PubMed:20540798 JSONTXT

{"project":"LitCoin-entities","denotations":[{"id":"7545","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"7546","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"7547","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7548","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"7549","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"7550","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7551","span":{"begin":260,"end":271},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7552","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7553","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7554","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"7555","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"7556","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"7557","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"7558","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"7559","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7560","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7561","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"7562","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"7563","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"7564","span":{"begin":1770,"end":1773},"obj":"OrganismTaxon"},{"id":"7565","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"7566","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"7567","span":{"begin":1990,"end":1998},"obj":"SequenceVariant"},{"id":"7568","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7569","span":{"begin":2036,"end":2039},"obj":"OrganismTaxon"},{"id":"7570","span":{"begin":2073,"end":2078},"obj":"OrganismTaxon"},{"id":"7571","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"7572","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"7573","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A7","pred":"db_id","subj":"7551","obj":"MESH:D050197"},{"id":"A2","pred":"db_id","subj":"7546","obj":"NCBIGene:5144"},{"id":"A10","pred":"db_id","subj":"7554","obj":"NCBITaxon:9606"},{"id":"A11","pred":"db_id","subj":"7555","obj":"NCBITaxon:9606"},{"id":"A22","pred":"db_id","subj":"7566","obj":"DBSNP:rs702553"},{"id":"A8","pred":"db_id","subj":"7552","obj":"MESH:D050197"},{"id":"A12","pred":"db_id","subj":"7556","obj":"NCBITaxon:9606"},{"id":"A21","pred":"db_id","subj":"7565","obj":"NCBITaxon:9606"},{"id":"A13","pred":"db_id","subj":"7557","obj":"DBSNP:rs702553"},{"id":"A14","pred":"db_id","subj":"7558","obj":"NCBIGene:5144"},{"id":"A27","pred":"db_id","subj":"7571","obj":"NCBIGene:5144"},{"id":"A16","pred":"db_id","subj":"7560","obj":"MESH:D020521"},{"id":"A24","pred":"db_id","subj":"7568","obj":"MESH:D020521"},{"id":"A4","pred":"db_id","subj":"7548","obj":"NCBIGene:5144"},{"id":"A25","pred":"db_id","subj":"7569","obj":"NCBITaxon:9606"},{"id":"A19","pred":"db_id","subj":"7563","obj":"NCBITaxon:9606"},{"id":"A1","pred":"db_id","subj":"7545","obj":"NCBIGene:5144"},{"id":"A9","pred":"db_id","subj":"7553","obj":"MESH:D020521"},{"id":"A28","pred":"db_id","subj":"7572","obj":"MESH:D020521"},{"id":"A15","pred":"db_id","subj":"7559","obj":"MESH:D020521"},{"id":"A17","pred":"db_id","subj":"7561","obj":"DBSNP:rs702553"},{"id":"A23","pred":"db_id","subj":"7567","obj":"DBSNP:rs702553"},{"id":"A6","pred":"db_id","subj":"7550","obj":"MESH:D020521"},{"id":"A20","pred":"db_id","subj":"7564","obj":"NCBITaxon:9606"},{"id":"A29","pred":"db_id","subj":"7573","obj":"MESH:D050197"},{"id":"A3","pred":"db_id","subj":"7547","obj":"MESH:D002340"},{"id":"A26","pred":"db_id","subj":"7570","obj":"NCBITaxon:9606"},{"id":"A18","pred":"db_id","subj":"7562","obj":"NCBITaxon:9606"},{"id":"A5","pred":"db_id","subj":"7549","obj":"NCBIGene:5144"}],"namespaces":[{"prefix":"_base","uri":"https://w3id.org/biolink/vocab/"},{"prefix":"MESH","uri":"http://id.nlm.nih.gov/mesh/"},{"prefix":"NCBITaxon","uri":"https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id="},{"prefix":"NCBIGene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"OMIM","uri":"https://www.omim.org/entry/"},{"prefix":"DBSNP","uri":"https://www.ncbi.nlm.nih.gov/snp/"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":91},"obj":"Sentence"},{"id":"T2","span":{"begin":92,"end":103},"obj":"Sentence"},{"id":"T3","span":{"begin":104,"end":190},"obj":"Sentence"},{"id":"T4","span":{"begin":191,"end":304},"obj":"Sentence"},{"id":"T5","span":{"begin":305,"end":476},"obj":"Sentence"},{"id":"T6","span":{"begin":477,"end":485},"obj":"Sentence"},{"id":"T7","span":{"begin":486,"end":634},"obj":"Sentence"},{"id":"T8","span":{"begin":635,"end":772},"obj":"Sentence"},{"id":"T9","span":{"begin":773,"end":898},"obj":"Sentence"},{"id":"T10","span":{"begin":899,"end":1077},"obj":"Sentence"},{"id":"T11","span":{"begin":1078,"end":1186},"obj":"Sentence"},{"id":"T12","span":{"begin":1187,"end":1363},"obj":"Sentence"},{"id":"T13","span":{"begin":1364,"end":1372},"obj":"Sentence"},{"id":"T14","span":{"begin":1373,"end":1490},"obj":"Sentence"},{"id":"T15","span":{"begin":1491,"end":1589},"obj":"Sentence"},{"id":"T16","span":{"begin":1590,"end":1740},"obj":"Sentence"},{"id":"T17","span":{"begin":1741,"end":1905},"obj":"Sentence"},{"id":"T18","span":{"begin":1906,"end":1974},"obj":"Sentence"},{"id":"T19","span":{"begin":1975,"end":2090},"obj":"Sentence"},{"id":"T20","span":{"begin":2091,"end":2103},"obj":"Sentence"},{"id":"T21","span":{"begin":2104,"end":2270},"obj":"Sentence"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":75,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":1402,"end":1406},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005311"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005311"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0021136"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-SeqVar","denotations":[{"id":"T1","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T2","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T3","span":{"begin":1990,"end":1998},"obj":"SequenceVariant"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-GeneOrGeneProduct-v0","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":272,"end":282},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":326,"end":331},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":332,"end":341},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":408,"end":417},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":477,"end":484},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":680,"end":684},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":706,"end":712},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":885,"end":891},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":937,"end":943},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1009,"end":1012},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1150,"end":1155},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":1196,"end":1201},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1219,"end":1224},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1402,"end":1406},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1483,"end":1489},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":1600,"end":1604},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":1634,"end":1640},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":1798,"end":1807},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":1975,"end":1984},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":2023,"end":2028},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-GeneOrGeneProduct-v2","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":326,"end":331},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":680,"end":684},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":885,"end":891},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":1150,"end":1155},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1196,"end":1201},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1402,"end":1406},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":2023,"end":2028},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":260,"end":271},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A9","pred":"originalLabel","subj":"T9","obj":"D020521"},{"id":"A1","pred":"originalLabel","subj":"T1","obj":"D002340"},{"id":"A10","pred":"originalLabel","subj":"T10","obj":"D050197"},{"id":"A6","pred":"originalLabel","subj":"T6","obj":"D020521"},{"id":"A7","pred":"originalLabel","subj":"T7","obj":"D020521"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"D020521"},{"id":"A4","pred":"originalLabel","subj":"T4","obj":"D050197"},{"id":"A3","pred":"originalLabel","subj":"T3","obj":"DISEASE"},{"id":"A8","pred":"originalLabel","subj":"T8","obj":"D020521"},{"id":"A5","pred":"originalLabel","subj":"T5","obj":"D020521"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":885,"end":891},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":75,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":629,"end":632},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":830,"end":833},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":933,"end":936},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":983,"end":986},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1568,"end":1571},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":1770,"end":1773},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1834,"end":1837},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T18","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":2036,"end":2039},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":2173,"end":2176},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A15","pred":"mondo_id","subj":"T15","obj":"0017169"},{"id":"A20","pred":"mondo_id","subj":"T20","obj":"0015798"},{"id":"A14","pred":"mondo_id","subj":"T14","obj":"0015798"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"0015798"},{"id":"A12","pred":"mondo_id","subj":"T12","obj":"0005098"},{"id":"A18","pred":"mondo_id","subj":"T18","obj":"0005098"},{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005311"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0017169"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005098"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"0015798"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005098"},{"id":"A19","pred":"mondo_id","subj":"T19","obj":"0017169"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"0017169"},{"id":"A21","pred":"mondo_id","subj":"T21","obj":"0005098"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0005311"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0015798"},{"id":"A17","pred":"mondo_id","subj":"T17","obj":"0015798"},{"id":"A13","pred":"mondo_id","subj":"T13","obj":"0017169"},{"id":"A11","pred":"mondo_id","subj":"T11","obj":"0005098"},{"id":"A16","pred":"mondo_id","subj":"T16","obj":"0015798"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0015798"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":260,"end":271},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A12","pred":"ID:","subj":"T12","obj":"DISEASE"},{"id":"A13","pred":"ID:","subj":"T12","obj":"D020521"},{"id":"A4","pred":"ID:","subj":"T4","obj":"DISEASE"},{"id":"A5","pred":"ID:","subj":"T5","obj":"D050197"},{"id":"A14","pred":"ID:","subj":"T14","obj":"DISEASE"},{"id":"A15","pred":"ID:","subj":"T14","obj":"D020521"},{"id":"A8","pred":"ID:","subj":"T8","obj":"DISEASE"},{"id":"A9","pred":"ID:","subj":"T8","obj":"D020521"},{"id":"A16","pred":"ID:","subj":"T16","obj":"D050197"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D002340"},{"id":"A6","pred":"ID:","subj":"T6","obj":"DISEASE"},{"id":"A7","pred":"ID:","subj":"T6","obj":"D020521"},{"id":"A10","pred":"ID:","subj":"T10","obj":"DISEASE"},{"id":"A11","pred":"ID:","subj":"T10","obj":"D020521"},{"id":"A2","pred":"ID:","subj":"T2","obj":"DISEASE"},{"id":"A3","pred":"ID:","subj":"T2","obj":"D020521"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"T6","span":{"begin":1770,"end":1773},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"T8","span":{"begin":2036,"end":2039},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":2073,"end":2078},"obj":"OrganismTaxon"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":260,"end":271},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A7","pred":"#label","subj":"T7","obj":"D020521"},{"id":"A9","pred":"#label","subj":"T9","obj":"D020521"},{"id":"A5","pred":"#label","subj":"T5","obj":"D020521"},{"id":"A10","pred":"#label","subj":"T10","obj":"D050197"},{"id":"A6","pred":"#label","subj":"T6","obj":"D020521"},{"id":"A1","pred":"#label","subj":"T1","obj":"D002340"},{"id":"A3","pred":"#label","subj":"T3","obj":"DISEASE"},{"id":"A4","pred":"#label","subj":"T4","obj":"D050197"},{"id":"A2","pred":"#label","subj":"T2","obj":"D020521"},{"id":"A8","pred":"#label","subj":"T8","obj":"D020521"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T1","span":{"begin":35,"end":52},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":108,"end":125},"obj":"ChemicalEntity"}],"attributes":[{"id":"A1","pred":"ID:","subj":"T1","obj":"D010727"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D010727"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"LitCoin-training-merged","denotations":[{"id":"T2","span":{"begin":108,"end":125},"obj":"ChemicalEntity"},{"id":"T1","span":{"begin":35,"end":52},"obj":"ChemicalEntity"},{"id":"T7","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":885,"end":891},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T20700","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T17844","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T95667","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T65416","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T86255","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T85028","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T89601","span":{"begin":260,"end":271},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20574","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T50333","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T71394","span":{"begin":2073,"end":2078},"obj":"OrganismTaxon"},{"id":"T50813","span":{"begin":2036,"end":2039},"obj":"OrganismTaxon"},{"id":"T57784","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"T38231","span":{"begin":1770,"end":1773},"obj":"OrganismTaxon"},{"id":"T67414","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"T81591","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"T14055","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T42261","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"T17795","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T84871","span":{"begin":1990,"end":1998},"obj":"SequenceVariant"},{"id":"T69829","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T70878","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"}],"attributes":[{"id":"A5730","pred":"#label","subj":"T20574","obj":"D020521"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D010727"},{"id":"A8","pred":"#label","subj":"T8","obj":"D020521"},{"id":"A5","pred":"#label","subj":"T86255","obj":"D020521"},{"id":"A3","pred":"#label","subj":"T89601","obj":"DISEASE"},{"id":"A55820","pred":"#label","subj":"T50333","obj":"D002340"},{"id":"A10","pred":"#label","subj":"T10","obj":"D050197"},{"id":"A9","pred":"#label","subj":"T9","obj":"D020521"},{"id":"A4","pred":"#label","subj":"T85028","obj":"D050197"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D010727"},{"id":"A7","pred":"#label","subj":"T95667","obj":"D020521"},{"id":"A6","pred":"#label","subj":"T65416","obj":"D020521"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":183,"end":189},"obj":"HP_0001297"},{"id":"T2","span":{"begin":460,"end":475},"obj":"HP_0002621"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"Allie","denotations":[{"id":"SS1_20540798_0_0","span":{"begin":35,"end":55},"obj":"expanded"},{"id":"SS2_20540798_0_0","span":{"begin":57,"end":62},"obj":"abbr"},{"id":"SS1_20540798_2_0","span":{"begin":108,"end":128},"obj":"expanded"},{"id":"SS2_20540798_2_0","span":{"begin":130,"end":135},"obj":"abbr"},{"id":"SS1_20540798_4_0","span":{"begin":319,"end":341},"obj":"expanded"},{"id":"SS2_20540798_4_0","span":{"begin":343,"end":346},"obj":"abbr"}],"relations":[{"id":"AE1_20540798_0_0","pred":"abbreviatedTo","subj":"SS1_20540798_0_0","obj":"SS2_20540798_0_0"},{"id":"AE1_20540798_2_0","pred":"abbreviatedTo","subj":"SS1_20540798_2_0","obj":"SS2_20540798_2_0"},{"id":"AE1_20540798_4_0","pred":"abbreviatedTo","subj":"SS1_20540798_4_0","obj":"SS2_20540798_4_0"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":260,"end":271},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T11","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"T12","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T13","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T14","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T18","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"T19","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"T20","span":{"begin":1770,"end":1773},"obj":"OrganismTaxon"},{"id":"T21","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"T22","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T23","span":{"begin":1990,"end":1998},"obj":"SequenceVariant"},{"id":"T24","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":2036,"end":2039},"obj":"OrganismTaxon"},{"id":"T26","span":{"begin":2073,"end":2078},"obj":"OrganismTaxon"},{"id":"T27","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T29","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-deepseek-nr-ng","denotations":[{"id":"T1","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":311,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":352,"end":358},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":486,"end":509},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":691,"end":697},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":911,"end":917},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":933,"end":936},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T14","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1468,"end":1474},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

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genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-deepseek-r-ng","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":311,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T11","span":{"begin":1986,"end":1998},"obj":"SequenceVariant"},{"id":"T12","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-deepseek-r-g","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":311,"end":347},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T10","span":{"begin":933,"end":936},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T12","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T13","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":1202,"end":1208},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T17","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"},{"id":"T18","span":{"begin":1886,"end":1888},"obj":"SequenceVariant"},{"id":"T19","span":{"begin":1891,"end":1893},"obj":"SequenceVariant"},{"id":"T20","span":{"begin":1986,"end":1998},"obj":"SequenceVariant"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gemini-nr-ng","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":108,"end":136},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":260,"end":279},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":311,"end":347},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":532,"end":543},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":691,"end":703},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":830,"end":833},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":911,"end":917},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T17","span":{"begin":1468,"end":1480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T18","span":{"begin":1619,"end":1631},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":1911,"end":1914},"obj":"OrganismTaxon"},{"id":"T21","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T22","span":{"begin":1932,"end":1944},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T23","span":{"begin":1986,"end":1998},"obj":"SequenceVariant"},{"id":"T24","span":{"begin":2023,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gemini-r-g","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":130,"end":141},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":311,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":532,"end":543},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T13","span":{"begin":691,"end":703},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":911,"end":928},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"T17","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T18","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T19","span":{"begin":1094,"end":1104},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T22","span":{"begin":1468,"end":1480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T23","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"T24","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"T25","span":{"begin":1600,"end":1604},"obj":"OrganismTaxon"},{"id":"T26","span":{"begin":1656,"end":1668},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T27","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"},{"id":"T28","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T29","span":{"begin":1770,"end":1773},"obj":"OrganismTaxon"},{"id":"T30","span":{"begin":1885,"end":1904},"obj":"SequenceVariant"},{"id":"T31","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"T32","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T33","span":{"begin":1932,"end":1944},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T34","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T35","span":{"begin":2023,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T36","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gemini-r-ng","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":108,"end":136},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":260,"end":279},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":311,"end":347},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T10","span":{"begin":691,"end":703},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":830,"end":833},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":911,"end":928},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"T15","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T16","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T17","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T20","span":{"begin":1468,"end":1480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"T22","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"T23","span":{"begin":1600,"end":1604},"obj":"OrganismTaxon"},{"id":"T24","span":{"begin":1656,"end":1668},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"},{"id":"T26","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T27","span":{"begin":1826,"end":1837},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T28","span":{"begin":1885,"end":1904},"obj":"SequenceVariant"},{"id":"T29","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"T30","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T31","span":{"begin":1932,"end":1944},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T32","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T33","span":{"begin":2023,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T34","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T35","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gpt-nr-ng","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":319,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T13","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gpt-nr-g","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":108,"end":136},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":311,"end":347},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T8","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T11","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"},{"id":"T12","span":{"begin":1885,"end":1904},"obj":"SequenceVariant"},{"id":"T13","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T14","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gpt-r-ng","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":108,"end":136},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":260,"end":279},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":311,"end":347},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":911,"end":928},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":933,"end":936},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T13","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T16","span":{"begin":1468,"end":1480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1619,"end":1631},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T18","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"},{"id":"T19","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":1779,"end":1790},"obj":"SequenceVariant"},{"id":"T21","span":{"begin":1834,"end":1837},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T22","span":{"begin":1885,"end":1904},"obj":"SequenceVariant"},{"id":"T23","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T24","span":{"begin":1932,"end":1944},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T26","span":{"begin":2023,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T27","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":2173,"end":2176},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T29","span":{"begin":2178,"end":2190},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T30","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T31","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gpt-r-g","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":75,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":311,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":933,"end":936},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T14","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T17","span":{"begin":1468,"end":1480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T18","span":{"begin":1619,"end":1631},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T19","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"},{"id":"T20","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T21","span":{"begin":1779,"end":1790},"obj":"SequenceVariant"},{"id":"T22","span":{"begin":1834,"end":1837},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T23","span":{"begin":1885,"end":1904},"obj":"SequenceVariant"},{"id":"T24","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":1932,"end":1944},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T26","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T27","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T28","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T29","span":{"begin":2173,"end":2176},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T30","span":{"begin":2178,"end":2190},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T31","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gemini-nr-g","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":108,"end":136},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":260,"end":279},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T10","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T11","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":2256,"end":2269},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gpt-r-m","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":75,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":128},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":130,"end":135},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":319,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":532,"end":538},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":544,"end":552},"obj":"OrganismTaxon"},{"id":"T13","span":{"begin":691,"end":703},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":796,"end":799},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T15","span":{"begin":911,"end":928},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":933,"end":936},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T17","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T18","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T20","span":{"begin":1219,"end":1224},"obj":"OrganismTaxon"},{"id":"T21","span":{"begin":1233,"end":1241},"obj":"OrganismTaxon"},{"id":"T22","span":{"begin":1274,"end":1282},"obj":"OrganismTaxon"},{"id":"T23","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T24","span":{"begin":1468,"end":1480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":1496,"end":1504},"obj":"OrganismTaxon"},{"id":"T26","span":{"begin":1605,"end":1613},"obj":"OrganismTaxon"},{"id":"T27","span":{"begin":1619,"end":1631},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T28","span":{"begin":1678,"end":1680},"obj":"SequenceVariant"},{"id":"T29","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T30","span":{"begin":1779,"end":1781},"obj":"SequenceVariant"},{"id":"T31","span":{"begin":1834,"end":1837},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T32","span":{"begin":1886,"end":1888},"obj":"SequenceVariant"},{"id":"T33","span":{"begin":1891,"end":1893},"obj":"SequenceVariant"},{"id":"T34","span":{"begin":1924,"end":1927},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T35","span":{"begin":1932,"end":1944},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T36","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T37","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T38","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"},{"id":"T39","span":{"begin":2173,"end":2176},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T40","span":{"begin":2178,"end":2190},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T41","span":{"begin":2195,"end":2201},"obj":"DiseaseOrPhenotypicFeature"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-gemini-r-m","denotations":[{"id":"T1","span":{"begin":35,"end":55},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":57,"end":62},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":108,"end":136},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":319,"end":341},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":343,"end":346},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":460,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":544,"end":552},"obj":"OrganismTaxon"},{"id":"T10","span":{"begin":629,"end":632},"obj":"OrganismTaxon"},{"id":"T11","span":{"begin":983,"end":986},"obj":"OrganismTaxon"},{"id":"T12","span":{"begin":991,"end":996},"obj":"OrganismTaxon"},{"id":"T13","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T14","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1156,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T16","span":{"begin":1219,"end":1224},"obj":"OrganismTaxon"},{"id":"T17","span":{"begin":1233,"end":1241},"obj":"OrganismTaxon"},{"id":"T18","span":{"begin":1266,"end":1282},"obj":"OrganismTaxon"},{"id":"T19","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T20","span":{"begin":1568,"end":1571},"obj":"OrganismTaxon"},{"id":"T21","span":{"begin":1583,"end":1588},"obj":"OrganismTaxon"},{"id":"T22","span":{"begin":1600,"end":1613},"obj":"OrganismTaxon"},{"id":"T23","span":{"begin":1678,"end":1680},"obj":"SequenceVariant"},{"id":"T24","span":{"begin":1758,"end":1761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T25","span":{"begin":1770,"end":1773},"obj":"OrganismTaxon"},{"id":"T26","span":{"begin":1826,"end":1837},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T27","span":{"begin":1886,"end":1888},"obj":"SequenceVariant"},{"id":"T28","span":{"begin":1891,"end":1893},"obj":"SequenceVariant"},{"id":"T29","span":{"begin":1909,"end":1914},"obj":"OrganismTaxon"},{"id":"T30","span":{"begin":1965,"end":1973},"obj":"SequenceVariant"},{"id":"T31","span":{"begin":1986,"end":1998},"obj":"SequenceVariant"},{"id":"T32","span":{"begin":2029,"end":2035},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T33","span":{"begin":2164,"end":2169},"obj":"GeneOrGeneProduct"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}

{"project":"biored-valid-deepseek-r-m","denotations":[{"id":"T1","span":{"begin":35,"end":63},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":67,"end":90},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":108,"end":141},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":183,"end":189},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":311,"end":347},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":352,"end":364},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":448,"end":475},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1078,"end":1086},"obj":"SequenceVariant"},{"id":"T9","span":{"begin":1094,"end":1099},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1150,"end":1162},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1421,"end":1429},"obj":"SequenceVariant"},{"id":"T12","span":{"begin":1678,"end":1689},"obj":"SequenceVariant"}],"text":"Sex-differential genetic effect of phosphodiesterase 4D (PDE4D) on carotid atherosclerosis.\nBACKGROUND: The phosphodiesterase 4D (PDE4D) gene was reported as a susceptibility gene to stroke. The genetic effect might be attributed to its role in modulating the atherogenic process in the carotid arteries. Using carotid intima-media thickness (IMT) and plaque index as phenotypes, the present study sought to determine the influence of this gene on subclinical atherosclerosis.\nMETHODS: Carotid ultrasonography was performed on 1013 stroke-free subjects who participated in the health screening programs (age 52.6 +/- 12.2; 47.6% men). Genotype distribution was compared among the high-risk (plaque index \u003e or = 4), low-risk (index = 1-3), and reference (index = 0) groups. We analyzed continuous IMT data and further dichotomized IMT data using mean plus one standard deviation as the cutoff level. Because the plaque prevalence and IMT values displayed a notable difference between men and women, we carried out sex-specific analyses in addition to analyzing the overall data. Rs702553 at the PDE4D gene was selected because it conferred a risk for young stroke in our previous report. Previous young stroke data (190 cases and 211 controls) with an additional 532 control subjects without ultrasonic data were shown as a cross-validation for the genetic effect.\nRESULTS: In the overall analyses, the rare homozygote of rs702553 led to an OR of 3.1 (p = 0.034) for a plaque index \u003e or = 4. When subjects were stratified by sex, the genetic effect was only evident in men but not in women. Comparing male subjects with plaque index \u003e or = 4 and those with plaque index = 0, the TT genotype was over-represented (27.6% vs. 13.4%, p = 0.008). For dichotomized IMT data in men, the TT genotype had an OR of 2.1 (p = 0.032) for a thicker IMT at the common carotid artery compared with the (AA + AT) genotypes. In women, neither IMT nor plaque index was associated with rs702553. Similarly, SNP rs702553 was only significant in young stroke men (OR = 1.8, p = 0.025) but not in women (p = 0.27).\nCONCLUSIONS: The present study demonstrates a sex-differential effect of PDE4D on IMT, plaque index and stroke, which highlights its influence on various aspects of atherogenesis."}