Apolipoprotein E phenotype, arterial disease, and mortality among older women: the study of osteoporotic fractures.

Abstract:

:This study is an investigation of the relationship between apolipoprotein E (apoE) phenotype, arterial disease, and mortality in a group of women (n = 1,751) aged 65 years and older enrolled in the Study of Osteoporotic Fractures. Crude mortality rates were highest among women with the 4-3 and 4-4 phenotypes but age-adjusted mortality showed no statistically significant variations across the phenotype groups. Using multivariate analysis, the mortality experience of women with 4-3 or 4-4 apoE phenotypes was compared to that of women with the 3-3 phenotype: no significant excess total mortality was found [relative risk (RR) = 1.2, 95% confidence interval (CI) 0.8, 1.8] among women with the epsilon 4 allele. Similarly, neither cardiovascular (RR = 0.9. 95% CI 0.5, 1.8) nor cancer (RR = 1.5, 95% CI 0.8, 2.8) mortality rates were significantly different in this group of women. Inclusion of cholesterol levels in the regression models did not change the relative mortality risks. Among women 65-69 year of age epsilon 4 was associated with an approximate doubling of RR for death due to both cardiovascular disease and cancer. No association was found between apoE phenotype and the presence of lower extremity arterial disease (defined as an ankle/arm index of 0.9 or less). These results suggest that women with the epsilon 4 who survive to age 70 years or beyond have a life expectancy that is similar to that for women homozygous for the 3 allele who comprise the majority of the population.

journal_name

Genet Epidemiol

journal_title

Genetic epidemiology

authors

Vogt MT,Cauley JA,Kuller LH

doi

10.1002/(SICI)1098-2272(1997)14:2<147::AID-GEPI4>3

subject

Has Abstract

pub_date

1997-01-01 00:00:00

pages

147-56

issue

2

eissn

0741-0395

issn

1098-2272

pii

10.1002/(SICI)1098-2272(1997)14:2<147::AID-GEPI4>3

journal_volume

14

pub_type

临床试验,杂志文章,多中心研究
  • Identifying genetic interactions in genome-wide data using Bayesian networks.

    abstract::It is believed that interactions among genes (epistasis) may play an important role in susceptibility to common diseases (Moore and Williams [2002]. Ann Med 34:88-95; Ritchie et al. [2001]. Am J Hum Genet 69:138-147). To study the underlying genetic variants of diseases, genome-wide association studies (GWAS) that sim...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.20514

    authors: Jiang X,Barmada MM,Visweswaran S

    更新日期:2010-09-01 00:00:00

  • Improving estimates of genetic maps: a meta-analysis-based approach.

    abstract::Inaccurate genetic (or linkage) maps can reduce the power to detect linkage, increase type I error, and distort haplotype and relationship inference. To improve the accuracy of existing maps, I propose a meta-analysis-based method that combines independent map estimates into a single estimate of the linkage map. The m...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.20221

    authors: Stewart WC

    更新日期:2007-07-01 00:00:00

  • Regressive logistic and proportional hazards disease models for within-family analyses of measured genotypes, with application to a CYP17 polymorphism and breast cancer.

    abstract::Various statistical methods have been proposed to evaluate associations between measured genetic variants and disease, including some using family designs. For breast cancer and rare variants, we applied a modified segregation analysis method that uses the population cancer incidence and population-based case families...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.10222

    authors: Cui JS,Spurdle AB,Southey MC,Dite GS,Venter DJ,McCredie MR,Giles GG,Chenevix-Trench G,Hopper JL

    更新日期:2003-04-01 00:00:00

  • A novel association test for multiple secondary phenotypes from a case-control GWAS.

    abstract::In the past decade, many genome-wide association studies (GWASs) have been conducted to explore association of single nucleotide polymorphisms (SNPs) with complex diseases using a case-control design. These GWASs not only collect information on the disease status (primary phenotype, D) and the SNPs (genotypes, X), but...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章,随机对照试验

    doi:10.1002/gepi.22045

    authors: Ray D,Basu S

    更新日期:2017-07-01 00:00:00

  • SimPEL: Simulation-based power estimation for sequencing studies of low-prevalence conditions.

    abstract::Power estimations are important for optimizing genotype-phenotype association study designs. However, existing frameworks are designed for common disorders, and thus ill-suited for the inherent challenges of studies for low-prevalence conditions such as rare diseases and infrequent adverse drug reactions. These challe...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.22129

    authors: Mak L,Li M,Cao C,Gordon P,Tarailo-Graovac M,Bousman C,Wang P,Long Q

    更新日期:2018-07-01 00:00:00

  • Generalization of the extended transmission disequilibrium test to two unlinked disease loci.

    abstract::The extended transmission disequilibrium test (ETDT) of Sham and Curtis [1995] is a powerful test of the null hypothesis of no linkage between a multi-allelic marker locus and a disease susceptibility locus of unknown location in the presence of association between alleles at the two loci. We propose a generalization ...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.13701707108

    authors: Morris A,Whittaker J

    更新日期:1999-01-01 00:00:00

  • Haplotype kernel association test as a powerful method to identify chromosomal regions harboring uncommon causal variants.

    abstract::For most complex diseases, the fraction of heritability that can be explained by the variants discovered from genome-wide association studies is minor. Although the so-called "rare variants" (minor allele frequency [MAF] < 1%) have attracted increasing attention, they are unlikely to account for much of the "missing h...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.21740

    authors: Lin WY,Yi N,Lou XY,Zhi D,Zhang K,Gao G,Tiwari HK,Liu N

    更新日期:2013-09-01 00:00:00

  • Improving power for rare-variant tests by integrating external controls.

    abstract::Due to the drop in sequencing cost, the number of sequenced genomes is increasing rapidly. To improve power of rare-variant tests, these sequenced samples could be used as external control samples in addition to control samples from the study itself. However, when using external controls, possible batch effects due to...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.22057

    authors: Lee S,Kim S,Fuchsberger C

    更新日期:2017-11-01 00:00:00

  • Pleiotropy and principal components of heritability combine to increase power for association analysis.

    abstract::When many correlated traits are measured the potential exists to discover the coordinated control of these traits via genotyped polymorphisms. A common statistical approach to this problem involves assessing the relationship between each phenotype and each single nucleotide polymorphism (SNP) individually (PHN); and t...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.20257

    authors: Klei L,Luca D,Devlin B,Roeder K

    更新日期:2008-01-01 00:00:00

  • Innovative approach to identify multigenomic and environmental interactions associated with birth defects in family-based hybrid designs.

    abstract::Genes, including those with transgenerational effects, work in concert with behavioral, environmental, and social factors via complex biological networks to determine human health. Understanding complex relationships between causal factors underlying human health is an essential step towards deciphering biological mec...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.22363

    authors: Lou XY,Hou TT,Liu SY,Xu HM,Lin F,Tang X,MacLeod SL,Cleves MA,Hobbs CA

    更新日期:2020-09-30 00:00:00

  • GAW10: simulated family data for a common oligogenic disease with quantitative risk factors.

    abstract::GAW10 Problem 2 involves a simulated common disease defined by imposing a threshold, T, on a quantitative trait, Q1. Every individual with a value of Q1 > or = T (where T = 40) is defined as affected. Also thought to be associated with the disease as intervening variables are four other quantitative traits (Q2, Q3, Q4...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/(SICI)1098-2272(1997)14:6<737::AID-GEPI29>

    authors: MacCluer JW,Blangero J,Dyer TD,Speer MC

    更新日期:1997-01-01 00:00:00

  • Linkage analysis in alcohol dependence.

    abstract::Alcohol dependence often is a familial disorder and has a genetic component. Research in causative factors of alcoholism is coordinated by a multi-center program, COGA [The Collaborative Study on the Genetics of Alcoholism, Begleiter et al., 1995]. We analyzed a subset of the COGA family sample, 84 pedigrees of Caucas...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.1370170768

    authors: Windemuth C,Hahn A,Strauch K,Baur MP,Wienker TF

    更新日期:1999-01-01 00:00:00

  • Multiethnic polygenic risk scores improve risk prediction in diverse populations.

    abstract::Methods for genetic risk prediction have been widely investigated in recent years. However, most available training data involves European samples, and it is currently unclear how to accurately predict disease risk in other populations. Previous studies have used either training data from European samples in large sam...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.22083

    authors: Márquez-Luna C,Loh PR,South Asian Type 2 Diabetes (SAT2D) Consortium.,SIGMA Type 2 Diabetes Consortium.,Price AL

    更新日期:2017-12-01 00:00:00

  • The power of iterated generalized least squares (GLS) method to detect direct relationships in the analysis of correlated quantitative traits.

    abstract::We examined the power of the stepwise iterated generalized least squares (GLS) method by modeling the relationship between quantitative traits and other variables using the simulated data for Problem 2A. The comparison between the generating model provided by the workshop and the results of the stepwise iterated GLS m...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/(SICI)1098-2272(1997)14:6<797::AID-GEPI39>

    authors: He Q,Nemesure BB,Mendell NR

    更新日期:1997-01-01 00:00:00

  • Parental transmission and D18S37 allele sharing in bipolar affective disorder.

    abstract::We combined the five chromosome 18 bipolar affective disorder data sets provided by GAW10, totaling 185 families with 3,394 individuals, and performed analysis of differential parental transmission and chromosome 18 marker allele sharing in families with transmission through fathers vs those through mothers. Results i...

    journal_title:Genetic epidemiology

    pub_type: 临床试验,杂志文章

    doi:10.1002/(SICI)1098-2272(1997)14:6<665::AID-GEPI19>

    authors: Lin JP,Bale SJ

    更新日期:1997-01-01 00:00:00

  • A general autosomal/X-linked model.

    abstract::This paper describes a general genetic model which encompasses both autosomal and X-linked inheritance as submodels. It allows one to test for X-linked inheritance of a trait by comparing the likelihood of X-linked inheritance to the likelihood of the general genetic model. The general model is formulated as two loci,...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.1370010105

    authors: Hasstedt SJ,Skolnick M

    更新日期:1984-01-01 00:00:00

  • A two-locus model for familial Alzheimer's disease?

    abstract::The present findings for familial Alzheimer's disease suggest a possible linkage to gene(s) on chromosome 21 for the early onset form and to chromosome 19 for the late onset. Since these results are not unequivocal, possible alternative hypotheses include the effect of genetic heterogeneity or of an oligogenic model o...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.1370100618

    authors: Macciardi F,Cavallini MC

    更新日期:1993-01-01 00:00:00

  • Model-based linkage analysis with imprinting for quantitative traits: ignoring imprinting effects can severely jeopardize detection of linkage.

    abstract::Genes with imprinting (parent-of-origin) effects express differently when inheriting from the mother or from the father. Some genes for development and behavior in mammals are known to be imprinted. We developed parametric linkage analysis that accounts for imprinting effects for continuous traits, implementing it in ...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.20321

    authors: Sung YJ,Rao DC

    更新日期:2008-07-01 00:00:00

  • Genetic epidemiology with a capital "E".

    abstract::Three characteristics of genetic epidemiology that distinguish it from its parent disciplines are a focus on population-based research, a focus on the joint effects of genes and the environment, and the incorporation of the underlying biology of the disease into its conceptual models. These principles are illustrated ...

    journal_title:Genetic epidemiology

    pub_type:

    doi:10.1002/1098-2272(200012)19:4<289::AID-GEPI2>3.0.C

    authors: Thomas DC

    更新日期:2000-12-01 00:00:00

  • Logistic transmission modeling for the simulated data of GAW10 problem 2.

    abstract::A recently developed nonparametric method is a generalization of the transmission disequilibrium test across all alleles of a locus. This approach has been applied to Problem 2 of GAW10 and has been extended to explore the combined contribution of neighboring loci for chromosomes 1, 5, and 8. When applied to the chrom...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/(SICI)1098-2272(1997)14:6<857::AID-GEPI49>

    authors: Neas BR,Moser KL,Harley JB

    更新日期:1997-01-01 00:00:00

  • Meta-Analysis of Rare Variant Association Tests in Multiethnic Populations.

    abstract::Several methods have been proposed to increase power in rare variant association testing by aggregating information from individual rare variants (MAF < 0.005). However, how to best combine rare variants across multiple ethnicities and the relative performance of designs using different ethnic sampling fractions remai...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.21939

    authors: Mensah-Ablorh A,Lindstrom S,Haiman CA,Henderson BE,Marchand LL,Lee S,Stram DO,Eliassen AH,Price A,Kraft P

    更新日期:2016-01-01 00:00:00

  • Phenotype validation in electronic health records based genetic association studies.

    abstract::The linkage between electronic health records (EHRs) and genotype data makes it plausible to study the genetic susceptibility of a wide range of disease phenotypes. Despite that EHR-derived phenotype data are subjected to misclassification, it has been shown useful for discovering susceptible genes, particularly in th...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.22080

    authors: Wang L,Damrauer SM,Zhang H,Zhang AX,Xiao R,Moore JH,Chen J

    更新日期:2017-12-01 00:00:00

  • Linkage analysis of asthma and atopy including models with genomic imprinting.

    abstract::Asthma and atopy are two closely related, common complex traits in which a number of genetic and environmental factors are suspected to play a role. We have performed parametric and nonparametric multi-marker linkage analysis for the Busselton data set, which is part of problem 1 of Genetic Analysis Workshop 12. In pa...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.2001.21.s1.s204

    authors: Strauch K,Bogdanow M,Fimmers R,Baur MP,Wienker TF

    更新日期:2001-01-01 00:00:00

  • Haplotype sharing analysis in affected individuals from nuclear families with at least one affected offspring.

    abstract::In diseases with a complex mode of inheritance, families with multiple affected individuals are difficult to ascertain. The haplotype sharing statistic (HSS) uses (hidden) co-ancestry between affected individuals from a founder population. These affected individuals will likely not only share the same mutation(s), but...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/(SICI)1098-2272(1997)14:6<915::AID-GEPI59>

    authors: Van der Meulen MA,te Meerman GJ

    更新日期:1997-01-01 00:00:00

  • Sib-pair linkage tests for disease susceptibility loci: common tests vs. the asymptotically most powerful test.

    abstract::Several statistical tests for linkage between a disease susceptibility locus and a marker locus for sib-pair data are examined analytically. Two common statistics, a test based on the mean number of marker alleles shared identical by descent by sib-pairs, and a test based on the proportion of sib-pairs sharing exactly...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.1370070506

    authors: Schaid DJ,Nick TG

    更新日期:1990-01-01 00:00:00

  • Combining family- and population-based imputation data for association analysis of rare and common variants in large pedigrees.

    abstract::In the last two decades, complex traits have become the main focus of genetic studies. The hypothesis that both rare and common variants are associated with complex traits is increasingly being discussed. Family-based association studies using relatively large pedigrees are suitable for both rare and common variant id...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.21844

    authors: Saad M,Wijsman EM

    更新日期:2014-11-01 00:00:00

  • Testing the utility of mod scores and sib-pair analysis to detect presence of disease susceptibility loci.

    abstract::Linkage analyses and association studies were employed to detect disease susceptibility loci leading to elevated Q1 levels in Problem 2B. Phenotypes were defined to be the dichotomous affection status, the quantitative value for Q1, and Q1 adjusted for covariates. The method of mod-scores (for the dichotomous phenotyp...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/(SICI)1098-2272(1997)14:6<1035::AID-GEPI79

    authors: Neuman RJ,Xian H

    更新日期:1997-01-01 00:00:00

  • Data mining and computationally intensive methods: summary of Group 7 contributions to Genetic Analysis Workshop 13.

    abstract::The Framingham Heart Study data, as well as a related simulated data set, were generously provided to the participants of the Genetic Analysis Workshop 13 in order that newly developed and emerging statistical methodologies could be tested on that well-characterized data set. The impetus driving the development of nov...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.10285

    authors: Costello TJ,Falk CT,Ye KQ

    更新日期:2003-01-01 00:00:00

  • Pooling data and linkage analysis in the chromosome 5q candidate region for asthma.

    abstract::We investigated a variety of methods for pooling data from eight data sets (n = 5,424 subjects) to validate evidence for linkage of markers in the cytokine cluster on chromosome 5q31-33 to asthma and asthma-associated phenotypes. Chromosome 5 markers were integrated into current genetic linkage and physical maps, and ...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章,meta分析

    doi:10.1002/gepi.2001.21.s1.s103

    authors: Jacobs KB,Burton PR,Iyengar SK,Elston RC,Palmer LJ

    更新日期:2001-01-01 00:00:00

  • Association and linkage analysis of ICD-10 diagnosis for alcoholism.

    abstract::We analyzed the GAW11 data on alcoholism provided by the Collaborative Study on the Genetics of Alcoholism (COGA) using an extension of a new test of linkage and association for quantitative traits developed by George et al. [1999]. This method determines linkage between marker loci and quantitative traits, when allel...

    journal_title:Genetic epidemiology

    pub_type: 杂志文章

    doi:10.1002/gepi.1370170758

    authors: Tiwari HK,Zhu X,Elston RC,Shu Y,George V

    更新日期:1999-01-01 00:00:00