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Masanobu Yamada

Researcher at Gunma University

Publications -  350
Citations -  6641

Masanobu Yamada is an academic researcher from Gunma University. The author has contributed to research in topics: Thyroid hormone receptor & Thyrotropin-releasing hormone. The author has an hindex of 35, co-authored 330 publications receiving 5799 citations. Previous affiliations of Masanobu Yamada include Dokkyo University.

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Identification of nesfatin-1 as a satiety molecule in the hypothalamus

TL;DR: It is shown that nesfatin, corresponding to NEFA/nucleobindin2 (NUCB2), a secreted protein of unknown function, is expressed in the appetite-control hypothalamic nuclei in rats and identified as a satiety molecule that is associated with melanocortin signalling in the hypothalamus.
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Peripheral Administration of Nesfatin-1 Reduces Food Intake in Mice: The Leptin-Independent Mechanism

TL;DR: The findings indicate that the midsegment of nesfatin-1 causes anorexia, possibly by activating POMC and CART neurons in the NTS via a leptin-independent mechanism after peripheral stimulation.
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Tertiary hypothyroidism and hyperglycemia in mice with targeted disruption of the thyrotropin-releasing hormone gene

TL;DR: The TRH-/- mice provide a model of exploiting tertiary hypothyroidism, and that TRH gene abnormalities cause disturbance of insulin secretion resulting in marked hyperglycemia, indicating a direct involvement of TRH in the regulation of thyrotrophs.
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Expression and mutations of KCNJ5 mRNA in Japanese patients with aldosterone-producing adenomas.

TL;DR: A significant number of patients with APA had somatic mutations of the KCNJ5 gene, and KC NJ5 mRNA levels were higher in the APA with mutations than those without, and the expression of KCNH5 mRNA was significantly higher in APA than cortisol-producing adenomas and pheochromocytomas.
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Thymic hyperplasia in patients with Graves' disease. Identification of thyrotropin receptors in human thymus.

TL;DR: Thymic hyperplasia is apparently associated with Graves' disease and it is suggested that thymic thyrotropin receptor may act as an autoantigen that may be involved in the pathophysiology of development of Graves’ disease.