维普中文期刊产品整合服务
3篇 您的检索式:作者名="Shuang Shuli"
    题名 作者 年代 出处 被引量
1A Sensitivi-ty Model(SM)Approach to Analyze Urban Developmentin Taiwan Based on Sustainability Indicators显示文摘Shuang Shuli Yeh C T Budd W W 2009Envi-ronmental Impact Assessment Review2009,29,2:1
2Targeting UDP-α-D-glucose 6-dehydrogenase alters the CNS tumor immune microenvironment and inhibits glioblastoma growth显示文摘Glioblastoma(GBM,WHO grade IV glioma)is the most common and lethal malignant brain tumor in aduts with a dismal prognosis.The extracellular matrix(ECM)supports GBM progression by promoting tumor cell proliferation,migration,and immune escape.Uridine diphosphate(UDP)-glucose 6-dehydrogenase(UGDH)is the rate-limiting enzyme that catalyzes the biosynthesis of glycosaminoglycans that are the principal component of the CNS ECM.We investigated how targeting UGDH in GBM infuence$the GBM immune microenvironment,including tumor-associated microglia/macrophages(TAMs)and T cells.TAMs are the main im-mune effector cells in GBM and can directly target tumor cells if properly activated.In co-cultures of GBM cells and human primary macrophages,UGDH knockdown in GBM cells pro-moted macrophage phagocytosis and M-like polarization.In orthotropic human GBM xeno-grafts and syngeneic mouse glioma models,targeting UGDH decreased ECM deposition,increased TAM phagocytosis marker expression,reduced M2-like TAMS and inhibited tumor growth.UGDH knockdown in GBM cells also promoted cytotoxic T cell ifltration and activa-tion in orthotopic syngeneic mouse glioma models.The potent and in-human-use small mole-cule GAG synthesis inhibitor 4-methylumbelliferone(4-MU)was found to inhibit GBM cell proliferation and migration in vitro,mimic the macrophage and T-cell responses to UGDH knockdown in vitro and in vivo and inhibit growth of orthotopic murine GBM.Our study shows that UGDH supports GBM growth through multiple mechanisms and supports the development of ECM-based therapeutic strategies to simultaneously target tumor cells and their microenvi-ronment.Daqian Zhan Fatih Yalcin Ding Ma Yi Fu Shuang Wei Bachchu Lal Yunqing Li Omar Dzaye John Laterra Mingyao Ying Hernando Lopez-Bertoni Shuli Xia 2022Genes & Diseases2022,9,3:1
3Expert consensus on difficulty assessment of endodontic therapy显示文摘Endodontic diseases are a kind of chronic infectious oral disease. Common endodontic treatment concepts are based on the removal of inflamed or necrotic pulp tissue and the replacement by gutta-percha. However, it is very essential for endodontic treatment to debride the root canal system and prevent the root canal system from bacterial reinfection after root canal therapy(RCT). Recent research, encompassing bacterial etiology and advanced imaging techniques, contributes to our understanding of the root canal system’s anatomy intricacies and the technique sensitivity of RCT. Success in RCT hinges on factors like patients, infection severity, root canal anatomy, and treatment techniques. Therefore, improving disease management is a key issue to combat endodontic diseases and cure periapical lesions. The clinical difficulty assessment system of RCT is established based on patient conditions, tooth conditions, root canal configuration, and root canal needing retreatment, and emphasizes pre-treatment risk assessment for optimal outcomes. The findings suggest that the presence of risk factors may correlate with the challenge of achieving the high standard required for RCT. These insights contribute not only to improve education but also aid practitioners in treatment planning and referral decision-making within the field of endodontics.Dingming Huang Xiaoyan Wang Jingping Liang Junqi Ling Zhuan Bian Qing Yu Benxiang Hou Xinmei Chen Jiyao Li Ling Ye Lei Cheng Xin Xu Tao Hu Hongkun Wu Bin Guo Qin Su Zhi Chen Lihong Qiu Wenxia Chen Xi Wei Zhengwei Huang Jinhua Yu Zhengmei Lin Qi Zhang Deqin Yang Jin Zhao Shuang Pan Jian Yang Jiayuan Wu Yihuai Pan Xiaoli Xie Shuli Deng Xiaojing Huang Lan Zhang Lin Yue Xuedong Zhou 2024International Journal of Oral Science2024,16,1:0
返回顶部 每页显示:
共1页 首页 上一页 第1页 下一页 末页 /1 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费