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Biomedical subjects

Alan James

Publications and source records attributed to Alan James.

5 recordsLinked to original sources
PubMed2006

Longitudinal study of risk factors for habitual snoring in a general adult population: the Busselton Health Study.

BACKGROUND: The aim of this longitudinal study was to identify body size, behavioral, and respiratory risk factors for the development of habitual snoring in a general adult population. METHODS: The sample for this study comprised 967 adults aged 25 to 74 years who reported not snoring in the 1981 Busselton Health Survey and who also attended the 1994-1995 follow-up survey. Logistic regression was used to identify and quantify the effect of baseline and change risk factors for the development of habitual snoring. RESULTS: A total of 13% had become habitual snorers by 1994-1995. Male gender (odds ratio [OR], 3.5) and baseline body mass index (OR, 1.4 per 3.4 kg/m(2)) were significant predictors of habitual snoring; after accounting for these variables, no other baseline body size, behavioral, or respiratory/allergy variables were significantly related to the development of habitual snoring. However, change in body mass index over the 14-year follow-up period (OR, 1.55 per 2.3 kg/m(2)), development of asthma (OR, 2.8), and commencement of smoking (OR, 2.2) were additional significant independent risk factors for development of habitual snoring. CONCLUSIONS: This study has confirmed male gender, obesity, and weight gain as key determinants of habitual snoring, and has indicated that development of asthma and taking up smoking also play a role. Maintaining a healthy weight and not smoking are recommended lifestyle preventive strategies to reduce the risk of sleep-disordered breathing and its sequelae.

Adult↗
PubMed2005

NOD1 variation, immunoglobulin E and asthma.

Asthma is a familial inflammatory disease of the airways of the lung. Microbial exposures in childhood protect against asthma through unknown mechanisms. The innate immune system is able to identify microbial components through a variety of pattern-recognition receptors (PRRs). NOD1 is an intracellular PRR that initiates inflammation in response to bacterial diaminopimelic acid (iE-DAP). The NOD1 gene is on chromosome 7p14, in a region that has been genetically linked to asthma. We carried out a systematic search for polymorphism in the gene. We found an insertion-deletion polymorphism (ND(1)+32656) near the beginning of intron IX that accounted for approximately 7% of the variation in IgE in two panels of families (P<0.0005 in each). Allele*2 (the insertion) was associated with high IgE levels. The same allele was strongly associated with asthma in an independent study of 600 asthmatic children and 1194 super-normal controls [odds ratio (OR) 6.3; 95% confidence interval (CI) 1.4-28.3, dominant model]. Differential binding of the two ND(1)+32656 alleles was observed to a protein from nuclei of the Calu 3 epithelial cell line. In an accompanying study, the deletion allele (ND(1)+32656*1) was found to be associated with inflammatory bowel disease. The results indicate that intracellular recognition of specific bacterial products affects the presence of childhood asthma.

Adaptor Proteins, Signal Transducing↗
PubMed2005

Airway remodeling in asthma.

PURPOSE OF REVIEW: This overview summarizes some the more recent studies of remodeling in patients with asthma, studies using animal models to study the interaction of cell types and mediators, and studies using in vitro models to assess the effects of mitogenic stimuli, including mechanical strain, on mesenchymal cells and extracellular matrix proteins. The aim is to demonstrate how the term remodeling is becoming increasingly less specific as reductionism is applied to this field of study. RECENT FINDINGS: Specific areas of recent interest include plasticity of airway smooth muscle and fibroblast phenotype; the role of the extracellular matrix and its relation to the function of the airway smooth muscle and the mechanical properties of the airway wall; mitogenic stimuli arising from damaged epithelium, fibroblasts, smooth muscle cells, mast cells, eosinophils, and mechanical stress; extracellular and intracellular signaling in fibroblasts and smooth muscle cells; and therapeutic targets among the many pathways of remodeling-pathways that may be distinct from those involved in inflammation. The potential functional consequences of some of these findings call into question the role of remodeling. In some respects, it may represent a continuum from inflammation to scarring, but it may also be a protective response to altered airway mechanics caused by ongoing tissue damage or by abnormal airway structure present from early in life. SUMMARY: The diverse areas of research in this field are increasingly making the term remodeling as useful (or not) as the word asthma, because both can be used to describe simultaneously a large number of processes that may or may not be related to each other.

Animals↗
PubMed2003

Atopy, respiratory function and HLA-DR in Aboriginal Australians.

The Class II genes of the MHC represent a major locus with quantified effects on atopic (allergic) phenotypes in many studies of westernized Caucasians. Although asthma is considered a disease of western societies, typical components of the asthma phenotype, such as elevations of the IgE, are seen with parasitic infestation. We have therefore investigated the effects of the HLA-DRB1 locus on asthma and its intermediate phenotypes in Aboriginal people from the Kimberly region of Australia who were suffering from endemic hookworm infection. Recognizable correlates of allergic asthma were present in the subjects, including skin test positivity to house dust mite (HDM), specific IgE responses to HDM, and the total serum IgE. HLA-DRB1 alleles did not predict the presence of asthma, but multi-allelic tests of association showed the locus accounted for approximately 33% of the variance of the total serum IgE concentration and 17% of the variance of the specific IgE titres to HDM. Genetic admixture was excluded as a cause of the results. These effects of the MHC on IgE levels were an order of magnitude greater than that seen in Caucasians, consistent with the hypothesis that the genetic predisposition to allergic disease may be driven by adaptation to helminth infection. The results further suggest that parasitism per se is not protective against asthma.

Adolescent↗