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8篇 您的检索式:作者名="Yuanliang Jiang"
    题名 作者 年代 出处 被引量
1Alternative splicing and expression of the insulin-like growth factor (IGF-1) gene in osteoblasts under mechanical stretch显示文摘(IGF-1 ) 像胰岛素的生长因素 1 支持造骨细胞区别和骨头形成,和它的表示被机械段导致,因此, IGF-1 被认为连接机械刺激和本地织物回答的一个受动器分子。在这研究,一台机械拉长设备被设计把生理的水平静电干扰或周期的拉长刺激用于造骨细胞。IGF-1 mRNA 的不同 isoforms 被 RT-PCR 用各自的教材从房间放大,这些放大产品被定序。产品被发现被造骨细胞有选择地在拉长刺激下面生产的拼接的 IGF-1 的 iso 形式。ThisIGF-1 isoform 与原来在肌肉细胞被识别的 mechano 生长因素(MGF ) 有相同顺序。肝类型 IGF (L.IGF-1 ) 和在在段刺激下面的造骨细胞的 MGF 的表示的规定进一步用半量的 RT-PCR 被学习。Stretchstimulation 被发现 IGF-1 (L.IGF-1 和 MGF ) 的表示到职业人员警句,并且为两 isoformsexpression,更多被周期的段有效地比静态的段刺激。MGF 仅仅在受到机械段的造骨细胞被检测,建议 MGF 是段敏感生长因素。MGF 的表示比 L.IGF-1 的早达到顶点,它类似于他们在肌肉的规定并且作为在肌肉房间在骨头建议了 MGF 和 L.IGF-1 的类似的角色。在造骨细胞的 MGF 和 L.IGF-1 的功能将被进一步试验性的研究建立。XIAN Chengyu WANG Yuanliang ZHANG Bingbing TANG Liling PAN Jun LUO Yanfeng JIANG Peng LI Dajun 2006Chinese Science Bulletin2006,51,22:7
2Theory of passive localization for underwater sources based on acoustic ray modeling显示文摘The theory of passive localization for underwater sources based on acoustic ray channel modeling is discussed. The principles of channel modeling in Ray-theory, determination of eigenrays which connect source and receiver, analysis of DOA arriving structure and time delay spectrum arriving structure, their relationship to source location are given in the paper. Source location is estimated by matching measured DOA and TDS to their calculated counterparts. The method of Ray-theory based passive localization features its simplicity, less calculation, short array aperture and robust performance to environment parameters, as compared with those methods based on Normal Mode theory.SUN Zhenge (National Laboratory of Acoustics Beijing 100080)MA Yuanliang TU Qingping and JIANG Xiaoquan(College of Marine Engineering, NPU Xi’an 710072) 1997Chinese Journal of Acoustics1997,16,3:2
3Immunoenhancement effect of rehmannia glutinosa polysaccharide on lymphocyte proliferation and dendritic cell显示文摘Yee Huang Chunmao Jiang Yuanliang Hu Xiaojuan Zhao Cheng Shi Yun Yu Cui Liu Yang Tao Huarong Pan Yibo Feng Jiaguo Liu Yi Wu Deyun Wang 2013Carbohydrate Polymers2013,,2:1
4The State of the art surveys for application of metal magnetic memory testing in remanufacturing显示文摘Zhang Yuanliang Zhou Di Jiang Pengsen 2011Advanced Materials Research2011,,:1
5Osteogenic Responses to Different Concentrations/Ratios of BMP-2 and bFGF in Bone Formation显示文摘Lei Wang Yuanliang Huang Kefeng Pan Xinquan Jiang Changsheng Liu 2010Annals of Biomedical Engineering2010,,1:1
6Osteogenic Responses to Different Concentrations/Ratios of BMP-2 and bFGF in Bone Formation显示文摘Lei Wang Yuanliang Huang Kefeng Pan Xinquan Jiang Changsheng Liu 2010Annals of Biomedical Engineering2010,,1:1
7Disabled homolog 2 is required for migration and invasion of prostate cancer cells显示文摘残废相当或相同的事物(DAB2 ) 2 经常被删除或 epigenetically 在许多人的癌症房间的 silenced。因此, DAB2 总是被认为是肿瘤 suppressor 基因。然而,在肿瘤前进和转移的 DAB2 的角色仍然保持不清楚。在这研究, DAB2 表示是与人的前列腺癌症(PCa ) 一起的 upregulated 前进。在 LNCaP 和 PC3 房间线的 DAB2 overexpression 或击倒的效果被验证在 PCa 前进和转移探讨 DAB2 的生物功能。LNCaP 和 PC3 房间线分别地与低、高的变形潜力从人的 PCa 房间被产生。结果显示出那 DAB2 shRNA 击倒能禁止 PC3 房间,以及 tumorigenicity 的迁移、侵略的能力,而 DAB2 overexpression 提高了 LNCaP 房间移植和侵略。进一步的调查证明 DAB2 调整了房间迁居在 PC3 房间的联系基因,和微分 DAB2 在 LNCaP 和 PC3 房间之间的表示被 histone 部分调整 4 acetylation。因此, DAB2 可以在 PCa 前进和转移起一个重要作用。Yinyin Xie Yuanliang Zhang Lu Jiang Mengmeng Zhang Zhiwei Chen Dan Liu Qiuhua Huang 2015Frontiers of Medicine2015,9,3:0
8COVID-19 and atherosclerosis: looking beyond the acute crisis显示文摘The novel coronavirus disease 2019(COVID-19)was firstly reported in Wuhan,China,and eventually identified on December 31,2019 and remains as an ongoing worldwide pandemic.Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)invades human alveolar epithelial cells in the nose and throat mainly through angiotensin-converting enzyme 2(ACE2),[1]inducing innate inflammation in the lungs largely mediated by pro-inflammatory macrophages and granulocytes.Zhang Shi Yuanliang Jiang Jonathan Weir-McCall Ximing Wang Zhongzhao Teng 2022Emergency and Critical Care Medicine2022,2,1:0
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