Makoto Mino
Osaka City University
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Featured researches published by Makoto Mino.
Pediatrics International | 1969
Makoto Mino; Yonosuke Ueda; Masaki Hayashi; Yukitsura Tanabe
The occurrence of posterior subcapsular cataract (PSC) in 25 of 45 cases received the corticosteroid therapy was observed. No cases in the non‐steroid group had PSC. The dosage and duration of systemic corticoid administration appeared to be the major determining factor in development of the PSC.
Pediatrics International | 1966
Makoto Mino; Toshio Takai
Studies on LDH‐isozyme during development of the human fetus were undertaken. In the heart and liver during the early fetal life, the activity was found to be predominant in the LDH‐3 area. In the heart the predominancy of LDH‐3 area was found to continue throughout the fetal life, while in the liver it decreased and LDH‐5 region increased at 5 months of gestation. A decrease in the activity of LDH‐3 in the heart was found to occur after birth. Changes in LDH isozyme pattern in the skeletal muscle were found to be approximate to those in the liver. No remarkable changes in the isozyme pattern were shown in the brain and kidney.
Pediatrics International | 1966
Makoto Mino; Toshio Takai
Activities of cytochrome oxidase and succinic dehydrogenase in the heart, liver and brain of the developing human fetus were determined.
Pediatrics International | 1967
Makoto Mino; Toshio Takai
Studies on fructose diphosphate aldolase during development of the human fetus were undertaken. Additionally, the relation of the activity of LDH and its isozymes to aldolase in developing tissues including the liver, skeletal muscle, heart and brain were observed.
Pediatrics International | 1968
Makoto Mino; Toshio Takai; Toru Yamaguchi
In studing the enzymatic development of the human fetus, it is necessary to consider placental function, which may affect fetal metabolism. Glucose-6-phosphatase which play an improtant role in the regulation of blood glucose levels early in development, for example, is absent in fetal liver but present in the placenta. The activity of the enzyme in placenta, however, decreases as gestation proceeds and finally reaches low levels at term. The glycogen content of placenta has also been reported to be very high at the earliest stage of gestation and decreases thereafter in parallel with placental glucose-6-phosphatase activity. The placenta could thus regulate blood glucose levels of the fetus during early gestation at a time of prior to formation of requisite enzymes in the fetal liver. Based on the above evidence1)-5), changes in the activity of lactate dehydrogenase (LDH) in the human placenta were examined throughout the gestation period as a coronary to a previous study61 in which changes in this enzyme were followed developing human fetal tissues.
Pediatrics International | 1967
Makoto Mino; Toru Takeuchi; Toshio Takai
The studies were undertaken to examine changes in glucose‐6‐phosphate dehydrogenase activity during development of human fetal liver and red cells. In the liver, high activity of glucose‐6‐phosphate dehydrogenase was observed through 6 months of gestation. Thereafter, the activity promptly decreased and remained in the range of the adult level. In the red cells, the highest level of enzyme activity was observed during the earliest fetal life. However, the activity of the enzyme in fetal liver was found to be about a thousand times greater than that of the fetal red cells. Accordingly, the high level of glucose‐6‐phosphate dehydrogenase activity in the human phosphate dehydrogenase activity in the human fetal liver may not be a consequence only of contamination by the erythrocyte enzyme.
Pediatrics International | 1967
Makoto Mino; Toshio Takai
Studies on GOT and its isozyme during development of the human fetus were undertaken.
Vitamins | 1962
Makoto Mino; Otosaburo Hishikawa
Pediatrics International | 1968
Tatsuya Tsuchida; Syozo Nakagawa; Katsuzi Shiomi; Yonosuke Ueda; Masaki Hayashi; Makoto Mino
Pediatrics International | 1966
Makoto Mino