PubMed:9555861 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":142,"end":273},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":274,"end":358},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":359,"end":501},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":502,"end":711},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":712,"end":786},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":787,"end":980},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":981,"end":1216},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":1217,"end":1507},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"T2","span":{"begin":142,"end":273},"obj":"Sentence"},{"id":"T3","span":{"begin":274,"end":358},"obj":"Sentence"},{"id":"T4","span":{"begin":359,"end":501},"obj":"Sentence"},{"id":"T5","span":{"begin":502,"end":711},"obj":"Sentence"},{"id":"T6","span":{"begin":712,"end":786},"obj":"Sentence"},{"id":"T7","span":{"begin":787,"end":980},"obj":"Sentence"},{"id":"T8","span":{"begin":981,"end":1216},"obj":"Sentence"},{"id":"T9","span":{"begin":1217,"end":1507},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants.\nPlasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels were significantly higher in men (P\u003c.001), alcohol drinkers (P\u003c.001), smokers (P=.009), and homozygotes for the PAI-1 gene deletion allele (4G/4G) (P=.012). Multivariate analysis documented the independent effect on PAI-1 plasma levels of body mass index (P\u003c.001), triglycerides (P\u003c.001), sex (P\u003c.001), PAI-1 4G/5G polymorphism (P=.019), smoking habit (P=.041), and ACE I/D genotype (P=.042). Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis."}

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{"project":"DisGeNet-2017-sample","denotations":[{"id":"T2170","span":{"begin":0,"end":5},"obj":"gene:5054"},{"id":"T2171","span":{"begin":73,"end":88},"obj":"disease:C0003850"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T2170","obj":"T2171"},{"id":"R2","pred":"associated_with","subj":"T2170","obj":"T2171"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants.\nPlasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels were significantly higher in men (P\u003c.001), alcohol drinkers (P\u003c.001), smokers (P=.009), and homozygotes for the PAI-1 gene deletion allele (4G/4G) (P=.012). Multivariate analysis documented the independent effect on PAI-1 plasma levels of body mass index (P\u003c.001), triglycerides (P\u003c.001), sex (P\u003c.001), PAI-1 4G/5G polymorphism (P=.019), smoking habit (P=.041), and ACE I/D genotype (P=.042). Thus, in addition to the markers of insulin resistance and smoking habit, gene variants of PAI-1 and ACE account for a significant portion of the between-individual variability of circulating PAI-1 antigen concentrations in a general population without clinical evidence of atherosclerosis."}