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- 저자 : Zhi-min Pan (검색결과 4 건)
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Virtual Presentation and Customization of Products Based on Internet
Pan Zhi-geng,Chen Tian,Zhang Ming-min,Xu Bin Society for Computational Design and Engineering 2004 International Journal of CAD/CAM Vol.4 No.1
Through reviewing and comparing the current virtual shopping malls web sites integrated VR into E-commerce, this paper analyzed both the advantages and disadvantages of two kinds of methods for product presentation: 2D image based and 3D model based presentation method. Using the virtual shopping mall (EasyMall) as a showcase, we presented the architecture of the system and the development technologies, especially those in the mixed presentation method. The presentation and customization methods in the two related modules, including the PhoneShow for mobile phone and EasyShow for textile products, were discussed. It indicated that the integration of E-commerce with VR could provide consumers with virtual experience and intelligent service for business activities. Furthermore, the product presentation methods can be made available for use in different cases.
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Zhang, Ying-Yao,Xu, Zhi-Na,Wang, Jun-Xi,Wei, Dong-Min,Pan, Xin-Liang Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.5
Objective: To investigate the prognostic role of antigen KI-67 (Ki-67) and G1/S-specific cyclin-D1 (cyclin-D1) in patients with laryngeal squamous cell carcinoma (LSCC). Methods: Immunohistochemical staining (IHS) was used to determine the protein expression of Ki-67 and cyclin-D1 in LSCC tissues. Kaplan-Meier survival curves was calculated with reference to Ki-67 and cyclin-D1 levels. Results: Cyclin-D1 and Ki67 were expressed in the nuclei of cancer cells. Among the total of 92 cancer tissues examined by immunohistochemistry, 60 (65.22%) had cyclin-D1 overexpression and 56 (60.87%) had Ki67 overexpression. Cyclin-D1 overexpression is associated with the advanced stage of the cancer (P=0.029), but not with gender, age, stage of cancer, histological differentiation, anatomical site, smoking history and alcohol consumption history. Ki67 overexpression is not associated with the advanced stage, gender, age, histological differentiation, anatomical site, smoking history and alcohol consumption history. A statistically significant correlation was found between lymph node status and the expression of Ki67 (p = 0.025). Overexpression of cyclin-D1 was correlated to shorter relapse-free survival period (P<0.001). Conclusions: Overexpression of cyclin-D1 can be used as a marker to predict relapse in patients with LSCC after primary curative resection.
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Jun-yi Hua,Yu-zhou He,Yun Xu,Xu-hong Jiang,Wu Ye,Zhi-min Pan 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-
Neointimal proliferation after vascular injury is a key mechanism of restenosis, a major cause of percutaneous transluminal angioplasty failure and artery bypass occlusion. Emodin, an anthraquinone with multiple physiological activities, has been reported to inhibit proliferation of vascular smooth muscle cells (VSMCs) that might cause intimal arterial thickening. Thus, in this study, we established a rat model of balloon-injured carotid artery and investigated the therapeutic effect of emodin and its underlying mechanism. Intimal thickness was analyzed by hematoxylin and eosin staining. Expression of Wnt4, dvl-1, β-catenin and collagen was determined by immunohistochemistry and/or western blotting. The proliferation of VSMC was evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and electron microscopy. MicroRNA levels were quantified by real-time quantitative PCR. Emodin relieved injury-induced artery intimal thickness. Results of western blots and immunohistochemistry showed that emodin suppressed expression of signaling molecules Wnt4/Dvl-1/β-catenin as well as collagen protein in the injured artery. In addition, emodin enhanced expression of an artery injury-related microRNA, miR-126. In vitro, MTT assay showed that emodin suppressed angiotensin II (AngII)-induced proliferation of VSMCs. Emodin reversed AngII-induced activation of Wnt4/Dvl-1/β-catenin signaling by increasing expression of miR-126 that was strongly supported by transfection of mimic or inhibitor for miR-126. Emodin prevents intimal thickening via Wnt4/Dvl-1/β-catenin signaling pathway mediated by miR-126 in balloon-injured carotid artery of rats.
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