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Biomedical subjects

M Uchihashi

Publications and source records attributed to M Uchihashi.

24 records · Page 2Linked to original sources
PubMed1982

Immunoreactive human epidermal growth factor in human pancreatic juice.

Human epidermal growth factor (hEGF), which stimulates the growth of a variety of cells in culture, has recently been isolated from human urine. In the present study, we identified significant amounts of immunoreactive (IR) hEGF (mean +/- SE, 2.3 +/- 0.09 ng/ml; n = 3) in human pancreatic juice. The IR-hEGF materials were immunologically indistinguishable from standard hEGF, although they were only 5% as active in receptor binding to human placental membrane as in RIA. Gel exclusion chromatography of the pancreatic juice under neutral and acidic conditions revealed three distinct IR-hEGF components with different molecular sizes. Incubation of 125I-labeled hEGF with either the pancreatic juice or the high molecular weight component(s) yielded no aggregation or degradation products. These data suggest that fully immunoreactive but much less bioactive hEGF-like substances which are heterogeneous in size are secreted into human pancreatic juice. Their tissue(s) of origin and physiological functions, if any, remain to be elucidated.

Adult↗
PubMed1982

Presence of human epidermal growth factor in human cerebrospinal fluid.

Human epidermal growth factor (gEGF), a potent stimulator of the growth of many tissues in culture, has been isolated from human urine and subsequently identified in many human biological fluids. We have partially purified and characterized hEGF-like substance(s) from human cerebrospinal fluid (CSF) and determined the concentrations of immunoreactive (IR) hEGF in CSF obtained from patients with a variety of neurological diseases. Competitive binding curves generated by the CSF samples appeared to be parallel to standard hEGF both in RIA and radioreceptor assays using human placental membrane. Sephadex G-50 gel exclusion chromatography of the CSF extract revealed a single peak of IR-hEGF which coeluted with standard hEGF. The apparent mol wt of the CSF hEGF-like substances(s) was estimated to be 8000 by sodium dodecyl sulfate poplyacrylamide gel electrophoresis, and its approximate pI was 4.5 as determined by isoelectric focusing. The concentrations of IR-hEGF in CSF from patients with pituitary and brain tumors and radiculomyelopathy were significantly higher than those from control subjects, while neither patients with hydrocephalus nor encephalomeningitis had CSF IR-hEGF levels statistically different from the control subjects. The presence of hEGF-like substance(s) in human CSF suggests that it may play an important physiological role in the function of the human nervous tissues but does not provide any evidence of its source.

Adolescent↗
PubMed1982

Specific binding sites for epidermal growth factor and its effect on human chorionic gonadotrophin secretion by cultured tumour cell lines: comparison between trophoblastic and non-trophoblastic cells.

Using human trophoblastic (SCH) and nontrophoblastic (HeLa S3) tumour cell lines, specific binding sites for epidermal growth factor (EGF), a potent stimulator of growth in many tissues, and its effect on secretion of human chorionic gonadotrophin (hCG) and/or its subunits were compared between these two tumour cells. Both SCH and HeLa S3 cells possessed two populations of specific binding sites for 125I-labelled EGF: the high affinity (Kd approximately 10(-10) M) and the low affinity (Kd approximately 7 x 10(-10) M) system. Tetradecanoyl phorbol acetate (TPA), a tumour promotor, showed a potent competitor of labelled tracer binding to its receptor sites in both cell lines. EGF stimulated both hCG-alpha and hCG and/or hCG-beta secretion in a dose-responsive manner from SCH cells, whereas it had no effect on hCG-alpha secretion from HeLa S3 cells. In contrast, dibutyryl cyclic AMP plus theophylline, a phosphodiesterase inhibitor, enhanced hCG-alpha secretion from both cells, while TPA had no effect in either cells. These data suggest that EGF may play a physiological role in hCG secretion from trophoblastic tissues and that the mechanism by which hCG and/or its subunits are secreted may differ between trophoblastic and non-trophoblastic tumour cells.

Bucladesine↗
PubMed1981

Presence of ectopic beta-adrenergic receptors on human adrenocortical cortisol-producing adenomas.

A direct binding study of radioligand [3H]dihydroalprenolol (DHA), a potent beta-adrenergic antagonist, was performed on the particulate fractions of four adrenocortical adenomas (three cortisol-producing adenomas and one aldosterone-producing adenoma) and normal adrenal tissues. The effect of epinephrine on cortisol production was also evaluated in vitro from the cultured tumor cells from one cortisol-producing adenoma. Saturable binding of [3H]DHA to the tumor membranes was observed in two of three cortisol-producing adenomas, but not in the aldosterone-producing adenoma or in normal adrenal tissues. Scatchard analysis of equilibrium binding of [3H]DHA revealed a single class of binding sites on the tumor membranes; the apparent dissociation constant (Kd) was 1 nM in each, and the numbers of binding sites were 108 and 45 fmol/mg protein, respectively. Competition by adrenergic agents with [3H]DHA for binding sites on the membranes from one cortisol-producing adenoma revealed that (+/-)propranolol, a beta-adrenergic antagonist, was about 350-fold more potent than phentolamine, an alpha-adrenergic antagonist, suggesting the beta-adrenergic nature of receptor sites. In addition, stereospecificity was demonstrated by about 1000-fold greater affinity of (-)alprenolol than to (+)alprenolol, both of which are stereoisomers of the beta-adrenergic antagonist. Furthermore, production of cortisol from the cultured tumor cells prepared from the same adenoma was significantly stimulated by epinephrine in addition to ACTH. These data indicate that ectopic beta-adrenergic receptor sites are present in some human adrenocortical tumors which may be functionally related to the activation of adenylate cyclase by catecholamines other than ACTH in those tumors, as previously demonstrated. The mechanism by which such altered cellular membrane characteristics occur in association with neoplastic alteration of the endocrine tissues remains unanswered.

Adenoma↗