PubMed:21911891 JSON TXT

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TEST-DiseaseOrPhenotypicFeature

TEST-ChemicalEntity

{"project":"TEST-ChemicalEntity","denotations":[{"id":"T1","span":{"begin":331,"end":338},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":490,"end":493},"obj":"ChemicalEntity"},{"id":"T4","span":{"begin":1009,"end":1022},"obj":"ChemicalEntity"}],"attributes":[{"id":"A1","pred":"ID:","subj":"T1","obj":"D006147"},{"id":"A2","pred":"ID:","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_16235"},{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_3416"},{"id":"A4","pred":"ID:","subj":"T4","obj":"D014280"},{"id":"A5","pred":"ID:","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_17855"}],"text":"Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease.\nBACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.\nAIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.\nMATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.\nRESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p \u003c 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).\nCONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients."}

TEST-OrganismTaxon

{"project":"TEST-OrganismTaxon","denotations":[{"id":"T1","span":{"begin":107,"end":115},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":670,"end":678},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":733,"end":741},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":1094,"end":1102},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":1170,"end":1178},"obj":"OrganismTaxon"},{"id":"T6","span":{"begin":1421,"end":1429},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":1477,"end":1485},"obj":"OrganismTaxon"},{"id":"T8","span":{"begin":1594,"end":1602},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":1692,"end":1700},"obj":"OrganismTaxon"},{"id":"T10","span":{"begin":2044,"end":2052},"obj":"OrganismTaxon"}],"text":"Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease.\nBACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.\nAIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.\nMATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.\nRESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p \u003c 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).\nCONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients."}

Test-GeneOrGeneProduct

{"project":"Test-GeneOrGeneProduct","denotations":[{"id":"T1","span":{"begin":0,"end":11},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":12,"end":21},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":172,"end":203},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":212,"end":217},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":413,"end":418},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":435,"end":440},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":524,"end":529},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":891,"end":896},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":1133,"end":1138},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1302,"end":1307},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1389,"end":1394},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":1535,"end":1540},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":1725,"end":1730},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1757,"end":1762},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1978,"end":1983},"obj":"GeneOrGeneProduct"}],"text":"Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease.\nBACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.\nAIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.\nMATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.\nRESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p \u003c 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).\nCONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients."}

Test-merged

Test-merged-2

DisGeNET

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":1389,"end":1394},"obj":"gene:5054"},{"id":"T1","span":{"begin":1494,"end":1508},"obj":"disease:C0239946"},{"id":"T2","span":{"begin":1389,"end":1394},"obj":"gene:5054"},{"id":"T3","span":{"begin":1435,"end":1449},"obj":"disease:C0239946"},{"id":"T4","span":{"begin":1389,"end":1394},"obj":"gene:5054"},{"id":"T5","span":{"begin":1415,"end":1420},"obj":"disease:C0028754"},{"id":"T6","span":{"begin":1535,"end":1540},"obj":"gene:5054"},{"id":"T7","span":{"begin":1619,"end":1633},"obj":"disease:C0239946"},{"id":"T8","span":{"begin":1978,"end":1983},"obj":"gene:5054"},{"id":"T9","span":{"begin":2038,"end":2043},"obj":"disease:C0028754"},{"id":"T10","span":{"begin":1978,"end":1983},"obj":"gene:5054"},{"id":"T11","span":{"begin":2020,"end":2034},"obj":"disease:C0239946"}],"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"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease.\nBACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.\nAIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.\nMATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.\nRESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p \u003c 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).\nCONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients."}

Allie

{"project":"Allie","denotations":[{"id":"SS1_21911891_2_0","span":{"begin":172,"end":210},"obj":"expanded"},{"id":"SS2_21911891_2_0","span":{"begin":212,"end":217},"obj":"abbr"},{"id":"SS1_21911891_5_0","span":{"begin":610,"end":643},"obj":"expanded"},{"id":"SS2_21911891_5_0","span":{"begin":645,"end":650},"obj":"abbr"}],"relations":[{"id":"AE1_21911891_2_0","pred":"abbreviatedTo","subj":"SS1_21911891_2_0","obj":"SS2_21911891_2_0"},{"id":"AE1_21911891_5_0","pred":"abbreviatedTo","subj":"SS1_21911891_5_0","obj":"SS2_21911891_5_0"}],"text":"Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease.\nBACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.\nAIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.\nMATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.\nRESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p \u003c 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).\nCONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients."}

DisGeNET5_gene_disease

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"21911891-14#33#38#gene5054","span":{"begin":1978,"end":1983},"obj":"gene5054"},{"id":"21911891-14#93#98#diseaseC0028754","span":{"begin":2038,"end":2043},"obj":"diseaseC0028754"}],"relations":[{"id":"33#38#gene505493#98#diseaseC0028754","pred":"associated_with","subj":"21911891-14#33#38#gene5054","obj":"21911891-14#93#98#diseaseC0028754"}],"text":"Plasminogen activator inhibitor type 1 serum levels and 4G/5G gene polymorphism in morbidly obese Hispanic patients with non-alcoholic fatty liver disease.\nBACKGROUND: The plasminogen activator inhibitor type-1 (PAI-1) has been implicated in the regulation of fibrinolysis and extracellular matrix components. The single base pair guanine insertion/deletion polymorphism (4G/5G) within the promoter region of the PAI-1 gene influences PAI-1 synthesis and may modulate hepatic fibrogenesis.\nAIM: To evaluate the influence of PAI-1 serum levels and 4G/5G polymorphism on the risk of liver fibrosis associated to non-alcoholic fatty liver disease (NAFLD) in morbidly obese patients.\nMATERIAL AND METHODS: Case-control study of 50 obese patients undergoing bariatric surgery and 71 non-obese subjects matched by age and sex. Anthropometric and biochemical measurements were performed, including PAI-1 serum levels. Genomic DNA was obtained to assess the presence of 4G/5G polymorphism.\nRESULTS: BMI, insulinemia, triglycerides, HOMA-IR, hypertension and diabetes were significantly higher in obese patients compared to control subjects. PAI-1 serum levels observed in obese patients were significantly lower (10.63 ± 4.82) compared to controls (14.26 ± 11.4; p \u003c 0.05). No differences were observed in the PAI-1 4G/5G promoter genotypes frequencies (p = 0.12). No differences were observed in PAI-1 plasma levels among obese patients with liver fibrosis (10.64 ± 4.35) compared to patients without liver fibrosis (10.61 ± 5.2; p = 0.985). PAI-1 4G/5G promoter genotypes frequencies were similar in patients with or without liver fibrosis associated to NASH (p = 0.6).\nCONCLUSIONS: Morbidly obese patients had significantly lower PAI-1 serum levels with similar PAI-1 4G/5G genotypes frequencies compared to non-obese subjects. The frequency of 4G/5G genotypes in Chilean Hispanic healthy subjects was similar to that described in other populations. No association was found between PAI-1 serum levels or 4G/5G genotype with liver fibrosis in obese patients."}