Lead Deposition in Bovine Enamel during a pH-Cycling Regimen Simulating the Caries Process

Like fluoride, lead (Pb) accumulates on the enamel surface pre-eruptively, but it is not yet known whether it also deposits on enamel while dental caries is developing. This study evaluates Pb distribution in bovine enamel slabs submitted to a pH-cycling regimen simulating the caries process. The slabs were subjected to 8 cycles of de- and remineralizing conditions, and Pb (as acetate salt) was added to the de- and remineralized solutions at concentrations of 30 mu g/l (experimental group, E1) and 300 mu g/l (experimental group, E2). The control group (C) consisted of solutions to which Pb was not added. After the pH cycling, 100-mu m sections of the slabs were analyzed by polarizing microscopy, to observe the extent of caries-like lesions, and these sections were used for Pb estimation by Synchrotron radiation X-ray microfluorescence. Caries lesions were observed along all superficial enamel surfaces to an extent of 120 mu m. A Pb concentration gradient was observed in enamel, which decreased toward dentine. The highest Pb signals were observed for group E2, and the differences were statistically significant at enamel depths of 0 (C vs. E2; p = 0.029) and 50 mu m (C vs. E2 and E1 vs. E2; p = 0.029). In conclusion, this study suggests that if Pb is present in the oral environment, it may deposit in enamel during the caries process. Copyright (C) 2011 S. Karger AG, Basel

Cigarette smoking and risk of epithelial ovarian cancer (Australia)

Objectives: We studied the association between cigarette smoking and ovarian cancer in a population-based case-control study. Methods: A total of 794 women with histologically confirmed epithelial ovarian cancer who were aged 18-79 years and resident in one of three Australian states were interviewed, together with 855 controls aged 18-79 years selected at random from the electoral roll from the same states. Information was obtained about cigarette smoking and other factors including age, parity, oral contraceptive use, and reproductive factors. We estimated the relative risk of ovarian cancer associated with cigarette smoking, accounting for histologic type, using multivariable logistic regression to adjust for confounding factors. Results: Women who had ever smoked cigarettes were more likely to develop ovarian cancer than women who had never smoked (adjusted odds ratio (OR) = 1.5; 95% confidence interval (CI) = 1.2-1.9). Risk was greater for ovarian cancers of borderline malignancy (OR = 2.4; 95% CI = 1.4-4.1) than for invasive tumors (OR = 1.7; 95% CI = 1.2-2.4) and the histologic subtype most strongly associated overall was the mucinous subtype among both current smokers (OR = 3.2; 95% CI = 1.8-5.7) and past smokers (OR = 2.3; 95% CI = 1.3-3.9). Conclusions: These data extend recent findings and suggest that cigarette smoking is a risk factor for ovarian cancer, especially mucinous and borderline mucinous types. From a public health viewpoint, this is one of the few reports of a potentially avoidable risk factor for ovarian cancer.

Reproduction-related risk factors for mucinous and nonmucinous epithelial ovarian cancer

The proposition that mucinous ovarian cancer has an etiology distinct from that of other histologic types has been evaluated using data from a population-based case-control study of epithelial ovarian cancer conducted in 1990-1993 among Australian women aged 18-79 years. The protective effects of parity and oral contraceptive use were greater in nonmucinous than in mucinous ovarian tumors. However, these differences appeared to be driven largely by the effect of ovulatory life, which was positively associated with nonmucinous tumors only. An association with family history of breast and/or ovarian cancer also appeared to be restricted to nonmucinous cancers. These results lend support to the hypothesis that mucinous and nonmucinous ovarian tumors develop via different causal mechanisms.

Long-term risk stratification for survivors of acute coronary syndromes - Results from the long-term intervention with pravastatin in ischemic disease (LIPID) study

OBJECTIVES We developed a prognostic strategy for quantifying the long-term risk of coronary heart disease (CHD) events in survivors of acute coronary syndromes (ACS). BACKGROUND Strategies for quantifying long-term risk of CHD events have generally been confined to primary prevention settings. The Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) study, which demonstrated that pravastatin reduces CHD events in ACS survivors with a broad range of cholesterol levels, enabled assessment of long-term prognosis in a secondary prevention setting. METHODS Based on outcomes in 8,557 patients in the LIPID study, a multivariate risk factor model was developed for prediction of CHD death or nonfatal myocardial infarction. Prognostic indexes were developed based on the model, and low-, medium-, high- and very high-risk groups were defined by categorizing the prognostic indexes. RESULTS In addition to pravastatin treatment, the independently significant risk factors included: total and high density lipoprotein cholesterol, age, gender, smoking status, qualifying ACS, prior coronary revascularization, diabetes mellitus, hypertension and prior stroke. Pravastatin reduced coronary event rates in each risk level, and the relative risk reduction did not vary significantly between risk levels. The predicted five-year coronary event rates ranged from 5% to 19% for those assigned pravastatin and from 6.4% to 23.6% fur those assigned placebo. CONCLUSIONS Long-term prognosis of ACS survivors varied substantially according to conventional risk factor profile. Pravastatin reduced coronary risk within all risk levels; however, absolute risk remained high in treated patients with unfavorable profiles. Our risk stratification strategy enables identification of ACS survivors who remain at very high risk despite statin therapy. CT Am Coil Cardiol 2001;38:56-63) (C) 2001 by the American College of Cardiology.

Study on the potential inhibition of root dentine wear adjacent to fluoride-containing restorations

The purpose of this in vitro study was to determine whether the vicinity of root dentine that had been restored with fluoride-releasing materials was at reduced risk for erosive/abrasive wear compared to root dentine restored with a non-fluoride-containing material. According to a randomized complete block design, standardized cavities prepared on the surface of 150 bovine root dentine slabs were restored with glass-ionomer cement, resin-modified glass ionomer, polyacid-modified resin composite, fluoride-containing or conventional composite. Specimens were coated with two layers of an acid-resistant nail varnish exposing half of the dentine surface and half of the restoration. Subsequently, specimens were either eroded in an acidic drink or left uneroded, then exposed to artificial saliva and abraded in a toothbrushing machine. Wear depth in the vicinity of restorations was quantified by a stylus profilometer, based on the nonabraded areas surrounding the erosion/abrasion region. Two-way ANOVA did not demonstrate significant interaction between restoratives and eroded-uneroded dentine (p = 0.5549) nor significant difference among restorative materials (p = 0.8639). Tukey`s test ascertained that the wear depth was higher for eroded than for uneroded groups. Fluoride-releasing materials seemed to negligibly inhibit wear in the vicinity of restored root dentine subjected to erosive/abrasive challenges.

Considerations in the design of a mixed-method cluster evaluation of a community programme for 'at-risk' young people

This article discusses the design of a comprehensive evaluation of a community development programme for young people 'at-risk' of self-harming behaviour. It outlines considerations in the design of the evaluation and focuses on the complexities and difficulties associated with the evaluation of a community development programme. The challenge was to fulfil the needs of the funding body for a broad, outcome-focused evaluation while remaining close enough to the programme to accurately represent its activities and potential effects at a community level. Specifically, the strengths and limitations of a mixed-method evaluation plan are discussed with recommendations for future evaluation practice.

Towards a molecular epidemiology of alcohol dependence analysing the interplay of genetic and environmental risk factors

Background Progress in identifying genetic factors protective against alcohol dependence (AlcD) requires a paradigm shift in psychiatric epidemiology. Aims To integrate analysis of research into the genetics of alcoholism. Method Data from prospective questionnaire and interview surveys of the Australian twin panel, and from a subsample who underwent alcohol challenge, were analysed. Results In men, effects of alcohol dehydrogenase ADH2*1/*2 genotype or high alcohol sensitivity (risk-decreasing), and of history of childhood conduct disorder, or having monozygotic co-twin or twin sister with AlcD (risk-increasing) were significant and comparable in magnitude. Religious affiliation (Anglican versus other) was associated with the ADH2 genotype, but did not explain the associations with AlcD symptoms. No protective effect of the ADH2*1/*2 genotype was observed in women. Conclusions The early onset and strong familial aggregation of AlcD, and opportunity for within-family tests of genetic association to avoid confounding effects, make epidemiological family studies of adolescents and young adults and their families a priority.

MC1R genotype modifies risk of melanoma in families segregating CDKN2A mutations

Mutations in the exons of the cyclin-dependent kinase inhibitor gene CDKN2A are melanoma-predisposition alleles which have high penetrance, although they have low population frequencies. In contrast, variants of the melanocortin-1 receptor gene, MC1R, confer much lower melanoma risk but are common in European populations. Fifteen Australian CDKN2A mutation-carrying melanoma pedigrees were assessed for MC1R genotype, to test for possible modifier effects on melanoma risk. A CDKN2A mutation in the presence of a homozygous consensus MC1R genotype had a raw penetrance of 50%, with a mean age at onset of 58.1 years. When an MC1R variant allele was also present, the raw penetrance of the CDKN2A mutation increased to 84%, with a mean age at onset of 37.8 years (P=0.1). The presence of a CDKN2A mutation gave a hazard ratio of 13.35, and the hazard ratio of 3.72 for MC1R variant alleles was also significant. The impact of MC1R variants on risk of melanoma was mediated largely through the action of three common alleles, Arg151Cys, Arg160Trp, and Asp294His, that have previously been associated with red hair, fair skin, and skin sensitivity to ultraviolet light.

Variation in Alcohol Pharmacokinetics as a Risk Factor for Alcohol Dependence

Background: The significant association between alcohol dehydrogenase (ADH)-2 genotype and alcohol-dependence risk, demonstrated in both Asian and non-Asian populations, suggests a link between the metabolism of alcohol (ethanol) and individual differences in susceptibility to dependence. Methods: We tested this hypothesis by following up on subjects who took part in the Alcohol Challenge Twin Study conducted in 1979-1981 and comparing the blood and breath alcohol results in that study between subjects who subsequently did or did not meet diagnostic criteria for lifetime alcohol dependence in 1992-1993. Results: Subjects who met DSM-III-R criteria for lifetime alcohol dependence at follow-up had higher blood and breath alcohol values after alcohol challenge than never-dependent subjects. Multivariate analysis showed independent effects of susceptibility to alcohol dependence and smoking status on blood alcohol concentrations, whereas habitual alcohol intake at the time of the initial study had marginally significant effects. The risk of alcohol dependence was 2-fold higher in men and 3-fold higher in women with blood or breath alcohol concentrations in the highest quartile than in the lowest quartile. Conclusions: In view of this association and the known genetic influences on both alcohol pharmacokinetics and alcohol dependence, it is probable that part of the heritability of dependence is mediated by genes (other than the known ADH2 and ADH3 polymorphisms) affecting alcohol metabolism.