Analysis of Melanoma Onset: Assessing Familial Aggregation by Using Estimating Equations and Fitting Variance Components via Bayesian Random Effects Models

We investigate whether relative contributions of genetic and shared environmental factors are associated with an increased risk in melanoma. Data from the Queensland Familial Melanoma Project comprising 15,907 subjects arising from 1912 families were analyzed to estimate the additive genetic, common and unique environmental contributions to variation in the age at onset of melanoma. Two complementary approaches for analyzing correlated time-to-onset family data were considered: the generalized estimating equations (GEE) method in which one can estimate relationship-specific dependence simultaneously with regression coefficients that describe the average population response to changing covariates; and a subject-specific Bayesian mixed model in which heterogeneity in regression parameters is explicitly modeled and the different components of variation may be estimated directly. The proportional hazards and Weibull models were utilized, as both produce natural frameworks for estimating relative risks while adjusting for simultaneous effects of other covariates. A simple Markov Chain Monte Carlo method for covariate imputation of missing data was used and the actual implementation of the Bayesian model was based on Gibbs sampling using the free ware package BUGS. In addition, we also used a Bayesian model to investigate the relative contribution of genetic and environmental effects on the expression of naevi and freckles, which are known risk factors for melanoma.

Application of a coupled ground-surface water flow model to simulate periodic groundwater flow influenced by a sloping boundary, capillarity and vertical flows

Theoretical developments as well as field and laboratory data have shown the influence of the capillary fringe on water table fluctuations to increase with the fluctuation frequency. The numerical solution of a full, partially saturated flow equation can be computationally expensive. In this paper, the influence of the capillary fringe on water table fluctuations is simplified through its parameterisation into the storage coefficient of a fully-saturated groundwater flow model using the complex effective porosity concept [Nielsen, P., Perrochet, P., 2000. Water table dynamics under capillary fringes: experiments and modelling. Advances in Water Resources 23 (1), 503-515; Nielsen, P., Perrochet, P., 2000. ERRATA: water table dynamics under capillary fringes: experiments and modelling (Advances in Water Resources 23 (2000) 503-515). Advances in Water Resources 23, 907-908]. The model is applied to sand flume observations of periodic water table fluctuations induced by simple harmonic forcing across a sloping boundary, analogous to many beach groundwater systems. While not providing information on the moisture distribution within the aquifer, this approach can reasonably predict the water table fluctuations in response to periodic forcing across a sloping boundary. Furthermore, he coupled ground-surface water model accurately predicts the extent of the seepage face formed at the sloping boundary. (C) 2005 Elsevier Ltd. All rights reserved.

Is mortality from heart failure increasing in Australia? An analysis of official data on mortality for 1997-2003

Objective To assess whether trends in mortality from heart failure(HF) in Australia are due to a change in awareness of the condition or real changes in its epidemiology. Methods We carried out a retrospective analysis of official data on national mortality data between 1997 and 2003. A death was attributed to HF if the death certificate mentioned HF as either the underlying cause of death (UCD) or among the contributory factors. Findings From a total of 907 242 deaths, heart failure was coded as the UCD for 29 341 (3.2%) and was mentioned anywhere on the death certificate in 135 268 (14.9%). Between 1997 and 2003, there were decreases in the absolute numbers of deaths and in the age-specific and age-standardized mortality rates for HF either as UCD or mentioned anywhere for both sexes. HF was mentioned for 24.6% and 17.8% of deaths attributed to ischaemic heart disease and circulatory disease, respectively, and these proportions remained unchanged over the period of study. In addition, HF as UCD accounted for 8.3% of deaths attributed to circulatory disease and this did not change materially from 1997 to 2003. Conclusion The decline in mortality from HF measured as either number of deaths or rate probably reflects a real change in the epidemiology of HF. Population-based studies are required to determine accurately the contributions of changes in incidence, survival and demographic factors to the evolving epidemiology of HF.