[Natural childbirth as the basis of obstetrics].
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Biomedical subjects
Publications and source records attributed to K Aoyagi.
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To clarify the metabolic pathway of guanidinosuccinic acid (GSA), we investigated the relationship between GSA synthesis and the urea cycle. In isolated rat hepatocytes, GSA formation increased as urea concentration was raised; the effect of urea was not modified by the addition of ammonium chloride. Other urea cycle intermediates, including arginine and cyanate, a degradation product of urea, failed to stimulate GSA synthesis. Ornithine and arginine, which stimulate urea synthesis, strongly inhibited urea-stimulated GSA synthesis in the presence of 10 mM ammonium chloride, but the inhibitory effect of ornithine was not observed when ammonium chloride was not present. Citrulline (5 mM) strongly inhibited urea-stimulated GSA synthesis with or without ammonium chloride. D,L-norvaline, which inhibits urea cycle enzymes, strongly inhibited GSA synthesis. Following urea injection, hepatic GSA levels also increased in vivo, but there was little change in hepatic arginine. However, the addition of ornithine or D,L-norvaline inhibited the production of hepatic GSA, although arginine was increased substantially. These results indicate that GSA synthesis occurs in rat hepatocytes and is stimulated by urea. The data also suggest that the urea cycle enzymes catalyze some of the biochemical reactions in the GSA synthetic pathway.
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The coexistence of hyperthyroidism and peptic ulcer is considered to be extremely rare. We have treated 24 patients with both hyperthyroidism and peptic ulcer during the years 1968-1978. With regard to the correlation between hyperthyroidism and peptic ulcer, we found that the mean value of gastric acid output was higher in the hyperthyroid patients than in the controls, and an extremely high gastric acid output was noted in 8 of the hyperthyroid patients. These results suggest that hyperthyroidism coexisting with peptic ulcer may not be so rare.
In 25 patients with prostatic cancer and 26 patients with benign prostatic hypertrophy, urinary hydroxyproline excretion as estimated by the method described by Cleary and Saunders. The patients were kept on a diet free of gelatin. Urinary creatinine was measured in all patients and serum acid phosphatase, prostatic acid phosphatase, alkaline phosphatase and calcium were measured in patients with prostatic cancer. Urinary hydroxyproline excretion and the hydroxyproline/creatinine ratio were both elevated in patients who had prostate cancer with bone metastasis when compared to values in patients who had benign prostatic hypertrophy or prostatic cancer without bone metastasis. These two were more sensitive indicators of bone metastasis than serum acid phosphatase, prostatic acid phosphatase, alkaline phosphatase and calcium. These results suggest that urinary hydroxyproline is a valuable index of bone metastasis in prostatic cancer.
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To study the gastrointestinal hormones in hyperthyroidism and the interrelations with the thyroid hormones, the preprandial serum gastrin and motilin were measured by radioimmunoassay in 104 patients before and after the treatments. The following results were obtained: 1) Serum gastrin concentration in hyperthyroidism was significantly higher than that of the control, and when the patients reached euthyroidism or hypothyroidism after the treatments, the gastrin concentrations in the serum decreased to the normal level. There was a positive correlation between the thyroid hormones and the serum gastrin. 2) Serum motilin concentration in hyperthyroidism was slightly lower than that of the control. As the patients reached the euthyroid or hypothyroid state after the treatments, an increasing tendency of motilin was observed, though the change was not significant. There was a slightly negative correlation in gastrin versus motilin and also in T4 versus motilin.
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Pent-4-enoate at 0.1 to 1.0 mM strongly inhibited urea synthesis in isolated rat hepatocytes. Pent-4-enoate at the same concentrations markedly decreased concentrations of N-acetyl-L-glutamate, an essential activator of carbamoyl-phosphate synthase-I (EC 2.7.2.5), and the decrease was well in parallel with the inhibition of urea synthesis by pent-4-enoate. This compound also lowered cellular concentrations of acetyl-CoA, a substrate of acetylglutamate synthase (EC 2.3.1.1). Pent-4-enoate in a dose of 1 mM did not significantly affect cellular concentrations of ATP, and had no direct effect on acetylglutamate synthase activity. These results suggest that the inhibition of urea synthesis by pent-4-enoate is due to decrease in N-acetyl-L-glutamate concentration and that the decrease is probably brought about by decreased rate of its synthesis due to the lowered concentration of cellular acetyl-CoA.
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