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  1. C100 医学部/医学系研究科
  2. C100b 紀要
  3. Nagoya journal of medical science
  4. 30(2)

Analysis of Constitutions by Mathematical Principles :I. The Analysis of Obese-Diabetic and Obese Normal Constitutions

https://doi.org/10.18999/nagjms.30.2.157
https://doi.org/10.18999/nagjms.30.2.157
e9ec2bff-1776-45bf-a9f4-17446fe6a708
名前 / ファイル ライセンス アクション
v30n2p157_168.pdf v30n2p157_168.pdf (1.6 MB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2013-09-25
タイトル
タイトル Analysis of Constitutions by Mathematical Principles :I. The Analysis of Obese-Diabetic and Obese Normal Constitutions
言語 en
著者 OGAWA, SYUHEI

× OGAWA, SYUHEI

WEKO 93956

en OGAWA, SYUHEI

Search repository
YAMADA, KOZO

× YAMADA, KOZO

WEKO 93957

en YAMADA, KOZO

Search repository
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
抄録
内容記述 There are numerous empirical knowledge in the field of clinical medicine. In this article the authors intend to analyze such knowledge logically. A mathematical structure of an organism is proposed, using the "theory of sets", and the development of axiom was adopted into practice for the analysis of obese-diabetic and obese·normal constitutions. Define X, Y and Z as the sets of genetic, environmental factors and of vital phenomena; x, y, and z the elements in each set and t as time factor of aging, when z can be shown by the formula: Of course, the law given to "correspondence" f is of paramount importance. An organism is at least representing itself as having the responses of fitness to y within some limits by its x at t in the physiologic state. Therefore, the authors gave correspondence f, the law, that an organism would fitly respond to y or its own x with deficiency of minimal type. This axiom should not be applied to the pathologic state-that is, vital phenomena with cancer, autoimmunity or functio laesa etc. A man with glucokinase (GK) deficiency and without others will become a hyperinsulinar obese-diabetic; a man with deficiencies of phosphofructokinase (PFK) or pyruvate kinase (PK) in the liver, or of both enzymes, will become a hyperinsulinar obese-normal subject. One will recognize hyperinsulinism (one element in set Z) to be a response of fitness (correspondence f) in a person with any deficiency of hepatic key glycolytic enzymes, GK, PFK, and PK, (one element in set X), because insulin is the inducer of biosynthesis of hepatic key glycolytic enzymes. It is well known that rats fed on high fat diet show a diabetic status. Weber et al. reported that the hepatic key glycolytic enzymes, GK, PFK, and PK, were inhibited by physiological concentrations of fatty acids. Without genetic deficiencies, however, these organisms will become normal by removal of the insults. Thus, diets of environmental factors in set Y can regulate the appearance of genetic factors quantitatively, but not qualitatively. An enzyme with deficient activity needs to be produced in a larger quantity in order to compensate for the deficiency. Therefore, a person with GK deficiency shows hyperinsulinism. It is reported that insular function of pancreas decreases with age even in normal man and suggested that senile changes in the insular apparatus are significant factors in the development of diabetes. A person with hyperinsulinism will show a decrease in insular function with age more rapidly than a normal man will. Therefore, diabetes and obesity are in conformity with the "wear and tear theory" as a mechanism underlying the aging process. Thus, a constitution is composed of combinations of abnormal key enzymes and the interrelations between these enzymes and neural or hormonal systems which work on these key enzymes. Furthermore, the great variety of combinations between abnormality of elements in set X and modifications by elements in set Y should decrease or increase the time factor "t" when a pathologic state should occur.
言語 en
内容記述タイプ Abstract
出版者
言語 en
出版者 Nagoya University School of Medicine
言語
言語 eng
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ departmental bulletin paper
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
ID登録
ID登録 10.18999/nagjms.30.2.157
ID登録タイプ JaLC
関連情報
関連タイプ isVersionOf
識別子タイプ URI
関連識別子 http://www.med.nagoya-u.ac.jp/medlib/nagoya_j_med_sci/302/302.html
ISSN(print)
収録物識別子タイプ PISSN
収録物識別子 0027-7622
ISSN(Online)
収録物識別子タイプ EISSN
収録物識別子 2186-3326
書誌情報 en : Nagoya Journal of Medical Science

巻 30, 号 2, p. 157-168, 発行日 1967-09
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