基本情報
研究キーワード
18経歴
3-
2017年4月 - 現在
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2013年4月 - 2017年3月
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2005年4月 - 2013年4月
学歴
3-
2000年4月 - 2005年3月
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1991年4月 - 1995年3月
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1989年4月 - 1991年3月
論文
136-
Circulation Journal 74(Suppl.I) 567-567 2010年3月
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Circulation journal : official journal of the Japanese Circulation Society 74(3) 503-509 2010年3月 査読有り
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Circulation journal : official journal of the Japanese Circulation Society 73(7) 1197-1198 2009年7月 査読有り
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Circulation journal : official journal of the Japanese Circulation Society 73(5) 912-917 2009年5月 査読有り
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Circulation journal : official journal of the Japanese Circulation Society 73(5) 885-891 2009年5月 査読有り
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Circulation Journal 73(Suppl.I) 160-160 2009年3月
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Circulation journal : official journal of the Japanese Circulation Society 73 160 2009年3月 査読有り
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Journal of atherosclerosis and thrombosis 16(1) 30-32 2009年3月 査読有り
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Hypertension research : official journal of the Japanese Society of Hypertension 32(2) 109-114 2009年2月 査読有り
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医療情報学 29(6) 245-254 2009年The objective of this study was to evaluate the efficacy of the Integrating the Healthcare Enterprise (IHE) Echocardiography profile in an environment that included legacy information systems. For this study, we developed an Ultrasound Image and Report Management System that was capable of supporting the IHE echocardiography profile. We then implemented this system at the real clinical environment and integrated it with the existing legacy hospital information system, department system, and picture archive and communication system (PACS). A gateway interface was used to convert the proprietary protocol and data from the legacy systems to support the standard HL7 data format and DICOM connectivity used in newer systems. After a year of operation, we evaluated the efficacy of IHE connectivity by collecting questionnaires and performing interviews to compare system performance before and after the integration. The assessment showed that IHE connectivity provided greater accuracy for measurement data as well as for patient and examination information on the report. The conclusion was that IHE connectivity is effective in environments that mix new standards-based systems with existing legacy information systems.
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Circulation journal : official journal of the Japanese Circulation Society 73(1) 78-85 2009年1月 査読有り
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International heart journal 49(2) 193-203 2008年3月 査読有り
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Journal of atherosclerosis and thrombosis 14(5) 226-234 2007年10月 査読有り
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Rheumatology 46(4) 597-603 2007年4月 査読有りObjectives. Periarticular osteoporosis and joint destruction are major complications in rheumatoid arthritis (RA), caused by osteoclast-mediated bone resorption. However, the mechanisms of monocyte/osteoclast maturation and role of RA endothelial cells (RAECs) in the control of osteoclastogenesis remain unclear. The present study was designed to determine the most important factors that influence monocyte accumulation and osteoclast formation among the many factors produced by RAEC. Methods. We analysed the expression profiles of various genes in human endothelial cells from various organs (RA synovium, umbilical vein, skin, liver sinusoid, renal glomerulus and brain) using oligonucleotide microarrays. Specifically, up-regulated gene in RAECs was assessed by real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assay and immunostaining of RA synovia. Migration of monocytes was assessed by the chemotactic chamber EZ-TAXIScan™. Tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cell (MNC) formation was observed by microscopy. Results. Among many epithelial-expressed factors, macrophage colony-stimulating factor (M-CSF) gene was abundantly expressed specifically in RAECs. Genes of fibroblast growth factor-2, interleukin-6 and osteoprotegerin were also overexpressed in RAECs. Migration of monocytes and osteoclast formation in co-cultures promoted by culture supernatants of RAECs were inhibited by M-CSF neutralizing antibody. Conclusions. M-CSF produced by RAECs is involved in osteoclastogenesis from monocytes, migration and TRAP-positive MNC formation. © 2007 Oxford University Press.
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Circulation Journal 71(Suppl.I) 307-307 2007年3月
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Hypertension research : official journal of the Japanese Society of Hypertension 29(9) 719-729 2006年9月 査読有り
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Circulation Journal 70(Suppl.I) 609-609 2006年3月
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Biochemical and biophysical research communications 337 534-539 2005年11月 査読有り
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Journal of Leukocyte Biology 78(2) 481-490 2005年 査読有りGranulocyte colony-stimulating factor (G-CSF) is a cytokine that stimulates myeloid progenitor cells to proliferate and differentiate into neutrophilic granulocytes. To identify genes induced by G-CSF during neutrophil differentiation, interleukin-3-dependent murine myeloid precursor FDC-P1 cells expressing the G-CSF receptor were stimulated with G-CSF, and the gene expression profile was characterized by DNA microarray analysis. In addition to known signal transducer and activator of transcription-3 target genes, such as suppressor of cytokine signaling-3 (SOCS3), JunB, and p19(INK4D), we newly identified several G-CSF targets, including genes for the CC chemokine receptor-2 (CCR2), raft proteins flotillin-1 and flotillin-2, and immunoglobulin-like receptor gp49B. Real-time, quantitative polymerase chain reaction analyses revealed that the expression of these genes was induced in various myeloid cell lines by G-CSF. Furthermore, when HoxA9-immortalized bone marrow progenitors were induced by G-CSF to differentiate into mature neutrophils, all of these genes were strongly activated. These genes could be categorized into three groups based on their time-course of expression: immediate-early (approximately 20 min, SOCS3), mid-early (2-4 h, flotillin-1/2 and gp49B), and late (>12 h, CCR2). This suggests that different transcriptional mechanisms are involved in the regulation of these genes. We show that bone marrow neutrophils express functional CCR2, which suggest that CC chemokines may play previously unknown roles in neutrophil activation and chemotaxis.
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The Journal of biological chemistry 279(48) 50537-50554 2004年11月 査読有り
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Physiological Genomics 15 199-208 2004年1月1日
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Journal of atherosclerosis and thrombosis 11(2) 88-97 2004年 査読有り
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Journal of cardiovascular pharmacology 42 Suppl 1 S1-6 2003年12月 査読有り
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Physiological genomics 15(3) 199-208 2003年11月 査読有り
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Journal of atherosclerosis and thrombosis 10(5) 304-313 2003年 査読有り
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Arteriosclerosis, thrombosis, and vascular biology 22(10) 1712-1719 2002年10月 査読有り
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Transplantation 73(9) 1480-1486 2002年5月 査読有り
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Journal of atherosclerosis and thrombosis 9(5) 224-232 2002年 査読有り
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Transplantation 72(2) 320-329 2001年
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Journal of Atherosclerosis and Thrombosis 7(1) 39-44 2000年
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Journal of Atherosclerosis and Thrombosis 7(3) 145-151 2000年
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Yonsei Medical Journal 41(6) 740-755 2000年 査読有りIn order to determine the precise mechanism of the interactions between different types of cells, which are common phenomena in tissues and organs, the importance of coculture techniques are becoming increasingly important. In the area of cardiology, artificial arteries have been developed, based on the understanding of physiological communication of the arterial smooth muscle cells (SMC), endothelial cells (EC), and the extracellular matrix (ECM). In the study of atherosclerosis, the modification of low-density lipoprotein. (LDL), which result in the recruitment and accumulation of white blood cells, especially, monocytes/macrophages, and foam cell formation, are hypothesized. Although there are well known animal models, an in vitro model of atherogenesis with a precisely known atherogenesis mechanism has not yet been developed. In this paper, an arterial wall reconstruction model using rabbit primary cultivated aortic SMCs and ECs, was shown. In addition, human peripheral monocytes were used and the transmigration of monocytes was observed by scanning electron and laser confocal microscopy. Monocyte differentiation into macrophages was shown by immunohistochemistry and comprehensive gene expression analysis. With the modified form of LDL, the macrophages were observed to accumulate lipids with a foamy appearance and differentiate into the foam cells in the ECM between the ECs and SMCs in the area of our coculture model.
MISC
67共同研究・競争的資金等の研究課題
4-
日本学術振興会 科学研究費助成事業 2014年4月 - 2017年3月
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日本学術振興会 科学研究費助成事業 2011年4月 - 2014年3月
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日本学術振興会 科学研究費助成事業 2010年 - 2012年
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日本学術振興会 科学研究費助成事業 2005年 - 2006年