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Biomedical subjects

T Mouri

Publications and source records attributed to T Mouri.

At least 91 records · Page 5Linked to original sources

Plasma concentrations of atrial natriuretic peptide in various diseases.

Using a radioimmunoassay for atrial natriuretic peptide (ANP) we studied plasma concentrations of immunoreactive ANP in order to investigate the pathophysiological role of ANP in patients with various diseases. Plasma ANP levels were elevated in patients with congestive heart failure (394 +/- 260 pg/ml, n = 8) and chronic renal failure (219 +/- 86 pg/ml, n = 11). In patients undergoing hemodialysis plasma ANP levels were markedly high and decreased after hemodialysis from 433 +/- 166 pg/ml to 204 +/- 92 pg/ml (n = 11). ANP was removed from blood to dialysate (21 +/- 13 pg/ml of dialysate, n = 6, dialysate flow: 500 ml/min). Plasma ANP level was conversely correlated with creatinine clearance (r = -0.812, p less than 0.001) in patients with renal diseases (n = 29). In patients with atrial fibrillation, pace maker implantation, lung disease, chronic glomerulonephritis, nephrotic syndrome, essential hypertension, liver disease and cerebrovascular disease, plasma ANP levels were not significantly different from those in normal subjects (70 +/- 32 pg/ml, n = 28). These results suggest that ANP may be a circulating hormone playing pathophysiological roles in congestive heart failure and chronic renal failure.

Adult↗

Presence of neurophysins in the human pituitary corticotrophs, Cushing's adenomas, and growth hormone-producing adenomas detected by immunohistochemical study.

Neurophysins have been recognized as the carrier proteins of vasopressin and oxytocin. The distribution of neurophysins is immunohistochemically confirmed in the hypothalamus, median eminence, and posterior lobe of the pituitary gland. The authors detected neurophysins in the human corticotrophs and pituitary adenomas with the use of the immunohistochemical method with antiserum to human neurophysins, which did not cross-react with adrenocorticotropic hormone (ACTH), beta-endorphin, and corticotropin-releasing factor. All of ten pituitary glands obtained by autopsy revealed the presence of neurophysin-positive cells in the anterior, intermediate, and the posterior lobes. The neurophysin-positive cells were similar to the corticotrophs in shape and distribution. Simultaneous staining for ACTH and neurophysins in the serial sections revealed that neurophysin-positive cells were also ACTH-positive. One hundred twenty-four cases of pituitary adenoma operated upon were investigated. All of 7 Cushing's adenomas were composed of neurophysin-positive cells. Six tumors with giantism showed sparsely distributed neurophysin-positive cells. No neurophysin-positive cells were observed in any other cases. This study is the first reported evidence of the presence of neurophysins in the human corticotrophs and pituitary adenomas.

Adenoma↗

Synergistic pressor action of neuropeptide Y and norepinephrine in conscious rats.

The interaction of neuropeptide Y (NPY) and norepinephrine (NE) was studied in conscious unrestrained rats. Neuropeptide Y, administered intravenously (i.v.) in doses of 110 pmol/kg to 1.1 nmol/kg increased the mean arterial pressure (MAP) and decreased the heart rate (HR) in a dose-dependent way. The pressor effect of NPY (1.1 nmol/kg) was not attenuated by i.v. phentolamine in a dose of 3.1 mumol/kg. Norepinephrine infused at a rate of 89 nmol/kg per h, which had no effect on MAP, did not modulate the pressor effect of NPY. A pressor dose of NE infused at a rate of 266 nmol/kg per h significantly potentiated the pressor effect of NPY. Neuropeptide Y infused at a rate of 3.5 nmol/kg per h had no effect on MAP, and significantly potentiated the pressor effect of i.v. NE. It is concluded from these results that NPY could modulate the cardiovascular action of NE in physiological conditions.

Animals↗

Determination by enzyme-linked immunosorbent assay (ELISA) of specific IgG antibody activities for diagnosis of farmer's lung disease.

The specific IgG antibodies to thermophilic actinomycetes in the sera from patients with farmer's lung disease were quantitated by an ELISA and the results thereof were compared with those obtained by the standard double immunodiffusion assay (Ouchterlony's method). All sera from patients with farmer's lung disease were precipitin positive to Thermoactinomyces vulgaris and/or Micropolyspora faeni by the Ouchterlony's method, and revealed significantly high levels of IgG antibody activities against these antigens by ELISA. We have found 18 precipitin-positive but asymptomatic subjects in a survey of the dairy farming population of the northern area of IWATE Prefecture. Their sera were precipitin positive to antigens related to the farmer's lung disease, however IgG antibody activities as determined by ELISA to these antigens was significantly lower in the group of asymptomatics than in the group of symptomatics. Precipitin negative dairy farming controls and normal controls living in the urban area revealed low antibody activities as determined by ELISA. From these studies, we concluded that the assay of specific IgG antibody activity to thermophilic actinomyces by ELISA is useful for the diagnosis and screening of farmer's lung disease.

Adult↗

Chemical and immunological characterization of salmon endorphins.

Five new peptides related to salmon N-acetyl endorphin II (N-Ac-EP II) were isolated from an acid acetone extract of the pituitary. They were identified as EP II and four N-terminal fragments of N-Ac-EP II, namely N-Ac-EP II (1-18), (1-19), (1-20), and (1-29). The sequence comparison with mammalian EPs revealed that N-Ac-EP II (1-18) and (1-19) corresponded to mammalian alpha- and gamma-EP, respectively. The occurrence of peptides similar to mammalian alpha-, beta-, and gamma-EP indicates that further processing of EP takes place in both the teleost and mammalian pituitaries by similar pathways. A radioimmunoassay for salmon EPs has been developed with rabbit antiserum raised against salmon N-Ac-EP II. It was demonstrated that the antiserum showed full cross-reactivity with salmon N-Ac-EP I, N-Ac-EP II (1-20), and N-Ac-EP II (1-18), but none with Met-enkephalin, human beta-EP, and human beta-LPH. Similarly, the salmon EPs did not cross-react with human beta-EP antiserum in the radioimmunoassay.

Amino Acid Sequence↗

Effect of dexamethasone on immunoreactive corticotropin-releasing factor in the rat median eminence and intermediate-posterior pituitary.

Immunoreactive ACTH (I-ACTH) concentrations in the anterior pituitary, intermediate-posterior pituitary (IP), and plasma and immunoreactive corticotropin-releasing factor (I-CRF) concentrations in the median eminence and IP were determined in rats receiving dexamethasone for various periods from 16 h to 10 days. Plasma I-ACTH concentrations were decreased 16 h after a single injection of dexamethasone. Anterior pituitary I-ACTH concentrations did not decrease until 4 days after the start of dexamethasone medication. IP I-ACTH concentrations did not change throughout these periods. I-CRF concentrations in median eminence and IP rapidly decreased after dexamethasone administration. These results raise the possibility that the source of I-CRF in the IP is hypothalamic.

Adrenocorticotropic Hormone↗

Immunoreactive corticotropin and corticotropin-releasing factor in human hypothalamus, adrenal, lung cancer, and pheochromocytoma.

Immunoreactive corticotropin-releasing factor (I-CRF) and ACTH (I-ACTH) were examined using RIA, immunoaffinity chromatography, and gel filtration chromatography in human hypothalamus, adrenal (cortex and medulla), lung cancer, and pheochromocytoma. I-CRF and I-ACTH were present in these tissues. Gel filtration of I-ACTH in the adrenal, pheochromocytoma, and lung cancer showed the presence of larger amounts of I-ACTH with large molecular weight forms in contrast to the hypothalamus. Gel filtration of I-CRF in these tissues showed the main peak eluted at the position of synthetic rat CRF. High performance liquid chromatography of this main peak showed two components which eluted in the positions of synthetic rat CRF and oxidized CRF. These elution positions were the same in all tissues and identical with those in the hypothalamus. These results suggest the presence of I-ACTH and I-CRF in these tissues and that CRF outside the brain is identical to hypothalamic CRF.

Adrenal Gland Neoplasms↗

Distribution and characterization of immunoreactive corticotropin-releasing factor in human tissues.

The distribution and characterization of immunoreactive corticotropin-releasing factor (I-CRF) in human tissues were examined using a rat CRF RIA, immunoaffinity chromatography, gel filtration chromatography, and high performance liquid chromatography. High concentrations of I-CRF were found in the hypothalamus and pituitary stalk. In addition, I-CRF was found in the posterior pituitary, thalamus, cerebral cortex, cerebellum, pons, medulla oblongata, spinal cord, and outside the brain and in the adrenal, lung, liver, stomach, duodenum, and pancreas. The major component of I-CRF from these tissues eluted in the position of rat CRF on gel filtration chromatography. High performance liquid chromatography of this major component showed two main peaks which eluted in the positions of CRF and oxidized CRF. These elution positions were the same in all tissues. These results indicate the presence of I-CRF outside the brain and suggest that this CRF is identical to hypothalamic CRF.

Adrenal Glands↗

Immunocytochemical identification of CRF in the human hypothalamus.

Immunoreactive ovine corticotropin-releasing factor (CRF) was revealed in the cell bodies of parvocellular neurons in the paraventricular nucleus of the human hypothalamus by an immunocytochemical technique. The immunoreactivity was negative in magnocellular neurons. Immunoreactive nerve fibers were found in the subependymal layers of the third ventricle and in the perivascular space of the primary plexus in the lower hypothalamus. No CRF immunoreactive cell bodies were found in the supraoptic nucleus.

Corticotropin-Releasing Hormone↗

Multiple forms of immunoreactive dynorphin in human pituitary and pheochromocytoma.

Multiple forms of immunoreactive dynorphin (I-Dy) in human pituitary and pheochromocytoma were examined utilizing gel filtration and high performance liquid chromatography (HPLC). Gel filtration of I-Dy from these tissues revealed the major component in the position of Dy(1-17) and other minor components with large molecular weight forms. HPLC profile of this major component from gel filtration showed a large peak corresponding to the position of Dy(1-17) and small peaks corresponding to the positions of Dy (1-13), (1-12) and other unknown peptides. These results strongly suggest the presence of Dy(1-17) as the major component, and Dy (1-13), (1-12) or other unknown peptides as the minor components in these human tissues.

Adrenal Gland Neoplasms↗

Effects of bilateral adrenalectomy on immunoreactive corticotropin-releasing factor in the rat median eminence and intermediate-posterior pituitary.

Immunoreactive ACTH (I-ACTH) concentrations in the anterior pituitary (AP), intermediate-posterior pituitary (IP) and plasma, and immunoreactive corticotropin-releasing factor (I-CRF) concentrations in the median eminence (ME) and IP, were determined in adrenalectomized rats from 3 h till 14 days after surgery. Plasma I-ACTH concentrations showed the typical triphasic response over time. AP I-ACTH concentrations decreased immediately after surgery, then increased to high concentrations 3 days after surgery. I-ACTH concentrations in IP did not change through these periods. I-CRF concentrations in ME and IP decreased immediately after surgery, then gradually increased to high concentrations (ME) or to control levels (IP) 14 days after surgery. These results raise the possibility that the I-CRF in IP is of hypothalamic origin.

Adrenalectomy↗

Effects of cyproheptadine, reserpine, and synthetic corticotropin-releasing factor on pituitary glands from patients with Cushing's disease.

Direct effects of cyproheptadine, reserpine, synthetic ovine corticotropin-releasing factor (CRF), dexamethasone, and lysine-8-vasopressin (LVP) on the secretion of immunoreactive ACTH and beta-endorphin from the adenoma and the nonadenomatous tissue of patients with Cushing's disease were examined using a superfusion system. Cyproheptadine and reserpine (10(-9)-10(-7) M of each) suppressed immunoreactive ACTH and beta-endorphin secretion from both tissues. CRF (10(10)-10(7) M) stimulated the secretion of both peptides from the nonadenomatous tissue, but only a high dose of CRF could stimulate the secretion of these peptides from some adenomas. Such CRF-induced secretion was partially suppressed by dexamethasone. LVP (10(-9)-10(-7) M) stimulated peptide secretion from both types of tissue. These results suggest direct inhibitory effects of cyproheptadine and reserpine on the secretion of these peptides from the pituitary of patients with Cushing's disease, a different stimulatory mechanism of LVP from that of CRF in these tissues, and low sensitivity of the adenoma to CRF.

Adenoma↗

Presence of immunoreactive corticotropin-releasing factor in human cerebrospinal fluid.

Immunoreactive corticotropin-releasing factor (I-CRF) was measured by radioimmunoassay and immunoaffinity chromatography in human hypothalamus and cerebrospinal fluid (CSF). Dilution curves of I-CRF in the hypothalamus and CSF were parallel to that of synthetic ovine CRF standard. I-CRF content in the hypothalamus was 643 and 281 fmol eq, respectively. I-CRF concentration in CSF was 7.4 +/- 1.1 fmol eq/ml. Sephadex G-75 column chromatography showed the main peak eluted at the position of synthetic CRF.

Chromatography, Affinity↗

Immunoreactive corticotropin-releasing factor concentrations in cerebrospinal fluid from patients with hypothalamic-pituitary-adrenal disorders.

The concentrations of immunoreactive corticotropin-releasing factor (I-CRF) in human cerebrospinal fluid (CSF) were measured utilizing immunoaffinity chromatography and RIA in patients with no endocrine disease, patients with Cushing's disease, Nelson's syndrome, Sheehan's syndrome, Addison's disease and steroid treated patients. On high performance liquid chromatography, the elution profile and retention time of I-CRF in CSF were not identical with ovine CRF. I-CRF concentrations in CSF from patients with Cushing's disease and Sheehan's syndrome were lower than those from normal subjects, however those from patients with Nelson's syndrome and Addison's disease were within the normal range. I-CRF concentrations in CSF from patients with Cushing's disease returned to normal levels 2-9 months after pituitary adenomectomy. These results suggest that CSF I-CRF concentrations are reduced by increased plasma corticosteroid levels.

Addison Disease↗