Tao Jiang

Beijing Neurosurgical Institute, Peping, Beijing, China

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Publications (296)1100.62 Total impact

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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; DOI:10.1007/s11060-015-1798-x · 2.79 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: 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 · 5.08 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
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    ABSTRACT: Wernicke's area is one of the most important language regions and has been widely studied in both basic research and clinical neurology. However, its exact anatomy has been controversial. In this study, we proposed to address the anatomy of Wernicke's area by investigating different connectivity profiles. First, the posterior superior temporal gyrus (STG), traditionally called “Wernicke's area”, was parcellated into three component subregions with diffusion MRI. Then, whole-brain anatomical connectivity, resting-state functional connectivity (RSFC) and meta-analytic connectivity modeling (MACM) analyses were used to establish the anatomical, resting-state and task-related coactivation network of each subregion to identify which subregions participated in the language network. In addition, behavioral domain analysis, meta-analyses of semantics, execution speech, and phonology and intraoperative electrical stimulation were used to determine which subregions were involved in language processing. Anatomical connectivity, RSFC and MACM analyses consistently identified that the two anterior subregions in the posterior STG primarily participated in the language network, whereas the most posterior subregion in the temporoparietal junction area primarily participated in the default mode network. Moreover, the behavioral domain analyses, meta-analyses of semantics, execution speech and phonology and intraoperative electrical stimulation mapping also confirmed that only the two anterior subregions were involved in language processing, whereas the most posterior subregion primarily participated in social cognition. Our findings revealed a convergent posterior anatomical border for Wernicke's area and indicated that the brain's functional subregions can be identified on the basis of its specific structural and functional connectivity patterns. Hum Brain Mapp, 2015. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 01/2015; 36(5). DOI:10.1002/hbm.22745 · 6.92 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 01/2015; 10(3):e0121380. DOI:10.1371/journal.pone.0121380 · 3.53 Impact Factor
  • Kun Yao, Xue-Ling Qi, Xi Mei, Tao Jiang
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    ABSTRACT: We describe a rare case of gliosarcoma with primitive neuroectodermal, osseous, cartilage and adipocyte differentiation. A 57-year-old man experienced a month history of headache, nausea and vomiting. Worse yet, the headache has become more severe for the past 6 days. Magnetic resonance (MR) images disclosed a lesion with operative indications located in the right frontal lobe. Then the tumor was macroscopically totally removed. Histologically, the tumor showed two kinds of components. One kind of the tumor cells appeared typical astrocytic tumor cells with anaplastic appearance. The other kind of the tumor cells appeared sheets of small round hyperchromatic cells, which presented a kind of pancreatic neuroendocrine tumor (PNET)-like structure. These sheets of small round cells were surrounded by a large number of relative-sparse-spindle cells. Multiple separate distinct areas of adipose tissue, osteoid matrix laid down and cartilage tissue were also identified. Immunohistochemically, a portion of typical astrocytic tumor cells and some small round hyperchromatic cells showed GFAP positivity. Small round hyperchromatic cells were positive for S-100, Fli-1, Nestin, MAP-2 and Syn. A large amount of relative sparse spindle cells (sarcomatous areas) were positive for vimentin. In addition, reticulin staining demonstrated expression of reticular fibers in relative-sparse-spindle cells areas but not in the astrocytic tumor cells and small round hyperchromatic cells areas. Molecular cytogenetic analyses demonstrated PTEN allele loss and no evidence of amplification of EGFR in both the astrocytic tumor cells, PNET-like structure and sparse spindle cells areas. These data suggest that this tumor was a gliosarcoma with primitive neuroectodermal, osseous, cartilage and adipocyte differentiation. To our knowledge, this is a rare gliosarcoma , reporting our additional new case would add to the better understanding of this tumor.
    International journal of clinical and experimental pathology 01/2015; 8(2):2079-84. · 1.78 Impact Factor
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    ABSTRACT: The majority of patients with low-grade glioma (LGG) experience epileptic seizures as their initial symptom, while the underlying mechanisms of tumor-related seizures are still far from being fully understood. In addition to tumor type and location, genetic changes of LGGs are considered to be influential factors in causing epileptic seizures. Nevertheless, the molecular biomarkers associated with tumor-related epilepsy have rarely been identified. RNA sequence data from 80 patients with histologically confirmed LGG were collected from the Chinese glioma genome atlas database and significant differences in expression levels of 33 genes were found. One of the genes, Very large G-protein-coupled receptor-1 (VLGR1), had been previously associated with seizures. Therefore, we investigated the association between LGG-related epilepsy and VLGR1, which played a role in idiopathic epilepsy. The level of VLGR1 expression was compared between patients with epileptic seizures and those without using the reads per kilobase transcriptome per million method. To evaluate the prognostic role of VLGR1 gene expression, the progression-free survival was determined by the Kaplan-Meier method and a multivariate Cox model. We demonstrated that VLGR1 had a significantly lower expression level in patients with epileptic seizures compared to seizure-free patients (p = 0.003). Furthermore, VLGR1 was highly associated with the presence of seizures in a multivariate statistical model. However, VLGR1 could not serve as an independent prognostic factor to determine progression-free survival of LGG patients. Based on RNA sequence data analysis, our results suggest that low expression of VLGR1 is a significant risk factor of epileptic seizures in patients with LGG.
    Journal of Neuro-Oncology 12/2014; 121(3). DOI:10.1007/s11060-014-1674-0 · 2.79 Impact Factor
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    ABSTRACT: The present paper aims to analyze the capabilities and limitations for retrieving vegetation water content from Landsat8 OLI (Operational Land Imager) sensor-new generation of earth observation program. First, the effect of soil background on canopy reflectance and the sensitive band to vegetation water content were analyzed based on simulated dataset from ProSail model. Then, based on vegetation water indices from Landsat8 OLI and field vegetation water content during June 1 2013 to August 14 2013, the best vegetation water index for estimating vegetation water content was found through comparing 12 different indices. The results show that: (1) red, near infrared and two shortwave infrared bands of OLI sensor are sensitive to the change in vegetation water content, and near infrared band is the most sensitive one; (2) At low vegetation coverage, solar radiation reflected by soil background will reach to spectral sensor and influence the relationship between vegetation water index and vegetation water content, and simulation results from ProSail model also show that soil background reflectance has a significant impact on vegetation canopy reflectance in both wet and dry soil conditions, so the optimized soil adjusted vegetation index (OSAVI) was used in this paper to remove the effect of soil background on vegetation water index and improve its relationship with vegetation water content; (3) for the 12 vegetation water indices, the relationship between MSI2 and vegetation water content is the best with the R-square of 0.948 and the average error of vegetation water content is 0.52 kg·m-2; (4) it is difficult to estimate vegetation water content from vegetation water indices when vegetation water content is larger than 2 kg·m-2 due to spectral saturation of these indices.
    Guang pu xue yu guang pu fen xi = Guang pu 12/2014; 34(12). DOI:10.3964/j.issn.1000-0593(2014)12-3385-06 · 0.27 Impact Factor
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    ABSTRACT: Patients with isocitrate dehydrogenase 1 (IDH1)-mutant glioblastoma exhibit increased survival compared with those with wild-type IDH1 tumors. The magnitude of this finding has led to the use of IDH1 mutations as diagnostic and prognostic biomarkers. However, the mechanisms underlying the reported correlation between the IDH1 mutation and increased survival have not been fully revealed. In this work, based on genome-wide transcriptional analyses of 69 Chinese patients with glioblastoma, we have found that the focal adhesion pathway is significantly downregulated in IDH1-mutant glioblastomas. The impaired focal adhesion leads to compromised cell migration and tumor invasion, contributing to the optimistic prognosis of these patients. Moreover, the signature genes of HIF-1α, the downstream factor of mutated IDH1, are found to be suppressed in IDH1-mutant gliomas. Given the role of HIF-1α in cell migration, we conclude that the attenuation of HIF-1α-dependent glioblastoma cell infiltration contributes to the better outcomes of patients with IDH1-mutant gliomas. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Cancer Letters 12/2014; 357(2). DOI:10.1016/j.canlet.2014.12.018 · 5.02 Impact Factor
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    ABSTRACT: Dengue has been well recognized as a global public health threat, but only sporadic epidemics and imported cases were reported in recent decades in China. Since July 2014, an unexpected large dengue outbreak has occurred in Guangdong province, China, resulting in more than 40000 patients including six deaths. To clarify and characterize the causative agent of this outbreak, the acute phase serum from a patient diagnosed with severe dengue was subjected to virus isolation and high-throughput sequencing (HTS). Traditional real-time RT-PCR and HTS with Ion Torrent PGM detected the presence of dengue virus serotype 2 (DENV-2). A clinical DENV-2 isolate GZ05/2014 was obtained by culturing the patient serum in mosquito C6/36 cells. The complete genome of GZ05/2014 was determined and deposited in GenBank under the access number KP012546. Phylogenetic analysis based on the complete envelope gene showed that the newly DENV-2 isolate belonged to Cosmopolitan genotype and clustered closely with other Guangdong strains isolated in the past decade. No amino acid mutations that are obviously known to increase virulence or replication were identified throughout the genome of GZ05/2014. The high homology of Guangdong DENV-2 strains indicated the possibility of establishment of local DENV-2 circulation in Guangdong, China. These results help clarify the origin of this epidemic and predict the future status of dengue in China.
    Science China. Life sciences 12/2014; 57(12):1149-55. DOI:10.1007/s11427-014-4782-3 · 1.51 Impact Factor

Publication Stats

3k Citations
1,100.62 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
  • 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
  • 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
  • 2003–2014
    • Beijing Institute of Microbiology and Epidemiology
      Peping, Beijing, China
    • Beijing Centers for Disease Control and Prevention
      Peping, Beijing, 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