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Hiroshi Demura

Researcher at Tohoku University

Publications -  367
Citations -  12438

Hiroshi Demura is an academic researcher from Tohoku University. The author has contributed to research in topics: Hypothalamus & Pituitary gland. The author has an hindex of 60, co-authored 367 publications receiving 12235 citations. Previous affiliations of Hiroshi Demura include Tokyo Institute of Technology & Hirosaki University.

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Anabolic effects of 1,25-dihydroxyvitamin D3 on osteoblasts are enhanced by vascular endothelial growth factor produced by osteoblasts and by growth factors produced by endothelial cells.

TL;DR: 1,25-(OH)2D3 exerts an anabolic effect on osteoblasts by enhancing their production of VEGF, which stimulates its receptors on endothelial cells, followed by increased production of osteotropic growth factors, such as insulin-like growth factor I and ET-1.
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The responses of plasma adrenocorticotropin and cortisol to corticotropin-releasing hormone (CRH) and cerebrospinal fluid immunoreactive CRH in anorexia nervosa patients

TL;DR: It is suggested that hypersecretion of CRH may occur in patients with anorexia nervosa, and the concentrations of immunoreactive CRH in cerebrospinal fluid were measured.
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Age-related changes in plasma growth hormone response to growth hormone-releasing factor in man.

TL;DR: Results suggest that somatotroph cells become less sensitive to growth hormone-releasing factor with aging, and plasma growth hormone increased markedly after hpGRF-44 injection in all men in their twenties and thirties.
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Intracerebroventricular administration of corticotropin-releasing factor inducesc-fos mRNA expression in brain regions related to stress responses: comparison with pattern ofc-fos mRNA induction after stress

TL;DR: It is suggested thatCRF produces c-fos mRNA expression in the brain areas related to stress response, and that CRF may induce behavioral and neuroendocrine responses through activating these brain structures, such as the limbic system and the hypothalamic nuclei.
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Interleukin-1 stimulates corticotropin-releasing factor gene expression in rat hypothalamus.

TL;DR: Results indicate that acute administration of IL-1 alpha and -beta stimulates gene expression of hypothalamic CRF and CRF release, which causes the stimulation of ACTH release and POMC gene expression in AP.