J
James J. Nordlund
Researcher at University of Cincinnati Academic Health Center
Publications - 189
Citations - 8822
James J. Nordlund is an academic researcher from University of Cincinnati Academic Health Center. The author has contributed to research in topics: Vitiligo & Melanocyte. The author has an hindex of 51, co-authored 189 publications receiving 8486 citations. Previous affiliations of James J. Nordlund include National Institutes of Health & Yale University.
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Book
The pigmentary system : physiology and pathophysiology
TL;DR: This chapter discusses thephysiology of the pigmentation system, an overview of human skin color and its disorders, and the treatment of pigmented diseases.
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Binding of melanotropic hormones to the melanocortin receptor MC1R on human melanocytes stimulates proliferation and melanogenesis
TL;DR: The results suggest that alpha- MSH, ACTH, and possibly beta-MSH, but not gamma-MSh, are capable of a physiological role in regulating human pigmentation, and that melanocytes in human skin are a specific target for these hormones.
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Vitiligo in patients with metastatic melanoma: a good prognostic sign.
James J. Nordlund,John M. Kirkwood,Bernadette M. Forget,Gerard Milton,Daniel M. Albert,Aaron B. Lerner +5 more
TL;DR: The data suggest that the appearance of vitiligo in patients with metastatic melanoma portends a longer survival than expected, and the patients with Vitiligo are not necessarily cured and eventually may succumb to metastatic disease.
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The pigmentary system: new interpretations of old data.
TL;DR: It has been stated that a patient can live essentially a "normal" life with nonfunctioning melanocytes (oculocutaneous albinism) or without any cutaneous melanocytes at all (piebaldism or total vitiligo) because pigment and pigment cells are involved in many important activities of the skin and other organs.
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The effects of oral melatonin on skin color and on the release of pituitary hormones.
TL;DR: Melatonin appeared to depress the level of luteinizing hormone (LH) in serum and may have inhibited in some patients the release of growth hormone from the pituitary gland after stimulation by stress or L-dopa.