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  Vol. 86 No. 2, August 1962 TABLE OF CONTENTS
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Glycogen Response in Human Epidermal Basal Cell

WALTER C. LOBITZ, JR., M.D.; DORIS BROPHY, Lic. es. Sc.; ALBERT E. LARNER, M.D., Ph.D.; FARRINGTON DANIELS, JR., M.D., Ph.D.

Arch Dermatol. 1962;86(2):207-211.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Living organisms can respond to a stimulus at 3 levels: (1) the cell; (2) the tissue; (3) the organism as a whole. Although the earliest response to a stimulus is at the cellular level, inflammation is basically a tissue response. By the time an inflammatory disease of the skin is apparent, however, it is too late to observe how the tissue responses evolve to produce the clinical lesion. The purpose of this paper is to present evidence that cytoplasmic glycogen in the human epidermal basal cell may indicate at the cellular level that an inflammatory stimulus has reached the skin before the tissue as a whole has reacted sufficiently to appear inflamed.

Three types of experimental stimuli were used: removal of the stratum corneum,1-4,8,10 minimal erythema from the sunburn wavelength of ultraviolet light,5,9 and a horizontal cut through the dermis below an intact epidermis.6,11

As previously described, . . . [Full Text PDF of this Article]


Author Affiliations

PORTLAND, ORE.; CHICAGO

Professor and Head, Division of Dermatology (Dr. Lobitz), Lic. es. Sc., Research Associate (Doris Brophy), National Institutes of Health Trainee (Dr. Larner), Division of Dermatology, University of Oregon Medical School; Associate Professor of Dermatology (Dr. Daniels), University of Illinois College of Medicine.


Footnotes

Read before the 82d Annual Meeting of the American Dermatological Association, Inc., Chandler, Ariz., March 30, 1962.

This investigation was supported (in part) by the U.S. Army Research and Development Command under contract DA-49-193-MD-2184; by a PHS training grant, 2A-5300, from the National Institute of Arthritis and Metabolic Diseases, Public Health Service; and by a PHS research grant, E-3102(C2), National Institute of Allergy and Infectious Diseases, Public Health Service.



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