Controlling leprosy.
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Biomedical subjects
Publications and source records attributed to C L Crawford.
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The effect of topical application of ascorbic acid (AA) and ascorbyl palmitate (AP) on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced tumor promotion in mouse skin was investigated. A single application of TPA decreased epidermal AA by 45%. Repetitive application of 6 and 28 mumol AA with 2 nmol TPA inhibited tumor multiplicity by 39% and 76%. Repetitive application of 0.16, 0.8, and 4.0 mumol AA with 5 nmol TPA inhibited tumor multiplicity by 16%, 46%, and 91%. Because AA may be poorly absorbed cutaneously, we evaluated the effect of dietary AA. Supplementation of drinking water with AA increased epidermal ascorbic acid levels by 50%. Dietary intake of AA did not inhibit TPA-induced tumor promotion. Preliminary data suggest that the mice not receiving AA developed increased epidermal AA levels in response to the tumor promoting regimen. Recently we have found that dietary AP inhibited TPA-induced biochemical parameters associated with tumor promotion.
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Rabbits previously sensitised by injection of human sensory peripheral nerve showed degeneration of somatic unmyelinated fibres at skin test sites when challenged by sensory nerve or certain non-myelin fractions prepared from human sensory nerve. Epithelioid cells were found in the endoneurium and may mediate the nerve damage. The degeneration was consistently found and lasted for at least 58 days. Phagocytosing macrophages were absent. Differences in the pattern of nerve damage to that of EAN and EAE are discussed.
We report the isolation of four independently selected mutations (scs) in the c17 promoter of phage lambda that reduce or eliminate the promoter activity. The c17 promoter is not normally present in lambda, and has been shown to be generated by a tandem duplication which creates a "Pribnow Box," a heptamer sequence implicated in promoter activity. This sequence is located upstream from the site of transcription initiation and is present, with some variation, in all promoters whose sequences have been determined. Analysis of the c17 duplications carrying the scs mutations reveals that three of these mutants carry single base-pair changes in the most highly conserved base pairs of the Pribnow Box and that the other mutation is a reversion to the wild type sequence in this region (i.e., a loss of the duplicated base pairs).
Epithelioid cell granulomas were induced in rabbits previously sensitised with human sensory peripheral nerve extract by skin testing with homogenate of sural nerve. Ultrastructurally some of the cells contained in their cytoplasm abundant and dilated rough endoplasmic reticulum filled with a moderately dense product while the cytoplasm of other cells contained numerous membrane-bound vesicles. These cells show all the ultrastructural characteristics of epithelioid cells found in human granulomatous disease and in human states of granulomatous hypersensitivity. Thus we have developed an animal model which supports the concept of granulomatous hypersensitivity as a distinct entity in humans to be differentiated from foreign body and delayed-type hypersensitivity reactions. The model may also prove important in elucidating the pathogenesis of granuloma formation in non-lepromatous leprosy and other granulomatous disease and in defining the nature of the products of epithelioid cells.
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