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Articles by Chen Zhang
Total Records ( 3 ) for Chen Zhang
  Yong Hang , Chen Zhang and Hui Li
  Evaluation of controlled airspace capacity based on the controllers’ workload is the most wildly used theoretical evaluation method of controlled airspace capacity currently in China. This method uses the aircraft sorties to be the only metric. It identifies some quantitative relationship between the metric of aircraft sorties and controllers’ workload. The method then figures out the controllers’ workload and evaluates the capacity value limited by the controllers’ workload ability in the controlled airspace according to the DORATASK method. But in actual operation, aircraft sorties is not the only Influencing factor of controllers’ workload. Therefore, a new evaluation method of controllers’ workload based on the metric of traffic complexity is proposed. This new method uses a group of multidimensional metric of air traffic complexity to research and solve the problem of evaluating the controllers’ workload, Instead of using a traditional single traffic measurement- aircraft sorties. The method is applied in the capacity evaluation project of control sector 02 in Shanghai. The evaluation results are recognized by the front-line ATC experts. Meanwhile they also verify the feasibility and correctness of the method applying to the airspace capacity evaluation.
  Jian Meng and Chen Zhang
  Background and Objective: Sepsis is a condition that causes multiple organ failure leading to mortality. Oxidative stress has a pivotal role in the development of sepsis causing organ failure. So, the aim of this study was to analyze the effect of vanillic acid on sepsis-induced liver damage in rats. Materials and Methods: Male Sprague Dawley rats were segregated into four groups; sham group, sepsis control group, vanillic acid control group and vanillic acid treated sepsis group. Sepsis was induced by cecal ligation and puncture (CLP). Rats were intraperitoneally (i.p.) injected with 100 mg kg–1 b.wt. vanillic acid in 0.5 mL kg–1 b.wt. saline upon sepsis induction and sacrificed after 24 h of treatment for biochemical and histopathological analysis. Results: The levels of reduced glutathione (GSH) and antioxidant enzymes (glutathione peroxidase, superoxide dismutase, catalase) were markedly reduced (p<0.05) in the sepsis control group. Malondialdehyde (MDA) levels, liver damage markers (AST, ALT, ALP) and pro-inflammatory cytokines (TNF-α, IL-6) in the liver tissues and plasma of rats were elevated (p<0.05) in sepsis control group. Treatment with vanillic acid significantly reversed (p<0.05) the effects of sepsis on oxidative stress markers and pro-inflammatory cytokine levels compared to sepsis control group. Histopathological changes in liver were observed in vanillic acid treated rats as compared to sepsis control group. Conclusion: So, it was concluded that vanillic acid is able to prevent the progression of sepsis and protect against oxidative liver injury. Further research is needed to ascertain the mechanism of vanillic acid in preventing sepsis-induced organ damage.
  Chengjian Mao , Nicole M. Patterson , Milu T. Cherian , Irene O. Aninye , Chen Zhang , Jamie Boney Montoya , Jingwei Cheng , Karson S. Putt , Paul J. Hergenrother , Elizabeth M. Wilson , Ann M. Nardulli , Steven K. Nordeen and David J. Shapiro
  Estrogen receptor α (ERα) plays an important role in several human cancers. Most current ERα antagonists bind in the receptor ligand binding pocket and compete for binding with estrogenic ligands. Instead of the traditional approach of targeting estrogen binding to ER, we describe a strategy using a high throughput fluorescence anisotropy microplate assay to identify small molecule inhibitors of ERα binding to consensus estrogen response element (cERE) DNA. We identified small molecule inhibitors of ERα binding to the fluorescein-labeled (fl)cERE and evaluated their specificity, potency, and efficacy. One small molecule, theophylline, 8-[(benzylthio)methyl]-(7CI,8CI) (TPBM), inhibited ERα binding to the flcERE (IC50 ~ 3 µM) and inhibited ERα-mediated transcription of a stably transfected ERE-containing reporter gene. Inhibition by TPBM was ER-specific, because progesterone and glucocorticoid receptor transcriptional activity were not significantly inhibited. In tamoxifen-resistant breast cancer cells that overexpress ERα, TPBM inhibited 17β-estradiol (E2)-ERα (IC50 9 µM) and 4-hydroxytamoxifen-ERα-mediated gene expression. Chromatin immunoprecipitation showed TPBM reduced E2·ERα recruitment to an endogenous estrogen-responsive gene. TPBM inhibited E2-dependent growth of ERα-positive cancer cells (IC50 of 5 µM). TPBM is not toxic to cells and does not affect estrogen-independent cell growth. TPBM acts outside of the ER ligand binding pocket, does not act by chelating the zinc in ER zinc fingers, and differs from known ERα inhibitors. Using a simple high throughput screen for inhibitors of ERα binding to the cERE, a small molecule inhibitor has been identified that selectively inhibits ERα-mediated gene expression and estrogen-dependent growth of cancer cells.
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