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図書 |
図書
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馬渕宏編集
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図書 |
図書
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馬渕宏著
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論文 |
論文
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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
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
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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.
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論文 |
論文
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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
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
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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
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論文
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Tada, Hayato ; Nohara, Atsushi ; Kawashiri, Masa-aki ; Inazu, Akihiro ; Mabuchi, Hiroshi ; Yamagishi, Masakazu ; 多田, 隼人 ; 野原, 淳 ; 川尻, 剛照 ; 稲津, 明広 ; 馬渕, 宏 ; 山岸, 正和
概要:
金沢大学医薬保健研究域医学系<br />We herein report a case of marked transient hypercholesterolemia in a man receiving low-dose mitotan
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e as adjuvant chemotherapy for adrenocortical carcinoma.A 58-year-old man without any clinical symptoms or history of hypercholesterolemia was admitted to our hospital to treat an adrenocortical carcinoma detected on general screening using computed tomography. He reported no chest symptom and did not exhibit any established risk factors for coronary artery disease, such as diabetes, obesity, hypertension or relevant family history, with the exception of current smoking, on admission. A stress electrocardiogram showed negative findings. The left adrenal tumor as well as left kidney, spleen and distal portion of the pancreas were subsequently resected using radical surgery. The histopathological findings confirmed the preoperative diagnosis of adrenocortical carcinoma. After the operation, treatment with low-dose mitotane (1g/day) was introduced as adjuvant chemotherapy. Interestingly, the patient developed marked hyper-LDL cholesterolemia at a level equivalent to that of familial hypercholesterolemia (LDL cholesterol level ~ 300 mg/ dL) following the introduction of mitotane, without evidence of primary or secondary hypercholesterolemia due to other causes. A coronary angiogram performed to assess the new-onset angina revealed three-vessel disease, which was later revascularized via percutaneous coronary intervention eight months after the start of mitotane therapy. The cholesterol level normalized with the suspension of mitotane. This case suggests that mitotane can cause severe hypercholesterolemia, potentially resulting in coronary atherosclerosis. © 2014, Japan Atherosclerosis Society. All rights reserved.<br />出版者照会後に全文公開
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論文 |
論文
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稲津, 明広 ; 馬渕, 宏 ; Inazu, Akihiro ; Mabuchi, Hiroshi
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金沢大学医薬保健研究域医学系
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論文
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Kitatani, Masako ; Koizumi, Junji ; Inazu, Akihiro ; Kajinami, Kouji ; Mabuchi, Hiroshi ; 小泉, 順二 ; 稲津, 明広 ; 梶波, 康二 ; 馬渕, 宏
概要:
金沢大学医薬保健研究域保健学系<br />A study was conducted to determine the clinical efficacy and tolerability of simvastatin, an inhibi
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tor of 3-hydroxy-3-methylglutaryl coenzyme A reductase in seven patients with heterozygous familial hypercholesterolemia (FH) (defined as primary hypercholesterolemia with tendon xanthoma or primary hypercholesterolemia without tendon xanthomas and at least one first-degree relative with familial hypercholesterolemia). These patients were administrated 10 mg/d of simvastatin for up to 4 years. Simvastatin significantly reduced levels of both total cholesterol and low-density lipoprotein cholesterol during treatment; respective reduction rates were 28% and 34% after 1 month and 32% and 40% after 4 years. Serum high-density lipoprotein cholesterol levels slightly and insignificantly increased. Serum triglyseride levels fell significantly by 24% at month 6. After this study, all xanthomas had reduced in size. No adverse events related to simvastatin were observed. We conclude that long-term simvastatin therapy is clinically useful and well tolerated in patients with FH. Copyright © 1985 Published by Elsevier Inc.
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論文
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Mabuchi, Hiroshi ; Nohara, Atsushi ; Higashikata, Toshinori ; Ueda, Kosei ; Bujo, H. ; Matsushima, Teruhiko ; Ikeda, Yoshihiko ; Nii, Masahiro ; 馬渕, 宏 ; 野原, 淳
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論文
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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
概要:
出版者照会後に全文公開
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論文
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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
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