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Dive into the research topics where Paula E. Beattie is active.

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Featured researches published by Paula E. Beattie.


Clinical and Experimental Dermatology | 2006

UVA1 phototherapy for genital lichen sclerosus

Paula E. Beattie; R.S. Dawe; J. Ferguson; Sally H. Ibbotson

Background.  Lichen sclerosus (LS) is characterized histologically by an inflammatory T‐cell infiltrate, sclerosis and thickening of the dermis, and epidermal atrophy. Ultraviolet (UV) A1 therapy has been shown to be effective in the management of morphea and scleroderma, diseases that have some histological and clinical similarities with LS, and more recently in extragenital LS.


Clinical and Experimental Dermatology | 2004

Lack of efficacy and tolerability of topical PDT for psoriasis in comparison with narrowband UVB phototherapy

Paula E. Beattie; R.S. Dawe; J. Ferguson; Sally H. Ibbotson

active as a result of this treatment. In an extensive literature review we found no references concerning the activation of an arteriovenous malformation after laser treatment. In conclusion, we present a singular association that has not previously been reported, between chylothorax and a vascular malformation of the back treated with flash-lamp pulsed dye laser. Dorsal cutaneous arteriovenous malformations may be associated with abnormalities of the thoracic lymphatic vessels. The dermatologist should be alert to the possibility of this complication, and in patients with vascular malformations of the back, the presence of associated lymphatic abnormalities should be ruled out by means of lymphography before programming any laser treatment.


Clinical and Experimental Dermatology | 2006

UVA1 phototherapy for treatment of necrobiosis lipoidica.

Paula E. Beattie; R.S. Dawe; Sally H. Ibbotson; J. Ferguson

The primary cause of collagen degeneration in necrobiosis lipoidica (NL) is proposed to be immunologically mediated vascular disease. Ultraviolet (UV)A1 has been used successfully to treat scleroderma in which both vascular damage and collagen dysregulation also occur. We treated six patients with NL [(five women; mean age of 32 years (range 22–70) and mean disease duration of 2.9 years (range 6 months to 5 years)] with a high‐output ultraviolet (UV)A1 2‐kW filtered metal halide source (Dr Hönle; Dermalight ultrA 1) having an emission spectrum of 340–440 nm. All patients had NL on the shins, which had been unresponsive to potent topical corticosteroid therapy (n = 6) and had responded minimally or not at all to TL‐01 UVB (n = 2), topical psoralen plus UVA (PUVA) soaking (n = 2) or oral PUVA (n = 1) therapy. Patients received a variable number of total exposures (15–51), given 3–5 times weekly. NL resolved completely in one patient; this patient had minimal improvement after the first course of 16 exposures, but after a further 13 exposures, resolution occurred 6 months later. Two subjects obtained moderate improvement in their overall disease severity after 15 and 24 exposures, while two had only minimal improvement after 15 and 51 exposures. The remaining patient had no improvement after 16 treatments. Patients with the shortest disease duration had the greatest response. UVA1 therapy may be of benefit for the treatment of NL as an adjuvant therapy to topical corticosteroids or as a second‐line alternative to other phototherapies, and may have a superior outcome in a proportion of patients.


British Journal of Dermatology | 2005

The effect of ultraviolet (UV) A1, UVB and solar-simulated radiation on p53 activation and p21Waf1/Cip1

Paula E. Beattie; L.E. Finlan; Neil M. Kernohan; G. Thomson; T.R. Hupp; Sally H. Ibbotson

Background  High‐dose ultraviolet (UV) A1 therapy (doses in the order of 130 J cm−2) is effective for atopic dermatitis and scleroderma. UVA1 has been shown to induce a dose‐dependent increase in p53 expression in keratinocytes.


British Journal of Dermatology | 2005

Differential effects of 5‐aminolaevulinic acid photodynamic therapy and psoralen + ultraviolet A therapy on p53 phosphorylation in normal human skin in vivo

L.E. Finlan; N.M. Kernohan; G. Thomson; Paula E. Beattie; T.R. Hupp; Sally H. Ibbotson

Background  Phosphorylation of the tumour suppressor p53 by the CK2/FACT pathway plays a central role in suppressing ultraviolet (UV)‐induced skin cancer in animal models. Although p53 protein stabilization is induced after solar‐simulated irradiation of human skin in vivo, p53 phosphorylation has not been defined.


British Journal of Dermatology | 2005

Can St John's wort (hypericin) ingestion enhance the erythemal response during high‐dose ultraviolet A1 therapy?

Paula E. Beattie; R.S. Dawe; N.J. Traynor; Julie A. Woods; J. Ferguson; Sally H. Ibbotson

Background  St Johns wort (SJW) is widely used as a treatment for depression. A phototoxic reaction, due to its content of hypericin, can occur in animals and in cell culture, and has been reported in humans. Hypericin displays absorption within the ultraviolet (UV) A1 spectrum and there may therefore be a potential for phototoxicity if taken during high‐dose UVA1 therapy.


Archives of Dermatology | 2003

Characteristics and Prognosis of Idiopathic Solar Urticaria: A Cohort of 87 Cases

Paula E. Beattie; R.S. Dawe; Sally H. Ibbotson; James Ferguson


Toxicology Letters | 2005

Photogenotoxicity of hypericin in HaCaT keratinocytes: implications for St. John's Wort supplements and high dose UVA-1 therapy.

N.J. Traynor; Paula E. Beattie; Sally H. Ibbotson; Harry Moseley; J. Ferguson; Julie A. Woods


Archives of Dermatology | 2005

Dose-Response and Time-Course Characteristics of UV-A1 Erythema

Paula E. Beattie; R.S. Dawe; James Ferguson; Sally H. Ibbotson


Journal of The American Academy of Dermatology | 2007

Can dietary furanocoumarin ingestion enhance the erythemal response during high-dose UVA1 therapy?

Paula E. Beattie; Murray J.V. Wilkie; Gillian Smith; J. Ferguson; Sally H. Ibbotson

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