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您选择的条件: Chen, Wei
  • AOL4PS: A Large-scale Data Set for Personalized Search

    分类: 计算机科学 >> 计算机科学的集成理论 提交时间: 2022-11-18 合作期刊: 《数据智能(英文)》

    摘要: Personalized search is a promising way to improve the quality of Websearch, and it has attracted much attention from both academic and industrial communities. Much of the current related research is based on commercial search engine data, which can not be released publicly for such reasons as privacy protection and information security. This leads to a serious lack of accessible public data sets in this field. The few publicly available data sets have not become widely used in academia because of the complexity of the processing process required to study personalized search methods. The lack of data sets together with the difficulties of data processing has brought obstacles to fair comparison and evaluation of personalized search models. In this paper, we constructed a large-scale data set AOL4PS to evaluate personalized search methods, collected and processed from AOL query logs. We present the complete and detailed data processing and construction process. Specifically, to address the challenges of processing time and storage space demands brought by massive data volumes, we optimized the process of data set construction and proposed an improved BM25 algorithm. Experiments are performed on AOL4PS with some classic and state-of-the-art personalized search methods, and the experiment results demonstrate that AOL4PS can measure the effect of personalized search models.

  • Fluorescence Biomembrane Force Probe: Concurrent Quantitation of Receptor-ligand Kinetics and Binding-induced Intracellular Signaling on a Single Cell

    分类: 生物学 >> 生物物理学 提交时间: 2016-05-11

    摘要: Membrane receptor-ligand interactions mediate many cellular functions. Binding kinetics and downstream signaling triggered by these molecular interactions are likely affected by the mechanical environment in which binding and signaling take place. A recent study demonstrated that mechanical force can regulate antigen recognition by and triggering of the T-cell receptor (TCR). This was made possible by a new technology we developed and termed fluorescence biomembrane force probe (fBFP), which combines single-molecule force spectroscopy with fluorescence microscopy. Using an ultra-soft human red blood cell as the sensitive force sensor, a high-speed camera and real-time imaging tracking techniques, the fBFP is of similar to 1 pN (10(-12) N), similar to 3 nm and similar to 0.5 msec in force, spatial and temporal resolution. With the fBFP, one can precisely measure single receptor-ligand binding kinetics under force regulation and simultaneously image binding-triggered intracellular calcium signaling on a single live cell. This new technology can be used to study other membrane receptor-ligand interaction and signaling in other cells under mechanical regulation.

  • Bortezomib enhances the therapeutic efficacy of dasatinib by promoting c-KIT internalization-induced apoptosis in gastrointestinal stromal tumor cells

    分类: 生物学 >> 生物物理学 >> 肿瘤学 提交时间: 2016-05-11

    摘要: Dasatinib-based therapy is often used as a second-line therapeutic strategy for imatinib-resistance gastrointestinal stromal tumors (GISTs); however, acquired aberrant activation of dasatinib target proteins, such as c-KIT and PDGFR13, attenuates the therapeutic efficiency of dasatinib. Combination therapy which inhibits the activation of dasatinib target proteins may enhance the cytotoxicity of dasatinib in GISTs. Bortezomib, a proteasome inhibitor, significantly inhibited cell viability and promoted apoptosis of dasatinib-treated GIST-TI cells, whereas GIST-TI cells showed little dasatinib cytotoxicity when treated with dasatinib alone, as the upregulation of c-KIT caused by dasatinib itself interfered with the inhibition of c-KIT and PDGFRI3 phosphorylation by dasatinib. Bortezomib induced internalization and degradation of c-KIT by binding c-KIT to Cbl, an E3 ubiquitin-protein ligase, and the subsequent release of Apaf-1, which was originally bound to the c-KIT-Hsp903-Apaf-1 complex, induced primary apoptosis in GISTTI cells. Combined treatment with bortezomib plus dasatinib caused cell cycle arrest in the G1 phase through inactivation of PDGFRP and promoted bortezomib-induced apoptosis in GIST-TI cells. Our data suggest that combination therapy exerts better efficiency for eradicating GIST cells and may be a promising strategy for the future treatment of GISTs. (C) 2015 Elsevier Ireland Ltd. All rights reserved.