• Archives of Pharmacal Research
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• v.21 no.3
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• pp.231-235
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• 1998

A sensitive enzyme immunoassay for serum TSH has been developed utilizing the tight binding between biotin and avidin, and three layered protein polystyrene beads as solid phase. To increase binding capacity of TSH and sensitivity of the assay, the polystyrene beads were coated sequentially with mouse immunoglobulin as first layer, rabbit antimouse immunoglobulin as second layer and monoclonal anti-TSH as third layer. A serum sample was incubated simultaneously with a monoclonal anti-TSH immobilized polystyrene beads and a second monoclonal anti-TSH covalently attached to biotin. After washing, the antibody bound serum TSH-anti-TSH-biotin complex is reacted with horseradish peroxidase (HRP)-labeled avidin. Following second wash, the bound HRP activity was measured calorimetrically. Reproducible results were obtained within 4 hours for serum TSH in the range between $0{\mu}\textrm{IU}$ml and ${50}{\mu}\textrm{IU}$ml with detection limit of $0.1{\mu}\textrm{IU}$ per test.

• The Korean Journal of Nuclear Medicine
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• v.13 no.1_2
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• pp.31-36
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• 1979

The TRH stimulation test was known as a highly diagnostic method in hypothalamopituitary disorders. To evaluate the location and the extension of the lesion, we estimated TSH response to TRH test in 27 patients. Correlation between volume of sella and TSH response was also studied. The results obtained were as follows: 1. In Sheehan's syndrome, TSH response after TRH test were not observed in all of 12 patients. 2. All 2 acromegaly patients showed normal TSH response. 3. In 4 cases of chromophobe adenoma, 2 cases showed no TSH response. In 2 responded cases, one patient whose tumor mass extended to suprasella region was hypothyroid state. 4. In craniopharyingioma 3 cases, the tumor which extended to intrasella showed hypothyroid and no TSH response. 5. Correlation between volume of sella and TSH response were valuable in 2 cases, but no diagnostic significance. 6. In diabetes inspidus, TSH response were all absent. 7. In primary amenorrhea, TSH response observed in 1 case, which conformed with isolated FSH deficiency.

• The Korean Journal of Nuclear Medicine
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• v.21 no.2
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• pp.143-150
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• 1987

To assess the analytic performance of immunoradiometric TSH assay (IRMA TSH), assay precision determined by intra and interassay variance, assay accuracy determined by dilution and recovery study, were evaluated by using two commercial kit $(Abott^{(R)}\;and\;Daichi^{(R)})$. Normal range of basal serum TSH and TRH stimulated TSH increment were also determined in 234 healthy subjects (male 110, female 124; age 20-70) and 30 voluteers (male 10, female 20; age 21-26). In addition, basal TSH levels of 70 patients with untreated hyperthyroidism, 50 untreated hypothyroidism, and 60 euthyroidism were measured to assess the clinical utility of IRMA TSH. The detection limit of IRMA TSH was 0.04 mU/l and 0.08 mU/l by Abott Kit and Daichi kit respectively. Using Abott kit, intra assay variance were 2.0, 3.1 and 1.4% in mean TSH concentration 2.4, 31.6 and 98.2 mU/l repectively and interassay variance were 2.0 and 3.2% in mean TSH concentration 2.3 and 31.3 mU/l. Mean recovery rate was 92.5% and dilution study showed nearly straight line. When Daichi kit was used, intrasssay variance were 5.6, 5.2 and 6.2% in mean TSH concentration of 2.4, 31.6 and 98.2 mU/l respectively and interassay variance were 7.1 and 7.4% in mean TSH of 2.3 and 31.3 mU/l. Mean recoveray rate was 89.9%. Normal range of basal TSH and TRH stimulated peak TSH were 0.38-4.02 mU/l and 2.85-30.8 mU/l repectively (95% confidence interval, Abott kit used). Sensitivity and specificity of basal TSH levels for diagnosing hypothyroidism as well as specificity for diagnosing hyperthyroidism were 100% by using both kit. Sensitivity of basal TSH level for diagnosing hyperthyroidism was 100% when TSH levels were measured by Abott kit while that was 80.9% when measured by Daichi kit. These results suggest that IRMA TSH was very precise and accurate method and might be used as a first line test in the evaluation of thyroid function.

• Korean Journal of Veterinary Research
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• v.32 no.2
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• pp.165-173
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• 1992

The present study was carried out to investigate the effects of dopaminergic drugs and the role of specific dopamine(DA) receptors on the release of TSH, $T_4$ and $T_3$. Serum TSH levels (cold-induced, $4{^{\circ}C}$) were determined using RIA(radioimmunoassay) at 30 min after administration of dopamine agonists and antagonists. Serum $T_4$ and $T_3$ levels were detected after these dopaminergic drugs were administered subcutaneously twice a day for a week. The results of the study are summarized as follows : Apomorphine, a nonspecific DA receptor agonist, produced a dose-depedent decrease in serum TSH, $T_4$ and $T_3$ levels. However, only low doses (0.3, 1.0mg/kg) of SKF38393, a specific $D_1$-receptor agonist, produced a decrease in serum lelvels of TSH. I,Y171555, a specific $D_2$-receptor agonist, produced a dose dependent decrease in serum TSH, $T_4$ and $T_3$ levels. However, SCH23390, a specific $D_1$-receptor antagonist, produced a decrease except in serum T levels which were increased dose dependently. High doses (1.0, 3.0mg/kg) of sulpiride, a specific $D_2$-receptor antagonist, made a increase in the serum levels of TSH and $T_3$. The effects of dopaminergic drugs in serum TSH and $T_4$ levels was potentiated by the pretreatment of apomorphine. The overall results of this study suggest that the regulation of TSH, $T_4$ and $T_3$ secretion were mediated via specific $D_1$ and $D_2$ receptor.

• International journal of thyroidology
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• v.10 no.2
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• pp.71-76
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• 2017

Background and Objectives: The role of thyroid-stimulating hormone (TSH) signaling on osteoblastic differentiation is still undetermined. The aim of this study was to investigate the effects of 5-aza-2'-deoxycytidine (5-azacytidine) on TSH-mediated regulations of osteoblasts. Materials and Methods: MG63, a human osteoblastic cell-line, was treated with 5-azacytidine before inducing osteogenic differentiation using osteogenic medium (OM) containing L-ascorbic acid and ${\beta}$-glyceophosphate. Bovine TSH or monoclonal TSH receptor stimulating antibody (TSAb) was treated. Quantitative real-time PCR analyses or measurement of alkaline phosphatase activities were performed for evaluating osteoblastic differentiation. Results: Studies for osteogenic-related genes or alkaline phosphatase activity demonstrated that treatment of TSH or TSAb alone had no effects on osteoblastic differentiation in MG63 cells. However, treatment of 5-azacytidine, per se, significantly increased osteoblastic differentiation and combination treatment of 5-azacytidine and TSH or TSAb in the condition of OM showed further significant increase of osteoblastic differentiation. Conclusion: Stimulating TSH signaling has little effects on osteoblastic differentiation in vitro. However, in the condition of epigenetic modification using inhibitor of DNA methylation, TSH signaling positively affects osteoblastic differentiation in human osteoblasts.

• The Korean Journal of Nuclear Medicine
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• v.9 no.2
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• pp.1-11
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• 1975

The serum concentrations of thyrotropin (TSH) were measured by means of radioimmunoassay, in 98 cases of normal controls, 51 cases of hyperthyroidism, 80 cases of primary hypothyroidism and 4 cases of secondary hypothyroidism to evaluate the diagnostic significance in various functional states of the thyroid. The obtained data were analyzed in correlation with other thyroid function test values in various phases of the functional thyroid diseases. The results were as follows: 1) The serum TSH concentration in normal control group was $<1.3{\sim}8.0{\mu}U/ml$. 2) The measurement of serum TSH was more significant in diagnostic accuracy compared with that of serum $T_4(75.0{\pm}12.2%)$. Free $T_4$ Index ($64.2{\pm}15.2%$), serum $T_3(41.0{\pm}21.0%)\;or\;T_3$ resin uptake ($41.1{\pm}15.8%$) in evaluation of primary hypothyroidism. 3) In case of overt hypothyroidism, the serum TSH and $T_4$ were both abnormal, compatible with the clinical diagnosis, while in case of preclinical or mild hypothyroidism, the serum $T_4(41.2{\pm}23.8%)\;or\;50.0{\pm}25.0%)$ was much less reliable than serum TSH. 4) In the treatment of primary hypothyroidism with desiccated thyroid, the administration of 1 grain of the hormone per day was sufficient to suppress the serum concentration of TSH to normal range. It showed that the measurement of serum TSH concentration was a significant criteria in evaluating the efficiency of the treatment of hypothyroidism. 5) The measurement of serum TSH concentration is a very significant method in the early detection of hypothyroidism induced during or after the treatment of the hyperthyroidism with antithyroid drugs or radioactive Iodine ($^{131}I$).

• The Korean Journal of Nuclear Medicine
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• v.6 no.2
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• pp.41-47
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• 1972

The radioimmunoassay of human thyrotropin was performed in various thyroid states, utilizing the anti-h-T.S.H. antibody and purified human thyrotropin supplied from National Institute of Arthritis and Metabolic Diseases, Bethesda, Ma., U.S.A., and human thyrotropin standard-A obtained from National Institute for Biologic Standards, Mill Hill, London, England. $^{131}I$ labelled h-TSH was prepared after the Chloramine-T method of Greenwood et al. This double antibody system had a assay sensitivity of about $1.0{\mu}U/ml$ of plasma HTS-A and could detect the plasma h-TSH level in the euthyroid patients. Plasma h-TSH level of the normal 26 Korean was $1.1{\pm}0.83{\mu}U/ml$, and that of the 8 hypothyroidisms were 8.3 to $67.5{\mu}U/ml$. In hyperthyroidisms, no cases showed the plasma h-TSH levels over $1.0{\mu}U/ml$. Between the hypothyroidism and euthyroidsm, no overlap is noticed on plasma h-TSH levels. A case of transient hypothyroid state identified by determination of plasma h-TSH level is presented. These results revealed that the radioimmunoassay of h-TSH in plasma could be a sensitive method to diagnose the hypothyroidsm, if not caused by a pituitary disease.

• Journal of Life Science
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• v.10 no.2
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• pp.150-156
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• 2000

This experiment was performed to evaluate the effect of TSH (thyroid-stimulating) on the ERp29 (endoplasmic reticulum resident 29 kDa protein) gene expression in the rat thyrocytes of FRTL-5 cells. Although ERp29 mRNA was constantly expressed, its expression began to increase remarkably from 10-9 M TSH. and its maximum expression was at 5×10-9 M TSH (about 3.5 fold). On the other hand, the effect of TSH on the abundance of ERp29 mRNA started within 6 h, and peaked at 8 h (about 2.5 fold). Actinomycin D (transcription inhibitor) strongly blocked this effect while cycloheximide (translation inhibitor) did not. The half-life of ERp29 mRNA was about 4.5 h in the presence or absence of TSH that was not affected by the stability of ERp29 mRNA. The effect of TSH on the ERp29 gene expression was specific, while other growth factors (transfferin, insulin, and hydrocortisone) did not alter its expression. Our data indicate for the first time that the expression of ERp29 is regulated transcriptionally by TSH in the thyrocytes.

• The Korean Journal of Nuclear Medicine
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• v.14 no.2
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• pp.53-60
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• 1980

The radioimmunoassay of TSH (human thyrotropin) was performed by utilizing anti-h-TSH antibody and purified human thyrotropin supplied from Daiichi Radioisotope company in Japan. From Jan. 1978 through Aug. 1980 the serum concentration of TSH was measured on 41 cases with various thyroid diseases, and 22 normal persons. Among 41 cases, 9(22%) were primary hypothyroidism, 17(41%) Graves' disease, 8(20%), subacute or chronic lymphocytic thyroiditis, and 7(17%) nodular goiter. The results were as follows: 1) The normal values of serum TSH in 22 cases of control group were $4.2{\pm}1.7{\mu}U/ml(1.9-7.4{\mu}U/ml)$, which were within normal range in kit used in this study. 2) The serum TSH concentration in 9 cases with primary hypothroidism were $97.1{\pm}116.4{\mu}U/ml(14.0-300{\mu}U/ml)$, which were significantly elevated as compared with normal control values. 3) The serum TSH concentration in 17 cases with Graves' disease were $1.5{\pm}0.6{\mu}U/ml(1.0-2.5{\mu}U/ml)$, which were below than normal control. 4) The serum TSH concentration in 8 cases with subacute or chronic lymphocytic thyroiditis. revealed wide ranges ($1.6-220{\mu}U/ml$) according to the state of thyroid function. 5) The serum TSH values in 7 cases with nodular goiters were $2.3{\pm}2.0{\mu}U/ml$, which were strictly within normal levels. 6) The serum TSH levels were elevated during prolonged treatment with Tapazole (Methimazole) without serial check of the serum TSH concentration in Graves' disease, so the serial measurement of serum TSH concentration was considered of available index of thyroid states.

• The Korean Journal of Nuclear Medicine
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• v.14 no.1
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• pp.1-8
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• 1980

Serum TSH levels were measured by radioimmunoassay before and after intravenous administration of synthetic thyrotropin-releasing hormone (TRH) to 15 normal subjects and 55 patients with primary thyroid disease (14 patients with euthyroidism, 24 patients with thyrotoxicosis and 17 patients with hypothyroidism) to evaluate pituitary TSH reserve and its diagnostic availability. The observed results were as follows. 1. In normal subjects, serum TSH responses to synthetic TRH were $3.2{\pm}1.0$ at 0min (baseline TSH level), $8.0{\pm}4.0$ at 10min, $11.7{\pm}5.0$ at 20min, $13.7{\pm}7.1$ at 30min, $9.7{\pm}5.0$ at 60min., $5.2{\pm}2.0$ at 120min. and $3.6{\pm}0.4{\mu}U/ml$ at 180 min. Serum TSH peaked at $20{\sim}30$ minutes and returned nearly to baseline at 180minutes. 2. In euthyroid group, serum TSH responses to synthetic TRH were $3.3{\pm}1.6$ at 0min, $8.6{\pm}8.0$ at 10min, $10.9{\pm}8.5$ at 20min, $12.5{\pm}8.4$ at 30min, $9.0{\pm}5.9$ at 60min, $5.6{\pm}2.6$ at 120min and $3.5{\pm}1.3{\mu}U/ml$ at 180min. No significant difference revealed between euthyroid group and normal subjects (p>0.05). 3. In hyperthyroid group, serum TSH responses to synthetic TRH were $1.5{\pm}0.6$ at 0min, $2.2{\pm}0.8$ at 10min., $2.3{\pm}1.0$ at 20min., $2.4{\pm}1.5$ at 30min., $2.1{\pm}1.1$ at 60min., $1.9{\pm}0.2$ at 120min. and $1.5{\pm}0.8{\mu}U/ml$ at 180min., No response to TRH showed. 4. In hypothyroid group, mean values of serum TSH response to synthetic TRH were 42.0 at 0min., 60.6 at 10min., 124.8 at 20min., 123.0 at 30min., 101.6 at 60min., 64.3 at 120min. and $15.5{\mu}U/ml$ at 180 min., Patients with primary hypothyroidism showed an exaggerated TSH response to synthetic TRH despite their high basal TSH. 5. Side effects attending synthetic TRH administration were transient nausea (59.0%), desire to micturate (59.0%), feeling of flushing(19.7%), dizziness (45.9%), metallic taste (9.8%) and headache (19.7%). Any side effect didn't show in 16.4%. These symptoms began almost immediately after TRH intravenous injection and lasted several minutes, and not related to dose or response in the person experiencing it.