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Sökning: WFRF:(Thelle Dag 1942)

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31.
  • Guron, Cecilia Wallentin, 1965, et al. (författare)
  • Usefulness of atrial size inequality as an indicator of abnormal left ventricular filling
  • 2005
  • Ingår i: Am J Cardiol. - : Elsevier BV. - 0002-9149. ; 95:12, s. 1448-52
  • Tidskriftsartikel (refereegranskat)abstract
    • Although pulsed Doppler echocardiography estimates current left ventricular (LV) filling, left atrial (LA) size reflects LV filling and pressure over time. However, the wide normal LA size range may blunt this diagnostic tool. Our objective was to compare the intraindividual atrial area difference (LA--right atrial [RA] area) and absolute LA area in their detection of a LA enlargement with respect to the degree of current LV filling impairment. We examined patients with acute coronary syndromes in sinus rhythm and without valvular disease (n = 154), and age- and gender-matched healthy controls (n=50) with echocardiography, applying pulsed Doppler international recommendations to group the patients according to the LV filling pattern: 0, normal; 1, delayed relaxation; 2, an isolated abnormal mitral pulmonary venous A-wave duration difference; 3, pseudonormal; and 4, restrictive. The LA and RA areas were measured in the 4-chamber view. Control values defined the normal range of: absolute LA area, LA area adjusted for body height, and LA-RA area. These areas indicated a LA enlargement in: (1) controls, 2%, 2%, and 4%, respectively; (2) patients with LV filling graded as normal/mildly impaired (groups 0 and 1), 15%, 17%, and 46%, respectively; moderately impaired (group 2), 26%, 29%, and 52%, respectively; and severely impaired (group 3 and 4), 42%, 38%, and 54%, respectively. Unequally sized atria appear to detect LA enlargement sensitively, especially when Doppler evidence of LV filling pathology is sparse. Clinically, with no obvious current cause for LA enlargement, a diagnosed "atrial size inequality" may still indicate a history of such causes.
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32.
  • Gustavsson, Jaana, 1974, et al. (författare)
  • Interaction of apolipoprotein E genotype with smoking and physical inactivity on coronary heart disease risk in men and women.
  • 2012
  • Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 220:2, s. 486-492
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Apolipoprotein E genotype (APOE) polymorphism affects lipid levels and coronary heart disease (CHD) risk. However, these associations may be modified by lifestyle factors. Therefore, we studied whether smoking, physical inactivity or overweight interact with APOE on cholesterol levels and CHD risk. METHODS: Combining two Swedish case-control studies yielded 1735 CHD cases and 4654 population controls (3747 men, 2642 women). Self-reported questionnaire lifestyle data included smoking (ever [current or former regular] or never) and physical inactivity (mainly sitting leisure time). We obtained LDL cholesterol levels and APOE genotypes. CHD risk was modelled using logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for relevant covariates. RESULTS: Smoking interacted with APOE on CHD risk; adjusted ORs for ever versus never smoking were 1.45 (95% CI 1.00-2.10) in ɛ2 carriers, 2.25 (95% CI 1.90-2.68) in ɛ3 homozygotes and 2.37 (95% CI 1.85-3.04) in ɛ4 carriers. Female ɛ4 carriers had OR 3.62 (95% CI 2.32-5.63). The adjusted ORs for physical inactivity were 1.09 (95% CI 0.73-1.61), 1.34 (95% CI 1.12-1.61), and 1.79 (95% CI 1.38-2.30) in ɛ2, ɛ3ɛ3 and ɛ4 groups, respectively. No interaction was seen between overweight and APOE for CHD risk, or between any lifestyle factor and APOE for LDL cholesterol levels. CONCLUSION: The APOE ɛ2 allele counteracted CHD risk from smoking in both genders, while the ɛ4 allele was seen to potentiate this risk mainly in women. Similar ɛ2 protection and ɛ4 potentiation was suggested for CHD risk from physical inactivity.
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33.
  • Haheim, Anne Lise Lund, et al. (författare)
  • Comparative analysis of antibodies to four major periodontal bacteria in respiratory diseases: a cohort study
  • 2024
  • Ingår i: BMJ OPEN. - 2044-6055. ; 14:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives To make a descriptive comparison of antibodies to four major periodontal bacteria and their relation to the respiratory diseases asthma and bronchitis/emphysema, and to cancer incidence. Methods The serum of a random sample of men with no history of cancer incidence (n=621) was analysed by the ELISA method for antibody levels of four periodontal bacteria; the anaerobes of the so-called red complex Tannerella forsythia (TF), Porphyromonas gingivalis (PG), and Treponema denticola (TD), and the facultative anaerobe Aggregatibacter actinomycetemcomitans (AA). The antibody readings were divided into quartiles and the distribution of cases of the relevant diseases as compared with the non-cases. Comparisons of the quartile distributions were by the Pearson chi(2) test. Data and serum from the Oslo II study of Norwegian men from 2000 were used. The ELISA analyses were performed on thawed frozen serum. Cancer data from 17.5 years of follow-up were provided by the Norwegian Cancer Registry. Results In all, 52 men had reported asthma and 23 men had bronchitis/emphysema at the health screening. Results on cancer incidence are given for all respiratory cancers, n=23, and bronchi and lung cancers separately, n=18. Stratified analyses were performed for the four endpoints showing significant association with low levels of TD antibodies for bronchitis; p=0.035. Both TF and TD were significant for low levels of antibodies among daily smokers; p=0.030 for TF and p<0.001 for TD in the analysis of the full study sample. For PG and AA, no such associations were observed. An association with respiratory cancers was not observed. Conclusion A low level of TD was associated with bronchitis/emphysema compared with the rest of the cohort. In the total study sample, low levels of antibodies to both TF and TD were associated with daily smoking.
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34.
  • Haheim, L. L., et al. (författare)
  • Low level of antibodies to the oral bacterium Tannerella forsythia predicts bladder cancers and Treponema denticola predicts colon and bladder cancers: A prospective cohort study
  • 2022
  • Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 17:8
  • Tidskriftsartikel (refereegranskat)abstract
    • This study explores the risk for cancer by level of antibodies to the anaerobe oral bacteria of periodontitis Tannerella forsythia (TF), Porphyromonas gingivalis (PG), and Treponema denticola (TD) all three collectively termed the red complex, and the facultative anaerobe bacterium Aggregatibacter actinomycetemcomitans (AA). The prospective cohort, the Oslo I I-study from 2000, the second screening of the Oslo study of 1972/73, has been followed for 17 1/2 years with regard to cancer incidence and mortality. A random sample of 697 elderly men comprised the study cohort. The antibody results measured by enzyme linked immunosorbent assay (ELISA) were used in the Cox proportional hazards analyses, and quartile risk on cancer incidence in a 17 1/2 years follow-up. Among the 621 participants with no prior cancer diagnoses, 221 men developed cancer. The incidence trend was inverse, and the results are shown as 1st quartile of highest value and 4th as lowest of antibody levels. The results of the Cox proportional regression analyses showed that TF inversely predicts bladder cancer (n = 22) by Hazard Ratio (HR) = 1.71 (95% CI: 1.12, 2.61). TD inversely predicts colon cancer (n = 26) by HR = 1.52 (95% CI: 1.06, 2.19) and bladder cancer (n = 22) by HR = 1.60 (95% CI: 1.05, 2.43). Antibodies to two oral bacteria, TF and TD, showed an inverse risk relationship with incidence of specific cancers: TF bladder cancer, TD bladder and colon cancer. Lowered immunological response to the oral infection, periodontitis, is shown to be a risk factor in terms of cancer aetiology.
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35.
  • Haheim, L. L., et al. (författare)
  • Oral health and cardiovascular disease risk factors and mortality of cerebral haemorrhage, cerebral infarction and unspecified stroke in elderly men: A prospective cohort study
  • 2020
  • Ingår i: Scandinavian Journal of Public Health. - : SAGE Publications. - 1403-4948 .- 1651-1905. ; 48:7, s. 762-769
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Stroke mortality comprises different specific diagnoses as cerebral infarction, different haemorrhagic conditions and unspecified stroke. This study seeks to explore the prediction of oral health indicators versus known cardiovascular disease risk factors for stroke mortality. Methods: Altogether, 12,764 men aged 58 to 77 years were invited to the health screening Oslo II in the year 2000. It included general medical measurements and questionnaire information. Mortality data were supplied by Statistics Norway for the 6530 attending men. Cox proportional hazards regression analyses were used to establish prediction models for mortality. Results: Oral health by number of tooth extractions >10 was found to be an independent predictor for cerebral infarction hazard ratio = 2.92, 95% confidence interval (1.24-6.89). This was independent of HDL-Cholesterol (inversely) hazard ratio = 0.21, 95% confidence interval (0.06-0.76), frequent alcohol consumption (drinking 4-7 times per week) hazard ratio = 3.58, 95% confidence interval (1.40-9.13) and diabetes hazard ratio = 4.28, 95% confidence interval (1.68-10.89). Predictors for cerebral haemorrhage were age, hs-C-reactive protein and body mass index (inversely). Age and total cholesterol (inversely) were predictors for unspecified stroke. Conclusions: Oral health measured by number of tooth extractions >10 was an independent predictor for cerebral infarction in addition to age, HDL-C, hs-C-reactive protein and diabetes. The pattern of risk factors varied between the specific stroke diagnoses.
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36.
  • Henriksson, Göran, et al. (författare)
  • Are manual workers at higher risk of death than non-manual employees when living in Swedish municipalities with higher income inequality?
  • 2007
  • Ingår i: Eur J Public Health. - : Oxford University Press (OUP). - 1101-1262 .- 1464-360X. ; 17:2, s. 139-44
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To test the hypothesis that manual workers are at higher risk of death than are non-manual employees when living in municipalities with higher income inequality. DESIGN: Hierarchical regression was used for the analysis were individuals were nested within municipalities according to the 1990 Swedish census. The outcome was all-cause mortality 1992-1998. The income measure at the individual level was disposable family income weighted against composition of family; the income inequality measure used at the municipality level was the Gini coefficient. PARTICIPANTS: The study population consisted of 1 578 186 people aged 40-64 years in the 1990 Swedish census, who were being reported as unskilled or skilled manual workers, lower-, intermediate-, or high-level non-manual employees. RESULTS: There was no significant association between income inequality at the municipality level and risk of death, but an expected gradient with unskilled manual workers having the highest risk and high-level non-manual employees having the lowest. However, in the interaction models the relative risk (RR) of death for high-level non-manual employees was decreasing with increasing income inequality (RR = 0.77; 95% CI, 0.63-0.93), whereas the corresponding risk for unskilled manual workers increased with increasing income inequality (RR = 1.24; 95% CI, 1.06-1.46). The RRs for skilled manual, low- and medium- level non-manual employees were not significant. Controlling for income at the individual level did not substantially alter these findings, neither did potential confounders at the municipality level. CONCLUSIONS: The findings suggest that there could be a differential impact from income inequality on risk of death, dependent on individuals' social position.
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37.
  • Henriksson, Göran, et al. (författare)
  • Income distribution and mortality: implications from a comparison of individual-level analysis and multilevel analysis with Swedish data
  • 2006
  • Ingår i: Scand J Public Health. - : SAGE Publications. - 1403-4948. ; 34:3, s. 287-94
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: This follow-up study analyses whether there is an association between income distribution in Swedish municipalities and risk of death from all causes in the total Swedish population aged 40-64 years and compares the results obtained with analyses performed on individual-level analysis and multilevel analysis. METHODS: Individual-level data on social and economic circumstances were obtained from various official records and were linked to the national cause-of-death register. Analyses were made with two methods, an individual-level regression and a multilevel regression. The study population comprised all people 40-64 years of age in the 1990 Swedish census, altogether 2.57 million people in 284 municipalities. RESULTS: The main results showed that in the individual-level regression the income distribution showed a positive and significant association (risk ratio = 1.29; 95% CI = 1.24-1.34) with higher mortality for those living in municipalities with higher income inequality. This association was not found in the multilevel regression analysis (RR = 1.03; 95%CI = 0.94-1.13). CONCLUSION: There seems to be no association between income distribution and mortality in Sweden when considering the possibility of clustering in municipalities. Further studies on the relationship between income inequality and health should aim at elucidate processes within area-level units.
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38.
  • Hägg, Daniel, 1974, et al. (författare)
  • Expression of chemokine (C-C motif) ligand 18 in human macrophages and atherosclerotic plaques
  • 2009
  • Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 204:2
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Using gene expression profiling, we aimed to identify genes that are predominantly expressed in human carotid atherosclerotic plaques. Such genes may be important in atherogenesis and pathophysiology of the plaque, and genes that encode for secreted proteins may be potential biomarkers for atherosclerosis and cardiovascular disease. METHODS: DNA microarray generated expression profiles of human carotid atherosclerotic plaques were compared to expression profiles of 80 different human tissues and cell types, to identify plaque-specific genes. RESULTS: We identified the chemokine (C-C motif) ligand 18 (CCL18) as predominantly expressed in human carotid plaque. Immunohistochemistry showed that CCL18 protein was localized to a subset of macrophages in carotid plaques. Monocyte-derived macrophages from subjects with atherosclerosis had threefold higher expression of CCL18 than macrophages from control subjects (p=0.012). Subjects with A/G genotype of the rs2015086 SNP in the promoter region of the CCL18 gene had threefold higher macrophage expression of CCL18 than subjects with A/A genotype (p=0.049), but we found no association of this SNP with an increased risk of coronary heart disease. We also compared serum levels of CCL18 from subjects with symptomatic carotid artery disease with control subjects. There were no differences in serum levels of CCL18 between the two groups, however CCL18 correlated with measurements of adiposity. CONCLUSION: CCL18 is predominantly expressed in human atherosclerotic plaques and may participate in the atherosclerotic plaque formation.
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39.
  • Hägg, Daniel, 1974, et al. (författare)
  • Expression profiling of macrophages from subjects with atherosclerosis to identify novel susceptibility genes.
  • 2008
  • Ingår i: International journal of molecular medicine. - 1107-3756 .- 1791-244X. ; 21:6, s. 697-704
  • Tidskriftsartikel (refereegranskat)abstract
    • Although a number of environmental risk factors for atherosclerosis have been identified, heredity seems to be a significant independent risk factor. The aim of our study was to identify novel susceptibility genes for atherosclerosis. The screening process consisted of three steps. First, expression profiles of macrophages from subjects with atherosclerosis were compared to macrophages from control subjects. Secondly, the subjects were genotyped for promoter region polymorphisms in genes with altered gene expression. Thirdly, a population of subjects with coronary heart disease and control subjects were genotyped to test for an association with identified polymorphisms that affected gene expression. Twenty-seven genes were differentially expressed in both macrophages and foam cells from subjects with atherosclerosis. Three of these genes, IRS2, CD86 and SLC11A1 were selected for further analysis. Foam cells from subjects homozygous for the C allele at the -765C-->T SNP located in the promoter region of IRS2 had increased gene expression compared to foam cells from subjects with the nonCC genotype. Also, macrophages and foam cells from subjects homozygous for allele 2 at a repeat element in the promoter region of SLC11A1 had increased gene expression compared to macrophages and foam cells from subjects with the non22 genotype. Genotyping of 512 pairs of subjects with coronary heart disease (CHD) and matched controls revealed that subjects homozygous for C of the IRS2 SNP had an increased risk for CHD; odds ratio 1.43, p=0.010. Immunohistochemical staining of human carotid plaques showed that IRS2 expression was localised to macrophages and endothelial cells in vivo. Our method provides a reliable approach for identifying susceptibility genes for atherosclerosis, and we conclude that elevated IRS2 gene expression in macrophages may be associated with an increased risk of CHD.
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40.
  • Johansen, K. R., et al. (författare)
  • Risk of atrial fibrillation and stroke among older men exposed to prolonged endurance sport practice: a 10-year follow-up. The Birkebeiner Ageing Study and the Tromso Study
  • 2022
  • Ingår i: Open Heart. - : BMJ. - 2053-3624. ; 9:2
  • Tidskriftsartikel (refereegranskat)abstract
    • AimsEndurance sport practice is associated with a high prevalence of atrial fibrillation (AF), which increases the risk of stroke in the general population. However, stroke risk in endurance athletes with AF is sparsely investigated. Most studies have been limited by design and are largely restricted to younger and middle-aged populations. Thus, we aimed to investigate AF and stroke risk in older athletes exposed to prolonged endurance training.MethodDuring a 10-year period, 505 male athletes aged >= 65 years frequently participating in a long-distance ski race were compared with 1867 men of the same age from the general population. The main exposure was endurance sport practice with self-reported AF and stroke as outcomes. Stroke risk was further examined by joint modelling of AF and endurance practice. Statistical analysis was conducted with a modified Poisson model.ResultsAthletes (median age: 68, range: 65-90) participated in a long-distance ski race over a median of 14 years (range: 1-53). Prevalence (28.5% vs 17.8%) and adjusted risk of AF (risk ratio (RR): 1.88, 95% CI: 1.49 to 2.37) were higher in athletes compared with non-athletes, whereas the prevalence (5.4% vs 9.7%) and risk of stroke were lower (RR: 0.60, 95% CI: 0.37 to 0.95). Compared with athletes without AF, risk of stroke was twofold in athletes (RR: 2.38, 95% CI: 1.08 to 5.24) and nearly fourfold in non-athletes (RR: 3.87, 95% CI: 1.98 to 7.57) with AF.ConclusionAlthough older male endurance athletes experienced an increased risk of AF, the long-term risk of stroke was substantially reduced compared with non-athletes.
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