A brief history of the Department of Dermatology, New York University.
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Biomedical subjects
Publications and source records attributed to B Burrall.
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Controversy still surrounds the recommendation for performing sentinel node biopsy (SLNB) in patients with primary melanoma 1mm or greater in thickness, but why? In the absence of widespread, metastatic disease, nodal status is the single most important prognostic factor which determines likelihood of survival. It allows early therapeutic removal of micrometastatic lymph node disease and identifies patients who are eligible for Interferon alfa-2b adjuvant therapy. SLNB is a requirement for current clinical trials.
Sweet's syndrome, or acute febrile neutrophilic dermatosis, is a condition characterized by the sudden onset of fever, leukocytosis, and tender,erythematous, well-demarcated papules and plaques which show dense neutrophilic infiltrates on histologic examination. Although it ma occur in the absence of other known disease, Sweet's syndrome is often associated with hematologic disease (including leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease). Treatment with systemic corticosteroids is usually successful. skin, Sweet syndrome, neutrophilic dermatosis, corticosteroids,
The present studies demonstrate that incubation of arachidonic acid (AA) with a 20,000 g homogenate (containing both microsomal and cytoplasmic fractions) from UVB-irradiated guinea pig epidermis (24-72 h) resulted in decreased transformation of the [14C]AA into the cyclooxygenase products (PGD2, PGE2, and PGF2 alpha) while the incorporation of 14C into lipoxygenase products (15-HETE and 12-HETE) increased. An investigation into the selective inhibition of the cyclooxygenase pathway revealed that the in vitro transformation of [14C]AA into [14C]-cyclooxygenase products by the 100,000 g particulate fraction prepared from normal unirradiated guinea pig epidermis was inhibited by the 100,000 g cytoplasmic extract prepared from a 24-h postirradiated guinea pig epidermis. These latter data imply that an endogenous inhibitor of the cyclooxygenase pathway is generated and released into the cytoplasm during UVB irradiation and it is likely that this selective inhibition of the cyclooxygenase pathway may contribute at least in part to the increased lipoxygenase products in the 24-h postirradiated skin specimens and possibly the recognized prolonged UVB-induced inflammatory process.