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Volume 61, Issue 1
Displaying 1-6 of 6 articles from this issue
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Masaaki SEKINE1985 Volume 61 Issue 1 Pages 1-13
Published: January 20, 1985
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSWe established a radioimmunoassay of 6-keto PG F1α, using 125 I-6-keto PG F1α-tyramide, which enabled us more easily to monitor the plasma levels of prostacyclin in clinical fields.
Antibodies against 6-keto PG F1α were obtained from rabbits immunized with 6-keto PG F1α-BSA complex, which could be used for RIA at a final dilution of 1 : 648,000.
The detection limit of 6-keto PG F1α was 50 - 1000 pg/ml. The cross reactivities between PG I2 and PG F1α were 26.6% and 1.62% respectively, but those between other prostaglandins were less than 1%.
Using this radioimmunoassay with 125 I-6-keto PG F1α crtyramide, plasma levels of 6-keto PG F1α were measured.
The recovery rate by this assay was 92.9%, and the intra- and inter-assay coefficients of variation determined were 9.9% and 27.1%, respectively.
The mean of plasma levels of 6-keto PG F1α revealed 126.2 ± 75.3 (mean ± S.D.) pg/ml in 46 healthy Japanese males, 122.7 ± 85.2 pg/ml in 60 females, and 124.2 ± 81.3 pg/ml in 106 Japanese of both sexes.View full abstractDownload PDF (1054K) -
Tsutomu KANDA, Makoto OTSUKI, Teruhisa AKEYAMA, Tatsuo MINAKAWA, Shuni ...1985 Volume 61 Issue 1 Pages 14-21
Published: January 20, 1985
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSLiver cirrhosis (LC) is often associated with osteomalacia and osteoporosis. Since it has been shown that serum levels of 25 hydroxy vitamin D (25-OH-D) are reduced in LC, defective hepatic hydroxylation of vitamin D has been postulated to be responsible for the low serum 25-OH-D levels and skeletal demineralization. This study was designed, therefore, to determine serum 25-OH-D and 1α, 25-(OH)2 -D levels in patients with LC. Further, the response of serum 1α, 25-(OH)2-D to a single oral dose of 1α-OH-D3(2μEg) was investigated.
In 5 patients with severe decompensated LC and 3 patients with compensated LC, serum 25-OH-D and 1α, 25-(OH)2-D levels were respectively measured by the modified method of Belsey and by that of Eisman.
Serum 25-OH-D in patients with compensated and decompensated LC was significantly higher than that in normals. Serum levels of 1α, 25-(OH)2-D in patients with decompensated LC were significantly lower than those in patients with compensated LC and normals.
After a single oral administration of 1α-OH-D3 at a dose of 2μg, the 1α, 25-(OH)2 -D rose in each patient within 6h, reaching the maximum levels at 12h. The percent increase over the basal value in decompensated LC was similar to that in compensated LC.
Since 25-OH-D is known to be hydroxylated to 1α, 25-(OH)2 -D in renal tubules, the relationship between renal function and serum 1α, 25-(OH)2 -D levels has been investigated, and a significant positive correlation was found between creatinine clearance and serum 1α, 25-(OH)2-D levels.
Contrary to the previous observations, the present study has demonstrated high serum 25-OH-D levels in patients with LC. Although the reason for this discrepancy is unknown, the modified method of Belsey for determining serum 25-OH-D levels might be responsible for the high serum 25-OH-D levels.
In this study, all 8 patients treated with 1α-OH-D3 responded with elevation of the serum 1α, 25-(OH)2-D. This observation has demonstrated that hepatic 25-hydroxylation is not impaired even in patients with severe LC.
To function physiologically, vitamin D must be hydroxylated in the liver to 25-OH-D and subsequently by the kidney to 1α, 25-(OH)2-D. A significant positive correlation was observed between creatinine clearance and serum 1α, 25-(OH)2 -D levels in LC. These results imply a defect in the la-hydroxylation step of vitamin D metabolism in LC, probably due to hepatorenal syndrome. Thus it may be conceivable that osteoporosis and osteomalacia associated with LC is due to a defect in the 1α-hydroxylation by the kidney rather than a hepatic hydroxylation defect.View full abstractDownload PDF (757K) -
Effect of Ovarian Steroids Implantation into the Forebrain and Basal Hypothalamus on Pulsatile LH Secretion in Ovariectomized RatsYoshikatsu TADOKORO1985 Volume 61 Issue 1 Pages 22-37
Published: January 20, 1985
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSRecent studies have demonstrated that ovarian steroids are involved in the regulation of pulsatile LH secretion. In order to identify the site of action of ovarian steroids in modulating pulsatile LH secretion, the effect of local administration of estradiol benzoate (EB) or progesterone (P) into various brain regions on the characteristic of LH pulses was investigated in ovariectomized rats.
Female rats of the Wistar strain were ovariectomized about 3-4 weeks before the experiment. Blood samples were obtained at 6-min intervals for 4h without anesthesia through the indwelling atrial catheter. The steroid was implanted into the brain via the chronically-implanted cannula 1h after the initiation of the bleeding. Serum LH concentrations were determined by radioimmunoassay. The following results were obtained.
(1) Pulsatile LH secretion occurred at intervals of approximately 20-30 min and mean LH pulse amplitude was 4.85-5.27 ng/ml h in intact ovariectomized rats. Implantation of cholesterol, as a control, in various brain areas did not induce any changes in the pattern of pulsatile LH secretion.
(2) Implantation of EB into the preoptic suprachiasrnatic area (POSC) rapidly de-creased the mean serum concentration of LH within 1h as compared to the pre-implantation value. The LH pulse frequency, but not the amplitude, was also decreased rapidly and significantly within 1h after EB was implanted into the POSC.
(3) In rats with EB implanted into the diagonal band of Broca (DBB), LH pulse frequency began to decrease with 2h, followed by a decline in the mean LH concentration within 3h after the implantation.
(4) Implantation of EB into the medial part of the amygdala (m-AMYG) decreased the pulse frequency within 2h, and lowered the average LH level within 3h. The mean amplitude of LH pulses did not change after the implantation.
(5) Mean LH concentrations and LH pulse amplitudes began to decrease 1-2h after EB was implanted into the medial basal hypothalamus (MBH), whereas there was no change in the pulse frequency.
(6) Rats with the EB implant in the bed nucleus of the stria terminaris, the medial preoptic area, the medial septal nucleus or the anterior hypothalamic area did not show any changes in either the amplitude or the frequency of pulsatile LH secretion.
(7) Implantation of P into the DBB, POSC or MBH of ovariectomized rats did not induce any significant change in the pattern of pulsatile LH secretion.
These results suggest that the sites of estradiol action in modulating characteristics of pulsatile LH secretion are not widespread but rather concentrated within the specific brain regions. The POSC, DBB and m-AMYG seem to have neural components which respond to estradiol and modulate LH pulse frequency, while the MBH and/or the pituitary seem to be involved in the mechanism regulating LH pulse amplitude.View full abstractDownload PDF (1394K) -
The Role of Occulted Hyperprolactinemia in AnovulationHiroyuki MORI, Kozo AISAKA, Ryo MATSUOKA, Tomonori KIGAWA1985 Volume 61 Issue 1 Pages 38-47
Published: January 20, 1985
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSIt has been well documented that ovulation was induced by Bromocriptine treatment in euprolactinemic anovulation. The present study has been carried out to clarify the underlying mechanism.
28 patients with euprolactinemia (PRL<25 ng/ml) were treated with a 5 mg daily administration of Bromocriptine. Ovulation was induced in 13 cases, which were determined by their BBT charts.
In the ovulated cases, PRL secreting capacities were increased, determined by TRH administration. On the other hand, PRL secreting capacities were normal in the anovulated cases. The studies of the circadian secretion of PRL revealed that a nocturnal hyperprolactinemic state occurred for several hours in the ovulated cases, which was not seen in the anovulated cases.
From these results, the mechanism of induction of ovulation by Bromocriptine in euprolactinemic anovulation exists on the suppression of the increased PRL secreting capacity, which may be related to the occulted hyperprolactinemia at night. Ovulated cases by Bromocriptine are seemingly euprolactinemia, but in truth they may be a kind of hyperprolactinemia.View full abstractDownload PDF (799K) -
Hiroyuki MORI, Kozo AISAKA, Ryo MATSUOKA, Tomonori KIGAWA1985 Volume 61 Issue 1 Pages 48-55
Published: January 20, 1985
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSIt is well known that an acute administration of Bromocriptine (dopamine agonist) suppresses the serum LH level either in normal women or in women with polycystic ovary syndrome, in whom the serum LH level is elevated. The present study was carried out to examine the effectiveness of Bromocriptine on anovulatory women with a high LH level (serum LH>30 mIU/ml). Bromocriptine was administered for 3 months, 5 mg daily, to 9 anovulatory women with euprolactinemia (serum PRL<25 ng/ml). Ovulation was observed by their BBT charts. Before and after the treatment of Bromocriptine, FSH, LH and PRL secreting capacities were tested by LHRH and TRH injection. Also, estrone, estradiol and testosterone levels were measured before and after the Bromocriptine administration.
Resting levels of LH, FSH and PRL were 45.4 ± 11.0 mIU/ml, 11.4 ± 3.0 mIU/ml, and 14.3 ± 4.7 ng/ml (M ± SD), respectively, before the treatment. As a result of the treatment, the LH level was markedly decreased to 27.3 ± 14.5 (M ± SD, PC0.05), and PRL decreased to 3.76 ± 4.2 ng/ml (M ± SD, P<0.005). On the other hand, FSH did not show a marked change. The responsiveness of LH to LHRH before the treatment showed a marked increase, which was suppressed by Bromocriptine. However, FSH showed no change. The responsiveness of PRL to TRH was suppressed by Bromocriptine. Serum estrone, estradiol and testosterone levels before the treatment were 115.5 ± 76.7 pg/ml, 93.7 ± 61.0 pg/ml and 0.809 ± 0.209 ng/ml (M ± SD), respectively, which showed no significant change after the treatment. Six cases out of 9 ovulated with Bromocriptine.
From these results, it was concluded that 1) Bromocriptine induces ovulation in anovulatory women with a high LH level and euprolactinemia. 2) the underlying mechanismexists on the LH suppressive effect of Bromocriptine, which is independent of the PRL suppressive effect of Bromocriptine.View full abstractDownload PDF (639K) -
Immunochemical Studies with Monoclonal Islet Cell Surface Antibody Using Hybridization of Spleen Lymhocytes from Non-obese Diabetic MiceJojij HARI1985 Volume 61 Issue 1 Pages 56-68
Published: January 20, 1985
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSThe production of monoclonal antibodies to islet cell surface antigens, using hybridization of spleen lymphocytes from non-obese diabetic (NOD) mice has been reported previously from our laboratory.
In the present study, the immunochemical characteristics of the monoclonal antibody (3A4) have been investigated using In-111 cells, a virus-induced insulinoma cell line derived from the Syrian golden hamster as target cells. The antibody 3A4 could be visually detected in the immunoenzymatic labelling of the surface of In-111 cells. To identify the molecular weight of target specific antigens reacting with 3A4, 125I-surface labelled In-111 cells were solubilized and extracts were absorbed with 3A4. The immunoprecipitates were subjected to polyacrylamide gel electrophoresis and autoradiography. 3A4 recognized two major polypeptides with apparent molecular weights of radioactive 64K and inactive 28K daltons. In order to evaluate antibody-mediated cytotoxic mechanisms of 3A4, complement-dependent antibody-mediated cytotoxicity (C'AMC) and antibody-dependent cellular cytotoxicity (ADCC) were tested, using a method of specific chromium release. In the study for C'AMC, even though over wide ranges of antibody concentration and rabbit complement, purified 3A4 had no apparent cytotoxic effects on In-111 cells. On the other hand, significant ADCC was observed at 10 μEg/ml antibody concentration and 1 : 40 target : effector cell ratio.
Finally, the effect of 3A4 on glucose-stimulated insulin release in isolated rat isletswas examined. At 16.7mM glucose concentration, 3A4 significantly inhibited the insulin release in the absence or presence of complement. Therefore, 3A4 can not only bind but also be active to the target cells in the cytotoxicity and suppression of insulin release, and it can be a useful tool to clarify the pathogenesis of type 1 diabetes mellitus. Furthermore, these results suggest that the relationship between islet cell surface antibody and cellmediated immunity, especially immunoresponse against certain antigenic determinants on pancreatic B cells, seems to be important in the pathogenesis of type 1 diabetes mellitus.View full abstractDownload PDF (1896K)
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