PubMed Health⌕ Search

Biomedical subjects

Rebecca Reynolds

Publications and source records attributed to Rebecca Reynolds.

12 recordsLinked to original sources
PubMed2006

Expanding the concept of parental control: a role for overt and covert control in children's snacking behaviour?

The existing literature on parental control and children's diets is confusing. The present paper reports two studies to explore an expanded conceptualisation of parental control with a focus on overt control which 'can be detected by the child' and covert control which 'cannot be detected by the child'. In study 1, 297 parents of children aged between 4 and 11 completed a measure of overt control and covert control alongside ratings of their child's snacking behaviour as a means to assess who uses either overt or covert control and how these aspects of parental control relate to a child's snacking behaviour. The results showed that lighter parents and those with children perceived as heavier were more likely to use covert control and those from a higher social class were more likely to use overt control. Further, whilst greater covert control predicted a decreased intake of unhealthy snacks, greater overt control predicted an increased intake of healthy snacks. In study 2, 61 parents completed the same measure of overt and covert control alongside the three control subscales of the Child Feeding Questionnaire [Birch, L.L., Fisher, J.O., Grimm-Thomas, Markey, C.N., Sawyer, R. (2001). Confirmatory factor analysis of the Child Feeding Questionnaire: A measure of parental attitudes, beliefs and practices about child feeding and obesity proneness. Appetite, 36, 201-210] to assess degrees of overlap between these measures. The results showed that although these five measures of control were all positively correlated, the correlations between the new and existing measures indicated a maximum of 21% shared variance suggesting that covert and overt control are conceptually and statistically separate from existing measures of control. To conclude, overt and covert control may be a useful expansion of existing ways to measure and conceptualise parental control. Further, these constructs may differentially relate to snacking behaviour which may help to explain some of the confusion in the literature.

Adult↗
PubMed2006

Cost-efficient higher-order crossover designs in comparative bioavailability studies.

BACKGROUND AND OBJECTIVE: Cost is an extremely important factor to consider when planning drug clinical trials. Higher-order crossover designs have recently drawn considerable attention in comparative bioavailability studies because of their desirable statistical properties. In this paper, we compared the cost efficiency of five commonly used higher-order crossover designs under certain cost function for comparative bioavailability studies. METHODS: Multivariate normal data were simulated under scenarios of a wide range of variability and correlations (coefficient of variation = 10-40%; correlation coefficient rho = 0.2-0.8). Monte Carlo simulations and mixed-effects models were carried out to obtain empirical sample sizes for each design using Schuirmann's two-one sided test procedure, under an 80% power and a 5% significance level, based on the US FDA bioequivalence criteria (80-125%). The five crossover designs studied were the two-period four-sequence (D2 x 4), the three-period two-sequence (D3 x 2), the three-period four-sequence (D3 x 4), the four-period two-sequence (D4 x 2), and the four-period four-sequence (D4 x 4). Costs for each design were then determined by a cost function, which takes into account costs for recruiting and screening, costs associated with period, and the overheads incurred for multiple sequences. Comparison of the costs for the above-mentioned designs was made under different scenarios. RESULTS: There was no single design uniformly dominating the others in terms of cost efficiency for comparative bioavailability studies. The designs D3 x 2 and D4 x 4 (especially the former) have the best overall performance in terms of cost efficiency for comparative bioavailability studies. They dominated the other designs under most of the scenarios. The design D2 x 4 showed the worst performance among the five crossover designs. CONCLUSIONS: A D3 x 2, and D4 x 2 crossover designs are recommended to achieve cost efficiency with a given power. The D2 x 4 crossover design is not recommended in general for comparative bioavailability studies.

Biological Availability↗
PubMed2006

Surveying the RHIO landscape. A description of current RHIO models, with a focus on patient identification.

Across the country, new RHIOs are being formed every day. The 21 RHIOs studied by the work group illustrate the variety of purposes, funding, and record linking methods RHIOs may adopt. As this trend continues to evolve and improve, RHIOs may prove to be a valuable stepping stone on the road to a national system in which a patient's medical data will be available anywhere, anytime. Accurate patient identification and linking are the foundation of health technology that is implemented in a RHIO or any similar network that shares patient information. Without accurate patient identification, patient safety and quality of care are compromised. When high percentages of duplication or overlaying of records occurs in electronic health record databases, physician trust in the system is lost. As HIM professionals, we must be involved in addressing the security and confidentiality of RHIO databases and in defining the record linking method appropriate to the RHIO. As professionals skilled in patient identification methods and possessing significant organizational skills and personnel management experience, HIM professionals should become involved in this process at the earliest opportunity in the RHIO formation. HIM professionals can participate in long-term planning, business plan development, and organizational structure definition. Future articles will address how HIM professionals can become involved, what particular attributes and skills they can bring to the table, and job descriptions appropriate to HIM professionals in the healthcare information sharing industry. The work group urges all HIM professionals to become involved personally in this exciting new field.

Humans↗
PubMed2005

Forensic casework analysis using the HVI/HVII mtDNA linear array assay.

The mitochondrial hypervariable regions I and II have proven to be a useful target for analysis of forensic materials, in which the amount of DNA is limited or highly degraded. Conventional mitochondrial DNA (mtDNA) sequencing can be time-consuming and expensive, limitations that can be minimized using a faster and less expensive typing assay. We have evaluated the exclusion capacity of the linear array mtDNA HVI/HVII region-sequence typing assay (Roche Applied Science) in 16 forensic cases comprising 90 samples. Using the HVI/HVII mtDNA linear array, 56% of the samples were excluded and thus less than half of the samples require further sequencing due to a match or inconclusive results. Of all the samples that were excluded by sequence analysis, 79% could be excluded using the HVI/HVII linear array alone. Using the HVI/HVII mtDNA linear array assay, we demonstrate the potential to decrease sequencing efforts substantially and thereby reduce the cost and the turn-around time in casework analysis.

Crime↗
PubMed2004

Haplotype analysis of the beta2 adrenergic receptor gene and risk of myocardial infarction in humans.

Polymorphisms in the beta2 adrenergic receptor (ADRB2), in particular G16R, Q27E, and T164I, have been implicated in the pathogenesis of cardiovascular and metabolic phenotypes. However, no prospective, genetic-epidemiological data are available on the risk of cardiovascular disease associated with these variants. Using DNA samples collected at baseline in a prospective cohort of 14,916 initially healthy American men, we evaluated the G16R, Q27E, and T164I polymorphisms among 523 individuals who subsequently developed myocardial infarction and among 2092 individuals who remained free of reported cardiovascular events during follow-up. The haplotype frequency distribution was significantly different among cases and controls (chi(2)(7d.f.) = 20.92, P = 0.0039). Haplotype-based logistic regression, adjusting for age, smoking, and randomized treatment group, indicated that G16-Q27-I164 (odds ratio 0.178, 95% C.I. 0.043-0.737, P = 0.017) and (non-G16-Q27)-T164 (odds ratio 1.235, 95% C.I. 1.031-1.480, P = 0.022) haplotypes were significantly associated with altered risk of myocardial infarction. These findings remained after further adjustment for BMI, history of hypertension, and presence or absence of diabetes. In conclusion, variation in haplotype frequencies for the beta2 adrenergic receptor gene was found to be associated with risk of myocardial infarction.

Cohort Studies↗
PubMed2004

Genetic variation in immunoregulatory pathways and atopic phenotypes in infancy.

BACKGROUND: Asthma is a chronic respiratory disease that often originates in early childhood. Although candidate gene studies have identified many potential asthma susceptibility genes in adult populations, few have studied associations with immune phenotypes in the first year that might be early clinical markers of asthma. OBJECTIVE: The aim of this study was to assess the contribution of genetic variation to cytokine response profiles and atopic phenotypes in the first year of life in the Childhood Origin of Asthma cohort. METHODS: Two hundred seven European American children participating in the Childhood Origin of Asthma study were genotyped for 61 single nucleotide polymorphisms in 35 genes involved in immune regulation. We examined the relationship between these single nucleotide polymorphisms and PHA-induced cytokine (IL-5, IL-10, IL-13, and IFN-gamma) response profiles at birth and at year 1, respiratory syncytial virus-induced wheezing and atopic dermatitis in the first year of life, and total IgE levels, peripheral blood eosinophil counts, and allergic sensitization at age 1 year. The data were analyzed by using censored regression for quantitative measurements and logistic regression for qualitative phenotypes. RESULTS: The 237Gly allele of the high-affinity IgE receptor beta chain (FCER1B) and a silent substitution in the nitric oxide synthase (NOS)2A gene were associated with reduced IL-13 responses in cord blood (P = .0025 and P = .0062, respectively). A significant gene-gene interaction between FCER1B 237Gly and NOS2A D346D was detected, with individuals carrying the minor allele for both polymorphisms having the lowest cord blood IL-13 levels. Furthermore, the IL13 110Gln allele showed an association with increased IgE levels at year 1 (P = .0026), and the colony-stimulating factor 2 (CSF2) 117Thr allele showed an association with a greater increase in IL-5 responses during the first year (P = .0092). The TGF-beta1 (TGFB1) -509T allele was associated with respiratory syncytial virus-related wheezing in the first year (P = .0005). None of the polymorphisms included in this study were associated with atopic dermatitis during the first year or a positive RAST result at 1 year of age. CONCLUSION: These data suggest that variations in genes involved in immune regulation are associated with biologic and clinical phenotypes in the first year of life that might increase the risk for the subsequent development of childhood asthma.

Alleles↗
PubMed2004

Are common disease susceptibility alleles the same in outbred and founder populations?

Founder populations have been the subjects of complex disease studies because of their decreased genetic heterogeneity, increased linkage disequilibrium and more homogeneous environmental exposures. However, it is possible that disease alleles identified in founder populations may not contribute significantly to susceptibility in outbred populations. In this study we examine the Hutterites, a founder population of European descent, for 103 polymorphisms in 66 genes that are candidates for cardiovascular or inflammatory diseases. We compare the frequencies of alleles at these loci in the Hutterites to their frequencies in outbred European-American populations and test for associations with cardiovascular disease-associated phenotypes in the Hutterites. We show that alleles at these loci are found at similar frequencies in the Hutterites and in outbred populations. In addition, we report associations between 39 alleles or haplotypes and cardiovascular disease phenotypes (P<0.05), with five loci remaining significant after adjusting for multiple comparisons. These data indicate that this founder population is informative and offers considerable advantages for genetic studies of common complex diseases.

Cardiovascular Diseases↗
PubMed2003

Polymorphism in the P-selectin and interleukin-4 genes as determinants of stroke: a population-based, prospective genetic analysis.

Candidate gene polymorphisms related to inflammation, thrombosis and lipid metabolism have been implicated in the development of ischemic stroke. Using DNA samples collected at baseline in a prospective cohort of 14 916 initially healthy American men, we genotyped 92 polymorphisms from 56 candidate genes among 319 individuals who subsequently developed ischemic stroke and among 2092 individuals who remained free of reported cardiovascular disease over a mean follow-up period of 13.2 years to prospectively determine whether candidate gene polymorphisms contribute to stroke risk. After adjustment for multiple comparisons and age, smoking, body mass index, hypertension, hyperlipidemia and diabetes, two related to inflammation [a val640leu polymorphism in the P-selectin gene (OR=1.63, 95% CI 1.22-2.17, P=0.001) and a C582T polymorphism in the interleukin-4 gene (OR=1.40, 95% CI 1.13-1.73, P=0.003)] were found to be independent predictors of thrombo-embolic stroke. In bootstrap replications, the inclusion of genetic information from these two polymorphisms improved prediction models for stroke based upon traditional risk factors alone (ROC 0.67 versus 0.64). Two polymorphisms related to thrombosis (an arg353gln polymorphism in the factor VII gene and a T11053G polymorphism in the plasminogen activator inhibitor type-1 gene) and one related to lipid metabolism [a C(-482)T polymorphism in the apolipoprotein CIII gene] achieved nominal significance, but were not found to be independent predictors after multiple comparison adjustment. Two inflammatory candidate gene polymorphisms were identified which were independently associated with incident stroke. These population-based data demonstrate the ability of prospective, epidemiological studies to test candidate gene associations for athero-thrombotic disease.

Aged↗
PubMed2003

Novel case-control test in a founder population identifies P-selectin as an atopy-susceptibility locus.

To avoid problems related to unknown population substructure, association studies may be conducted in founder populations. In such populations, however, the relatedness among individuals may be considerable. Neglecting such correlations among individuals can lead to seriously spurious associations. Here, we propose a method for case-control association studies of binary traits that is suitable for any set of related individuals, provided that their genealogy is known. Although we focus here on large inbred pedigrees, this method may also be used in outbred populations for case-control studies in which some individuals are relatives. We base inference on a quasi-likelihood score (QLS) function and construct a QLS test for allelic association. This approach can be used even when the pedigree structure is far too complex to use an exact-likelihood calculation. We also present an alternative approach to this test, in which we use the known genealogy to derive a correction factor for the case-control association chi2 test. We perform analytical power calculations for each of the two tests by deriving their respective noncentrality parameters. The QLS test is more powerful than the corrected chi2 test in every situation considered. Indeed, under certain regularity conditions, the QLS test is asymptotically the locally most powerful test in a general class of linear tests that includes the corrected chi2 test. The two methods are used to test for associations between three asthma-associated phenotypes and 48 SNPs in 35 candidate genes in the Hutterites. We report a highly significant novel association (P=2.10-6) between atopy and an amino acid polymorphism in the P-selectin gene, detected with the QLS test and also, but less significantly (P=.0014), with the transmission/disequilibrium test.

Alleles↗
PubMed2003

A polymorphism in the TCF7 gene, C883A, is associated with type 1 diabetes.

Type 1 diabetes is an autoimmune disease with a Th1 phenotype in which insulin-producing beta-cells in the pancreas are destroyed. The T-cell-specific transcription factor TCF7 activates genes involved in immune regulation and is a candidate locus for genetic susceptibility to type 1 diabetes. A nonsynonymous single nucleotide polymorphism (SNP) (Pro to Thr) in the TCF7 gene, C883A, was examined in samples from 282 Caucasian multiplex type 1 diabetic families. HLA-DRB1 and -DQB1 genotypes were previously determined for these samples, allowing data stratification based on HLA-associated risk. The transmission disequilibrium test showed significant overtransmission of the A allele from fathers (64.1%, P < 0.007) and nonsignificant overtransmission (57.4%, P < 0.06) of the A allele to patients who do not carry the highest-risk HLA-DR3/DR4 genotype. Elliptical sib pair analysis showed significant associations of the A allele with type 1 diabetes in paternal transmissions (P < 0.03), transmissions to male children (P < 0.04), and in the non-DR3/DR4 group (P < 0.04). These data also suggest that TCF7 C883A may affect age of disease onset. Analysis of genotype data from surrounding SNPs suggests that this TCF7 polymorphism may itself represent a risk factor for type 1 diabetes.

Adenine↗
PubMed2002

Induction of tissue factor expression in human endothelial cells by CD40 ligand is mediated via activator protein 1, nuclear factor kappa B, and Egr-1.

Induction of tissue factor expression in endothelial cells via ligation of CD40 probably figures prominently in the pathogenesis of prevalent inflammatory diseases, including atherosclerosis. However, the molecular mechanisms of tissue factor gene expression triggered by CD40 ligand (CD40L) in this cell type remain unknown. We demonstrate here that the tissue factor promoter region -278 bp to +121 bp contains the CD40L-responsive elements, consisting of activator protein 1 (AP-1)+/-, nuclear factor (NF) kappaB-, and Egr-1-binding sites. Mutations of either the AP-1- or NF-kappaB-binding sites markedly reduced the CD40L-dependent promoter activation. The AP-1 and NF-kappaB sites displayed constitutive and CD40L-enhanceable DNA binding activity, respectively. Of note, mutation of the Egr-1-binding sites, previously not associated with CD40 signaling, impaired activation of the tissue factor promoter. Accordingly, CD40L strongly induced Egr-1 protein expression and DNA binding activity to all three bindings sites. In contrast to CD40L, other established inducers of tissue factor in endothelial cells, interleukin-1beta or tumor necrosis factor alpha, did not increase the expression of Egr-1. In conclusion, induction of tissue factor gene expression in human endothelial cells by CD40L involves AP-1 and NF-kappaB as well as Egr-1, a pathway previously not implicated in CD40 signaling and distinct from that employed by certain other proinflammatory cytokines.

Base Sequence↗