Tao Zhang

Peking University, Peping, Beijing, China

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Publications (140)365.44 Total impact

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    ABSTRACT: Fetuses and infants are vulnerable to perchlorate toxicity. We assessed fetal and infantile exposure to perchlorate in two Chinese cities (Nanchang and Tianjin). Perchlorate was widely found (82%-100%) in breast milk, dissolved infant formula, infants' urine, maternal and cord blood samples. Perchlorate levels in infants' urine (mean ± standard deviation: 22.4 ± 35.6 ng mL(-1)), breast milk (36.6 ± 48.1 ng mL(-1)), and cord blood (3.18 ± 3.83 ng mL(-1)) samples collected from Nanchang and Tianjin were approximately an order of magnitude higher than those reported for the U.S. Perchlorate concentrations in cord blood were comparable to that in maternal blood, indicating that perchlorate is transferred from mother to fetus through placenta. Among all infants providing urine samples, the average daily intake of perchlorate (DOSEU) was estimated to be 1.17 ± 1.57 μg kg(-1) bw d(-1), and 40% of these infants had DOSEU exceeding the RfD (0.7 μg kg(-1) bw d(-1)) recommended by U.S. EPA. However, approximately 70% of exclusively breast-fed infants had perchlorate exposure dose via breast milk exceeding the RfD. For breast-fed infants, breast milk was the overwhelmingly predominant exposure pathway; while infant formula and indoor dust ingestion were major perchlorate exposure sources for formula-fed infants. To our knowledge, this is the first report to assess the fetal and infantile exposure to perchlorate in China.
    Chemosphere 02/2016; 144:948-954. DOI:10.1016/j.chemosphere.2015.09.073 · 3.34 Impact Factor
  • Hui Wang · Na Gao · Wen Li · Zhuo Yang · Tao Zhang
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    ABSTRACT: Context: Melamine, as an industrial chemical, was blended illegally with infant formula to counterfeit the illusion of more abundant protein content in 2008. Due to its nephrotoxicity, thousands of children underwent kidney disease. Objective: It was to investigate whether melamine could affect autophagy in mesangial cells (MCs) via oxidative stress and whether autophagy played a positive role in protecting MCs impaired by melamine. Materials and methods: MCs were used as a mesangium model. The cell viability was measured by MTT assay. Intracellular hydrogen peroxide (H2O2) was assessed by using H2O2 assay kit. The Western blot assay was employed to measure the expression of autophagy-related proteins. Results: MTT assay showed that melamine induced MCs death in a concentration-dependent and time-dependent manner. The measurement of H2O2 demonstrated that melamine decreases H2O2 level of MCs. Meaningfully, treatment of a type of ROS scavenger formulation named N-(mercaptopropionyl)-glycine (N-MPG) could inhibit MCs death induced by melamine. Meanwhile, Western blot analysis indicated that melamine enhanced the ratio of LC3-II/LC3-I and Beclin-1 level in MCs, and N-MPG down-regulated autophagy in melamine-treated MCs. The cell viability of MCs with melamine and an autophagy inhibitor named 3-methyladenine (3-MA) showed that autophagy could protect melamine-treated MCs. Conclusions: The study showed that melamine-enhanced autophagy by increasing ROS levels in MCs, and autophagy could protect melamine-treated MCs. Improving autophagy may become a new potential clinical application to relieve melamine-induced renal injury.
    Toxicology mechanisms and methods 09/2015; DOI:10.3109/15376516.2015.1053655 · 1.52 Impact Factor
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    ABSTRACT: The transient receptor potential canonical (TRPC) 6 channel is an important ion channel located in podocytes, which plays an essential role in regulating calcium homeostasis of the cell signaling. Podocytes are specialized, terminally differentiated cells surrounding glomerular capillaries, and are the subject of keen interest because of their key roles in kidney development and disease. Here we wonder whether TRPC6 channels undergo developmental changes in the expression and function during the podocyte differentiation, and whether they contribute to the maturation of podocytes. Using morphological, immunohistochemical and electrophysiological techniques, we investigated the development of distribution and expression of TRPC6 in conditionally immortalized mouse podocyte cell line. Our results showed that the distribution of TRPC6 channels changed with the maturity of podocyte differentiation. The fluorescent intensity of TRPC6 on cell surface increased, which was accompanied by a corresponding increase in the density of current flowing through the channels. TRPC6 inhibition by TRPC6 siRNA or SKF-96365, a blocker or TRP cation channels, resulted in F-actin cytoskeleton disruption only on the developmental stage of podocytes. These results strongly support the conclusion that TPRC6 is an essential component of the slit diaphragm and is required for development of glomerulus.
    Cell calcium 09/2015; DOI:10.1016/j.ceca.2015.09.001 · 3.51 Impact Factor
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    ABSTRACT: Background: Senile plaques consisting of amyloid-beta (Aβ) are the major pathological hallmark of Alzheimer's disease (AD) and have been the primary therapeutic target. Immunotherapies, which are designed to remove brain Aβ deposits, increased levels of soluble Aβ and accelerated brain atrophy in some clinical trials, suggesting that the solubilization of Aβ deposition might facilitate the formation of more toxic Aβ oligomers and enhance neurotoxicity. Methods: The capacity of antibodies against different epitopes of Aβ to disaggregate preformed Aβ fibrils was investigated. The co-incubation of antibodies and Aβ fibrils was then tested for neurotoxicity both in vitro and in vivo. Results: After the incubation of preformed Aβ fibrils with the N-terminal antibody 6E10, the fibrils were decreased, while the oligomers, mostly dimers and trimers, were significantly increased. However, no such effects were observed for antibodies targeting the middle domain (4G8) and C-terminus of Aβ (8G7). The co-incubates of preformed Aβ fibrils with 6E10 were more neurotoxic, both in vitro and in vivo, than the co-incubates with 4G8 and 8G7. Conclusions: Our results indicate that the antibody targeting the N-terminus of Aβ promoted the transformation of Aβ from fibrils into oligomers and increased neurotoxicity. Immunotherapies should take into consideration the enhanced neurotoxicity associated with the solubilization of Aβ deposits by antibodies against the Nterminus of Aβ.
    Journal of Neuroinflammation 08/2015; 12(1):153. DOI:10.1186/s12974-015-0379-4 · 5.41 Impact Factor
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    ABSTRACT: The imbalance between ß-amyloid (Aß) generation and clearance plays a fundamental role in the pathogenesis of Alzheimer's disease (AD). The sporadic form of AD is characterized by an overall impairment in Aß clearance. Immunotherapy targeting Aß clearance is believed to be a promising approach and is under active clinical investigation. Autophagy is a conserved pathway for degrading abnormal protein aggregates and is crucial for Aß clearance. We previously reported that oral vaccination with a recombinant AAV/Aß vaccine increased the clearance of Aß from the brain and improved cognitive ability in AD animal models, while the underlying mechanisms were not well understood. In this study, we first demonstrated that oral vaccination with rAAV/Aß decreased the p62 level and up-regulated the LC3B-II/LC3B-I ratio in APP/PS1 mouse brain, suggesting enhanced autophagy. Further, inhibition of the Akt/mTOR pathway may account for autophagy enhancement. We also found increased anti-Aß antibodies in the sera of APP/PS1 mice with oral vaccination, accompanied by elevation of complement factors C1q and C3 levels in the brain. Our results indicate that autophagy is closely involved in oral vaccination-induced Aß clearance, and modulating the autophagy pathway may be an important strategy for AD prevention and intervention.
    Neuroscience Bulletin 08/2015; 31(4):491-504. DOI:10.1007/s12264-015-1546-4 · 2.51 Impact Factor
  • Chunhua Liu · Xiaxia Xu · Jing Gao · Tao Zhang · Zhuo Yang
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    ABSTRACT: Our previous study has demonstrated that hydrogen sulfide (H2S) attenuates neuronal injury induced by vascular dementia (VD) in rats, but the mechanism is still poorly understood. In this study, we aimed to investigate whether the neuroprotection of H2S was associated with synaptic plasticity and try to interpret the potential underlying mechanisms. Adult male Wistar rats were suffered the ligation of bilateral common carotid arteries. At 24 h after surgery, rats were administered intraperitoneally with sodium hydrosulfide (NaHS, 5.6 mg·kg(-1)·day(-1)), a H2S donor, for 3 weeks in the VD+NaHS group and treated intraperitoneally with saline in the VD group respectively. Our results demonstrated that NaHS significantly decreased the level of glutamate. It obviously ameliorated cognitive flexibility as well as the spatial learning and memory abilities by Morris water maze. Moreover, NaHS significantly improved the long-term depression (LTD), and was able to elevate the expression of N-methyl-D-aspartate receptor subunit 2A, which plays a pivotal role in synaptic plasticity. Interestingly, NaHS decreased the phosphorylation of Akt, and it could maintain the activity of glycogen synthase kinase-3β (GSK-3β). Surprisingly, NaHS triggered the canonical Notch pathway by increasing expressions of Jagged-1 and Hes-1. These findings suggest that NaHS prevents synaptic plasticity from VD-induced damage partly via Akt/GSK-3β pathway and Notch signaling pathway.Hydrogen sulfide modulated the ratio of NMDAR 2A/2B and improved the synaptic plasticity via Akt/GSK-3β pathway and Notch signaling pathway in VD rats.
    Molecular Neurobiology 07/2015; DOI:10.1007/s12035-015-9324-x · 5.14 Impact Factor
  • Lei An · Tao Zhang
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    ABSTRACT: Chronic prenatal ethanol exposure (CPEE) can impair long-term potentiation (LTP) in the male hippocampus. Sexually specific alterations were frequently reported in female animals that had been prenatally exposed to ethanol. This study aimed to examine the effects of CPEE on spatial learning and memory, as well as on hippocampal synaptic plasticity in female adolescent rats. Female offspring were selected from dams that had been exposed to 4 g/kg/day of ethanol throughout the gestational period. Subsequently, performance in the Morris water maze (MWM) was determined, while LTP and depotentiation were measured in the hippocampal CA3-CA1 pathway. In the behavioral test, the escape latencies in both initial and reversal training stages were significantly prolonged. Interestingly, LTP was considerably enhanced while depotentiation was significantly depressed. Our results suggest a critical role of synaptic plasticity balance, which may prominently contribute to the cognitive deficits present in CPEE offspring. Copyright © 2015 Elsevier Inc. All rights reserved.
    Alcohol (Fayetteville, N.Y.) 07/2015; 49(6). DOI:10.1016/j.alcohol.2015.05.004 · 2.01 Impact Factor
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    ABSTRACT: Phospholipid transfer protein (PLTP) is a widely expressed lipid transfer protein participating in the transport of cholesterol and other lipids in the plasma and peripheral tissues. Recently, elevated amyloid β (Aβ) in young and aged PLTP-deficient brains had been reported. However, the role of PLTP in amyloid precursor protein (APP) processing and Alzheimer's disease (AD) pathology remains elusive. Here we first found that deficiency of PLTP accelerated memory dysfunction in APP/PS1ΔE9 AD model mice at the age of 3 months. Further characterization showed that PLTP deficiency increased soluble Aβ peptides, and intracellular accumulation of Aβ was illustrated, which might be due to disrupted APP turnover and the enhanced amyloidogenic pathway. Besides, reduced brain-derived neurotrophic factor (BDNF) was found in PLTP deficient APP/PS1ΔE9 mice, and BDNF level was negatively correlated with Aβ42 content, instead of Aβ40 content. In addition, autophagic dysfunction was found in the PLTP deficient APP/PS1ΔE9 mice. Our data presented a novel model to link phospholipid metabolism to APP processing, and also suggested that PLTP played an important role in Aβ metabolism and would be useful to further elucidate functions of PLTP in AD susceptibility. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Human Molecular Genetics 07/2015; DOI:10.1093/hmg/ddv262 · 6.39 Impact Factor
  • Qun Li · Ning Cheng · Tao Zhang
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    ABSTRACT: Neural oscillatory phenomenon generally exists in the nervous system through a dynamic form. It plays a very important role in the brain, especially in the higher cognitive activities, such as information processing, transfer and integration, consolidating memory and so on. Furthermore, the specific activity pattern of neural oscillations is often associated with cognitive functions and their alterations. Accordingly, how to quantitatively analyze the pattern of neural oscillations becomes one of the fundamental issues in the computational neuroscience. In this review, we addressed a variety of analytic algorithms, which are commonly employed in our recent studies to investigate the issues of neurobiology and cognitive science. In addition, we tried to classify these analytic algorithms by distinguishing their different metrics, synchronization and coupling modes. Finally, multidimensional analytic algorithms for potential application have also been discussed.
    Sheng li xue bao: [Acta physiologica Sinica] 04/2015; 67(2):143-54.
  • Lei An · Jingxuan Fu · Tao Zhang
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    ABSTRACT: Previous studies showed that the spatial cognitive deficits of rats were induced by chronic melamine exposure, which was associated with the hippocampal oxidative damage. Currently, we examined the antioxidative effect of vitamins C and E combination on cognitive function in melamine-treated rats. Melamine was oral administrated to male adolescent Wistar at a dosage of 300 mg/kg/day for 28 days. After that, animals received vitamins C and E at a dose of 150 and 200 mg/kg respectively, intraperitoneally for the next 7 days. Cognitive behaviors were investigated using the Morris water maze test. The biochemical indexes were detected in the hippocampal homogenate. The treatment with vitamin complex significantly ameliorated cognitive deficits induced by melamine. ROS, MDA, NO contents were almost back to normal, while SOD, CAT, GSH-Px, NOS activities were improved as well. The neural apoptosis in the hippocampus were ameliorated by regulating the expression of anti-apoptotic protein (Bcl-2) and caspase-3. Additionally, histological observation showed that vitamin complex effectively alleviated the injuries of hippocampal neurons. These results suggest that the potential therapeutic for oxidative damage induced neuronal apoptosis after treatment of vitamins C and E combination, which is most likely related to the antioxidative effects. Copyright © 2015. Published by Elsevier Inc.
    Pharmacology Biochemistry and Behavior 03/2015; 132. DOI:10.1016/j.pbb.2015.03.009 · 2.78 Impact Factor
  • Xiaxia Xu · Chunhua Liu · Zhanyong Li · Tao Zhang
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    ABSTRACT: Our previous study showed that hydrogen sulfide (H2S) could alleviate the cognitive deficits in vascular dementia (VD) rats associated with the improvement of synaptic plasticity. Neural oscillations are reported to interact with each other through either identical-frequency or cross-frequency coupling. This study examined whether impaired neural couplings could be alleviated by H2S in the hippocampal CA3-CA1 of VD rats and explored its possible mechanism. A VD rat model was established by two-vessel occlusion. Sodium hydrosulfide (NaHS), a kind of H2S donor, was administered intraperitoneally (5.6 mg/kg/day) for 3 weeks. Local field potentials were simultaneously collected in the hippocampal CA3 and CA1. The effects of NaHS on the modulation of theta-gamma coupling were evaluated by using the measurements of both phase-phase coupling and phase-amplitude coupling, while several other approaches including behavior, electrophysiology, western blot, immunofluorescence staining were also employed. The results showed that NaHS significantly prevented spatial learning and memory impairments (p < 0.01). NaHS considerably alleviated the impairment of neural coupling in VD rats in an identical-frequency rhythm and between cross-frequency bands. Moreover, the expression of cystathionine-β-synthase (CBS) was markedly attenuated in VD rats. NaHS elevated the expression of CBS to maintain the intrinsic balance of H2S. Interestingly, it was observed that NaHS increased the protein expression of N-methyl-D-aspartic acid receptor 2A (NMDAR2A) in VD rats. In conclusion, the data suggest that NaHS played the neuroprotective role partly via modulating the expression of NMDAR2A in order to alleviate the impairments of neural couplings in VD rats.
    Brain Topography 03/2015; DOI:10.1007/s10548-015-0430-x · 3.47 Impact Factor
  • Hui Wang · Na Gao · Zhigui Li · Zhuo Yang · Tao Zhang
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    ABSTRACT: Since melamine was illegally added to raw milk for increasing the apparent protein content, such a scandal has not been quite blown out. Previous studies showed that melamine induced apoptosis and oxidative damage in both in vivo and in vitro experiments. It is well known that autophagy is closely related to oxidative stress. In the present study, we examined whether autophagy played an important role in protecting PC12 cells, which were damaged by melamine. Immunofluorescence assay showed that melamine enhanced the number of punctuate dot, indicating the increase of autophagosomes. Western blot assay presented that melamine significantly elevated the expression level of autophagy markers including LC3-II/LC3-I ratio, beclin-1, and Atg 7. Rapamycin further enhanced the effect, whereas 3-methyadenine (3-MA) inhibited it. MTT assay exhibited that rapamycin significantly enhanced the cell viability (P < 0.01), while 3-MA considerably reduced it in melamine-treated PC12 cells (P < 0.01). Furthermore, flow cytometry assay showed that rapamycin considerably reduced the reactive oxygen species (ROS) level of the cells (P < 0.01), but 3-MA increased the generation of ROS (P < 0.01). Additionally, the superoxide dismutase (SOD) activity was notably increased by rapamycin in melamine-treated PC12 cells (P < 0.01), while the activity of which was prominently decreased by 3-MA (P < 0.01). Malondialdehyde (MDA) assay showed that rapamycin remarkably decreased the MDA level of the cells (P < 0.05), while 3-MA increased it (P < 0.01). Consequently, this study demonstrated that autophagy protected PC12 cells from melamine-induced cell death via inhibiting the excessive generation of ROS. Regulating autophagy may become a new targeted therapy to relieve the damage induced by melamine.
    Molecular Neurobiology 03/2015; DOI:10.1007/s12035-014-9073-2 · 5.14 Impact Factor
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    Chenguang Zheng · Tao Zhang
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    ABSTRACT: It is believed that phase synchronization facilitates neural communication and neural plasticity throughout the hippocampal-cortical network, and further supports cognition and memory. The pathway from ventral hippocampus to medial prefrontal cortex (mPFC) is thought to play a significant role in emotional memory processing. Therefore, the information transmission on the pathway was hypothesized to be disrupted in depressive state, which could be related to its impaired synaptic plasticity. In this study, local field potentials (LFPs) from both ventral CA1 (vCA1) and mPFC were recorded in both normal and chronic unpredictable stress (CUS) model rats under the urethane anesthesia. The LFPs of all rats were recorded before and after the long term potentiation (LTP) induced on vCA1-mPFC pathway in order to figure out the correlation of oscillatory synchronization of LFPs and synaptic plasticity. Our results showed the vCA1-to-mPFC unidirectional phase coupling of theta rhythm, rather than the power of either region, was significantly enhanced by LTP induction, with less enhancement in the CUS model rats compared to that in the normal rats. In addition, theta phase coupling was positively correlated with synaptic plasticity on vCA1-mPFC pathway. Moreover, the theta-slow gamma phase-amplitude coupling in vCA1 was long-term enhanced after high frequency stimulation. These results suggest that the impaired synaptic plasticity in vCA1-mPFC pathway could be reflected by the attenuated theta phase coupling and theta-gamma cross frequency coupling of LFPs in depression state. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 02/2015; 292. DOI:10.1016/j.neuroscience.2015.01.071 · 3.36 Impact Factor
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    ABSTRACT: In an effort to accelerate translational bioinformatics research, this study presents a universal software tool, named as Sequence Relation Drawing program (SRD). It can be used to dynamically visualize the relationship between molecular sequences and their categories based on undirected graphs in similarity analysis of gene and protein sequences. SRD consists of two components: a Window-based application and a computerized database. Researchers can import their datasets into the database, which will make the software run faster and occupy less memory. Pre-computed sequence relations and other user-defined information can also be imported into the system, and then be visualized in several interactive perspectives. Sequences could be partitioned into several categories, and several windows are provided and linked for the visualization involving intro-category, extra-category and category-category relationships, respectively. An example is also provided, which is HIV Pestiferous Map Analysis. Given the sequences of the envelope glycoprotein gene and their similarities, SRD could help to investigate traits of the spread of the AIDS disease, which may help biologists or clinicians to control the AIDS disease transmission in molecular epidemiology study. The SRD software can be download from http://www.nkbiox.com/srd/index.htm. - See more at: http://eurekaselect.com/129304#sthash.rpvOz0il.dpuf
    Current Bioinformatics 02/2015; 10(5):69-78. DOI:10.2174/157489361001150309141803 · 0.92 Impact Factor
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    ABSTRACT: AimsThis study explored whether surgical stress-induced glucocorticoid receptor (GR) phosphorylation is related to postoperative cognitive dysfunction (POCD) in aged individuals. Inhibition of GR activation could be an effective treatment for POCD.MethodsA laparotomy was given to C57/BL6 mice in POCD group both 20 and 6 months old. Animals in control group were treated in identical manners except for laparotomy. Cognitive function was evaluated by Morris water maze and elevated plus maze. Western blot and Elisa assay were used to detect related molecules. Mifepristone and roscovitine were treated as inhibitions of GR phosphorylation.ResultsThe cognitive function was impaired, and brain-derived neurotrophic factor (BDNF) was found reduced in aged POCD group. GR translocation into nucleus and elevated GR phosphorylation were found in prefrontal cortex of aged POCD mice. Cyclin-dependent Kinase 5 (CDK5), kinase for GR phosphorylation also elevated in aged POCD mice. With GR antagonist and CDK5 inhibitor, reduction of BDNF and cognitive dysfunction in aged mice were both rescued.Conclusion These results presented a mechanism that surgical stress-induced GR phosphorylation contributes to POCD in aged individuals. Inhibition of GR activation and phosphorylation might be a potential treatment target of POCD.
    CNS Neuroscience & Therapeutics 01/2015; 21(5). DOI:10.1111/cns.12368 · 3.93 Impact Factor
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    ABSTRACT: Abstract Perchlorate is used in fireworks and China is the largest fireworks producer and consumer in the world. Information regarding human exposure to perchlorate is scarce in China, and exposure via indoor dust ingestion (EDIindoor dust) has rarely been evaluated. In this study, perchlorate was found in indoor dust (detection rate: 100%, median: 47.4 µg/g), human urine (99%, 26.2 ng/mL), drinking water (100%, 3.99 ng/mL), and dairy milk (100%, 12.3 ng/mL) collected from cities that have fireworks manufacturing areas (Yueyang and Nanchang) and in cities that do not have fireworks manufacturing industries (Tianjin, Shijiazhuang, Yuxi and Guilin) in China. In comparison with perchlorate levels reported for other countries, perchlorate levels in urine samples from fireworks sites and non-fireworks sites in China were higher. Median indoor dust perchlorate concentrations were positively correlated (r = 0.964, p < 0.001) with outdoor dust perchlorate levels reported previously. The total daily intake (EDItoal) of perchlorate, estimated based on urinary levels, ranged from 0.090 to 27.72 µg/kg body weight (bw)/day for all studied participants; the percentage of donors who had EDItotal exceeding the reference dose (RfD) recommended by the United States Environmental Protection Agency (US EPA) was 79%, 48%, and 25% for toddlers (median: 1.829 µg/kg bw/day), adults (0.669 µg/kg bw/day), and children (median: 0.373 µg/kg bw/day), respectively. Toddlers (0.258 µg/kg bw/day) had the highest median EDIindoor dust, which was 2 to 5 times greater than the EDIindoor dust calculated for other age groups (the range of median values: 0.044 to 0.127 µg/kg bw/day). Contribution of indoor dust to EDItotal was 26%, 28%, and 7% for toddlers, children, and adults, respectively. Indoor dust contributed higher percentage to EDItotal than that by dairy milk (0.5-5%).
    Environmental Science and Technology 01/2015; 49(4). DOI:10.1021/es504444e · 5.33 Impact Factor
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    ABSTRACT: We have previously reported that presynaptic dysfunction and cognitive decline have been found in lipoprotein lipase (LPL) deficient mice, but the mechanism remains to be elucidated. Accumulating evidence supported that α-synuclein (α-syn) and ubiquitin C-terminal hydrolase L1 (UCHL1) are required for normal synaptic and cognitive function. In this study, we found that α-syn aggregated and the expression of UCHL1 decreased in the brain of LPL deficient mice. Reduction of UCHL1 was resulted from nuclear retention of DNA cytosine-5-methyltransferase 1 in LPL knockout mice. Reverse changes were found in cultured cells overexpressing LPL. Furthermore, deficiency of LPL increased ubiquitination of α-syn. These results indicated that aggregation of α-syn and reduction of UCHL1 expression in LPL deficient mice may affect synaptic function. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 01/2015; 290. DOI:10.1016/j.neuroscience.2014.12.068 · 3.36 Impact Factor
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    ABSTRACT: Mutations of glucocerebrosidase (GBA) confer susceptibility to Parkinson's disease in several ethnical populations, with a high incidence especially in the Ashkenazi Jewish population. Although there are several studies that have investigated a similar association in a Chinese population, small sample sizes and few positive outcomes have made it difficult to obtain conclusive results from these individual studies. Therefore, the present study used a meta-analysis approach, pooling the appropriate data from published studies to investigate the association of GBA mutations and Parkinson's disease in a Chinese population. Nine studies containing 6536 Chinese subjects (3438 cases and 3098 healthy controls) and examining the GBA mutations of L444P, N370S and several other mutations were included. Review Manager 5.2 software was applied to analyze the pooled odds ratios (ORs) and 95% confidence intervals (CIs). The results showed a significant association of Parkinson's disease risk with overall GBA mutations (OR = 6.34, 95% CI = 3.77-10.68, p<0.00001), and with the subgroup of L444P mutation (OR = 11.68, 95% CI = 5.23-26.06, p<0.00001). No such association was observed for the subgroup with N370S mutation or other mutations, in part because of the small sample size or rare events. Thus, for the rare occurrence of GBA mutations, studies with larger sample size are necessary to minimize the sampling error and to obtain convincing results.
    PLoS ONE 12/2014; 9(12):e115747. DOI:10.1371/journal.pone.0115747 · 3.23 Impact Factor
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    ABSTRACT: Surgical stress induced depression and anxiety like behavior are common complications among aged individuals suffering from surgery. Recent studies proposed that accumulation of oxidative stress is involved in the etiology of stress induced depression and anxiety. Dapsone possesses antioxidant properties, however, whether dapsone is effective in modulating surgical stress induced brain oxidative damage remains uncertain. The present study aimed to investigate the effect of dapsone on surgical stress induced depressive and anxiety like behavior, and brain oxidative stress in a well-established surgical stress model. Depressive and anxiety like behavior accompanied by elevated brain oxidative stress were observed in aged mice underwent abdominal surgery. Pretreatment with 5mg/kg dapsone significantly improved the behavioral disorder and ameliorated brain oxidative stress in this model. Further investigation, revealed that surgical stress increased brain NADPH oxidase level, while pretreatment with dapsone abrogated the elevation of NADPH oxidase triggered by surgical stress. These findings suggest that dapsone is effective in improving surgical stress induced brain oxidative damage via down-regulating NADPH oxidase level in aged mice. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Neuroscience Letters 11/2014; 585. DOI:10.1016/j.neulet.2014.11.045 · 2.03 Impact Factor
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    ABSTRACT: Although levels of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) in human blood are well documented, information on elimination of these chemicals is limited. In this study, PFOS and PFOA were analyzed in 81 whole blood-urine paired samples from general adults and pregnant women in Tianjin, China. PFOS and PFOA were detected in 48 and 76 % of adult urine (AU) samples, with geometric mean (GM) concentrations of 0.011 and 0.008 ng/mL, respectively; whereas relatively low PFOS and PFOA concentrations were found in maternal urine (MU) samples, with GM concentrations of 0.006 and 0.003 ng/mL, respectively. For PFOA, the coefficients of Pearson's correlation between whole blood concentrations and creatinine-adjusted and creatinine-unadjusted urinary concentrations were 0.348 (p = 0.013) and 0.417 (p = 0.002), respectively. The GM urinary elimination rates of PFOS (PFOSUER) and PFOA (PFOAUER) were 16 and 25 %, respectively, for adults. These results indicate that urine is an important pathway of excretion of perfluoroalkyl substances (PFASs). The partitioning ratios of PFAS concentration between urine and whole blood (PFASU/B) in pregnant women (PFOSU/B, 0.0004; PFOAU/B, 0.0011) were significantly lower (p = 0.025 for PFOSU/B, p = 0.017 for PFOAU/B) than the ratios found in non-pregnant women (PFOSU/B, 0.0013; PFOAU/B, 0.0028). Furthermore, our results suggest a clear gender difference in the urinary elimination of PFOA, with male adults (31 %) having significantly higher PFOAUER than that of female adults (19 %). PFOSUER was significantly inversely correlated with age (r = -0.334, p = 0.015); these findings suggest that urinary elimination of PFOS is faster in young adults than in the elderly.
    Environmental Science and Pollution Research 11/2014; 22(7). DOI:10.1007/s11356-014-3725-7 · 2.83 Impact Factor

Publication Stats

1k Citations
365.44 Total Impact Points


  • 2014–2015
    • Peking University
      • Laboratory of Neuroscience
      Peping, Beijing, China
    • Sun Yat-Sen University
      • School of Environmental Science and Engineering
      Shengcheng, Guangdong, China
    • Peking University Health Science Center
      Peping, Beijing, China
  • 2005–2015
    • Nankai University
      • • College of Environmental Science and Engineering
      • • College of Life Sciences
      • • Key Laboratory of Bioactive Materials
      T’ien-ching-shih, Tianjin Shi, China
  • 2013–2014
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
    • Chinese Academy of Medical Sciences
      Peping, Beijing, China
  • 2010–2012
    • Peking Union Medical College Hospital
      Peping, Beijing, China
  • 2002–2007
    • University of Birmingham
      • Group of Medical Science and Education
      Birmingham, England, United Kingdom