PMID- 11255244
OWN - NLM
STAT- MEDLINE
DCOM- 20010607
LR  - 20151119
IS  - 0741-0395 (Print)
IS  - 0741-0395 (Linking)
VI  - 20
IP  - 3
DP  - 2001 Apr
TI  - Gibbs sampling-based segregation analysis of asthma-associated quantitative 
      traits in a population-based sample of nuclear families.
PG  - 356-72
AB  - Asthma is a common, complex human disease. Elevated serum immunoglobulin E (IgE) 
      levels, elevated blood eosinophil counts, and increased airway responsiveness are 
      physiological traits that are characteristic of asthma. Few studies have 
      investigated major gene effects for these traits in a population-based sample. 
      Further, it is not known if any putative major genes may be common to two or more 
      of these traits. We investigated the existence and nature of major genes 
      modulating asthma-associated quantitative traits in an Australian 
      population-based sample of 210 Caucasian nuclear families. The sharing of these 
      major genes was also investigated. Segregation analysis was based upon a Markov 
      Chain Monte Carlo (Gibbs sampling) approach as implemented in the program BUGS 
      v0.6. All models included adjustment for age, height, tobacco smoke exposure, and 
      gender. The segregation of total IgE levels, blood eosinophil counts, and 
      dose-response slope (DRS) of methacholine challenge were all consistent with 
      major loci at which a recessive allele acted to increase or decrease the 
      phenotype. The respective estimated frequencies of the recessive alleles were 68% 
      (total IgE), 10% (blood eosinophil count), and 27% (DRS). Extensive modelling 
      suggested that the major loci controlling total serum IgE levels, blood 
      eosinophil counts, and airway responsiveness represent different genes. These 
      data provide evidence, for the first time, of the existence of at least 3 
      distinct genetic pathways involving major gene effects on physiological traits 
      closely associated with asthma. These results have implications for gene 
      discovery programs.
CI  - Copyright 2001 Wiley-Liss, Inc.
FAU - Palmer, L J
AU  - Palmer LJ
AD  - Genetic Epidemiology Unit, Division of Population Sciences, TVW Telethon 
      Institute for Child Health Research, Perth, Western Australia. 
      lyle@ichr.uwa.edu.au
FAU - Cookson, W O
AU  - Cookson WO
FAU - James, A L
AU  - James AL
FAU - Musk, A W
AU  - Musk AW
FAU - Burton, P R
AU  - Burton PR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genet Epidemiol
JT  - Genetic epidemiology
JID - 8411723
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Asthma/blood/*genetics/physiopathology
MH  - Australia
MH  - Child
MH  - Eosinophils/cytology
MH  - Family Health
MH  - Female
MH  - Forced Expiratory Volume
MH  - Humans
MH  - Immunoglobulin E/blood
MH  - Male
MH  - *Models, Genetic
MH  - Models, Statistical
MH  - Nuclear Family
MH  - *Quantitative Trait, Heritable
MH  - Sampling Studies
MH  - Smoking
MH  - Surveys and Questionnaires
EDAT- 2001/03/20 10:00
MHDA- 2001/06/19 10:01
CRDT- 2001/03/20 10:00
PHST- 2001/03/20 10:00 [pubmed]
PHST- 2001/06/19 10:01 [medline]
PHST- 2001/03/20 10:00 [entrez]
AID - 10.1002/gepi.6 [pii]
AID - 10.1002/gepi.6 [doi]
PST - ppublish
SO  - Genet Epidemiol. 2001 Apr;20(3):356-72. doi: 10.1002/gepi.6.