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Articles by Ling Wang
Total Records ( 6 ) for Ling Wang
  Liping Wan , Chun Wang , Lin Liu , Xiaoqiong Tang , Jinghua Wang , Yue Guan , Ming Jiang , Xianlin Duan , Xiaoyan Ke , Hongmei Jing , Jiong Hu , Ling Wang , Yuming Li and Li Geng
  Invasive Fungal Disease (IFD) is a major cause of death in severe neutropenic patients with hematologic malignancies. Micafungin, a new echinocandin antifungal drug, is effective in treating IFD. However, the efficacy and safety of micafungin in preventing IFD in severe neutropenic patients with hematologic malignancies have not been demonstrated. A prospective and multicenter clinical study was conducted to evaluate the efficacy and safety of micafungin as prophylaxis for IFD. Micafungin 50 mg daily was administered intravenously to 117 high-risk patients with hematologic malignancies undergoing intensive chemotherapy or Hematopoietic Stem Cell Transplantation (HSCT), for a median of 24 days. Successful prophylaxis (no proven, probable or possible IFD up to 1 week after the end of prophylactic treatment) was achieved in 88.54% patients. No patient developed proven IFD during treatment and only 2.08% had probable IFD and 9.38% possible IFD. Micafungin potentially accounted for adverse events in 6.84% of patients. No severe adverse events attributable to micafungin were seen. Micafungin 50 mg daily is a promising prophylactic antifungal therapy for neutropenic patients with hematologic malignancies.
  Zhaohui Jin , Yanran Wang , Xiaoqun Ren , Huiru Xie , Yangyang Gao , Ling Wang and Shichang Gao
  Ganoderic acid A is one of the important active triterpenoid components of Ganoderma lucidum, however the study on pharmacokinetics and oral bioavailability of it is still lacking. The present study aims to investigate pharmacokinetic properties and the absolute oral bioavailability of Ganoderic acid A. A sensitive and selective LC-MS/MS method was developed for the determination of Ganoderic acid A. The validated method was successfully applied to the quantification of Ganoderic acid A in rat plasma after oral and intravenous administrations of triterpenoid extract from Ganoderma lucidum with different single dosages. Ganoderic acid A was rapidly absorbed with the time to maximum concentration (Cmax) <0.611 h after oral administrations for all oral dosage groups. The Cmax after oral administration were 358.733, 1378.20 and 3010.40 ng mL-1 for 100, 200, 400 mg kg-1 dosages, respectively. Area under the concentration-time curve from time zero to the last time point were 954.732, 3235.07 and 7197.236 h ng mL-1 after oral administration for 100, 200, 400 mg kg-1 dosages and 880.950, 1751.076 and 7129.951 h ng mL-1 after intravenous administration for 10, 20, 40 mg kg-1 dosages, respectively. The half-life ranged from 0.363- 0.630 h and 2.183 to 2.485 h after intravenous and oral administration, respectively. Absolute bioavailability ranged from 10.38-17.97%.
  Ling Wang , Feng Yang , Xiaojuan Wei , Yongjiang Luo , Xuzhen Zhou , Wenzhu Guo , Jiangrong Niu and Zhiting Guo
  The objective of this study was to determine the prevalence of mastitis, identify the frequency alteration of predominant pathogens related to clinical and subclinical mastitis in Gansu and Ningxia Province of China. The 29 dairy farms comprising 2000 lactating cows enrolled from April 2012 to November 2014 of which 43.0% (860/2000) were found positive for mastitis by physical examination and Lanzhou Mastitis Test (LMT), the prevalence of Clinical Mastitis (CM) and Subclinical Mastitis (SCM) at cow level were 5.10 and 37.90%, respectively. The proportion of samples contained major pathogens were 97.60% and 871 isolates obtained from 860 milk samples. The common isolates from CM were E. coli (26.89%), S. agalactiae (21.01%) and S. aureus (19.33%) while from SCM were S. agalactiae, S. dysgalactiae and S. aureu, accounted for 30.45, 18.62 and 14.89%, respectively. The contagious pathogens had showed to predominate over the environmental pathogens and the Streptococcus sp. was found the predominant species which remains a significant cause of mastitis in local cattle herds.
  Jiashun Zhang , Rongjie Lv and Ling Wang
  With the rapid development of intelligent system, real time optimization become more and more urgent. Particle Swarm Optimization (PSO) is one of the most effective algorithms in solving such problems. Considered the complexity of intelligent system optimization, speed-up technique is needed. As many optimization problems can be converted to travelling salesman problem, the standard benchmark problem of TSP with 31 cities is employed to analyze the relationship between optimal solution and different parameters. The effect on average of the optimal solution, optimal solution, convergence speed and stability of the optimal solution of different parameters are analyzed. Finally, a comparation with ant colony algorithm is conducted and suitable values of parameters are proposed.
  Stella Maris Ranuncolo , Ling Wang , Jose M. Polo , Tania Dell’Oso , Jamil Dierov , Terry J. Gaymes , Feyruz Rassool , Martin Carroll and Ari Melnick
  The BCL6 oncogenic transcriptional repressor is required for development of germinal center centroblasts, which undergo simultaneous genetic recombination and massive clonal expansion. Although BCL6 is required for survival of centroblasts, its expression in earlier B-cells is toxic. Understanding these opposing effects could provide critical insight into normal B-cell biology and lymphomagenesis. We examined the transcriptional and biological effects of BCL6 in various primary cells. BCL6 repression of ATR was previously shown to play a critical role in the centroblast phenotype. Likewise, we found that BCL6 could impose an ATR-dependent phenotype of attenuated DNA damage sensing and repair in primary fibroblasts and B-cells. BCL6 induced true genomic instability because DNA repair was delayed and was qualitatively impaired, which could be critical for BCL6-induced lymphomagenesis. Although BCL6 can directly repress TP53 in centroblasts, BCL6 induced TP53 expression in primary fibroblasts and B-cells, and these cells underwent p53-dependent growth arrest and senescence in the presence of physiological levels of BCL6. This differential ability to trigger a functional p53 response explains at least in part the different biological response to BCL6 expression in centroblasts versus other cells. The data suggest that targeted re-activation of TP53 could be of therapeutic value in centroblast-derived lymphomas.
  Ling Wang , Jie Gao , Wei Dai and Luo Lu
  Hypoxia/reoxygenation stress induces the activation of specific signaling proteins and activator protein 1 (AP-1) to regulate cell cycle regression and apoptosis. In the present study, we report that hypoxia/reoxygenation stress activates AP-1 by increasing c-Jun phosphorylation and DNA binding activity through activation of Polo-like-kinase 3 (Plk3) resulting in apoptosis. The specific effect of hypoxia/reoxygenation stress on Plk3 activation resulting in c-Jun phosphorylation was the opposite of UV irradiation-induced responses that are meanly independent on activation of the stress-induced JNK signaling pathway in human corneal epithelial (HCE) cells. The effect of hypoxia/reoxygenation stress-induced Plk3 activation on increased c-Jun phosphorylation and apoptosis was also mimicked by exposure of cells to CoCl2. Hypoxia/reoxygenation activated Plk3 in HCE cells to directly phosphorylate c-Jun proteins at phosphorylation sites Ser-63 and Ser-73, and to increase DNA binding activity of c-Jun, detected by EMSA. Further evidence demonstrated that Plk3 and phospho-c-Jun were immunocolocalized in the nuclear compartment of hypoxia/reoxygenation stress-induced cells. Increased Plk3 activity by overexpression of wild-type and dominantly positive Plk3 enhanced the effect of hypoxia/reoxygenation on c-Jun phosphorylation and cell death. In contrast, knocking-down Plk3 mRNA suppressed hypoxia-induced c-Jun phosphorylation. Our results provide a new mechanism indicating that hypoxia/reoxygenation induces Plk3 activation instead of the JNK effect to directly phosphorylate and activate c-Jun, subsequently contributing to apoptosis in HCE cells.
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