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Dive into the research topics where D A Scott is active.

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Featured researches published by D A Scott.


European Journal of Clinical Investigation | 2002

Effect of nicotine replacement and quitting smoking on circulating adhesion molecule profiles (sICAM-1, sCD44v5, sCD44v6)

Richard Palmer; J A Stapleton; G. Sutherland; Paula Y. Coward; R F Wilson; D A Scott

Background Soluble ICAM‐1 (sICAM‐1; sCD54), sCD44v5 and sCD44v6 are circulating adhesion molecules, with immunomodulatory potential, that have been frequently attributed diagnostic, prognostic and aetiological significance in a number of inflammatory and malignant diseases. We have previously shown that systemic concentrations of these molecules are increased significantly in tobacco smokers, but reduce to within normal levels at 12 months following successful quitting.


Journal of Dental Research | 2001

Elevated Systemic Concentrations of Soluble ICAM-1 (sICAM) are Not Reflected in the Gingival Crevicular Fluid of Smokers with Periodontitis

H S Fraser; Richard Palmer; Ron Wilson; Paula Y. Coward; D A Scott

Raised serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) in smokers could have immunomodulatory effects in periodontitis. The aim of this study was to compare serum and gingival crevicular fluid (GCF) concentrations of sICAM-1 in smokers and non-smokers with periodontal disease. sICAM-1 in serum and GCF collected from age- and gender-matched smokers (n = 14) and non-smokers (n = 14) with periodontitis were measured by ELISA. Mean serum sICAM-1 concentrations were significantly elevated in smokers (331 ng mL-1), compared with non-smokers (238 ng mL-1, p = 0.008). However, the concentration of sICAM-1 in the GCF was significantly lower in the smokers (83 ng mL -1), compared with non-smokers (212 ng mL-1, p = 0.013). The difference between concentrations of sICAM-1 in GCF and serum was significant only in smokers (p < 0.001). Since GCF is a serum-derived tissue exudate, these results suggest that, in smokers, circulating sICAM-1 molecules are affected either in their passage from the periodontal microvasculature or within the periodontal tissues.


Tobacco Induced Diseases | 2003

The influence of tobacco smoking on adhesion molecule profiles

D A Scott; Richard Palmer

Sequential interactions between several adhesion molecules and their ligands regulate lymphocyte circulation and leukocyte recruitment to inflammatory foci. Adhesion molecules are, therefore, central and critical components of the immune and inflammatory system. We review the evidence that tobacco smoking dysregulates specific components of the adhesion cascade, which may be a common factor in several smoking-induced diseases. Smoking causes inappropriate leukocyte activation, leukocyte-endothelial adhesion, and neutrophil entrapment in the microvasculature, which may help initiate local tissue destruction. Appropriate inflammatory reactions may thus be compromised. In addition to smoke-induced alterations to membrane bound endothelial and leukocyte adhesion molecule expression, which may help explain the above phenomena, smoking has a profound influence on circulating adhesion molecule profiles, most notably sICAM-1 and specific sCD44 variants. Elevated concentrations of soluble adhesion molecules may simply reflect ongoing inflammatory processes. However, increasing evidence suggests that specific soluble adhesion molecules are immunomodulatory, and that alterations to soluble adhesion molecule profiles may represent a significant risk factor for several diverse diseases. This evidence is discussed herein.


International Journal of Gynecology & Obstetrics | 2003

Recrudescent herpes labialis during and prior to early pregnancy

D A Scott; S Moore; Mark Ide; Paula Y. Coward; R Baylis; E Borkowska

Objectives: To assess the experience of recrudescent herpes labialis (RHL) before and during early pregnancy. Methods: History of RHL prior to and during the first trimester of pregnancy was obtained from 3738 women attending at 10–15 weeks’ gestation. The influence of age, ethnicity, socioeconomic group, smoking behavior, and alcohol intake on RHL was assessed. Results: 1066 women (28.5%) reported a history of RHL lesions, with reduced incidence of RHL during pregnancy (0.111 lesions/subject per month) compared with outside pregnancy (0.19 lesions/subject per month) (P<0.0001). Those who did report lesions during pregnancy (n=296) experienced them at a higher monthly rate (0.41 lesions/subject per month) than before pregnancy (0.25 lesions/subject per month) (P<0.0001). RHL rate in early pregnancy was related solely to the previous rate of lesion recrudescence (P<0.001). Conclusion: Pregnant women with a history of RHL report reduced incidence of RHL during pregnancy.


Tobacco Induced Diseases | 2003

Analysis of circulating insulin-like growth factor-1 (IGF-1) and IGF binding protein-3 (IGFBP-3) in tobacco smokers and non-smokers

Richard Palmer; Ron Wilson; Paula Y. Coward; D A Scott

BackgroundIGF-1 and the major serum IGF-1 binding protein, IGFBP-3, are under extensive investigation as potential prognostic markers of specific malignancies and vascular diseases. However, there is conflicting evidence that tobacco smoking may influence systemic concentrations of IGF-1 and IGFBP-3.Subjects and methodsSerum concentrations of IGF-1 and IGFBP-3 were measured in 20 smokers and 20 non-smokers, matched for age and gender. Serum concentrations of cotinine, the major metabolite of nicotine, and ICAM-1, known to exhibit a dose-dependent relationship with cotinine, were also assayed.ResultsThere was no difference between the systemic concentrations of IGF-1 or IGFBP-3 found in smokers and non-smokers (IGF-1: mean [s.d]; 104 [29] vs 101 [24] ng ml-1, respectively; and IGFBP-3: 2562 [522] vs 2447 [570] ng ml-1, respectively). Similarly, there was no correlation between serum cotinine and IGF-1 or IGFBP-3 concentrations in smokers. Soluble ICAM-1 concentrations were significantly increased in smokers, compared to non-smokers (mean [s.d]; 258 [60] vs 194 [50] ng ml-1, respectively; p = 0.002).ConclusionThere was no relationship noted between tobacco smoking and either IGF-1 or IGFBP-3. These data suggest that smoking would not appear to be a major confounder of the reported clinical associations between IGF-1, IGFBP-3, or IGF-1/IGFBP-3 ratios and specific disease entities.


Journal of Clinical Periodontology | 2001

Validation of smoking status in clinical research into inflammatory periodontal disease

D A Scott; Richard Palmer; J A Stapleton


Journal of Clinical Periodontology | 2000

Laser Doppler flowmeter measurement of relative gingival and forehead skin blood flow in light and heavy smokers during and after smoking

T. N. Meekin; Ron Wilson; D A Scott; Mark Ide; Richard Palmer


Journal of Clinical Periodontology | 2003

Gingival bleeding on probing increases after quitting smoking.

P Nair; G Sutherland; Richard Palmer; Ron Wilson; D A Scott


Journal of Oral Pathology & Medicine | 2002

Expression of ICAM-1 and E-selectin in gingival tissues of smokers and non-smokers with periodontitis

K Rezavandi; Richard Palmer; D A Scott; Ron Wilson


Journal of Periodontal Research | 1999

Potential mechanisms of susceptibility to periodontitis in tobacco smokers

Richard Palmer; D A Scott; T. N. Meekin; Robin Poston; Edward W. Odell; Ron Wilson

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Mark Ide

King's College London

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R Baylis

King's College London

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