Urinary SLI was measured every six hours for twenty four hours in rats fed a regular diet. Previously, we found that the urinary SLI increased after the administration of TRH intravenously. In the present study, in order to reveal the localization of increased SLI, we measured the contents in the hypothalamus, pituitary, thyroid, stomach and pancreas after the oral TRH administration.
(1) The rat urinary SLI levels showed a circadian rhythm. The maximum level of SLI was collected from 0.00-6.00 a.m. (89.4 ± 8.6 pg/6 hrs) (mean±SEM). This level was reduced during the daytime 6.00 a.m.-6.00 p.m. The minimum level was obtained from 6.00 p.m. -0.00 a.m. (49.3 ± 7.2 pg/6 hrs).
(2) The rats were decapitated at three and six hours after the oral TRH (500 μg/ml) administration. The SLI content was measured by RIA after extraction from each organ with 2.5 ml of 2M acetic acid. The pituitary SLI content was reduced three hours after the oral TRH administration.
(3) The thyroid SLI content was reduced six hours after the oral TRH administration.
(4) The hypothalamic, gastric and pancreatic SLI contents didn't change at three and six hours after the oral TRH administration.
As the result, the data suggest that augmentation by the oral TRH administration of urinary SLI was caused by its effect on the both the pituitary and the thyroid.

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Partial thyroxine-binding globulin (TBG) deficiency in a family is described. A 43-year-old male was admitted because of the association of low thyroxine level but markedly elevated triiodothyronine resin-uptake despite his complaints of palpitation and excessive sweating. TBG was low (6 μg/ml) by radioimmunoassay. His free thyroxine level was normal. ¹²³I uptake at 24 hours was normal and was suppressed following oral administration of triiodothyronine. Serum TSH level was normal and responded normally to TRH stimulation. Similar low level (6 μg/ml) in TBG was found in his elder brother who had no complaints. Another brother and 3 sisters had normal TBG levels.
According to the classification of the TBG deficiency proposed by Barbosa et al., a family described here is considered to have the type II TBG deficiency which shows a much lower TBG level in male than in female with X-linked inheritance.

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A 58-year-old man with primary aldosteronism associated with chronic chronic renal failure was treated with CAPD, oral administrations of Trilostane and furosemide. No adverse clinical or laboratory response could be attributed to these combination therapies. After subsequent removal of aldosterone-producing adenoma from left adrenal gland, his clinical symptoms were slightly improved. This case, still received CAPD treatment, is a unique presentation for primary aldosteronism without showing suppressed plasma renin activity.

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R 1881 binding receptor and DHT concentrations in human prostatic cytosol were assayed in surgically removed prostatic tissues of benign prostatic hyperplasia (BPH) and of the normal prostate. The normal prostates were obtained from totally cystectomized male patients with bladder cancer.
Cytosols were incubated with 0.25-8.0 nM (6 points) of ³H-R 1881 in the presence or absence of excess radioinert R 1881 at 4°C for 20 hours, thereafter treated with 0.5% dextran coated charcoal. Specific bindings were analysed in the form of scatchard plot analysis. Cytosol DHT levels were determined by radioimmunoassay reported previously.
Steroid specificity studies revealed that R 1881 binding receptor was inhibited not only by androgens but also by progesterone, however, an addition of 1000 fold excess triamcinolone acetonide (TCA) reduced the inhibition by progesterone. As R 1881-receptor complex was eluted at the void volume of sephacryl S-200 chromatography, the receptor was considered to be 8-9S protein.
Cytosol DHT levels were 35.5±13.6 pg/mg cytosol protein in BPH and 18.9 ±7.1 pg/mg protein in the normal prostates, showing a significantly higher value in the former (p<0.01). Kd and NBS of R 1881 receptor in BPH were 0.73 ±0.21 nM and 30.1± 9.0 fmol/mg cytosol protein and those in normal prostate were 0.68±0.28 nM, 10.2± 4.2 fmol/mg protein, respectively. NBS were also higher in BPH compared to the normal prostate (p<0.001). Moreover, DHT levels (y) and NBS (x) showed a significant correlation (y=0.631 X + 15.764, r=0.506). It was considered that both methods might posess almost equal ability to clarify the androgen dependency of prostatic tissues.

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A syndrome which is known as plasma cell dyscrasia with polyneuropathy and various endocrine manifestations or plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, abnormal M protein and skin changes is very interesting because this syndrome has miscellaneous manifestations such as skin hyperpigmentation, hypertrichosis, polyneuropathy, M protein abnormality, plasma cell dyscrasia and endocrine disturbances. Miscellaneous endocrine abnormalities which have not been described so far are reported here.
A 47 year old female was admitted with the chief complaints of edema and gait disturbance. Past and family histories were noncontributory. In April 1981, edema appeared in her face and legs. In June she noticed paresthesia in her legs. Edema increased gradually and she had difficulty walking. Her skin became pigmented and hairy. In October she was admitted because of polyneuropathy with increased cerebrospinal fluid protein without pleocytosis. Prednisolone was started. Walking improved slightly, but edema and paresthesia remained unchanged. Prednisolone was stopped at the end of the following March. In May 1982, she was admitted for further evaluation of edema and polyneuropathy.
The patient was alert and cooperative. On standing the skin of her legs became cyanotic. There was hypertrichosis on the arms and legs. Her fingers were clubbed. A moderate swelling of the cervical lymph nodes was noted. There was mild hepatomegaly without splenomegaly. All tendon reflexes were lost. Plantar response was flexor. Muscular strength diminished mildly. She complained of paresthesia on the soles. Superficial sensation was normal. Vibratory sense decreased mildly. Cerebellar function and cranial nerves were normal. There was no sphincter disturbance.
The examination of urine, stool and peripheral blood was normal. The repeatedly examined value of total cholesterol, total serum protein, CPK and choline esterase decreased. A mild increase in IgA (lambda type) and lambda type light chain was immunoelectrophoretically shown. Serum IgG were normal. Increased protein without pleocytosis was noted in the cerebrospinal fluid. Motor and sensory conduction velocities in the median nerve slowed. The evoked potential was not obtained in the sural nerve. Amyloid deposit could not be observed in the rectal biopsy. Myelin destruction (segmental demyelination) with relatively intact axon was microscopically and electron-microscopically shown in the sural nerve. The number of myelinated fibers was preserved. Antinuclear antibody (homogeneous pattern) was mildly positive.
Endocrinologically, T₃ was low and rT₃ increased. The basal level of TSH was slightly increased and TSH was also mildly hyperresponsive for TRH. Elevated plasma ACTH and low urinary excretion of 17KS were present. Plasma DOC, lldeoxycortisol, corticosterone and serum DHEA-S decreased. A staircase increase of 17OHCS was observed for ACTH stimulation for three days. The circadian rhythm of plasma cortisol was reduced. These findings suggested the presence of latent adrenocortical failure. But whether this failure was due to the syndrome itself or the result of using prednisolone could not be concluded. It will be necessary to accumulate evidence and further investigate this syndrome. Urinary excretion of estrogens (E₃ and occasionally E₂) increased. Plasma testosterone and progesterone were mildly reduced. There was a mildly impaired glucose tolerance with a slowed peak of IRI. Plasma renin activity was low. Plasma aldosterone was normal. PRL was slightly hyperresponsive for TRH. The basal level of LH and FSH was high, and LH and FSH were hyperresponsive for LHRH. Urinary excretion of catecholamines, cPTH, nPTH, calcitonin and alpha MSH were normal.
To our knowledge, this is the first report of this syndrome in which miscellaneous endocrine examinations have been performed with abnormal results.

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It has been well demonstrated that C-cells are the source of the hypocalcemic polypeptide hormone calcitonin (CT), and that they are the origin of medullary thyroid carcinoma. However, our knowledge of the morphology of normal human C-cells is still primitive. The purpose of this study is to present a detailed report concerning the morphology, distribution and population of C-cells in fresh normal thyroid glands using the high specificity immunoperoxidase staining method.
In addition, the carcinoembryonic antigen (CEA) activity in the C-cells and the solid cell nest are studied.
Fifteen fresh thyroid glands with no abnormal histological or laboratory findings were examined for C-cells by Sternberger's PAP method, and five thyroid glands obtained at autopsy 6-8 hours after death with no evidence of thyroid or parathyroid disease were examined as the control group. The CEA activity in the C-cells was examined by the anti-CEA and anti-CT double staining method.
The C-cells were detected in all 15 fresh glands examined. They were oval, spindle or polygonal in shape, and at the interfollicular or parafollicular position. Except for one gland which contained very rare C-cells, no C-cells were detected in the control autopsy glands. C-cells were most numerous at the junction of the upper and middle third of the lateral lobe, and in these areas the C-cell population ranged from 47 to 111 per section. Morphologically, the C-cells appeared not only singly but in groups in a parafollicular position as clusters or enclosing the follicular epithelium in the form of lamina.
Solid cell nests were easily distinguished from follicular epithelium by a routine H-E staining examination. None of these areas revealed a positive reaction with anti-CT, although scattered C-cells were seen occasionally in the neighboring area.
CEA activity in the C-cells was evident from the brown color by a DAB reaction product, while the CT was indicated by the violet color using a 4-chloro-1-naphthol reaction product. These two colors were identified in the same cells simultaneously.
From these results, it is concluded :
1) The autopsy thyroids obtained a few hours after death were not suitable for C-cell examination by the immunoperoxidase staining method.
2) The most numerous C-cells were distributed at the junction of the upper and middle third rather than the middle third of the lateral lobe, and the population in these areas averaged from 47 to 111 per section, or about 3 times as many as reported before.
3) C-cell clusters and lamina were clearly observable in the fresh thyroid glands, so the conventional C-cell hyperplasia approach must be reconsidered.
4) The solid cell nest was different from the cluster of C-cells, probably deriving from the metaplasia of follicular epithelium.
5) CEA activity in normal C-cells was confirmed.

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A very simple method for the evaluation of the interaction between thyroxine binding globulin (TBG) and thyroxine (T₄) has been developed and evaluated in 6 healthy subjects and 5 pregnant women.
Rabbit anti-human TBG antiserum was precipitated with 50% anmonium sulfate followed by passing a DEAE-cellulose column. Immunoglobulin G (IgG) fraction thus prepared was covalently attached on a Sepharose CL-4B and used as an immunoadsorbent of serum TBG.
After treatment with charcoal to remove endogeneous thyroid hormones, 10 μl of sera from 6 healthy subjects and 5 pregnant women were incubated with ¹²⁵I-T4 and various concentrations of cold T₄ followed by immunoadsorption with anti-TBG-Sepharose, and association constants (Ka) between TBG and T₄ were calculated in each subject using Scatchard's plot.
The Ka value thus obtained in 6 healthy subjects was 1.47 × 10⁸M^-1 (SD = 0.24), and in 5 pregnant women it was 0.82 × 10⁸M^-1 (SD = 0.21) which was significantly lower than that of healthy subjects (P<0.001).
Our present method does not need purification of TBG from serum to investigate its functions, especially in relation to the binding with thyroid hormones. Also, only a very small amount (100-150 μl) of serum is enough for the calculation of Ka between T₄ and TBG. The whole procedure is very easy to perform and can be done in a relatively short time, and therefore we consider this method clinically relevant and useful.

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In previous experiments it was found that PGF₂α originating from the uterine endometrium plays a physiologically important role in corpus luteum regression. The present study was undertaken to investigate the regulation of PGF₂α release from the uterus in luteolysis.
The effect of ovariectomy on PGF₂α release was examined. Bilateral ovariectomy was performed on day 14 of pseudopregnancy. PGF₂α urinary metabolite excretion was almost constant from day 15 to 22, although a significant increase of PGF₂αUM excretion could be seen in the control rabbits.
Ovariectomy was performed on day 17. Levels of PGF₂αUM excretion increased from day 15 to 17, however, an abrupt decrease occurred after ovariectomy. This indicates that the ovaries are necessary for PGF₂α release from the uterus.
The effect of steroids on PGF₂α release was examined. No significant increase in PGF₂αUM excretion could be seen in the ovariectomized pseudopregnant rabbits by the administration of estradiol and/or progesterone, although they are reported to be involved in other species.
The effect of the ligation of the vessels between the uterus and ovaries on PGF₂α release was investigated. The ligation was performed on day 9. No increase in the production of PGF₂α occurred after ligation. Luteal life span was prolonged by 6 days. Endometrial perifusion was carried out to investigate PGF₂α production activity on day 18 of the pseudopregnant rabbits after the ligation of the vessels between the uterus and ovaries. PGF₂α production activity in the treated rabbits was lower than in the controls.
These results indicate that a non-steroidal regulator may regulate PGF₂α release via the circulation of the uterus and ovaries in the pseudopregnant rabbit.

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Increased sympathetic nervous activity may play an important role in the pathogenesis of essential hypertension. It is well-known that both dietary sodium intake and age influence plasma norepinephrine (P-NE). There are many reports on comparative studies of P-NE in patients with essential hypertension and normotensive controls. However, there are few studies on changes in plasma catecholamines in both the aging and salt intake states. The present study was undertaken to evaluate the effect of age on sympathetic nervous activity in patients with essential hypertension and normal controls under low (U_NaV 29±3 mEq/ day), regular (U_NaV 133±8 mEq/day) and high (U_NaV 324±12 mEq/day) sodium regimens. The catecholamine levels were analyzed by THI methods after HPLC separation. Twenty-four hour urinary norepinephrine, epinephrine and electrolyte (Na⁺, K⁺) excretion on day 5 of each regimen was also determined. On day 6 morning, supine and upright P-NE, plasma epinephrine and plasma renin activity were determined after blood pressure and pulse rate measurement. Subjects were separated according to age as follows : young (<40 y.o.), middle-aged (40-60 y.o.) and old (>60 y.o.). P-NE in hypertensives was significantly higher than in normals under any three sodium intakes. There was a significantly positive correlation between age and P-NE, but only in normal controls under three sodium intakes and not in hypertensive patients under any three sodium regimens. In the young group of hypertensive patients, P-NE was significantly higher than that of normal controls.
These results suggest that the increased sympathetic nervous activity plays an important role in the pathogenesis and maintenance of essential hypertension, and this is particularly obvious in young patients.

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It has been said that the frontal lobe neocortex regulates the secretion of pituitary hormones. In the present study, the nerve circuit including the frontal lobe neocortex which is concerned in regulating the secretion of pituitary gonadotropin was studied in the 4-day vaginal cycle of female Wistar rats.
1. Electric stimulation (monophasic pulse wave, 1Hz, 6-9V) of the dorsal part of the anterior frontal lobe neocortex induced evoked potential in the thalamic dorsomedial nucleus (DM), the basolateral amygdaloid nucleus (basolateral-AMYG), the medial septal nucleus (m-SEPT) and the anterior border of the diagonal band of Broca (DBB).
2. Multiple unit activity (MUA) recorded in the DM, basolateral-AMYG and m-SEPT showed a fluctuation with the estrous cycle in which the minimum level was observed on the day of proestrus and the maximum level was observed on the day of estrus. But MUA did not show a distinct fluctuation with the estrous cycle in the frontal lobe neocortex.
3. A horizontal circular cut of the median region in the forebrain-limbic area including the m-SEPT and the anterior border of the DBB on the day of diestrus II induced vaginal cornification on the following day.
4. Excision of the dorsal region of the anterior frontal lobe neocortex on the day of diestrus II increased the serum concentrations of luteinizing hormone (LH) in the afternoon of that day and induced vaginal cornification on the following day.
5. Electrochemical stimulation (DC 120 μA, 30 sec) of the anterior frontal lobe neocortex just before the critical period of ovulation on the day of proestrus blocked the preovulatory surge of LH.
6. Electrochemical stimulation of the anterior frontal lobe neocortex just after excision of the lateral amygdaloid nucleus (lateral-AMYG) including the basolateral-AMYG did not block the preovulatory surge of LH and ovulation. Electrochemical stimulation of the frontal neocortex after excision of the DM did not block the preovulatory LH surge. Excision of the m-SEPT showed a similar effect, but it had little effect on the blockade of the inhibition of LH secretion induced by electrochemical stimulation of the anterior frontal lobe neocortex.
It became clear that the dorsal region of the anterior frontal lobe neocortex has an inhibitory function on the secretion of LH and ovulation through the nerve circuit including the DM, the basolateral-AMYG and the median region of the septal area. Then the anterior frontal lobe neocortex probably participates in the periodical rhythm of LH secretion with the estrous cycle.

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