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Javier Llorca

Publications and source records attributed to Javier Llorca.

77 records · Page 5Linked to original sources
PubMed2002

Visualising exposure-disease association: the Lorenz curve and the Gini index.

BACKGROUND: It has been suggested that the summary index of the Lorenz curve, the Gini index, should be used to characterize the exposure-disease association, rather than relative and attributable risks. Nevertheless, the sampling behavior of the Gini index in epidemiological settings, and the relationships between the Lorenz curve and the usual indices of risk, need to be more deeply understood. MATERIAL/METHODS: The present paper analyzes the geometrical relationships between the Lorenz curve and the relative and attributable risks based on two of the main sampling schemes (cohort and case-control designs). Examples for both designs are provided. Gini index confidence intervals are obtained by bootstrap. RESULTS: The Gini index is a function of the proportion of the population at each level of exposure, relative risk and attributable risk. If exposure is ordered by increasing levels of risk, the Lorenz curve contains all the information about relative and attributable risks and distribution of exposure in the population. Therefore, the Lorenz curve easily allows both risks and their distribution in the analyzed population to be visualised. CONCLUSIONS: The Lorenz curve and the Gini index can complement the information provided by relative and attributable risks.

Case-Control Studies↗
PubMedDate not supplied

CD14 receptor polymorphism and Alzheimer's disease risk.

Activation of microglial cells is involved in the inflammatory component of Alzheimer's disease (AD), and it may be triggered by infectious pathogens. CD14, a receptor upregulated in activated microglia, plays a central role in innate immunity through recognition of bacterial lipopolysaccharide and initiation of inflammatory response. A polymorphism in the promoter region (-260) of the CD14 receptor has been found to be related to increased risk of bacterial infections and inflammatory diseases such as atherosclerosis. In a case-control study utilizing a clinically well-defined group of 310 sporadic AD patients and 310 control subjects, we investigated whether the CD14 (-260) polymorphism might be responsible for susceptibility to AD, and we also examined the combined gene effects between CD14 and APOE and several other proinflammatory cytokine genes. The current study does not demonstrate an association between CD14 (-260) polymorphism and AD, neither through an independent effect nor through interaction with APOE epsilon4 allele or interleukin (IL)-1A, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and intercellular adhesion molecule-1 polymorphisms.

Aged↗
PubMedDate not supplied

[Survival analysis with competing risks: estimating failure probability].

OBJECTIVE: To show the impact of competing risks of death on survival analysis. METHOD: We provide an example of survival time without chronic rejection after heart transplantation, where death before rejection acts as a competing risk. Using a computer simulation, we compare the Kaplan-Meier estimator and the multiple decrement model. RESULTS: The Kaplan-Meier method overestimated the probability of rejection. Next, we illustrate the use of the multiple decrement model to analyze secondary end points (in our example: death after rejection). Finally, we discuss Kaplan-Meier assumptions and why they fail in the presence of competing risks. CONCLUSIONS: Survival analysis should be adjusted for competing risks of death to avoid overestimation of the risk of rejection produced with the Kaplan-Meier method.

Graft Rejection↗
PubMedDate not supplied

[Competing risks of death and Hardy-Weinberg equilibrium in case-control studies of gene-disease association].

OBJECTIVE: To study the impact of competing risks on Hardy-Weinberg equilibrium and their consequences in case-control studies of gene-late onset disease association. METHODS: Based on a population born in Hardy-Weinberg equilibrium for a particular gene, the genetic composition when the gene is associated with a lethal early-onset disease and its consequences on a late-onset disease can be deduced. Odds ratios estimates are unbiased in case-control studies when controls are sampled by density, even if the controls are in Hardy-Weinberg disequilibrium. RESULTS: An example in which a mutant gene is associated with early mortality is presented, producing a departure from Hardy-Weinberg equilibrium; as a result, controls in later ages are in disequilibrium, producing an odds ratio equal to 1.61. CONCLUSION: Although the main causes of Hardy-Weinberg disequilibrium in controls are selection bias or genotyping error, a competing risk of death associated with the mutant gene would also result in Hardy-Weinberg disequilibrium among controls.

Aged↗