Linked Life Data

9475280

Source:http://linkedlifedata.com/resource/pubmed/id/9475280

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-3-31
pubmed:abstractText
Deficiency of the lipoprotein complex, surfactant, can lead to respiratory distress syndrome (RDS) in the prematurely born infant. The surfactant proteins (SP) play important roles in the function of surfactant. Previously, we have characterized four allelic variants of the SP-A1 gene (6A, 6A2, 6A3, and 6A4) and five allelic variants of the SP-A2 gene (1A, 1A0, 1A1, 1A2, and 1A3). We hypothesized that specific SP-A alleles/genotypes are associated with increased risk of RDS. Because race, gestational age (GA), and sex are risk factors for RDS, we first studied the distribution and frequencies of SP-A alleles/genotypes while adjusting for these factors as confounders or effect modifiers in control (n = 86 white and 12 black subjects) and RDS (n = 106 white and 37 black subjects) populations with GAs ranging from 24 wk to term. Although the odds ratios of several alleles and genotypes were in the opposite directions for black and white subjects, the homogeneity of odds ratio reached statistical significance only in the case of 6A3/6A3. Although differences were observed in subgroups with different GAs (< or =28 and >28 wk) of the RDS white population, definitive conclusions cannot be made regarding the effect of modification by GA. No differences were observed as a function of sex. Second, we compared the frequencies of SP-A genotypes and alleles between control (n = 83) and RDS (n = 82) patients in the >28-wk white population. Differences between the two groups were observed for the 1A0 allele and 1A0 genotypes. Moreover, a significant synergistic positive association was observed between 1A0 allele + SP-B polymorphic variant and RDS. We conclude that 1) the genetic analyses of RDS and SP-A locus should be performed separately for black and white populations and 2) SP-A alleles/genotypes and SP-B variant may contribute to the etiology of RDS and/or may serve as markers for disease subgroups.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0031-3998
pubmed:author
pubmed:issnType
Print
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
169-77
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9475280-African Continental Ancestry Group, pubmed-meshheading:9475280-Alleles, pubmed-meshheading:9475280-European Continental Ancestry Group, pubmed-meshheading:9475280-Female, pubmed-meshheading:9475280-Gene Frequency, pubmed-meshheading:9475280-Genotype, pubmed-meshheading:9475280-Gestational Age, pubmed-meshheading:9475280-Glycoproteins, pubmed-meshheading:9475280-Humans, pubmed-meshheading:9475280-Infant, Newborn, pubmed-meshheading:9475280-Male, pubmed-meshheading:9475280-Polymorphism, Genetic, pubmed-meshheading:9475280-Proteolipids, pubmed-meshheading:9475280-Pulmonary Surfactant-Associated Protein A, pubmed-meshheading:9475280-Pulmonary Surfactant-Associated Proteins, pubmed-meshheading:9475280-Pulmonary Surfactants, pubmed-meshheading:9475280-Respiratory Distress Syndrome, Newborn
pubmed:year
1998
pubmed:articleTitle
Association of pulmonary surfactant protein A (SP-A) gene and respiratory distress syndrome: interaction with SP-B.
pubmed:affiliation
Department of Cellular and Molecular Physiology, The Pennsylvania State University, Hershey 17033, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.