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您的检索式：作者名="MASAMITSU Fujii"
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| 1 | The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury显示文摘Inflammatory stimuli,such as a microbes or lipopolysaccharides,induce a rapid release of neutrophils from the bone marrow and promote neutrophil migration into inflamed sites to promote host defense.However,an excess accumulation and retention of neutrophils in inflamed tissue can cause severe tissue injuries in the later stages of inflammation.Recent studies have reported that both CXCL12 levels in injured lungs and its receptor,CXCR4,on accumulated neutrophils in injured lungs,increased;furthermore,these studies showed that the CXCL12/CXCR4 signaling pathway participated in neutrophil accumulation in the later stages of lipopolysaccharide(LPS)-induced lung injury.However,the mechanisms underlying this increase in surface CXCR4 expression in neutrophils remain unclear.In this study,we found that surface CXCR4 expression increased in extravascular,but not intravascular,neutrophils in the lungs of LPS-induced lung injury model mice.Furthermore,ex vivo studies revealed that CXCL12 acted not only as a chemoattractant,but also as a suppressor of cell death for the lung neutrophils expressing CXCR4.Sulfatide,one of the native ligands for L-selectin,induced the increase of surface CXCR4 expression on isolated circulating neutrophils,suggesting that the activation of L-selectin may be involved in the increase in surface CXCR4.Our findings show that surface CXCR4 levels on neutrophils increase after extravasation into injured lungs,possibly through the activation of L-selectin.The CXCL12/CXCR4 signaling pathway plays an important role in the modulation of neutrophil activity during acute lung injury,not only by promoting chemotaxis but also by suppressing cell death. | Mitsuhiro Yamada Hiroshi Kubo Seiichi Kobayashi Kota Ishizawa Mei He Takaya Suzuki Naoya Fujino Hiroyuki Kunishima Masamitsu Hatta Katsushi Nishimaki Tetsuji Aoyagi Kouichi Tokuda Miho Kitagawa Hisakazu Yano Hirokazu Tamamura Nobutaka Fujii Mitsuo Kaku | 2011 | Cellular & Molecular Immunology2011，8，4： | 6 |
| 2 | Repetitive administration of cultured human CD34+cells improve adenine-induced kidney injury in mice显示文摘BACKGROUND There is no established treatment to impede the progression or restore kidney function in human chronic kidney disease(CKD).AIM To examine the efficacy of cultured human CD34+cells with enhanced proliferating potential in kidney injury in mice.METHODS Human umbilical cord blood(UCB)-derived CD34+cells were incubated for one week in vasculogenic conditioning medium.Vasculogenic culture significantly increased the number of CD34+cells and their ability to form endothelial progenitor cell colony-forming units.Adenineinduced tubulointerstitial injury of the kidney was induced in immunodeficient non-obese diabetic/severe combined immunodeficiency mice,and cultured human UCB-CD34+cells were administered at a dose of 1×106/mouse on days 7,14,and 21 after the start of adenine diet.RESULTS Repetitive administration of cultured UCB-CD34+cells significantly improved the time-course of kidney dysfunction in the cell therapy group compared with that in the control group.Both interstitial fibrosis and tubular damage were significantly reduced in the cell therapy group compared with those in the control group(P<0.01).Microvasculature integrity was significantly preserved(P<0.01)and macrophage infiltration into kidney tissue was dramatically decreased in the cell therapy group compared with those in the control group(P<0.001).CONCLUSION Early intervention using human cultured CD34+cells significantly improved the progression of tubulointerstitial kidney injury.Repetitive administration of cultured human UCB-CD34+cells significantly improved tubulointerstitial damage in adenine-induced kidney injury in mice via vasculoprotective and anti-inflammatory effects. | Takayasu Ohtake Shoichi Itaba Amankeldi A Salybekov Yin Sheng Tsutomu Sato Mitsuru Yanai Makoto Imagawa Shigeo Fujii Hiroki Kumagai Masamitsu Harata Takayuki Asahara Shuzo Kobayashi | 2023 | World Journal of Stem Cells2023，15，4： | 0 |
| 3 | Electric Field Enhancement of Nano Gap of Silver Prisms显示文摘用数字计算,我们在本地轻紧张改进上与圆角落检验一双 nano 差距银棱柱的差距距离的效果。二座山峰由于局部性的表面电浆子(LSP ) ,刺激从 900mn to300nm 在一个波长范围被观察。结果证明那达到顶点在一更长并且更短的波长通信了象 todipole 一样和像四极的 LSP 回声分别地。在 to20nm 上面的差距距离比单个银 nano 棱柱的向更大的轻紧张改进提供圆角落,这被发现。而且, nano 差距银棱柱被直接集中的离子横梁处理制作,并且我们由一个共焦的光系统测量一双 nano 棱柱的散布轻光谱。然而,因为 nano 的尺寸豁开,二座 LSP 山峰没在可见范围被观察,棱柱太大。 | KENZO Yamaguchi TOMOHIRO Inoue MASAMITSU Fujii MASANOBU Haraguchi TOSHIHIRO Okamoto MASUO Fukui SHU Seki SEIICHI Tagawa | 2007 | Chinese Physics Letters2007，24，10： | 0 |
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