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Volume 64, Issue 12
Displaying 1-13 of 13 articles from this issue
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Familial Multiple Endorcrine Neoplasia Type 1G.D. AURBACH, S.J. MARX, K. SAKAGUCHI, M. ZIMERING, M.L. BRANDI1988 Volume 64 Issue 12 Pages 1209-1213
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
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The Role of Growth Factors on the Expression of Differentiated Functions of the Ovary and PlacentaTakeshi MARUO1988 Volume 64 Issue 12 Pages 1214-1222
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
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A Paraneoplastic Syndrome of Hypercalcemia and Leukocytosis Associated with Solid Tumors : Production of Interleukin 1 Alpha (IL-1α) and Granulocyte Colony-Stimulating Factor (G-CSF) by Clonal SKanji SATO1988 Volume 64 Issue 12 Pages 1223-1227
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSWe have demonstrated that T3M-1 cells and T3M-5 cells, derived from squamous carcinomas of patients with leukocytosis and hypercalcemia, produced excessively G-CSF, IL-1α and a small amount of PTH-like factor. We confirmed that G-CSF and IL-1α (hemopoietin 1) enhanced granulocytopoiesis and caused marked leukocytosis in vivo
Furthermore, we also demonstrated that PTH-rP and IL-1α (a potent osteoclastactivating factor) synergistically stimulated bone resorption in vitro and also synergistically increased serum calcium concentration in vitro.
Since we have demonstrated that at least two clonal cell lines derived from patients with hypercalcemia and leukocytosis produced G-CSF and IL-la, we presume that hypercalcemia and leukocytosis associated with some solid tumors may constitute a new paraneoplastic syndrome.View full abstractDownload PDF (501K) -
Expression of Major Histocompatibility Complex Class II Antigen on Target Cells in Autoimmune Endocrine DiseaseToshiaki HANAFUSA1988 Volume 64 Issue 12 Pages 1228-1232
Published: December 20, 1988
Released on J-STAGE: November 09, 2012
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Marc R. MONTMINY1988 Volume 64 Issue 12 Pages 1233-1235
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
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H. Okamoto1988 Volume 64 Issue 12 Pages 1236-1237
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
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The 61st Annual Meeting of the Japan Endocrine Society Symposium Cellular Mechanism of Hormon ActionInositol Phosphate Metabolism and Its Relationship to Calcium SignallingArlene R. HUGHES, Debra A. HORSTMAN, James W. PURNEY Jr.1988 Volume 64 Issue 12 Pages 1238-1242
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
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Masato KASUGA, Tetsuro IZUMI, Kazuuki TOBE, Takashi KADOWAKI, Kaoru MO ...1988 Volume 64 Issue 12 Pages 1243-1249
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
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Parathyroid Hormone -Quo vadis?Takuo FUJITA1988 Volume 64 Issue 12 Pages 1250-1257
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSParathyroid hormone is the most important calcium regulating hormone, especially in the process of aging. As a compensation for progressive calcium deficiency in aging, PTH secretion progressively rises. Heterogeneity of PTH in peripheral blood indicates the importance of understanding the degradation mechanism throughout the life cycle of the hormone. In addition to cathepsin B and D which degrades PTH in the liver, kidney and parathyroid gland, a new neutral PTH ase was found in the cytosolic fraction of rat kidney cells. PTH responsive bone and kidney cell lines, UMR-106 and OK cells, were found to degrade PTH by a chymotrypsin-like enzyme on the plasma membrane through a receptor mediated mechanism. This process was inhibited by cyclic AMP-A-kinase system and augmented by C-kinase system, suggesting an intimate relationship between PTH action and degradation and also a new physiological significance of PTH degradation.View full abstractDownload PDF (791K) -
Yoshihisa TAKADA, Kiyohide NAKAO, Saburo YANA1988 Volume 64 Issue 12 Pages 1258-1272
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSWe examined the mechanism of loss and recovery of steroid binding activity (inactivation and reactivation) of the rat liver glucocorticoid receptor (GR) in the cell free condition.
Male Sprague-Dawly rats were adrenectomized 2 days before the hepatectomy for the experiments, and were fed with normal diet and saline. The cytosol was prepared in 10mM phosphate buffer (pH 7.4) containing 10% glycerol (PG buffer). The nuclei were isolated by centrifuging at 800 × g for 20 min at 4°C in 10mM phosphate buffer (pH 7.4) containing 0.32M sucrose, 3mM MgCl2, then centrifuged again at 40,000 × g for 20 min at 4°C in 10mM phosphate buffer (pH 7.4) containing 1.8M sucrose, 3mM MgCl2. The glucocorticoid receptor was partially purified by affinity chromatography with DOC-Sepharose 6B, and column chromatography with Sephacryl S-300 and DEAE-cellulose in the presence of molybdate throughout the procedure.
The steroid binding activity of the cytosol prepared in PG buffer was inactivated by following procedures; either 1) treatment with 1% activated charcoal, 2) dialysis against 500 volumes of PG buffer, 3) incubation at 37°C for 30 min, or 4) incubation in high salt condition (0.4M KCl) at 0°C for 16h. When the steroid binding activity was inactivated by incubation at 0°C for 16hr and charcoal treatment, dithiothreitol (DTT) and NADPH were effective on reactivation, while glutathione (reduced form) was ineffective. Antipain increased the reactivated steroid binding activity in these cases. The steroid binding activity, which was inactivated by dialysis, was slightly recovered by DTT or NADPH, but antipain was ineffective. We could not reactivate steroid binding activity which was inactivated by incubation at 37°C for 30 min or high salt (0.4M KCl) treatment with any reagent we tested. Leupeptin, however, partially prevented the high salt inactivation. When the cytosol prepared in PG buffer was labeled with 3H-dexamethasone (Dex) and then incubated at 25°C for 30 min, 3H-Dex labeled steroid receptor was transformed and it also lost its steroidbinding activity partially. DTT or NADPH increased steroid binding activity, but did not increase nuclear binding activity. Interestingly, by dialysis, the cytosol glucocorticoid receptor was not transformed in the PG buffer.
We also examined the reactivation of steroid receptor using the partially purified receptor. To remove molybdate, the partially purified receptor was dialyzed against PG buffer. Large part of steroid binding activity was lost during the dialysis. DTT, however, reactivated steroid binding activity without molybdate, and also S-value of reactivated receptor was undistinguishable from the untransformed (molybdate stabilized) receptor.
The results of the present studies suggest that steroid binding activity is reactivated by DTT in a direct manner, futhermore, reactivated glucocorticoid receptor is the untransformed form which has no ability to bind with the nuclei.View full abstractDownload PDF (1296K) -
Taisuke IWAOKA, Teruhisa UMEDA, Shojiro NAOMI, Miho OHONO, Fumihiro MI ...1988 Volume 64 Issue 12 Pages 1273-1280
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSFour lateralising methods were carried out in 14 patients with primary aldosteronism (PA) : ultrasonography, CT scan, adrenal scintiscan and determination of adrenal venous aldosterone levels. In all cases, unilateral aldosterone-producing adenomas were verified by surgery. Of four lateralising methods, determination of adrenal venous aldosterone, in spite of high diagnostic value, has two big problems : difficulty in selective catheterization of right adrenal vein and dilution of adrenal vein efflux from nonadrenal sources. To solve these problems, cortisol (C, μg/dl) levels along with aldosterone (A, ng/dl) were determined in samples from the left adrenal vein (LAV) and the inferior vena cava (IVC) in 8 patients with PA, and the (LAV A/C) / (IVC A/C) ratio was calculated. That ratio was also obtained in 7 patients with other types of hypertension for comparison.
Accuracy of lateralisation by ultrasonography, CT scan and adrenal scintiscan was 23%, 64% and 69% respectively, in the first studies. Those rates changed to 23%, 93% and 85% when the second studies were performed. Venous blood was obtained from both adrenal veins in 46% (6/13), while lateralisation of adenoma was also predicted in 46% (6/13) by the measurement of aldosterone concentrations alone. On the other hand, (LAV A/C) / (IVC A/C) ratios were 3.54 - 6.98 in the cases of left APA, 0.15 - 0.98 in those of right APA and 1.10 - 2.86 in cases of other types of hypertension. There was no overlap of ratios among the three groups, resulting in correct prediction of lateralisation in all cases (8/8) of APA. In 2 of 8 cases, tumors were not detected with either CT scan or adrenal scintiscan until the second studies, probably because of the small size of the tumors. The lateralisation in these two cases, however, could have been predicted in the first studies with use of the (LAV A/C) / (IVC A/C) ratio.
Consequently, the (LAV A/C) / (IVC A/C) ratio enables predictive lateralisation of APA with more ease and accuracy, especially in early diagnosis.View full abstractDownload PDF (832K) -
Masayuki YAMASAKI, Noriaki WATANABE, Toshihiko INOUE, Shiro SAITO1988 Volume 64 Issue 12 Pages 1281-1292
Published: December 20, 1988
Released on J-STAGE: November 09, 2012
JOURNAL FREE ACCESSNature of insulin-like growth factor (IGF) binding on rat hepatocytes of primary monolayer culture and its regulation by IGF-related peptides were studied. The specific binding of 125I-IGF-I to the rat hepatocytes was saturable and dependent on incubation time and temperature.
The optimal pH of incubation medium was 7.8-8.2. The steady-state binding was attained at 20°C for 6h, and averaged 12% per 4×105 cells. Fifty percent displacement of the 125 I-IGF-I binding was observed at concentrations of 10ng/ml of IGF-I and 5 ng/ml of IGF-II, but insulin (10ng/ml-10μg/ml) did not inhibit the binding. IGF-II inhibited the binding of 125 to the hepatocytes half maximally at concentrations of 2 ng/ml. A Scatchard plot of the data of binding was linear, and indicated association constant of 1.0 X 109M-1 and a binding site of 44,000 per cell.
Preincubation of the hepatocytes with either IGFs or insulin at 37°C for 24 h resulted in the reduction of 125 I-IGF-I binding to the hepatocytes in a dose-related manner, being dependent on incubation time and insulin concentrations. The binding was reduced to 20% of the control value in the presence of 10-7M IGF-I, and to 85% of the control in the presence of 5×10-8M IGF-II. Although insulin showed no affinity to the type II IGF receptors, 125 I-IGF-I binding to the hepatocytes was decreased to 60% of the control after preincubation with 10 -10M insulin.
These results indicate that 1) the hepatocytes of primary monolayer cultures have only type II IGF binding, 2) preincubation of the cells with IGF-I, IGF-II or insulin induces the reduction of 125I-IGF-I binding to the cells, indicating down-regulation of the binding, and 3) this binding site of rat hepatocytes is regulated by not only IGF-I and IGF-II but also insulin of physiological concentrations.View full abstractDownload PDF (1057K) -
Shuichi UENO1988 Volume 64 Issue 12 Pages 1293-1312
Published: December 20, 1988
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSTo clarify the role of the sympatho-adrenomedullary and renin-angiotensin-aldosterone systems, and catecholamine receptors, in the pathogenesis of orthostatic hypotension in diabetes mellitus (DM), urinary excretion of catecholamines, and plasma levels of norepinephrine (PNE), epinephrine (PE), renin activity (PRA), aldosterone (PAC), cyclic AMP (PcAMP) and cyclic GMP (PcGMP) were measured in 16 normal subjects (N) and 50 diabetic patients with or without orthostatic hypotension (DMOH (+), DMOH (-)). Changes in PNE, PE, PRA, PAC, PcAMP and PcGMP by standing, glucagon (G) adminsitration and cold pressor test were examined. Furthermore, the effect of metoclopramide on catecholamine levels and blood pressure was investigated before and after cold pressor test. The results were following;
(1) Urinary free norepinephrine excretion was significantly lower in DMOH (+), while urinary total norepinephrine excretion was normal in the two DM groups. Urinary free and total epinephrine excretions were lower in DMOH (+) than in N and DMOH (-).
(2) PNE and PE were elevated after standing in all groups tested, and more pronounced in some cases of DMOH (+). Although PRA and PAC were elevated normally after standing in all groups, a dissociation between the two parameters was seen in some cases of DM. PcAMP after standing was correlated with PE (r=0.829). Basal PcGMP was high in manycases of DMOH (+). However, no difference in the elevation of PcGMP after standing was noted between N and the two DM groups.
(3) Systolic blood pressure (SBP) rose markedly in only DMOH (+) from 146 ± 27mmHg to 178 ± 34mmHg 5 minutes after G administration. The increment of PNE and PE 5 minutes after G administration were similar in all groups. In only DMOH (+), the increase in PcAMP 15 minutes after G test was proportional (r=0.498) to that of epinephrine.
(4) Responses of SBP, PNE, PE and PAC to cold pressor test apparently improved after administration of metoclopramide (MC) in some patients with DM.
These results suggest that not only organic disturbance of sympathetic nerves but also functional inhibition of norepinephrine release mediated by dopamine receptor, may play an important role in the pathogenesis of orthostatic hypotension in diabetes mellitus. It is considered that catecholamine secretion from the adrenal medulla in DMOH (+) is increased by hypotension induced by standing. Furthermore, the vascular response to catecholamines may be accelerated through the increment of the extrajunctional receptor in DMOH (+).
In conclusion, for the purpose of finding any abnormality in blood pressure regulation in the early stages of diabetes mellitus, it is necessary to clarify the sympathetic and dopamine activities by orthostatic, glucagon loading and cold pressor tests. Therefore, it is suggested that sympathetic stimulants are useful for patients with sympathetic dysfunction; and antidopaminergic drugs for those diabetic patients with the hyperdopaminergic state.View full abstractDownload PDF (2077K)
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