PubMed:17981284 JSON TXT

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Inflammaging

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":111},"obj":"Sentence"},{"id":"T2","span":{"begin":112,"end":123},"obj":"Sentence"},{"id":"T3","span":{"begin":124,"end":214},"obj":"Sentence"},{"id":"T4","span":{"begin":215,"end":522},"obj":"Sentence"},{"id":"T5","span":{"begin":523,"end":543},"obj":"Sentence"},{"id":"T6","span":{"begin":544,"end":665},"obj":"Sentence"},{"id":"T7","span":{"begin":666,"end":804},"obj":"Sentence"},{"id":"T8","span":{"begin":805,"end":951},"obj":"Sentence"},{"id":"T9","span":{"begin":952,"end":1151},"obj":"Sentence"},{"id":"T10","span":{"begin":1152,"end":1274},"obj":"Sentence"},{"id":"T11","span":{"begin":1275,"end":1388},"obj":"Sentence"},{"id":"T12","span":{"begin":1389,"end":1484},"obj":"Sentence"},{"id":"T13","span":{"begin":1485,"end":1497},"obj":"Sentence"},{"id":"T14","span":{"begin":1498,"end":1759},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":111},"obj":"Sentence"},{"id":"T2","span":{"begin":112,"end":123},"obj":"Sentence"},{"id":"T3","span":{"begin":124,"end":214},"obj":"Sentence"},{"id":"T4","span":{"begin":215,"end":522},"obj":"Sentence"},{"id":"T5","span":{"begin":523,"end":543},"obj":"Sentence"},{"id":"T6","span":{"begin":544,"end":665},"obj":"Sentence"},{"id":"T7","span":{"begin":666,"end":804},"obj":"Sentence"},{"id":"T8","span":{"begin":805,"end":951},"obj":"Sentence"},{"id":"T9","span":{"begin":952,"end":1151},"obj":"Sentence"},{"id":"T10","span":{"begin":1152,"end":1274},"obj":"Sentence"},{"id":"T11","span":{"begin":1275,"end":1388},"obj":"Sentence"},{"id":"T12","span":{"begin":1389,"end":1484},"obj":"Sentence"},{"id":"T13","span":{"begin":1485,"end":1497},"obj":"Sentence"},{"id":"T14","span":{"begin":1498,"end":1759},"obj":"Sentence"}],"text":"Variation in inflammation-related genes and risk of incident nonfatal myocardial infarction or ischemic stroke.\nBACKGROUND: From initiation to plaque rupture, immune system components contribute to atherosclerosis. We investigated variation in inflammation-related genes - interleukin (IL)-1beta, IL-6, C-reactive protein (CRP), IL-10, IL-18, and the tumor necrosis factor (TNF) superfamily [lymphotoxin(LT)-alpha, TNF-alpha, LT-beta] - with respect to nonfatal incident myocardial infarction (MI) or ischemic stroke risk.\nMETHODS AND RESULTS: A population-based case-control study recruited postmenopausal and/or hypertensive Group Health members aged 30-79 years. We chose a subset of single nucleotide polymorphisms (SNPs) to describe common gene-wide variation on the basis of linkage disequilibrium. 36 SNPs, describing 38 common haplotypes for 5 genes and a 3-gene cluster, were genotyped among 856 MI cases, 368 stroke cases, and 2688 controls. Associations of SNPs or PHASE-inferred haplotypes and risk were estimated using logistic regression; significance of gene-level associations was assessed with global Wald tests and permutation tests. Gene-wide IL-18 variation was associated with higher MI risk and an IL-1B haplotype was associated with lower stroke risk. In secondary analyses of SNPs, we observed associations of several IL-1B polymorphisms with risk of MI or stroke. IL-6, CRP, IL-10, and TNF superfamily gene variation was not associated with MI or stroke risk.\nCONCLUSIONS: Our results support prior reports associating an IL-18 gene variant and MI risk, contribute additional evidence to reports of IL-1B and cardiovascular risk, and fail to confirm risk differences previously observed for CRP, IL-6, and TNF-alpha promoter variants."}

PMID_GLOBAL

DisGeNET

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":198,"end":213},"obj":"HP_0002621"},{"id":"T2","span":{"begin":351,"end":356},"obj":"HP_0002664"},{"id":"T3","span":{"begin":471,"end":492},"obj":"HP_0001658"},{"id":"T4","span":{"begin":501,"end":516},"obj":"HP_0002140"},{"id":"T5","span":{"begin":510,"end":516},"obj":"HP_0001297"}],"text":"Variation in inflammation-related genes and risk of incident nonfatal myocardial infarction or ischemic stroke.\nBACKGROUND: From initiation to plaque rupture, immune system components contribute to atherosclerosis. We investigated variation in inflammation-related genes - interleukin (IL)-1beta, IL-6, C-reactive protein (CRP), IL-10, IL-18, and the tumor necrosis factor (TNF) superfamily [lymphotoxin(LT)-alpha, TNF-alpha, LT-beta] - with respect to nonfatal incident myocardial infarction (MI) or ischemic stroke risk.\nMETHODS AND RESULTS: A population-based case-control study recruited postmenopausal and/or hypertensive Group Health members aged 30-79 years. We chose a subset of single nucleotide polymorphisms (SNPs) to describe common gene-wide variation on the basis of linkage disequilibrium. 36 SNPs, describing 38 common haplotypes for 5 genes and a 3-gene cluster, were genotyped among 856 MI cases, 368 stroke cases, and 2688 controls. Associations of SNPs or PHASE-inferred haplotypes and risk were estimated using logistic regression; significance of gene-level associations was assessed with global Wald tests and permutation tests. Gene-wide IL-18 variation was associated with higher MI risk and an IL-1B haplotype was associated with lower stroke risk. In secondary analyses of SNPs, we observed associations of several IL-1B polymorphisms with risk of MI or stroke. IL-6, CRP, IL-10, and TNF superfamily gene variation was not associated with MI or stroke risk.\nCONCLUSIONS: Our results support prior reports associating an IL-18 gene variant and MI risk, contribute additional evidence to reports of IL-1B and cardiovascular risk, and fail to confirm risk differences previously observed for CRP, IL-6, and TNF-alpha promoter variants."}

DisGeNET5_gene_disease

Wangshuguang

{"project":"Wangshuguang","denotations":[{"id":"T1","span":{"begin":289,"end":295},"obj":"B-Variation"},{"id":"T2","span":{"begin":351,"end":356},"obj":"B-Molecular_Activity"},{"id":"T3","span":{"begin":357,"end":365},"obj":"I-Molecular_Activity"},{"id":"T4","span":{"begin":366,"end":372},"obj":"I-Molecular_Activity"},{"id":"T5","span":{"begin":407,"end":413},"obj":"B-Variation"},{"id":"T6","span":{"begin":1041,"end":1051},"obj":"B-Variation"},{"id":"T7","span":{"begin":1334,"end":1341},"obj":"B-Molecular_Activity"},{"id":"T8","span":{"begin":1342,"end":1347},"obj":"I-Molecular_Activity"},{"id":"T9","span":{"begin":1348,"end":1361},"obj":"B-Molecular_Activity"},{"id":"T10","span":{"begin":1367,"end":1371},"obj":"B-Cell_Physiological_Activity"},{"id":"T11","span":{"begin":1372,"end":1374},"obj":"I-Cell_Physiological_Activity"},{"id":"T12","span":{"begin":1613,"end":1620},"obj":"B-Variation"}],"text":"Variation in inflammation-related genes and risk of incident nonfatal myocardial infarction or ischemic stroke.\nBACKGROUND: From initiation to plaque rupture, immune system components contribute to atherosclerosis. We investigated variation in inflammation-related genes - interleukin (IL)-1beta, IL-6, C-reactive protein (CRP), IL-10, IL-18, and the tumor necrosis factor (TNF) superfamily [lymphotoxin(LT)-alpha, TNF-alpha, LT-beta] - with respect to nonfatal incident myocardial infarction (MI) or ischemic stroke risk.\nMETHODS AND RESULTS: A population-based case-control study recruited postmenopausal and/or hypertensive Group Health members aged 30-79 years. We chose a subset of single nucleotide polymorphisms (SNPs) to describe common gene-wide variation on the basis of linkage disequilibrium. 36 SNPs, describing 38 common haplotypes for 5 genes and a 3-gene cluster, were genotyped among 856 MI cases, 368 stroke cases, and 2688 controls. Associations of SNPs or PHASE-inferred haplotypes and risk were estimated using logistic regression; significance of gene-level associations was assessed with global Wald tests and permutation tests. Gene-wide IL-18 variation was associated with higher MI risk and an IL-1B haplotype was associated with lower stroke risk. In secondary analyses of SNPs, we observed associations of several IL-1B polymorphisms with risk of MI or stroke. IL-6, CRP, IL-10, and TNF superfamily gene variation was not associated with MI or stroke risk.\nCONCLUSIONS: Our results support prior reports associating an IL-18 gene variant and MI risk, contribute additional evidence to reports of IL-1B and cardiovascular risk, and fail to confirm risk differences previously observed for CRP, IL-6, and TNF-alpha promoter variants."}

123123123

{"project":"123123123","denotations":[{"id":"T1","span":{"begin":289,"end":295},"obj":"B-Variation"},{"id":"T2","span":{"begin":351,"end":356},"obj":"B-Molecular_Activity"},{"id":"T3","span":{"begin":357,"end":365},"obj":"I-Molecular_Activity"},{"id":"T4","span":{"begin":366,"end":372},"obj":"I-Molecular_Activity"},{"id":"T5","span":{"begin":407,"end":413},"obj":"B-Variation"},{"id":"T6","span":{"begin":1041,"end":1051},"obj":"B-Variation"},{"id":"T7","span":{"begin":1334,"end":1341},"obj":"B-Molecular_Activity"},{"id":"T8","span":{"begin":1342,"end":1347},"obj":"I-Molecular_Activity"},{"id":"T9","span":{"begin":1348,"end":1361},"obj":"B-Molecular_Activity"},{"id":"T10","span":{"begin":1367,"end":1371},"obj":"B-Cell_Physiological_Activity"},{"id":"T11","span":{"begin":1372,"end":1374},"obj":"I-Cell_Physiological_Activity"},{"id":"T12","span":{"begin":1613,"end":1620},"obj":"B-Variation"}],"text":"Variation in inflammation-related genes and risk of incident nonfatal myocardial infarction or ischemic stroke.\nBACKGROUND: From initiation to plaque rupture, immune system components contribute to atherosclerosis. We investigated variation in inflammation-related genes - interleukin (IL)-1beta, IL-6, C-reactive protein (CRP), IL-10, IL-18, and the tumor necrosis factor (TNF) superfamily [lymphotoxin(LT)-alpha, TNF-alpha, LT-beta] - with respect to nonfatal incident myocardial infarction (MI) or ischemic stroke risk.\nMETHODS AND RESULTS: A population-based case-control study recruited postmenopausal and/or hypertensive Group Health members aged 30-79 years. We chose a subset of single nucleotide polymorphisms (SNPs) to describe common gene-wide variation on the basis of linkage disequilibrium. 36 SNPs, describing 38 common haplotypes for 5 genes and a 3-gene cluster, were genotyped among 856 MI cases, 368 stroke cases, and 2688 controls. Associations of SNPs or PHASE-inferred haplotypes and risk were estimated using logistic regression; significance of gene-level associations was assessed with global Wald tests and permutation tests. Gene-wide IL-18 variation was associated with higher MI risk and an IL-1B haplotype was associated with lower stroke risk. In secondary analyses of SNPs, we observed associations of several IL-1B polymorphisms with risk of MI or stroke. IL-6, CRP, IL-10, and TNF superfamily gene variation was not associated with MI or stroke risk.\nCONCLUSIONS: Our results support prior reports associating an IL-18 gene variant and MI risk, contribute additional evidence to reports of IL-1B and cardiovascular risk, and fail to confirm risk differences previously observed for CRP, IL-6, and TNF-alpha promoter variants."}