j. Soc. Cosmet. Chem., 39, 321-328 (September/October 1988) Abstracts The Annual Scientific Meetings and Seminars of the Society of Cosmetic Chemists are important venues for informing the participants about the state of the art and recent technical advances in the field of Cosmetic Science. To provide broader dissemination of that information, the Publi- cations Committee has decided to publish abstracts of the technical presentations made at these Meetings and Seminars in the Journal.--The Editor. Society of Cosmetic Chemists Annual Meeting December 1-2, 1988 Waldorf-Astoria Hotel, New York City Program arranged by the Society's Committee on Scientific Affairs Morton Pader, Ph.D., Chairman, 1988 SESSION A ADVANCES IN THE BIOCHEMISTRY OF SKIN Mechanisms of cutaneous photosensitization by psoralens Jeffrey D. Laskin, Ph.D., Department of Environ- mental and Community Medicine, UMDNJ- Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854 The psoralens in combination with ultraviolet light (UVA) are currently used in photomedicine as tan- ning agents and for the treatment of skin disorders such as psoriasis. Our laboratory has been interested in elucidating the mechanism of action of the pso- talens and UVA light in the skin. We have found that these compounds act by binding to specific high-affinity receptors located in the cytoplasm and membranes of responsive cell types. Exposure to UVA light induces receptor alkylation and initiates a biological response. We have found that one im- portant biological response resulting from psoralen receptor alkylation is the inhibition of epidermal growth factor (EGF) binding. The EGF receptor is a transmembrane glycoprotein processing intrinsic tyrosine kinase activity. Inhibition of EGF binding by the psoralens is associated with alterations in the activity of the EGF receptor kinase. Since the EGF receptor is important in regulating epidermal cell growth, the ability of the psoralens and UVA light to modulate its function may underlie the biological effects of these agents in the skin. The role of the epidermal keratinocyte in the measurement of skin immunocompetence and immunosurveillance Fredika M. Robertson, Ph.D., Department of Sur- gery, UMDNJ-Robert Wood Johnson Medical School, Academic Health Sciences Center, New Brunswick, NJ 08903 Our laboratory has been interested in the cellular mechanisms involved in epidermal immunocompe- tence and immunosurveillance. We have recently found that human epidermal keratinocytes can be induced to act functionally like macrophages after exposure to soluble factors from lymphocytes and macrophages, such as gamma interferon and tumor necrosis factor. We found that human keratinocytes can express the class II major histocompatibility an- tigen, process and present antigen to T lympho- cytes, produce elevated levels of interleukin-1, and undergo respiratory burst to produce hydrogen per- oxide. Morphological examination of keratinocytes and macrophages treated with gamma intefferon 321

322 JOURNAL OF THE SOCIETY OF COSMETIC CHEMISTS and tumor necrosis factor alone and in combination revealed similar dramatic increases in cytoplasmic vacuolization in both cell types. These observations strongly implicate the role of the keratinocyte in the maintenance of immunosurveillance, particu- larly in disease states with elevated levels of gamma interferon, such as psoriasis, as well as in the cuta- neous eruptions, infections, and diminished wound-healing abilities of AIDS/ARC patients. SESSION B FRONTIERS OF SCIENCE LECTURE (Spon- sored by Felton Worldwide, Inc.) Growth factors, signal transduction, and pro- tooncogenes in psoriasis John J.Voorhees, M.D., Department of Derma- tology, University of Michigan Medical Center, Ann Arbor, MI 48109-0314 Important participants in the psoriatic lesion are activated keratinocytes, immunocytes, fibroblasts, and endothelial cells. Activated keratinocytes within lesions are characterized by chronically in- creased signal transduction. Work from our labora- tories has shown increased polyphosphoinositide hydrolysis resulting in the formation of increased levels of diacylglycerol (DAG) and inositol tris- phosphate (IP3) in lesions. This increased hydrolysis is due to two phospholipase C (PLC) activities, one that is GTP-dependent and one that is not. DAG and phorbol ester (TPA) activate protein kinase C (PKC) with subsequent down-regulation by binding to the same regulatory domain on the PKC molecule. Thus endogenous DAG levels within le- sions via activation of PKC, in theory, would be analogous to chronic treatment of skin with TPA. TPA treatment of skin leads to hyperplasia, poly- amine formation, eicosanoid release, accelerated ter- minal differentiation, and increased plasminogen activator activity. Biochemical abnormalities similar to those seen in TPA-treated mouse skin are present in psoriatic le- sions, supporting the concept that chronic activa- tion of PKC and resultant down-regulation by DAG in psoriatic lesions is a key regulatory abnor- mality and thus a key location for pharmacological attack. In fact, the simultaneous application of TPA and sphingosine or cyclosporine A (CSA) to mouse skin markedly inhibits the TPA clinical lesion and hyperplasia, polyamine formation, eicosanoid re- lease, and the accelerated terminal differentiation induced by application of TPA. However, sphingo- sine blocks the activation of PKC by DAG, whereas CSA blocks not PKC activation but rather inhibits PKC-inducible molecular events which are distal to PKC activation. PKC activity induces TGF-alpha gene transcription but not the transcription of the TGF-beta. In pso- riatic lesions TGF-alpha messenger RNA and pro- tein are increased, whereas TGF-beta protein is un- detectable. Since TGF-alpha promotes and TGF-beta inhibits epidermal growth, the TGF-alpha overex- pression in psoriatic lesions may be an important participant in the hyperplastic component of the psoriatic process. As well, the lesional levels of c-myc and c-Hras protooncogene messenger RNA are increased. Since these two protooncogenes are intimately involved in the regulation of cell growth, the overexpression of these genes may also be key components of the hyperplastic process in psoriasis. SESSION C GENERAL PAPERS ON HAIR Dandruff: Etiology and response to treatment --A new method to quantify scaling of the scalp D. Saint-Leger, Laboratories de Recherche Avanc•e de L'Oreal, Department de Biophysique, Aulnay- Sous-Bois, France Dandruff is scaling without visible inflammation. The level of dandruff may be quantified by filtering and weighing the dried scales collected by a thor- ough washing of the scalp. Scale productions (mg) per two days highly correlates with clinical gradings. After sonicating the scales into a suspen- sion of single cells, the percentage of nucleated (parakeratotic) cells may be determined, providing a measure of the underlying inflammatory process, which, in turn, correlates with the clinical severity of dandruff. Such a method allows us to demon- strate that: though clinically absent, dandruff has a clear inflammatory origin the percentage of cells with retained nuclei correlates with the size of scales and every scalp (included non-dandruff) pro- duces nucleated scales. The difference between dan- druff and non-dandruff is solely the degree of scaling among the resident flora of the scalp, only P. ovale is of any account. Keeping P. ovale at a low level will prevent recurrence of dandruff the method may be used to assess the effectiveness of anti-fungal agents such as Octopiros © or Omadi- ness© in a shampoo base, though scaling may be suppressed by other means (anti-inflammatory or cytostatic agents) P. ovale is a necessary but insuffi- cient agent for the development of dandruff. Re- garding dandruff as a straightforward infection by P. ovale is an oversimplification. In the light of these findings and examination of histological slides, a new clinical and objective description of dandruff will be discussed.