Wei Zhang

Third Military Medical University, Ch’ung-ch’ing-shih, Chongqing Shi, China

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Publications (487)1285.53 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Recent cases of human infection with avian influenza H5N1 and H7N9 viruses underscore an urgent need for techniques that can rapidly assess their potential threat to the humans. Determination of the receptor-binding property of influenza virus is crucial to direct viral control and prevention measures. Current methods to perform this analysis are dependent on immunoanalytical strategies that use instable biological components and complex procedures. We have developed a facile colorimetric assay to determine the interaction of the viral hemagglutinin (HA) protein with host glycan receptors using glycan-functionalized gold nanoparticles (gGNPs). This method is based on the color and absorbance changes of gold probes when the solution is simply mixed with HAs or intact viruses. The resulting sensitivity and selectivity has enabled HAs/viruses binding to various glycan structures to be differentiated visually and rapidly. Using this system, we have screened, in parallel, the receptor specificity of eight representative human and avian viral HAs, and three whole viruses including an emerging H7N9 strain. Our results reveal the detailed receptor-binding profiles of H7N9 virus and its HA, and show that they effectively bind to human-type receptors. This gGNP-based assay represents a strategy that would be helpful for developing simple and sensitive systems to probe glycan-mediated biological processes.
    ACS Nano 04/2014; · 12.06 Impact Factor
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    ABSTRACT: 2,4,6-Trinitrotoluene (TNT) is a widely used nitroaromatic explosive with significant detrimental effects on the environment and human health. Its detection is of great importance. In this study, both electrochemiluminescence (ECL)-based detection of TNT through the formation of a TNT-amine complex and the detection of TNT through electrochemiluminescence resonance energy transfer (ECRET) are developed for the first time. 3-Aminopropyltriethoxysilane (APTES)-modified [Ru(phen)3 ](2+) (phen=1,10-phenanthroline)-doped silica nanoparticles (RuSiNPs) with uniform sizes of (73±3) nm were synthesized. TNT can interact with APTES-modified RuSiNPs through charge transfer from electron-rich amines in the RuSiNPs to the electron-deficient aromatic ring of TNT to form a red TNT-amine complex. The absorption spectrum of this complex overlaps with the ECL spectrum of the APTES-modified RuSiNPs/triethylamine system. As a result, ECL signals of the APTES-modified RuSiNPs/triethylamine system are turned off in the presence of TNT owing to resonance energy transfer from electrochemically excited RuSiNPs to the TNT-amine complex. This ECRET method has been successfully applied for the sensitive determination of TNT with a linear range from 1×10(-9) to 1×10(-6) M with a fast response time within 1 min. The limit of detection is 0.3 nM. The method exhibits good selectivity towards 2,4-dinitrotoluene, p-nitrotoluene, nitrobenzene, phenol, p-quinone, 8-hydroxyquinoline, p-phenylenediamine, K3 [Fe(CN)6 ], Fe(3+) , NO3 (-) , NO2 (-) , Cr(3+) , Fe(2+) , Pb(2+) , SO3 (2-) , formaldehyde, oxalate, proline, and glycine.
    Chemistry 03/2014; · 5.93 Impact Factor
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    ABSTRACT: A facile seedless growth method for high-yield synthesis of monodisperse gold nanorods using binary surfactant mixtures is reported for the first time. In comparison with other seedless methods, the present method enables the preparation of gold nanorods with much better monodispersity. Moreover, the present seedless growth method enables the preparation of not only thin gold nanorods but also thick gold nanorods which cannot be prepared by other reported seedless methods. Dark-field microscopy measurements of a single gold nanorod indicate that the thicker gold nanorod shows enhanced scattering properties.
    Nanotechnology 02/2014; 25(12):125601. · 3.84 Impact Factor
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    ABSTRACT: Spinal cord injury (SCI) usually leads to severe sensory and motor deficits below the spinal lesion. Previous animal models have shown significant atrophic changes in the neural sensorimotor system following SCI. However, specific anatomical changes in the human brain following SCI remain poorly understood. The purpose of the present study was to investigate structural changes during the early stage of SCI, and to investigate further the association between the structural changes and patients' sensorimotor functions. The study participants included 20 patients with SCI and 30 matched healthy controls. The mean period post-SCI was 8.9 ± 2.7 weeks (range 4-12 weeks). Voxel-based morphometry was used to investigate the regions with grey and white matter volume changes. Compared to healthy controls, patients with SCI showed significant grey matter atrophy in the primary motor cortex (M1), primary somatosensory cortex (S1), supplementary motor area (SMA), and thalamus, as well as white matter atrophy in the corticospinal tracts at the level of the bilateral cerebral peduncles. In addition, grey matter volume in the primary motor cortex was positively correlated with the total American Spinal Injury Association motor score in patients with SCI. In conclusion, our findings suggest that SCI causes significant anatomical changes in the human sensorimotor system, and that these anatomical changes may occur in the early phase of SCI. Future treatments that aim to restore sensorimotor functions following SCI need to attend to these anatomical changes in the brain.
    Neuroscience 02/2014; · 3.12 Impact Factor
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    ABSTRACT: Octahedrally shaped NiO powders have been synthesized via a one-step composite-hydroxide-mediated method without any surfactant. The synthesized materials are characterized by XRD, EDS, TEM and FESEM techniques. Each particle exhibited a nearly perfect octahedron shape with sharp edges and corners as well as smooth surfaces. The octahedral NiO particles performed better gas-sensitivity toward ethanol than that of NiO nanopowders, which was attributed to the exposed {111} facets of octahedron. The result was confirmed by the first-principle calculation which indicated that the (111) facet was more active than (100) and (110) facet.
    Crystal Research and Technology 02/2014; · 1.12 Impact Factor
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    ABSTRACT: Ticagrelor (TIC) is the first reversible P2Y12 receptor antagonist that exhibits rapid antiplatelet effect by indirect inhibition of the GPIIb/IIIa complex. Polymorphisms in genes coding GPIIb/IIIa, namely ITGA2B and ITGB3, are associated with aspirin resistance and risk for thrombotic diseases. We assessed whether ITGA2B and ITGB3 polymorphisms can influence the ex vivo antiplatelet activity of ticagrelor in Chinese population. A total of 196 healthy Chinese male individuals were recruited. ADP-induced platelet aggregation was determined using optical aggregometry at baseline and after incubation of the platelet-rich plasma with 15 and 50 μM ticagrelor, respectively. Single nucleotide polymorphisms in ITGA2B (rs5911 G>T) and ITGB3 (rs4642 A>G and rs4634 G>A) were genotyped by sequencing. TIC at both concentrations of 15 and 50 μM decreased ADP-induced platelet aggregation significantly (P < 0.05, respectively). As compared to ITGA2B rs5911 GG homozygotes, individuals with the rs5911 TG genotype showed significantly increased inhibition of platelet aggregation (IPA) by both 15 and 50 μM ticagrelor incubation (P < 0.05, respectively). Neither rs4642 nor rs4634 polymorphism affected ticagrelor-induced IPA. We suggest that the ITGA2B rs5911 GG genotype is associated with decreased ex vivo antiplatelet activity of ticagrelor in healthy Chinese male subjects.
    International journal of hematology 01/2014; · 1.17 Impact Factor
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    ABSTRACT: Pseudoginsenoside-F11 (PF11), an ocotillol-type ginsenoside, has been shown to possess significant neuroprotective activity. Since microglia-mediated inflammation is critical for induction of neurodegeneration, this study was designed to investigate the effect of PF11 on activated microglia. PF11 significantly suppressed the release of ROS and proinflammatory mediators induced by LPS in a microglial cell line N9 including NO, PGE2, IL-1β, IL-6 and TNF-α. Moreover, PF11 inhibited interaction and expression of TLR4 and MyD88 in LPS-activated N9 cells, resulting in an inhibition of the TAK1/IKK/NF-κB signaling pathway. PF11 also inhibited the phosphorylation of Akt and MAPKs induced by LPS in N9 cells. Importantly, PF11 significantly alleviated the death of SH-SY5Y neuroblastoma cells and primary cortical neurons induced by the conditioned-medium from activated microglia. At last, the effect of PF11 on neuroinflammation was confirmed in vivo: PF11 mitigated the microglial activation and proinflammatory factors expression obviously in both cortex and hippocampus in mice injected intrahippocampally with LPS. These findings indicate that PF11 exerts anti-neuroinflammatory effects on LPS-activated microglial cells by inhibiting TLR4-mediated TAK1/IKK/NF-κB, MAPKs and Akt signaling pathways, suggesting its therapeutic implication for neurodegenerative disease associated with neuroinflammation.
    Neuropharmacology 01/2014; · 4.11 Impact Factor
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    ABSTRACT: Studies implicate a potential role for EAF1 in MLL-ELL induced leukemogenesis; however the biological function of EAF1 in this process remains unknown. In this study, we show that knockdown of zebrafish eaf1 by morpholinos caused serious defects in both primitive and definitive hematopoiesis. Using microarray analysis, we identified foxo3b as a target gene suppressed by eaf1. Ectopic expression of foxo3b in embryos mimicked the phenotypes exhibited in eaf1 morphants, except that foxo3b had no effect on runx1 and c-myb expression while eaf1 morphants did not express these markers in the ventral wall of dorsal aorta. Subsequent experiments showed that a dominant negative form of foxo3b (dn-foxo3b) partially restored primitive hematopoietic defects in eaf1 morphants, suggesting that foxo3b might serve as a key factor for mediating eaf1 function in primitive hematopoiesis. Furthermore, we observed that foxo3b inhibited the transcriptional activity of gata1 and spi1 through protein-protein interaction. Our findings not only suggest a function of eaf1 on hematopoiesis in vivo, but also reveal a novel regulatory pathway, eaf1-foxo3b-gata1/spi1, that may shed light on the role of EAF1 in MLL-ELL induced leukemogenesis.
    Developmental Biology 01/2014; · 3.87 Impact Factor
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    ABSTRACT: Acute lymphoblastic leukemia (ALL) is the most frequently occurring malignant neoplasm in children. Despite advances in treatment and outcomes for ALL patients, the pathogenesis of the disease remains unclear. Microarray analysis of samples from 100 Chinese children with ALL revealed the up-regulation of CTCF (CCCTC binding factor). CTCF is a highly conserved 11-zinc finger protein that is involved in many human cancers; however, the biological function of CTCF in pediatric ALL is unknown. The expression patterns of CTCF were evaluated in matched newly diagnosed (ND), complete remission (CR), and relapsed (RE) bone marrow samples from 28 patients. The potential oncogenic mechanism of CTCF and related pathways in leukemogenesis were investigated in leukemia cell lines. We identified significant up-regulation of CTCF in the ND samples. Importantly, the expression of CTCF returned to normal levels after CR but rebounded in the RE samples. In the pre-B ALL cell line Nalm-6, siRNA-mediated silencing of CTCF expression promoted cell apoptosis and reduced cell proliferation; accordingly, over-expression of a cDNA encoding full-length CTCF protected cells from apoptosis and enhanced cell proliferation. Furthermore, inhibition or activation of the nuclear factor-kappa B (NF-kappaB) pathway resulted in marked variations in the levels of CTCF mRNA and protein in leukemic cells, indicating that CTCF may be involved downstream of the NF-kappaB pathway. Moreover, inhibition of the NF-kappaB pathway increased cell apoptosis, which was partially rescued by ectopic over-expression of CTCF, suggesting that CTCF may play a significant role in the anti-apoptotic pathway mediated by NF-kappaB. Our results indicate that CTCF serves as both an anti-apoptotic factor and a proliferative factor in leukemic cells. It potentially contributes to leukemogenesis through the NF-kappaB pathway in pediatric ALL patients.
    Molecular Cancer 01/2014; 13(1):5. · 5.13 Impact Factor
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    ABSTRACT: We report the nucleotide sequence of a novel blaKPC-2-harboring IncNplasmid, pECN580, from a multidrug-resistant Escherichia coli ST131 isolate recovered from Beijing, China. pECN580 harbors multiple antimicrobial resistance genes, including blaKPC-2, blaCTX-M-3, blaTEM-1, aac(6')-Ib-cr, qnrS1, arr-3 and dfrA14 that confer β-lactam, aminoglycoside, quinolone, rifampin and trimethoprim resistance. The emergence of blaKPC-2-harboring multidrug-resistant plasmid in epidemic E. coli ST131 clone poses a significant potential threat for both community and hospital settings.
    Antimicrobial Agents and Chemotherapy 01/2014; · 4.57 Impact Factor
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    ABSTRACT: Researches have revealed that the endothelial nitric oxide synthase (eNOS) gene G894T polymorphism is associated with the risk of Myocardial infarction (MI), but the results remain conflicting. A meta-analysis was conducted to investigate the association between eNOS G894T polymorphism and MI. Published studies from PubMed, Embase, CNKI and CBM databases were retrieved. The pooled odds ratios (ORs) for the association between eNOS G894T polymorphism and MI and their corresponding 95% confidence intervals (CIs) were estimated using the random- or fixed- effect model. A total of 34 studies including 8229 cases and 12839 controls were identified for the meta-analysis. The eNOS G894T polymorphism was significantly associated with MI under a homozygous genetic model (OR = 1.41, 95% CI = 1.08-1.84; P = 0.012), a recessive genetic model (OR = 1.35, 95% CI = 1.06-1.70; P = 0.014), a dominant genetic model (OR = 1.18, 95% CI = 1.04-1.34; P = 0.009). In the subgroup analysis by ethnicity (non-Asian and Asian), no significant association was observed between eNOS G894T polymorphism and MI risk among non-Asians (P>0.05), but a positive significant association was found among Asians (P<0.05). The eNOS G894T polymorphism is associated with increased MI risk in Asians. The results indicate that ethnicity plays important roles in the association between eNOS G894T polymorphism and MI.
    PLoS ONE 01/2014; 9(1):e87196. · 3.73 Impact Factor
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    ABSTRACT: The androgen receptor (AR) plays a pivotal role in prostate homeostasis and prostate cancer development. To understand the mechanism underlying the regulation of AR holds a promise for developing novel therapeutic approaches for prostate cancer. Here, we show that the Von Hippel-Lindau gene product, pVHL, physically interacts with AR and inhibits AR transcription activity, but does not induce AR turnover. Moreover, pVHL also suppresses androgen-induced cell proliferation, implicating a physiological role of pVHL in androgen-induced signaling pathway. In addition, we provide evidences to show that pVHL actually enhance AR de-ubiquitination instead of inducing AR ubiquitination, uncovering a non-canonical role of pVHL in the ubiquitin proteasome pathway. Our data reveal a novel function of pVHL in the regulation of AR transcription activity, which may expand the scope of pVHL in tumor suppression and provide mechanistic insight into prostate cancer initiation and progression.
    Molecular Endocrinology 01/2014; · 4.75 Impact Factor
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    ABSTRACT: Combination of low doses of histone deacetylases inhibitors and chemotherapy drugs is considered as one of the most promising strategies to increase the anticancer efficacy. Chidamide is a novel benzamide chemical class of HDAC inhibitor that selectively inhibited HDAC1, 2, 3 and 10. We sought to determine whether chidamide may enhance platinum-induced cytotoxicity in NSCLC cells. In this study, the combination of chidamide with carboplatin showed a good synergism on growth inhibition with the mean combination index value as 0.712 and 0.639 in A549 and NCI-H157 cells, respectively. The used concentration of chidamide was non-toxic on cells by itself as low as 0.3 μM. All of our experiments were comparisons between combination regimen and single carboplatin regimen in A549 and NCI-H157 cell lines. Phosphorylated histone H2A.X (γH2A.X), a hall marker of DNA damage response, was dramatically increased by the combination treatment. Cell cycle analysis by flow cytometry and phosphorylation level analysis of histone H3 (Ser10) by western blotting showed that combination treatment significantly increased the percentage of G2/M phase of cells. Mitochondrial membrane potential and cleaved-PARP1 level analysis indicate that chidamide synergistically enhances carboplatin-induced apoptosis. Additionally, synergistic effects of chidamide were found when it was combined with two other platinum drugs (cisplatin and oxaliplatin). The results suggest that Chidamide in combination with platinum drugs may be a novel therapeutic option for NSCLC.
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 01/2014; · 2.24 Impact Factor
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    ABSTRACT: Abstract An orthogonal experiment (form L16(45)) was used to investigate how the soil nematode community (density, diversity, and faunal structure) and soil health were affected by hybrid napiergrass management. The experiment included four levels of the each of the following main factors: nitrogen fertilization, cutting frequency, cutting intensity, and irrigation. The soil nematode community was affected more by nitrogen fertilization and irrigation than by cutting frequency and cutting intensity. Hybrid napiergrass develops a large root system and the carbon stored in the roots might have buffered any adverse effects of cutting on soil nematodes in the present study. The responses to fertilization indicated that fertilization had both positive and negative effects on the soil community and that the net effect depended on the level of fertilization. Additional water applied in irrigation was detrimental to soil nematode communities in that it might reduce the oxygen content of soil and also increases the potential for the leaching of nutrients from soil. Additionally, we suggest that moderate N fertilization (460 kg ha−1 yr−1), moderate irrigation (one time yr−1 during the dry season), and cutting (three times per year at 20 cm height) will maintain soil health and provide substantial hybrid napiergrass yields.
    Applied Soil Ecology 01/2014; 75:134-144. · 2.11 Impact Factor
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    ABSTRACT: The population of the plateau zokor (Myospalax fontanierii) rapidly increases on the degraded alpine meadows of Qinghai–Tibetan Plateau. The burrowing and feeding activities of plateau zokor exert huge effects on the plant community and soil properties. However, the possible effects on the production and consumption of greenhouse gases have not been investigated. To evaluate the effects, we measured the ecosystem respiration (Re), soil methane (CH4) and nitrous oxide (N2O) fluxes and the main soil, vegetation and environmental factors of zokor mounds of different excavation years (one-, two- and three to five-year, hereafter referred to as ZM1, ZM2 and ZM3–5) and surrounding control meadow (CM) in a typical Kobresia humilis meadow from July to November 2012. The cumulative Re, CH4 uptake and N2O emissions were 1.82 ± 0.28, 2.83 ± 0.48, 3.13 ± 0.13 and 3.91 ± 0.27 ton C ha−1, 1.55 ± 0.27, 1.33 ± 0.15, 1.20 ± 0.16 and 1.02 ± 0.25 kg C ha−1 and 0.23 ± 0.02, 0.10 ± 0.04, 0.08 ± 0.01 and 0.07 ± 0.02 kg N ha−1 for ZM1, ZM2, ZM3–5 and CM, respectively. The soil CH4 uptake and N2O emission were stimulated and the Re was inhibited for ZM1, ZM2 and ZM3–5 as compared to the CM. If the distribution area of zokor mounds increased from 2% to 6%, the combined CO2-equivalent of CH4 and N2O exchanges strengthened 3.2 times. Furthermore, the composition of plant community altered; the plant biomass, topsoil organic carbon content, temperature and moisture decreased; and the topsoil gas permeability, inorganic nitrogen and dissolved organic carbon contents increased on zokor mounds as compared to the CM (P < 0.05). The recovery process of the vegetation and soil organic carbon pools of zokor mounds requires many years (>10 years). In view of the loss of soil organic carbon and the stimulation of N2O emission, the increasing distribution area of zokor mounds weaken the function of alpine meadows on the Qinghai–Tibetan Plateau as a greenhouse gas sink.
    Soil Biology and Biochemistry 01/2014; 71:105–112. · 3.65 Impact Factor
  • Hao Li, Wei Zhang, Honghao Zhou
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    ABSTRACT: An antibody-based electrochemical biosensing platform was developed and used for the detection of protein. In the presence of the target, antibody pair bound to the protein simultaneously, which caused two oligo-DNA conjugated with antibody pair to hybridize each other and became a big "stem-loop" structure. Subsequently, the longer oligo-DNA of the "stem" with a methylene blue (MB) label at the terminal hybridized stably with capture DNA due to the enhancement of base stacking. The strong redox current signal of MB was used for protein quantification. Using Alfa-fetoprotein (AFP) as a model, the proposed method could detect AFP at a concentration as low as 2 pg mL(-1) with a dynamic range of 4 orders of magnitude, which approached to the traditional assays such as enzyme-linked immunosorbent assay (ELISA).
    Analytical Biochemistry 12/2013; · 2.58 Impact Factor
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    ABSTRACT: ELL was first identified as a translocation partner of MLL in acute myeloid leukemia; however, the exact mechanism of its action has remained elusive. In this study, we identified ELL as a direct downstream target gene of E2F1. Co-immunoprecipitation assays show that ELL interacted with E2F1 in vitro and in vivo, leading to inhibition of E2F1 transcriptional activity. In addition, ELL enhanced E2F1 deacetylation via recruitment of HDAC1. Notably, MLL-ELL fusion protein lost the inhibitory role on E2F1 transcriptional activity. Furthermore, DNA damage induced ELL in an E2F1-dependent manner and ELL protected cell against E2F1-dependent apoptosis. Our findings not only connect ELL to E2F1 function and uncover a novel role of ELL in response to DNA damage, but also provide an insight into the mechanism for MLL-ELL associated leukemogenesis.
    Molecular and cellular biology 12/2013; · 6.06 Impact Factor
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    ABSTRACT: The glutathione and cysteine conjugates of microcystin (MC-GSH and MC-Cys, respectively) are two important metabolites in the detoxification of microcystins (MCs). Although studies have quantitated both conjugates, the reason why the amounts of MC-GSH are much lower than those of MC-Cys in various animal organs remains unknown. In this study, MC-RR-GSH and MC-RR-Cys were respectively i.p. injected into the cyanobacteria-eating bighead carp (Aristichthys nobilis), to explore the biotransformation and detoxification mechanisms of the two conjugates. The contents of MC-RR, MC-RR-GSH, MC-RR-Cys and MC-RR-N-acetyl-cysteine (MC-RR-Nac, the acetylation product of MC-RR-Cys) in the liver, kidney, intestine and blood of bighead carp in both groups were quantified via liquid chromatography electrospray ionization mass spectrometry (LC-ESI-MS). In the MC-RR-GSH-treated group, the MC-RR-Cys content in the kidney increased 96.7-fold from 0.25 to 0.5h post-injection, demonstrating that MC-RR-GSH acts as a highly reactive intermediate and is rapidly converted to MC-RR-Cys. The presence of MC-RR in both MC-RR-GSH- and MC-RR-Cys-treated groups indicates, for the first time, that MC conjugation with the thiol of GSH/Cys is a reversible process in vivo. Total MC-RR concentrations dissociated from MC-RR-Cys were lower than those from MC-RR-GSH, suggesting that MC-RR-Cys is more capable of detoxifying MC-RR. MC-RR-Cys was the most effectively excreted form in both the kidney and intestine, as the ratios of MC-RR-Cys to MC-RR reached as high as 15.2, 2.9 in the MC-RR-GSH-treated group and 63.4, 19.1 in the MC-RR-Cys-treated group. Whereas MC-RR-Nac could not be found in all of the samples of the present study. Our results indicate that MC-RR-GSH was rapidly converted to MC-RR-Cys and then excreted, and that both glutathione and cysteine conjugates could release MC-RR. This study quantitatively proves the importance of the GSH detoxification pathway and furthers our understanding of the biochemical mechanism by which bighead carp are resistant to toxic cyanobacteria.
    Aquatic toxicology (Amsterdam, Netherlands) 12/2013; 147C:18-25. · 3.12 Impact Factor
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    ABSTRACT: Gliomas are the most common primary brain tumors in adults and a significant cause of cancer-related mortality. A 9-gene signature was identified as a novel prognostic model reflecting survival situation obviously in gliomas. To identify an mRNA expression signature to improve outcome prediction for patients with different glioma grades. We used whole-genome mRNA expression microarray data of 220 glioma samples of all grades from the Chinese Glioma Genome Atlas (CGGA) database (http://www.cgga.org.cn) as a discovery set and data from Rembrandt and GSE16011 for validation sets. Data from every single grade were analyzed by the Kaplan-Meier method with a two-sided log-rank test. Univariate Cox regression and linear risk score formula were applied to derive a gene signature with better prognostic performance. We found that patients who had high risk score according to the signature had poor overall survival compared with patients who had low risk score. Highly expressed genes in the high-risk group were analyzed by gene ontology (GO) and gene set variation analysis (GSVA). As a result, the reason for the divisibility of gliomas was likely due to cell life processes and adhesion. This 9-gene-signature prediction model provided a more accurate predictor of prognosis that denoted patients with high risk score have poor outcome. Moreover, these risk models based on defined molecular profiles showed the considerable prospect in personalized cancer management.
    CNS Neuroscience & Therapeutics 11/2013; · 4.46 Impact Factor
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    ABSTRACT: Parkinson's disease (PD) patients have excessive iron depositions in substantia nigra (SN). Neuroinflammation characterized by microglial activation is pivotal for dopaminergic neurodegeneration in PD. However, the role and mechanism of microglial activation in iron-induced dopaminergic neurodegeneration in SN remain unclear yet. This study aimed to investigate the role and mechanism of microglial β-nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) activation in iron-induced selective and progressive dopaminergic neurodegeneration. Multiple primary midbrain cultures from rat, NOX2(+/+) and NOX2(-/-) mice were used. Dopaminergic neurons, total neurons, and microglia were visualized by immunostainings. Cell viability was measured by MTT assay. Superoxide (O2 (·-)) and intracellular reactive oxygen species (iROS) were determined by measuring SOD-inhibitable reduction of tetrazolium salt WST-1 and DCFH-DA assay. mRNA and protein were detected by real-time PCR and Western blot. Iron induces selective and progressive dopaminergic neurotoxicity in rat neuron-microglia-astroglia cultures and microglial activation potentiates the neurotoxicity. Activated microglia produce a magnitude of O2 (·-) and iROS, and display morphological alteration. NOX2 inhibitor diphenylene iodonium protects against iron-elicited dopaminergic neurotoxicity through decreasing microglial O2 (·-) generation, and NOX2(-/-) mice are resistant to the neurotoxicity by reducing microglial O2 (·-) production, indicating that iron-elicited dopaminergic neurotoxicity is dependent of NOX2, a O2 (·-)-generating enzyme. NOX2 activation is indicated by the increased mRNA and protein levels of subunits P47 and gp91. Molecules relevant to NOX2 activation include PKC-σ, P38, ERK1/2, JNK, and NF-КBP65 as their mRNA and protein levels are enhanced by NOX2 activation. Iron causes selective and progressive dopaminergic neurodegeneration, and microglial NOX2 activation potentiates the neurotoxicity. PKC-σ, P38, ERK1/2, JNK, and NF-КBP65 are the potential molecules relevant to microglial NOX2 activation.
    Molecular Neurobiology 11/2013; · 5.47 Impact Factor

Publication Stats

3k Citations
1,285.53 Total Impact Points


  • 2014
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2010–2014
    • Texas Biomedical Research Institute
      San Antonio, Texas, United States
    • The Hong Kong University of Science and Technology
      • Division of Life Science
      Chiu-lung, Kowloon City, Hong Kong
    • Qingdao University
      • College of Physics
      Tsingtao, Shandong Sheng, China
    • Peninsula Cancer Institute
      Williamsburg, Virginia, United States
    • National Institute for the Control of Pharmaceutical and Biological Products
      Peping, Beijing, China
    • The Third Xiangya Hospital of the Central South University
      Ch’ang-sha-shih, Hunan, China
    • Northwest A & F University
      • College of Life Sciences
      Yangling, Shaanxi Sheng, China
    • Peking University Third Hospital
      Peping, Beijing, China
    • University of Texas MD Anderson Cancer Center
      • Department of Pathology
      Houston, TX, United States
  • 2008–2014
    • Chinese Academy of Sciences
      • • Institute of Hydrobiology
      • • Institute of Biophysics
      • • Institute of Plasma Physics
      Peping, Beijing, China
    • Second Military Medical University, Shanghai
      Shanghai, Shanghai Shi, China
    • IBM
      Armonk, New York, United States
  • 2013
    • University of California, Los Angeles
      • Department of Materials Science and Engineering
      Los Angeles, California, United States
    • Guangdong Pharmaceutical University
      Shengcheng, Guangdong, China
  • 2012–2013
    • Peking Union Medical College Hospital
      Peping, Beijing, China
    • RWTH Aachen University
      Aachen, North Rhine-Westphalia, Germany
    • China Academy of Engineering Physics
      Peping, Beijing, China
    • Government of the People's Republic of China
      Peping, Beijing, China
    • Renmin University of China
      Peping, Beijing, China
  • 2011–2013
    • Guangzhou First People's Hospital
      Shengcheng, Guangdong, China
    • Hebei Medical University
      • School of Public Health
      Chentow, Hebei, China
    • Capital institute of Pediatrics
      Peping, Beijing, China
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
    • Chinese Research Academy of Environmental Sciences
      Peping, Beijing, China
    • Jinan University (Guangzhou, China)
      Shengcheng, Guangdong, China
    • Beijing Centers for Disease Control and Prevention
      Peping, Beijing, China
    • Wannan Medical College
      Wu-hu-shih, Anhui Sheng, China
    • Guangdong Province Ceramic Research Institute
      Swatow, Guangdong, China
    • Beijing University of Technology
      Peping, Beijing, China
  • 2009–2013
    • Fourth Military Medical University
      • • Department of Biopharmaceutics
      • • Department of Gynaecology and Obstetrics
      Xi’an, Liaoning, China
    • Tsinghua University
      • School of Materials Science and Engineering
      Peping, Beijing, China
    • Research Triangle Park Laboratories, Inc.
      Raleigh, North Carolina, United States
    • Harbin Institute of Technology
      Charbin, Heilongjiang Sheng, China
    • Xi'an Jiaotong University
      Ch’ang-an, Shaanxi, China
    • Capital Medical University
      Peping, Beijing, China
    • Taiyuan University of Technology
      Yangkü, Shanxi Sheng, China
    • University of Shanghai for Science and Technology
      • Library
      Shanghai, Shanghai Shi, China
  • 2008–2013
    • China Agricultural University
      • • College of Veterinary Medicine
      • • Department of Genetic Breeding and Reproduction
      Beijing, Beijing Shi, China
    • Shanghai Institutes for Biological Sciences
      Shanghai, Shanghai Shi, China
  • 2007–2013
    • Jilin University
      • State Key Lab of Theoretical and Computational Chemistry
      Yung-chi, Jilin Sheng, China
    • Shenyang Pharmaceutical University
      • Department of Pharmacy
      Feng-t’ien, Liaoning, China
    • University of Illinois at Chicago
      • Department of Medicine (Chicago)
      Chicago, IL, United States
  • 2006–2013
    • Northeast Institute of Geography and Agroecology
      • • State Key Laboratory of Electroanalytical Chemistry
      • • Institute of Biophysics
      • • Institute of Subtropical Agriculture
      • • National Center for Drug Screening
      Beijing, Beijing Shi, China
    • University of Washington Seattle
      • Department of Pathology
      Seattle, WA, United States
  • 2005–2013
    • Central South University
      • • Institute of Clinical Pharmacology
      • • School of Public Health
      Changsha, Hunan, China
    • Peking University School of Stomatology
      Peping, Beijing, China
    • Dalian Medical University
      Lü-ta-shih, Liaoning, China
  • 2004–2013
    • Beijing Tiantan Hospital
      Peping, Beijing, China
    • Guangxi Medical University
      • Department of Gynecologic Oncology
      Nanning, Guangxi Zhuangzu Zizhiqu, China
    • Sun Yat-Sen University
      • • School of Pharmaceutical Science
      • • State Key Laboratory of Oncology
      • • Key Laboratory of Stem Cell Biology and Tissue Engineering
      • • Section of Histology and Embryology
      Shengcheng, Guangdong, China
    • Guangxi University
      Yung-ning, Guangxi Zhuangzu Zizhiqu, China
  • 2011–2012
    • Sichuan University
      Hua-yang, Sichuan, China
  • 2010–2012
    • Beijing University of Posts and Telecommunications
      • • State Key Laboratory of Information Photonics and Optical Communications
      • • National Engineering Laboratory for Disaster Backup and Recovery
      Peping, Beijing, China
    • Huazhong (Central China) Normal University
      • College of Life Sciences
      Wuhan, Hubei, China
  • 2008–2012
    • Tianjin University of Traditional Chinese Medicine
      T’ien-ching-shih, Tianjin Shi, China
  • 2010–2011
    • University of Jinan (Jinan, China)
      Chi-nan-shih, Shandong Sheng, China
    • Fudan University
      • Department of Optical Science and Engineering
      Shanghai, Shanghai Shi, China
    • Peking University People's Hospital
      Peping, Beijing, China
  • 2009–2011
    • Peking University
      • Department of Chemical Biology
      Beijing, Beijing Shi, China
    • Yale University
      • Department of Pharmacology
      New Haven, CT, United States
  • 2008–2011
    • Virginia Polytechnic Institute and State University
      • Department of Biomedical Sciences and Pathobiology
      Blacksburg, VA, United States
  • 2006–2011
    • The Ohio State University
      • • Ohio Agricultural Research and Development Center
      • • Department of Veterinary Preventive Medicine
      Columbus, OH, United States
  • 2009–2010
    • Zhejiang University of Technology
      Hang-hsien, Zhejiang Sheng, China
  • 2007–2010
    • Mount Sinai School of Medicine
      • Department of Medicine
      Manhattan, NY, United States
  • 2006–2010
    • Huazhong University of Science and Technology
      • • Radiology Department
      • • Department of Hepatic Surgery
      Wuhan, Hubei, China
  • 2008–2009
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 2004–2008
    • National Institutes of Health
      • • Chemical Biology Laboratory
      • • Section of Molecular Neuropharmacology
      • • Section on Molecular Neurobiology
      Bethesda, MD, United States
  • 2003–2007
    • National Institute of Environmental Health Sciences
      • Laboratory of Toxicology and Pharmacology (LTP)
      Durham, North Carolina, United States
  • 2003–2006
    • China Institute for Radiation Protection
      Peping, Beijing, China