Overview
- Editors:
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Akitane Mori
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Okayama University Medical School, Okayama, Japan
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Burton D. Cohen
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The Bronx Lebanon Hospital Center, Bronx, USA
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Hikaru Koide
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Juntendo University School of Medicine, Tokyo, Japan
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Table of contents (41 chapters)
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Involvement of Giuanidino Compounds in Renal Dysfunction
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- Masato Inouchi, Tomoya Fujino, Takeo Sato, Takashi Yasuda, Hitoshi Tomita, Tsukasa Kanazawa et al.
Pages 277-288
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- Makoto Ishizaki, Hiroshi Kitamura, Hisako Sugai, Kazuyuki Suzuki, Kosei Kurosawa, Gen Futaki et al.
Pages 289-297
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- Burton D. Cohen, Harini Patel
Pages 299-301
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- Shuei Nakayama, Masahiro Junen, Ikuo Kiyatake, Hikaru Koide
Pages 303-311
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- Shuei Nakayama, Ikuo Kiyatake, Yoshio Shirokane, Hikaru Koide
Pages 313-322
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- Kazuyuki Tasaki, Kazukiyo Yoshida, Fumitake Gejyo, Masaaki Arakawa
Pages 323-329
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- Yoshiharu Tsubakihara, Eiji Yamato, Kenji Yokoyama, Eisaku Kitamura, Noriyuki Okada, Isao Nakanishi et al.
Pages 331-336
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- Kazuo Isoda, Tetsuya Mitarai, Noritsugu Imamura, Hidehiko Honda, Ryoji Nagasawa, Satoru Hirose et al.
Pages 337-344
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Back Matter
Pages 345-365
About this book
Guanidine is named for its similarity to the purine guanine which, in turn, is named for its principal source guano, which comes from the Inca word, huano, for dung. Guanidine, therefore, translates into dung-like, which is hardly a genteel way to introduce a subject. On the other hand, texts are seldom inspirational, "frequently crude and rarely literary and should be judged on how successfully they assemble, organize and present current data. I am impressed that the material which fol]ows goes a long way toward successfully achieving those goals. Tue International Guanidine Society is a synthesis of three groups of investigators: biologists studying guanidines as phosphagens, neurologists interested in guanidines as convulsants and nephrologists involved with guanidines as toxins. As a member of the latter group. I am gratified by the considerable progress this book represents. To begin with. there now appears to be a common theme which unifies current speculation concerning the metabolic origin of the guanidines in uremia. At the First International Congress in 1983, evidence was presented which supported the theory that certain guanidines were products of the mixed function oxidation of urea. This year's meeting brings together overwhelming data showing that methyl guanidine is an effect of active oxygen reacting with creatinine. An idolatry, worshipped throughout biochemistry, that urea and creatinine are inert byproducts of protein metabolism, is shown to have feet of clay.
Editors and Affiliations
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Okayama University Medical School, Okayama, Japan
Akitane Mori
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The Bronx Lebanon Hospital Center, Bronx, USA
Burton D. Cohen
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Juntendo University School of Medicine, Tokyo, Japan
Hikaru Koide