By Dirkje S. Postma, Scott T. Weiss
Responding to the large progress that has taken position within the box over the last decade, this reference offers an in-depth assessment of present proposal at the genetics and genomics of bronchial asthma and COPD relating to their pathogenesis and therapy. With contributions by way of an esteemed workforce of foreign professionals at the subject, this resource spans the newest advancements within the usage of microarray concepts, linkage and organization stories, mapping recommendations, comparative genetics, microarray options, proteomics, and pharmacogenomics.
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Extra resources for Genetics of Asthma and Chronic Obstructive Pulmonary Disease (Lung Biology in Health and Disease 218)
Sample text
Within a given family, individuals who share the disease phenotype will also share alleles at markers near the disease gene. If allele sharing occurs significantly more often than expected by chance, linkage of the particular marker with the disease can be assumed, indicating that the chromosomal region containing the marker also contains a gene that contributes to the disease trait. Results of linkage analysis are reported as logarithm of the odds (LOD) of sharing a chromosomal region. A positive LOD score is indicative of a region linked to the disease.
Genome-Wide Linkage Analysis Genome-wide linkage analysis is an approach to identify which chromosomal areas are involved in disease. This method compares the inheritance of disease with inheritance of genetic markers in families with multiple affected members. If the disease is coinherited with the marker, this suggests that a disease susceptibility gene is located close to the marker of that chromosome. The first studies on linkage analyses for COPD were performed in the Boston severe early-onset COPD population.
2 Genetic Epidemiology of Reduced Lung Function CLEO C. VAN DIEMEN and H. MARIKE BOEZEN Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands I. Introduction Genetic epidemiology of respiratory disease focuses on identifying genetic determinants of disease development taking environmental factors that preclude, affect, or enhance this development, into account. The respiratory disease chronic obstructive pulmonary disease (COPD) is almost fully attributable to the environmental factor, smoking, with the exception of the genetical predominance of a1-antitrypsine (AAT) deficiency gene, which carriers need no further environmental smoke exposure to develop a phenotypic expression of COPD.