Within their first days of life, newborns' skin undergoes various adaptation processes needed to accommodate the transition from the wet uterine environment to the dry atmosphere. The skin of newborns and infants is considered as a physiological fragile skin, a skin with lower resistance to aggressions. Fragile skin is divided into four categories up to its origin: physiological fragile skin (age, location), pathological fragile skin (acute and chronic), circumstantial fragile skin (due to environmental extrinsic factors or intrinsic factors such as stress) and iatrogenic fragile skin. Extensive research of the past 10 years have proven evidence that at birth albeit showing a nearly perfect appearance, newborn skin is structurally and functionally immature compared to adult skin undergoing a physiological maturation process after birth at least throughout the first year of life. This article is an overview of all known data about fragility of epidermis in 'fragile populations': newborns, children and adolescents. It includes the recent pathological, pathophysiological and clinical data about fragility of epidermis in various dermatological diseases, such as atopic dermatitis, acne, rosacea, contact dermatitis, irritative dermatitis and focus on UV protection .

Bacterial infections (e.g., with Staphylococcus aureus) are serious problems in skin with a compromised barrier, such as in patients with atopic dermatitis. Previously, it was shown that tight junction (TJ) proteins are influenced by staphylococcal infection, and TJ function is impaired after infection of the keratinocyte cell line HaCaT. However, functional studies in cells or models more similar to human skin are missing. Therefore, we investigated bacterial colonialization and infection with live S. aureus in primary human keratinocytes and reconstructed human epidermis (RHE). We show that short-term inoculation results in increased TJ barrier function-which could not be seen in HaCaT cells-hinting at an early protective effect. This is accompanied by occludin phosphorylation and sustained localization of occludin and claudin-4 at cell membranes. Long-term incubation resulted in decreased presence of claudin-1 and claudin-4 at cell membranes and decreased TJ barrier function. The agr regulon of S. aureus plays a role in the increasing but not in the decreasing effect. Proinflammatory cytokines, which are produced as a result of S. aureus inoculation, influence both phases. In summary, we show here that S. aureus can have short-term promoting effects on the TJ barrier, while in the long term it results in disturbance of TJs.

ORS cell-based reconstructed epidermis is a valid and reproducible model for human epidermis and it may be used to evaluate the effects of active substances and cosmetic formulations.

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The use of L-dopa in the treatment of Parkinsonism represents a great advance but we are becoming increasingly aware of the problems involved with its lo.ng-term use-side effects, abnormal involuntary movements, diurnal oscillations in performance ("on-off" effects), and loss of therapeutic efficiency after several years' treatment. Therefore, other substances are being sought to replace or to be used in conjunction with L-dopa. It is for these reasons that dopaminergic agonists have been synthesised: apomorphine, piribedil, lergotrile, N-propyl-aporphine and, more recently, bromocriptine (CB 154 Sandoz; Parlodel).First used for its inhibitory properties on prolactin secretion, bromocriptine also stimulates the postsynaptic (Corrodi et al., 1973) and presynaptic (Snider et al., 1976) central dopaminergic receptors which renders it suitable for the treatment of Parkinson's disease. Bromocriptine also seems to have a stimulating action on the serotoninergic receptors (Corrodi et al., 1975; Snider et al., 1976).Since the first clinical trials done by Calne and co-workers (1974a, b), bromocriptine has been the object of numerous studies. It improves the extrapyramidal symptoms (mainly tremor and rigidity) not only at low doses (20 to 30 mg) in conjunction Address for reprint requests: Professor A. Rascol,