Search PubMed⌕ Search

Biomedical subjects

E Ogata

Publications and source records attributed to E Ogata.

At least 289 records · Page 16Linked to original sources
PubMed1985

A case of biliary cystadenocarcinoma with recurrent jaundice. Diagnostic evaluation of computed tomography.

A 73-year-old male patient with biliary cystadenocarcinoma and episodes of recurrent jaundice is reported. This very rare tumor was suggested as a possible diagnosis by the computed tomographic findings showing intrahepatic cystic masses with septations and papillary projections. The diagnosis of the mucin-producing tumor was supported by aspiration of mucinous bile with a cannule inserted endoscopically via the major duodenal papilla. The computed tomographic findings and the diagnosis were verified by pathologic studies made on the material obtained surgically. The mucinous bile is assumed to have been responsible for the recurrent jaundice.

Aged↗
PubMed1985

Hyperpolarizing membrane potential changes in a cloned monkey kidney cell line.

Electrophysiological properties of a cloned monkey kidney cell line, JTC-12, were studied. The mean resting potential and input resistance were -15.3 mV and 78 M omega, respectively. Spontaneous hyperpolarizations with increased membrane conductance were observed. Similar hyperpolarization could be elicited by mechanical and electrical stimulations. The mean reversal potential of these hyperpolarizations was -72.7 mV. Hyperpolarization could be also elicited in a chloride-free solution. These data indicate that: JTC-12 cells exhibit spontaneous and induced hyperpolarizations, and occurrence of hyperpolarization is related to an increase in membrane permeability to potassium ions.

Animals↗
PubMed1985

Antihypertensive therapy with a single daily dose of acebutolol in essential hypertension, response and ophthalmological assessment in the Japanese.

Twenty patients with essential hypertension were given 400 mg acebutolol once daily for 24 weeks. In order to study if side effects resembling the "Practolol syndrome" developed, ocular effects were sought and antinuclear antibody (ANA) in blood was assessed before and after treatment. ANA was negative both before and after the study in 17 patients; in one patient ANA was positive, but the titre (1:10) was low and did not change during the study. Acebutolol produced no undesirable effects on cornea, conjunctiva or lens. During acebutolol treatment, tear secretion was reduced but tear lysozyme concentration was not significantly altered. Overall, acebutolol had no undesirable action similar to the practolol-induced syndrome, nor did it cause such common clinical ocular symptoms such as dry or gritty eyes.

Acebutolol↗
PubMed1985

Growth hormone-releasing factor reduces voltage-gated Ca2+ channel current in rat GH3 cells.

The action of GRF on GH3 cell membrane was examined by patch electrode techniques. Under current clamp with patch electrode, spontaneous action potentials were partially to totally eliminated by application of GRF. In the case of partial elimination, the duration of remaining spontaneous action potentials was prolonged and the amplitude of afterhyperpolarization was decreased. The evoked action potential in the cells which did not show spontaneous action potentials was also eliminated by GRF. In order to examine what channels were affected by GRF, voltage-clamp analysis was performed. It was revealed that voltage-gated Ca2+ channel current and Ca2+-induced K+ channel current were decreased by GRF, while voltage-gated Na+ channel and delayed K+ channel were not affected. The decrease of Ca2+-induced K+ channel current was considered to be a consequence of the decrease of voltage-gated Ca2+ channel current. Therefore it is likely that the effect of GRF on GH3 cells was due to the block of voltage-gated Ca2+ channels. The elimination of action potential under current clamp corresponded to the block of voltage-gated Ca2+ channels and the prolongation of action potential could be explained by the decrease of Ca2+-induced K+ channel current. The amplitude decrease of afterhyperpolarization could also be explained by the reduction of Ca2+-induced K+ channel current. Thus the results under current clamp well coincide with the results under voltage clamp. Hormone secretion from GH3 cells was not stimulated by GRF. However, the finding that GRF solely blocked voltage-gated Ca2+ channel suggested the specific action of GRF on GH3 cell membranes.

Action Potentials↗
PubMed1985

Differentiated properties characteristic of renal proximal epithelium in a cell line derived from a normal monkey kidney (JTC-12).

The JTC-12 cell, an established cell line derived from a normal monkey kidney, was studied in an attempt to characterize the epithelial qualities. Phase contrast microscopy showed dome formation in confluent monolayers and electron microscopic examinations revealed the presence of numerous microvilli on the apical membranes and desmosome between cells. Sonicated cells showed activities of gamma-glutamyl transpeptidase, leucine aminopeptidase, alkaline phosphatase, and trehalase, marker enzymes of renal proximal epithelium. Alkaline phosphatase activity exhibited the characteristics of a renal type isozyme. Furthermore, confluent JTC-12 monolayers exhibited Na+-dependent transport of hexose, amino acid as well as inorganic phosphate. These findings indicate that JTC-12 cells in monolayer culture maintain ultrastructural, biochemical, and physiological properties of renal proximal epithelial cells. This cell line will be useful for further studies on cellular functions of renal proximal epithelium.

Alkaline Phosphatase↗
PubMed1985

Influence of extracellular phosphate concentrations on the regulation of hepatic glucose output.

Experiments were carried out to investigate the role of extracellular phosphate in the hormonal regulation of glycogenolysis in perfused fed-rat liver. Omission of phosphate from the perfusate did not affect the ATP, ADP and AMP contents of the tissue and the basal glucose output from the perfused liver. However, it inhibited significantly the glycogenolysis induced by glucagon, cyclic AMP, phenylephrine and vasopressin but not that induced by 2,4-dinitrophenol. In the absence of perfusate phosphate, the increase in phosphorylase a activity caused by the addition of glucagon, phenylephrine and vasopressin was significantly less than that observed in the presence of perfusate phosphate. Insulin inhibition of the glucagon- or cyclic AMP-induced glycogenolysis was abolished when the perfusion was carried out with the phosphate-free buffer. However, the inhibitory effect of insulin on phenylephrine-induced glycogenolysis was clearly demonstrated even when the perfusate contained no phosphate. These data indicate that in the phosphate-depleted liver, the hormonal control of phosphorylation and dephosphorylation of phosphorylase is impaired. The difference in the phosphate dependency of insulin action on glucagon-and alpha-adrenergic agonist-induced glycogenolysis suggests that the mechanism or site of insulin action on glucagon and phenylephrine is different.

Adenine Nucleotides↗
PubMed1985

Inhibition by prostaglandin E2 of renal effects of calcitonin in rats.

To investigate the possible role of prostaglandin E2 (PGE2) in modulating the actions of PTH and calcitonin (CT) in the kidney, the effects of PGE2 were examined on the in vivo conversion of [3H]25-hydroxyvitamin D3 to [3H]1,25-dihydroxyvitamin D3 ([3H]1,25-(OH)2D3) in vitamin D-deficient thyroparathyroidectomized (T-PTX) rats and on the urinary excretion of phosphate (Pi) in vitamin D-replete T-PTX rats in the presence of either PTH or CT. Plasma accumulation of [3H] 1,25-(OH)2D3 increased from 12.2 +/- 0.6 pmol/100 ml in controls to 19.5 +/- 1.1 (P less than 0.01) by 20 micrograms/h PGE2 to 29.8 +/- 1.8 (P less than 0.001) by 7.5 U/h PTH, and to 23.3 +/- 0.7 (P less than 0.01) by 500 mU/h CT. Administration of PGE2 inhibited CT-stimulated accumulation of 1,25-(OH)2D3 to levels not different from those by PGE2 alone (17.8 +/- 1.0 pmol/100 ml). In contrast, PGE2 had no effect on PTH-stimulated 1,25-(OH)2D3 accumulation. PTH and CT caused an increase in urinary Pi excretion and a decrease in plasma Pi levels. PGE2 abolished the effects of CT, but not of PTH, on both urinary Pi excretion and plasma Pi levels. Administration of PGE2 alone caused no significant changes in plasma Pi levels and only minimal increase in urinary Pi excretion. PGE2 did not suppress urinary cAMP excretion stimulated by CT. These results demonstrate that PGE2 specifically suppresses the effects of CT to stimulate synthesis of [3H]1,25-(OH)2D3 from [3H]25-hydroxyvitamin D3 and to inhibit tubular reabsorption of Pi without affecting urinary cAMP excretion. Since CT appears to stimulate 1 alpha-hydroxylase and inhibit Pi reabsorption in proximal tubules, nephron segments devoid of CT-sensitive adenylate cyclase, these data suggest that PGE2 modulates the actions of CT, but not of PTH, on proximal tubular functions.

Animals↗
PubMed1985

Calcium metabolism in paravertebral ligamentous ossification.

Twenty-eight patients with paravertebral ligamentous ossification (PVLO) and 11 control subjects were studied in an attempt to examine possible involvement of disturbances in mineral metabolism in the development of PVLO. No significant difference in baseline serum calcium and fasting urinary calcium excretion was found between patients with PVLO and controls. Patients with PVLO showed lower serum inorganic phosphate (Pi) and tubular reabsorptive capacity for Pi (TmP/GFR) than controls. Basal nephrogenous cyclic 3',5'-AMP (NcAMP) was elevated in some patients with PVLO. A significant inverse relationship was found between basal TmP/GFR and NcAMP in patients with PVLO (r = -0.50; P less than 0.01). Compared with controls, patients with PVLO had significantly lower calciuric responses to an oral calcium load (P less than 0.05), suggesting decreased intestinal calcium absorption. Furthermore, a significant inverse correlation was found between basal NcAMP and the calciuric response in patients with PVLO (r = -0.42; P less than 0.05). Serum 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D (1,25(OH)2D) levels were not significantly different between the two groups. The size of ossified areas in paravertebral ligaments estimated from spinal radiograms inversely correlated with the calciuric response to the oral calcium load (r = -0.50; P less than 0.01). These data demonstrate that the development of PVLO is associated with decreased intestinal calcium absorption in the face of normal serum 1,25(OH)2D level. Thus, together with previous observations showing a high incidence of PVLO in patients with hypoparathyroidism or familial hypophosphataemic rickets/osteomalacia, the present results suggest that the defect in the action of 1,25(OH)2D may underlie the development of PVLO.

Calcifediol↗
PubMed1985

Adaptation to phosphorus depletion: effect of streptozotocin-induced diabetes mellitus.

The effect of streptozotocin-induced diabetes mellitus (DM) on the adaptive response to phosphorus depletion (PD) was investigated in order to examine if DM has any influence on the adaptation to PD in rats. PD for 7 days caused a marked reduction in serum phosphate (Pi) levels and increase in serum calcium (Ca) concentrations in control rats. In contrast, the increase in serum Ca concentration caused by PD was almost entirely eliminated in DM rats. Similarly, while bone Ca and P content was decreased by 7 days of PD in control rats, no significant changes in bone mineral contents were observed in DM rats during PD. There was a marked reduction in fractional excretion of Pi and an increase in fractional excretion of Ca during PD in both control and DM rats. Serum somatomedin A levels measured by radioreceptor assay were lower in DM rats compared to those in control rats, but PD caused no significant changes in either group of animals. These results demonstrate that the development of hypercalcaemia and reduction in bone mineral content in response to PD were inhibited while the renal tubular responses to PD were not affected in DM rats. It is suggested that the inhibition of the hypercalcaemic response to PD in DM rats is mainly due to an inhibition of the resorptive response of bone to PD, and that insulin either directly or indirectly may play a permissive role in the development of the resorptive response of bone to PD.

Adaptation, Physiological↗
PubMed1985

Effect of vitamin D metabolites on bone metabolism in a rat model of postmenopausal osteoporosis.

A rat model of postmenopausal osteoporosis was introduced, using ovariectomized rats on a low Ca diet. CT treatment of these animals for one month prevented the decrease in both mineral contents and physical properties of the femoral bone. Treatment of the animals with 1,25(OH)2D3 was effective in increasing bone mineral contents and maintaining positive mineral balance, but did not increase the physical tolerance of bones. In contrast, 24,25(OH)2D3 increased the breaking force of the femoral bone, with minimal effect on bone mineral contents and mineral balance. These results suggest that 1,25(OH)2D3 and 24,25(OH)2D3 act differently on the matrix phase and mineral phase of bones, but that they act together to maintain mineral balance and structural integrity of bones. The mechanism of how these vitamin D metabolites affect bone metabolism remain to be clarified.

24,25-Dihydroxyvitamin D 3↗
PubMed1984

[Standard procedure and the diagnostic criteria for the Ellsworth-Howard test using human PTH-(1-34)].

The present study was undertaken to establish a standard method to perform the Ellsworth-Howard test using human PTH-1-34). For this purpose we made a survey of literature concerning the Ellsworth-Howard test and then examined the data of the Ellsworth-Howard tests performed on 178 hypoparathyroid patients using human PTH-(1-34). The main items of investigation were: (i) to determine the appropriate dose of PTH for administration to adults and children; and (ii) to define the criteria of practical usefulness for the differential diagnosis of the types of hypoparathyroidism. From the analysis of the data, the following findings and conclusions were obtained. The dose of human PTH-(1-34) appropriate for diagnostic use is 100 U per person for adults and 100 U per body surface area of one square meter (100 U/m2) for children. The criteria of positive response in the Ellsworth-Howard test are defined as follows. a) phosphaturic response: (U4 + U5) - (U2 + U3) = more than 35 mg/2 h b) cyclic AMP response: U4 - U3 = more than 1 mumol/h, and U4/U3 = more than 10 times. In the above formula, U2 - U5 represent the urine samples collected hourly in order. PTH is injected at the time between U3 and U4. For the application of the criteria in children, one should use the values corrected for body surface area of one square meter. It is necessary to confirm the following conditions before the application of the criteria: the presence of hypocalcemia and hyperphosphatemia; the lack of phosphate deficiency (basal urinary phosphate excretion more than 10 mg/2 h); the accuracy of timed urine collections (ratio of creatinine excretion during 2 hours before PTH to that after PTH administration in the range from 0.8 to 1.2); and the absence of marked diurnal variation in phosphate excretion (difference in phosphate excretion between the two basal hourly urine less than 17.5 mg/h). To ensure the above conditions, medications such as phosphate-binding antacids should be withheld for at least 1 week before the test, and the test should be performed according to the standard procedure described in this paper. The diagnosis of pseudohypoparathyroidism Type II should be done cautiously. It is necessary to take account of the high basal urinary cyclic AMP excretion and the elevated serum PTH level along with the results of the Ellsworth-Howard test (positive cyclic AMP response and negative phosphaturic response) for a definite diagnosis of this entity.

Adolescent↗
PubMed1984

Alterations of oxidative phosphorylation reactions in mitochondria isolated from hypothyroid rat liver.

Several parameters of oxidative phosphorylation reaction were studied in vitro in isolated liver mitochondria from hypothyroid rats. When succinate was employed as a respiratory substrate for mitochondria incubated in a mannitol/sucrose/phosphate buffer, and measurements were performed during initial additions of ADP, the magnitude of state 3 and state 4 respiration was not different between mitochondria from the hypothyroid and those from the control rats. During the course of repetitive additions of ADP and consequently of sequential transitions from state 4 to state 3 and back to state 4, mitochondria from hypothyroid animals showed a gradual decline in the rate of both state 3 and state 4 respiration whereas those from normal animals did not. The total succinate dehydrogenase activity was not different between the two types of mitochondria, and the decline in state 3 and state 4 respiration was not accompanied by any change in the apparent Km for ADP or in the corrected ADP/O ratio [Biochem. Biophys. Res. Commun. (1973) 53, 988]. The amount of oxygen consumed during the state-4----3----4 transition was lower in the hypothyroid than in the control mitochondria. These alterations were reversed if the hypothyroid animals were injected with thyroxine intraperitoneally (2 micrograms/100 g body weight) for 3 weeks before isolation of mitochondria. These results indicate that the fall of respiratory activity in hypothyroidism may result from the decrease not only of respiratory activities of state 3 and state 4, but also of the energy spent in the process of the state-4----3----4 transition, while the coupling efficiency per se remains normal. These properties become manifest when mitochondria respond to pulses of ADP load, a situation likely to occur in situ.

Adenosine Diphosphate↗
PubMed1984

[Urinary phosphate and cyclic adenosine monophosphate response to intravenous administration of synthetic human parathyroid hormone-(1-34) in idiopathic hypoparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism and normal subjects].

The response to exogenous parathyroid hormone (PTH) with urinary excretion of phosphate and cyclic adenosine monophosphate (cAMP) was tested by the use of synthetic human parathyroid hormone (1-34) [hPTH-(1-34)] on 59 patients with hypocalcemia and normal or high serum inorganic phosphorus and normal renal function without a history of parathyroidectomy for differentiation between idiopathic hypoparathyroidism (IHP), pseudohypoparathyroidism (PHP) and related diseases along with 18 normal subjects. A positive phosphaturic response to exogenous PTH was defined as the increment of 2 hours phosphate excretion (delta P) of more than 35 mg. A positive urinary cAMP response to exogenous PTH was defined as the increment by more than 1 mumole per one hour (delta cAMP) and the increase of 1 hour excretion by more than 10 times. Increments of 2 hours urinary phosphate excretion in response to hPTH-(1-34) 100 units were 60.5 +/- 7.7 mg (mean +/- SEM) in 27 patients with IHP, 23.5 +/- 5.9 mg in 21 patients with PHP type I and 24.9 +/- 4.0 mg in 17 normal subjects. Increments of 1 hour urinary cAMP excretion in response to hPTH-(1-34) 100 units were 12.0 +/- 1.5 mumole in 27 patients with IHP, 0.33 +/- 0.10 mumole in patients with PHP type I and 23.6 +/- 5.8 mumole in 15 normal subjects. Ratios of 1 hour urinary cAMP excretion were 97 +/- 10 in 27 patients with IHP, 3.6 +/- 0.5 in 21 patients with PHP type I and 54 +/- 14 in 15 normal subjects. Positive phosphaturic and negative urinary cAMP response was encountered in 3 out of 21 patients with PHP type I in response to hPTH-(1-34). This exaggerated phosphaturic response should be considered as due to the influence of treatment with Ca or vitamin D derivatives.

Adolescent↗
PubMed1984

Effects of glucagon on the redox states of cytochromes in mitochondria in situ in perfused rat liver.

The effects of glucagon on the respiratory function of mitochondria in situ were investigated in isolated perfused rat liver. Glucagon at the concentrations higher than 20 pM and cyclic AMP (75 microM) stimulated hepatic respiration, and shifted the redox state of pyridine nucleotide (NADH/NAD) in mitochondria in situ to a more reduced state as judged by organ fluorometry and beta-hydroxybutyrate/acetoacetate ratio. The organ spectrophotometric study revealed that glucagon and cyclic AMP induced the reduction of redox states of cytochromes a(a3), b and c+c1. Atractyloside (4 micrograms/ml) abolished the effects of glucagon on these parameters and gluconeogenesis from lactate. These observations suggest that glucagon increases the availability of substrates for mitochondrial respiration, and this alteration in mitochondrial function is crucial in enhancing gluconeogenesis.

Animals↗
PubMed1984

Ossification of the paravertebral ligaments: a frequent complication of hypoparathyroidism.

Various forms of paravertebral ligamentous ossification (PVLO) were detected radiologically in 9 (53%) of 17 consecutive patients with hypoparathyroidism. A significant correlation was found between the period during which the patient was untreated and the incidence of ossification. Serum levels of calcium, phosphate, and their ionic product appeared not to influence the incidence. All the patients with PVLO exhibited evidence of ectopic calcification. The fact that ectopic ossification, which is histologically distinct from ectopic calcification, is frequently associated with hypoparathyroidism suggests that similar pathogenetic mechanisms are responsible for the development of these two conditions. The high incidence of PVLO in hypoparathyroid patients in this study may explain some of the neurologic findings in hypoparathyroidism that have been hard to explain simply on the basis of altered neuromuscular excitability.

Adult↗
PubMed1984

Vitamin D deficiency and renal calcium transport in the rat.

To examine the role of vitamin D in the renal tubular handling of calcium, clearance studies were performed in three groups of rats: group A rats fed a standard vitamin D-deficient diet (Ca 0.45%, P 0.3%) for 6 wk, were hypocalcemic with secondary hyperparathyroidism; group B rats fed the same diet as in group A but with high calcium (Ca 1.4%) and 20% lactose, were normocalcemic and without secondary hyperparathyroidism; group C rats fed the same diet as in group A but supplemented with 25 U of vitamin D3 orally twice a week, were normocalcemic, vitamin D-replete, and euparathyroid. After thyroparathyroidectomy (TPTX), each rat was infused intravenously with an electrolyte solution that contained a fixed concentration of calcium (0-30 mM) with or without parathyroid hormone (PTH; 0.75 or 2.5 U/h) at a rate of 3 ml/h. Urinary calcium excretion and serum calcium concentrations were measured between 16 and 19 h of the infusion, and the apparent threshold of calcium excretion was determined. The threshold of calcium excretion was lower in vitamin D-deficient TPTX rats (groups A and B) than in vitamin D-replete TPTX rats (group C), and not different between group A and group B. Administration of PTH at a dose of 0.75 U/h increased the threshold of calcium excretion by approximately 0.6 mM in group C, but did not alter the threshold either in group A or group B. Administration of a higher dose of PTH (2.5 U/h) raised the threshold similarly in both group A and group B to the extent comparable with that in group C, when it was given 0.75 U/h of PTH. These results demonstrate that the renal threshold of calcium excretion is decreased in the vitamin D-deficient rats independent of the secondary hyperparathyroidism, and that the higher dose of PTH was necessary to raise the calcium threshold in vitamin D-deficient rats. Thus, present study indicates the presence of dual effects of vitamin D on renal tubular handling of calcium; the one is to facilitate renal calcium reabsorption and the other is to enhance the responsiveness of the tubule to PTH.

Animals↗
PubMed1984

Oxygenation of 18-hydroxycorticosterone as the final reaction for aldosterone biosynthesis.

Incubation of 18-hydroxycorticosterone with the sonicated mitochondrial preparation of bovine adrenal glomerulosa tissue leads to the production of aldosterone, as measured by radioimmunoassay. The in vitro production of aldosterone from 18-hydroxycorticosterone requires both molecular oxygen and NADPH, and is inhibited by carbon monoxide. Cytochrome P-450 inhibitors such as metyrapone, SU 8000, SU 10603, SKF 525A, amphenone B and spironolactone decrease the biosynthesis of aldosterone from 18-hydroxycorticosterone. These results support the conclusion that the final reaction in aldosterone synthesis from 18-hydroxycorticosterone is catalyzed by an oxygenase, but not by 18-hydroxysteroid dehydrogenase. By the same preparation, the production of [3H]aldosterone but not [3H]18-hydroxycorticosterone from [1,2-3H]corticosterone is decreased in a dose-dependent manner by addition of non-radioactive 18-hydroxycorticosterone.

18-Hydroxycorticosterone↗