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Langton A.K.,Dermatological science | Sherratt M.J.,University of Manchester | Griffiths C.E.M.,Dermatological science | Watson R.E.B.,Dermatological science
International Journal of Cosmetic Science | Year: 2010

Cutaneous ageing is the result of two distinct, biological processes which may occur concurrently: (i) the passage of time, termed intrinsic ageing and (ii) environmental influences, termed extrinsic ageing. Intrinsic ageing of the skin is a slow process which causes changes in tissue structure and impairs function in the absence of additional biological, chemical and physical factors. The clinical features of intrinsically aged skin are not usually evident until old age when, although smooth and unblemished, the skin surface appears pale and is characterized by fine wrinkles with occasional exaggerated expression lines. Functionally, intrinsically aged skin is dry and less elastic than more youthful skin. In contrast, extrinsically aged skin is exemplified by deep, coarse wrinkles, mottled hyperpigmentation and a marked loss of elasticity and recoil. The two major environmental influences which induce extrinsic ageing are: (i) chronic exposure to solar ultraviolet (UV) irradiation (termed photoageing) and (ii) smoking. This review discusses the changes associated with the ageing process in the skin, with particular emphasis on the role played by the elastic fibre network in maintaining dermal function. The review concludes with a discussion of a short-term assay for independent assessment of the efficacy of anti-ageing cosmetic products using the elastic fibre component fibrillin-1 as a biomarker of extracellular matrix repair. © 2010 Society of Cosmetic Scientists and the Société Française de Cosmétologie. Source

Laws P.,Dermatological science | Barton A.,University of Manchester | Warren R.B.,Dermatological science
Journal of the European Academy of Dermatology and Venereology | Year: 2010

Psoriasis is commonly associated with a co-existent arthritis known as psoriatic arthritis (PsA). Although there is some treatment overlap for psoriasis and psoriatic arthritis, it is possible that dermatologists may not diagnose or treat appropriately patients who are developing psoriatic arthritis at an early stage of the disease process when joint damage may be preventable. In this article we review the criteria for diagnosis of this sero-negative arthritis, look at the clinical indications for referral to a rheumatologist and discuss evolving treatment options relevant to both conditions. © 2010 The Authors. Source

Bowes J.,University of Manchester | Ho P.,University of Manchester | Flynn E.,University of Manchester | Ali F.,Dermatological science | And 13 more authors.
Annals of the Rheumatic Diseases | Year: 2012

Objective: A number of rheumatoid arthritis (RA) susceptibility genes have been identified in recent years. Given the overlap in phenotypic expression of synovial joint inflammation between RA and psoriatic arthritis (PsA), the authors explored whether RA susceptibility genes are also associated with PsA. Methods: 56 single nucleotide polymorphisms (SNPs) mapping to 41 genes previously reported as RA susceptibility loci were selected for investigation. PsA was defined as an inflammatory arthritis associated with psoriasis and subjects were recruited from the UK and Ireland. Genotyping was performed using the Sequenom MassArray platform and frequencies compared with data derived from large UK control collections. Results: Significant evidence for association with susceptibility to PsA was found to a SNP mapping to the REL (rs13017599, p trend = 5.2 × 104) gene, while nominal evidence for association (ptrend < 0.05) was found to seven other loci including PLCL2 (rs4535211, p = 1.7 × 10-3); STAT4 (rs10181656, p = 3.0 × 10-3) and the AFF3, CD28, CCL21, IL2 and KIF5A loci. Interestingly, three SNPs demonstrated opposite effects to those reported for RA. Conclusions: The REL gene, a key modulator of the NFκB pathway, is associated with PsA but the allele conferring risk to RA is protective in PsA suggesting that there are fundamental differences in the aetiological mechanisms underlying these two types of inflammatory arthritis. Source

Kleyn C.E.,Dermatological science | McKie S.,University of Manchester | Ross A.,Dermatological science | Elliott R.,University of Manchester | Griffiths C.E.M.,Dermatological science
British Journal of Dermatology | Year: 2012

Background Pruritus, or itch, is the most prevalent symptom of allergic and inflammatory skin disease. Although it is known that itch induces activation of a neural network in the brain, the temporal dynamics of the network as well as the pathophysiology and neurobiology are not well understood. Objectives The study aimed to elucidate (i) the temporal dynamics of the itch response identified in earlier studies and (ii) the relationship between central and subjective responses to itch. Methods Using a novel time-series analysis, we performed a double-blind, placebo-controlled, randomized, within-subject functional magnetic resonance imaging (fMRI) study of the cerebral processing of histamine-induced itch in healthy volunteers (n = 16) by tracking the 8-min period following a single skin prick. Results Histamine-induced itch compared with saline resulted in significant area under the curve blood oxygen level dependent (BOLD) signal changes in the middle/superior temporal gyrus and right inferior frontal gyrus/insula. We observed negative itch-induced BOLD signal changes compared with saline in (i) the pregenual anterior cingulate cortex (ACC)/medial frontal gyrus, (ii) subgenual ACC/ventral striatum, (iii) bilateral temporal pole/parahippocampal gyrus and (iv) several regions within the cerebellum. We noted a trend significance in the left precentral gyrus part of the motor cortex. The BOLD signal change in several of these regions correlated with perception of itch intensity. Conclusions In contrast to other fMRI studies we observed a multifocal negative signal. An improved understanding of both activated and deactivated brain regions during the itch response may in the long term facilitate development of more effective management strategies. © 2012 The Authors. BJD © 2012 British Association of Dermatologists. Source

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