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5 results on '"Tetsurou Satoh"'

1. Mice Lacking the Thyrotropin-Releasing Hormone Gene: What Do They Tell Us?

Author

Masatomo Mori, Tetsurou Satoh, and Masanobu Yamada

Subjects
endocrine system, medicine.medical_specialty, Pituitary gland, endocrine system diseases, Hormone Replacement Therapy, Endocrinology, Diabetes and Metabolism, Thyrotropin, Thyrotropin-releasing hormone, Endogeny, Biology, Peptides, Cyclic, Piperazines, Embryonic and Fetal Development, Mice, Endocrinology, Hypothyroidism, Pituitary Gland, Anterior, Internal medicine, medicine, Animals, Secretion, Hormone replacement therapy, Cloning, Molecular, Protein Precursors, Thyrotropin-Releasing Hormone, Mice, Knockout, Brain, Embryo, Embryo, Mammalian, Thyroxine, Phenotype, medicine.anatomical_structure, Hypothalamus, hormones, hormone substitutes, and hormone antagonists, Hormone
Abstract

Thyrotropin-releasing hormone (TRH) is localized in the brain hypothalamus and stimulates the secretion and synthesis of pituitary thyrotropin (TSH). Although TRH deficiency caused by artificial hypothalamic destructions has been reported to result in significant decreases in TSH secretion in rodents, clinical observations from the patients with possible TRH deficiency did not entirely agree with these animal results. Because of its ubiquitous distribution throughout the brain and in the peripheral tissues, TRH has been suggested to possess a wide variety of functions in these regions. However, the neurobehavioral and peripheral actions of TRH still remains to be established. It has been, therefore, anticipated that detailed analysis of TRH-knockout mice might provide insight into the physiological significance of endogenous TRH. The present review focuses on the phenotypic findings of mice deficient in TRH.

Published
2003

2. Correction

Author

Tsuyoshi Kouki, Masatomo Mori, Atsushi Suzuki, Tetsurou Satoh, Tadao Iburi, Ritei Uehara, Kumiko Tsuboi, Masaki Nagai, Osamu Isozaki, Hajime Otani, Yoshikazu Nakamura, Shu Wakino, Tsuyoshi Monden, Takashi Akamizu, and Satoshi Teramukai

Subjects
Pediatrics, medicine.medical_specialty, Pathology, Endocrinology, medicine.anatomical_structure, business.industry, Endocrinology, Diabetes and Metabolism, Incidence (epidemiology), Thyroid, medicine, Thyroid storm, business
Published
2012

3. Diagnostic criteria and clinico-epidemiological features of thyroid storm based on a nationwide survey

Author

Masaki Nagai, Atsushi Suzuki, Satoshi Teramukai, Tsuyoshi Monden, Yoshikazu Nakamura, Hajime Otani, Tetsurou Satoh, Shu Wakino, Kumiko Tsuboi, Masatomo Mori, Ritei Uehara, Takashi Akamizu, Osamu Isozaki, Tsuyoshi Kouki, and Tadao Iburi

Subjects
medicine.medical_specialty, Endocrinology, business.industry, Endocrinology, Diabetes and Metabolism, Environmental health, Epidemiology, Thyroid storm, Medicine, business, Nationwide survey
Published
2012

4. Resistance to Thyroid Hormone Due to a Novel Thyroid Hormone Receptor Mutant in a Patient with Hypothyroidism Secondary to Lingual Thyroid and Functional Characterization of the Mutant Receptor.

Author

Yasuyo Nakajima, Masanobu Yamada, Kazuhiko Horiguchi, Tetsurou Satoh, Koshi Hashimoto, Etsuro Tokuhiro, Kazuhiko Onigata, and Masatomo Mori

Subjects
DRUG resistance, HYPOTHYROIDISM, THYROID hormones, HORMONE receptors, NEONATAL diseases, TRIIODOTHYRONINE, PATIENTS
Abstract

Background:We describe a rare case of congenital hypothyroidism and an extremely high serum thyrotropin (TSH) level caused by a combination of resistance to thyroid hormone (RTH) and a lingual thyroid. As the RTH mutant, R316C, was new, the optimum dose of levothyroxine was unclear. To aid in assessment of the therapy, we characterized the mutant R316C thyroid hormone receptor (TR) and compared it with a common mutant, R316H, using in vitrostudies.Summary:The patient was a newborn female having severe hypothyroidism with a free thyroxine level of 0.36 ng/dL and a serum TSH level of 177 μU/mL. A scintiscan showed ectopic lingual thyroid tissue without a normal thyroid gland. Supplementation with levothyroxine at a dose of >350 μg/day did not normalize the serum TSH level; however, the patient showed normal growth and intelligence at 14 years of age. Consistent with the results of a computer analysis, the binding of R316C to triiodothyronine (T3) was significantly decreased to 38% that of the wild type. Electrophoretic mobility shift assay demonstrated that like R316H, R316C did not form a homodimer, but formed a heterodimer with RXR. However, a glutathione-S-transferase pull-down assay showed reduced binding of R316C with NCoR in the absence of T3 and impaired release in the presence of T3. In addition, transient transfection experiments demonstrated that unlike R316H, R316C had severe impairment of transcriptional activity on genes both positively and negatively regulated by thyroid hormone. It also had a clear dominant negative effect on genes negatively, but not positively, regulated by thyroid hormone, including the TSH-releasing hormone and TSHβ genes.Conclusion:This is the first reported case of a R316C TR mutation. The characteristics of the R316C mutant differed from those of the R316H mutant. Our findings suggest that R316C causes reduced association with and impaired release of NCoR, resulting in RTH predominantly at the pituitary level, and that slightly elevated serum TSH level with high dose of levothyroxine might be optimum for normal growth. [ABSTRACT FROM AUTHOR]

Published
2010
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