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Prepuberal castration of male rabbits of the New Zealand White breed arrests growth and leads after about 10 weeks to regressive changes in the auricular sebaceous glands. Treatment of such castrates with high doses of a depot androgen preparation (Triolandren® i.m.) for 4 weeks, on the other hand, causes hyperplasia of the auricular glands, which already begins to develop after a few injections, though it does not reach its maximum until some weeks after the androgen treatment has been withdrawn. This experimental model consequently seems well suited for the evaluation of inhibitors and stimulators of the activity of the sebaceous glands.

Local application of alpha-l-fucose on the ear before elicitation of contact allergy to dinitrofluorobenzene (DNFB) in BALB/c mice results in a suppression of the contact allergic response. However, local application of alpha-l-fucose at the sensitization site on the abdominal wall before sensitizing the animals with DNFB had no inhibitory effect on contact allergy. Alpha-l-fucose has been demonstrated to inhibit lymphokine activity in vitro and manifestation of cellular immunity in vivo. Our results suggest that alpha-l-fucose suppresses contact allergy by locally inhibiting the efferent phase of the cellular immune response.

Epidermal thinning of mouse tail skin was compared for commercial preparations of clobetasol propionate (Dermovate), clobetasone butyrate (Eumovate), fluocinonide (Metosyn), and hydrocortisone butyrate (Locoid). The thickness measurements were ranked with those for hydrocortisone (1%), betamethasone valerate (Betnovate), triamcinolone acetonide (Ledercort), fluocinolone acetonide (Synalar), and prednisolone stearoylglycolate (Sinistrone) obtained in a previous study (Spearman and Jarrett, 1975). All steroids caused epidermal thinning, except clobetasone butyrate. Some cream and ointment vehicles were also assayed. Epidermal thickening was caused by the cream and ointment vehicles used for Eumovate and also by the cream employed for Locoid formulation.