Search

Objective To elicit a patient's willingness to participate in a diabetes pay-for-performance for patient (P4P4P) program using a discrete choice experiment method. Methods The survey was conducted in March 2013. Our sample was drawn from patients with diabetes at five hospitals in Taiwan ( International Classification of Diseases, Ninth Revision, Clinical Modification code 250). The sample size was 838 patients. The discrete choice experiment questionnaire included the attributes monthly cash rewards, exercise time, diet control, and program duration. We estimated a bivariate probit model to derive willingness-to-accept levels after accounting for the characteristics (e.g., severity and comorbidity) of patients with diabetes. Results The preferred program was a 3-year program involving 30 minutes of exercise per day and flexible diet control. Offering an incentive of approximately US $67 in cash per month appears to increase the likelihood that patients with diabetes will participate in the preferred P4P4P program by approximately 50%. Conclusions Patients with more disadvantageous characteristics (e.g., elderly, low income, greater comorbidity, and severity) could have less to gain from participating in the program and thus require a higher monetary incentive to compensate for the disutility caused by participating in the program's activities. Our result demonstrates that a modest financial incentive could increase the likelihood of program participation after accounting for the attributes of the P4P4P program and patients' characteristics.

It remains unclear whether the GSTM1 genotype interacts with tobacco smoke exposure (TSE) in asthma development. This study aimed to investigate the interactions among GSTM1 genotype, gender, and prenatal TSE with regard to childhood asthma development. In a longitudinal birth cohort in Taiwan, 756 newborns completed a 6-year follow-up, and 591 children with DNA samples available for GSTM1 genotyping were included in the study,and the interactive influences of gender-GSTM1 genotyping-prenatal TSE on childhood asthma development were analyzed. Among these 591 children, 138 (23.4%) hadphysician-diagnosed asthmaat 6 years of age, and 347 (58.7%) werenull-GSTM1. Prenatal TSE significantly increased the prevalence of childhood asthma innull-GSTM1children relative to those withpositiveGSTM1. Further analysis showed that prenatal TSE significantly increased the risk of childhood asthma in girls withnull-GSTM1. Furthermore, among the children without prenatal TSE, girls withnull-GSTM1had a significantly lower risk of developing childhood asthma and a lower total IgE level at 6 years of age than those withpositiveGSTM1. This study demonstrates that the GSTM1 null genotype presents a protective effect against asthma development in girls, but the risk of asthma development increases significantly under prenatal TSE.

Methods A birth cohort in southern Taiwan was studied. Information about parental allergic histories, gender, prematurity, TSE, and childhood allergic disease ever diagnosed by a physician were acquired from questionnaire during follow up. Children were asked to follow up at 6 years of age for allergic questionnaire and sensitization examination (CAP system). Results In this cohort study, 748 of the children with complete data were analyzed. 217 (29%) of children had positive parental allergic history, 191 (25.5%) of children had TSE history, and 186 (24.9%) of children had been diagnosed as asthma by a physician in the first 6 years of life. In a regression analysis, physician diagnosed asthma ever in the first 6 years of life were significantly associated with male gender (OR: 1.941, 95% CI: 1.371-2.748, p 0.5). Besides, TSE and parental allergic history had synergistic influence on the physician diagnosed asthma ever in the 6 years of life. This synergistic influence was significant in girls, rather than in boys (Table 1).

Elevation of serum IgE levels has long been associated with allergic diseases. Many genes have been linked to IgE production, but few have been linked to the developmental aspects of genetic association with IgE production. To clarify developmental genetic association, we investigated what genes and gene-gene interactions affect IgE levels among fetus, infancy and childhood in Taiwan individuals. A birth cohort of 571 children with completion of IgE measurements from newborn to 1.5, 3, and 6 years of age was subject to genetic association analysis on the 384-customized SNPs of 159 allergy candidate genes. Fifty-three SNPs in 37 genes on innate and adaptive immunity, and stress and response were associated with IgE production. Polymorphisms of the IL13, and the HLA-DPA1 and HLA-DQA1 were, respectively, the most significantly associated with the IgE production at newborn and 6 years of age. Analyses of gene-gene interactions indentified that the combination of NPSR1, rs324981 TT with FGF1, rs2282797 CC had the highest risk (85.7%) of IgE elevation at 1.5 years of age (P=1.46 × 10(-4)). The combination of IL13, CYFIP2 and PDE2A was significantly associated with IgE elevation at 3 years of age (P=5.98 × 10(-7)), and the combination of CLEC2D, COLEC11 and CCL2 was significantly associated with IgE elevation at 6 years of age (P=6.65 × 10(-7)). Our study showed that the genetic association profiles of the IgE production among fetus, infancy and childhood are different. Genetic markers for early prediction and prevention of allergic sensitization may rely on age-based genetic association profiles.