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Volume 67 (1991)
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Volume 68, Issue 11
Displaying 1-8 of 8 articles from this issue
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Takahide MORI, Masatsune FUKUOKA1992 Volume 68 Issue 11 Pages 1151-1157
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSAlthough it is well established that the pituitary gonadotropins and prolactin are the primary regulators of ovarian function, steroidal and nonsteroidal molecules produced locally in the ovary have been implicated in the modulation of gonadotropin action as autocrine or paracrine regulators. Recent studies suggest that the cells of the immune system play important roles in regulating ovarian function, and the immune regulation of ovarian function has become one of the topics in the field of ovarian physiology. Since it has become clear that the immune factors, cytokines, show a wide range of biological functions, not only on immune cells but also on nonimmune cells, the physiological significance of the resident immune cells, the widespread distribution of which in mammalian ovaries has been known for a long time, has reattracted attention as a third kind of regulator of ovarian function. In this article, current knowledge of the regulatory roles of immune cells as well as the cytokines in ovarian physiology is reviewed.View full abstractDownload PDF (775K) -
Physiological and Pathological Roles of Estrone Sulfate and Estradiol 17-SulfateHideo HONJO, Hiroji Okada1992 Volume 68 Issue 11 Pages 1158-1166
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSPlasma ethinylestradiol increases 47.6% when taken with ascorbic acid because of competition in producing sulfate conjugation. Thus the role of sulfates may be important.
Serum and urinary estrone sulfate (E1-S)in pregnancy and non - pregnancy were analyzed. Its serum peak during the menstrual cycle was 2.67±0.37ng/ml (mean±SE) and about ten times that of estradiol -17β. E1-S showed lower levels in malignant tissues of breast cancer and endometrial cancer. Increased sulfatase activity in the malignant tissue hydrolizes E1-S to E1, which may develop the tumors.
Serum estradiol 17-sulfate (E2-17-S) in pregnancy was first measured. As E2-17-S decreased, lipid peroxides increased. E2-17-S is converted to 2-OH or 4-OH E2-17-S, which act as lipid peroxide scavengers. Pregnancy-induced hypertension showed lower levels of E2-17-S. In vitro study using the human endothelial cell of the aorta, E2-17-S and 2-OH E2-17-S strongly suppressed lipid peroxidation, which precedes atheloscrelotic change.View full abstractDownload PDF (668K) -
Takao OBARA1992 Volume 68 Issue 11 Pages 1167-1176
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSPrimary hyperparathyroidism is nowadays not uncommon in Japan. The incidence is considered to be one in every 2,500 to 5,000 persons. Many advances have occurred in diagnosis, localization study, and treatment of the disease. Surgery remains the treatment of choice for patients with primary hyperparathyroidism. Notwithstanding, there are still controversies concerning the management of primary hyperparathyroidism. One of the current disputable points is whether the use of localization study in patients who are undergoing and initial operation is justified or not.
Another is whether unilateral exploration is justified or not. The basic reasons for these persistent controversies is the lack of consensus about incidence of multiglandular hyperplasia or double adenomas. Our observation implies that the incidence of hyperplasia or double adenomas among all the patients with primary hyperparathyroidism in Japan is lower than that in western countries. Since diagnostic accuracy of noninvasive localization studies has recently improved, it seems reasonable to adopt unilateral neck exploration in our country. It is also characteristic in Japan that the incidence of parathyroid carcinoma is relatively high (6%) compared with that reported in many other countries.View full abstractDownload PDF (1049K) -
Kiyonobu TANAKA, [in Japanese]1992 Volume 68 Issue 11 Pages 1177-1187
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSThe aim of the present study is to explore whether the renal and cardiovascular response to clonidine in type II diabetic patients is different from that in control subjects, and to clarify the role of central α2-receptor in the regulation of cardiovascular response and sodium handling in type II diabetes mellitus (DM).
Thirty-five diabetic inpatients aged 30-71 years (54.1±9.7) and ten control subjects (N) were enrolled in this study after their fasting plasma glucose had been improved. To evaluate the peripheral sympathetic nerve activity, 24-hour urinary catecholamine was measured, and pulse rate (PR) responses to a 30-second standing test was determined. On another day, blood pressure (BP), PR, plasma norepinephrine (PNE), cyclic AMP (p-cAMP), renin activity (PRA), aldosterone (PAC) and growth hormone (p-GH) were measured at 0, 30, 60, 90, 120, 150, 180 minutes following the oral administration of clonidine (150μg). Type II DM were classified as DM with hyper-response (DM-HR, n=12) when their PR decreased after clonidine more than that of N, and if not, they were classified as DM with normal response (DM-NR, n=23).
Urinary catecholamine excretions in type II DM were within the normal range. BP, PNE and p-cAMP were markedly decreased with clonidine in similar fashion in DM-NR, DM-HR and N. The percent changes of PNE were correlated positively with the changes of p-cAMP in both N and DM- NR (r=0.660 and 0.449, respectively), but not in DM-HR. No significant difference in the changes of p-GH (Δp-GH) and J GH (the area under the curve) following clonidine administration was observed in the three groups. The decrease in PR was correlated with neither Δp-GH (N: r=0.082, DM- NR: r=-0.400, DM-HR: r= 0.242) or∫GH (N : r= 0.191, DM-NR: r= 0.382, DM-HR: r= 0.162). The fractional excretion of sodium (FENa) decreased in N (p<0.01), increased in DM-NR (p<0.05) and did not change in DM-HR. The changes of FENa were not correlated with those of PRA and PAC.
These results suggest that there is an abnormal response to the central α2-adrenoceptor stimulation in some diabetic patients exhibiting a normal sympathetic response to standing, and that an abnormal renal sodium handling, probably resulting from altered α- adrenoceptor density in not only the central nervous system but also peripheral tissues, exists in the patients without peripheral sympathetic neuropathy.View full abstractDownload PDF (1116K) -
Tetsuro KAWANO, Kohei MATSUURA, Ritsuo HONDA, Hiroshi NISHIMURA, Nobuy ...1992 Volume 68 Issue 11 Pages 1188-1196
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSTo investigate the usefulness of a semi-quantitative assay of urinary luteinizing hormone (LH) for predicting ovulation, the relationship among urinary LH, serum LH, serum estradiol (E2) and ultrasonographic observations of follicles were examined in 32 infertile women (35 cycles) at spontaneous (7), clomiphene (13) or cyclofenil (3) induced or hMG (12) induced cycles. Their urine samples were collected 3 times a day for LH assay, starting from about the 10th cycle day or when follicles having a diameter of 10mm or more were detected to the day of ultrasonographical confirmation of follicle ruptures. In the morning on these days, blood was taken twice daily for LH and E2 determination at intervals of 30 min. In spontaneous cycles, urinary LH was (P<0.001) correlated to a significant extent with the serum LH and E2 levels, and follicle rupture was observed 1.9 days after the urine LH surge. In contrast, there was no significant correlation between the urine LH and serum LH or E2 levels in the ovulation induced cycles. In addition, the period from urine LH positive to follicle rupture was significantly (P<0.05) prolonged in those cycles compared with that in spontaneous cycles. These results suggested that the urine LH determination was good for predicting ovulation in spontaneous cycles, but it was also necessary to monitor the follicle sizes by ultrasonography in ovulation induced cycles.View full abstractDownload PDF (807K) -
Koichi YANO, Yoshiya ITOH, Fumie INYAKU, Tetsuo TAGUCHI, Masatoshi TAK ...1992 Volume 68 Issue 11 Pages 1197-1204
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSTwo sisters with athyreotic congenital hypothyroidism are described. This is the fifth report on athyreotic congenital hypothyroidism in siblings. The elder sister is 14 years old and the younger one is 12. The parents have no consanguinity or family history of thyroid disease. Both of the patients were born before the start of neonatal screening tests for congenital hypothyroidism. After birth, they had jaundice, abdominal distention and constipation, which are typical symptoms of congenital hypothyroidism. Serum T4 levels were decreased, and the serum TSH levels were markedly increased. Therefore we diagnosed them as having congenital hypothyroidism. They have received replacement therapy with thyroxine since diagnosis and have shown normal development physically and psychologically. They were tested for thyroid scintigram when the elder sister was 9 years old and the younger one was 7. 123I thyroid uptakes were 0.69% and 0.64%, respectively. The thyroid scans demonstrated no focus of accumulation of 123I. They do not have trapping defect of iodine, because 123I of saliva and serum were 41.3 and 46.3, respectively. From these results, we diagnosed them as having athyreotic congenital hypothyroidism. They and their mother do not have any antithyroid antibodies. We suppose that some genetic factor is responsible for the athyreotic congenital hypothyroidism.View full abstractDownload PDF (1094K) -
Syoh-ichi YAMAGISHI, Hisatsugu MIYAKOSHI, Yukihiro NAGAI, Kenso OHSAWA ...1992 Volume 68 Issue 11 Pages 1205-1214
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSSpuriously high value of serum free triiodothyronine (FT3: Amerlex free T3 kit, Amersham, UK.) was noted accidentally on routine laboratory examination of two clinically euthyroid patients (case 1: FT3; 18.5pg/ml, FT4; 1.1ng/dl, T3; 103ng/dl, T4; 8.2μg/dl, TSH; 1.74μU/ml, case 2: FT3; 8.5pg/ml, FT4; 1.1ng/dl, T3; 137ng/dl, T4; 8.9μg/dl, TSH; 1.45μU/ml), the former with poorly controlled diabetes (FBG 253mg/dl, HbAic 12.1%) and the latter with essential hypertension (184/108mmHg). Although the hypertensive patient showed mild diffuse goiter, there was no evidence that the patients had autoimmune thyroid diseases because anti-thyroglobulin antibody tests measured by radioimmunoassay and MCHA, TGHA or TBII were all negative. Their serum levels of TBG were within the normal range. Further studies revealed that both patients' sera had unusual binding activity to labelled polyaminocarboxy T3 (125I-aT3) but not labelled T3 (125I-T3). Furthermore, this binding protein was precipitated by goat anti-human immunoglobulin G (IgG). The IgG purified from both patients' sera also showed strong binding activity to 125I-aT3, which was inhibited by unlabelled T3 in a dose dependent manner.
In conclusion, we found anti-T3 antibody in two clinically euthyroid patients with no apparent evidence of complicating autoimmune thyroid diseases. The stronger binding activity to polyaminocarboxy T3 rather than T3 may lead to the spuriously high value of serum FT3. The mechanisms of the production of such autoantibodies in our cases should be further investigated.View full abstractDownload PDF (789K) -
Aoi YOSHIIWA, Takashi NABATA, Shigeto MORIMOTO, Katsuhiko SAKAGUCHI, H ...1992 Volume 68 Issue 11 Pages 1215-1223
Published: November 20, 1992
Released on J-STAGE: September 24, 2012
JOURNAL FREE ACCESSThis report describes a 48-year old female patient with Hashimoto's thyroiditis, distal-type renal tubular acidosis (d-RTA), Sjögren syndrome (SjS), and empty sella syndrome (ESS). She has been receiving replacement of thyroxine for Hashimoto's thyroiditis since 1967. She felt muscle weakness and numbness in the extremities and was found to have low serum potassium (2.9mEq/l) in 1987. Since then she has been administrated potassium chloride orally. She was admitted to our hospital because of recurrence of muscle weakness and numbness of the extremities in November 1990. Laboratory examination revealed that her serum levels of antimicrosomal antibody and anti-thyroglobulin antibody were highly positive (MCHA: x 210 x 100, and TGHA: x 100). Furthermore, she was revealed to have 1) d-RTA by oral tolerance tests with the administration of NH4Cl and NaHCO3, 2) SjS by Schirmer test and sialography, and 3) ESS by computed tomography and magnetic resonance imaging examinations of the pituitary. Association of Hashimoto's thyroiditis, d-RTA, SjS and ESS in this case may possibly be caused by common autoimmune mechanism.View full abstractDownload PDF (1543K)
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