PubMed:8488520 JSONTXT

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    sentences

    {"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":78},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":79,"end":100},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":101,"end":124},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":125,"end":218},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":219,"end":307},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":308,"end":316},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":317,"end":581},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":582,"end":729},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":730,"end":738},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":739,"end":893},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":894,"end":1066},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1067,"end":1136},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":1137,"end":1370},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1371,"end":1511},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1512,"end":1612},"obj":"Sentence"},{"id":"TextSentencer_T16","span":{"begin":1613,"end":1858},"obj":"Sentence"},{"id":"TextSentencer_T17","span":{"begin":1859,"end":1871},"obj":"Sentence"},{"id":"TextSentencer_T18","span":{"begin":1872,"end":2072},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":78},"obj":"Sentence"},{"id":"T2","span":{"begin":79,"end":100},"obj":"Sentence"},{"id":"T3","span":{"begin":101,"end":124},"obj":"Sentence"},{"id":"T4","span":{"begin":125,"end":218},"obj":"Sentence"},{"id":"T5","span":{"begin":219,"end":307},"obj":"Sentence"},{"id":"T6","span":{"begin":308,"end":316},"obj":"Sentence"},{"id":"T7","span":{"begin":317,"end":581},"obj":"Sentence"},{"id":"T8","span":{"begin":582,"end":729},"obj":"Sentence"},{"id":"T9","span":{"begin":730,"end":738},"obj":"Sentence"},{"id":"T10","span":{"begin":739,"end":893},"obj":"Sentence"},{"id":"T11","span":{"begin":894,"end":1066},"obj":"Sentence"},{"id":"T12","span":{"begin":1067,"end":1136},"obj":"Sentence"},{"id":"T13","span":{"begin":1137,"end":1370},"obj":"Sentence"},{"id":"T14","span":{"begin":1371,"end":1511},"obj":"Sentence"},{"id":"T15","span":{"begin":1512,"end":1612},"obj":"Sentence"},{"id":"T16","span":{"begin":1613,"end":1858},"obj":"Sentence"},{"id":"T17","span":{"begin":1859,"end":1871},"obj":"Sentence"},{"id":"T18","span":{"begin":1872,"end":2072},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. A case-control study.\nBACKGROUND AND PURPOSE: Apolipoprotein E polymorphism may influence the early development of coronary artery disease. We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction.\nMETHODS: The apolipoprotein E phenotypes of 69 patients (mean +/- SD age, 72 +/- 11 years) who had suffered completed stroke or a transient ischemic attack and 68 sex- and age-matched control subjects free of cerebrovascular disease were determined by isoelectric focusing. The relative frequency of the apolipoprotein E phenotypes in the general population was estimated in 498 healthy blood donors (mean age, 37 years).\nRESULTS: The prevalences of hypertension, diabetes mellitus, obesity, and intermittent claudication were significantly higher in patients than in control subjects. Serum lipid and apolipoprotein B concentrations and the composition of very low density lipoproteins were not significantly different between patients and control subjects. Apolipoprotein A-I and E levels were significantly lower in patients. Cholesterol levels were higher in male patients than in male control subjects (5.10 +/- 1.46 versus 4.41 +/- 0.80 mmol/L; p = 0.036), and the ratio of apolipoprotein A-I to B was lower (0.77 +/- 0.29 versus 1.03 +/- 0.37; p \u003c 0.001). The E3/E3 phenotype was more frequent in control subjects (85%) than in patients (72.5%; p \u003c 0.05) and healthy blood donors (64%; p \u003c 0.02). The E3/E2 phenotype was more frequent in patients (10.1%) than in control subjects (1.4%; p \u003c 0.05). A stepwise logistic regression showed that the presence of stroke was significantly related to high blood pressure (p \u003c 0.0001), low apo E levels (p \u003c 0.008), obesity (p \u003c 0.041), the apo E phenotype (p \u003c 0.05), and diabetes mellitus (p \u003c 0.05).\nCONCLUSIONS: The E3/E3 phenotype may protect against early vascular morbidity, and the epsilon 2 gene may be a risk factor for cerebrovascular morbidity, possibly related to diabetes, hypertension, and/or obesity."}

    DisGeNET

    {"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":125,"end":141},"obj":"gene:348"},{"id":"T1","span":{"begin":194,"end":217},"obj":"disease:C0010054"},{"id":"T2","span":{"begin":125,"end":141},"obj":"gene:348"},{"id":"T3","span":{"begin":194,"end":217},"obj":"disease:C0010068"},{"id":"T4","span":{"begin":125,"end":141},"obj":"gene:348"},{"id":"T5","span":{"begin":194,"end":217},"obj":"disease:C1956346"}],"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"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. A case-control study.\nBACKGROUND AND PURPOSE: Apolipoprotein E polymorphism may influence the early development of coronary artery disease. We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction.\nMETHODS: The apolipoprotein E phenotypes of 69 patients (mean +/- SD age, 72 +/- 11 years) who had suffered completed stroke or a transient ischemic attack and 68 sex- and age-matched control subjects free of cerebrovascular disease were determined by isoelectric focusing. The relative frequency of the apolipoprotein E phenotypes in the general population was estimated in 498 healthy blood donors (mean age, 37 years).\nRESULTS: The prevalences of hypertension, diabetes mellitus, obesity, and intermittent claudication were significantly higher in patients than in control subjects. Serum lipid and apolipoprotein B concentrations and the composition of very low density lipoproteins were not significantly different between patients and control subjects. Apolipoprotein A-I and E levels were significantly lower in patients. Cholesterol levels were higher in male patients than in male control subjects (5.10 +/- 1.46 versus 4.41 +/- 0.80 mmol/L; p = 0.036), and the ratio of apolipoprotein A-I to B was lower (0.77 +/- 0.29 versus 1.03 +/- 0.37; p \u003c 0.001). The E3/E3 phenotype was more frequent in control subjects (85%) than in patients (72.5%; p \u003c 0.05) and healthy blood donors (64%; p \u003c 0.02). The E3/E2 phenotype was more frequent in patients (10.1%) than in control subjects (1.4%; p \u003c 0.05). A stepwise logistic regression showed that the presence of stroke was significantly related to high blood pressure (p \u003c 0.0001), low apo E levels (p \u003c 0.008), obesity (p \u003c 0.041), the apo E phenotype (p \u003c 0.05), and diabetes mellitus (p \u003c 0.05).\nCONCLUSIONS: The E3/E3 phenotype may protect against early vascular morbidity, and the epsilon 2 gene may be a risk factor for cerebrovascular morbidity, possibly related to diabetes, hypertension, and/or obesity."}

    DisGeNet-2017-sample

    {"project":"DisGeNet-2017-sample","denotations":[{"id":"T1013","span":{"begin":125,"end":141},"obj":"gene:348"},{"id":"T1014","span":{"begin":194,"end":217},"obj":"disease:C0010054"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T1013","obj":"T1014"},{"id":"R2","pred":"associated_with","subj":"T1013","obj":"T1014"},{"id":"R3","pred":"associated_with","subj":"T1013","obj":"T1014"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. A case-control study.\nBACKGROUND AND PURPOSE: Apolipoprotein E polymorphism may influence the early development of coronary artery disease. We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction.\nMETHODS: The apolipoprotein E phenotypes of 69 patients (mean +/- SD age, 72 +/- 11 years) who had suffered completed stroke or a transient ischemic attack and 68 sex- and age-matched control subjects free of cerebrovascular disease were determined by isoelectric focusing. The relative frequency of the apolipoprotein E phenotypes in the general population was estimated in 498 healthy blood donors (mean age, 37 years).\nRESULTS: The prevalences of hypertension, diabetes mellitus, obesity, and intermittent claudication were significantly higher in patients than in control subjects. Serum lipid and apolipoprotein B concentrations and the composition of very low density lipoproteins were not significantly different between patients and control subjects. Apolipoprotein A-I and E levels were significantly lower in patients. Cholesterol levels were higher in male patients than in male control subjects (5.10 +/- 1.46 versus 4.41 +/- 0.80 mmol/L; p = 0.036), and the ratio of apolipoprotein A-I to B was lower (0.77 +/- 0.29 versus 1.03 +/- 0.37; p \u003c 0.001). The E3/E3 phenotype was more frequent in control subjects (85%) than in patients (72.5%; p \u003c 0.05) and healthy blood donors (64%; p \u003c 0.02). The E3/E2 phenotype was more frequent in patients (10.1%) than in control subjects (1.4%; p \u003c 0.05). A stepwise logistic regression showed that the presence of stroke was significantly related to high blood pressure (p \u003c 0.0001), low apo E levels (p \u003c 0.008), obesity (p \u003c 0.041), the apo E phenotype (p \u003c 0.05), and diabetes mellitus (p \u003c 0.05).\nCONCLUSIONS: The E3/E3 phenotype may protect against early vascular morbidity, and the epsilon 2 gene may be a risk factor for cerebrovascular morbidity, possibly related to diabetes, hypertension, and/or obesity."}

    UBERON-AE

    {"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":194,"end":209},"obj":"http://purl.obolibrary.org/obo/UBERON_0001621"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":203,"end":209},"obj":"http://purl.obolibrary.org/obo/UBERON_0001637"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":695,"end":700},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1482,"end":1487},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":1713,"end":1718},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. A case-control study.\nBACKGROUND AND PURPOSE: Apolipoprotein E polymorphism may influence the early development of coronary artery disease. We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction.\nMETHODS: The apolipoprotein E phenotypes of 69 patients (mean +/- SD age, 72 +/- 11 years) who had suffered completed stroke or a transient ischemic attack and 68 sex- and age-matched control subjects free of cerebrovascular disease were determined by isoelectric focusing. The relative frequency of the apolipoprotein E phenotypes in the general population was estimated in 498 healthy blood donors (mean age, 37 years).\nRESULTS: The prevalences of hypertension, diabetes mellitus, obesity, and intermittent claudication were significantly higher in patients than in control subjects. Serum lipid and apolipoprotein B concentrations and the composition of very low density lipoproteins were not significantly different between patients and control subjects. Apolipoprotein A-I and E levels were significantly lower in patients. Cholesterol levels were higher in male patients than in male control subjects (5.10 +/- 1.46 versus 4.41 +/- 0.80 mmol/L; p = 0.036), and the ratio of apolipoprotein A-I to B was lower (0.77 +/- 0.29 versus 1.03 +/- 0.37; p \u003c 0.001). The E3/E3 phenotype was more frequent in control subjects (85%) than in patients (72.5%; p \u003c 0.05) and healthy blood donors (64%; p \u003c 0.02). The E3/E2 phenotype was more frequent in patients (10.1%) than in control subjects (1.4%; p \u003c 0.05). A stepwise logistic regression showed that the presence of stroke was significantly related to high blood pressure (p \u003c 0.0001), low apo E levels (p \u003c 0.008), obesity (p \u003c 0.041), the apo E phenotype (p \u003c 0.05), and diabetes mellitus (p \u003c 0.05).\nCONCLUSIONS: The E3/E3 phenotype may protect against early vascular morbidity, and the epsilon 2 gene may be a risk factor for cerebrovascular morbidity, possibly related to diabetes, hypertension, and/or obesity."}

    performance-test

    {"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":695,"end":700},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":1482,"end":1487},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1713,"end":1718},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":894,"end":899},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":203,"end":209},"obj":"http://purl.obolibrary.org/obo/UBERON_0001637"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":194,"end":209},"obj":"http://purl.obolibrary.org/obo/UBERON_0001621"}],"text":"Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. A case-control study.\nBACKGROUND AND PURPOSE: Apolipoprotein E polymorphism may influence the early development of coronary artery disease. We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction.\nMETHODS: The apolipoprotein E phenotypes of 69 patients (mean +/- SD age, 72 +/- 11 years) who had suffered completed stroke or a transient ischemic attack and 68 sex- and age-matched control subjects free of cerebrovascular disease were determined by isoelectric focusing. The relative frequency of the apolipoprotein E phenotypes in the general population was estimated in 498 healthy blood donors (mean age, 37 years).\nRESULTS: The prevalences of hypertension, diabetes mellitus, obesity, and intermittent claudication were significantly higher in patients than in control subjects. Serum lipid and apolipoprotein B concentrations and the composition of very low density lipoproteins were not significantly different between patients and control subjects. Apolipoprotein A-I and E levels were significantly lower in patients. Cholesterol levels were higher in male patients than in male control subjects (5.10 +/- 1.46 versus 4.41 +/- 0.80 mmol/L; p = 0.036), and the ratio of apolipoprotein A-I to B was lower (0.77 +/- 0.29 versus 1.03 +/- 0.37; p \u003c 0.001). The E3/E3 phenotype was more frequent in control subjects (85%) than in patients (72.5%; p \u003c 0.05) and healthy blood donors (64%; p \u003c 0.02). The E3/E2 phenotype was more frequent in patients (10.1%) than in control subjects (1.4%; p \u003c 0.05). A stepwise logistic regression showed that the presence of stroke was significantly related to high blood pressure (p \u003c 0.0001), low apo E levels (p \u003c 0.008), obesity (p \u003c 0.041), the apo E phenotype (p \u003c 0.05), and diabetes mellitus (p \u003c 0.05).\nCONCLUSIONS: The E3/E3 phenotype may protect against early vascular morbidity, and the epsilon 2 gene may be a risk factor for cerebrovascular morbidity, possibly related to diabetes, hypertension, and/or obesity."}