Ying Wang

Tongji Hospital, Wu-han-shih, Hubei, China

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Publications (315)999.53 Total impact

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    ABSTRACT: The tumor microenvironment (TME) is being increasingly recognized as a key factor in multiple stages of disease progression, particularly local resistance, immune-escaping, and distant metastasis, thereby substantially impacting the future development of frontline interventions in clinical oncology. An appropriate understanding of the TME promotes evaluation and selection of candidate agents to control malignancies at both the primary sites as well as the metastatic settings. This review presents a timely outline of research advances in TME biology and highlights the prospect of targeting the TME as a critical strategy to overcome acquired resistance, prevent metastasis, and improve therapeutic efficacy. As benign cells in TME niches actively modulate response of cancer cells to a broad range of standard chemotherapies and targeted agents, cancer-oriented therapeutics should be combined with TME-targeting treatments to achieve optimal clinical outcomes. Overall, a body of updated information is delivered to summarize recently emerging and rapidly progressing aspects of TME studies, and to provide a significant guideline for prospective development of personalized medicine, with the long term aim of providing a cure for cancer patients.
    BMC Medicine 12/2015; 13(1):278. DOI:10.1186/s12916-015-0278-7 · 7.28 Impact Factor
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    ABSTRACT: Application of the sepsis resuscitation bundle is limited by clinician knowledge, skills, and experience. We used the adjusted first-hour basic care tasks in pediatric patients in three tertiary hospitals in Shanghai, China. The aim of this study is to survey the compliance of the adjusted tasks and to evaluate in situ simulation team training on improving the compliance. A prospective observational study was performed with the survey checklists from May 2011 to January 2012 in three pediatric intensive care units. A simulated case scenario was administered to the practitioners in one hospital. Seventy-three patients were enrolled, including 47 patients in one simulation hospital (SH) and 26 patients in two nonsimulation hospitals (NSH). The total compliance of the tasks was 47.9% (35/73). The compliance in the SH was significantly higher compared to that in the NSHs (61.7% [29/47] vs. 23.1% [6/26], p < 0.01). Compared to the SH, the main problems in the NSH were giving intravenous or intraosseous fluid resuscitation in a longer time (35.3 min vs. 19.9 min, p = 0.000), a smaller percentage of measurement of accurate urine output (38.5% vs. 68.1%, p = 0.027), delivering high-flow oxygen (73.1% vs. 93.6%, p = 0.028), and measurement of lactate (69.2% vs. 100%, p = 0.000). In situ simulation team training is an effective method of teaching the tasks of septic shock care to clinicians and nurses on the front line and of improving the compliance of the tasks. Copyright © 2015 Elsevier Inc. All rights reserved.
    Journal of Emergency Medicine 08/2015; DOI:10.1016/j.jemermed.2015.05.040 · 1.18 Impact Factor
  • Yizong Wang · Xueguan Lu · Ying Wang · Jun Zhou
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    ABSTRACT: To determine the clinical effect of Radiofrequency Ablation (RFA) for residual lung metastases from breast cancer after systemic chemotherapy. An experimental study. The Second Affiliated Hospital of Soochow University, Suzhou, Fudan University Shanghai Cancer Center, Shanghai, China, from January 2008 to October 2014. Thirty-five breast cancer patients with 67 pulmonary metastases were involved in this study. All lesions were treated by RFAand followed by CT-scan. Primary endpoint of this clinical study was local control; secondary endpoints were overall survival and treatment-related toxicities. Complete Response (CR) was observed in 59 lesions, with Partial Response (PR) in 4 lesions, Stable Disease (SD) in 1 lesion and Progression Disease (PD) in 3 lesions. The lesion diameter > 2 cm was related to poor local control (p=0.04). The median Overall Survival (OS) was 33 months (95%CI: 21.6 - 44.4). One-, 2-, and 3-year OS rates were 88.6%, 59.3% and 42.8% respectively. The mumber of pulmonary metastases (≥2), the diameter of lesion (> 2 cm) and coexisting with liver metastases were significantly correlated to poor OS by multivariate analysis. Log-rank test showed statistically significant difference of OS in diameter of lesion and coexisting with other metastases. RFAis a promising treatment option for patients with residual lung metastases from breast cancer after systemic chemotherapy in selected patients.
    08/2015; 25(8):602-605.
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    ABSTRACT: The high-mobility group box 1 (HMGB1) protein is a DNA-binding nuclear protein, which is overexpressed in leukemia cells. Cordycepin is characterized by strong antileukemic properties and is regarded as an effective natural compound for leukemia therapy. The aim of the present study was to investigate the impact of HMGB1 knockdown and cordycepin treatment on proliferation, apoptosis, reactive oxygen species (ROS) levels and adhesion of K562 human chronic myeloid leukemia cells. The Cell Counting kit‑8 assay was used to determine the proliferation of K562 cells. The cell cycle and apoptosis of K562 cells was determined using flow cytometric analysis. In addition, a cell adhesion assay was performed. Western blotting was used to determine the protein expression of cyclooxygenase 2, Bax, receptor for advanced glycation end-products and Bcl‑2. The data collected demonstrated that HMGB1 knockdown combined with cordycepin treatment had significant anti‑proliferative and pro‑apoptotic effects. In addition, it increased the ROS levels and reduced the adhesion of K562 cells. It was also identified that HMGB1 knockdown had synergistic effects with cordycepin, which aided in accelerating apoptosis, and inhibiting proliferation and adhesion in chronic myeloid leukemia cells. These results indicated that HMGB1 may be used as a potential therapeutic target, with cordycepin having potential as an auxiliary drug. Therefore, it is suggested that HMGB1 knockdown and corycepin treatement may present a promising therapeutic strategy for leukemia.
    Molecular Medicine Reports 06/2015; DOI:10.3892/mmr.2015.3928 · 1.48 Impact Factor
  • Wei Cao · Kai Cao · Jianchang Cao · Ying Wang · Yufang Shi
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    ABSTRACT: Over the past decade, our understanding of the regulatory role of mesenchymal stem cells (MSCs) in adaptive immune responses through both preclinical and clinical studies has dramatically expanded, providing great promise for treating various inflammatory diseases. Most studies are focused on the modulatory effects of these cells on the properties of T cell-mediated immune responses, including activation, proliferation, survival, and subset differentiation. Interestingly, the immunosuppressive function of MSCs was found to be licensed by IFN-γ and TNF-α produced by T cells and that can be further amplified by cytokines such as IL-17. However, the immunosuppressive function of MSCs can be reversed in certain situation, such as suboptimal levels of inflammatory cytokines, or in the presence of immunosuppressive molecules. Here we review the influence of MSCs on adaptive immune system, especially their bidirectional interaction in tuning the immune microenvironment and subsequently repairing damaged tissue. Understanding MSC-mediated regulation of T cells is expected to provide fundamental information for guiding appropriate applications of MSCs in clinical settings. Copyright © 2015. Published by Elsevier B.V.
    Immunology letters 06/2015; DOI:10.1016/j.imlet.2015.06.003 · 2.37 Impact Factor
  • Xiaodong Chen · Yurun Gan · Ying Wang · Yufang Shi
    Cytotherapy 06/2015; 17(6):S48-S50. DOI:10.1016/j.jcyt.2015.03.477 · 3.10 Impact Factor
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    ABSTRACT: The quest for high-efficiency heat-to-electricity conversion has been one of the major driving forces towards renewable energy production for the future. Efficient thermoelectric devices require careful material engineering such as high voltage generation from a temperature gradient, and high electrical conductivity while maintaining a low thermal conductivity. Significant progress in the thermoelectric performance of materials has been made by exploring the ultralow thermal conductivity at high temperature, reducing the thermal conductivity by nanostructuring, resonant doping and energy-dependent scattering. For a given thermal conductivity and temperature, thermoelectric powerfactor is determined by the electronic structure of the material. Low dimensionality (1D and 2D) opens new routes to high powerfactor due to their unique density of states of confined electrons and holes. Emerging 2D transition metal dichalcogenide (TMDC) semiconductors represent a new class of thermoelectric materials not only from their discretized density of states, but especially due to their large effective masses and high carrier mobilities, different from gapless semi-metallic graphene. Here we report a measured powerfactor of $MoS_2$ as large as $8.5 mWm^{-1}K^{-2}$ at room temperature, the highest among all thermoelectric materials and twice that of commercial thermoelectric material $Bi_2Te_3$. For the first time, the measurement of the thermoelectric properties of monolayer $MoS_2$ allows us to determine the quantum confined 2D density of states near the conduction band edge, which cannot be measured by electrical conductivity alone. The demonstrated record high powerfactor in 2D TMDCs holds promise for efficient thermoelectric energy conversion.
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    ABSTRACT: Our previous study has proved glucagon-like peptide-1 (GLP-1), which is developed to treat type 2 diabetes, has a significant effect on neuroprotection against AGE-induced neuronal insult in vitro models of diabetes-related Alzheimer's disease (AD). However, the molecular mechanisms remain to be elucidated and it is not clear whether GLP-1 receptor mediates the down-regulation effects on AGE-induced AD-like changes in vivo. This study aims to explore the effect and mechanisms of GLP-1 receptor agonists (GLP-1RA) against the AGE-dependent signaling pathway both in vitro and in vivo. In this study, We demonstrated GLP-1RA could inhibit oxidative stress and repair the mitochondrial damage in addition to decreasing tau hyperphosphorylation in PC12 cells treated with AGEs. Importantly, we first observed AGEs in the circulatory system could induce tau hyperphosphorylation after we injected AGEs (1 μg/kg bodyweight) into the mice tail vein. We found GLP-1RA could promote mitochondrial biogenesis and antioxidant system via regulating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) signaling pathway in vivo besides down-regulating the activity of glycogen synthase kinase 3β (GSK-3β) to reverse tau hyperphosphorylation directly. Collectively, our results suggest that GLP-1RA protects neurons against AGE-induced tau hyperphosphorylation via regulating GSK-3β and PGC-1α two cooperative signaling pathways. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 05/2015; 300. DOI:10.1016/j.neuroscience.2015.05.023 · 3.33 Impact Factor
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    ABSTRACT: Epstein-Barr virus (EBV) can infect both susceptible B lymphocytes and non-susceptible epithelial cells (ECs). Viral tropism analyses have revealed two intriguing means of EBV infection, either by a receptor-mediated infection of B cells or by a cell-to-cell contact-mediated infection of non-susceptible ECs. Herein, we report a novel "in-cell infection" mechanism for EBV infection of non-susceptible ECs through the formation of cell-in-cell structures. Epithelial CNE-2 cells were invaded by EBV-infected Akata B cells to form cell-in-cell structures in vitro. Such unique cellular structures could be readily observed in the specimens of nasopharyngeal carcinoma. Importantly, the formation of cell-in-cell structures led to the autonomous activation of EBV within Akata cells and subsequent viral transmission to CNE-2 cells, as evidenced by the expression of viral genes and the presence of virion particles in CNE-2 cells. Significantly, EBV generated from in-cell infected ECs displayed altered tropism with higher infection efficacy to both B cells and ECs. In addition to CNE-2 tumor cells, cell-in-cell structure formation could also mediate EBV infection of NPEC1-Bmi1 cells, an immortalized nasopharyngeal epithelial cell line. Furthermore, efficient infection by this mechanism involved the activation of the PI3K/AKT signaling pathway. Thus, our study identified "in-cell infection" as a novel mechanism for EBV infection. Given the diversity of virus-infected cells and the prevalence of cell-in-cell structures during chronic infection, we speculate that "in-cell infection" is likely a general mechanism for EBV and other viruses to infect non-susceptible ECs.Cell Research advance online publication 28 April 2015; doi:10.1038/cr.2015.50.
    Cell Research 04/2015; 25(7). DOI:10.1038/cr.2015.50 · 11.98 Impact Factor
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    ABSTRACT: Interleukin (IL) 17-producing T helper (Th17) cells play critical roles in the clearance of extracellular bacteria and fungi as well as the pathogenesis of various autoimmune diseases, such as multiple sclerosis, psoriasis, and ulcerative colitis. Although a global transcriptional regulatory network of Th17 cell differentiation has been mapped recently, the participation of epigenetic modifications in the differentiation process has yet to be elucidated. We demonstrated here that histone H3 lysine-27 (H3K27) demethylation, predominantly mediated by the H3K27 demethylase Jmjd3, crucially regulated Th17 cell differentiation. Activation of naïve CD4+ T cells immediately induced high expression of Jmjd3. Genetic depletion of Jmjd3 in CD4+ T cells specifically impaired Th17 cell differentiation both in vitro and in vivo. Ectopic expression of Jmjd3 largely rescued the impaired differentiation of Th17 cells in vitro in Jmjd3-deficient CD4+ T cells. Importantly, Jmjd3-deficent mice were resistant to the induction of experimental autoimmune encephalomyelitis (EAE). Furthermore, inhibition of the H3K27 demethylase activity with the specific inhibitor GSK-J4 dramatically suppressed Th17 cell differentiation in vitro. At the molecular level, Jmjd3 directly bound to and reduced the level of H3K27 trimethylation (me3) at the genomic sites of Rorc, which encodes the master Th17 transcription factor Rorγt, and Th17 cytokine genes such as Il17, Il17f, and Il22. Therefore, our studies established a critical role of Jmjd3-mediated H3K27 demethylation in Th17 cell differentiation and suggest that Jmjd3 can be a novel therapeutic target for suppressing autoimmune responses.
    Journal of Molecular Cell Biology 04/2015; DOI:10.1093/jmcb/mjv022 · 8.43 Impact Factor
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    ABSTRACT: Optical selection rule fundamentally determines the optical transition between energy states in a variety of physical systems from hydrogen atoms to bulk crystals such as GaAs. It is important for optoelectronic applications such as lasers, energy-dispersive X-ray spectroscopy and quantum computation. Recently, single layer transition metal dichalcogenide (TMDC) exhibits valleys in momentum space with nontrivial Berry curvature and excitons with large binding energy. However, it is unclear how the unique valley degree of freedom combined with the strong excitonic effect influences the optical excitation. Here we discover a new set of optical selection rules in monolayer WS2,imposed by valley and exciton angular momentum. We experimentally demonstrated such a principle for second harmonic generation (SHG) and two-photon luminescence (TPL). Moreover, the two-photon induced valley populations yield net circular polarized photoluminescence after a sub-ps interexciton relaxation (2p->1s) and last for 8 ps. The discovery of this new optical selection rule in valleytronic 2D system not only largely extend information degrees but sets a foundation in control of optical transitions that is crucial to valley optoeletronic device applications such as 2D valley-polarized light emitting diodes (LED), optical switches and coherent control for quantum computing.
  • PLoS ONE 03/2015; 10(3):e0117429. DOI:10.1371/journal.pone.0117429 · 3.23 Impact Factor
  • Yongtao Xiao · Weihui Yan · Lina Lu · Ying Wang · Wei Lu · Yi Cao · Wei Cai
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    ABSTRACT: Although our previous studies have provided evidence that oxidative stress has an essential role in total parenteral nutrition (TPN)-associated liver injury, the mechanisms involved are incompletely understood. Here, we show the existence of crosstalk between the miR-200 family of microRNAs and oxidative stress. The members of the miR-200 family are markedly enhanced in hepatic cells by hydrogen peroxide (H2O2) treatment. The upregulation of miR-200-3p in turn modulates the H2O2-mediated oxidative stress response by targeting p38α. The enhanced expression of miR-200-3p mimics p38α deficiency and promotes H2O2-induced cell death. Members of the miR-200 family that are known to inhibit the epithelial to mesenchymal transition (EMT) are induced by the tumour suppressor p53. Here, we show that p53 phosphorylation at Ser 33 contributes to H2O2-induced miR-200s transcription. In addition, we show that p38α can directly phosphorylate p53 at serine 33 upon H2O2 exposure. Thus, we suggest that in liver cells, the oxidative stress-induced, p38α-mediated phosphorylation of p53 at Ser33 is essential for the functional regulation of oxidative stress-induced miR-200 transcription by p53. Collectively, our data indicate that the p53-dependent expression of miR-200a-3p promotes cell death by inhibiting a p38/p53/miR-200 feedback loop.
    Cell cycle (Georgetown, Tex.) 03/2015; 14(10). DOI:10.1080/15384101.2015.1026491 · 5.01 Impact Factor
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    ABSTRACT: The aim of this work was to screen miRNA signatures dysregulated in tuberculosis to improve our understanding of the biological role of miRNAs involved in the disease. Datasets deposited in publically available databases from microarray studies on infectious diseases and malignancies were retrieved, screened, and subjected to further analysis. Effect sizes were combined using the inverse-variance model and between-study heterogeneity was evaluated by the random effects model. 35 miRNAs were differentially expressed (12 up-regulated, 23 down-regulated; p < 0.05) by combining 15 datasets of tuberculosis and other infectious diseases. 15 miRNAs were found to be significantly differentially regulated (7 up-regulated, 8 down-regulated; p < 0.05) by combining 53 datasets of tuberculosis and malignancies. Most of the miRNA signatures identified in this study were found to be involved in immune responses and metabolism. Expression of these miRNA signatures in serum samples from TB subjects (n = 11) as well as healthy controls (n = 10) was examined by TaqMan miRNA array. Taken together, the results revealed differential expression of miRNAs in TB, but available datasets are limited and these miRNA signatures should be validated in future studies. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Tuberculosis (Edinburgh, Scotland) 03/2015; 95(4). DOI:10.1016/j.tube.2015.02.043 · 3.50 Impact Factor
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    ABSTRACT: Pulmonary oligometastases can be treated by local treatment options, such as resection, radiofrequency ablation (RFA), and radiotherapy, in selected patients. In the present study, 67 patients with 115 pulmonary metastases were treated, and all the lesions were treated by RFA and followed with a computed tomography scan. The local control, overall survival (OS), progression-free survival (PFS) and treatment-related toxicity were observed. Median follow-up duration after the initial RFA was 24 months (range, 3-39 months). The median PFS from RFA was 14 months [95% confidence interval (CI), 11.6-16.4]. The 6-, 12- and 18-month PFS rates were 82.1, 55.7 and 27.5%, respectively. The median OS rate from RFA was 24 months (95% CI, 18.2-29.8). The 1-, 2- and 3-year OS rates were 83.6, 46.3 and 14.3%, respectively. Primary tumor was significantly correlated to PFS and OS on multivariate analysis, and other variates showed no significance. Therefore, RFA is safe for patient treatment and can be considered as a promising treatment option for patients with pulmonary metastases.
    Molecular and Clinical Oncology 03/2015; 3(3). DOI:10.3892/mco.2015.525
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    ABSTRACT: Alzheimer's disease (AD) is a common neurodegenerative disease affecting cognitive function in the elderly, which is characterized by the presence of extracellular deposits of insoluble amyloid-β plaques and neuronal loss. Modern pharmacology and drug development usually follow a single-target principle, which might contribute to the failure of most compounds in clinical trials against AD. Considering AD is a multifactorial disease, a combination therapeutic strategy that applies drugs with different mechanisms would be an alternative way. Smart Soup (SS), a Traditional Chinese Medicine formula, is composed of three herbaceous plants and has been applied in the treatment of amnesia in China for hundreds of years. In this work, we studied the clinical potency of the combination of SS and Aricept in AD therapy. In the in vivo model, both longevity and locomotive activity of AD transgenic Drosophila were improved remarkably in the combined medicine treated group. We also observed less amyloid-β deposition and retarded neuronal loss following the combined drug treatment. In the retrospective cohort study, we found the combination therapy exerted better therapeutic effect on AD patients. Our study revealed that combination therapy with multiple drug targets did have a better therapeutic outcome. It provides a new strategy to develop an optimum pharmaceutical approach against AD.
    Journal of Alzheimer's disease: JAD 02/2015; DOI:10.3233/JAD-143183 · 4.15 Impact Factor
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    ABSTRACT: Tuberculosis (TB) is a communicable disease of major global importance and causes metabolic disorder of the patients. In a previous study, we found that the plasma metabolite profile of TB patients differs from that of healthy control subjects based on nuclear magnetic resonance (NMR) spectroscopy. In order to evaluate the TB specificity of the metabolite profile, a total of 110 patients, including 40 with diabetes, 40 with malignancy, and 30 with community-acquired pneumonia (CAP), assessed by NMR spectroscopy, and compared to those of patients with TB. Based on the orthogonal partial least-squares discriminant analysis (OPLS-DA), the metabolic profiles of these diseases were significant different, as compared to the healthy controls and TB patients, respectively. The score plots of the OPLS-DA model demonstrated that TB was easily distinguishable from diabetes, CAP and malignancy. Plasma levels of ketone bodies, lactate, and pyruvate were increased in TB patient compared to healthy control, but lower than CAP and malignancy. We conclude that the metabolic profiles were TB-specific and reflected MTB infection. Our results strongly support the NMR spectroscopy-based metabolomics could contribute to an improved understanding of disease mechanisms and may offer clues to new TB clinic diagnosis and therapies. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Tuberculosis (Edinburgh, Scotland) 02/2015; 95(3). DOI:10.1016/j.tube.2015.02.038 · 3.50 Impact Factor
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    ABSTRACT: CPS-F, a polysaccharide derived from Cordyceps sinensis, is a potential anti-inflammatory and anti-oxidative agent. We demonstrated that CPS-F not only inhibits platelet-derived growth factor BB (PDGF-BB)-induced intracellular reactive oxygen species (ROS) generation, and up-regulation of tumor necrosis factor-α (TNF-α), TNF-α receptor 1 (TNFR1), and monocyte chemotactic protein-1 (MCP-1), but also acts synergistically in combination with MAPK/ERK inhibitor U0126 and PI3K/Akt inhibitor LY294002. Additionally, up-regulation of pro-inflammatory factors was reversed by use of a combination of CPS-F and NADPH oxidase (NOX) inhibitor diphenyleneiodonium chloride (DPI) or silencing of NOX1. Furthermore, CPS-F prevents the PDGF receptor β (PDGFRβ) promoter activity induced by PDGF-BB in transfected cells and ameliorates increased levels of TNF-α, TNFR1, and MCP-1 when PDGFRβ is silenced, thereby suggesting that CPS-F possesses a bidirectional regulatory function. Our findings suggest CPS-F may exert its therapeutic effect for the treatment of glomerulonephritis related to human mesangial cells (HMCs) through the ERK1/2/Akt pathways. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Carbohydrate Polymers 02/2015; 125. DOI:10.1016/j.carbpol.2015.02.012 · 4.07 Impact Factor
  • Jin Wang · Ying Wang · Guo-Ping Zhao
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    ABSTRACT: GlnR has been characterized as a central regulator governing most nitrogen metabolisms in many important actinomycetes. So far, the GlnR binding consensus sequences have been extensively studied, but with different motifs proposed, which has therefore brought confusion and impeded the understanding of the in-depth molecular mechanisms of GlnR-mediated transcriptional regulation. Here, a 30-nt GlnR-protected DNA sequence in the promoter of glnA in A. mediterranei was employed for precise characterization of GlnR binding consensus sequences. Site-by-site mutagenesis strategy combining with the Electrophoretic Mobility Shift Assay were employed, and a 5-nt GlnR Box was precisely defined as the basic unit for GlnR binding.
    Biochemical and Biophysical Research Communications 02/2015; 458(3). DOI:10.1016/j.bbrc.2015.02.010 · 2.28 Impact Factor
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    ABSTRACT: Invasive yeast infections cause significant morbidity and mortality. Surveillance for the infection is necessary to detect trends in species distribution and antifungal resistance. We performed this retrospective study of yeast infection at Jinling Hospital, Nanjing in China, from year of 2010 to 2012. A total of 341 yeast isolates were obtained from patients with invasive infections in the period. Among these isolates, Candida spp. comprised of the highest percentage of yeast strains (91.8 %), followed by Cryptococcus neoformans (5.9 %) and other non-Candida yeast strains (2.3 %). Bloodstream isolates made up 41.3 % of yeast strains and the isolates from CVC made up 17.3 %. Among Candida spp., C. albicans was the most common species identified from non-blood clinical specimens (42.9 %), but appeared in only 20.8 % of blood isolates (P < 0.001). C. tropicalis was the most prevalent Candida species in the blood samples (28.5 %). Candida spp. was mainly isolated from specimens of the ICU patients, while C. neoformans was mainly isolated from specimens in medical wards. Resistance to FLC occurred in 3.7 % of C. albicans, 9.9 % of C. tropicalis, 74.0 % of C. glabrata, and 4.4 % of C. parapsilosis. Most (>92 %) isolates of C. albicans, C. tropicalis, C. parapsilosis, and C. neoformans strains were susceptible to VRC; However, 26.7 % of isolates of C. glabrata were VRC resistant.
    Mycopathologia 01/2015; 179(5-6). DOI:10.1007/s11046-015-9858-5 · 1.55 Impact Factor

Publication Stats

3k Citations
999.53 Total Impact Points


  • 2015
    • Tongji Hospital
      Wu-han-shih, Hubei, China
  • 2012–2015
    • Harbin Medical University
      • • Department of Hematology
      • • Department of Anesthesiology
      Charbin, Heilongjiang Sheng, China
    • Yale-New Haven Hospital
      New Haven, Connecticut, United States
  • 2011–2015
    • Ruijin Hospital North
      Shanghai, Shanghai Shi, China
    • Tianjin Institute of Urban Construction
      T’ien-ching-shih, Tianjin Shi, China
  • 2008–2015
    • Shanghai Institute of Technology
      Shanghai, Shanghai Shi, China
    • China Pharmaceutical University
      • School of Life Science and Technology
      Nan-ching-hsü, Jiangxi Sheng, China
    • Zhejiang Medical University
      • Department of Neurobiology
      Hang-hsien, Zhejiang Sheng, China
  • 2006–2015
    • Renji Hospital
      Shanghai, Shanghai Shi, China
    • Sichuan University of Science and Engineering
      Tzu-kung, Sichuan, China
  • 2004–2015
    • Chinese Academy of Sciences
      • • Biophysics Laboratory
      • • Institute of Health Sciences
      • • Institute of Semiconductors
      Peping, Beijing, China
    • Fudan University
      • • State Key Laboratory of Genetic Engineering
      • • Department of Microbiology and Microbial Engineering
      • • Department of Chemistry
      Shanghai, Shanghai Shi, China
  • 2003–2015
    • Shanghai Jiao Tong University
      • • Department of Clinical Nutrition
      • • Department of Plastic and Reconstructive Surgery
      Shanghai, Shanghai Shi, China
    • Shanghai University
      Shanghai, Shanghai Shi, China
  • 2014
    • University of Illinois at Chicago
      • School of Public Health
      Chicago, Illinois, United States
    • Chinese National Human Genome Center at Shanghai
      Shanghai, Shanghai Shi, China
    • Massachusetts General Hospital
      • Wellman Center for Photomedicine
      Boston, Massachusetts, United States
    • Northeast Normal University
      • Institute of Grassland Science
      Hsin-ching, Jilin Sheng, China
    • Shanghai Institute of Applied Physics
      Shanghai, Shanghai Shi, China
    • Qingdao University
      • College of Automation Engineering
      Tsingtao, Shandong Sheng, China
  • 2013–2014
    • Tianjin University
      • School of Chemical Engineering and Technology
      T’ien-ching-shih, Tianjin Shi, China
    • Harvard University
      Cambridge, Massachusetts, United States
    • Northeast Petroleum University
      Sa-erh-t’u, Heilongjiang Sheng, China
    • Shanghai's Children's Medical Center
      Shanghai, Shanghai Shi, China
    • Harvard Medical School
      • Department of Dermatology
      Boston, Massachusetts, United States
    • Zhengzhou University
      Cheng, Henan Sheng, China
    • Shanghai Institutes for Biological Sciences
      • Institute of Health Sciences
      Shanghai, Shanghai Shi, China
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 2011–2014
    • Baylor College of Medicine
      • Department of Molecular & Cellular Biology
      Houston, Texas, United States
  • 2006–2014
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China
  • 2003–2014
    • Second Military Medical University, Shanghai
      Shanghai, Shanghai Shi, China
  • 2012–2013
    • Nanjing University
      • • School of Medicine
      • • Department of Physics
      Nan-ching, Jiangsu Sheng, China
  • 2010–2013
    • East China Normal University
      • School of Life Sciences
      Shanghai, Shanghai Shi, China
    • Jilin University
      • • Department of Animal Science
      • • College of Chemistry
      Yung-chi, Jilin Sheng, China
    • Wenzhou Medical College
      • Department of Laboratory Medicine
      Yung-chia, Zhejiang Sheng, China
    • Nanjing University of Traditional Chinese Medicine
      Nan-ching, Jiangsu Sheng, China
  • 2009–2013
    • Texas A&M University System Health Science Center
      • Institute of Biosciences and Technology
      Bryan, Texas, United States
    • University of Texas Health Science Center at Houston
      Houston, Texas, United States
    • Yangzhou University
      Chiang-tu, Jiangsu Sheng, China
    • Beijing University of Aeronautics and Astronautics (Beihang University)
      • Department of Physics
      Peping, Beijing, China
    • Tianjin Medical University
      T’ien-ching-shih, Tianjin Shi, China
  • 2008–2013
    • Nanjing University of Science and Technology
      Nan-ching, Jiangsu Sheng, China
  • 2011–2012
    • Changhai Hospital, Shanghai
      Shanghai, Shanghai Shi, China
  • 2010–2012
    • The Chinese University of Hong Kong
      • • Prince of Wales Hospital
      • • Department of Microbiology
      Hong Kong, Hong Kong
  • 2009–2012
    • Kunming Institute of Zoology CAS
      Yün-nan, Yunnan, China
  • 2009–2011
    • Capital Medical University
      • Department of Biochemistry and Molecular Biology
      Peping, Beijing, China
  • 2008–2010
    • Texas A&M University
      • Department of Molecular and Cellular Medicine
      College Station, Texas, United States
  • 2005–2008
    • Hunan University
      Ch’ang-sha-shih, Hunan, China