Biomedical subjects

S Iida

Publications and source records attributed to S Iida.

618 records · Page 35Linked to original sources

PubMedDate not supplied

Accelerated decline of blood glucose after intravenous glucose injection in a patient with Cowden disease having a heterozygous germline mutation of the PTEN/MMAC1 gene.

The PTEN/MMAC1, a putative tumor suppressor, has been demonstrated to dephosphorylate phosphatidylinositol 3, 4, 5-triphosphate, a key molecule involved in the insulin signaling pathway. The PTEN may act, therefore, as a negative regulator of insulin signaling. The patient with Cowden disease, having a heterozygous PTEN/MMAC1 gene mutation, a C to T substitution of a single base at codon 130, was suspected to have decreased amount of PTEN protein with phosphatase signature motif. We thought that the patient might be more sensitive to insulin than normal subjects. As expected, administration of a bolus of glucose resulted in a more rapid clearance of blood glucose than was observed in 5 control subjects, indicating the presence of insulin hypersensitivity in the patient. The euglycemic hyperinsulinemic clamp study provided additional evidence.

Adult↗

PubMedDate not supplied

Rounding of cultured human carcinoid tumor cells by forskolin.

A primary culture of carcinoid cells obtained from a metastasized brain tumor of a 30 year old man was established. Rounding of carcinoid cells was induced by the addition of 20 microM forskolin or 1 mM dibutyryl cyclic AMP to the culture medium. The cyclic AMP content in carcinoid cells was increased thirtyfold by the addition of 20 microM forskolin. The results provided evidence that cyclic AMP might also be involved in rounding of human malignant carcinoid cells.

Adult↗

PubMedDate not supplied

Transport of acetaminophen conjugates in isolated rat hepatocytes.

The membrane permeabilities of acetaminophen glucuronide and sulfate produced through conjugative metabolism were examined in isolated rat hepatocytes. The glucuronide formed in hepatocytes was gradually released into the medium and its intracellular level decreased. Release of the sulfate formed in hepatocytes occurred more rapidly and its intracellular level remained almost constant. The permeability of acetaminophen was so rapid that it caused instantaneous equilibrium between hepatocytes and the medium. Its intracellular level thus decreased by conjugation reactions, but compensation for this decrease from the medium was soon made so that a constant intracellular level was resumed. The uptake of both preformed glucuronide and sulfate into hepatocytes indicated carrier-mediated transport. From these results, a pharmacokinetic model is proposed in which conjugative metabolism occurs in two consecutive steps: conjugative reactions of the parent compound taken up instantaneously into hepatocytes and membrane transport of conjugates into the medium. Changes in the amount of acetaminophen, its glucuronide, and its sulfate in the hepatocytes and medium as a function of time simulated according to the model closely agreed with those actually observed. Consequently, membrane permeability of the conjugates was concluded to be essential for conjugative metabolism.

Acetaminophen↗

PubMedDate not supplied

Functional characteristics of transplantable rat pituitary tumor MtT SA5 inducing pronounced adrenal hyperplasia.

Transplantable rat pituitary tumor MtT SA5 is characterized by the induction of pronounced adrenal enlargement. In spite of remarkable elevation of plasma ACTH levels, serum corticosterone levels in hypophysectomized tumor-bearing rats were lower than those in intact control rats. No immunohistochemical alterations were seen in corticotrophs of the pituitary in tumor-bearing rats. Ratio of bioactive ACTH (Bio-ACTH) to immunoreactive ACTH (Ir-ACTH) in the tumor tissues was 0.2%, being extraordinarily lower than in the pituitary tissues (23%). Gel chromatography of the tumor tissue showed large molecular weight forms of Ir-ACTH, which seem to result from abnormal processing of proopiomelanocortin, and are responsible for the lower levels of Bio-ACTH compared to Ir-ACTH. The MtT SA5 tumor is suggested to secrete ACTH-related peptides which induce pronounced adrenal enlargement with little or no stimulation of glucocorticoid production.

Adrenal Glands↗

PubMedDate not supplied

Induction of differentiation of human phaeochromocytoma cells in culture by epidermal growth factor and insulin.

A primary culture of malignant phaeochromocytoma cells obtained from a left adrenal tumor of a 56 year old woman complaining of occasional palpitation and headache was established. The addition of epidermal growth factor (EGF) and insulin to the culture medium induced a profound development of network formation of axon-like processes. At the same time, the secretion of catecholamines from cultured cells was also increased. EGF and insulin were demonstrated to induce the differentiation of malignant phaeochromocytoma cells in primary culture.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

A somatic mutation of the p21(Waf1/Cip1) gene in a human adrenocortical adenoma.

The p21(Waf1/Cip1) protein, an inhibitory protein of cellular growth and DNA replication, is induced by the p53 tumour suppressor protein. Any mutations or deletions inactivating the protein may result in unregulated cellular growth. In one aldosterone secreting adrenocortical adenoma, we found a heterozygous deletion of a 111-base-pair (bp) fragment of the p21 cDNA. This deletion resulted in a truncated p21 protein lacking 37 amino acids from codon 65 to 101. The deletion was a somatic mutation, because it was not detected in the DNA of cultured fibroblasts obtained from the same patient. The results suggest that an alteration of the p21 protein may be relevant in inducing an adrenocortical adenoma, a well differentiated and slowly growing benign tumour.

Adenoma↗