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Biomedical subjects

G Yamamoto

Publications and source records attributed to G Yamamoto.

At least 55 records · Page 3Linked to original sources
PubMed1984

Somatostatin desensitization in rat anterior pituitary cells.

The possibility that desensitization to the inhibitory effects of somatostatin (SS) might develop following chronic exposure to this tetradecapeptide was examined in cultured rat anterior pituitary cells. Pretreatment with 1 microM SS for 48 h caused a shift in the IC50 of SS to inhibit 3-isobutyl-1-methylxanthine (IBMX) or growth hormone-releasing factor (GRF)-induced growth hormone (GH) and TRH + IBMX-induced thyroid-stimulating hormone (TSH) release by more than 2 orders of magnitude. Refractoriness developed after 12 h of exposure to doses of SS of 10 nM or more and became maximal at 48 h. Restoration of SS responsiveness followed a similar time-course upon removal of the peptide. In superfused cells, 10 nM SS lowered GH secretion rates to less than 5 ng/min within 2 h, but GH release began to rise after 16 h despite the continued presence of SS. However, when somatostatin was delivered in pulses, it remained fully effective for more than 36 h. Somatostatin-28 was also capable of inducing refractoriness in cultured pituitary cells. However, cells made refractory to either SS-14 or SS-28 were not made refractory to the same extent to the other form of somatostatin. These results indicate that the pituitary can become desensitized to the inhibitory actions of somatostatin just as it does to the stimulatory actions of the other hypothalamic releasing hormones.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Effects of synthetic ovine corticotropin-releasing factor, glucocorticoids, catecholamines, neurohypophysial peptides, and other substances on cultured corticotropic cells.

Synthetic ovine corticotropin-releasing factor (CRF) is a 41-residue peptide with high potency and intrinsic activity to stimulate the secretion of ACTH and beta-endorphin-like immunoactivity (beta-End-LI) by cultured adenohypophysial corticotropic cells. The action of CRF in vitro can be potentiated by the weaker secretagogues, vasopressin, oxytocin, epinephrine, norepinephrine, and angiotensin II. CRF-mediated secretion of ACTH and beta-End-LI is noncompetitively inhibited by pretreatment of cells with glucocorticoids. Long term exposure of adenohypophysial cells to CRF results in an increase in total medium plus cell ACTH in the cultures, suggesting that CRF can enhance rates of ACTH synthesis as well as release. CRF also stimulates the secretion of beta-End-LI by corticotropic cells cultured from the neurointermediate lobe. Higher concentrations of CRF are required to stimulate secretion by this cell type than by anterior lobe corticotropic cells. These in vitro results are consistent with CRF playing a major physiological role in the neuroregulation of secretion by anterior lobe corticotropic cells, where the peptide may interact with other modulators.

Adrenocorticotropic Hormone↗
PubMed1978

[103Ru for tumor scanning--a comparative study on tissue distributions of 103Ru-chloride and 103Ru-citrate in tumor-bearing animals (author's transl)].

Biological distribution of 103Ru in mice bearing Ehlrich's solid tumor and rats bearing AH-130 solid tumor were studied with two compounds of 103Ru, the chloride and citrate. The radioactivity of 103Ru-chloride showed slower excretion and higher tumor concentration than that of citrate. The tumor-to-muscle ratios of chloride were always higher, but the tumor-to-blood ratios were always lower than those of citrate. No significant difference was founds between 103Ru-chloride and citrate as tumor scanning agents.

Animals↗
PubMed1976

Studies on ferrous ion-induced lipid peroxidation of rat liver mitochondria. II. Relationship to incubation temperature.

Ferrous ion-induced lipid peroxidation in rat liver mitochondria has a lag in the induction period. The characteristics of the lag were investigated under various conditions. This lag period lengthened proportionally to increased temperature (4 degrees approximately 37 degrees C). In the presence of inorganic phosphate the lag period lengthened, reaching a maximum at about 20 degrees C, and then shortened with increased temperatute. Elongated lag periods were shown in heat-treated or protein digested mitochondria. Shortened lag periods were shown in snake venom-treated mitochondria. On the other hand, almost no lag was observed in the peroxidation of the lipid extracted from mitochondria. The lag period also varied with incubation temperature. The results suggested that certain factors, which determined lag of the induction period in membrane lipid peroxidation associate with reaction-temperature and the lipo-protein structure in mitochondrial membranes.

Animals↗
PubMed1975

Tissue distributions of 97Ru and 103Ru in subcutaneous tumor of rodents.

Mice bearing Ehrlich tumor were administered 97Ru-chloride or 103Ru-chloride intravenously. Examinations of various tissues indicated similar distributions by the two radionuclides. The levels were higher in the lung, liver and kidney than in the tumor tissue. Rats bearing AH-130 tumor were administered 103Ru-chloride intravenously. The 103Ru distribution in rats was highest in the spleen, followed by the liver and kidney; however, the radioactive distribution in the tumor tissue exceeded the muscle level by about 5-fold. Tumors were delineated in rats by scintigraphy. The findings indicate that ruthenium radionuclides may be a useful clinical agent in the delineation of some types of tumors. Ruthenium-97 would be favored in possible clinical usage due to its shorter physical half-life and lower levels of gamma energy.

Animals↗