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論文

論文
Tada, Hayato ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Yasuda, Kenji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; Hayashi, Kenshi ; 多田, 隼人 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 小林, 淳二 ; 馬淵, 宏 ; 山岸, 正和 ; 林, 研至
出版情報: Journal of Atherosclerosis and Thrombosis.  24  pp.338-345,  2017.  日本動脈硬化学会 = Japan Atherosclerosis Society
URL: http://hdl.handle.net/2297/00053012
概要: 金沢大学附属病院循環器内科<br />Aim: The Japan Atherosclerosis Society (JAS) guidelines for the prevention of atherosclerotic disease s 2012 (JAS2012) proposed lipid management targets; however, less data is available regarding the attainment rates of each target in community-based settings. Therefore, we assessed the attainment rates of lipid management targets among subjects who underwent Japanese specific health checkups.\nMethods: A total of 85,716 subjects (male=29,282, 34.2%) aged 40–74 years who underwent specific health checkups from 2012 to 2014 in Kanazawa city, Japan, were included in this study. We evaluated the attainment rates of the lipid management targets according to the JAS2012 guideline and investigated the clinical characteristics of the subjects without achieving the targets.\nResults: The target for LDL cholesterol (LDL-C) was the least attained in all risk categories, 89, 72, 50, and 34% for category I, II, III, and secondary prevention, respectively, in 2014. In addition, these rates inversely correlated with the grade of risk categories (p-value for trends <0.001). Attainment rate of the LDL-C target in the suspected chronic kidney disease (CKD) group was significantly lower than in the groups with diabetes, stroke, or absolute risk in category III (49.2, 60.3, 63.5, 54.4%, respectively, p-value <0.001 for each). Moreover, the attainment rate of the LDL-C target was significantly lower in subjects that did not receive lipid-lowering therapy than in those who received it in the secondary prevention (27.7 and 40.6%, respectively, p-value <0.001).\nConclusions: Lipid management is inadequate in community-based settings, particularly, in subjects with CKD and secondary prevention.<br />This article distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License. 続きを見る
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Imamura, S. ; Kobayashi, Junji ; Sakasegawa, S. ; Nohara, Atsushi ; Nakajima, Kenichi ; Kawashiri, Masa-aki ; Inazu, Akihiro ; Yamagishi, Masakazu ; Koizumi, Junji ; Mabuchi, Hiroshi ; 小林, 淳二 ; 野原, 淳 ; 中嶋, 憲一 ; 川尻, 剛照 ; 稲津, 明広 ; 山岸, 正和 ; 小泉, 順二 ; 馬渕, 宏
出版情報: Journal of Lipid Research.  48  pp.453-457,  2007-02.  American Society for Biochemistry and Molecular Biology
URL: http://hdl.handle.net/2297/00050262
概要: 金沢大学医薬保健研究域医学系<br />The objective of this study was to establish a hepatic lipase (HL) assay method that can be applied to automatic clinical analyzers. Seventy-four hyperlipidemic subjects (men/women 45/29) were recruited. Lipase activity was assayed measuring the increase in absorbance at 546 nm due to quinonediimine dye production. Reaction mixture R-1 contained 50 mM Tris-HCl (pH 9.5), 0.5 mM glycerol-1,2-dioleate, 0.4% (unless otherwise noted) polyoxyethylenenonylphenylether, 3 mM ATP, 3 mM MgCl2, 1.5 mM CaCl2, monoacylglycerol-specific lipase, glycerol kinase, glycerol-3-phosphate oxidase, 0.075% N,N-bis-(4-sulfobutyl)-3-methylaniline-2 Na, peroxidase, ascorbic acid oxidase. Reaction mixture R-2 contained 50 mM Tris-HCl (pH9.5), 0.15% 4-aminoantypirine. Automated assay for activity was performed with a Model 7080 Hitachi analyzer. In the lipase assay, 160 μl of R-1 was incubated at 37°C with 3 μl of samples for 5 min, and 80 μl of R-2 was added. Within-run coefficient of variations was 0.9-1.0%. Calibration curve of lipase activity was linear (r = 0.999) between 0 and 320 U/l. Analytical recoveries of purified HL added to plasma were 96.6-99.8%. HL activity in postheparin plasma measured in this method had a closer correlation with HL mass by a sandwich ELISA (r = 0.888, P , 0.0001) than those in the conventional method using [ 14C-]triolein (r = 0.730, P < 0.0001). This assay method for HL activity can be applied to an automatic clinical analyzer. Copyright © 2007 by the American Society for Biochemistry and Molecular Biology, Inc. 続きを見る
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論文
Tada, Hayato ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Inazu, Akihiro ; Kobayashi, Junji ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; 多田, 隼人 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 小林, 淳二 ; 馬渕, 宏 ; 山岸, 正和
出版情報: Journal of Atherosclerosis and Thrombosis.  22  pp.1-9,  2015.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/00050270
概要: 金沢大学医薬保健研究域医学系<br />Autosomal recessive hypercholesterolemia (ARH) is an extremely rare inherited disorder, the cause of which is mutations in the low-density lipoprotein (LDL) receptor adaptor protein 1 (LDLRAP1) gene. Only 36 families with 14 different mutations have been reported in the literature to date. The clinical phenotype of ARH is milder than that of homozygous familial hypercholesterolemia (FH) caused by LDL receptor gene mutations. Recently, the lipoprotein metabolism of ARH was investigated in both humans and mice by several investigators, including ourselves. Based on these findings the preserved clearance of LDL receptor-dependent very-LDL (VLDL) may be a possible mechanism underlying the responsiveness to statins and the milder phenotype of ARH. Although ARH has been described as being “recessive,” several studies, including ours, have indicated that a heterozygous carrier status of the LDLRAP1 gene is associated with mild hypercholesterolemia and exacerbates the phenotype of FH resulting from LDL receptor gene mutations. This review summarizes current understanding regarding ARH and its causative gene, LDLRAP1, and attempts to provide new insight into novel pharmacological targets for treating dyslipidemic patients. © Journal of Atherosclerosis and Thrombosis. All right received.<br />出版者照会後に全文公開 続きを見る
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Mabuchi, Hiroshi ; Higashikata, Toshinori ; Nohara, Atsushi ; Lu, Hong ; Yu, Wen Xin ; Nozue, Tsuyoshi ; Noji, Yoshihiro ; Katsuda, Shoji ; Kawashiri, Masa-aki ; Inazu, Akihiro ; Kobayashi, Junji ; Koizumi, Junji ; 馬渕, 宏 ; 野原, 淳 ; 川尻, 剛照 ; 稲津, 明広
出版情報: Journal of Atherosclerosis and Thrombosis.  12  pp.35-40,  2005-02-23.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48755
概要: 出版者照会後に全文公開
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Mabuchi, Hiroshi ; Higashikata, Toshinori ; Kawashiri, Masa-aki ; Katsuda, Shoji ; Mizuno, Mihoko ; Nohara, Atsushi ; Inazu, Akihiro ; Koizumi, Junji ; Kobayashi, Junji ; 馬渕, 宏 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 小泉, 順二 ; 小林, 淳二
出版情報: Journal of Atherosclerosis and Thrombosis.  12  pp.111-119,  2005-06-07.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48756
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Kobayashi, Junji ; 小林, 淳二
出版情報: Journal of Atherosclerosis and Thrombosis.  22  pp.658-659,  2015-07-23.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48757
概要: 出版者照会後に全文公開
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Kobayashi, Junji ; 小林, 淳二
出版情報: Journal of Atherosclerosis and Thrombosis.  11  pp.1-5,  2004-03-01.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48758
概要: 出版者照会後に全文公開
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Kobayashi, Junji ; Miyashita, Kazuya ; Nakajima, Katsuyuki ; Mabuchi, Hiroshi ; 小林, 淳二 ; 馬渕, 宏
出版情報: Journal of Atherosclerosis and Thrombosis.  22  pp.1001-1011,  2015-10-01.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48759
概要: 出版者照会後に全文公開
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Kobayashi, Junji ; Murano, Shunichi ; Kawamura, Isao ; Nakamura, Fumie ; Murase, Yuko ; Kawashiri, Masa-aki ; Nohara, Atsushi ; Asano, Akimichi ; Inazu, Akihiro ; Mabuchi, Hiroshi ; 小林, 淳二 ; 川尻, 剛照 ; 野原, 淳 ; 稲津, 明広 ; 馬渕, 宏
出版情報: Journal of Atherosclerosis and Thrombosis.  13  pp.221-226,  2006-11-02.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48760
概要: 出版者照会後に全文公開
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論文
Kobayashi, Junji ; Sasaki, Takeyoshi ; Watanabe, Mitsuyo ; 小林, 淳二
出版情報: Journal of Atherosclerosis and Thrombosis.  11  pp.173-179,  2004-07-09.  Japan Atherosclerosis Society = 日本動脈硬化学会
URL: http://hdl.handle.net/2297/48761
概要: 出版者照会後に全文公開