Masaru Iwai
Shiga University of Medical Science
10 Papers
58 Citations
Masaru Iwai is an academic researcher from Shiga University of Medical Science. The author has contributed to research in topics: Glucuronosyltransferase & Crigler–Najjar syndrome. The author has an hindex of 8, co-authored 10 publications.
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Papers
UDP-glucuronosyltransferase 1A4 polymorphisms in a Japanese population and kinetics of clozapine glucuronidation.
TL;DR: The importance of identifying patients with the L48V polymorphism when calculating dosage, and when considering the potential adverse effects of drugs that are substrates of UGT1A4, is shown.
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Two linked polymorphic mutations (A(TA)7TAA and T-3279G) of UGT1A1 as the principal cause of Gilbert syndrome
Yoshihiro Maruo,Carlos D'Addario,Asami Mori,Masaru Iwai,Hiroko Takahashi,Hiroshi Sato,Yoshihiro Takeuchi +6 more
TL;DR: The linkage of the two mutations, A(TA)7TAA and T-3279G, indicated that the decrease in transcription caused by both mutations together may be essential to the syndrome.
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Effect of D256N and Y483D on propofol glucuronidation by human uridine 5'-diphosphate glucuronosyltransferase (UGT1A9).
TL;DR: This study shows the importance of D256N in differences between individuals concerning adverse effects of drugs that are catalysed primarily by UGT1A9, and carriers of D 256N may be at risk of suffering adverse results of propofol and other substrates that are primarily metabolized by U GT1A 9.
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Co-occurrence of three different mutations in the bilirubin UDP-glucuronosyltransferase gene in a Chinese family with Crigler-Najjar syndrome type I and Gilbert's syndrome.
Yoshihiro Maruo,K K-H Poon,Masaki Ito,Masaru Iwai,H Takahashi,A Mori,H Sato,Yoshihiro Takeuchi +7 more
TL;DR: The present results indicate that carriers of the nonsense mutation could be normal for plasma bilirubin concentration, Gilbert's syndrome and Crigler–Najjar syndrome type II.
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Chemotherapy-induced unconjugated hyperbilirubinemia caused by a mutation of the bilirubin uridine-5'-diphosphate-glucuronosyltransferase gene.
Yoshihiro Maruo,Hiroshi Sato,Noriko Bamba,Masaru Iwai,Hiroko Sawa,Hidetoshi Fujino,Takashi Taga,Shigeru Ota,Morimi Shimada +8 more
TL;DR: An identical heterozygous missense mutation in exon 1 (211G→A: G71R) may be the basis of chemotherapy-induced unconjugated hyperbilirubinemia.
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