The effect of synthetic alpha-human atrial natriuretic polypeptide (α-hANP) on the in vivo and in vitro release of ACTH and corticosterone was examined. In the in vivo study ACTH and corticosterone responses to rapid 2-ml/rat hemorrhage were measured in sixteen conscious rats after α-hANP administration. The hemorrhage increased plasma ACTH and corticosterone concentrations in the control group of rats (p>0.01). ANP inhibited hemorrhageinduced ACTH secretion (p<0.05), but the plasma corticosterone response was not affected. In the in vitro study a high concentration of ANP (1 μM) reduced basal corticosterone secretion from the isolated rat adrenal gland (p<0.05), but the response to ACTH (10 ng/ml) and dibutyryl cyclic AMP (0.5 mM, 5.0 mM) was not affected. Our data suggest that ANP inhibits hemorrhage-induced ACTH secretion from the anterior pituitary but inhibits corticosterone secretion from the adrenal gland very weakly.

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In order to prove the acute stimulatory effects of estrogen on pituitary gonadotropin release, we have performed the present experiments in 8 women with a hypergonadotropic state due to surgical castration or primary ovarian failure. They received gonadotropin releasing hormone (Gn-RH) for 12-21 h at the constant rate of 20 μg/h. In 5 of the women, estradiol-17β was concomitantly administered at the rate of 20 μg/h from 6 h after the start of Gn-RH infusion. Blood samples were collected frequently throughout the experiments for the analysis of LH, FSH and estradiol.
In response to the sole stimulation of Gn-RH, remarkable and prompt rises in LH (313.5%), but to a lesser degree in FSH (194.2%), were abserved within the initial 3 h, and their high levels were maintained throughout the experimental period. However, the additional administration of estradiol brought on a further sudden rise in both gonadotropins levels: 178.3% for LH and 163.5% for FSH within 2 h. These high levels were sustained during estradiol infusions. In 2 of them, blood samples were obtained for several hours after cessation of estradiol infusion. The circulating gonadotropin level dropped precipitously close to the baseline level within 3 h after estradiol infusions.
Our data indicate that estrogen has an acute and strong augmentative effect on Gn-RH induced gonadotropin release in addition to its conventional negative and positive feedback effects.

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³H-Dexamethasone (Dex)-receptor complexes prepared from the rat liver cytosol efficiently bound to the nuclear matrix from the same tissue. The binding was increased with the concentration of the ³H-Dex-receptor complex added and reached a maximum plateau. However, when the partially purified ³H-Dex-receptor complex was used, saturation of the binding sites in the nuclear matrix was not observed in the range of concentration of ³H-Dex-receptor complex used. Therefore, it was considered that the apparent saturability observed in the binding of the unpurified receptor complexes is caused by the translocation inhibitor (s) in the cytosol. When the binding capacity was expressed on the basis of unit weight of DNA, the nuclear matrix exhibited 20 times more of that the unfractionated nuclei. However, no line of evidence of enrichment of the binding sites in the DNA isolated from the nuclear matrix was observed. These observations show that the role of the nuclear matrix in the action of glucocorticoid is quite uncertain.

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Monolayer cultures of the pancreas of the neonatal rat were maintained in TCM 199 medium, supplemented with 5.5 mM glucose, with or without 5 mM 3-amino-3-deoxyglucose, and perifused to examine the changes which occurred in the insulin secretory response during culture. On day 0, B cells showed a monophasic insulin secretion in response to 16.7 mM glucose, whereas in the presence of 200 nM 12-o-tetradecanoyl phorbol-13-acetate, 40 μM lysophosphatidylcholine, 10 μM forskolin or 1 mM 3-isobutyl-1-methylxanthine, the same dose of glucose stimulated insulin secretion in a biphasic fashion. Under culture conditions without 3-amino-3-deoxyglucose, the response to glucose totally disappeared after 7 days, and that to 10 mM of either leucine or 2-ketoisocaproate was as low as that of day O. In contrast, B cells that had been cultured for 7 days in medium with 3-amino-3-deoxyglucose showed an adult-like biphasic pattern in response to glucose. When stimulated by glucose at a linear gradient concentration running from 0 to 20 mM, the B cells responded to increasing concentrations of glucose in a dose-dependent fashion. Further, the response of cAMP to glucose was increased by adding forskolin or 3-isobutyl-1-methylxanthine, which also enhanced the secretion of insulin under either a step-wise or slow-rise stimulation with glucose. The effect of 12-o-tetradecanoyl phorbol-13-acetate was also outstanding. Likewise, the addition of either leucine or 2-keptoisocaproate induced a striking increase in the secondary phase secretion as well as promoting the rates of glutamine oxidation within the cells. In conclusion, it is suggested that the high response to a wider variety of stimuli may represent the reaction of neonatal B cells to the cultural milieu rather than a process of physiological development, and these effects exhibited by 3-amino-3-deoxyglucose would be related to a change in the constituents of glycoproteins in the cells.

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A 59 year-old patient had lumbago and pain in hip joints, knees, and ribs of long duration. Severe hypophosphatemia and high serum ionized calcium were found in spite of normal level of total serum calcium. The serum parathyroid hormone and alkaline phosphatase levels were elevated, and diffuse demineralization of the bones and renal stones were found by x-ray examination. Parathyroid adenoma was diagnosed from the subtraction image of the ^99mTcO₄^- and ²⁰¹Tl-Cl₂ scintigrams. Osteomalacia was demonstrated by bone biopsy at the right iliac crest. A right lower parathyroid adenoma of 2.0×1.8 cm, weighing 4.0 g was removed. The long standing phosphate depletion and hypophosphatemia, due to hyperparathyroidism causing renal damage with nephrocalcinosis and reduced synthesis of active vitamin D, and milk intolerance due to gastroduodenostomy were probably responsible for producing the clinical picture of normocalcemic hyperparathyroidism complicated with osteomalacia.

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In order to examine whether substrate specificity of angiotensin-converting enzyme (ACE) exists or not for N-terminal substituted angiotensin I (ANG I) in man, biological activities of sarcosine¹-angiotensin I (Sar¹-ANG I) and the effects of an ACE inhibitor, captopril, on the Sar¹-ANG I activities were studied in 5 normal men. The following 3 experiments were done at 1 week intervals.(1) Sarcosine¹-angiotensin II (Sar¹-ANG II) was infused iv at a rate of 5 pmol/kg·min from 0900 h to 0930 h in 5 normal men in a recumbent position. Blood pressure rose remarkably and the average increment was 38/31 mmHg at 30 min (p<0.001). Average duration of the pressor action after the cessation of the infusion (T) was 40 min for systolic and 50 min for diastolic and much longer than T of isoleucine⁵-angiotensin II. Plasma renin activity (PRA) decreased (p<0.01) and plasma aldosterone (PA) increased significantly (p<0.01).(2): Sar¹-ANG I was infused iv at a rate of 5 pmol/kg·min from 0900 h to 0930 h. Blood pressure rose to the same extent as in (1)(p<0.001). T was 40 min for both systolic and diastolic and much longer than T of ANG I in man. PRA decreased (p<0.01) and PA increased (p<0.01) significantly.(3): Oral 100 mg captopril was given at 0800 h and Sar¹-ANG I was infused iv at a rate of 5 pmol/kg·min from 0900 h to 0930 h. Blood pressure showed no significant change. Sixty minutes after captopril PRA increased markedly (p<0.001) and PA decreased (p<0.001). At 30 min of Sar¹-ANG I infusion PRA decreased to the pre-captopril level (p<0.001) and PA was kept at the preinfusion level. From these results it is concluded that the conversion of Sar¹-ANG I to Sar¹-ANG II is almost complete in normal men and even if N-terminal aspartic acid of ANG I is substituted by sarcosine, substrate specificity of ACE is not demonstrated in man. Sar¹-ANG I may possibly inhibit renin release in normal men.

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Sixty-two patients with pituitary dwarfism were treated with three different preparations of methionyl hGH (m-hGH) for 3 to 14 months. They were given 0.5 IU/kg/week intramuscularly. The growth rate during treatment with the three different preparations was the same for each and increased from 3.5±0.9 to 8.2±1.7 cm/year. A high incidence of hGH antibody formation was observed following the treatment, but the titer of antibody was decreased according to the purity of m-hGH preparations. At the end of 12 month treatment with a highly purified preparation (Somatonorm III), 76.2% of the patients had hGH antibody. However, the presence of antibodies did not affect the growth rate except in one patient. No clinical or laboratory sideeffects were observed following the treatment with m-hGH. Thus, m-hGH was considered to he useful for the treatment of GH deficient children.

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Follicular fluid from small porcine follicles was filtrated through an Amicon XM-50 membrane to obtain a filtrate less than 50, 000 MW. The filtrate was eluted through a Sephadex G-25 column (1.5×70 cm) using 0.01 N CH₃COOH, pH 4.0, as elution buffer, and divided to five fractions. To test the inhibitory activity of these fractions on the in vitro estradiol and progesterone secretion, each fraction was added into a rat granulosa cell culture with FSH and testosterone in the medium. Two of five fractions exerted a significant inhibitory activity on the estradiol and progesterone secretions by the granulosa cells. They were in a range of low molecular weight fractions (MW 1, 000-3, 000) on the elution profile. Whether the in vitro active fractions are capable of inhibiting the in vivo estradiol and progesterone secretions by the ovary was assessed using the hypophysectomized DES-treated immature rat with hMG stimulation and the testosterone-treated immature rat with PMSG stimulation. The administration of the fractions to the former animal significantly suppressed the increases due to gonadotropin in the ovarian and serum estradiol concentrations. The administration of the fractions to the latter animal significantly suppressed the increases due to gonadotropin in the estradiol and progesterone concentrations of the ovary and serum. These results suggest that a low molecular weight substance from porcine small follicular fluid is capable of inhibiting the estradiol and progesterone biosyntheses in the follicle of the rat ovary.

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Serum and urinary concentrations of methimazole (MMI) were measured by high-performance liquid chromatography (HPLC) with an electrochemical detector (ECD) in 10 normal subjects and 43 hyperthyroid patients after intravenous and oral administration of the drug.
The pharmacokinetic parameters of MMI were estimated in 5 normal subjects and 15 hyperthyroid patients according to a two-compartment model after intravenous injection of a 10 mg dose. The mean half-life of the distribution phase (T_1/2α) was 2.7 ±1.0 h (mean±SD) and 3.1 ± 1.4 h and that of the slower-phase (T_1/2β) was 20.7±9.6 h and 18.5±12.9 h in normal subjects and hyperthyroid patients, respectively.There were no significant differences between pharmacokinetic parameters of normal subjects and those of hyperthyroid patients.No correlations between free T₄ index (FT₄I) and pharmacokinetic parameters were observed.
Maximum serum MMI concentrations (C_max)(213±84 and 299±92 ng/ml) were attained 1.8±1.4 h and 2.3±0.8 h after a single dose of 10 mg in 5 normal subjects and in 15 hyperthyroid patients, respectively.In hyperthyroid patients the time taken to reach the peak concentration (T_max) after a single dose of 10 mg was similar to that after a single 15 mg and 30 mg dose.The pharmacokinetic parameters, except C_max and the area under the curve (AUC), were not affected by the administered dose and those, except C_max, were not affected by the thyroid function.
All urine was collected at intervals of 3 h for the first 12 h and then at 24 h and 48 h after intravenous and oral administration of MMI.In all subjects, MMI rapidly appeared in the urine and the rate of excretion was highest in the first 3 h.The cumulative urinary excretion of MMI was 5.5-8.5% of administered doses in normal subjects and hyperthyroid patients.
These findings in the present study are compatible with the assumption that the extent of absorption of MMI is high, if not complete, and hyperthyroidism does not affect the kinetics of MMI, and that interindividual variation is observed in the time taken to reach the peak concentration after oral administration.

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Neural lobe function in male rats of the Wistar/Tw strain was studied at 3, 7 and 16-18 months of age.A significant rise in the serum arginine vasopressin (AVP) level was noted in 16-18-month-old rats showing polydipsia and polyuria.The content and concentration of AVP in the neural lobe of aged rats were significantly less than those of younger animals (3 and 7 months).These results point out an enhancement of AVP release from the neural lobe of aged rats.The reduction in urinary volume in aged rats subjected to 24 hours of water deprivation was less than those in younger animals.No increase in urinary sodium, potassium and chloride concentrations was observed in aged rats, and the decrease in electrolyte excretion from urine during the dehydration period was less in aged rats than younger ones.These results suggest that the antidiuretic response to osmotic stimuli was reduced in aged rats.The administration of AVP to aged rats resulted in a significant decrease in water intake and urinary volume, but AVP administration did not induce any change in the electrolyte balance.Therefore, it is concluded that the main cause of the development of polydipsia and polyuria is the decline in renal function but not in neurosecretory activity, although exogenous AVP can effectively reduce water intake and urinary output in aged rats.

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Murine monoclonal antibody (mAb 16.3.2) to human thyroglobulin whichbound equally to various thyroglobulins derived from nine species was oqtainedfrom the fusion of C3H/He spleen cells sensitized with normal human thyroglobulin.Characterization of mAb 16.3.2 revealed that both L-thyroxine (T₄) and reverse triiodo-L-thyorine (rT₃) were very efficient in the competitivebinding inhibition test and that a molar ratio between T₄ and rT₃ needed for 50% inhibition of binding to immunized thyroglobulin was about 1: 1.Further studies on the idiotype of mAb 16.3.2 using both binding and competitivebinding inhibition tests showed that mAb 16.3.2 had a unique idiotypenot cross-reacting with other monoclonal antibodies to thyroglobulins.Therefore, a possible explanation offered was that mAb 16.3.2 was endowed with aunique idiotype to be regulated by a distinct idiotype network from those ofother mAbs.

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Seventeen patients with moderately severe ophthalmopathy due to Graves'disease were treated by cobalt or supervoltage radiotherapy.All patientscomplained of diplopia.The mean proptosis value was 21.4 mm.Threepatients (18%) showed good response, 7 (41%) moderate and 7 minimal orno response.Improvement was noted mainly in soft tissue changes anddiplopia, while proptosis decreased in only 5 patients.All except one patientwho had marked extraocular muscle involvement revealed by computed tomographyresponded to treatment.These data indicate that radiotherapy may beindicated in patients with progressive opthalmopathy, especially in those whoare associated with extraocular muscle enlargement.

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Antisera to purified porcine follicullar fluid inhibin of 32 K protein (pFF 32 K inhibin) were raised in rabbits.Increasing doses of an antiserum withhigh titer could neutralize the maximal suppression of FSH secretion caused by 10 ng of pFF 32 K inhibin from rat anterior pituitary cells in culture.A radioimmunoassay was developed using the antiseum and ¹²⁵I-labelled pFF 32 K inhibin.Specificity of the antiserum was examined by comparing immunologicaland biological potencies of various inhibin preparations.Cross-reactivity tests revealed that the antiserum almost recognizes rat ovarian inhibinpreparations.The antiserum also recognizes purified bovine follicular fluidinhibin of 32 K protein (bFF 32 K inhibin), but with a cross-reactivity ofapproximately 20%.Cross-reactivity of human follicular fluid to the antiserumwas less than 10%.The antiserum also recognizes inhibin forms of highermolecular weights, 100 K, 80 K, and 55 K proteins, which have previously been identified by gel filtration or SDS-PAGE of crude pFF inhibin preparationsunder protein-dissociating conditions, indicating that these inhibin forms have common or closely related immunodetermining sites.

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Detailed oro-maxillofacial studies using dental cast, pantomogram and cephalogram were performed in 43 patients with GH deficiency aged 7-17 years and compared statistically to the results from 62 short children with normal GH secretion.The dental age was retarded as compared to the choronological age in patients with GH deficiency by a mean of 2.0±1.3 years.This value did not differ statistically from that observed in normal short children (1.7±0.8 years) However the bone age was significantly retarded in patients with GH deficiency (3.2±1.7 yrs vs 1.5±1.1 yrs, p<0.001).There was no difference between tooth size or cephalogram analysis results in the children in the two groups.The coronal arch length, basal arch width and basal arch length were shorter in patients with GH deficiency.These data indicate underdevelopment of the maxilla in patients with GH deficiency.

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The effect of sialylated TBG and desialylated TBG on thyroxine (T₄) uptake by human peripheral mononuclear cells was investigated in vitro.[¹²⁵I]-T₄ uptake was observed when the cells were incubated with free [¹²⁵I]-T₄.The uptake was inhibited in a concentration dependent manner when TBG was added.During the incubation, [¹²⁵I]-T₄ binding to TBG was observed.[¹²⁵I]-T₄ incorporation into cells was also observed when the cells were incubated with [¹²⁵I]-T₄-sialylated TBG or with [¹²⁵I]-T₄-desialylated TBG complex.The uptake was related to the temperature and length of time of the incubation.desialylated TBG during the early 0-20 min.incubation, whereas the amount of [¹²⁵I]-T₄ incorporated into the cells incubated with [¹²⁵I]-T₄-desialylated TBG became greater than that into the cells incubated with [¹²⁵I]-T₄-sialyted TBG after 20 min.of incubation.Pretreatment of the cells with methylamine blocked [¹²⁵I]-T₄ uptake in both cases, i.e.incubated with [¹²⁵I]-T₄-sialylated TBG and incubated with [¹²⁵I]-T₄-desialylated TBG.The results suggest that TBG plays a role not only as a carrier protein for T₄ in circulation but also as a protein which can transport T₄ from the extracellular into the intracellular space, so that the mechanism of T₄ transport mediated by desialylated TBG is different from that mediated by sialylated TBG, and that the T₄ transport system in both cases, mediated by sialylated TBG and by desialylated TBG, may be related to the internalization of T4-TBG-TBG receptor complex or of T₄-T₄ receptor complex if TBG receptors are present in the outer surface of the cell membrane.

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The effect of an injection of thyrotrophin releasing hormone (TRH) on plasma levels of thyroid hormones was studied in dwarf and normal Rhode Island Red chickens with similar genotypes othei than for the sex-linked dwarf gene dw.The sex-linked dwarf chickens had different plasma iodothyronine levels from control normal chickens: high thyroxine (T4), low triiodothyronine (T3) and similar reverse T3 (rT3) levels.The injection of TRH (10 μg/kg) in 5-day- and 5-week-old normal chickens increased the plasma T4 within 30 min without a significant increase in T3, whereas the injection of TRH in 11-and 26-week-old normal chickens increased plasma T3 60 min later.In dwarfs the response of T4 to TRH was the same as that in normals but no increased T3 response was observed.The plasma level of rT3 was not influenced by the TRH injection in either strain.These results suggest that although in the sex-linked dwarfs thyroidal response to exogenous TRH is similar to that of normals, the dwarf gene dw inhibits the conversion of T4 to T3 in peripheral tissues without any inhibitory effect on rT3 production.

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The acute effects of methylmercury chloride (MMC) on the endocrine functions were investigated with doses too small to cause any typical neurological dysfunctions. The hormones included PRL, LH, TSH, ACTH, corticosterone (Bk), testosterone (TLI), total thyroxine (T4) and free thyroxine (free T4). The changes in serum hormone levels from 1 hour through 10 days after a single injection of MMC (12 mg/kg s. c.)(Exp. 1), and dose-response relationships between MMC doses (2 to 16 mg/kg s. c.) and the serum hormone levels at 25 hours after MMC injection (Exp. 2) were examined. The acute effects revealed, which were all reversible, are summarized as follows; 1) MMC might directly inhibit thyroxine synthesis; 2) MMC could affect only stimulatively the pituitary-adrenal axis and PRL synthesis/release, the primary action site for which may be the CNS; and 3) the effects of the pituitary-gonadal axis were inconsistent and, therefore, this axis seems to be relatively resistent to MMC. On the other hand, the responses of PRL and TSH to TRH loading, which were examined for both groups in Exp. 3, suggested that MMC could not affect the metabolizing activity for serum PRL and TSH. The hormone levels of the MMC group enhanced by TRH recovered very rapidly as in the control group.
Thus, these acute and reversible endocrine effects seem to indicate relatively earlier development of possible chronic and irreversible effects on the endocrine functions when exposed to methylmercury chronically, and these should be examined further.

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A new radioimmunoassay (RIA) for human Chorionic Gonadotropin (hCG) was developed using murine monoclonal antibody to the β-subunit of hCG (β-hCG). The IgG fraction of the monoclonal antibody which did not react with ¹²⁵I-β-hCG was purified from hybridoma ascites, and covalently coupled to Sepharose 4B. This solid-phase antibody was incubated with standard hCG or serum sampled for 48 hours. The reaction medium was then removed by centrifugation and ¹²⁵I-β-hCG and anti-β-hCG rabbit polyclonal antibody were added to the precipitate. The alcohol precipitation method was used for separating “bound” and “free” forms in the second reaction.
The sensitivity for hCG in this assay system was 0.5 mIU/ml serum and the cross-reactivity with human Luteinizing Hormone (hLH) was 0.4%. This assay system was shown to be clinically applicable. Serial serum samples from two patients with trophoblastic disease were assayed and minute amounts of hCG, which could not be determined by conventional assay methods, could be assayed by this new RIA.

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A 76-year-old female patient with known Hashimoto's thyroiditis had 12 episodes of acute exacerbation, characterized by high fever and spontaneous pain in the thyroid over a period of 4 months. Percutaneous needle biopsies were performed before and serially after local steroid injection. Histological examination of the thyroid tissue involved obtained before steroid administration revealed quite a unique localized edematous and inflammatory appearance with rich but loosely arranged collagen. fibers, and destruction of follicular structures and swollen degenerated epithelia. Neither remarkable cellular infiltrations nor granulomatous changes were observed in the area involved. Ultrasonogram showed an extremely hypoechoic lesion coincident with the location of pain and tenderness. Intrathyroidal administration of triamcinolone acetate (40 mg) resulted in an immediate relief of pain, fever and localized swelling. Surprisingly, remarkable histological improvements were observed even on the day following the injection. However, clinical manifestations as well as histological changes were reversed again within one week or so. After various therapeutic means, total thyroidectomy was performed which induced disappearance of the manifestations.
The etiology remains unclear, but pathological findings observed in this patient may provide an insight into the pathogenesis of this rare but intractable condition.

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In order to clarify the diurnal pattern of secretion of plasma immunoreactive (IR) proopiomelanocortin (POMC)-derived peptides, IR-N-terminal peptide (Nt), IR-β-endorphin (Ep), IR-β-lipotropin (LPH), and IR-ACTH (ACTH) in normal subjects and in patients with Adisson's disease and Cushing's disease, we measured these 4 peptides in the same plasma obtained at 0900 h and then every three hours until 0600 h at the next day.
All four peptides showed diurnal rhythms with the peaks at 0600 h, and the nadirs of ACTH, LPH, Ep and Nt were at 0000 h, 0000 h, 1800 h and 0300, respectively in normal subjects. In patients with Addison's disease, these four peptides also showed diurnal rhythms with the peaks at 0600 h for ACTH and Ep and at 0900 h for LPH and Nt, and the nadirs at 2100 h for ACTH and Ep and at 0000 h for LPH and Nt. The molar ratios of Ep/ACTH, LPH/ACTH and Nt/ACTH in plasma also presented diurnal variations in normal subjects and in patients with Addison's disease. On the other hand, in patients with Cushing's disease, ACTH, LPH and Nt showed no rhythmicity or change in molar ratios of Ep/ACTH, LPH/ACTH or Nt/ACTH. Only Ep showed diurnal variation. The molar ratios of Ep/ACTH, LPH/ACTH and Nt/ACTH in patients with Cushing's disease were significantly higher than those in normal subjects and in patients with Addison's disease at 0000 h In patients with Cushing's disease, the molar ratios of Ep/ACTH, LPH/ACTH and Nt/ACTH differed in each case and there was no remarkable change in these molar ratios during the 24 hours of a day. These phenomena might be in part due to different half-lives of POMC derived peptides and/or different processing of POMC in each case or at each time during a day.

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Response of growth hormone (GH) release to metoclopramide (MCP), a dopamine antagonist, was evaluated in normal women, hyperprolactinemicamenorrheic patients with pituitary microadenoma and normoprolactinemicamenorrheic patients. Mean basal concentrations of serum GH and prolactin (PRL) in amenorrheic patients were not significantly different from those in normal women except PRL concentrations in hyperprolactinemic patients. Serum GH concentrations significantly increased after MCP administration in normal women and normoprolactinemic-amenorrheic patients, but not in hyperprolactinemic patients. Dopamine causes modest and transient GH secretion in some subjects. Therefore MCP is not likely to stimulate GH secretion through its effect as a dopamine antagonist, and the mechanism of action of MCP on GH secretion is not known. Although the cause of the absence of GH response to MCP in hyperprolactinemic patients is unclear, it may be related to the increased hypothalamic dopaminergic tone which is operative in such patients or it may reflect a direct action of PRL on hypothalamic-pituitary GH regulation.

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Human chorionic gonadotropin (hCG) is considered to be one of the factors which regulate relaxin secretion in humans. Serum immunoreactive relaxin levels are increased and are detectable by radioimmunoassay both in normal and molar pregnancy. Circulating hCG levels are increased in trophoblastic disease. In the present study, relaxin and hCG levels were sequentially measured in patients with invasive mole, choriocarcinoma and presistent trophoblastic disease. Serum relaxin levels were detectable by radioimmunoassay in these patients before treatment, though they were significantly lower than in normal pregnancy. The corpus luteum of pregnancy is the main source of circulating relaxin in normal pregnancy. The existence of a corpus luteum was confirmed in the 2 patients who underwent laparotomy. Consequently, the corpus luteum may also be the main source of circulating relaxin in trophoblastic disease. Parallel changes in hCG and relaxin levels were observed during the courses of trophoblastic disease. The finding suggests that relaxin secretion is dependent on hCG stimulation in trophoblastic disease in the presence of corpus luteum.

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Serum levels of thyrotrophin (TSH), prolactin (PRL), free thyroxine (FT₄) and free triiodothyronine (FT₃) were determined before and after physical exercise in 21 normal male subjects. The subjects were divided into 3 groups as follows: group I-light exercise (exercise on the Mijnhardt bicycle ergometer at 100 Watts for 15 min); group II-moderate exercise (a 5 km marathon); group III-heavy exercise (a 10 km marathon). In group I, TSH level rose from 1.96±0.42μu/ml (mean±SEM) to 2.52±0.30 μu/ml (p<0.01), and PRL levels rose from 11.0±2.0 ng/ml to 19.0±5.2ng/ml (p<0.01). In group II, TSH rose from 2.11±0.51 μu/ml to 2.62±0.56 μu/ml (p<0.05), and PRL rose from 11.2±1.6 ng/ml to 24.0±5.2 ng/ml (p<0.01). In group III, TSH rose from 2.01±0.41μu/ml to 2.36±0.45 μu/ml (p<0.02), and PRL rose from 12.1±2.0 ng/ml to 47.7±9.3ng/ml (p<0.01).
The serum levels of FT4 showed different results among the three groups: Group I showed an increased response from 1.60±0.12ng/dl to 1.72±0.12 ng/dl (p<0.01); Group II showed no significant difference; and group III demonstrated a diminished response from 1.61±0.14 ng/dl to 1.45±0.16 ng/dl (p<0.05). FT:, levels increased in group I from 4.50±0.16 ng/dl to 4.77±0.22 ng/dl (p<0.02), but no statistically significant change was observed in groups II and III. The present investigation demonstrates that physical exercise leads to increased TSH and PRL, whereas short-term continued light exercise results in rises in FT₃ and FT₄ levels, but long-term continued heavy exercise results in the damping of FT₄ levels. TBG levels did not change during the experiment.
He results indicate that the change in the TSH level is not regulated by the feedback mechanism of the hypothalmo-pituitary-thyroid axis alone but that a more complex, but as yet unidentified, mechanism is involved.

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