Biomedical subjects

C C Holmes

Publications and source records attributed to C C Holmes.

3 recordsLinked to original sources

PubMed2003

Generalized monotonic regression using random change points.

We introduce a procedure for generalized monotonic curve fitting that is based on a Bayesian analysis of the isotonic regression model. Conventional isotonic regression fits monotonically increasing step functions to data. In our approach we treat the number and location of the steps as random. For each step level we adopt the conjugate prior to the sampling distribution of the data as if the curve was unconstrained. We then propose to use Markov chain Monte Carlo simulation to draw samples from the unconstrained model space and retain only those samples for which the monotonic constraint holds. The proportion of the samples collected for which the constraint holds can be used to provide a value for the weight of evidence in terms of Bayes factors for monotonicity given the data. Using the samples, probability statements can be made about other quantities of interest such as the number of change points in the data and posterior distributions on the location of the change points can be provided. The method is illustrated throughout by a reanalysis of the leukaemia data studied by Schell and Singh.

Bayes Theorem↗

PubMed2001

Bayesian partitioning for estimating disease risk.

This paper presents a Bayesian nonlinear approach for the analysis of spatial count data. It extends the Bayesian partition methodology of Holmes, Denison, and Mallick (1999, Bayesian partitioning for classification and regression, Technical Report, Imperial College, London) to handle data that involve counts. A demonstration involving incidence rates of leukemia in New York state is used to highlight the methodology. The model allows us to make probability statements on the incidence rates around point sources without making any parametric assumptions about the nature of the influence between the sources and the surrounding location.

Bayes Theorem↗

PubMed1998

Dietary chitosan inhibits hypercholesterolaemia and atherogenesis in the apolipoprotein E-deficient mouse model of atherosclerosis.

Chitosan, the deacetylated form of chitin, is extracted from the shells of crustaceans. The strong positive charge carried by the chitosan molecule causes it to bind negatively charged substrates such as lipids. Orally administered chitosan binds fat in the intestine, blocking absorption, and has been shown to lower blood cholesterol in animals and humans. As a result it has been proposed that dietary supplementation with chitosan may inhibit the formation of atherosclerotic plaque. We have tested this hypothesis using the apolipoprotein E-deficient mouse model of atherosclerosis. This hypercholesterolaemic animal develops atherosclerosis without the need for dietary or surgical intervention. The apolipoprotein E-deficient mouse therefore provides an ideal model in which to study the effects of dietary chitosan on both blood cholesterol and atherosclerosis. Animals were fed for 20 weeks on a diet containing 5% chitosan or on a control diet. Blood cholesterol levels were significantly lower in the chitosan fed animals throughout the study, and at 20 weeks were 64% of control levels. When the area of aortic plaque in the two groups was compared a highly significant inhibition of atherogenesis, in both the whole aorta and the aortic arch, was observed in the chitosan fed animals--42 and 50%, respectively. Body growth was significantly greater in the chitosan fed animals. This study is the first to show a direct correlation between lowering of serum cholesterol with chitosan and inhibition of atherogenesis, and suggests that the agent could be used to inhibit the development of atherosclerosis in individuals with hypercholesterolaemia.

Animals↗