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- Lindberg, Anne, et al.
(författare)
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Seven-year cumulative incidence of COPD in an age-stratified general population sample.
- 2006
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Ingår i: Chest. - : Elsevier BV. - 0012-3692 .- 1931-3543. ; 129:4, s. 879-885
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To estimate the cumulative incidence of COPD and risk factors related to the development of COPD, including evaluation of the relationship between Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 0 (ie, respiratory symptoms and normal lung function) and the development of COPD, in an age-stratified general population sample of middle-aged and elderly individuals. METHOD: The third survey of the Obstructive Lung Disease in Northern Sweden studies cohort I (three age strata born in 1919 to 1920, 1934 to 1935, and 1949 to 1950) was performed in 1996, and 5,189 subjects (88%) responded to the postal questionnaire. Of the responders, a random sample (1,500 subjects) was invited to an examination in 1996 and in 2003. A total of 963 subjects performed spirometry on both occasions. COPD was defined according to the spirometric criteria of the GOLD. Two levels of disease severity, grade I and higher (GOLD criteria, FEV(1)/FVC ratio of < 0.70) and also grade II and higher (GOLD II criteria, FEV(1)/FVC ratio of < 0.70 and FEV(1) <80% predicted). RESULTS: The 7-year cumulative incidence of COPD was 11.0% and 4.9%, respectively, according to GOLD and GOLD II, and was significantly related to smoking (smokers, 18.8% and 10.6%, respectively; ex-smokers, 10.5% and 5.2%, respectively; non-smokers, 7.6% and 1.6%, respectively). Incident COPD according to GOLD, but not according to GOLD II, was significantly associated with increasing age. Most respiratory symptoms at study entry were markers of increased risk for incident COPD when analyzed in a multivariate model adjusting for confounders. CONCLUSION: The GOLD criteria yielded a higher cumulative incidence (11.0%) compared to the GOLD II (4.9%). Smoking, but not gender, was associated with incident COPD. Most respiratory symptoms at the beginning of the observation period marked an increased risk for developing COPD, thus the classification GOLD stage 0 seems relevant among middle-aged and elderly persons.
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- Lundbäck, Bo, 1948, et al.
(författare)
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A 20-year follow-up of a population study-based COPD cohort-report from the obstructive lung disease in Northern Sweden studies.
- 2009
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Ingår i: COPD: Journal of Chronic Obstructive Pulmonary Disease. - : Informa UK Limited. - 1541-2563 .- 1541-2555. ; 6:4, s. 263-71
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Tidskriftsartikel (refereegranskat)abstract
- Mortality and other long-term outcomes of COPD from epidemiological studies of cohorts based on the general population are still rare. In contrast, data from follow-ups of patients from hospitals and general practices are more common and demonstrate often a 5-year mortality of about 50% and even higher. The aim was to study 20-year outcomes, mainly mortality, in a COPD cohort derived from a population study. The Obstructive Lung Disease in Northern Sweden (OLIN) Study's first postal survey was performed in 1985, and 5698 subjects (86%) responded. A stratified sample of symptomatic subjects and controls was invited to clinical examinations including lung function tests in 1986, 1506 (91%) of the invited participated and 266 subjects fulfilled the GOLD criteria of COPD. All alive and possible to trace had participated at least at two follow-up examinations. Of the 266 subjects with COPD 46% were still alive after 20 years. The proportion of survived among subjects with severe and very severe COPD at entry was 19%. Death was significantly related to age, male sex, disease severity and concomitant ischemic heart disease or cardiac failure at entry. Socioeconomic status (manual workers) was significant in the univariate analysis, but failed to reach statistical significance in the multivariate model. The annual decline in FEV(1) among survivors was low to normal. Long-term follow-ups of subjects with COPD derived from population studies provide data reflecting the course of COPD in society better than follow-ups of hospital recruited patients, who represent the top of the iceberg. Surprisingly many with severe COPD were still alive after 20 years.
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- Mälarstig, Anders, et al.
(författare)
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Variants of the interferon regulatory factor 5 gene regulate expression of IRF5 mRNA in atherosclerotic tissue but are not associated with myocardial infarction
- 2008
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Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - 1079-5642 .- 1524-4636. ; 28:5, s. 975-982
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Signaling events after activation of toll-like receptors (TLRs) are important mechanisms promoting inflammation in the atherosclerotic plaque. INF regulatory factor 5 (IRF5) is one of the mediators of downstream effects of TLRs. Several single nucleotide polymorphisms (SNPs) in the IRF5 gene have been found to be associated with systemic lupus erythematosus. METHODS AND RESULTS: We examined IRF5 mRNA expression in carotid atherosclerotic tissue (n=99) and the case-control association between SNPs in the IRF5 gene with myocardial infarction (MI) (n=376+387) and unstable coronary artery disease (CAD) (n=3101+445). Among unstable CAD patients, association of IRF5 SNPs with recurrent coronary events (n=401) was also investigated. The IRF5 mRNA expression was increased in atherosclerotic tissue compared with control tissue (P<0.001). Significant associations with IRF5 expression was observed for 6 of 10 SNPs in the study. However, the IRF5 SNPs examined were neither associated with the risk of precocious MI, nor with unstable CAD or risk of recurrent cardiovascular events in unstable CAD patients. CONCLUSIONS: IRF5 mRNA is expressed in cells in atherosclerotic tissue and its expression is modified by SNPs in the IRF5 gene. Genetic variation at the IRF5 locus was, however, not associated with CAD or related phenotypes.
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- Olofsson, P. S., et al.
(författare)
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Genetic variants of TNFSF4 and risk for carotid artery disease and stroke
- 2009
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Ingår i: Journal of Molecular Medicine. - New York : Springer. - 0946-2716 .- 1432-1440. ; 87:4, s. 337-346
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Tidskriftsartikel (refereegranskat)abstract
- In two independent human cohorts, the minor allele of SNP rs3850641 in TNFSF4 was significantly more frequent in individuals with myocardial infarction than in controls. In mice, Tnfsf4 expression is associated with increased atherosclerosis. The expression of TNFSF4 in human atherosclerosis and the association between genotype and cerebrovascular disease have not yet been investigated. TNFSF4 messenger RNA (mRNA) levels were significantly higher in human atherosclerotic lesions compared with controls (730∈±∈30 vs 330∈±∈65 arbitrary units, p∈<∈0.01). TNFSF4 was mainly expressed by macrophages in atherosclerotic lesions. In cell culture, endothelial cells upregulated TNFSF4 in response to tumor necrosis factor alpha (TNF-α; 460∈±∈110 vs 133∈±∈8 arbitrary units, p∈<∈0.001 after 6 h of stimulation). We analyzed the TNFSF4 gene in 239 patients who had undergone carotid endarterectomy and 138 matching controls from The Biobank of Karolinska Carotid Endarterectomies and Stockholm Heart Epidemiology Program cohorts and 929 patients and 1,382 matching controls from the Sahlgrenska Academy Study on Ischemic Stroke and Case Control Study of Stroke cohorts, limiting inclusion to patients with ischemic stroke. Participants were genotyped for the rs3850641 SNP in TNFSF4. Genotype associations were neither found with TNFSF4 mRNA levels nor with atherosclerosis associated systemic factors or risk for stroke. This study shows that TNFSF4 is expressed on antigen-presenting cells in human carotid atherosclerotic lesions but provides no evidence for an association of TNFSF4 gene variation with the risk for ischemic stroke.
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