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D R Blake

Publications and source records attributed to D R Blake.

293 records · Page 17Linked to original sources
PubMedDate not supplied

Is home tooth bleaching gel cytotoxic?

Tooth whitening systems are widely used clinically and for home usage. The aim of this study was to determine the effects of two bleaching gels, each containing 10 percent and 15 percent carbamide peroxide, respectively, a 'bleaching gel' without carbamide peroxide, and carbamide peroxide alone on the viability of human endothelial cells in vitro in comparison with culture medium that acted as a negative control. The incubation period used was 30 minutes. A colorimetric viability assay (MTT assay) was employed. The results showed that the gel without carbamide peroxide is not cytotoxic compared to the negative control, while carbamide peroxide on its own and 10 percent and 15 percent carbamide peroxide bleaching gels were cytotoxic, but there were no significant differences (p greater than 0.05) among these latter three test groups. These data indicate that 10 percent and 15 percent carbamide peroxide bleaching gels are cytotoxic and that carbamide peroxide is the component responsible for this cytotoxic effect. This paper also discusses why this in vitro cytotoxic effect appears not to be significant in vivo.

Analysis of Variance↗
PubMedDate not supplied

Understanding pain.

Explore the source record for details and available documents.

Arthritis↗
PubMedDate not supplied

Inactivation of xanthine oxidoreductase is associated with increased joint swelling and nitrotyrosine formation in acute antigen-induced arthritis.

OBJECTIVE: Arthritis is associated with increased articular formation of nitrotyrosine, which may contribute to injury. Nitrotyrosine is formed by nitration of tyrosine by reactive nitrogen species such as peroxynitrite, the formation of which may be enhanced by xanthine oxidoreductase (XOR), since it can generate nitric oxide from nitrite/nitrate, and superoxide during xanthine metabolism. We hypothesized that inactivation of XOR would protect against antigen-induced arthritis (AIA) and decrease nitrotyrosine formation. METHODS: AIA was induced with methylated bovine serum albumin (mBSA) in three groups of Wistar rats: animals fed on (1) tungsten-enriched chow (0.7 g/kg) (TG), which inactivates XOR, (2) standard chow (SG), and (3) rats treated with allopurinol (50 mg/kg/day; p.o.) (AG). Nitrotyrosine in patella-synovium was quantified by mass spectrometry three weeks after intra-articular (i.a.) antigen injection. RESULTS: Treatment with tungsten, but not allopurinol, suppressed plasma and articular XOR activity at < or = 0.9% of normal levels. XOR inactivation was associated with increased knee swelling 24-48 hrs post i.a. mBSA, compared with controls (mean increase +/- SEM of knee diameter from baseline of 3.3 +/- 0.5, 2.0 +/- 0.3 and 1.9 +/- 0.2 mm in TG, SG and AG (n = 14 each group), respectively; p < 0.05, TG vs SG, ANOVA). Mean ratio of articular nitrotyrosine-tyrosine (+/- SEM) was increased in the XOR-inactivated group, compared with controls: 12.3 +/- 0.7, 9.6 +/- 0.8 and 10.4 +/- 0.5 pg/microg in TG, SG and AG, respectively; p < 0.05, TG vs SG. CONCLUSION: Contrary to expectation, XOR inactivation was associated with increased joint swelling and articular tyrosine nitration in acute AIA, suggesting a novel, protective role for XOR in inflammatory arthritis.

Allopurinol↗
PubMedDate not supplied

Serum sulphydryl levels in early synovitis.

The determination of serum sulphydryl levels has been assessed as a diagnostic/prognostic indicator of rheumatoid arthritis in patients attending an early synovitis clinic. This simple assay has been compared with other test systems including C-reactive protein, plasma viscosity, IgM rheumatoid factor and immune complexes. Results show that a low serum sulphydryl at presentation is a useful prognostic indicator for development of persistent synovitis. Patients with normal sulphydryl levels suffered only mild or transient symptoms. These results suggest that, since stimulated phagocytes generate the oxygen-derived species responsible for sulphydryl oxidation, such cells are active before the patient develops persistent symptoms.

Arthritis, Rheumatoid↗