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Chambers ; J. S. Kooner ; D. P. Strachan ; H. Campbell ; J. N. Hirschhorn ; M. Perola ; O. Polasek ; J. F. Wilson
    Nature Publishing Group (NPG)
    Published 2015
    Staff View
    Publication Date:
    2015-07-02
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Biological Evolution ; Blood Pressure/genetics ; Body Height/*genetics ; Cholesterol, LDL/genetics ; *Cognition ; Cohort Studies ; Educational Status ; Female ; Forced Expiratory Volume/genetics ; Genome, Human/genetics ; *Homozygote ; Humans ; Lung Volume Measurements ; Male ; Phenotype
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Staff View
    ISSN:
    1365-2222
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Medicine
    Notes:
    Background Allergic asthma is a multifactorial disease for which there is a widely assessed, although poorly understood, genetic involvement. Genome-wide screens reported evidence for linkage of allergic asthma-related phenotypes to several chromosomal locations. Markers on chromosome 19 have been linked to allergic asthma phenotypes in different populations in independent studies.Objective The aim of this study was to perform a genetic linkage analysis on chromosome 19 to search for DNA markers linked to phenotypes related to allergic asthma.Methods Using non-parametric multipoint linkage analysis on a total of 22 random DNA markers in 2 stages, a sample of 111 families (542 subjects) from north-eastern Italy, recruited through an asthmatic allergic proband, was investigated. Phenotypes examined were: clinical asthma, total serum elevated IgE, skin prick test positivity, bronchial hyper-responsiveness, and atopy defined as skin prick test positivity and/or elevated IgE. Simulation studies were performed to confirm the significance of the results.Results A novel linkage of atopy and skin prick test positivity to marker D19S601 (19q13.3) was found. Modest evidence for linkage of atopy, skin prick test positivity, and IgE was also found to marker D19S591 (19p13.3). Simulation analysis for atopy gave an NPL-Z 〉 3.326 in 2 replicates out of 1000 (P = 0.002) for D19S601, and an NPL-Z 〉 2.56 in 16 replicates out of 1000 (P = 0.016) for D19S591.Conclusions On chromosome 19, suggestive linkage of atopy and skin prick test positivity with marker D19S601 (19q13.3) and modest evidence of linkage of marker D19S591 (19p13.3) to the atopic phenotypes investigated were found. These results suggest that these regions may contain susceptibility loci associated to atopic phenotypes.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1046/j.1365-2222.2001.01132.x

    Articles: DFG German National Licenses
  3. 3
    Staff View
    ISSN:
    1432-0827
    Keywords:
    Key words: COLIA1 — CTR — Genetics — Bone mass — Osteoporosis
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Biology
    Medicine
    Physics
    Notes:
    Abstract. The variability of bone mass and bone strength is in part genetically determined. The pathophysiology of the disease is complex and its heritability is almost certainly polygenic. In a large group of women from north eastern Italy, homogeneous for calcium intake and other risk factors for osteoporosis, we investigated three different genetic polymorphic markers that have been associated with bone mineral density (BMD). The study includes 663 postmenopausal (aged 48–85 years) and 52 perimenopausal (aged 47–53 years) women. Lumbar spine and hip BMD were measured by dual energy X-ray absorptiometry (DXA). After DNA extraction, the restriction enzymes utilized were MscI for the SP1 site of the collagen type I regulatory region (COLIA1), AluI for the calcitonin receptor (CTR) gene, and BsmI for the Vitamin D receptor (VDR) gene. COLIA1 genotype was significantly associated with age-adjusted hip BMD, with the highest values in the SS group and the lowest in the ss group (p 〈 0.05). The COLIA1 effect was not visible until the sixth decade of life, but it increased thereafter with aging, becoming statistically significant also at the lumbar spine in subjects aged 〉70 years. CTR genotype was also significantly related to bone mass in the CC group, with the lowest age and weight-adjusted BMD values at the spine (p 〈 0.05). The CTR genotype effect was greater in the younger subset of women. This suggests that the CTR genotype might influence the process of acquiring peak bone mass rather than the process of bone loss along aging. No trend association was found between BMD values and VDR genotype. These findings suggest an association between the COLIA1 gene polymorphism more with the age-related rate of bone loss than with peak bone mass, which apparently is somewhat affected by CTR gene polymorphism.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s002230001160

    Articles: DFG German National Licenses