| Project/Area Number |
02454498
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | Gifu University |
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Principal Investigator |
NOMA Akio School of Medicine Professor, 医学部, 教授 (30208384)
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| Co-Investigator(Kenkyū-buntansha) |
OKUNO Masataka University Hospital Assistant, 医学部附属病院, 助手 (10204140)
SEISHIMA Mitsuru School of Medicine Assistant, 医学部, 助手 (10171315)
ABE Akira University Hospital Lecturer, 医学部附属病院, 講師 (30175898)
SHIMOKAWA Kuniyasu School of Medicine Assistant Professor, 医学部, 助教授 (70021376)
中村 容子 岐阜大学, 医学部, 助手 (90227950)
牧野 和彦 岐阜大学, 医学部, 助手 (80181618)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥5,600,000 (Direct Cost: ¥5,600,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1990: ¥4,300,000 (Direct Cost: ¥4,300,000)
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| Keywords | Lipoprotein(a) / Lp(a) phenotype / Coronary artery disease / Acute phase reactant / Interleukin-6 / Coagulation / Fibrinolysis / Plasminogen / 血液凝固線溶系 / 組織修復 / リポ蛋白(a)[Lp(a)] / ELISA法 / 糖尿病 / アポ(a)表現型 / トリグリセリド・リッチ・リポ蛋白 / イオン強度 |
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| Research Abstract |
1) Lp(a) assay method and normal value in Japan. We evaluated the ELISA kit for Lp(a) determination, and the immunological interference by plasminogen on the assay. Results obtained by this assay method were compared with those by our polyclonal ELISA method. Serum Lp(a) was determined in 1513 healthy Japanese with use of the assay method.
2) Lp(a) phenotype frequencies in healthy Japanese and in patients with CAD. The distribution of Lp(a) levels, mean and median values, and Lp(a) phenotype and allele frequencies in healthy Japanese were not significantly different from the results for Europeans, whereas they were significantly different from other Asian populations. The frequencies of Lp(a) alleles in the CAD patients were not significantly different from those in the healthy subjects. Lp(a) levels in the patients were higher than those in the healthy subjects with the same phenotype.
3) Change as an acute phase reactant. Although IL-6, CRP and alpha_1-antitrypsin reached the maximal levels 1-2 days, 3 days and 4-5 days after the episodes, respectively, the peak time of Lp(a) levels delayed some extent in myocardial infarction and surgical operated groups. Studying on the transient increases of Lp(a) levels as a function of apo(a) isoforms, the higher density Lp(a) particles preferentially containing high molecular weight apo(a) isoforms were more increased than the lower density Lp(a) particles.
4) Relationship between Lp(a) and clinical parameters in the hemostatic process. Plasma concentrations of Lp(a), TAT, t-PA, PAI-1, t-PA-PAI-1 complex and PIC were determined in healthy subjects and in patients with CAD. Lp(a) levels showed a significant positive correlation with PIC values in the healthy group, whereas this correlation was disappeared in the CAD group. These results suggest that Lp(a) has the potential to regulate the coagulation-fibrinolytic system and that it may interfere with the fibrinolytic system in patients with CAD.
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