PubMed:20415560 JSONTXT

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":112},"obj":"Sentence"},{"id":"T2","span":{"begin":113,"end":118},"obj":"Sentence"},{"id":"T3","span":{"begin":119,"end":250},"obj":"Sentence"},{"id":"T4","span":{"begin":251,"end":471},"obj":"Sentence"},{"id":"T5","span":{"begin":472,"end":492},"obj":"Sentence"},{"id":"T6","span":{"begin":493,"end":737},"obj":"Sentence"},{"id":"T7","span":{"begin":738,"end":782},"obj":"Sentence"},{"id":"T8","span":{"begin":783,"end":983},"obj":"Sentence"},{"id":"T9","span":{"begin":984,"end":992},"obj":"Sentence"},{"id":"T10","span":{"begin":993,"end":1149},"obj":"Sentence"},{"id":"T11","span":{"begin":1150,"end":1163},"obj":"Sentence"},{"id":"T12","span":{"begin":1164,"end":1186},"obj":"Sentence"},{"id":"T13","span":{"begin":1187,"end":1302},"obj":"Sentence"},{"id":"T14","span":{"begin":1303,"end":1466},"obj":"Sentence"},{"id":"T15","span":{"begin":1467,"end":1602},"obj":"Sentence"},{"id":"T16","span":{"begin":1603,"end":1614},"obj":"Sentence"},{"id":"T17","span":{"begin":1615,"end":1778},"obj":"Sentence"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

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E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":18,"end":40},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":61,"end":78},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":141,"end":158},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":227,"end":249},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":690,"end":711},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1415,"end":1433},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0004995"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005015"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005015"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0004995"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005068"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005068"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-GeneOrGeneProduct-v0","denotations":[{"id":"T28","span":{"begin":1249,"end":1251},"obj":"GeneOrGeneProduct"},{"id":"T29","span":{"begin":1292,"end":1295},"obj":"GeneOrGeneProduct"},{"id":"T30","span":{"begin":1296,"end":1301},"obj":"GeneOrGeneProduct"},{"id":"T31","span":{"begin":1320,"end":1322},"obj":"GeneOrGeneProduct"},{"id":"T32","span":{"begin":1379,"end":1385},"obj":"GeneOrGeneProduct"},{"id":"T33","span":{"begin":1379,"end":1381},"obj":"GeneOrGeneProduct"},{"id":"T34","span":{"begin":1507,"end":1513},"obj":"GeneOrGeneProduct"},{"id":"T35","span":{"begin":1507,"end":1509},"obj":"GeneOrGeneProduct"},{"id":"T36","span":{"begin":1596,"end":1601},"obj":"GeneOrGeneProduct"},{"id":"T37","span":{"begin":1678,"end":1680},"obj":"GeneOrGeneProduct"},{"id":"T38","span":{"begin":1714,"end":1720},"obj":"GeneOrGeneProduct"},{"id":"T39","span":{"begin":1714,"end":1716},"obj":"GeneOrGeneProduct"},{"id":"T40","span":{"begin":1750,"end":1756},"obj":"GeneOrGeneProduct"},{"id":"T1","span":{"begin":10,"end":17},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":61,"end":69},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":87,"end":98},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":141,"end":149},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":172,"end":183},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":184,"end":192},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":185,"end":187},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":286,"end":288},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":291,"end":300},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":327,"end":331},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":449,"end":455},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":449,"end":451},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":484,"end":491},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":496,"end":510},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":511,"end":513},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":559,"end":563},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":568,"end":573},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":615,"end":617},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":846,"end":851},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":900,"end":904},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":905,"end":909},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":923,"end":927},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":993,"end":997},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1087,"end":1090},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":1091,"end":1096},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":1100,"end":1106},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":1100,"end":1102},"obj":"GeneOrGeneProduct"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-GeneOrGeneProduct-v2","denotations":[{"id":"T1","span":{"begin":61,"end":69},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":87,"end":98},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":141,"end":149},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":172,"end":183},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":185,"end":187},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":286,"end":288},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":291,"end":300},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":449,"end":455},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":449,"end":451},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":511,"end":513},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":615,"end":617},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":905,"end":909},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":993,"end":997},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1100,"end":1106},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1100,"end":1102},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1249,"end":1251},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":1320,"end":1322},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1379,"end":1385},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1379,"end":1381},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1507,"end":1513},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":1507,"end":1509},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":1678,"end":1680},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":1714,"end":1720},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1714,"end":1716},"obj":"GeneOrGeneProduct"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":18,"end":40},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":61,"end":78},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":141,"end":158},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":160,"end":162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":227,"end":249},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":456,"end":458},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":526,"end":528},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":682,"end":688},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":690,"end":711},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":731,"end":736},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1107,"end":1109},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1336,"end":1338},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1415,"end":1433},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":1435,"end":1441},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":1460,"end":1465},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1514,"end":1516},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1655,"end":1657},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A11","pred":"originalLabel","subj":"T11","obj":"D003920"},{"id":"A9","pred":"originalLabel","subj":"T9","obj":"D009203"},{"id":"A5","pred":"originalLabel","subj":"T5","obj":"D002318"},{"id":"A4","pred":"originalLabel","subj":"T4","obj":"D003920"},{"id":"A3","pred":"originalLabel","subj":"T3","obj":"D003920"},{"id":"A6","pred":"originalLabel","subj":"T6","obj":"D003920"},{"id":"A16","pred":"originalLabel","subj":"T16","obj":"D003920"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"D003920"},{"id":"A8","pred":"originalLabel","subj":"T8","obj":"D020521"},{"id":"A14","pred":"originalLabel","subj":"T14","obj":"D020521"},{"id":"A12","pred":"originalLabel","subj":"T12","obj":"D003920"},{"id":"A13","pred":"originalLabel","subj":"T13","obj":"D009203"},{"id":"A7","pred":"originalLabel","subj":"T7","obj":"D003920"},{"id":"A17","pred":"originalLabel","subj":"T17","obj":"D003920"},{"id":"A10","pred":"originalLabel","subj":"T10","obj":"D003643"},{"id":"A1","pred":"originalLabel","subj":"T1","obj":"D002318"},{"id":"A15","pred":"originalLabel","subj":"T15","obj":"D003643"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":18,"end":40},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":61,"end":78},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":141,"end":158},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":160,"end":162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":185,"end":187},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":227,"end":249},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":286,"end":288},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":449,"end":451},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":456,"end":458},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":511,"end":513},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":526,"end":528},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":615,"end":617},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":682,"end":688},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":690,"end":711},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T18","span":{"begin":974,"end":976},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1100,"end":1102},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":1107,"end":1109},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T22","span":{"begin":1249,"end":1251},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T23","span":{"begin":1320,"end":1322},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T24","span":{"begin":1336,"end":1338},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T26","span":{"begin":1379,"end":1381},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T27","span":{"begin":1415,"end":1433},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T28","span":{"begin":1435,"end":1441},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T29","span":{"begin":1507,"end":1509},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T30","span":{"begin":1514,"end":1516},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T32","span":{"begin":1655,"end":1657},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T34","span":{"begin":1678,"end":1680},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T35","span":{"begin":1714,"end":1716},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0008185"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"0008185"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0016367"},{"id":"A5","pred":"mondo_id","subj":"T4","obj":"0005015"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"0016367"},{"id":"A11","pred":"mondo_id","subj":"T10","obj":"0005015"},{"id":"A23","pred":"mondo_id","subj":"T23","obj":"0008185"},{"id":"A19","pred":"mondo_id","subj":"T19","obj":"0008185"},{"id":"A16","pred":"mondo_id","subj":"T16","obj":"0005098"},{"id":"A13","pred":"mondo_id","subj":"T13","obj":"0016367"},{"id":"A14","pred":"mondo_id","subj":"T13","obj":"0005015"},{"id":"A28","pred":"mondo_id","subj":"T28","obj":"0005098"},{"id":"A22","pred":"mondo_id","subj":"T22","obj":"0008185"},{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0004995"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0004995"},{"id":"A12","pred":"mondo_id","subj":"T12","obj":"0008185"},{"id":"A17","pred":"mondo_id","subj":"T17","obj":"0005068"},{"id":"A32","pred":"mondo_id","subj":"T32","obj":"0016367"},{"id":"A33","pred":"mondo_id","subj":"T32","obj":"0005015"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005015"},{"id":"A27","pred":"mondo_id","subj":"T27","obj":"0005068"},{"id":"A29","pred":"mondo_id","subj":"T29","obj":"0008185"},{"id":"A20","pred":"mondo_id","subj":"T20","obj":"0016367"},{"id":"A21","pred":"mondo_id","subj":"T20","obj":"0005015"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"0008185"},{"id":"A35","pred":"mondo_id","subj":"T35","obj":"0008185"},{"id":"A18","pred":"mondo_id","subj":"T18","obj":"0004992"},{"id":"A34","pred":"mondo_id","subj":"T34","obj":"0008185"},{"id":"A30","pred":"mondo_id","subj":"T30","obj":"0016367"},{"id":"A31","pred":"mondo_id","subj":"T30","obj":"0005015"},{"id":"A15","pred":"mondo_id","subj":"T15","obj":"0008185"},{"id":"A24","pred":"mondo_id","subj":"T24","obj":"0016367"},{"id":"A25","pred":"mondo_id","subj":"T24","obj":"0005015"},{"id":"A26","pred":"mondo_id","subj":"T26","obj":"0008185"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005015"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":18,"end":40},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":61,"end":78},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":141,"end":158},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":160,"end":162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":227,"end":249},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":456,"end":458},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":526,"end":528},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":682,"end":688},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":690,"end":711},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":731,"end":736},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":1107,"end":1109},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1336,"end":1338},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1415,"end":1433},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":1435,"end":1459},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":1460,"end":1465},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T22","span":{"begin":1514,"end":1516},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T24","span":{"begin":1655,"end":1657},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A19","pred":"ID:","subj":"T19","obj":"D009203"},{"id":"A4","pred":"ID:","subj":"T4","obj":"DISEASE"},{"id":"A5","pred":"ID:","subj":"T4","obj":"D003920"},{"id":"A15","pred":"ID:","subj":"T15","obj":"DISEASE"},{"id":"A16","pred":"ID:","subj":"T15","obj":"D003920"},{"id":"A13","pred":"ID:","subj":"T13","obj":"D009203"},{"id":"A24","pred":"ID:","subj":"T24","obj":"DISEASE"},{"id":"A25","pred":"ID:","subj":"T24","obj":"D003920"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D002318"},{"id":"A7","pred":"ID:","subj":"T7","obj":"DISEASE"},{"id":"A8","pred":"ID:","subj":"T7","obj":"D003920"},{"id":"A14","pred":"ID:","subj":"T14","obj":"D003643"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D003920"},{"id":"A17","pred":"ID:","subj":"T17","obj":"DISEASE"},{"id":"A18","pred":"ID:","subj":"T17","obj":"D003920"},{"id":"A21","pred":"ID:","subj":"T21","obj":"D003643"},{"id":"A22","pred":"ID:","subj":"T22","obj":"DISEASE"},{"id":"A23","pred":"ID:","subj":"T22","obj":"D003920"},{"id":"A11","pred":"ID:","subj":"T11","obj":"DISEASE"},{"id":"A12","pred":"ID:","subj":"T11","obj":"D020521"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D002318"},{"id":"A9","pred":"ID:","subj":"T9","obj":"DISEASE"},{"id":"A10","pred":"ID:","subj":"T9","obj":"D003920"},{"id":"A20","pred":"ID:","subj":"T20","obj":"D009203"},{"id":"A3","pred":"ID:","subj":"T3","obj":"D003920"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":18,"end":40},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":61,"end":78},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":141,"end":158},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":160,"end":162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":227,"end":249},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":456,"end":458},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":526,"end":528},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":682,"end":688},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":690,"end":711},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1107,"end":1109},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":1336,"end":1338},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1415,"end":1433},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T18","span":{"begin":1435,"end":1459},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1514,"end":1516},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":1655,"end":1657},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A21","pred":"#label","subj":"T21","obj":"DISEASE"},{"id":"A22","pred":"#label","subj":"T21","obj":"D003920"},{"id":"A7","pred":"#label","subj":"T7","obj":"DISEASE"},{"id":"A8","pred":"#label","subj":"T7","obj":"D003920"},{"id":"A1","pred":"#label","subj":"T1","obj":"D002318"},{"id":"A13","pred":"#label","subj":"T13","obj":"DISEASE"},{"id":"A14","pred":"#label","subj":"T13","obj":"D003920"},{"id":"A15","pred":"#label","subj":"T15","obj":"DISEASE"},{"id":"A16","pred":"#label","subj":"T15","obj":"D003920"},{"id":"A6","pred":"#label","subj":"T6","obj":"D002318"},{"id":"A3","pred":"#label","subj":"T3","obj":"D003920"},{"id":"A17","pred":"#label","subj":"T17","obj":"D009203"},{"id":"A11","pred":"#label","subj":"T11","obj":"D020521"},{"id":"A18","pred":"#label","subj":"T18","obj":"D009203"},{"id":"A12","pred":"#label","subj":"T12","obj":"D009203"},{"id":"A2","pred":"#label","subj":"T2","obj":"D003920"},{"id":"A4","pred":"#label","subj":"T4","obj":"DISEASE"},{"id":"A5","pred":"#label","subj":"T4","obj":"D003920"},{"id":"A19","pred":"#label","subj":"T19","obj":"DISEASE"},{"id":"A20","pred":"#label","subj":"T19","obj":"D003920"},{"id":"A9","pred":"#label","subj":"T9","obj":"DISEASE"},{"id":"A10","pred":"#label","subj":"T9","obj":"D003920"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T1","span":{"begin":0,"end":9},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":258,"end":269},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":368,"end":379},"obj":"ChemicalEntity"},{"id":"T4","span":{"begin":380,"end":389},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":602,"end":611},"obj":"ChemicalEntity"},{"id":"T6","span":{"begin":1127,"end":1136},"obj":"ChemicalEntity"},{"id":"T7","span":{"begin":1265,"end":1274},"obj":"ChemicalEntity"},{"id":"T8","span":{"begin":1391,"end":1400},"obj":"ChemicalEntity"},{"id":"T9","span":{"begin":1494,"end":1503},"obj":"ChemicalEntity"},{"id":"T10","span":{"begin":1726,"end":1735},"obj":"ChemicalEntity"}],"attributes":[{"id":"A1","pred":"ID:","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_18145"},{"id":"A2","pred":"ID:","subj":"T2","obj":"ChemicalEntity"},{"id":"A3","pred":"ID:","subj":"T3","obj":"ChemicalEntity"},{"id":"A4","pred":"ID:","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A6","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A7","pred":"ID:","subj":"T7","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A8","pred":"ID:","subj":"T8","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A9","pred":"ID:","subj":"T9","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A10","pred":"ID:","subj":"T10","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":974,"end":981},"obj":"OrganismTaxon"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":87,"end":98},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":172,"end":183},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":185,"end":187},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":286,"end":288},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":291,"end":300},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":449,"end":455},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":511,"end":513},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":615,"end":617},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":993,"end":997},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1100,"end":1106},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":1249,"end":1251},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1320,"end":1322},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1379,"end":1385},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":1507,"end":1513},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1678,"end":1680},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1714,"end":1720},"obj":"GeneOrGeneProduct"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

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red":"ID:","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A3","pred":"ID:","subj":"T3","obj":"ChemicalEntity"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"},{"id":"A2","pred":"ID:","subj":"T2","obj":"ChemicalEntity"},{"id":"A6","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_33234"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":87,"end":98},"obj":"gene:3240"},{"id":"T1","span":{"begin":61,"end":78},"obj":"disease:C0011849"},{"id":"T2","span":{"begin":87,"end":98},"obj":"gene:3240"},{"id":"T3","span":{"begin":18,"end":40},"obj":"disease:C0007222"},{"id":"T4","span":{"begin":185,"end":190},"obj":"gene:283297"},{"id":"T5","span":{"begin":227,"end":249},"obj":"disease:C0007222"},{"id":"T6","span":{"begin":185,"end":190},"obj":"gene:283297"},{"id":"T7","span":{"begin":141,"end":162},"obj":"disease:C0011849"},{"id":"T8","span":{"begin":172,"end":183},"obj":"gene:3240"},{"id":"T9","span":{"begin":227,"end":249},"obj":"disease:C0007222"},{"id":"T10","span":{"begin":172,"end":183},"obj":"gene:3240"},{"id":"T11","span":{"begin":141,"end":162},"obj":"disease:C0011849"},{"id":"T12","span":{"begin":1379,"end":1383},"obj":"gene:283297"},{"id":"T13","span":{"begin":1415,"end":1433},"obj":"disease:C0027051"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"},{"id":"R5","pred":"associated_with","subj":"T8","obj":"T9"},{"id":"R6","pred":"associated_with","subj":"T10","obj":"T11"},{"id":"R7","pred":"associated_with","subj":"T12","obj":"T13"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":141,"end":158},"obj":"HP_0000819"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"Allie","denotations":[{"id":"SS1_20415560_2_0","span":{"begin":141,"end":158},"obj":"expanded"},{"id":"SS2_20415560_2_0","span":{"begin":160,"end":162},"obj":"abbr"},{"id":"SS1_20415560_2_1","span":{"begin":172,"end":183},"obj":"expanded"},{"id":"SS2_20415560_2_1","span":{"begin":185,"end":187},"obj":"abbr"}],"relations":[{"id":"AE1_20415560_2_0","pred":"abbreviatedTo","subj":"SS1_20415560_2_0","obj":"SS2_20415560_2_0"},{"id":"AE1_20415560_2_1","pred":"abbreviatedTo","subj":"SS1_20415560_2_1","obj":"SS2_20415560_2_1"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"20415560-0#87#98#gene3240","span":{"begin":87,"end":98},"obj":"gene3240"},{"id":"20415560-0#18#40#diseaseC0007222","span":{"begin":18,"end":40},"obj":"diseaseC0007222"},{"id":"20415560-0#61#78#diseaseC0011849","span":{"begin":61,"end":78},"obj":"diseaseC0011849"},{"id":"20415560-1#66#71#gene283297","span":{"begin":185,"end":190},"obj":"gene283297"},{"id":"20415560-1#108#130#diseaseC0007222","span":{"begin":227,"end":249},"obj":"diseaseC0007222"},{"id":"20415560-3#122#124#gene3240","span":{"begin":615,"end":617},"obj":"gene3240"},{"id":"20415560-3#189#195#diseaseC0038454","span":{"begin":682,"end":688},"obj":"diseaseC0038454"},{"id":"20415560-8#76#80#gene283297","span":{"begin":1379,"end":1383},"obj":"gene283297"},{"id":"20415560-8#112#130#diseaseC0027051","span":{"begin":1415,"end":1433},"obj":"diseaseC0027051"},{"id":"20415560-9#40#44#gene283297","span":{"begin":1507,"end":1511},"obj":"gene283297"},{"id":"20415560-9#47#49#diseaseC0011849","span":{"begin":1514,"end":1516},"obj":"diseaseC0011849"}],"relations":[{"id":"87#98#gene324018#40#diseaseC0007222","pred":"associated_with","subj":"20415560-0#87#98#gene3240","obj":"20415560-0#18#40#diseaseC0007222"},{"id":"87#98#gene324061#78#diseaseC0011849","pred":"associated_with","subj":"20415560-0#87#98#gene3240","obj":"20415560-0#61#78#diseaseC0011849"},{"id":"66#71#gene283297108#130#diseaseC0007222","pred":"associated_with","subj":"20415560-1#66#71#gene283297","obj":"20415560-1#108#130#diseaseC0007222"},{"id":"122#124#gene3240189#195#diseaseC0038454","pred":"associated_with","subj":"20415560-3#122#124#gene3240","obj":"20415560-3#189#195#diseaseC0038454"},{"id":"76#80#gene283297112#130#diseaseC0027051","pred":"associated_with","subj":"20415560-8#76#80#gene283297","obj":"20415560-8#112#130#diseaseC0027051"},{"id":"40#44#gene28329747#49#diseaseC0011849","pred":"associated_with","subj":"20415560-9#40#44#gene283297","obj":"20415560-9#47#49#diseaseC0011849"}],"text":"Vitamin E reduces cardiovascular disease in individuals with diabetes mellitus and the haptoglobin 2-2 genotype.\nAIMS: Individuals with both diabetes mellitus (DM) and the Haptoglobin (Hp) 2-2 genotype are at increased risk of cardiovascular disease. As the antioxidant function of the Hp 2-2 protein is impaired, we sought to test the pharmacogenomic hypothesis that antioxidant vitamin E supplementation would provide cardiovascular protection to Hp 2-2 DM individuals.\nMATERIALS \u0026 METHODS: We determined the Hp genotype on DM participants from two trials (HOPE and ICARE) and assessed the effect of vitamin E by Hp genotype on their common prespecified outcome, the composite of stroke, myocardial infarction and cardiovascular death. Data was analyzed with a fixed-effect model. These results were input into a simulation model, the Evidence Based Medicine Integrator, in order to estimate their long-term implications in a real-world population from Kaiser Permanente (CA, USA).\nRESULTS: Meta-analysis of the two trials demonstrated a significant overall reduction in the composite end point in Hp 2-2 DM individuals with vitamin E (odds ratio: 0.58; 95% CI: 0.40-0.86; p = 0.006). There was a statistically significant interaction between the Hp genotype and vitamin E on the composite end point. In these trials, Hp typing of 69 DM individuals and treating those with the Hp 2-2 with vitamin E prevented one myocardial infarct, stroke or cardiovascular death. Lifelong administration of vitamin E to Hp 2-2 DM individuals in the Kaiser population would increase their life expectancy by 3 years.\nCONCLUSION: A pharmacogenomic strategy of screening DM individuals for the Hp genotype and treating those with Hp 2-2 with vitamin E appears to be highly clinically effective."}