Tao Jiang

Beijing Neurosurgical Institute, Peping, Beijing, China

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Publications (305)1140.33 Total impact

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    ABSTRACT: The highly pathogenic H5N1 avian influenza virus is one of the greatest influenza pandemic threats since 2003. The association of the receptor binding domain (RBD) with the virulence of influenza virus is rarely addressed, particularly of H5N1 influenza viruses. In this study, BALB/c mice were intranasally infected with A/Vietnam/1194/2004 (VN1194, H5N1). The mouse lung-adapted variants were isolated and the mutation of E190G (H3 numbering) in the RBD was recognized. The recombinant virus, rVN-E190G carrying E190G in hemagglutinin (HA) was designed and rescued using reverse genetics techniques. The receptor binding activity, growth curve and pathogenicity in mice of the rVN-E190G were investigated. Results demonstrated that rVN-E190G virus increased the binding avidity to α2,6 SA (sialic acid) and reduced the affinity to α2,3 SA, meanwhile weakened the viral replication in vitro. Moreover, the virulence assessment demonstrated that rVN-E190G was attenuated in mice. These results indicated that the mutation E190G in HA decreases H5N1 viral replication in vitro and significantly attenuates virulence in vivo. These findings identify one of the determinants in RBD which can be associated with H5N1 virulence in mice. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Medical Virology 06/2015; DOI:10.1002/jmv.24257 · 2.22 Impact Factor
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    ABSTRACT: Therapeutics targeting the Nogo-A signal pathway hold promise to promote recovery following brain injury. Based on the temporal characteristics of Nogo-A expression in the process of cerebral ischemia and reperfusion, we tested a novel asynchronous treatment, in which TAT-M9 was used in the early stage to decrease neuronal loss, and TAT-NEP1-40 was used in the delayed stage to promote neurite outgrowth after bilateral common carotid artery occlusion (BCCAO) in mice. Both TAT-M9 and TAT-NEP1-40 were efficiently delivered into the brains of mice by intraperitoneal injection. TAT-M9 treatment promoted neuron survival and inhibited neuronal apoptosis. Asynchronous therapy with TAT-M9 and TAT-NEP1-40 increased the expression of Tau, GAP43 and MAP-2 proteins, and enhanced short-term and long-term cognitive functions. In conclusion, the asynchronous treatment had a long-term neuroprotective effect, which reduced neurologic injury and apoptosis, promoted neurite outgrowth and enhanced functional recovery after ischemia. It suggests that this asynchronous treatment could be a promising therapy for cerebral ischemia in humans.
    Journal of Drug Targeting 06/2015; DOI:10.3109/1061186X.2015.1052070 · 2.72 Impact Factor
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    ABSTRACT: Infection in airspaces and lung parenchyma may cause acute lung injury and multiple organ dysfunction syndrome due to acute inflammatory response, leading to organ failure and high mortality. ZC3H12D has been shown to modulate Toll-like receptor signaling. This study aimed to investigate the change of ZC3H12D during acute lung injury and its role in inflammation processes. Mice were challenged with lipopolysaccharides (LPS) intratracheally. The expression levels of Zc3h12d, NF-κB, and cytokines were analyzed by quantitative real-time PCR (qPCR), ELISA, and Western blot. The mRNA stability was assessed by qPCR after cells were treated with actinomycin D for specified times. The 3' untranslated region (3'-UTR) of c-fos was cloned immediately downstream of the luciferase coding sequence driven by CMV promoter and luciferase activity was measured with a Luciferase Assay kit. Upon LPS treatment, ZC3H12D levels were reduced in mouse immune cells, whereas levels of NF-κB, IL-6, and TNF-α were significantly increased. Knockdown Zc3h12d in THP1 cells resulted in the upregulation of NF-κB while overexpression of Zc3h12d inhibited NF-κB expression. Ectopic Zc3h12d significantly reduced the mRNA stability of c-fos, NF-κB, TNF-α, IL-1β, and IL-6. Attachment of the c-fos 3'-UTR made luciferase expression levels sensitive to levels of ZC3H12D. The data indicated that ZC3H12D could suppress both the initial inflammation storm and chronic inflammation by targeting the mRNA of cytokines as well as NF-κB and c-fos. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Molecular Immunology 06/2015; DOI:10.1016/j.molimm.2015.05.018 · 3.00 Impact Factor
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    ABSTRACT: Internal ribosomal entry site (IRES)-mediated translation initiation is constitutively activated during stress conditions such as tumorigenesis and hypoxia. The RNA editing enzyme ADAR1 plays an important role in physiology and pathology. Initially, we found that the ADAR1 p150 or p110 transcript levels were decreased in glioma cells compared with normal astrocyte cells. In contrast, protein levels of ADAR1 p110 were significantly upregulated in glioma tissues and cells. This expression pattern indicated translationally controlled regulation. We identified an 885-nt sequence that was located between AUG1 and AUG2 within the ADAR1 mRNA that exhibited IRES-like activity. Furthermore, we confirmed that the translational mode of ADAR1 p110 was mediated by PTBP1 in glioma cells. The protein levels of PTBP1 and ADAR1 were cooperatively expressed in glioma tissues and cells. Knocking down ADAR1 p110 significantly decreased cell proliferation in three types of glioma cells (T98G, U87MG and A172). The removal of a minimal IRES-like sequence in a p150-overexpression construct could effectively abolish p110 induction and resulted in the slight suppression of cell proliferation compared with ADAR1-p150 overexpression in siPTBP1-treated T98G cells. In summary, our study revealed a mechanism whereby ADAR1 p110 can be activated by PTBP1 through an IRES-like element in glioma cells, and ADAR1 is essential for the maintenance of gliomagenesis.
    Cellular and Molecular Life Sciences CMLS 06/2015; DOI:10.1007/s00018-015-1938-7 · 5.86 Impact Factor
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    ABSTRACT: Live attenuated influenza vaccines (LAIV) are now available for the prevention of influenza, with LAIV strains generally derived from serial passaging in cultures or by reverse genetics. The receptor binding domain (RBD) in the hemagglutinin (HA) of influenza virus is responsible for viral binding to avian type, α2,3-linked or human type α2,6-linked sialic acid receptor; however the virulence determinants in the RBD of H5N1 virus remain largely unknown. In the present study, serial passaging of H5N1 virus A/Vietnam/1194/2004 (VN1194) in MDCK cells resulted in the generation of adapted variants with large-plaque morphology, and genomic sequencing of selected variants revealed two specific amino acid substitutions (K193E and G225E) in the RBD. Reverse genetics (RG) was used to generate H5N1 viruses containing either single or double substitutions in the HA. The RG virus containing K193E and G225E mutations (rVN-K193E/G225E) demonstrated large plaque morphology, enhanced replication, and genetic stability after serial passaging, without changing the receptor binding preference. Importantly, in vivo virulence assessment demonstrated that rVN-K193E/G225E was significantly attenuated in mice. Microneutralization and hemagglutination inhibition assays demonstrated that immunization with rVN-K193E/G225E efficiently induced a robust antibody response against wild type H5N1 virus in mice. Taken together, our experiments demonstrate that K193E and G225E mutations synergistically attenuated H5N1 virus without enhancing the receptor binding avidity, and that the RG virus rVN-K193E/G225E represents a potential H5N1 LAIV strategy that deserves further development. These findings identify the RBD as novel attenuation target for live vaccine development and highlight the complexity of RBD interactions.
    Journal of General Virology 05/2015; DOI:10.1099/vir.0.000193 · 3.53 Impact Factor
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    ABSTRACT: Both age of patients and tumor location are associated with tumor origin, genetic characteristics, and prognosis. The objective of this study was to investigate the relationship between tumor location and age at diagnosis in a large cohort of patients with a primary diagnosis of glioma. We consecutively enrolled a cohort of 200 adults with glioblastoma and another cohort of 200 adults with diffuse low-grade gliomas. The magnetic resonance images of all tumors were manually segmented and then registered to a standard brain space. By using voxel-by-voxel regression analysis, specific brains regions associated with advanced age at tumor diagnosis were localized. In the low-grade gliomas cohort, the brain regions associated with advanced age at tumor diagnosis were mainly located in the right middle frontal region, while a region in the left temporal lobe, particularly at the subgranular zone, was associated with lower age at tumor diagnosis. In the glioblastoma cohort, the brain regions associated with advanced age at tumor diagnosis were mainly located in the temporal lobe, particularly at the posterior region of the subventricular zones. A region in the left inferior frontal region was associated with lower age at tumor diagnosis. Significant differences in the age of patients were found between tumors located in the identified regions and those located elsewhere in both cohorts. The current study demonstrated the correlation between tumor location and age at diagnosis, which implies differences in the origin of gliomas in young and older patients.
    Journal of Neuro-Oncology 05/2015; 123(2). DOI:10.1007/s11060-015-1798-x · 2.79 Impact Factor
  • PLoS ONE 05/2015; 10(5):e0126022. DOI:10.1371/journal.pone.0126022 · 3.53 Impact Factor
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    ABSTRACT: Loss of ATRX leads to epigenetic alterations, including abnormal levels of DNA methylation at repetitive elements such as telomeres in murine cells. We conducted an extensive DNA methylation and mRNA expression profile study on a cohort of 82 patients with astrocytic tumors to study whether ATRX expression was associated with DNA methylation level in astrocytic tumors and in which cellular functions it participated. We observed that astrocytic tumors with lower ATRX expression harbored higher DNA methylation level at chromatin end and astrocytic tumors with ATRX-low had distinct gene expression profile and DNA methylation profile compared with ATRX-high tumors. Then, we uncovered that several ATRX associated biological functions in the DNA methylation and mRNA expression profile (GEP), including apoptotic process, DNA-dependent positive regulation of transcription, chromatin modification, and observed that ATRX expression was companied by MGMT methylation and expression. We also found that loss of ATRX caused by siRNA induced apoptotic cells increasing, reduced tumor cell proliferation and repressed the cell migration in glioma cells. Our results showed ATRX-related regulatory functions of the combined profiles from DNA methylation and mRNA expression in astrocytic tumors, and delineated that loss of ATRX impacted biological behaviors of astrocytic tumor cells, providing important resources for future dissection of ATRX role in glioma.
    Oncotarget 05/2015; · 6.63 Impact Factor
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    ABSTRACT: PTPRZ1-MET (ZM) proteins are a group of fusion proteins identified in human gliomas by high-throughput transcriptome sequencing. ZM fusions are associated with poor prognosis in afflicted glioma patients and mediate oncogenic effects in assays. In this study, we show that ZM-carrying patients have increased MET mRNA expression levels induced by fusion with receptor-type tyrosine-protein phosphatase zeta (PTPRZ1). Furthermore, ZM fusions preserve fundamental properties of wild-type MET with respect to processing and dimerization, and enhance phosphorylation in an HGF-dependent and independent manner. Our findings suggest that ZM induces gliomas through elevated expression and phosphorylation of the MET oncoprotein. Copyright © 2015. Published by Elsevier B.V.
    FEBS letters 04/2015; DOI:10.1016/j.febslet.2015.04.032 · 3.34 Impact Factor
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    ABSTRACT: High density electrocorticogram (ECoG) of motor cortex was recorded during awake surgeries of two subjects with respectively epilepsy and brain tumor. Subjects were asked to execute spontaneous hand movements: extension and flexion during the experiments. We investigated the ECoG in time frequency plane during these hand movements and computed event-related desynchronization (ERD) and event-related synchronization (ERS) levels of beta (8-32 Hz) and gamma frequency bands. The distribution of ERD and ERS over channels provided an idea about the spatial distribution of the cortical activity within each task. In both subjects, consistently, the scale of power changes in beta and gamma band was larger in hand flexion compared to hand extension. In addition, the spatial distribution of ERD in beta and ERS in gamma band during flexion was larger than extension but highly overlapped between these tasks. Gamma band was more spatially localized than beta band activity and cortical patterns were more distinct between the tasks. Our preliminary results indicate that the high density ECoG can be effectively used in awake surgery for functional mapping.
    7th International IEEE/EMBS Conference on Neural Engineering; 04/2015
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    ABSTRACT: Adversity, particularly in early life, can cause illness. Clues to the responsible mechanisms may lie with the discovery of molecular signatures of stress, some of which include alterations to an individual's somatic genome. Here, using genome sequences from 11,670 women, we observed a highly significant association between a stress-related disease, major depression, and the amount of mtDNA (p = 9.00 × 10(-42), odds ratio 1.33 [95% confidence interval [CI] = 1.29-1.37]) and telomere length (p = 2.84 × 10(-14), odds ratio 0.85 [95% CI = 0.81-0.89]). While both telomere length and mtDNA amount were associated with adverse life events, conditional regression analyses showed the molecular changes were contingent on the depressed state. We tested this hypothesis with experiments in mice, demonstrating that stress causes both molecular changes, which are partly reversible and can be elicited by the administration of corticosterone. Together, these results demonstrate that changes in the amount of mtDNA and telomere length are consequences of stress and entering a depressed state. These findings identify increased amounts of mtDNA as a molecular marker of MD and have important implications for understanding how stress causes the disease. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.
    Current biology: CB 04/2015; 25(9). DOI:10.1016/j.cub.2015.03.008 · 9.92 Impact Factor
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    ABSTRACT: Contrast enhancement is a crucial radiologic feature of malignant brain tumors, which are associated with genetic changes of the tumor. The purpose of the current study was to investigate the potential relationship among tumor contrast enhancement with MR imaging, vascular endothelial growth factor (VEGF) expression, and survival outcome in anaplastic gliomas. MR images from 240 patients with histologically confirmed anaplastic gliomas were retrospectively analyzed. The volumes of T2 hyperintense, contrast enhanced regions and necrotic regions on postcontrast T1-weighted images were measured. The ratio of the enhanced volume to necrotic volume was compared between patients with high versus low levels of VEGF expression and was further used in the survival analysis. The volumetric ratio of enhancement to necrosis was significantly higher in patients with low VEGF expression than in those with high VEGF expression (Mann-Whitney, p = 0.009). In addition, the enhancement/necrosis ratio was identified as a significant predictor of progression-free survival (Cox regression model, p = 0.004) and overall survival (Cox regression model, p = 0.006) in the multivariate analysis. These results suggest that the volumetric ratio of enhancement to necrosis could serve as a noninvasive radiographic marker associated with VEGF expression and that this ratio is an independent predictor for progression-free survival and overall survival in patients with anaplastic gliomas.
    PLoS ONE 03/2015; 10(3):e0121380. DOI:10.1371/journal.pone.0121380 · 3.53 Impact Factor
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    ABSTRACT: Accumulating evidence demonstrates that defining molecular subtypes based on objective genetic alterations may permit a more rational, patient-specific approach to molecular targeted therapy across various cancers. The objective of this study was to subtype primary glioblastoma (pGBM) based on microRNA (miRNA) profiling in Chinese population. Here, miRNA expression profiles from 82 pGBM samples were analyzed and 78 independent pGBM samples were used for qRT-PCR validation. We found that two distinct subgroups with different prognosis and chemosensitivities to temozolomide (TMZ) in Chinese pGBM samples. One subtype is TMZ chemoresistant (termed the TCR subtype) and confers a poor prognosis. The other subtype is TMZ-chemosensitive (termed the TCS subtype) and confers a relatively better prognosis compared with the TCR subtype. A classifier consisting of seven miRNAs was then identified (miR-1280, miR-1238, miR-938 and miR-423-5p (overexpressed in the TCR subtype); and let-7i, miR-151-3p and miR-93 (downregulated in the TCR subtype)), which could be used to assign pGBM samples to the corresponding subtype. The classifier was validated using both internal and external samples. Meanwhile, the genetic alterations of the TCR and TCS subtypes were also analyzed. The TCR subtype was characterized by no IDH1 mutation, and EGFR and Ki-67 overexpression. The TCS subtype displayed the opposite situation. Taken together, the results indicate a distinct subgroup with poor prognosis and TMZ-chemoresistance.
    Oncotarget 03/2015; · 6.63 Impact Factor
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    ABSTRACT: HOTAIR is a negative prognostic factor and is overexpressed in multiple human cancers including glioblastoma multiform (GBM). Survival analysis of Chinese Glioma Genome Atlas (CGGA) patient data indicated that high HOTAIR expression was associated with poor outcome in GBM patients. NLK (Nemo-like kinase), a negative regulator of the β-catenin pathway, was negatively correlated with HOTAIR expression. When the β-catenin pathway was inhibited, GBM cells became susceptible to cell cycle arrest and inhibition of invasion. Introduction of the HOTAIR 5' domain in human glioma-derived astrocytoma induced β-catenin. An intracranial animal model was used to confirm that HOTAIR depletion inhibited GBM cell migration/invasion. In the orthotopic model, HOTAIR was required for GBM formation in vivo. In summary, HOTAIR is a potential therapeutic target in GBM.
    Oncotarget 03/2015; · 6.63 Impact Factor
  • Huimin Hu, Yanwei Liu, Tao Jiang
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    ABSTRACT: Cancer is the greatest challenge to human health in our era. Perturbations of receptor tyrosine kinase (RTK) function contribute to a large chunk of cancer etiology. Current evidence supports that mutations in RTKs mediate receptor dimerization and result in ligand-independent kinase activity and tumorigenesis, indicating that mutation-introduced receptor dimerization is a critical component of oncogenesis RTK mutations. However, there are no specialized reviews of this important principle. In the current review, we discuss the physiological and harmless RTK function and subsequently examine mutation-introduced dimerization of RTKs and the role of these mutations in tumorigenesis. We also summarize the protein structure characteristics that are important for dimerization and introduce research methods and tools to predict and validate the existence of oncogenic mutations introduced by dimerization in RTKs.
    Tumor Biology 03/2015; 36(3). DOI:10.1007/s13277-015-3287-4 · 2.84 Impact Factor
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    ABSTRACT: Non-obstructive azoospermia (NOA), a severe form of male infertility, is often suspected to be linked to currently undefined genetic abnormalities. To explore the genetic basis of this condition, we successfully sequenced ~650 infertility-related genes in 757 NOA patients and 709 fertile males. We evaluated the contributions of rare variants to the etiology of NOA by identifying individual genes showing nominal associations and testing the genetic burden of a given biological process as a whole. We found a significant excess of rare, non-silent variants in genes that are key epigenetic regulators of spermatogenesis, such as BRWD1, DNMT1, DNMT3B, RNF17, UBR2, USP1 and USP26, in NOA patients (P = 5.5 × 10(-7)), corresponding to a carrier frequency of 22.5% of patients and 13.7% of controls (P = 1.4 × 10(-5)). An accumulation of low-frequency variants was also identified in additional epigenetic genes (BRDT and MTHFR). Our study suggested the potential associations of genetic defects in genes that are epigenetic regulators with spermatogenic failure in human.
    Scientific Reports 03/2015; 5:8785. DOI:10.1038/srep08785 · 5.58 Impact Factor
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    ABSTRACT: Human leukocyte antigen-G (HLA-G) is a tumor microenvironment molecule that is involved in the escape of cancerous tumors from host immune recognition and destruction. This study investigated the potential relationship between HLA-G expression levels and the sharpness of low-grade glioma tumor borders in magnetic resonance images. Preoperative T2-weighted images from 72 patients were retrospectively examined by manually segmenting the hyperintensive tumor areas and subsequently registering them to a standard brain template. Then, the intensity of the voxels inside the tumor border (tumor voxels) was compared with that of the voxels outside the tumor border (paratumor voxels). The radiologic sharpness of a tumor was defined as the mean ratio of the intensity of the tumor voxels to the intensity of the paratumor voxels. Tumors with high HLA-G expression were associated with larger tumors and lower mean hyperintensive contrast. These findings suggest that tumors with blurred boundaries may be those prone to diffuse invasion. Additionally, patients with tumors having high HLA-G expression were less likely to have undergone complete resections. Thus, this study is the first to identify an association between HLA-G expression and the radiologic morphology of the tumor border, and may further our understanding of the role of the HLA gene in immune escape in patients with low-grade gliomas. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 03/2015; 282. DOI:10.1016/j.jneuroim.2015.02.013 · 2.79 Impact Factor
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    ABSTRACT: OBJECTIVE To detect the pathogenic mutation in a patient with methylmalonic acidemia using IonTorrent Personal Genome Machine (PGM) and assess the feasibility of such technology for analyzing complex monogenic diseases. METHODS Peripheral blood sample was collected from the patient. Genomic DNA was isolated using a standard method and subjected to targeted sequencing using an Ion Ampliseq Inherited Disease Panel. DNA fragment was ligated with a barcoded sequencing adaptor. Template preparation, emulsion PCR, and Ion Sphere Particles enrichment were carried out using the Ion One Touch system. Data from the PGM runs were processed using Ion Torrent Suite 3.2 software to generate sequence reads. All variants were filtered against dbSNPl37. DNA sequences were visualized with an Integrated Genomics Viewer. RESULTS After data analysis and database filtering, a previously reported nonsense mutation, c.586C>T (p.R196X), and a novel mutation c.898C>T (p.R300X) were identified in the MMAA gene in this patient. Both mutations were verified by conventional Sanger sequencing. Conclusion Pathogenic MMAA mutations have been identified in a patient with methylmalonic acidemia. This new-generation targeted sequencing on the PGM sequencers can be applied for genetic diagnosis of hereditary diseases.
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    ABSTRACT: Glioblastoma multiforme (GBM) is classified into primary (pGBM) or secondary (sGBM) based on clinical progression. However, there are some limits to this classification for insight into genetically and clinically distinction between pGBM and sGBM. The aim of this study is to characterize pGBM and sGBM associating with differential molecular subtype distribution. Whole transcriptome sequencing data was used to assess the distribution of molecular subtypes and genetic alterations in 88 pGBM and 34 sGBM in a Chinese population-based cohort, and the biological progression and prognostic impact were analyzed by combining clinical information. Forty-one percentage of pGBM were designated as Mesenchymal subtype, while only 15% were the Proneural subtype. However, sGBM displayed the opposite ratio of Mesenchymal (15%) and Proneural (44%) subtypes. Mutations in isocitrate dehydrogenase-1 (IDH1) were found to be highly concentrated in the Proneural subtypes. In addition, patients with sGBM were 10 years younger on average than those with pGBM, and exhibited clinical features of shorter overall survival and frontal lobe tumor location tendency. Furthermore, in sGBM, gene sets related to malignant progression were found to be enriched. Overall, these results reveal the intrinsic distinction between pGBM and sGBM, and provide insight into the genetic and clinical attributes of GBM.
    Oncotarget 01/2015; · 6.63 Impact Factor

Publication Stats

3k Citations
1,140.33 Total Impact Points

Institutions

  • 2010–2015
    • Beijing Neurosurgical Institute
      Peping, Beijing, China
    • Qingdao University of Science and Technology
      Tsingtao, Shandong Sheng, China
  • 2005–2015
    • Beijing Tiantan Hospital
      Peping, Beijing, China
  • 2003–2015
    • Beijing Institute of Microbiology and Epidemiology
      Peping, Beijing, China
    • Beijing Centers for Disease Control and Prevention
      Peping, Beijing, China
  • 2014
    • Chinese Academy of Sciences
      Peping, Beijing, China
    • Sichuan University
      • State Key Laboratory of Biotherapy
      Hua-yang, Sichuan, China
    • University of Oklahoma Health Sciences Center
      • Department of Surgery
      Oklahoma City, Oklahoma, United States
    • Xinjiang Medical University
      Ouroumtchi, Xinjiang Uygur Zizhiqu, China
    • Southern Medical University
      • Department of Anesthesiology
      Shengcheng, Guangdong, China
  • 2012–2014
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
    • FAW Group Corporation
      Changchun, Fujian, China
    • National Human Genome Research Institute
      Maryland, United States
    • Anhui Medical University
      • Institute of Dermatology
      Luchow, Anhui Sheng, China
    • Xinjiang Agricultural University
      新阳, Shaanxi, China
  • 2011–2014
    • Harbin Medical University
      • • Department of General Surgery
      • • Department of Neurosurgery
      Charbin, Heilongjiang Sheng, China
  • 2009–2014
    • Fourth Military Medical University
      • Department of Thoracic Surgery
      Xi’an, Liaoning, China
    • Southwest University in Chongqing
      Pehpei, Chongqing Shi, China
  • 2008–2014
    • Capital Medical University
      • Department of Neurosurgery
      Peping, Beijing, China
    • Nanjing Medical University
      • • Key Laboratory of Reproductive Medicine
      • • Department of Pediatrics
      Nan-ching, Jiangsu Sheng, China
  • 2013
    • Guangzhou Medical University
      Shengcheng, Guangdong, China
    • Beijing Shijitan Hospital
      Peping, Beijing, China
  • 2011–2013
    • Beijing Genomics Institute
      Bao'an, Guangdong, China
  • 2011–2012
    • Tianjin Medical University
      • Department of Radiology
      T’ien-ching-shih, Tianjin Shi, China
  • 2010–2012
    • Shandong University of Science and Technology
      Tsingtao, Shandong Sheng, China
  • 2009–2011
    • Jilin University
      • • College of Material Science and Engineering
      • • State Key Lab of Superhard Materials
      • • Department of Material Science and Engineering
      Yung-chi, Jilin Sheng, China
  • 2006–2008
    • Academy of Military Medical Sciences
      T’ien-ching-shih, Tianjin Shi, China