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Iain L C Chapple

Publications and source records attributed to Iain L C Chapple.

4 recordsLinked to original sources
PubMed2006

Prediction of serum total antioxidant activity from the concentration of individual serum antioxidants.

BACKGROUND: Redox mechanisms are implicated in the pathogenesis of many diseases and several assays of total antioxidant capacity (TAOC) have been reported. Large epidemiological databases contain information on individual serum antioxidants as well as disease-specific phenotypic data. However, antioxidants work co-operatively in biological systems and it is important to be able to translate individual antioxidant measures into those of global antioxidant defence. Models therefore need developing to quantify contributions made by individual species to global antioxidant defence. OBJECTIVE: To develop a predictive model that translates individual antioxidant concentrations into an index of TAOC, enabling interrogation of epidemiological databases that contain information about individual antioxidants, but not about TAOC. METHODS: Sera from 256 volunteers were simultaneously assayed for key antioxidants and TAOC by enhanced chemiluminescence (TAOC(ECL)). A predictive model was developed for serum TAOC using multiple linear regression analysis. RESULTS: The model explained 86% of TAOC(ECL) variability in serum. The strongest predictor of TAOC(ECL) was uric acid (1 SD increase associated with TAOC(ECL) increase of 103 micromol/l Teq-95% CI: 96.8-109), followed by vitamins A, C, E. CONCLUSIONS: The reported model represents a powerful tool for interrogating databases where individual serum antioxidant concentrations are known, and TAOC measures are required.

Antioxidants↗
PubMed2004

Crevicular fluid levels of TGFbeta1 in drug-induced gingival overgrowth.

OBJECTIVE: To determine if local, gingival crevicular fluid (GCF) levels of TGFbeta1 were altered in drug-induced gingival overgrowth. PATIENTS AND METHODS: GCF samples were collected on Periopaper strips from 45 renal transplant recipients who had been medicated with cyclosporin or cyclosporin in combination with other putative overgrowth-inducing drugs for a minimum of 6 months. Twenty-two subjects had gingival overgrowth while the other 23 patients showed no signs of gingival changes and constituted the medicated control group. Non-medicated controls consisted 20 periodontally healthy individuals who had never taken overgrowth-inducing drugs. GCF levels of TGFbeta1 and alkaline phosphatase, a marker of inflammation, were determined by enhanced chemiluminescence ELISA and enzyme activity assays, respectively. RESULTS: TGFbeta1 levels in GCF from overgrowth and non-overgrowth sites in overgrowth sufferers did not differ. However, there were significant differences in median concentration (P = 0.001) and GCF levels of TGFbeta1 per sample (P = 0.05) between study groups with overgrowth patients having higher amounts per sample and lower concentrations than medicated and healthy controls. Median levels of alkaline phosphatase per GCF sample differed between site (P = 0.01) with higher levels present at overgrowth sites. Despite this, the concentration of enzyme in GCF did not differ between site or patient group. CONCLUSIONS: GCF TGFbeta1 detected in overgrowth patients could reflect a higher level of gingival inflammation because of difficulties in plaque control consequent on the development of overgrowth. However, the higher local levels of total TGFbeta1 in overgrowth patients could indicate that it is a risk factor for developing gingival overgrowth.

Adult↗