Li Zhang

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (180)810.94 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: A facile and quick route for the chemical reduction of graphene oxide (GO) using In powder as a reductant has been established. The reduction of GO by In powder is traced by UV-visible absorption spectroscopy, and the obtained reduced graphene oxide (rGO) is analyzed. The In3+ ions produced during the reaction between the GO and the In powder are chemically transformed to In2O3 and then form In2O3/rGO hybrids. The In2O3/rGO hybrids are used as electrode materials and their electrochemical performance are studied using cyclic voltammetry and galvanostatic charge/discharge. The In2O3/rGO hybrids demonstrate excellent electrochemical performance and their highest specific capacitance is 178.8 F g-1 which is much higher than that of either In2O3 or rGO. In addition, the In2O3/rGO hybrids are also very stable.
    10/2014;
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    ABSTRACT: The relationship between hydrophobicity and the protective effect of whey protein hydrolysates (WPHs) against oxidative stress was studied. Whey protein was first hydrolysed by pepsin and trypsin to obtain WPHs. After absorbed by macroporous adsorption resin DA201-C, three fractions named as M20, M40, and M60 were eluted by various concentrations of ethanol. The hydrophobicity showed a trend of increase from M20 to M60. Antioxidant ability test in vitro indicated that all the three components of WPHs displayed reasonably good antioxidant ability. Moreover, with the increase of hydrophobicity, antioxidant ability of WPHs improved significantly. Then rat pheochromocytoma line 12 (PC12) cells oxidative model was built to evaluate the suppression of oxidative stress of three components on PC12 cells induced by H2O2. Morphological alterations, cell viability, apoptosis rate, and intracellular antioxidase system tests all indicated that WPHs exert significant protection on PC cells against H2O2-induced damage. Among them, M60 had the highest protective effect by increasing 19·3% cell survival and reducing 28·6% cell apoptosis. These results suggested hydrophobicity of WPHs was contributing to the antioxidant ability and the protective effect against oxidative damage.
    Journal of Dairy Research 10/2014; · 1.34 Impact Factor
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    ABSTRACT: Podocyte damage and loss together have an important role in the pathogenesis and progression of glomerulonephritis. Glomerulonephritis patients and healthy controls were enrolled in this study. Biochemical, clinical and experimental procedures included measurement of total urinary protein, renal biopsy and gene expression analysis of the receptor activator of NF-kappaB (RANK). The urinary mRNA levels of RANK were significantly higher in the glomerulonephritis group compared to the controls. The urinary RANK level of glomerular subtypes was correlated significantly with proteinuria. The calculated area of RANK mRNA levels under the curve was 0.61 for minimal change disease (MCD), 0.97 for membranous nephropathy (MN), 0.65 for IgA nephropathy (IgAN), 0.70 for lupus nephritis (LN) and 0.70 for focal segmental glomerulosclerosis (FSGS). The urinary mRNA of RANK might be used to differentiate histologic subtypes of glomerulonephritis, particularly between MCD and MN.
    Biomarkers 08/2014; · 1.88 Impact Factor
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    ABSTRACT: Phenotype modulation of pulmonary artery smooth muscle cells (PASMCs) plays an important role during hypoxia-induced vascular remodeling and pulmonary hypertension (PAH). We had previously shown that calcium-sensing receptor (CaSR) is expressed in rat PASMCs. However, little is known about the role of CaSR in phenotypic modulation of PASMCs in hypoxia-induced PAH as well as the underlying mechanisms. In this study, we investigated whether CaSR induces the proliferation of PASMCs in small pulmonary arteries from both rats and human with PAH. PAH was induced by exposing rats to hypoxia for 7-21 days. The mean pulmonary arterial pressure (mPAP), right ventricular hypertrophy index (RVI), the percentage of medial wall thickness to the external diameter (WT %), and cross-sectional total vessel wall area to the total area (WA %) of small pulmonary arteries were determined by hematoxylin and eosin (HE), masson trichrome and Weigert's staining. The protein expressions of matrix metalloproteinase (MMP)-2 and MMP-9, the tissue inhibitors of metalloproteinase (TIMP)-3, CaSR, proliferating cell nuclear antigen (PCNA), phosphorylated extracellular signal-regulated kinase (p-ERK), and smooth muscle cell (SMC) phenotype marker proteins in rat small pulmonary arteries, including calponin, SMα-actin (SMAα), and osteopontin (OPN), were analyzed by immunohistochemistry and Western blotting, respectively. In addition, immunohistochemistry was applied to paraffin-embedded human tissues from lungs of normal human and PAH patients with chronic heart failure (PAH/CHF). Compared with the control group, mPAP, RVI, WT % and WA % in PAH rats were gradually increased with the prolonged hypoxia. At the same time, the expressions of CaSR, MMP-2, MMP-9, TIMP-3, PCNA, OPN, and p-ERK were markedly increased, while the expressions of SMAα and calponin were significantly reduced in lung tissues or small pulmonary arteries of PAH rats. Neomycin (an agonist of CaSR) enhanced but NPS2390 (an antagonist of CaSR) weakened these hypoxic effects. We further found that the expression change of CaSR, PCNA, and SMC phenotypic marker proteins in PAH/CHF lungs was similar to those in PAH rats. Our data suggest that CaSR is involved in the pulmonary vascular remodeling and PAH by promoting phenotypic modulation of small pulmonary arteries.
    Molecular and Cellular Biochemistry 07/2014; · 2.33 Impact Factor
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    ABSTRACT: Astrocytic excitatory amino acid transporters (EAATs) regulate extracellular glutamate concentrations and play a role in preventing neuroexcitotoxicity. Since δ-opioid receptor (DOR) is neuroprotective against excitotoxic injury, we asked if DOR activation upregulates EAAT expression and function.
    British Journal of Pharmacology 07/2014; · 5.07 Impact Factor
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    ABSTRACT: -The KCNH2 gene encodes the Kv11.1 potassium channel that conducts the rapidly activating delayed rectifier current in the heart. The relative expression of the full-length Kv11.1a isoform and the C-terminally truncated Kv11.1a-USO isoform play an important role in regulation of channel function. The formation of C-terminal isoforms is determined by competition between the splicing and alternative polyadenylation of KCNH2 intron 9. It is not known whether changes in the relative expression of Kv11.1a and Kv11.1a-USO can cause long QT syndrome.
    Circulation Cardiovascular Genetics 07/2014; · 6.73 Impact Factor
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    ABSTRACT: A simple method to fabricate Bi nanoparticles by using redox reactions between sodium borohydride and ammonium bismuth citrate in the presence of soluble starch in water phase was developed. The results show that soluble starch is better than PVP in stabilizing Bi nanoparticles. The as-prepared Bi nanoparticles were characterized by Fourier transform infrared spectroscopy, transmission electron microscopy, energy-dispersive X-ray, and powder X-ray diffraction. The catalytic performance of the Bi nanoparticles for the reduction of 4-nitrophenol (4-NP) to 4-aminophenol (4-AP) in the presence of sodium borohydride was studied. The effects of sodium borohydride concentration, initial 4-NP concentration, catalyst dose, and reduction temperature were also investigated.
    Industrial & Engineering Chemistry Research. 06/2014; 53(26):10576–10582.
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    ABSTRACT: Aging is associated with exacerbated brain injury after ischemic stroke. Herein, we explored the possible mechanisms underlying the age-associated exacerbated brain injury after ischemic stroke and determined whether therapeutic intervention with anesthetic post-conditioning would provide neuroprotection in aged rats. Male Fisher 344 rats (young, 4 months; aged, 24 months) underwent 2 h of middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion, with or without sevoflurane post-conditioning for 15 min immediately at the onset of reperfusion. Compared with young rats, aged rats showed larger infarct size, worse neurological scores and more TUNEL positive cells in the penumbral cerebral cortex at 24 h after MCAO. However, edema formation and motor coordination were similar in both groups. Sevoflurane reduced the infarct size, edema formation, and TUNEL positive cells, and improved the neurological outcome in young rats but not in aged rats. Molecular studies revealed that basal expression of the anti-apoptotic molecule B-cell lymphoma-2 (Bcl-2) in the brain was lower in aged rats compared with young rats before MCAO, while basal expression of the pro-apoptotic molecule Bcl-2 associated X protein (Bax) showed similar levels in both groups. MCAO reduced Bcl-2 expression and increased Bax expression in both groups; however, Bax increase was more pronounced in aged rats. In young rats, sevoflurane reversed the above MCAO-induced changes. In contrast, sevoflurane failed to enhance Bcl-2 expression but decreased Bax expression in aged rats. These findings suggest that aging-associated reduction in basal Bcl-2 expression in the brain contributes to increased neuronal injury by enhancing cell apoptosis after ischemic stroke. Sevoflurane post-conditioning failed to provide neuroprotection in aged rats, probably due to its inability to increase Bcl-2 levels and prevent apoptosis in the brain.
    Neuroscience 06/2014; · 3.12 Impact Factor
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    ABSTRACT: Oxidative stress has been implicated in both normal aging and various neurodegenerative disorders and it may be a major cause of neuronal death. Chaperone-mediated autophagy (CMA) targets selective cytoplasmic proteins for degradation by lysosomes and protects neurons against various extracellular stimuli including oxidative stress. MEF2A (myocyte enhancer factor 2A), a key transcription factor, protects primary neurons from oxidative stress-induced cell damage. However, the precise mechanisms of how the protein stability and the transcriptional activity of MEF2A are regulated under oxidative stress remain unknown. In this study, we report that MEF2A is physiologically degraded through the CMA pathway. In pathological conditions, mild oxidative stress (200 μM H 2O 2) enhances the degradation of MEF2A as well as its activity, whereas excessive oxidative stress (> 400 μM H 2O 2) disrupts its degradation process and leads to the accumulation of nonfunctional MEF2A. Under excessive oxidative stress, an N-terminal HDAC4 (histone deacetylase 4) cleavage product (HDAC4-NT), is significantly induced by lysosomal serine proteases released from ruptured lysosomes in a PRKACA (protein kinase, cAMP-dependent, catalytic, α)-independent manner. The production of HDAC4-NT, as a MEF2 repressor, may account for the reduced DNA-binding and transcriptional activity of MEF2A. Our work provides reliable evidence for the first time that MEF2A is targeted to lysosomes for CMA degradation; oxidative stress-induced lysosome destabilization leads to the disruption of MEF2A degradation as well as the dysregulation of its function. These findings may shed light on the underlying mechanisms of pathogenic processes of neuronal damage in various neurodegenerative-related diseases.
    Autophagy 06/2014; 10(6):1015-1035. · 12.04 Impact Factor
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    ABSTRACT: The effect of dexamethasone on post-dural puncture headache (PDPH) after spinal anesthesia has not been well elucidated. This randomized, double-blind, placebo-controlled trial was carried out in patients undergoing a cesarean at the Qilu Hospital, Shandong University. The subjects were randomly divided into a placebo and a dexamethasone group. The incidences of PDPH on the first, second, third and seventh postoperative day were studied, and the severity of PDPH was assessed using a visual analog scale. Studies in PubMed, Embase and the Cochrane Library database were searched and included in the present meta-analysis. Summary estimates of weighted mean differences and 95 % confidence intervals (CIs) were obtained using random-effects models. We included 307 participants in the dexamethasone group and 309 in the placebo group for analysis. The results indicated that prophylactic administration of 8 mg dexamethasone did not have any protective effect against PDPH (31 vs. 18, P = 0.054) and even increased the incidence of PDPH in the first 24 h in parturient patients (25 vs. 11, P = 0.016). Furthermore, the meta-analysis also showed that dexamethasone did not prevent the incidence of PDPH in the postoperative follow-up days (RR 1.05; 95 % CI 0.46-2.38; P = 0.91) and may even have increased the trend in the first 24 h. Prophylactic administration of 8 mg dexamethasone does not have any protective effect against PDPH and may even increase the incidence of PDPH in the first 24 h in patients with spinal anesthesia.
    Acta neurologica Belgica. 05/2014;
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    ABSTRACT: RVF (Arg-Val-Phe), a peptide derived from wheat germ, shows antioxidant properties. Here, the neuroprotective efficacies of RVF were investigated in human neuroblastoma cells (SH-SY5Y) that were pretreated with RVF (150-250 μM, 4 h) and exposed to H2O2 (200 μM). RVF increased viable cell numbers by 37 % and reduced the release of lactate dehydrogenase. Pretreatment with RVF also inhibited H2O2-induced accumulation of reactive oxygen species and maintained the mitochondrial transmembrane potential as well as preventing intracellular Ca(2+) dysregulation during H2O2 exposure. Furthermore, pretreatment with RVF increased the Bcl-2/Bax ratio and blocked cleavage poly(ADP-ribose) polymerase by inhibiting caspase-3 activation, thus decreasing apoptosis.
    Biotechnology Letters 04/2014; · 1.85 Impact Factor
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    ABSTRACT: An environmentally friendly new approach to prepare reduced graphene oxide (RGO) was developed by using glycylglycine (gly-gly) as both a reducing and stabilizing agent. Graphene oxide (GO) was transformed to RGO with the appropriate pH, temperature and reducing agent/GO ratio. The RGO was characterized by ultraviolet-visible spectroscopy, Fourier transform infrared spectroscopy, Raman spectroscopy, thermo-gravimetric analysis, x-ray diffraction, x-ray photoelectron spectroscopy (XPS), and transmission electron microscopy. The RGO aqueous suspension showed extraordinary stability in the absence of any external stabilizing reagents. The XPS analysis showed that this excellent stability is due to modifications of the RGO nanosheets by the gly-gly molecules. The modified RGO complex with copper shows good catalytic performance for reduction of 4-nitrophenol to 4-aminophenol.
    Nanotechnology 03/2014; 25(13):135707. · 3.84 Impact Factor
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    ABSTRACT: Intermittent hypoxia/reoxygenation (IHR) induces proinflammatory cytokines, contributing to the pathogenic process of atherosclerosis associated with obstructive sleep apnea (OSA). Two transcription factors, nuclear factor‑κB (NF‑κB) and hypoxia‑inducible factor‑1 (HIF‑1), have been indicated to mediate proinflammatory cytokines during IHR. The anti‑inflammatory effects of propofol have attracted increasing attention in regard to the treament of multiple diseases associated with inflammation. The present study examined whether propofol inhibits NF‑κB and HIF‑1 activity in vascular endothelial cells during IHR. EA.hy926 endothelial cells were exposed to IHR for 64 cycles with or without propofol treatment. Gene knockdown by transfection of siRNA against p38 mitogen‑activated protein kinase (MAPK) was also used to investigate the molecular mechanisms. Compared with the control group, IHR exposure significantly induced the activation of NF‑κB and HIF‑1, enhanced the mRNA expression of proinflammatory cytokines and increased the activation of p38 MAPK. Propofol dose‑dependently inhibited the IHR‑induced activation of NF‑κB, but did not change the activation of HIF‑1, which was accompanied by decreased levels of proinflammatory cytokines. In addition, IHR‑induced p38 MAPK activity was attenuated by propofol in a similar manner to the reduction in NF‑κB activity. Furthermore, knockdown of p38 MAPK with siRNA significantly reduced the IHR‑induced activation of NF‑κB, while not affecting HIF‑1. These data demonstrate that propofol selectively attenuates the IHR‑induced activation of NF‑κB, but not HIF‑1, in vascular endothelial cells, and these beneficial effects are likely to be based on the inhibition of the p38 MAPK signaling pathway. Propofol may have the potential to prevent atherosclerosis in patients with OSA by inhibiting NF‑κB‑mediated inflammation in the vascular endothelium.
    Molecular Medicine Reports 02/2014; · 1.17 Impact Factor
  • Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi 02/2014; 35(2):218-20.
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    ABSTRACT: Ornithine decarboxylase (ODC) is the first rate-limiting enzyme in polyamine biosynthesis, which is essential for cell survival. We hypothesized that the ODC/polyamine system is involved in ischemic preconditioning (IPC)-mediated cardioprotection through the activation of Erk1/2 and Akt and through the inhibition of the mitochondrial permeability transition (mPT). Isolated rat hearts were subjected to 40 min of ischemia either with or without IPC (3 cycles of 5-min global ischemia), and ODC protein expression, polyamine content, and Akt and Erk1/2 phosphorylation were evaluated after 30 min of reperfusion. IPC significantly upregulated the ODC/polyamine pathway, promoted Erk1/2 and Akt phosphorylation, and reduced the infarct size and heart dysfunction after reperfusion. An inhibitor of ODC, α-difluoromethylornithine (DFMO), abolished the IPC-induced cardioprotection. Moreover, the inhibition of the IPC-induced activation of Erk1/2 and Akt using PD98059 or wortmannin downregulated the ODC/polyamine system. In separate studies, the Ca(2+) load required to open the mPT pore was significantly lower in DFMO-treated cardiac mitochondria than in mitochondria from IPC hearts. Furthermore, spermine or spermidine significantly inhibited the mPT induced by CaCl2. These results suggest that IPC upregulates the ODC/polyamine system and mediates preconditioning cardioprotection, which may depend on the phosphorylation/activation of Erk1/2 and Akt and on the inhibition of the mPT during reperfusion.
    Molecular and Cellular Biochemistry 01/2014; · 2.33 Impact Factor
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    ABSTRACT: Bimetallic palladium–silver nanoparticles (NPs) supported on reduced oxide graphene (RGO) with different Pd/Ag ratios (Pd–Ag/RGO) were prepared by an easy green method which did not use any additional reducing agents or a dispersing agent. During the process, simultaneous redox reactions between AgNO3, K2PdCl4 and graphene oxide (GO) led to bimetallic Pd–Ag NPs. The morphology and composition of the Pd–Ag/RGO were characterized by transmission electron microscopy, X-ray diffraction, X-ray photoelectron spectroscopy, thermogravimetric analysis and Raman spectroscopy. Cyclic voltammetry and chronoamperometry were used to investigate the electrochemical activities and stabilities of these Pd–Ag/RGO catalysts for the electro-oxidation of methanol and ethanol in alkaline media. Among the different Pd/Ag ratios, the Pd–Ag (1:1)/RGO had the best catalytic activities and stability. So it is a promising catalyst for direct alcohol fuel cell applications.
    Journal of Power Sources 01/2014; 263:13–21. · 5.26 Impact Factor
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    ABSTRACT: A new approach to prepare reduced graphene oxide was developed by using sodium diphenylamine sulphonic acid salt as both a reducing and stabilizing agent. Graphene oxide was transformed to reduced graphene oxide with the appropriate pH, temperature and reducing agent/graphene oxide ratio. The reduced graphene oxide was characterized by ultraviolet-visible spectroscopy, Fourier transform infrared spectroscopy, Raman spectroscopy, thermo-gravimetric analysis, X-ray diffraction, X-ray photoelectron spectroscopy, and transmission electron microscopy. The reduced graphene oxide aqueous suspension showed extraordinary stability in the absence of any external stabilizing reagents. The X-ray photoelectron spectroscopy analysis showed that this excellent stability is due to modifications of the reduced graphene oxide nanosheets by the sodium diphenylamine sulphonic acid salt molecules. The modified reduced graphene oxide aqueous suspension shows good catalytic performance for the synthesis of isoamyl benzoate.
    Science of Advanced Materials 01/2014; 6(4). · 2.51 Impact Factor
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    ABSTRACT: Neuroblastoma is the most common and deadly solid tumor in children, and there is currently no effective treatment available for neuroblastoma patients. The repressor element-1 silencing transcription (REST) factor has been found to play important roles in the regulation of neural differentiation and tumorigenesis. Recently, a REST signature consisting of downstream targets of REST has been reported to have clinical relevance in both breast cancer and glioblastoma. However it remains unclear how the REST signature works in neuroblastoma. Publicly available datasets were mined and bioinformatic approaches were used to investigate the utility of the REST signature in neuroblastoma with both preclinical and real patient data. The REST signature was found to be associated with drug sensitivity in neuroblastoma cell lines. Further, neuroblastoma patients with enhanced REST activity are significantly associated with higher clinical stages. Loss of heterozygosity on chromosome 11q23, which occurs in a large subset of high-risk neuroblastomas, tends to be correlated with high REST activity, with marginal significance. In conclusion, the REST signature has important implications for targeted therapy, and it is a prognostic factor in neuroblastoma patients.
    International Journal of Molecular Sciences 01/2014; 15(7):11220-11233. · 2.46 Impact Factor
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    ABSTRACT: Topographical modification at micro- and nanoscale is widely applied to enhance the tissue integration properties of biomaterials, but the underlying molecular mechanism is poorly understood. The biomaterial topography modulates cell functions via mechanotransduction of direct and indirect. We propose that N-cadherin may play a role in the topographically induced indirect mechanotransduction by regulating the β-catenin signaling. For confirmation, the cell functions, N-cadherin expression and β-catenin signaling activation of osteoblasts on titanium (Ti) surfaces with micro- or/and nanotopography are systemically compared with naive and N-cadherin down-regulating MC3T3-E1 cells. We find that the N-cadherin expression is reversely related to the intracellular β-catenin signaling and the N-cadherin/β-catenin signaling is modulated differentially by the micro- and nanotopography. The nanotopography significantly up-regulates the N-cadherin expression leading to lower β-catenin signaling activity and consequently depressed differentiation, whereas the microtopography down-regulates the N-cadherin expression resulting in enhanced β-catenin signaling and thus osteoblast differentiation. Artificial down-regulation of the N-cadherin expression can significantly up-regulate the β-catenin signaling and consequently enhance the osteoblast differentiation on all the Ti surfaces. The study for the first time clarifies the involvement of the N-cadherin/β-catenin interaction in the micro/nanotopography induced indirect mechanotransduction and provides a potentially new approach for biomaterial modification and biofunctionalization by down-regulating the cell N-cadherin expression to achieve improved clinical performance.
    Biomaterials 01/2014; 35(24):6206–6218. · 8.31 Impact Factor
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    ABSTRACT: An easy and efficient method to reduce graphene oxide (GO) with manganese powder under mildly acidic conditions with ultrasonication for 30 min at room temperature has been developed. The reduction process was traced by UV-visible absorption spectroscopy, and the obtained reduced graphene was characterized by X-ray diffraction (XRD), Raman microscope, thermo-gravimetric analysis (TGA) and X-ray photoelectron spectroscopy (XPS). The results showed that Mn powder is an efficient reducing agent for the reduction of GO. The Mn2+ ions produced during the redox reaction between GO and the manganese powder were chemically transformed to MnO2 and then formed MnO2/RGO composites. The MnO2/RGO composites were used as electrode materials and their capacitance was studied by cyclic voltammetry and galvanostatic charge/discharge. The MnO2/RGO composites showed excellent electrochemical performance with a highest specific capacitance of about 330 F.g−1.
    Electrochimica Acta. 01/2014; 130:305–313.

Publication Stats

4k Citations
810.94 Total Impact Points

Institutions

  • 2014
    • Fourth Military Medical University
      • School of Stomatology
      Xi’an, Liaoning, China
    • Shandong University
      Chi-nan-shih, Shandong Sheng, China
  • 2013–2014
    • Tianjin University
      • • Department of Chemistry
      • • School of Science
      T’ien-ching-shih, Tianjin Shi, China
    • Xi'an Jiaotong University
      Ch’ang-an, Shaanxi, China
    • Chinese Center For Disease Control And Prevention
      Peping, Beijing, China
    • Shanghai Jiao Tong University
      • Center of Instrumental Analysis
      Shanghai, Shanghai Shi, China
  • 2011–2014
    • Lankenau Institute for Medical Research
      Wynnewood, Oklahoma, United States
    • Tohoku University
      • Department of Electronic Engineering
      Sendai, Kagoshima-ken, Japan
    • Peking University
      Peping, Beijing, China
  • 2007–2014
    • China-Japan Friendship Hospital
      Peping, Beijing, China
    • Harbin Medical University
      • • Department of Pathophysiology
      • • Department of Cardiology
      Charbin, Heilongjiang Sheng, China
    • Jiangsu Institute of Nuclear Medicine
      Jiangqun, Qinghai Sheng, China
    • Tsinghua University
      • Department of Environmental Engineering
      Peping, Beijing, China
  • 2012–2013
    • Jiangnan University
      • School of Food Science and Technology
      Wuxi, Jiangsu Sheng, China
    • Logistical College of Chinese People's Armed Police Force
      T’ien-ching-shih, Tianjin Shi, China
  • 2009–2013
    • Peking University People's Hospital
      • Heart Center
      Peping, Beijing, China
    • Wenzhou Medical College
      • School of Pharmaceutical Science
      Yung-chia, Zhejiang Sheng, China
  • 2006–2013
    • University Center Rochester
      • Department of Medicine
      Rochester, Minnesota, United States
  • 2006–2012
    • Northeast Institute of Geography and Agroecology
      • State Key Laboratory of Drug Research
      Beijing, Beijing Shi, China
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2007–2011
    • Oregon Health and Science University
      • Division of Cardiovascular Medicine
      Portland, OR, United States
  • 2005–2011
    • Stanford University
      • • Department of Chemistry
      • • Department of Materials Science and Engineering
      Stanford, CA, United States
  • 2002–2010
    • University of Utah
      • • School of Medicine
      • • Department of Internal Medicine
      Salt Lake City, Utah, United States
  • 2007–2009
    • University of Science and Technology, Beijing
      Peping, Beijing, China
  • 2006–2009
    • Shanghai Institutes for Biological Sciences
      Shanghai, Shanghai Shi, China
  • 2008
    • Case Western Reserve University
      Cleveland, Ohio, United States
  • 2005–2006
    • Nanjing University
      • State Key Laboratory of Pharmaceutical Biotechnology
      Nanjing, Jiangsu Sheng, China
  • 2000
    • Beijing University of Aeronautics and Astronautics (Beihang University)
      Peping, Beijing, China