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  • 1
    In: Human Heredity, S. Karger AG, Vol. 68, No. 3 ( 2009), p. 209-219
    Abstract: 〈 i 〉 Objective: 〈 /i 〉 While multiple lines of evidence suggest the importance of genetic contributors to risk of preterm birth, the nature of the genetic component has not been identified. We perform segregation analyses to identify the best fitting genetic model for gestational age, a quantitative proxy for preterm birth. 〈 i 〉 Methods: 〈 /i 〉 Because either mother or infant can be considered the proband from a preterm delivery and there is evidence to suggest that genetic factors in either one or both may influence the trait, we performed segregation analysis for gestational age either attributed to the infant (infant’s gestational age), or the mother (by averaging the gestational ages at which her children were delivered), using 96 multiplex preterm families. 〈 i 〉 Results: 〈 /i 〉 These data lend further support to a genetic component contributing to birth timing since sporadic (i.e. no familial resemblance) and nontransmission (i.e. environmental factors alone contribute to gestational age) models are strongly rejected. Analyses of gestational age attributed to the infant support a model in which mother’s genome and/or maternally-inherited genes acting in the fetus are largely responsible for birth timing, with a smaller contribution from the paternally-inherited alleles in the fetal genome. 〈 i 〉 Conclusion: 〈 /i 〉 Our findings suggest that genetic influences on birth timing are important and likely complex.
    Type of Medium: Online Resource
    ISSN: 0001-5652 , 1423-0062
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2009
    detail.hit.zdb_id: 1482710-4
    SSG: 12
    Location Call Number Limitation Availability
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  • 2
    In: Human Heredity, S. Karger AG, Vol. 59, No. 1 ( 2005), p. 34-40
    Abstract: 〈 i 〉 Objective: 〈 /i 〉 Despite the well known genetic component influencing plasma lipid-lipoprotein levels and the observed correlations among these traits, little is known about pleiotropic heritable determinants among them. Our aim is to investigate pair-wise polygenic and environmental correlations among lipid-lipoprotein levels at baseline and in response to regular exercise in Whites and Blacks. 〈 i 〉 Methods: 〈 /i 〉 Common pair-wise genetic and environmental correlations among levels of total cholesterol (TC), LDL-C, ApoB, HDL-C (also HDL 〈 sub 〉 2 〈 /sub 〉 -C and HDL 〈 sub 〉 3 〈 /sub 〉 -C), triglycerides (TG, HDL-TG and LDL-TG) and ApoA-1 were investigated at baseline and again after a 20-week endurance exercise program using a variance-components-decomposition. 〈 i 〉 Results: 〈 /i 〉 With a few exceptions, all lipid phenotypes were heritable at baseline and for training responses in Blacks and Whites. Strong to high genetic and environmental correlations (0.4 〈 ρ 〈 sub 〉 g 〈 /sub 〉 〈 0.7) were observed for the majority of the baseline pair-wise traits. For training responses, many of the same patterns were noted, although fewer genetic correlations were significant as compared to the baseline results. 〈 i 〉 Conclusions: 〈 /i 〉 Results suggest that the observed phenotypic correlations among many of these traits may be due to in part to pleiotropic genes, in particular between LDL-C and ApoB and between TG and HDL-C. This shared genetic architecture should be considered in follow-up gene finding studies.
    Type of Medium: Online Resource
    ISSN: 0001-5652 , 1423-0062
    RVK:
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2005
    detail.hit.zdb_id: 1482710-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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