2004 Fiscal Year Final Research Report Summary
Basic research to detect vulnerable atherosclerotic plaque aimed for clinical PET examination
| Project/Area Number |
15591290
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | Yokohama City University, Hospital |
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Principal Investigator |
TAKAHASHI Nobukazu Yokohama City University, Hospital, Department of Radiology, Assistant Professor, 医学部附属病院, 講師 (20295512)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Tamio Yokohama City University Hospital, Department of Radiology, Professor, 医学(系)研究院, 教授 (80134295)
TAKAHASHI Megumi Kitazato University, School of Medicine, Department of Psychiatry, Assistant Professor, 医学部附属病院, 講師 (00305476)
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| Project Period (FY) |
2003 – 2004
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| Keywords | vulnerable plaque / F-18 FDG / F-18 Annexin V |
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| Research Abstract |
Unstable atherosclerotic plaque and its rupture are considered to be the cause of acute myocardial infarction and sudden death. It is reported that vascular remodeling, adventitial inflammation and apoptosis of the macrophage are the cause of unstable atherosclerotic plaque. The development of the imaging technology for apoptosis is clinically useful for diagnosis and decision making of therapy. Positron emission tomography (PET) using the positron tracer is an excellent imaging technique and it shows the highest sensitivity for imaging of the molecular biology such as apoptosis.
In this study, We evaluate the F-18 FDG (FDG) accumulation for the apoptotic phenomenon of the atherosclerosis. FDG is the tracer of glucose metabolic imaging it has already been applied clinically in Yokohama City University. And we examine the possibility of F-18 labeled Annexin V for a new apoptosis-detecting tracer.
FDG and F-18 Annexin V were injected with the apolipoprotein E deficit atheriosclerosis model
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mice and the control mice, we evaluated the relation between these two tracers accumulation and the appearance of apoptosis. Unstable atherosclerotic plaque was confirmed by histological examination by using TUNEL staining and the MOMA-1 antibody.
Apoptosis was induced by 5Gy gamma ray irradiation to HL60 cell, we compared the accumulation of F-18 Annexin V between irradiated cell group and control group to evaluate the accumulation of F-18 Annexin V was depend upon the presence of apoptosis.
F-18 Annexin V was synthesized as followed. The aqueous solution of Annexin V was transferred Sep-Pak columns (Waters Corp., Milford, MA), and overnight freeze-dried. F-18 labeled F2 by the ^<20>Ne(d, alpha) 18F reaction, was drawn into the column with a stream of helium gas. And the loaded Sep-Pak cartridge was washed with buffer and F-18 labeled Annexin V was corrected in vial. We confirmed that radioactive peak corresponded to the point of UV peak of cold Annexin V based on the results of HPLC analysis.
The causal relation between these of FDG and F-18 Annexin accumulation and the appearance of apoptosis was clear in the animal model study.
It revealed that higher accumulation of F-18 Annexin V was seen those group of the presence of apoptotic cells in unstable atherosclerotic plaque with model mice.
F-18 Annexine V showed higher counting to the apoptotic cell induces by irradiation. Especially the usefulness of F-18 Annexin V for PET tracer was shown, and it is necessary of the in vivo animal experiment for a clinical application. Less
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Research Products
(4 results)
