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Urea is a major component of many daily skincare products which is widely used. Its role in the treatment of, for example atopic skin, atopic eczema, psoriasis and ichthyosis, is undisputed. However, the mode of action of urea is partly still elusive and goes far beyond its assumed passive role. This article shall elucidate biophysical characteristics and properties of molecular biology that explain how urea affects healthy skin and exerts efficacy in various skin diseases. Knowledge about the mode of action of urea enables physicians to better understandthe appropriate use of urea in clinical routine.Urea is a well-known moisturiser and keratolytic topical agent. As it is widely used in dermatology, several formulations at different concentrations have been marketed lotions, creams, foams, ointments, gels and lacquers. Availability of different vehicles and concentration may vary in different countries, but in general products at low, medium and high urea concentration are accessible worldwide. The proper formulation should be chosen according to the disorder to treat, its severity, body areas involved and patients' preference.Urea-based topical compounds at medium concentrations (15%-30%) represent useful dermatological agents for their humectant and keratolytic effects by enhancing stratum corneum hydration and by loosening epidermal keratin, respectively. The aim of this paper is to review the clinical evidences of the use of 15%-30% urea as single topical agent. Although limited evidence supports the use of these concentrations of urea in skin disorders characterised by xerosis and hyperkeratosis, in clinical practice they are largely used especially in xerosis of limited skin areas, in which the side effects are tolerable, or hyperkeratosis involving large or more sensitive (eg, face, genital region, etc) areas, in which higher concentration may be irritant. In addition, urea at medium concentrations is used in combination with other substances including topical antifungals as penetration enhancer.Urea, also known as carbamide, is a polar, hygroscopic molecule produced by the human body that was first discovered in urine in 1773 by the French chemist Hilaire Rouelle and was artificially synthesised from inorganic precursors in 1828 by the German chemist Friedrich Wöhler. The importance of urea in dermatology is twofold it primarily has a physiological key role for the maintenance of skin hydration, and it secondarily has been used for more than a century in different topical preparation and concentration in various skin conditions. One of the first uses of urea was the topical treatment of wounds because of its antibacterial and proteolytic properties. Since the second part of the 20th century, urea became one of the most common moisturisers and keratolytic agents, useful for the treatment of xerosis, atopic dermatitis, ichthyosis and psoriasis.Urea is a hygroscopic molecule that, because of its moisturising properties, is topically used for the treatment of skin dryness at concentrations ranging from 2% to 12% in different formulations. Based on existing literature, low-concentration urea-containing products are effective in the treatment and/or prevention of xerosis in some skin disorders such as ichthyosis, atopic dermatitis and psoriasis, or unrelated to specific skin diseases. Generally, urea formulations at low concentration are well-tolerated and suited for the treatment of large skin areas, once or twice daily, even for a long period of time. selleckchem At low concentrations stinging and burning sensation is rare and transient, whit no reported sensitisation despite its widespread use.Pemphigus is a group of immune-mediated blistering diseases of skin and mucus membrane caused by destruction of the intercellular junction (desmosomes) by autoantibodies. Pemphigus vulgaris (PV) is considered the most common type of all pemphigus family. Various cytokines play a major role in pemphigus pathogenesis. Interleukin-33 (IL-33) role has been studied in various autoimmune diseases as; psoriasis and rheumatoid arthritis, yet it has not been studied in Egyptian patients with PV. The study aimed to evaluate the possible role of IL-33 in PV by assessing its level in the serum using ELISA and to detect its correlation with activity score using Pemphigus Disease Area Index (PDAI). Forty-four patients with PV and 36 age and sex-matched healthy controls were enrolled in the study. After full history taking and complete dermatological examination, the severity score was calculated using PDAI, then serum samples were taken from each patient and control subjects and subjected to quantitative measurement of serum IL-33 using ELISA. Serum level of IL-33 is significantly raised in PV patients compared to control subjects (P-value = .007). The level of IL-33 was found to be strongly correlated with the activity of the disease measured by PDAI. IL-33 might have a role in PV pathogenesis as shown by its rising level in PV patients. In addition, serum level of IL-33 is strongly correlated with the activity of PV. Thus, we suspect that IL-33 can be used as marker for monitoring PV severity and measuring treatment efficacy.Previously, we identified differentially expressed proteins, including ADFP, between lung adenocarcinoma (LAC) tissue and paired normal bronchioloalveolar epithelium. In this study, we investigated the role of ADFP in LAC. ADFP levels in the serum of patients with lung cancer and benign diseases were measured by enzyme-linked immunosorbent assays (ELISA). shRNA was used to knock-down or overexpress ADFP in A549 and NCI-H1299 cells. The biological function of ADFP and its underlying mechanisms was evaluated in vivo and in vitro. ADFP was highly expressed in the serum of lung cancer patients, especially those with LAC. ADFP promoted cell proliferation and up-regulated the p-Akt/Akt ratio in A549 and NCI-H1299 cells in vitro. Furthermore, in nude mice, ADFP promoted tumour formation with high levels of p-Akt/Akt, Ki67 and proliferating cell nuclear antigen (PCNA). Similar to the effect of ADFP knock-down, MK-2206 (a phosphorylation inhibitor of Akt) reduced A549 and NCI-H1299 cell proliferation. In ADFP-overexpressing A549 and NCI-H1299 cells, proliferation was suppressed by MK-2206 and returned to the control level.
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