[A practicing midwife in the countryside].
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Biomedical subjects
Publications and source records attributed to S Sakuma.
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Both the inhibitory and stimulatory guanine nucleotide-binding proteins of the adenylate cyclase complex were measured in erythrocyte membranes from patients with pseudohypoparathyroidism (PHP). The inhibitory guanine nucleotide-binding protein (Ni) of adenylate cyclase was measured by incorporation of [32P]ADP-ribose from [32P]NAD into the 39K subunit of Ni catalyzed by pertussis toxin. The ADP-ribosyltransferase activity of the toxin was expressed through incubation with dithiothreitol and erythrocyte membranes. Erythrocytes from 12 patients with PHP type I (PHP-I) had Ni values similar to those of 9 normal subjects and 2 patients with pseudopseudohypoparathyroidism. In 6 PHP-I patients, decreased activity of the stimulatory guanine nucleotide-binding protein (Ns) of adenylate cyclase, as determined by reconstitution of adenylate cyclase in the Ns-deficient membranes of cyc-S49 cells, corresponded with the reduced degree of ADP-ribosylation of the 42K subunit of Ns catalyzed by cholera toxin. These data suggest that the defect of Ns results in reduced stimulation of adenylate cyclase in some PHP-I patients, and that enhanced inhibition of the enzyme due to an increase in the 39K subunit of Ni does not account for the biochemical lesion in PHP-I patients.
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Chemoendocrine therapy was performed on a man with advanced breast cancer, and partial response was observed for 11 months. Estrogen receptor in cancer tissue was detected before and after the therapy. Progesterone receptor, however, was not detected after the treatment, whether it had been there or not prior to it. The serum estrone level was continuously high during the treatment, but the serum testosterone level was obviously decreased after that.
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Following local anesthetic use, maternal and umbilical serum levels of lidocaine were determined at delivery by means of a gas-chromatography-mass-spectrometry technique in 13 cases. In six cases, where delivery was performed by cesarean section, lidocaine was used for epidural analgesia. The dose given averaged 4.0 +/- 1.7 mg/kg, and the time between analgesia and delivery was 22.0 +/- 4.5 minutes. The mean umbilical serum level of lidocaine was 1.19 +/- 0.79 micrograms/ml and that of the maternal serum was 2.18 +/- 1.25 micrograms/ml. The fetal to maternal ratio was 0.52 +/- 0.18. Lidocaine levels of neonatal plasma were followed at 3, 6, 12, and 24 hours after delivery, and the mean half-life was found to be 6.7 +/- 1.3 hours. In the other seven cases, lidocaine was given in normal vaginal delivery for pudendal nerve block, and the dose was as small as 0.79 +/- 0.06 mg/kg. The mean umbilical and maternal serum concentrations of lidocaine were 0.064 +/- 0.039 micrograms/ml and 0.143 +/- 0.071 micrograms/ml, respectively, and the ratio was 0.45 +/- 0.16. Lidocaine given to the mothers crossed to the fetuses readily and resulted in neonatal plasma levels that were half those of the mothers'. The elimination of lidocaine from the newborn after birth was prolonged so that it might prevent the adaptation of the infant to postnatal circumstances. Viewed from the standpoint of infant care, anesthetics at delivery should be given to the mother only when the benefit obtained by their use outweighs any possible disadvantages.
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