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Sökning: WFRF:(Bennet AM)

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2.
  • Bennet, Anna M., et al. (författare)
  • Decreased risk for myocardial infarction and lower tumor necrosis factor-alpha levels in carriers of variants of the PDCD1 gene
  • 2006
  • Ingår i: Human Immunology. - 0198-8859 .- 1879-1166. ; 67:9, s. 700-705
  • Tidskriftsartikel (refereegranskat)abstract
    • Increasing interest has been directed toward the inflammatory mechanisms involved in the pathogenesis of myocardial infarction (MI). In the search for genetic mechanisms underlying these inflammatory components, we studied variants of programmed cell death-1 (PDCD1), an immunoinhibitory receptor that inhibits lymphocyte activation and cytokine production, previously shown to be associated with several autoimmune disorders. The PD1.1, PD1.3, and PD1.6 polymorphisms of the PDCD1 gene were typed in the Stockholm Heart Epidemiology Program, a population-based clinical material consisting of 1179 first-time MI case patients and 1528 unaffected control subjects. Individual alleles and haplotypes were studied for association with levels of the inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-6, and C-reactive protein and risk for MI. We observed a weak protective effect of PD1.3A allele for MI (odds ratio: 0.78, 95% confidence interval: 0.61-0.98). We also observed decreased levels of TNF-alpha in carriers of the PD1.1A/PD1.3G/PD1.6A haplotype, which is consistent with our previous observation that this haplotype may be protective from autoimmune conditions. Carriers of variants of the PDCD1 gene exhibit a decreased risk for nonfatal myocardial infarction, and PDCD1 mediates variation in TNF-alpha levels.
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3.
  • Bennet, Anna M, et al. (författare)
  • Genetic association of sequence variants near AGER/NOTCH4 and dementia.
  • 2011
  • Ingår i: Journal of Alzheimer's disease : JAD. - 1875-8908. ; 24:3, s. 475-84
  • Tidskriftsartikel (refereegranskat)abstract
    • We performed a survey of sequence variation in a series of 20 genes involved in inflammation-related pathways for association with dementia risk in twin and unrelated case-control samples consisting in total of 1462 Swedish dementia casesand 1929 controls. For a total of 218 tested genetic markers, strong evidence was obtained implicating a region near AGER and NOTCH4 on chromosome 6p with replication across both samples and maximum combined significance at marker rs1800625 (OR = 1.37, 95% CI 1.19–1.56, p = 1.36×10(–6)). Imputation of the associated genomic interval provided an improved signal atrs8365, near the 3UTR of AGER (p = 7.34×10(–7)). The associated region extends 120 kb encompassing 11 candidate genes.While AGER encodes a key receptor for amyloid-β protein, an analysis of network context based upon genes now confirmed to contribute to dementia risk (AβPP, PSEN1, PSEN2, CR1, CLU, PICALM, and APOE) suggested strong functional coupling to NOTCH4, with no significant coupling to the remaining candidates. The implicated region occurs in the broad HLA locus on chromosome 6p, but associated markers were not in strong LD with known variants that regulate HLA gene function, suggesting that this may represent a signal distinct from immune-system pathways.
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4.
  • Bennet, Anna M, et al. (författare)
  • Pleiotropy in the Presence of Allelic Heterogeneity: Alternative Genetic Models for the Influence of APOE on Serum LDL, CSF Amyloid-β42, and Dementia.
  • 2010
  • Ingår i: Journal of Alzheimer's disease : JAD. - 1875-8908. ; 22:1, s. 129-134
  • Tidskriftsartikel (refereegranskat)abstract
    • The two genetic polymorphisms, rs7412 and rs429358, that collectively form the ε2, ε3, and ε4 alleles of apolipoprotein E (APOE) are among the most widely studied sequence variants in the genome. The predominant model for testing APOE involves the haplotype combinations of ε2, ε3, and ε4 and has been basis of associations with dementia, atherosclerosis, and serum lipid levels. Here, we demonstrate the functional independence of these two component sites, with rs7412 contributing to the majority of variance in serum LDL (p=10-20), whereas rs429358 alone influences variance in CSF amyloid-β42 (Aβ42) (p=10-17). This latter relationship is also reflected in the association of APOE with dementia, where rs429358 strongly influences disease (p=10-67), but rs7412 does not. Models based upon ε2, ε3, and ε4 explained less variance for both dementia risk and CSF Aβ42 than did rs429358 alone. When adjusted for CSF Aβ42, the association of rs429358 with dementia is greatly reduced but remains significant indicating that APOE polymorphism influences disease by additional mechanisms distinct from Aβ42 metabolism. We reach four principal conclusion from this study: 1) rs429358 alone is responsible for the association of APOE with dementia; 2) The association of APOE with dementia is substantially mediated by its effect on CNS Aβ42 levels; 3) The association of APOE with dementia is not mediated by its impact on peripheral lipid metabolism; and 4) The dichotomy of effects of rs429358 and rs7412 represents one of the best examples of genetic pleiotropy for complex traits known and illustrates the importance of allelic heterogeneity in APOE.
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5.
  • Bennet, Anna M, et al. (författare)
  • The risk of myocardial infarction is enhanced by a synergistic interaction between serum insulin and smoking.
  • 2002
  • Ingår i: European Journal of Endocrinology. - 0804-4643 .- 1479-683X. ; 147:5, s. 641-7
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: To evaluate the relationship between levels of serum insulin, the homeostasis model assessment (HOMA) and IGF-binding protein-1 (IGFBP-1) as factors related to myocardial infarction (MI) risk, and their interaction with lifestyle-related risk factors. DESIGN: The Stockholm epidemiology programme (SHEEP), a case-control study, consisting of 749 first-time MI cases (510 men, 239 women) and 1101 healthy controls (705 men, 396 women) was used. METHODS: The risk of developing MI was assessed by calculating odds ratios (OR) and synergistic interactions (SI) between serum insulin, IGFBP-1, HOMA and other variables related to MI risk (including smoking) in men and women. RESULTS: Subjects with elevated levels of insulin and HOMA (>75th percentile) had increased MI risks when compared with individuals with low levels. ORs for elevated insulin and HOMA (adjusted for age and residential area) for men: insulin 1.6 (95% confidence interval (CI) 1.3-2.1) and HOMA 1.5 (95% CI 1.1-1.9) and for women: insulin 2.1 (95% CI 1.5-2.9) and HOMA 1.9 (95% CI 1.3-2.8). Women with low levels of IGFBP-1 (<10th percentile) showed a tendency towards elevated MI risk even if this was not statistically significant (OR 1.5 (95% CI 0.9-2.6)). Smokers with high levels of serum insulin had greatly increased MI risk (OR for men: 4.7 (95% CI 3.0-7.2) and OR for women: 8.1 (95% CI 4.5-14.8)). SI scores based upon these interactions were statistically significant. CONCLUSIONS: These results might have preventive cardiovascular implications as they clearly suggest that subjects with insulin resistance are particularly susceptible to the hazards of smoking.
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6.
  • Janszky, Imre, et al. (författare)
  • Alcohol and long-term prognosis after a first acute myocardial infarction : the SHEEP study
  • 2008
  • Ingår i: European Heart Journal. - 0195-668X .- 1522-9645. ; 29:1, s. 45-53
  • Tidskriftsartikel (refereegranskat)abstract
    • CONTEXTFew studies have investigated the relation between alcohol consumption, former drinking, and prognosis after an acute myocardial infarction (AMI), particularly for non-fatal outcomes.OBJECTIVETo investigate the prognostic importance of drinking habits among patients surviving a first AMI.DESIGN, SETTINGS, AND PATIENTSA total of 1346 consecutive patients between 45-70 years with a first non-fatal AMI underwent a standardized clinical examination and were followed for over 8 years.MAIN OUTCOME MEASURESTotal and cardiac mortality and hospitalization for non-fatal cardiovascular disease in relation to individual alcoholic beverage consumption at the time of AMI and 5 years before inclusion, assessed by a standardized questionnaire administered during hospitalization.RESULTSWe recorded 267 deaths, and 145 deaths from cardiac causes, during the follow-up period. After adjustment for several potential confounders, hazard ratios for total and cardiac mortality were 0.77 (0.51-1.15) and 0.61 (0.36-1.02) for those drinking >0-<5 g per day, 0.77 (0.50-1.18) and 0.62 (0.36-1.07) for those drinking 5-20 g per day, and 0.89 (0.56-1.40) and 0.69 (0.38-1.25) for those drinking over 20 g per day. Risk of hospitalization for recurrent non-fatal AMI, stroke, or heart failure generally showed a similar pattern to that of total and cardiac mortality. Recent quitters at the time of AMI had a hazard ratio of 4.55 (2.03-10.20) for total mortality. Measures of insulin sensitivity appeared to be the strongest mediators of this association.CONCLUSIONSModerate alcohol drinking might have beneficial effects on several aspects of long-term prognosis after an AMI. Our findings also highlight that former drinkers should be examined separately from long-term abstainers. The potential mechanisms that underlie this association still need to be elucidated.
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7.
  • Karlsson, Ida K., et al. (författare)
  • Apolipoprotein E ε4 genotype and the temporal relationship between depression and dementia
  • 2015
  • Ingår i: Neurobiology of Aging. - : Elsevier. - 0197-4580 .- 1558-1497. ; 36:4, s. 1751-1756
  • Tidskriftsartikel (refereegranskat)abstract
    • To investigate how apolipoprotein E (. APOE) affects the temporal relationship between depression and dementia, we conducted a nested case-control study with longitudinal depression and dementia evaluations from several population studies by using 804 dementia cases and 1600 matched controls, totaling 1519 unique individuals. Depression within 10 years of onset of dementia was strongly associated with dementia diagnosis regardless of APOE status (incidence rate ratio [IRR] 5.25, 95% confidence interval [95% CI] 3.32-8.31 for ε4 carriers, IRR 4.40, 95%CI 3.23-5.99 for noncarriers). However, we found a significant interaction between depression more than 10 years before the onset of dementia and APOE (. p= 0.01), with depression more distal to dementia being a risk factor only in ε4 carriers (IRR 3.39, 95% CI 1.69-6.78 for carriers, IRR 1.01, 95% CI 0.60-1.70 for noncarriers). Thus, depression with onset close in time to dementia onset is associated with disease irrespective of APOE genotype, whereas depression more distal to dementia onset is a risk factor only in ε4-carriers. This is the first study to show the interaction between APOE and depression to be dependent on timing of depression onset.
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10.
  • McGale, Paul, et al. (författare)
  • Incidence of heart disease in 35,000 women treated with radiotherapy for breast cancer in Denmark and Sweden
  • 2011
  • Ingår i: Radiotherapy and Oncology. - Amsterdam : Elsevier. - 0167-8140 .- 1879-0887. ; 100:2, s. 167-175
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: To study incidence of radiation-related heart disease in a large population of breast cancer patients followed for up to 30 years. Material and methods: 72,134 women diagnosed with breast cancer in Denmark or Sweden during 1976-2006 and followed prospectively. Radiation-related risk was studied by comparing women with left-sided and right-sided tumours. Results: 34,825 women (48%) received radiotherapy. Among unirradiated women tumour laterality had little relevance to heart disease. Among irradiated women mean dose to the whole heart was 6.3 Gy for left-sided tumours and 2.7 Gy for right-sided tumours. Mortality was similar in irradiated women with left-sided and right-sided tumours, but incidence ratios, left-sided versus right-sided, were raised: acute myocardial infarction 1.22 (95% CI 1.06-1.42), angina 1.25 (1.05-1.49), pericarditis 1.61 (1.06-2.43), valvular heart disease 1.54 (1.11-2.13). Incidence ratios for all heart disease were as high for women irradiated since 1990 (1.09 [1.00-1.19]) as for women irradiated during 1976-1989 (1.08 [0.99-1.17]), and were higher for women diagnosed with ischaemic heart disease prior to breast cancer than for other women (1.58 [1.19-2.10] versus 1.08 [1.01-1.15], p for difference = 0.01). Conclusions: Breast cancer radiotherapy has, at least until recently, increased the risk of developing ischaemic heart disease, pericarditis and valvular disease. Women with ischaemic heart disease before breast cancer diagnosis may have incurred higher risks than others. (C) 2011 Elsevier Ireland Ltd. All rights reserved. Radiotherapy and Oncology 100 (2011) 167-175
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