Changes in serum isozymes in breeding Japanese black heifer with Ibaraki disease.
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Biomedical subjects
Publications and source records attributed to Y Oki.
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Administration of monosodium aspartate (MSA) to neonatal voles, Microtus arvalis Pallas induced neuronal necrosis in several brain regions including the arcuate and ventromedial hypothalamic nuclei. In the growing stage, 56.7% showed glycosuria. In the mild diabetic voles, blood glucose concentrations rose to 180 mg/dl (72 mg/dl in normal), and plasma insulin levels were also increased to 112 microU/ml (21 microU/ml in normal). In the severe diabetic voles, on the other hand, blood glucose concentrations rose over 250 mg/dl, and plasma insulin levels decreased under 10 microU/ml. Histopathological examination of the pancreatic islets revealed moderately enlarged islets, and nuclear hypertrophy and partial degranulation of B cells in the mild diabetic voles, and moderately to markedly enlarged islets, and marked degranulation, vacuolation and accumulation of glycogen granules of B cells in the severe diabetic voles. These results indicated that the diabetic syndrome in herbivorous voles was induced by administration of MSA and diabetic voles fell into marked insulin deficiency in the severe stage.
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The aim of this study was to determine whether atrial natriuretic peptide (ANP) alters beta-endorphin (beta-END) secretion from rat intermediate pituitary and whether this effect is a direct action on the intermediate pituitary or an indirect one mediated by hypothalamic factor(s). We studied the release of beta-END from rat neuro-intermediate lobes of the pituitary (NIL) and from the hypothalamo-neurohypophysial complex (HNC), which consists of the hypothalamus, pituitary stalk, intermediate and posterior lobes of the pituitary, by means of an in vitro perifusion system. NIL and HNC were prepared from male Wistar rats and individually perifused for 30 min with perifusion medium followed by 20 min perifusion with medium containing alpha-rat ANP and/or dopamine (DA). Samples of perifusion medium were collected every 5 min and subjected to RIA for beta-END. The basal release of beta-END from NIL was 180% of that from HNC (p less than 0.01), which provides further support for the presence of hypothalamic factors that inhibit beta-END release from the intermediate pituitary. The perifusion of HNC with ANP at 10(-7) and 10(-6) M increased the beta-END concentration by 25 and 50%, respectively (p less than 0.01). In contrast, ANP (10(-8) to 10(-6) M) had no effect on beta-END release from NIL. The inhibitory effect of DA (10(6) M) on beta-END release from NIL and HNC (51% and 50% of the basal release, respectively, p less than 0.01) was confirmed. However, this inhibitory effect was not reversed by ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
We examined effects of sodium valproate, a gamma amino butyric acid (GABA)-transaminase inhibitor, on the secretion of immunoreactive (IR)-ACTH and IR-beta-endorphin/LPH from cultured rat anterior pituitary cells to determine whether sodium valproate has a direct action on the secretion of ACTH and its related peptides from the cultured rat anterior pituitary gland. During the 3 h incubation, the basal secretion of IR-ACTH and IR-beta-endorphin/LPH decreased to 50.8% and 58.3%, respectively, of the control concentration after adding 10(-7) M sodium valproate into the incubation media and to 67.7% and 69.3%, respectively, of the control levels with 10(-8) M sodium valproate. However, sodium valproate at a concentration of 10(-6) M or 10(-9) M did not affect the basal concentration of IR-ACTH and IR-beta-endorphin/LPH. Sodium valproate at a concentration of 10(-7) M significantly attenuated the stimulated release of IR-ACTH and IR-beta-endorphin/LPH by 10(-9) or 10(-10) M of ovine corticotrophin releasing factor. These results indicate that sodium valproate could directly effect rat anterior pituitary cells to suppress both basal and stimulated release of proopiomelanocortin derived peptides and this supports the hypothesis that sodium valproate has a direct effect at the pituitary corticotroph in reducing plasma ACTH.
Obese diabetes was induced by monosodium aspartate (MSA) administration in KK male mice and the diabetic KK mice were divided into two groups, younger (12-week-old) and older (35-week-old). The diabetic KK mice were castrated and administered with androgen and effect of androgen on glycosuria appearance was investigated. Androgen dependent tear proteins (Mtp-M) were detected by the method of polyacrylamide gel electrophoresis. Blood androgen level was estimated by observation of change of the pattern of Mtp-M. In the younger mice group, glycosuria disappeared temporarily after castration and then appeared naturally again. The Mtp-M declined with castration, but did not disappear in this experimental period. In the older mice group, glycosuria and Mtp-M disappeared completely and blood glucose level decreased considerably after castration. However, in the castrated older mice, the glycosuria and the Mtp-M appeared again after the administration of dehydroepiandrosterone (DHEA), and the increasing of blood glucose level was observed. These results strongly suggested that androgen had an important role in the onset of diabetes in the KK mice treated with MSA.
Nuclear protein antigens to the antinuclear antibodies in serum of non-obese diabetic (NOD) mice were investigated. In the serum of diabetic NOD female mice (20 weeks old), the antinuclear antibodies were detected by indirect immunofluorescence assay using frozen sections of liver of C 57 BL/6 J or NOD mice as antigen. Nuclei were separated from the liver of C 57 BL/6 J mice and solubilized. Solubilized nuclear antigens were analyzed by SDS PAGE-Western immunoblotting techniques. Nuclear protein antigens with molecular weights of 26,000, 32,000 and 65,000 showed strongly positive reactions with the antinuclear antibodies in the serum of the NOD mouse.
Extractable nuclear antigens (ENA) were prepared from liver of C57BL/6J mouse and analyzed by SDS PAGE Western-immunoblotting techniques. Some protein components of the ENA, with molecular weights of 94 K, 65 K, 32 K, and 26 K, reacted with antinuclear antibodies in the sera of NOD mice. Incidence of antinuclear antibodies in the sera of NOD mice with aging were measured by ELISA method using the ENA as antigen. The antinuclear antibodies were not detected in young NOD mice (10 weeks old). However, the incidence increased with aging and reached 100% in the female NOD mice of 40 weeks. In the male NOD mice, the incidence of antinuclear antibodies was delayed and low in comparison with that in female.
Concentrations of lactose in milk of Microtus montebelli were measured with the method using with the methylamine reaction. In this method, a small amount of sample (0.5 g) was sufficient for assay, and reproducibility and sensitivity were excellent. This method was very useful for measuring of lactose concentrations in experimental small animals. The average lactose concentration in milk of Microtus montebelli was 1.57g/100g, considerably low in comparison with the value of ICR mice (2.70g/100g). The low concentration of lactose in milk was considered to be one of metabolic characteristics of Microtus montebelli as a herbivorous animal.
A 47-year-old man was admitted with a cough on January 4, 1986. A chest X-ray film showed a mass shadow in the left lower lung, which was revealed to be a bronchogenic cyst by CT scanning and ultrasonography. Thoracotomy was performed on March 3, 1986 because cytologic tests on the fluid in the cyst suggested malignancy. A cyst, two tumors on the diaphragm and pleural thickening were revealed. Microscopic examination showed a benign bronchogenic cyst and a mixed-type malignant mesothelioma. In spite of chemotherapy (ADR, Cis-DPP, 5-fluorouracil) and immunotherapy (OK-432, PSK), the pleural thickening progressed, as was demonstrated by CT scanning and ultrasonography. Although cardiac tamponade due to invasion by the malignant mesothelioma developed, this was improved by cardiocentesis. The patient died of pneumonia on March 28, 1987. We studied the concentration of mineral fibers in lung and tumor tissues of this case by Energy Dispersive X-ray Analyser because asbestos or non-asbestos inorganic fibers might cause malignant mesothelioma. This case of malignant pleural mesothelioma accompanied by a bronchogenic cyst is very rare.
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The activity of an enzyme involved in decyanation of cyanocobalamin was found in the cell homogenate of Euglena gracilis. The enzyme essentially required FAD or FMN, and NADPH as cofactors. The apparent Km for cyanocobalamin and NADPH were 7.1 microM and 0.2 mM, respectively. The enzyme reaction obeyed allosteric kinetics towards FAD ([FAD]0.5 = 30 microM, n = 2.7; as calculated by the Hill plots). The Euglena enzyme was located in the mitochondria.
Tear proteins were detected by polyacrylamide gel electrophoresis in the vole, Microtus arvalis. The tear proteins were separated to 6 to 8 bands and the bands were divided to three regions on the anodic side. In the adult male vole, a male specific band (Vtp-1) was detected in the first region. The first region of adult female and immature voles contained two specific bands (Vtp-2, 3). In the castrated adult males or adult males injected with estrogen, the male specific hand, Vtp-1, disappeared and Vtp-2 and 3 bands appeared. In all castrated voles, the Vtp-1 band appeared and Vtp-2 and 3 bands disappeared after the administration of testosterone. Thus, sex hormone-dependent proteins are present in vole tears.
A sensitive and specific radioimmunoassay for cholecystokinin (CCK) has been developed. Synthetic unsulfated carboxy-terminal fragment, CCK-8, was radioiodinated by the conventional Chloramine-T method. Antibodies were raised against sulfated CCK-8 covalently coupled to bovine thyroglobulin via 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide. By purification, highly immunoreactive 125I-labeled CCK-8 was obtained. The antiserum was highly avid, and plasma could be assayed directly. The detection limit of the assay was 5 pmol of sulfated CCK-8 per liter. The assay measured fragments CCK-8, CCK-33, and CCK-39 with equimolar potency. CCK-4, gastrin, and vasoactive intestinal polypeptide were not detected, even at higher concentrations. The concentration of CCK, as the sum of these CCK peptides, in plasma during fasting was low (10.5 +/- 2.1 pmol/L, mean +/- SEM) but still detectable in all normal subjects examined (range, 6.4-20.1 pmol/L). After ingestion of a test meal, CCK in plasma increased rapidly, peaking at 41.3 (SEM 5.7) pmol/L at 40 min and remaining high for 3 h after the meal. This supports the concept that CCK has important roles in digestion and absorption.
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