PubMed:9125598
Annnotations
sentences
{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":244},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":245,"end":256},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":257,"end":364},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":365,"end":505},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":506,"end":614},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":615,"end":781},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":782,"end":795},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":796,"end":1024},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":1025,"end":1086},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":1087,"end":1389},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":1390,"end":1440},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1441,"end":1449},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":1450,"end":1611},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1612,"end":1726},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1727,"end":1907},"obj":"Sentence"},{"id":"TextSentencer_T16","span":{"begin":1908,"end":2041},"obj":"Sentence"},{"id":"TextSentencer_T17","span":{"begin":2042,"end":2143},"obj":"Sentence"},{"id":"TextSentencer_T18","span":{"begin":2144,"end":2345},"obj":"Sentence"},{"id":"TextSentencer_T19","span":{"begin":2346,"end":2358},"obj":"Sentence"},{"id":"TextSentencer_T20","span":{"begin":2359,"end":2620},"obj":"Sentence"},{"id":"TextSentencer_T21","span":{"begin":2621,"end":2797},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":244},"obj":"Sentence"},{"id":"T2","span":{"begin":245,"end":256},"obj":"Sentence"},{"id":"T3","span":{"begin":257,"end":364},"obj":"Sentence"},{"id":"T4","span":{"begin":365,"end":505},"obj":"Sentence"},{"id":"T5","span":{"begin":506,"end":614},"obj":"Sentence"},{"id":"T6","span":{"begin":615,"end":781},"obj":"Sentence"},{"id":"T7","span":{"begin":782,"end":795},"obj":"Sentence"},{"id":"T8","span":{"begin":796,"end":1024},"obj":"Sentence"},{"id":"T9","span":{"begin":1025,"end":1086},"obj":"Sentence"},{"id":"T10","span":{"begin":1087,"end":1389},"obj":"Sentence"},{"id":"T11","span":{"begin":1390,"end":1440},"obj":"Sentence"},{"id":"T12","span":{"begin":1441,"end":1449},"obj":"Sentence"},{"id":"T13","span":{"begin":1450,"end":1611},"obj":"Sentence"},{"id":"T14","span":{"begin":1612,"end":1726},"obj":"Sentence"},{"id":"T15","span":{"begin":1727,"end":1907},"obj":"Sentence"},{"id":"T16","span":{"begin":1908,"end":2041},"obj":"Sentence"},{"id":"T17","span":{"begin":2042,"end":2143},"obj":"Sentence"},{"id":"T18","span":{"begin":2144,"end":2345},"obj":"Sentence"},{"id":"T19","span":{"begin":2346,"end":2358},"obj":"Sentence"},{"id":"T20","span":{"begin":2359,"end":2620},"obj":"Sentence"},{"id":"T21","span":{"begin":2621,"end":2797},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Insulin-like growth factor binding protein-1 at the maternal-fetal interface and insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1 in the circulation of women with severe preeclampsia.\nOBJECTIVES: Preeclampsia is characterized by maternal hypertension, proteinuria, edema, and shallow placental invasion. Insulin-like growth factor binding protein-1, abundant in maternal decidua, is believed to play a role in limiting trophoblast invasiveness. In this study we addressed the hypothesis that this binding protein is aberrantly expressed in preeclampsia. We also investigated circulating levels of insulin-like growth factor-I and insulin-like growth factor-II in subjects with severe preeclampsia compared with controls.\nSTUDY DESIGN: Insulin-like growth factor binding protein-1 was investigated by immunohistochemistry at the maternal-fetal interface of eight pregnancies complicated by severe preeclampsia and six controls between 21 and 34 weeks of gestation. Cell types were identified with use of cell-specific markers. Circulating levels of insulin-like growth factor binding protein-1, insulin-like growth factor-I, and insulin-like growth factor-II in 16 patients with severe preeclampsia and 29 controls at the same gestational age were determined by an immunoradiometric assay and correlated with clinical parameters. Data were analyzed by t test and Pearson's method.\nRESULTS: Insulin-like growth factor binding protein-1 was highly expressed on syncytiotrophoblasts, cytotrophoblasts, and decidual cells but not on placental fibroblasts. Immunostaining was greater at the maternal-fetal interface in severe preeclamptic patients compared with controls. Circulating insulin-like growth factor binding protein-1 levels in subjects with severe preeclampsia were 428.3 +/- 85.9 ng/ml compared with 76.6 +/- 11.8 in controls (p = 0.0007). Circulating insulin-like growth factor-I levels were 80.9 +/- 17.2 ng/ml compared with 179.4 +/- 28.2 ng/ml in controls (p = 0.0001). In contrast, insulin-like growth factor-II levels were not significantly different in the two groups. In subjects with severe preeclampsia insulin-like growth factor binding protein-1 levels correlated with diastolic blood pressure (r = 0.498, p 0.049) and aspartate transcarbamylase (0.621, p = 0.010).\nCONCLUSIONS: The abundance of insulin-like growth factor binding protein-1 at the maternal-fetal interface in severely preeclamptic pregnancies suggests that the binding protein may participate in the pathogenesis of the shallow placental invasion observed in this disorder. Low circulating insulin-like growth factor-I and elevated insulin-like growth factor binding protein-1 levels may contribute to restricted placental and therefore fetal growth."}
Preeclampsia
{"project":"Preeclampsia","denotations":[{"id":"PD-Preeclampsia-B_T1","span":{"begin":231,"end":243},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T2","span":{"begin":257,"end":269},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T3","span":{"begin":601,"end":613},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T4","span":{"begin":745,"end":757},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T5","span":{"begin":957,"end":969},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T6","span":{"begin":1246,"end":1258},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T7","span":{"begin":1681,"end":1702},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T8","span":{"begin":1815,"end":1827},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T9","span":{"begin":2168,"end":2180},"obj":"ORPHA:275555"}],"namespaces":[{"prefix":"ORPHA","uri":"www.orpha.net/consor/cgi-bin/OC_Exp.php?lng=EN\u0026Expert="}],"text":"Insulin-like growth factor binding protein-1 at the maternal-fetal interface and insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1 in the circulation of women with severe preeclampsia.\nOBJECTIVES: Preeclampsia is characterized by maternal hypertension, proteinuria, edema, and shallow placental invasion. Insulin-like growth factor binding protein-1, abundant in maternal decidua, is believed to play a role in limiting trophoblast invasiveness. In this study we addressed the hypothesis that this binding protein is aberrantly expressed in preeclampsia. We also investigated circulating levels of insulin-like growth factor-I and insulin-like growth factor-II in subjects with severe preeclampsia compared with controls.\nSTUDY DESIGN: Insulin-like growth factor binding protein-1 was investigated by immunohistochemistry at the maternal-fetal interface of eight pregnancies complicated by severe preeclampsia and six controls between 21 and 34 weeks of gestation. Cell types were identified with use of cell-specific markers. Circulating levels of insulin-like growth factor binding protein-1, insulin-like growth factor-I, and insulin-like growth factor-II in 16 patients with severe preeclampsia and 29 controls at the same gestational age were determined by an immunoradiometric assay and correlated with clinical parameters. Data were analyzed by t test and Pearson's method.\nRESULTS: Insulin-like growth factor binding protein-1 was highly expressed on syncytiotrophoblasts, cytotrophoblasts, and decidual cells but not on placental fibroblasts. Immunostaining was greater at the maternal-fetal interface in severe preeclamptic patients compared with controls. Circulating insulin-like growth factor binding protein-1 levels in subjects with severe preeclampsia were 428.3 +/- 85.9 ng/ml compared with 76.6 +/- 11.8 in controls (p = 0.0007). Circulating insulin-like growth factor-I levels were 80.9 +/- 17.2 ng/ml compared with 179.4 +/- 28.2 ng/ml in controls (p = 0.0001). In contrast, insulin-like growth factor-II levels were not significantly different in the two groups. In subjects with severe preeclampsia insulin-like growth factor binding protein-1 levels correlated with diastolic blood pressure (r = 0.498, p 0.049) and aspartate transcarbamylase (0.621, p = 0.010).\nCONCLUSIONS: The abundance of insulin-like growth factor binding protein-1 at the maternal-fetal interface in severely preeclamptic pregnancies suggests that the binding protein may participate in the pathogenesis of the shallow placental invasion observed in this disorder. Low circulating insulin-like growth factor-I and elevated insulin-like growth factor binding protein-1 levels may contribute to restricted placental and therefore fetal growth."}
Preeclampsia-compare
{"project":"Preeclampsia-compare","denotations":[{"id":"PD-Preeclampsia-B_T1","span":{"begin":231,"end":243},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T2","span":{"begin":257,"end":269},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T3","span":{"begin":601,"end":613},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T4","span":{"begin":745,"end":757},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T5","span":{"begin":957,"end":969},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T6","span":{"begin":1246,"end":1258},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T7","span":{"begin":1681,"end":1693},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T8","span":{"begin":1815,"end":1827},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T9","span":{"begin":2168,"end":2180},"obj":"ORPHA:275555"},{"id":"PD-Preeclampsia-B_T10","span":{"begin":2465,"end":2477},"obj":"ORPHA:275555"}],"namespaces":[{"prefix":"ORPHA","uri":"www.orpha.net/consor/cgi-bin/OC_Exp.php?lng=EN\u0026Expert="}],"text":"Insulin-like growth factor binding protein-1 at the maternal-fetal interface and insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1 in the circulation of women with severe preeclampsia.\nOBJECTIVES: Preeclampsia is characterized by maternal hypertension, proteinuria, edema, and shallow placental invasion. Insulin-like growth factor binding protein-1, abundant in maternal decidua, is believed to play a role in limiting trophoblast invasiveness. In this study we addressed the hypothesis that this binding protein is aberrantly expressed in preeclampsia. We also investigated circulating levels of insulin-like growth factor-I and insulin-like growth factor-II in subjects with severe preeclampsia compared with controls.\nSTUDY DESIGN: Insulin-like growth factor binding protein-1 was investigated by immunohistochemistry at the maternal-fetal interface of eight pregnancies complicated by severe preeclampsia and six controls between 21 and 34 weeks of gestation. Cell types were identified with use of cell-specific markers. Circulating levels of insulin-like growth factor binding protein-1, insulin-like growth factor-I, and insulin-like growth factor-II in 16 patients with severe preeclampsia and 29 controls at the same gestational age were determined by an immunoradiometric assay and correlated with clinical parameters. Data were analyzed by t test and Pearson's method.\nRESULTS: Insulin-like growth factor binding protein-1 was highly expressed on syncytiotrophoblasts, cytotrophoblasts, and decidual cells but not on placental fibroblasts. Immunostaining was greater at the maternal-fetal interface in severe preeclamptic patients compared with controls. Circulating insulin-like growth factor binding protein-1 levels in subjects with severe preeclampsia were 428.3 +/- 85.9 ng/ml compared with 76.6 +/- 11.8 in controls (p = 0.0007). Circulating insulin-like growth factor-I levels were 80.9 +/- 17.2 ng/ml compared with 179.4 +/- 28.2 ng/ml in controls (p = 0.0001). In contrast, insulin-like growth factor-II levels were not significantly different in the two groups. In subjects with severe preeclampsia insulin-like growth factor binding protein-1 levels correlated with diastolic blood pressure (r = 0.498, p 0.049) and aspartate transcarbamylase (0.621, p = 0.010).\nCONCLUSIONS: The abundance of insulin-like growth factor binding protein-1 at the maternal-fetal interface in severely preeclamptic pregnancies suggests that the binding protein may participate in the pathogenesis of the shallow placental invasion observed in this disorder. Low circulating insulin-like growth factor-I and elevated insulin-like growth factor binding protein-1 levels may contribute to restricted placental and therefore fetal growth."}
UBERON-AE
{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":432,"end":439},"obj":"http://purl.obolibrary.org/obo/UBERON_0002450"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":480,"end":491},"obj":"http://purl.obolibrary.org/obo/UBERON_0000088"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1519,"end":1539},"obj":"http://purl.obolibrary.org/obo/UBERON_0000371"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1541,"end":1557},"obj":"http://purl.obolibrary.org/obo/UBERON_0000319"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":2259,"end":2264},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"Insulin-like growth factor binding protein-1 at the maternal-fetal interface and insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1 in the circulation of women with severe preeclampsia.\nOBJECTIVES: Preeclampsia is characterized by maternal hypertension, proteinuria, edema, and shallow placental invasion. Insulin-like growth factor binding protein-1, abundant in maternal decidua, is believed to play a role in limiting trophoblast invasiveness. In this study we addressed the hypothesis that this binding protein is aberrantly expressed in preeclampsia. We also investigated circulating levels of insulin-like growth factor-I and insulin-like growth factor-II in subjects with severe preeclampsia compared with controls.\nSTUDY DESIGN: Insulin-like growth factor binding protein-1 was investigated by immunohistochemistry at the maternal-fetal interface of eight pregnancies complicated by severe preeclampsia and six controls between 21 and 34 weeks of gestation. Cell types were identified with use of cell-specific markers. Circulating levels of insulin-like growth factor binding protein-1, insulin-like growth factor-I, and insulin-like growth factor-II in 16 patients with severe preeclampsia and 29 controls at the same gestational age were determined by an immunoradiometric assay and correlated with clinical parameters. Data were analyzed by t test and Pearson's method.\nRESULTS: Insulin-like growth factor binding protein-1 was highly expressed on syncytiotrophoblasts, cytotrophoblasts, and decidual cells but not on placental fibroblasts. Immunostaining was greater at the maternal-fetal interface in severe preeclamptic patients compared with controls. Circulating insulin-like growth factor binding protein-1 levels in subjects with severe preeclampsia were 428.3 +/- 85.9 ng/ml compared with 76.6 +/- 11.8 in controls (p = 0.0007). Circulating insulin-like growth factor-I levels were 80.9 +/- 17.2 ng/ml compared with 179.4 +/- 28.2 ng/ml in controls (p = 0.0001). In contrast, insulin-like growth factor-II levels were not significantly different in the two groups. In subjects with severe preeclampsia insulin-like growth factor binding protein-1 levels correlated with diastolic blood pressure (r = 0.498, p 0.049) and aspartate transcarbamylase (0.621, p = 0.010).\nCONCLUSIONS: The abundance of insulin-like growth factor binding protein-1 at the maternal-fetal interface in severely preeclamptic pregnancies suggests that the binding protein may participate in the pathogenesis of the shallow placental invasion observed in this disorder. Low circulating insulin-like growth factor-I and elevated insulin-like growth factor binding protein-1 levels may contribute to restricted placental and therefore fetal growth."}
preeclampsia_genes
{"project":"preeclampsia_genes","denotations":[{"id":"PD-PreeclampsiaGenes-B_T1","span":{"begin":0,"end":7},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T2","span":{"begin":81,"end":88},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T3","span":{"begin":111,"end":118},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T4","span":{"begin":146,"end":153},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T5","span":{"begin":365,"end":372},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T6","span":{"begin":658,"end":665},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T7","span":{"begin":691,"end":698},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T8","span":{"begin":796,"end":803},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T9","span":{"begin":1109,"end":1116},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T10","span":{"begin":1155,"end":1162},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T11","span":{"begin":1189,"end":1196},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T12","span":{"begin":1450,"end":1457},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T13","span":{"begin":1739,"end":1746},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T14","span":{"begin":1920,"end":1927},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T15","span":{"begin":2055,"end":2062},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T16","span":{"begin":2181,"end":2188},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T17","span":{"begin":2376,"end":2383},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T18","span":{"begin":2637,"end":2644},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T19","span":{"begin":2679,"end":2686},"obj":"HGNC:INS"},{"id":"PD-PreeclampsiaGenes-B_T20","span":{"begin":0,"end":26},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T21","span":{"begin":81,"end":107},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T22","span":{"begin":111,"end":137},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T23","span":{"begin":146,"end":172},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T24","span":{"begin":365,"end":391},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T25","span":{"begin":658,"end":684},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T26","span":{"begin":691,"end":717},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T27","span":{"begin":796,"end":822},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T28","span":{"begin":1109,"end":1135},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T29","span":{"begin":1155,"end":1181},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T30","span":{"begin":1189,"end":1215},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T31","span":{"begin":1450,"end":1476},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T32","span":{"begin":1739,"end":1765},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T33","span":{"begin":1920,"end":1946},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T34","span":{"begin":2055,"end":2081},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T35","span":{"begin":2181,"end":2207},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T36","span":{"begin":2376,"end":2402},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T37","span":{"begin":2637,"end":2663},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T38","span":{"begin":2679,"end":2705},"obj":"HGNC:IGF2"},{"id":"PD-PreeclampsiaGenes-B_T39","span":{"begin":0,"end":26},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T40","span":{"begin":81,"end":107},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T41","span":{"begin":111,"end":137},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T42","span":{"begin":146,"end":172},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T43","span":{"begin":365,"end":391},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T44","span":{"begin":658,"end":684},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T45","span":{"begin":691,"end":717},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T46","span":{"begin":796,"end":822},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T47","span":{"begin":1109,"end":1135},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T48","span":{"begin":1155,"end":1181},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T49","span":{"begin":1189,"end":1215},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T50","span":{"begin":1450,"end":1476},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T51","span":{"begin":1739,"end":1765},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T52","span":{"begin":1920,"end":1946},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T53","span":{"begin":2055,"end":2081},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T54","span":{"begin":2181,"end":2207},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T55","span":{"begin":2376,"end":2402},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T56","span":{"begin":2637,"end":2663},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T57","span":{"begin":2679,"end":2705},"obj":"HGNC:IGF1"},{"id":"PD-PreeclampsiaGenes-B_T58","span":{"begin":0,"end":42},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T59","span":{"begin":146,"end":188},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T60","span":{"begin":365,"end":407},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T61","span":{"begin":796,"end":838},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T62","span":{"begin":1109,"end":1151},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T63","span":{"begin":1450,"end":1492},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T64","span":{"begin":1739,"end":1781},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T65","span":{"begin":2181,"end":2223},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T66","span":{"begin":2376,"end":2418},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T67","span":{"begin":2679,"end":2721},"obj":"HGNC:IGFBP7"},{"id":"PD-PreeclampsiaGenes-B_T68","span":{"begin":0,"end":42},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T69","span":{"begin":146,"end":188},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T70","span":{"begin":365,"end":407},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T71","span":{"begin":796,"end":838},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T72","span":{"begin":1109,"end":1151},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T73","span":{"begin":1450,"end":1492},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T74","span":{"begin":1739,"end":1781},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T75","span":{"begin":2181,"end":2223},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T76","span":{"begin":2376,"end":2418},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T77","span":{"begin":2679,"end":2721},"obj":"HGNC:IGFBP3"},{"id":"PD-PreeclampsiaGenes-B_T78","span":{"begin":0,"end":42},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T79","span":{"begin":146,"end":188},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T80","span":{"begin":365,"end":407},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T81","span":{"begin":796,"end":838},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T82","span":{"begin":1109,"end":1151},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T83","span":{"begin":1450,"end":1492},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T84","span":{"begin":1739,"end":1781},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T85","span":{"begin":2181,"end":2223},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T86","span":{"begin":2376,"end":2418},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T87","span":{"begin":2679,"end":2721},"obj":"HGNC:IGFBP2"},{"id":"PD-PreeclampsiaGenes-B_T88","span":{"begin":0,"end":42},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T89","span":{"begin":146,"end":188},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T90","span":{"begin":365,"end":407},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T91","span":{"begin":796,"end":838},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T92","span":{"begin":1109,"end":1151},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T93","span":{"begin":1450,"end":1492},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T94","span":{"begin":1739,"end":1781},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T95","span":{"begin":2181,"end":2223},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T96","span":{"begin":2376,"end":2418},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T97","span":{"begin":2679,"end":2721},"obj":"HGNC:IGFBP4"},{"id":"PD-PreeclampsiaGenes-B_T98","span":{"begin":0,"end":42},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T99","span":{"begin":146,"end":188},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T100","span":{"begin":365,"end":407},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T101","span":{"begin":796,"end":838},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T102","span":{"begin":1109,"end":1151},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T103","span":{"begin":1450,"end":1492},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T104","span":{"begin":1739,"end":1781},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T105","span":{"begin":2181,"end":2223},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T106","span":{"begin":2376,"end":2418},"obj":"HGNC:IGFBP5"},{"id":"PD-PreeclampsiaGenes-B_T107","span":{"begin":2679,"end":2721},"obj":"HGNC:IGFBP5"}],"text":"Insulin-like growth factor binding protein-1 at the maternal-fetal interface and insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1 in the circulation of women with severe preeclampsia.\nOBJECTIVES: Preeclampsia is characterized by maternal hypertension, proteinuria, edema, and shallow placental invasion. Insulin-like growth factor binding protein-1, abundant in maternal decidua, is believed to play a role in limiting trophoblast invasiveness. In this study we addressed the hypothesis that this binding protein is aberrantly expressed in preeclampsia. We also investigated circulating levels of insulin-like growth factor-I and insulin-like growth factor-II in subjects with severe preeclampsia compared with controls.\nSTUDY DESIGN: Insulin-like growth factor binding protein-1 was investigated by immunohistochemistry at the maternal-fetal interface of eight pregnancies complicated by severe preeclampsia and six controls between 21 and 34 weeks of gestation. Cell types were identified with use of cell-specific markers. Circulating levels of insulin-like growth factor binding protein-1, insulin-like growth factor-I, and insulin-like growth factor-II in 16 patients with severe preeclampsia and 29 controls at the same gestational age were determined by an immunoradiometric assay and correlated with clinical parameters. Data were analyzed by t test and Pearson's method.\nRESULTS: Insulin-like growth factor binding protein-1 was highly expressed on syncytiotrophoblasts, cytotrophoblasts, and decidual cells but not on placental fibroblasts. Immunostaining was greater at the maternal-fetal interface in severe preeclamptic patients compared with controls. Circulating insulin-like growth factor binding protein-1 levels in subjects with severe preeclampsia were 428.3 +/- 85.9 ng/ml compared with 76.6 +/- 11.8 in controls (p = 0.0007). Circulating insulin-like growth factor-I levels were 80.9 +/- 17.2 ng/ml compared with 179.4 +/- 28.2 ng/ml in controls (p = 0.0001). In contrast, insulin-like growth factor-II levels were not significantly different in the two groups. In subjects with severe preeclampsia insulin-like growth factor binding protein-1 levels correlated with diastolic blood pressure (r = 0.498, p 0.049) and aspartate transcarbamylase (0.621, p = 0.010).\nCONCLUSIONS: The abundance of insulin-like growth factor binding protein-1 at the maternal-fetal interface in severely preeclamptic pregnancies suggests that the binding protein may participate in the pathogenesis of the shallow placental invasion observed in this disorder. Low circulating insulin-like growth factor-I and elevated insulin-like growth factor binding protein-1 levels may contribute to restricted placental and therefore fetal growth."}
performance-test
{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":2259,"end":2264},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":345,"end":354},"obj":"http://purl.obolibrary.org/obo/UBERON_0001987"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":1589,"end":1598},"obj":"http://purl.obolibrary.org/obo/UBERON_0001987"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":2575,"end":2584},"obj":"http://purl.obolibrary.org/obo/UBERON_0001987"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":2760,"end":2769},"obj":"http://purl.obolibrary.org/obo/UBERON_0001987"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":480,"end":491},"obj":"http://purl.obolibrary.org/obo/UBERON_0000088"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":432,"end":439},"obj":"http://purl.obolibrary.org/obo/UBERON_0002450"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":1519,"end":1539},"obj":"http://purl.obolibrary.org/obo/UBERON_0000371"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1541,"end":1557},"obj":"http://purl.obolibrary.org/obo/UBERON_0000319"}],"text":"Insulin-like growth factor binding protein-1 at the maternal-fetal interface and insulin-like growth factor-I, insulin-like growth factor-II, and insulin-like growth factor binding protein-1 in the circulation of women with severe preeclampsia.\nOBJECTIVES: Preeclampsia is characterized by maternal hypertension, proteinuria, edema, and shallow placental invasion. Insulin-like growth factor binding protein-1, abundant in maternal decidua, is believed to play a role in limiting trophoblast invasiveness. In this study we addressed the hypothesis that this binding protein is aberrantly expressed in preeclampsia. We also investigated circulating levels of insulin-like growth factor-I and insulin-like growth factor-II in subjects with severe preeclampsia compared with controls.\nSTUDY DESIGN: Insulin-like growth factor binding protein-1 was investigated by immunohistochemistry at the maternal-fetal interface of eight pregnancies complicated by severe preeclampsia and six controls between 21 and 34 weeks of gestation. Cell types were identified with use of cell-specific markers. Circulating levels of insulin-like growth factor binding protein-1, insulin-like growth factor-I, and insulin-like growth factor-II in 16 patients with severe preeclampsia and 29 controls at the same gestational age were determined by an immunoradiometric assay and correlated with clinical parameters. Data were analyzed by t test and Pearson's method.\nRESULTS: Insulin-like growth factor binding protein-1 was highly expressed on syncytiotrophoblasts, cytotrophoblasts, and decidual cells but not on placental fibroblasts. Immunostaining was greater at the maternal-fetal interface in severe preeclamptic patients compared with controls. Circulating insulin-like growth factor binding protein-1 levels in subjects with severe preeclampsia were 428.3 +/- 85.9 ng/ml compared with 76.6 +/- 11.8 in controls (p = 0.0007). Circulating insulin-like growth factor-I levels were 80.9 +/- 17.2 ng/ml compared with 179.4 +/- 28.2 ng/ml in controls (p = 0.0001). In contrast, insulin-like growth factor-II levels were not significantly different in the two groups. In subjects with severe preeclampsia insulin-like growth factor binding protein-1 levels correlated with diastolic blood pressure (r = 0.498, p 0.049) and aspartate transcarbamylase (0.621, p = 0.010).\nCONCLUSIONS: The abundance of insulin-like growth factor binding protein-1 at the maternal-fetal interface in severely preeclamptic pregnancies suggests that the binding protein may participate in the pathogenesis of the shallow placental invasion observed in this disorder. Low circulating insulin-like growth factor-I and elevated insulin-like growth factor binding protein-1 levels may contribute to restricted placental and therefore fetal growth."}