• Title/Summary/Keyword: Thyrotropin

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A Study on Radiolabelling Method in Radioimmunoassay -Part 1, A New Method for the $^{125}I-Labelling$ of Human Thyrotropin under Mild Conditions- (방사면역측정(放射免疫測定)에서 방사성(放射性) 동위원소(同位元素) 표식법(標識法) 개발에 관한 연구(硏究) -제1편(第1編). Human Thyrotropin의 온화한 조건하 $^{125}I$-표지를 위한 새로운 방법-)

  • Suh, Jung-Hun;Cho, Bo-Yeon;Park, Yong-Ja;Kim, Byong-Kook;Koh, Chang-Soon
    • The Korean Journal of Nuclear Medicine
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    • v.15 no.2
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    • pp.27-33
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    • 1981
  • Human thyrotropin(h-TSH)의 $^{125}I$-표지를 실온서 소량의 Chloramine T를 산화제로 사용하여 수행하였다. 이 방법은 다량의 Chloramine T를 사용하는 종래의 방법과 비교하여 균일한 방사능 표지를 용이하게 하고 강력한 산화제인 Chloramine T에 의한 h-TSH의 파손을 줄여 주었다. 새로운 방법에 의해 합성된 $h-TSH^*$는 항체에 대한 친화도와 유효기간에 있어서 Daiichi 회사의 상품에 비교하여 손색이 없었다.

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Process Development for Large Scale Synthesis of TRH (TRH의 대량합성 제조법 개발)

  • Kim, Dong-Hyeon;Thapa, Pritam;Karki, Radha;Jahng, Yurng-Dong;Lee, Eung-Seok
    • YAKHAK HOEJI
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    • v.51 no.6
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    • pp.490-494
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    • 2007
  • TRH (thyrotropin-releasing hormone) was chemically synthesized utilizing solution phase peptide chemistry for the process development of large scaled synthesis. All the synthetic steps performed in relatively mild conditions, higher yields, easier preparations, minimum racemizations, and separation and purification by recrystallizations.

Radioimmunoassay of Human Thyrotropin - Part 1. Plasma TSH levels in various thyroid functions (갑상선자극(甲狀腺刺戟)홀몬의 방사면역측정(放射免疫測定) - 제1편(第1編) 각종(各種) 갑상선질환(甲狀腺疾患)에 있어서 혈중(血中) TSH의 변동(變動))

  • Koh, Chang-Soon;Lee, Hong-Kyu;Ro, Heung-Kyu;Lee, Mun-Ho
    • 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.

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Enzymatic Degradation and Stabilization of Thyrotropin Releasing Hormone in Various Rabbit Mucosa Extracts (점막 추출액중 치로트로핀 유리호르몬의 효소적 분해 및 안정화)

  • Chun, In-Koo;Shin, Dong-Won
    • Journal of Pharmaceutical Investigation
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    • v.27 no.2
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    • pp.99-108
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    • 1997
  • To evaluate the feasibility of mucosal delivery of thyrotropin releasing hormone (TRH) through various mucosae, enzymatic degradation and stabilization of TRH in the nasal, rectal and duodenal extracts of rabbits were studied. TRH in the extracts was assayed by HPLC and its degradation was found to follow apparent first-order kinetics. The residual concentrations of TRH in the mucosal extracts of nasal, rectal and duodenal segments after 24 hr of incubation were found to be $65.1({\pm}1.1),\;19.7({\pm}2.7)$ and 0%, and in the serosal extracts, $65.6({\pm}5.5),\;75.2({\pm}1.1)$ and $68.7({\pm}1.4)%$, respectively. This result suggests that there is a significant difference in the activity of TRH-degrading enzymes among the sites of administration. The inhibition of TRH degradation in the mucosa extracts was kinetically investigated using various additives such as thimerosal, benzalkonium chloride, disodium edetate, ${\sigma}-phenanthroline$, dithiothreitol and dithioerythritol, and $IC_{50}$ values of inhibitors were calculated. The results obtained showed that thimerosal (0.5 mM) and benzalkonium chloride (0.141 mM) protected TRH from the enzymatic degradation in all the mucosa extracts more than 95% after 24 hr of incubation.

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Enhanced Transmucosal Permeation of Thyrotropin-releasing Hormone (치로트로핀 유리 호르몬의 점막 투과 증진)

  • 전인구;신동원
    • Biomolecules & Therapeutics
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    • v.7 no.3
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    • pp.263-270
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    • 1999
  • The in vitro permeation of thyrotropin-releasing hormone (TRH) through rabbit nasal, rectal and duodenal mucosae was studied in the absence and presence of an enzyme inhibitor and permeation enhancer. TRH in the donor and receptor solutions was assayed by HPLC. When thimerosal (TM, 0.5 mM) was added to the donor cell as an inhibitor, the permeation rate of TRH (200 $\mu\textrm{g}$/ml) increased linearly as a function of time. Fluxes of TRH through the nasal, rectal and duodenal mucosae were found to be 33.3$\pm$5.9, 11.8$\pm$1.9 and 9.6$\pm$0.7 $\mu\textrm{g}$/$\textrm{Cm}^2$/hr, respectively. The addition of sodium glycocholate, glycyrrhizic acid ammonium salt, sodium taurodihydrofusidate or L-$\alpha$-lysophosphatidylcholine to the donor solution containing TM did not result in the significant increase of permeation flux except for the duodenal mucosa, comparing with that in the presence of TM alone. Consequently, it was suggested that the nasal route was advantageous for systemic delivery of TRH, and the addition of TM and/or an enhancer was necessary to maximize the transmucosal permeation of TRH.

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Hyperthyroidism Caused by a Mutation in the Thyrotropin Receptor Gene in Two Brothers (형제에서 발생한 갑상선 자극호르몬 수용체 유전자 돌연변이에 의한 갑상선 항진증 2례)

  • Kim, Jae Hyun;Lee, Sung Soo;Lim, Jung Sup;Shin, Choong Ho;Yang, Sei Won
    • Clinical and Experimental Pediatrics
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    • v.48 no.3
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    • pp.337-341
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    • 2005
  • Thyrotropin receptor(TSHR) mutations must be considered when congenital hyperthyroidism has persisted, but there has been no evidence for autoimmunity. TSHR mutations leading to constitutive activation of the thyroid gland were identified as the molecular cause of autosomal dominant nonautoimmune hyperthyroidism and sporadic congenital hyperthyroidism. We report two cases of hyperthyroidism caused by germline TSHR mutation who presented with exessive sweating and no evidence of autoimmune thyroid disease. They were brothers and their mother had undergone thyroidectomy because of hyperthyroidism. Direct sequencing of the polymerase chain reaction-amplified exon 10 of the TSHR genomic DNA revealed a transition of GCT to GTT, resulting in an exchange of alanine 627 to valine in the patients and their mother. This might be a novel mutation or polymorphism, but we did not perform any functional gene study. But considering the clinical profiles, we can conclude that hyperthyroidism of these two brothers might come from the point mutation described above.