regression analysis indicated that education level and Hoehn & Yahr stage were associated with cognitive impairment in PD. Cognitive impairment is common in the early and middle stages of PD without dementia; executive function is the most common domain impaired in a Chinese PD population. Cognitive impairment might be predicted by lower education level and higher Hoehn and Yahr stage.
    Parkinsonism & Related Disorders 02/2012; 18(2):161-5. · 3.27 Impact Factor
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    ABSTRACT: To investigate the clinical features of Vogt-Koyanagi-Harada (VKH) disease presenting as acute angle closure glaucoma at onset. Retrospective non-comparative case series. Four hundred and eighty-six VKH patients seen from February 2001 to March 2010. The history and clinical findings of all patients were reviewed. Auxiliary examinations, including ultrasound biomicroscopy, fundus fluorescein angiography and optical coherence tomography, were performed in certain cases. Corticosteroids with or without cyclosporine A were used to treat these patients. Patients' demographics, clinical presentation and auxiliary examination findings. Eight out of 486 VKH patients were misdiagnosed as acute angle closure glaucoma. The mean age of these eight patients was 55.6 years. Six patients were female. The mean intraocular pressure (IOP) at disease onset was 32.9 mmHg. All of these patients had a shallow anterior chamber and a narrow or closed angle at their first visit. The complaints of these patients were mostly headache and sudden decreased vision in both eyes. Alterations shown on ultrasound biomicroscopy included detachment of the ciliary body and peripheral choroid. The increased IOP did not respond to anti-glaucoma therapy, but resolved following treatment with corticosteroids. The eye of one patient was enucleated after failed trabeculectomies prior to referral to our uveitis centre. VKH disease presenting with a bilateral increased IOP mostly occurs in older women. The strikingly decreased visual acuity associated with mild to moderate increased IOP is a clue to the diagnosis. The increased IOP responded well to corticosteroids but not to anti-glaucoma treatment.
    Clinical and Experimental Ophthalmology 09/2011; 39(7):639-47. · 1.96 Impact Factor
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    ABSTRACT: Parkinson's disease is the second most common neurodegenerative disease, and environmental toxins such as rotenone play an important role in causing degeneration of dopaminergic neurons. Melatonin, a major secretory product of pineal, is recently reported to protect against rotenone-induced cell death in animal models. Yet, the mechanism involved in this protection needs to be elucidated. Here, we report that rotenone treatment (0-100 μM) decreased cell survival of Hela cells in a dose-dependent manner. At concentrations ranging from 0.1 to 100 μM, rotenone induced a dose-dependent increase in the expression of microtubule-associated protein 1 light chain 3 (LC3)-II, a protein associated with the autophagosomal membrane. Knockdown of Bax or Omi using shRNA inhibited 1 μM rotenone-induced autophagy. To determine whether melatonin would protect cells against rotenone-induced cell death and autophagy, we pretreated Hela cells with 250 μM melatonin for 24 hr in the presence of rotenone. Melatonin inhibited Bax expression and the release of the omi/HtrA2 into the cytoplasm induced by 1 μM rotenone. Melatonin 250 μM treatment also suppressed cell death induced by 0.1-100 μM rotenone and protected against the formation of LC3-II in cells exposed to 1 μM rotenone. This work demonstrates a novel role for melatonin as a neuroprotective agent against rotenone.
    Journal of Pineal Research 07/2011; 52(1):120-7. · 7.30 Impact Factor
  • Parkinsonism & Related Disorders 05/2011; 17(4):291-2. · 3.27 Impact Factor
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    ABSTRACT: Inflammation is closely linked to angiogenesis, and Toll-like receptors (TLRs) are the key mediators of inflammatory responses. However, the impact of TLRs on angiogenesis is incompletely understood. In this study, we determined the involvement of TLRs in angiogenesis. In a mouse model of alkali-induced corneal neovascularization (CNV), we found that CNV was attenuated in TLR4-/- but not TLR2-/- mice. Further study revealed that the absence of TLR4 led to decreased production of proangiogenic factors in association with reduced accumulation of macrophages at the site of wounds, which was associated with reduced expression of high-mobility group box-1 (HMGB1) protein, an endogenous ligand for TLR4. Topical application of HMGB1 to the injured cornea promoted CNV with increased macrophage accumulation in wild-type mice but not in TLR4-/- mice. HMGB1 treatment in vitro also promoted the production of proangiogenic factors by mouse macrophages in a TLR4-dependent manner. Furthermore, antagonists of HMGB1 and TLR4 reduced CNV and macrophage recruitment in the injured cornea of wild-type mice. Our results suggest that the release of HMGB1 in the wounds initiates TLR4-dependent responses that contribute to neovascularization. Thus, targeting HMGB1-TLR4 signaling cascade may constitute a novel therapeutic approach to angiogenesis-related diseases.
    Arteriosclerosis Thrombosis and Vascular Biology 03/2011; 31(5):1024-32. · 6.34 Impact Factor
  • Xiangrong Ren, Hongyan Zhou, Bing Li, Shao Bo Su
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    ABSTRACT: Viral components can trigger autoimmunity, but the involved mechanisms remain to be elucidated. Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNA (dsRNA) and appears to play an important role in this context. Our previous studies showed that signaling of TLR2, TLR3, TLR4 and TLR9 is highly redundant in the adjuvant effect needed to induce experimental autoimmune uveitis (EAU), an animal model of human autoimmune eye disease. In this study, we analyzed the effects of systemic delivery of polyinosinic:polycytidylic acid (poly(I:C)), a mimic of viral dsRNA, in the induction of EAU. We found that TLR3 agonist poly(I:C) enhanced EAU scores, DTH responses and Ag-specific T cell proliferation. In addition, Ag-specific Interleukin 17 (IL-17) and interferon gamma (IFN-γ) production by draining lymph node cells was markedly increased in the poly(I:C)-treated group. Our results suggest that activation of innate immune system mediated by TLR3 signaling pathway is of importance in the pathogenesis of virus-induced autoimmune diseases.
    International immunopharmacology 02/2011; 11(6):769-73. · 2.21 Impact Factor
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    ABSTRACT: High-mobility group box-1 (HMGB1) plays important roles in inflammation, immune responses, and tumor progression. Since HMGB1 and its components have been shown to be mediators of a number of diseases but several sources of recombinant HMGB1 showed controversial biological activity, it is important to obtain recombinant HMGB1 with properties that resemble the native protein. For this purpose, we cloned genes coding for human HMGB1 and its active components A box and B box by PCR and inserted the cloned genes into pET28a vectors for transformation of Escherichia coli BL21. The E. coli expressed proteins were then purified with a Ni(2+)-NTA column and the endotoxin content was removed. Recombinant human HMGB1 (rhHMGB1) and its B box thus obtained stimulated, but A box inhibited, the production of the chemokine CXCL8/IL-8 by THP-1 monocytic cell line. We also used purified rhHMGB1 to immunize rabbits and generated potent anti-sera, which was capable of neutralizing the activity of rhHMGB1 in vitro and detecting the increased HMGB1 expression in inflammatory tissues in mice and humans. Thus, we have established essential means to produce biologically active rhHMGB1 that will facilitate us to study its role in diseases and to explore its potential as a therapeutic agent.
    International immunopharmacology 01/2011; 11(6):646-51. · 2.21 Impact Factor
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    ABSTRACT: IL-23 has been shown to be involved in the pathogenesis of Behcet's disease (BD) through promoting IL-17 production. This study examined whether IL-23R polymorphisms were associated with susceptibility to this disease in a Chinese Han population. Four single-nucleotide polymorphisms (SNP), rs7517847, rs11209032, rs 1343151 and rs17375018 were genotyped in 338 BD patients and 407 age, sex and ethnically matched healthy controls using a PCR restriction fragment length polymorphism assay. A significantly increased prevalence of the homozygous rs17375018 GG genotype and G allele was found in BD patients compared with controls (corrected p (p(c))<0.001,odds ratio (OR) 1.86, 95% CI 1.39 to 2.49; p(c)<0.001, OR 1.57, 95% CI 1.25 to 1.98, respectively). The frequencies of the AA genotype and A allele of the SNP rs11209032 were significantly higher in BD patients compared with controls (p(c)=0.024, OR 1.69, 95% CI 1.21 to 2.35; p(c)<0.001, OR 1.48, 95% CI 1.21 to 1.82, respectively). In addition, the results showed a significantly decreased frequency of the AGCG haplotype in BD patients compared with controls (p(c)=0.0016, OR 0.59, 95% CI 0.45 to 0.77). This study, for the first time, identified a strong association of an SNP of IL-23R, rs17375018, with BD. The results also suggested that both rs11209032 AA and rs17375018 GG of IL-23R are predisposing genotypes for BD and that the AGCG haplotype may provide protection against BD.
    Annals of the rheumatic diseases 04/2010; 69(7):1325-8. · 8.11 Impact Factor
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    ABSTRACT: Polymorphisms of interleukin-23 receptor (IL23R) gene have recently been reported to be associated with the susceptibility to several immune-related diseases. The aim of this study was to determine the association of IL23R polymorphisms with Vogt-Koyanagi-Harada (VKH) syndrome, a disease presumably mediated by autoimmune response. A total of 382 Chinese Han patients with VKH syndrome and 407 healthy controls were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method. Data were analyzed by chi(2) analysis. All genotype distributions in healthy controls were in Hardy-Weinberg equilibrium. There was no difference among the investigated four single nucleotide polymorphisms concerning the linkage disequilibrium between the tested samples and those available in the international HapMap. The genotype and allele frequencies of rs17375018, rs7517847, rs11209032, and rs1343151 were not different between patients with VKH syndrome and healthy controls. Analysis according to gender and clinical findings did not show any association of the four polymorphisms with these parameters. In conclusion, the tested IL23R gene polymorphisms are not associated with the susceptibility to VKH syndrome in the Chinese Han population.
    Human immunology 04/2010; 71(4):414-7. · 2.55 Impact Factor
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    ABSTRACT: To investigate the role of Foxp3-positive regulatory T cells in the development of experimental autoimmune uveoretinitis (EAU). B10RIII mice were immunized with 50 microg IRBP(161-180) in complete Freund's adjuvant (CFA) to induce EAU. EAU was evaluated clinically and pathologically on days 0, 7, 14, 21, and 28. Foxp3 mRNA levels were detected using reverse transcription-PCR (RT-PCR) and the frequencies of CD4(+)Foxp3(+) T cells and CD4(+)CD25(+)Foxp3(+) T cells in splenocytes were assessed by flow cytometry at the aforementioned time points. The first clinical signs of EAU were observed on day 8-9, worsened up to day 14, and then gradually resolved. Histopathologic results showed that inflammatory signs occurred on day 7, reached their peak on day 14, and then gradually decreased. The levels of Foxp3 mRNA and the frequencies of CD4(+)Foxp3(+) T cells and CD4(+)CD25(+)Foxp3(+) T cells in splenocytes increased on day 7, reached a peak on day 14, and then maintained at a high level until day 28. An upregulation of Foxp3 expression is induced in EAU and paralleled with disease activity, suggesting a role for this lymphocyte subpopulation in the regression of this experimental uveitis model.
    Ocular immunology and inflammation 01/2010; 18(1):38-43. · 0.72 Impact Factor
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    ABSTRACT: The aim of the study was to investigate the association of polymorphisms of the interleukin-23 receptor (IL23R) gene with Fuchs' syndrome in a Chinese Han population. Three single-nucleotide polymorphisms (SNPs), rs7517847, rs11209032 and rs17375018 of IL23R were genotyped in 138 Chinese Han patients with Fuchs' syndrome and 407 healthy controls by using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Data were analyzed by χ(2) analysis. All genotype and allele distributions in patients with Fuchs' syndrome and healthy controls were in Hardy-Weinberg equilibrium. The frequency of the rs11209032 AA genotype was significantly increased in patients with Fuchs' syndrome as compared to controls (corrected p [pc]=0.036, OR 1.86, 95%CI 1.21 to 2.86). There were no statistically significant differences between patients and healthy controls concerning the other two tested SNPs (rs17375018 and rs7517847). The haplotypes of the tested SNPs were not different between patients and controls. Additionally, analysis according to gender did not show any influence of sex on the association of IL23R with Fuchs' syndrome. Our results suggested that the rs11209032 AA genotype of the IL23R gene may predispose for Fuchs' syndrome in Chinese patients.
    Molecular vision 01/2010; 16:2585-9. · 1.99 Impact Factor
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    ABSTRACT: To investigate the role of CD4(+)CD25(+) Treg cells in the development of experimental autoimmune uveoretinitis (EAU). EAU was induced in B10RIII mice by immunization with IRBP(161-180) in complete Freund's adjuvant and evaluated clinically and pathologically on days 0, 7, 14, 21, and 28. Lymphocytes from draining lymph nodes (LNs) were subjected to flow cytometry to analyze the frequency of CD4(+)CD25(+) Treg cells. CD4(+)CD25(+) Treg cells and CD4(+)CD25(-) T cells were separated by means of magnetic-assisted cell sorting and cocultured or crossover cultured for 3 days. Proliferation of CD4(+)CD25(-) T cells was measured using a modified MTT assay. The levels of IFN-gamma and IL-17 in the supernatants were determined by enzyme-linked immunosorbent assay. Clinical and histopathologic results showed a severe intraocular inflammation in the immunized mice. The frequency of CD4(+)Foxp3(+) T cells and CD4(+)CD25(+)Foxp3(+) T cells in the draining LN lymphocytes was increased on day 7, reached its peak on day 14, and maintained a high level up to day 42. CD4(+)CD25(+) Treg cells obtained from mice on days 14 and 28 after immunization showed a stronger inhibitory effect on the proliferation of CD4(+)CD25(-) T cells and the production of IFN-gamma by CD4(+)CD25(-) T cells compared with those obtained from control mice. CD4(+)CD25(+) Treg cells did not affect IL-17 production. Transfer of CD4(+)CD25(+) Treg cells obtained from EAU mice was able to suppress EAU induction by IRBP(161-180) that was not observed after transfer of cells from mice that had received CFA alone, suggesting antigen specificity of the Treg response. A significantly increased frequency and immunoregulatory action of CD4(+)CD25(+) Treg cells is associated with the development and regression of EAU, suggesting that CD4(+)CD25(+) Treg cells are induced during EAU and may be involved in its regression.
    Investigative ophthalmology & visual science 09/2009; 51(1):383-9. · 3.43 Impact Factor
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    ABSTRACT: Recent studies in Caucasian uveitis patients have shown an association with the -2518 A/G polymorphism of the monocyte chemoattractant protein (MCP)-1 gene. It is unknown whether this polymorphism is also associated with ocular Behçet's disease (BD) in Chinese populations. The aim of the current study was therefore to investigate the possible involvement of MCP-1 in the susceptibility to ocular BD in Chinese Han individuals. A case control association study was performed in 296 ocular BD patients and 319 geographically and age-matched healthy controls using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Binary logistic regression analysis revealed a decreased frequency of the homozygous AA genotype and an increased frequency of AG genotype of the MCP-1 -2518 polymorphism in ocular BD patients compared with healthy controls, when adjusted for gender (p = 0.048, p = 0.028, respectively). However, when segregated on the basis of several clinical findings, no any association was found between this polymorphism and ocular BD. In conclusion, the present study suggests that the MCP-1 -2518 AA genotype seems to display a protective association with ocular BD, whereas the -2518 AG genotype might be a susceptible factor for ocular BD in the Chinese Han population.
    Human immunology 09/2009; 71(1):79-82. · 2.55 Impact Factor

Publication Stats

595 Citations
125.85 Total Impact Points

Institutions

  • 2005–2014
    • Sun Yat-Sen University
      • State Key Laboratory of Oncology
      Shengcheng, Guangdong, China
  • 2011
    • Shantou University
      Swatow, Guangdong, China
  • 2008–2010
    • Chongqing Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Sun Yat-Sen University Cancer Center
      Shengcheng, Guangdong, China
  • 2002
    • Zhongshan University
      中山, Guangdong, China