Tao Jiang

Xinjiang Medical University, Ouroumtchi, Xinjiang Uygur Zizhiqu, China

Are you Tao Jiang?

Claim your profile

Publications (151)431.15 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Studies of gene rearrangements and the consequent oncogenic fusion proteins have laid the foundation for targeted cancer therapy. To identify oncogenic fusions associated with glioma progression, we catalogued fusion transcripts by RNA-seq of 272 WHO grade II, III, and IV gliomas. Fusion transcripts were more frequently found in high grade gliomas, in the classical subtype of gliomas, and in gliomas treated with radiation / temozolomide. 67 in-frame fusion transcripts were identified, including three recurrent fusion transcripts: FGFR3-TACC3, RNF213-SLC26A11, and PTPRZ1-MET (ZM). Interestingly, the ZM fusion was found only in grade III astrocytomas (1/13; 7.7%) or secondary GBMs (sGBMs, 3/20; 15.0%). In an independent cohort of sGBMs, the ZM fusion was found in 3 of 20 (15%) specimens. The fusion was additionally detected in 3 of 19 (16%) glioblastoma cell lines, confirming the recurrent nature of this transcript. Genomic analysis revealed that the fusion arose from translocation events involving introns 3 or 8 of PTPRZ and intron 1 of MET. ZM fusion transcripts were found in GBMs irrespective of isocitrate dehydrogenase 1 (IDH1) mutation status. sGBMs harboring ZM fusion showed higher expression of genes required for PIK3CA signaling and lowered expression of genes that suppressed RB1 or TP53 function. Expression of the ZM fusion was mutually exclusive with EGFR over-expression in sGBMs. Exogenous expression of the ZM fusion in the U87MG glioblastoma line enhanced cell-migration and invasion. Clinically, patients afflicted with ZM fusion harboring glioblastomas survived poorly relative to those afflicted with non-ZM harboring sGBMs (p<0.001). Our study profiles the shifting RNA landscape of gliomas during progression and reveled ZM as a novel, recurrent fusion transcript in sGBMs.
    Genome research. 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Glioblastoma (GBM) is the most aggressive and malignant glioma. Currently, a few modern surgical and medical therapeutic strategies are applied for GBM, but the prognosis of GBM patients remains poor, and the average median survival time is only 14.6 months. In this study, we for the first time found that the levels of miR-320a were decreased in both GBM patients and glioma cells. In GBM patients, elevated miR-320a expression was associated with better prognosis. In addition, insulin-like growth factor-1 receptor (IGF-1R) was identified as a key direct target of miR-320a. Overexpression of miR-320a led to the inhibition of cell proliferation, migration, invasion, as well as tumorigenesis by targeting IGF-1R, and thus regulated the signaling pathways downstream, including PI3K/AKT and MAPK/ERK. In tumor orthotopic xenograft experiment, the tumor growth was depressed and survival time of mice model was prolonged when miR-320a was overexpressed. Therefore, our results suggested that miR-320a could suppress tumor development and growth by targeting IGF-1R, and miR-320a might serve as a new effective target for anti-cancer therapy strategies.
    Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine. 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the present study, we assessed the efficiency of four BMSC transplantation methods as a therapy for liver failure. A rat model (80 Sprague-Dawley rats) of D-galactosamine (D-gal)/lipopolysaccharide (LPS)-induced acute liver failure (ALF) was established and the rats were divided into 5 groups: a hepatic artery injection group, a portal vein injection group, a vena caudalis injection group, an intraperitoneal injection group and a control group (16 per group). Following transplantation, the liver tissue and blood samples were collected on days 1, 3 and 7, we detected the EdU (5-ethynyl-2'-deoxyuridine)-labeled cells homing to the liver tissue and assessed the proliferating cell nuclear antigen (PCNA) and cysteine-containing aspartate-specific protease (caspase)-3 expression in the liver tissue and detected the levels of stromal cell-derived factor 1 (SDF-1) and hepatocyte growth factor (HGF) in the liver tissues. Compared with the control group, the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and damage to the liver tissue in the hepatic artery group, the portal vein group and the vena caudalis group improved in vivo. The expression of PCNA and HGF in the liver was higher and caspase-3 expression was lower in the hepatic artery injection group, the portal vein injection group and the vena caudalis injection group than that in the intraperitoneal injection and control groups. The EdU-labeled BMSCs were only observed homing to the liver tissue in these three groups. However, no significant differences were observed between these three groups. Liver function in the rats with ALF was improved following BMSC transplantation via 3 endovascular implantation methods (through the hepatic artery, portal vein and vena caudalis). These 3 methods were effective in transplanting BMSCs for the treatment of ALF. However, the selection of blood vessel in the implantation pathway does not affect the transplantation outcome. Transplantation via intraperitoneal injection showed no therapeutic effect in our animal experiments.
    International Journal of Molecular Medicine 08/2014; · 1.96 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Accumulating evidence has suggested that tumor location is linked to the genetic profile of gliomas. Therefore, the aim of this study was to investigate the anatomical characteristics of p53-mutated glioblastomas. We also sought to provide new insight into the possible niche locations of cells of glioblastoma origin. In order to accomplish this, preoperative magnetic resonance images from 163 patients with primary glioblastomas were retrospectively analyzed. All tumors were manually marked and registered to the standard space. Using the voxel-based lesion-symptom mapping approach, voxels exhibiting the strongest correlations with p53 mutants were identified. T-values of voxels that were greater than 95% of the permutations were factored into the results of the mapping analysis. Distinct anatomical characteristics between p53-mutated and wild-type glioblastomas were demonstrated using this approach. More specifically, we found that p53-mutated glioblastomas were preferentially located in the frontal lobe in the area surrounding the rostral extension of the lateral ventricles. The distinct anatomical characteristics of p53-mutated and wild-type glioblastomas provide further evidence that these gliomas arise from distinct niche locations.
    Journal of the neurological sciences. 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: O6-methylguanine DNA methyltransferase (MGMT) is one of the important tumor-related biomarkers and is considered to be a prognostic factor for glioblastoma. This study aimed to investigate the anatomical location of tumor-related MGMT protein expression in histologically confirmed de novo glioblastoma multiforme (GBM). Preoperative magnetic resonance images were retrospectively examined from GBM patients. Tumor tissues were manually segmented based on the structural image of each patient and subsequently registered to a standard brain atlas. Superimposition of the tumor tissues was carried out in patients with and without epigenetic changes. We used voxel-based lesion symptom mapping (VLSM) to identify the specific brain regions that were associated with level of MGMT protein expression. The tumors with low expression of MGMT protein and those with high expression of MGMT protein showed not significant differences in tumor size on T2 imaging. The VLSM analysis demonstrated that tumors with low expression of MGMT protein were more likely to occur in the right temporal-parietal lobe, while tumors with high expression of MGMT protein occurred more often in the left frontal lobe. Based upon VLSM data, our results suggest that the epigenetic changes, which occur during tumorigenesis, may have anatomical specificity. The identified correlation between molecular biomarkers and anatomical distribution underscores the current understanding of the biological characteristics of glioblastoma.
    Journal of Neuro-Oncology 07/2014; · 3.12 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Patients afflicted with low-grade glioma (LGG) frequently suffer from seizures. The mechanisms of seizure initiation in these patients remain poorly understood. Tumor location has been correlated with seizure initiation. However, these correlative studies relied on dichotomized data analysis based on arbitrary lobe assignments. As a result, the lesion-symptom correlation may be incorrectly interpreted. Here, we present the first study that used a voxel-wise quantitative lesion analysis to investigate the spatial correlation between tumor location and seizure susceptibility.
    Neuro-oncology. 07/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: As a crucial homologous recombination repair gene, RAD52 participates in maintenance of genomic stability and prevention of tumorigenesis. Although several cancer susceptibility RAD52 single nucleotide polymorphisms (SNPs) have been identified previously, little was known on how the RAD52 SNPs are involved in glioma development in Han Chinese. Therefore, we examined the association between five RAD52 SNPs (rs1051669, rs10774474, rs11571378, rs7963551 and rs6489769) and glioma risk using a case-control design. Odds ratios (ORs) and 95 % confidence intervals (CIs) were estimated by logistic regression. We found that only the RAD52 rs7963551 SNP was significantly associated with glioma risk, with the odds of having the rs7963551 AC or CC genotype in patients was 0.49 (95 % CI 0.37-0.65, P = 9.2 × 10(-6)) or 0.39 (95 % CI 0.18-0.81, P = 0.012) compared with the AA genotype. These data are consistent with functional relevance of allelic regulation of RAD52 expression by the rs7963551 SNP and miRNA let-7 in cancer cells. Stratified analyses elucidated that statistically significant association between glioma and rs7963551 SNP only existed in either astrocytic tumors (P = 6.3 × 10(-6)) or oligoastrocytic tumors (P = 0.002). In conclusion, our results support the hypothesis that genetic variants influencing miRNA-mediated regulation of tumor suppressor genes or oncogenes may contribute glioma susceptibility.
    Journal of Neuro-Oncology 07/2014; · 3.12 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Increasing evidence has indicated that microRNAs (miRNAs) are strongly implicated in the initiation and progression of glioblastoma multiforme (GBM). Here, we identified a novel tumor suppressive miRNA, miR-377, and investigated its role and therapeutic effect for GBM.
    Neuro-oncology. 06/2014;
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Aspergillosis of the central nervous system is a rare fungal infection that is mainly reported in patients with immune deficiency, such as AIDS patients and organ transplant patients treated with immunosuppressive agents, and is uncommon among patients with intact immune function. We report here a rare case of intracranial aspergillosis in a patient who had previously undergone a parietal lobe tumorectomy. Aspergillus fumigatus was confirmed by histopathology, and susceptibility tests reported that this infection should respond to voriconazole. We believe the immunosuppression resulting from surgical trauma and glucocorticosteroid treatment may be contributing to the infection, and therefore management of these two factors may improve the prognosis.
    World Journal of Surgical Oncology 06/2014; 12(1):181. · 1.09 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The death receptors Fas, p75(NTR) and DR6 are key components of extrinsically activated apoptosis. Characterization of how they interact with the adaptors is crucial in order to unravel the signalling mechanisms. However, the exact conformation that their intracellular death domain adopts upon binding downstream partners remains unclear. One model suggests that it adopts a typical compact fold, whilst a second model proposed an open conformation. Calmodulin (CaM), a major calcium sensor, has previously been reported to be one of the Fas adaptors that modulate apoptosis. This work reports that CaM also binds directly to the death domains of p75(NTR) and DR6, indicating that it serves as a common modulator of the death receptors. Two crystal structures of CaM in complexes with the corresponding binding regions of Fas and p75(NTR) are also reported. Interestingly, the precise CaM-binding sites were mapped to different regions: helix 1 in Fas and helix 5 in p75(NTR) and DR6. A novel 1-11 motif for CaM binding was observed in p75(NTR). Modelling the complexes of CaM with full-length receptors reveals that the opening of the death domains would be essential in order to expose their binding sites for CaM. These results may facilitate understanding of the diverse functional repertoire of death receptors and CaM and provide further insights necessary for the design of potential therapeutic peptide agents.
    Acta Crystallographica Section D Biological Crystallography 06/2014; 70(Pt 6):1604-1613. · 12.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: As a commonly mutated form of the epidermal growth factor receptor, EGFRvIII strongly promotes glioblastoma (GBM) tumor invasion and progression, but the mechanisms underlying this promotion are not fully understood.
    Neuro-oncology. 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Glioma is one of the most aggressive and lethal human brain tumors. Accumulating evidence shows that microRNAs play important roles in cancers, including glioma. Previous studies reported that miR-124 levels were downregulated in glioma specimens. Here, we further investigate the potential role of miR-124 in glioma.
    Neuro-oncology. 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recent genome-wide association studies have identified several leukocyte telomere length (LTL)-related single nucleotide polymorphisms (SNPs). Our previous data demonstrated that two SNPs (rs398652 on 14q21 and rs621559 on 1p34.2) were associated with LTL and risk of esophageal squamous cell carcinoma in Chinese. However, the role of these genetic variants on glioma risk is still unknown. Therefore, we examined if these genetic variants have impact on the genetic susceptibility of glioma in Chinese. On the basis of analyzing 404 glioma patients and frequency-matched 820 controls, we found that subjects having the 1p34.2 rs621559 AG or GG genotype had an OR of 1.82 (95 % CI = 1.07-3.09, P = 0.026) or 2.12 (95 % CI = 1.26-3.56, P = 0.005) for developing glioma, respectively, compared with subjects having the rs621559 AA genotype. Similarly, the 14q21 rs398652 AG or GG genotype was associated with increased glioma risk (OR = 1.39, 95 % CI = 1.07-1.80, P = 0.012; OR = 1.52, 95 % CI = 1.04-2.20, P = 0.029) compared to AA genotype. In all, our results highlight the possible role of telomere in carcinogenesis.
    Journal of Neuro-Oncology 05/2014; · 3.12 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypermethylation of tumor suppressor promoters is generally accepted to indicate poor prognosis in glioma; however, the DNA methylation patterns associated with different glioma prognoses remain to be elucidated. In the present study, promoter methylation and gene expression microarrays were used to screen candidate genes between different grades of glioma. Survival analysis was performed using the Kaplan‑Meier (KM) method. Promoter methylation and protein expression of phosphodiesterase 4C (PDE4C) was examined in different grade gliomas and the correlation between PDE4C and wild-type (WT) p53 was evaluated in glioma cell lines. In addition, gene ontology and gene set variation analysis were used to examine PDE4C function. We found PDE4C exhibited promoter hypermethylation in high-grade glioma samples and hypomethylation in low-grade glioma, with PDE4C expression levels showing the reverse. This indicated PDE4C may be a candidate glioma biomarker. Through studies of PDE4C methylation and expression status in an independent cohort of 124 patient samples (56 low-grade and 63 high-grade glioma and 5 normal brain), we identified PDE4C as having significant promoter methylation and lower expression in high-grade glioma. Hypermethylation and reduced PDE4C protein expression were associated with grade progression and overall survival. In glioma cell lines, PDE4C was upregulated by demethylation treatment with 5-Aza-2'-deoxycytidine and WT p53 expression was downregulated after PDE4C siRNA suppression. Finally, we found PDE4C promoted apoptosis and inhibited migration in a U87 cell line. On the basis of these observations and the results from subset analysis, it is reasonable to conclude that PDE4C may function as a tumor suppressor by promoting apoptosis through the WT p53 pathway and inhibiting cell migration. The data show that PDE4C is downregulated through promoter hypermethylation in glioma.
    Oncology reports. 05/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: MGMT expression is a critical determinant for therapeutic resistance to DNA alkylating agents. We previously demonstrated that MGMT expression is post-transcriptionally regulated by miR-181d and other miRNAs. Here, we performed a genome-wide screen to identify MGMT regulating miRNAs. Candidate miRNAs were further tested for inverse correlation with MGMT expression in clinical specimens. We identified 15 candidate miRNAs and characterized the top candidate, miR-603. Transfection of miR-603 suppressed MGMT mRNA/protein expression in vitro and in vivo; this effect was reversed by transfection with antimiR-603. miR-603 affinity-precipitated with MGMT mRNA and suppressed luciferase activity in an MGMT-3'UTR-luciferase assay, suggesting direct interaction between miR-603 and MGMT 3'UTR. miR-603 transfection enhanced the temozolomide (TMZ) sensitivity of MGMT-expressing glioblastoma cell lines. Importantly, miR-603 mediated MGMT suppression and TMZ resistance were reversed by expression of an MGMT cDNA. In a collection of 74 clinical glioblastoma specimens, both miR-603 and miR-181d levels inversely correlated with MGMT expression. Moreover, a combined index of the two miRNAs better reflected MGMT expression than each individually. These results suggest that MGMT is co-regulated by independent miRNAs. Characterization of these miRNAs should contribute toward strategies for enhancing the efficacy of DNA alkylating agents.
    Oncotarget 05/2014; · 6.64 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: VgrG proteins form the spike of the type VI secretion system (T6SS) syringe-like complex. VgrG3 of Vibrio cholerae degrades the peptidoglycan cell wall of rival bacteria via its C-terminal region (VgrG3C) through its muramidase activity. VgrG3C consists of a peptidoglycan-binding domain (VgrG3C(PGB)) and a putative catalytic domain (VgrG3C(CD)), and its activity can be inhibited by its immunity protein partner TsiV3. Here, the crystal structure of V. cholerae VgrG3C(CD) in complex with TsiV3 is presented at 2.3 Å resolution. VgrG3C(CD) adopts a chitosanase fold. A dimer of TsiV3 is bound in the deep active-site groove of VgrG3C(CD), occluding substrate binding and distorting the conformation of the catalytic dyad. Gln91 and Arg92 of TsiV3 are located in the centre of the interface and are important for recognition of VgrG3C. Mutation of these residues destabilized the complex and abolished the inhibitory activity of TsiV3 against VgrG3C toxicity in cells. Disruption of TsiV3 dimerization also weakened the complex and impaired the inhibitory activity. These structural, biochemical and functional data define the molecular mechanism underlying the self-protection of V. cholerae and expand the understanding of the role of T6SS in bacterial competition.
    Acta Crystallographica Section D Biological Crystallography 04/2014; 70(Pt 4):1094-103. · 12.67 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective To investigate the changes in the expression levels of CCCH zinc finger type-containing 12D(Zc3h12d) gene in lung tissues of rats with acute lung injury (ALI) induced by small intestinal ischemia-reperfusion (IIRI). Methods Forty healthy male Sprague-Dawley (SD) rats were equally randomized into sham-operated group (control), 30-minute IIRI group, 60-minute IIRI group, 120-minute IIRI group. Rats in the IIRI groups were subjected to 60 minutes of superior mesenteric artery (SMA) occlusion and to reperfusion for 30, 60 and 120 minutes, respectively. Then the rats were sacrificed. Their lung tissues and sera were obtained, respectively. The lung tissues were examined for wet/dry (W/D) lung mass ratios and pathological changes through HE staining. The levels of TNF-α and IL-1β in sera and lung tissue homogenates were detected by ELISA. The dynamic expression of Zc3h12d mRNA and protein in lung tissues was assayed by real-time quantitative PCR (qRT-PCR), immunohistochemistry and Western blotting. Results Compared with the control group, IIRI groups presented the thickening of alveolar wall, the hemorrhage of alveolar space and the increased W/D ratios (P<0.05). qRT-PCR, immunohistochemistry and Western blotting showed that the expression of Zc3h12d mRNA and protein significantly decreased (P<0.05) after 120-minute reperfusion. Conclusion IIRI can down-regulate Zc3h12d gene expression in lung tissue, which implies that Zc3h12d protein may protect rats from IIRI-induced ALI.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 04/2014; 30(4):355-9.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Astrocytic tumors are the most common primary brain tumors in adults. ATRX mutations have been identified in gliomas and are correlated with its loss of expression, which causes alternative lengthening of telomeres (ALT) leading to genomic instability. In this study, we aimed to explore the role of ATRX mRNA expression alteration in the progression and subclassification of astrocytic tumors and examine its impact on clinical outcome. We investigated ATRX mRNA expression and its association with IDH1 and IDH2 mutations in 169 adult astrocytic tumors using whole transcriptome sequencing. In our cohort, low ATRX mRNA expression was detected in 68% of astrocytomas, 50% of anaplastic astrocytomas and 41.6% of glioblastomas. Low ATRX expression closely overlapped with mutations in IDH1/2 (P<0.0001) in astrocytic tumors across WHO grades II-IV. Significant association between low ATRX expression and longer overall survival was identified in our cohort (P<0.01). ATRX combined with IDH1/2 and Ki-67 was used to re-classify patients with astrocytic tumors: group A1 containing IDH1/2 mutations and low ATRX expression predicted a better prognostic outcome, whereas group A3 carrying wild-type IDH1/2 and high Ki-67 expression had the shortest overall survival; IDH-mutant tumors with low ATRX expression and IDH-wild-type tumors with high Ki-67 expression were grouped into group A2. In summary, our results showed that ATRX in cooperation with IDH1/2 and Ki-67 defines three subgroups of astrocytic tumors regardless of the conventional WHO grades consensus. The molecular stratification in astrocytic tumors may aid in treatment strategy selection, therapeutic trial design, and clinical prognosis evaluation.
    Oncotarget 03/2014; · 6.64 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Epidermal growth factor receptor (EGFR) is amplified in 40% of human glioblastomas. However, most glioblastoma patients respond poorly to anti-EGFR therapy. MicroRNAs can function as either oncogenes or tumor suppressor genes, and have been shown to play an important role in cancer cell proliferation, invasion and apoptosis. Whether microRNAs can impact the therapeutic effects of EGFR inhibitors in glioblastoma is unknown. miR-566 expression levels were detected in glioma cell lines, using real-time quantitative RT-PCR (qRT-PCR). Luciferase reporter assays and Western blots were used to validate VHL as a direct target gene of miR-566. Cell proliferation, invasion, cell cycle distribution and apoptosis were also examined to confirm whether miR-566 inhibition could sensitize anti-EGFR therapy. In this study, we demonstrated that miR-566 is up-regulated in human glioma cell lines and inhibition of miR-566 decreased the activity of the EGFR pathway. Lentiviral mediated inhibition of miR-566 in glioblastoma cell lines significantly inhibited cell proliferation and invasion and led to cell cycle arrest in the G0/G1 phase. In addition, we identified von Hippel-Lindau (VHL) as a novel functional target of miR-566. VHL regulates the formation of the beta-catenin/hypoxia-inducible factors-1alpha complex under miR-566 regulation. miR-566 activated EGFR signaling and its inhibition sensitized glioblastoma cells to anti-EGFR therapy.
    Molecular Cancer 03/2014; 13(1):63. · 5.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dissolved organic matter (DOM) is a very important component in terrestrial ecosystem, which also plays a key role in geo-environmental chemistry. A number of DOM samples were extracted from soils and sediments samples obtained from typical water-level fluctuation zones of Three Gorges reservoir areas. Ultraviolet-visible (UV-Vis) absorption spectra were recorded for unveiling the geochemical characteristics of DOM based on specific absorption parameters and fitting models. Through the results of specific absorption parameters, it was suggested that the aromaticity, hydrophobicity and humification degree were lower in soils than in the surface sediments, which were also independent of the sampling location height and land-use types. Among the four absorption models selected, model 2 was the optimal. Meanwhile, different models and fitting wavelengths also significantly affected the absorption spectral slope (S value): S increased with the decreasing wavelength. Additionally, the correlation among different S values obtained from different fitting wavelength ranges was significantly different suggesting that the S values in various wavelength ranges only indicated the tip of the iceberg of DOM characteristics instead of the entirety. Furthermore, the ratio of specific spectral slope (S(R)) indicated lower degradation (photo-bleaching or microbial degradation) degree in the surface sediments as compared to those in soils and older sediments. The surface sediments had higher aromaticity, hydrophobicity, molecular weight and photochemical/ biodegradation activity potentials, suggesting fresher DOM, lower effect of photobleaching and microbial degradation activities.
    03/2014; 35(3):933-41.

Publication Stats

906 Citations
431.15 Total Impact Points

Institutions

  • 2014
    • Xinjiang Medical University
      Ouroumtchi, Xinjiang Uygur Zizhiqu, China
  • 2013–2014
    • Chinese Academy of Sciences
      • Institute of Biophysics
      Peping, Beijing, China
  • 2010–2014
    • Fourth Military Medical University
      • • Department of Thoracic Surgery
      • • Department of Pharmacology
      Xi’an, Liaoning, China
    • Southwest University in Chongqing
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Beijing Neurosurgical Institute
      Peping, Beijing, China
  • 2005–2014
    • Beijing Tiantan Hospital
      Peping, Beijing, China
  • 2012–2013
    • Beijing Shijitan Hospital
      Peping, Beijing, China
    • Capital Medical University
      • Department of Neurosurgery
      Beijing, Beijing Shi, China
    • Tianjin Huanhu Hospital
      T’ien-ching-shih, Tianjin Shi, China
  • 2011–2013
    • Nanjing Medical University
      • Department of Neurosurgery
      Nanjing, Jiangsu Sheng, China
  • 2007–2013
    • Northeast Institute of Geography and Agroecology
      • • National Laboratory of Biomacromolecules
      • • Institute of Automation
      Peping, Beijing, China
  • 2008–2012
    • Harbin Medical University
      • • Department of Neurosurgery
      • • Department of Immunology
      Harbin, Heilongjiang Sheng, China
  • 2010–2011
    • Tianjin Medical University
      T’ien-ching-shih, Tianjin Shi, China