Irritant contact dermatitis (ICD) is common and poses a significant problem in high-risk populations. In most cases, ICD resolves despite continued exposure in a process known as 'hardening', allowing individuals to continue with their work. Those who cannot clear ICD develop chronic ICD, which is a significant source of emotional, physical, and financial distress for affected individuals. While hardening is well known among labourers and clinicians, its mechanism remains to be elucidated. Much can be learned from the study of self-healing processes like the hardening phenomenon. This overview briefly documents the pathogenesis of ICD, focuses on the latest advances pertaining to the hardening phenomenon in ICD, and then highlights potential avenues of productive research. A better understanding of the 'hardening' process in the skin will hopefully lead to advances for the treatment of ICD.Key words: accommodation; contact dermatitis; hardening; hyporeactivity; irritant; irritant contact dermatitis; skin hyporeactivity. # Blackwell Munksgaard, 2009. Accepted for publication 9 November 2008Irritant contact dermatitis (ICD) is common and poses a significant problem in high-risk populations. As many as 35% of junior hairdressers developed ICD during their first training year (1). In most cases, ICD resolves in spite of continued exposure in a process known as 'hardening', allowing individuals to continue with their work: 90% of hairdressing apprentices who initially suffered from hand eczema during their training period had clearance of the eczema by the end of the training. The eczema persisted in only 10% (2). Those who cannot clear ICD develop chronic ICD. Chronic ICD often manifests on the hands as red, dry, scaly, and fissured skin (3) and is a significant problem for those working in high-risk occupations such as hairdressing, health care, metal work, and cleaning (3). Due to lost workdays and emotional distress, chronic ICD has severe economic implications for workers, companies, and social security systems (4). Most ICD resolves without intervention in a process known as 'hardening' or 'accommodation'. The existence of this self-resolving phenomenon is accepted among labourers and clinicians, but its mechanism remains elusive. While extensive research and a textbook opine on the pathogenesis of irritation and its related factors, research is sparse pertaining to factors that contribute to non-irritated and non-sensitive skin (5). This is likely because the institution of modern science largely focuses on the mechanisms of active disease rather than those of non-disease and illnesses that self-resolve. Much can be learned, however, by studying these self-healing processes. The process of 'hardening' is an example of one of these self-resolving phenomena.This overview briefly documents the pathogenesis of ICD, focuses on the latest advances pertaining to the hardening phenomenon in ICD, and then highlights possible productive areas of research. A better understanding of the 'hardening' process in skin will ho...

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Tetracyclines (TCN) have powerful anti-inflammatory properties in addition to their antimicrobial effects. These anti-inflammatory effects are thought to play a role in inhibiting cutaneous inflammation in patients with rosacea and acne; however, the mechanism(s) of this action remains poorly understood. We have previously shown that adenosine-5′-triphosphate (ATP)γS, a hydrolysis-resistant ATP analogue, augments secretion of pro-inflammatory messengers by a human dermal microvascular endothelial cell line (HMEC-1). ATP released by the sympathetic nerves during stress may stimulate release of pro-inflammatory chemokines by dermal vessel endothelial cells, resulting in recruitment of inflammatory cells and exacerbation of inflammatory skin disease. Here we demonstrate that TCN inhibits ATPγS-induced release of proinflammatory mediators by HMEC-1 cells and primary human dermal microvascular endothelial cells. TCN dose-dependently inhibited ATPγS-induced augmentation of CXCL8 (interleukin-8) and CXCL1 (growth-regulated oncogene-α) production by HMEC-1 cells and primary human dermal endothelial cells in vitro. TCN and ATPγS did not affect HMEC-1 cell viability as determined by trypan-blue exclusion and cell counts. Inhibition of production of inflammatory mediators by endothelial cells may be one mechanism by which TCN improves inflammatory skin diseases. The ability to inhibit release of inflammatory mediators induced in HMEC-1 cells by purinergic agonists may be a useful way to screen for potential therapeutic agents for cutaneous inflammation.

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Dexamethasone treatment of ewes at 70% of gestation results in decreased regional brain water content in the fetuses after multiple but not single treatment courses, in somatic tissues (kidney, liver, muscle, and skin) after multiple courses, and in the liver after a single course.