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Biomedical subjects

I Adachi

Publications and source records attributed to I Adachi.

At least 271 records · Page 15Linked to original sources
PubMed1979

[Calcitonin].

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Calcitonin↗
PubMed1979

Family study of serum carcinoembryonic antigen in inherited medullary carcinoma of the thyroid.

Serum carcinoembryonic antigen (CEA) and calcitonin were assayed in 8 patients with medullary carcinoma of the thyroid (MCT) and 14 unaffected family members, from 4 pedigrees of Sipple's syndrome and one pedigree with inherited MCT. Serum CEA ranged from 5.4 to 44.5 ng/ml in the patients, but less than 2.5 ng/ml in the unaffected. This is in contrast with retinoblastoma and cancer family syndrome, where not only the patients but also unaffected family members show high serum CEA, and cytoplasmic or selective maternal inheritance of serum CEA level is presumed. In inheritable MCT, serum CEA increases in association with the development of MCT, and serum CEA level per se is not inherited.

Adolescent↗
PubMed1977

Immunohistochemical and ultrastructural analysis of medullary carcinoma of the thyroid in relation to hormone production.

Eighteen cases of medullary carcinoma of the thyroid were analyzed immunohistochemically for calcitonin- and ACTH-containing cells, and tumor cells in 8 cases were examined by an electron microscope and analyzed by manual and computer procedures with particular attention paid to the size and quality of secretory granules. Calcitonin- and ACTH-containing cells were found singly or in clusters in 14 and 11 tumors, respectively. In 4 cases, calcitonin-positive cell clusters and an increase in number of singly scattered C cells were seen apart from the main tumor, suggesting a multicentric nature of certain medullary carcinomas. Some ACTH-containing cells were apparently also positive for calcitonin. In a case of familial Sipple disease, follicular lining cells were replaced in areas with ACTH-containing cells. Three to five frequency distribution curves of the size of secretory granules were obtained in all of 6 cases analyzed, and at least two different types of granule matrix were identified.

Adrenocorticotropic Hormone↗
PubMed1977

Production of calcitonin, adrenocorticotropic hormone, and beta-melanocyte-stimulating hormone in tumors derived from amine precursor uptake and decarboxylation cells.

The tumor production of human calcitonin (CT) was examined by radioimmunoassay, and it was found that 50 of 85 (59%) tumor tissues collected at random contained immunoreactive CT. These tumors were grouped as to whether they were derived from the amine precursor uptake and decarboxylation (APUD) series. The group that was derived from APUD cells showed appreciable amounts of CT in 30 of 31 (97%) of these tumors or in 20 of 21 (95%) when the medullary carcinomas of the thyroid were excluded. However, of the non-APUD group of tumors only 20 of 54 (37%) were found to contain CT, so that the difference between these two groups was highly significant (p less than 0.001). Of the tumors with ectopic adrenocorticotropic hormone-melanocyte-stimulating hormone production, 12 of 14 were shown to contain CT. These data indicate that CT is a common product of the APUD tumors and that tumor production of CT is often associated with that of adrenocorticotropic hormone and beta-melanocyte-stimulating hormone.

APUD Cells↗
PubMed1976

Plasma human calcitonin (hCT) levels in normal and pathologic conditions, and their responses to short calcium or tetragastrin infusion.

Plasma hCT levels were less than 50 pg/ml in 50 normal subjects. In 16 patients with medullary carcinoma of the thyroid (MCT), plasma hCT levels were distinctively elevated and they fell significantly after total thyroidectomy, but in 11 of them plasma levels were still high, indicating the presence of metastases. In 74 patients with the other types of malignancy, plasma hCT levels were found to be high in 9 cases (3 oat cell carcinoma of the lung, 4 malignant carcinoids, one malignant pheochromocytoma and one acute myelocytic leukemia). Except for the leukemic case, all these tumors were derived from neural crest. In 12 patients with primary hyperparathyroidism, plasma hCT levels were less than 20 pg/ml. In 13 hypoparathyroid patients, two with pseudohypoparathyroidism and one with pseudoidiopathic hypoparathyroidism, plasma hCT levels were slightly elevated. Some patients with uremia had elevated plasma hCT levels, but there was no relation between plasma levels of hCT and those of PTH, urea nitrogen or creatinine. In response to Ca (4.5 mg/kg/10 min) or tetragastrin (4 mug/kg/5 min) infusion, a marked increase in plasma hCT was observed in all patients with MCT, but not in normal subjects. In 5 hypoparathyroid patients, a significant increase to both stimuli was also observed in all cases. Two patients with pseudopseudohypoparathyroidism responded to the Ca load. These results indicate that the determination of plasma hCT levels especially after a short Ca or tetragastrin infusion is important to study various pathological conditions.

Calcitonin↗
PubMed1975

Radioimmunoassay specific for amino (N) and carboxyl (C) terminal portion of parathyroid hormone.

A radioimmunoassay specific for the amino (N) terminal portion of the parathyroid hormone (PTH) molecule (N-PTH radioimmunoassay) has been developed by iodinating synthetic 1-34bovine PTH (1-34bPTH) and using commercially available bPTH antiserum. A radioimmunoassay specific for the carboxyl (C) terminal (C-PTH radioimmunoassay) has been carried out by adding enough amount of 1-34bPTH to the PTH radioimmunoassay system. The data obtained from N- and C-PTH radioimmunoassay were compared with those obtained from the PTH radioimmunoassay. It was observed that plasma levels of N-PTH, indicating biologically active PTH, were only one 8th to 32th to those of PTH and those of C-PTH were almost equal to those of PTH. These data corresponded well with those reported previously by using the antiserum specific for each terminal of the PTH molecule from the other laboratory. The half life of plasma N-PTH and C-PTH determined following the removal of parathyroid adenoma was less than 10 min and about 45 min respectively. These data indicate that the N-PTH radioimmunoassay can be done by iodinating 1-34bPTH and using commercially available antiserum.

Adenoma↗