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11篇 您的检索式:作者名="Yasuko Suzuki"
    题名 作者 年代 出处 被引量
1Bisphenol A in combination with TNF-a selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity显示文摘Bisphenol A(BPA)is a monomer used in manufacturing a wide range of chemical products,including epoxy resins and polycarbonate.BPA,an important endocrine disrupting chemical that exerts estrogen-like activities,is detectable at nanomolar levels in human serum worldwide.The pregnancy associated doses of 17b-estradiol(E2)plus tumor-necrosis factor-a(TNF-a)induce distorted maturation of human dendritic cells(DCs)that result in an increased capacity to induce T helper(Th)2 responses.The current study demonstrated that the presence of BPA during DC maturation influences the function of human DCs,thereby polarizing the subsequent Th response.In the presence of TNF-a,BPA treatment enhanced the expression of CC chemokine ligand 1(CCL1)in DCs.In addition,DCs exposed to BPA/TNF-a produced higher levels of IL-10 relative to those of IL-12p70 on CD40 ligation,and preferentially induced Th2 deviation.BPA exerts the same effect with E2 at the same dose(0.01–0.1 mM)with regard to DC-mediated Th2 polarization.These findings imply that DCs exposed to BPA will provide one of the initial signals driving the development and perpetuation of Th2-dominated immune response in allergic reactions.Hongchuan Guo Tianyi Liu Yasushi Uemura Shunchang Jiao Deqing Wang Zilin Lin Yayoi Narita Motoharu Suzuki Narumi Hirosawa Yasuko Ichihara Osamu Ishihara Hirosato Kikuchi Yasushi Sakamoto Satoru Senju Qiuhang Zhang Feng Ling 2010Cellular & Molecular Immunology2010,7,3:6
2Spermatogenesis in aged rats after prenatal 3,3′,4,4′,5-pentachlorobiphenyl exposure显示文摘Shin Wakui Fumio Takagi Tomoko Muto Kiyofumi Yokoo Shyou Hirono Yasuko Kobayashi Kinji Shirota Fumiaki Akahori Yoshihiko Suzuki Hiroshi Hano Hitoshi Endou Yoshikatsu Kanai 2007Toxicology2007,,2:3
3Inducing sleep by remote control facilitates memory consolidation in drosophila 显示文摘Jeffrey M Donlea Matthew S Thimgan Yasuko Suzuki 2011Science2011,332,6037:1
4Mirror therapy activates outside of cerebellum and ipsilateral M1显示文摘Nobusada Shinoura Yuichi Suzuki Yasuko Watanabe Ryozi Yamada Yusuke Tabei Kuniaki Saito Kazuo Yagi 2008Neurorehabilitation2008,,3:1
5Histopathological analyses of the antitumor activity of anti-glypican-3 antibody (GC33) in human liver cancer xenograft models: The essential role of macrophages显示文摘Hirotake Takai Atsuhiko Kato Yasuko Kinoshita Takahiro Ishiguro Yayoi Takai Yoshimi Ohtani Masamichi Sugimoto Masami Suzuki 2009Cancer Biology & Therapy2009,,:1
6The perilipin homologue,lipid storage droplet 2,regulates sleep homeostasis and prevents learning impairments following sleep loss显示文摘Matthew S Thimgan Yasuko Suzuki Laurent Seugnet 0,,08:1
7Role of Nitric Oxide-cGMP Pathway in Adrenomedullin-Induced Vasodilation in the Rat显示文摘Hiroshi Hayakawa Yasunobu Hirata Masao Kakoki Yasuko Suzuki Hiroaki Nishimatsu Daisuke Nagata Etsu Suzuki Kazuya Kikuchi Tetsuo Nagano Kenji Kangawa Hisayuki Matsuo Tsuneaki Sugimoto Masao Omata 1999Hypertension1999,,2:1
8Development of thin film thermocouple for measurement of instantaneous heat flux flowing into cast iron combustion chamber wall 显示文摘Masahiko Emi Yasuko Suzuki Yuichi Yamada 2002Transaction of Society of Automotive Engineers of Japan2002,33,3:1
9Plasma adenosine levels and P-selectin expression on platelets in preeclampsia显示文摘Yoshio Yoneyama Shunji Suzuki Rintaro Sawa Yasuko Kiyokawa Gordon G Power Tsutomu Araki 2001Obstetrics & Gynecology2001,,3:1
10Measuring Vehicle Speed at a License Plate Using a Pair of Line-scan Cameras 显示文摘Satoshi Sakuma Yasuko Takahashi Akira Suzuki 2004Electronics and Communications in Japan Translated from Denshi doho Tsushin Gakkai Ronbunshi(S1942-9541)2004,7,6:1
11Tumor-derived insulin-like growth factor-binding protein-1 contributes to resistance of hepatocellular carcinoma to tyrosine kinase inhibitors显示文摘Background:Antiangiogenic tyrosine kinase inhibitors(TKIs)provide one of the few therapeutic options for effective treatment of hepatocellular carcinoma(HCC).However,patients with HCC often develop resistance toward antiangiogenic TKIs,and the underlying mechanisms are not understood.The aim of this study was to determine the mechanisms underlying antiangiogenic TKI resistance in HCC.Methods:We used an unbiased proteomic approach to define proteins that were responsible for the resistance to antiangiogenic TKIs in HCC patients.We evaluated the prognosis,therapeutic response,and serum insulin-like growth factor-binding protein-1(IGFBP-1)levels of 31 lenvatinib-treated HCC patients.Based on the array of results,a retrospective clinical study and preclinical experiments using mouse and human hepatoma cells were conducted.Additionally,in vivo genetic and pharmacological gain-and loss-of-function experiments were performed.Results:In the patient cohort,IGFBP-1 was identified as the signaling molecule with the highest expression that was inversely associated with overall survival.Mechanistically,antiangiogenic TKI treatment markedly elevated tumor IGFBP-1 levels via the hypoxia-hypoxia inducible factor signaling.IGFBP-1 stimulated angiogenesis through activation of the integrinα5β1-focal adhesion kinase pathway.Consequently,loss of IGFBP-1 and integrinα5β1 by genetic and pharmacological approaches re-sensitized HCC to lenvatinib treatment.Conclusions:Together,our data shed light onmechanisms underlying acquired resistance of HCC to antiangiogenic TKIs.Antiangiogenic TKIs induced an increase of tumor IGFBP-1,which promoted angiogenesis through activating the IGFBP-1-integrinα5β1 pathway.These data bolster the application of a new therapeutic concept by combining antiangiogenic TKIs with IGFBP-1 inhibitors.Hiroyuki Suzuki Hideki Iwamoto Takahiro Seki Toru Nakamura Atsutaka Masuda Takahiko Sakaue Toshimitsu Tanaka Yasuko Imamura Takashi Niizeki Masahito Nakano Shigeo Shimose Tomotake Shirono Yu Noda Naoki Kamachi Miwa Sakai Kazutoyo Morita Masamichi Nakayama Tomoharu Yoshizumi Ryoko Kuromatsu Hirohisa Yano Yihai Cao Hironori Koga Takuji Torimura 2023Cancer Communications2023,43,4:0
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