| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-50 |
Sentence |
denotes |
Angiogenic balance (sFlt-1/PlGF) and preeclampsia. |
| T1 |
0-50 |
Sentence |
denotes |
Angiogenic balance (sFlt-1/PlGF) and preeclampsia. |
| T2 |
51-177 |
Sentence |
denotes |
Preeclampsia is a hypertensive disorder of pregnancy associated with important maternal and perinatal mortality and morbidity. |
| T2 |
51-177 |
Sentence |
denotes |
Preeclampsia is a hypertensive disorder of pregnancy associated with important maternal and perinatal mortality and morbidity. |
| T3 |
178-369 |
Sentence |
denotes |
Although symptomatic management has improved, there is currently no curative treatment, and only childbirth and delivery of the placenta, usually prematurely, alleviate the mother's symptoms. |
| T3 |
178-369 |
Sentence |
denotes |
Although symptomatic management has improved, there is currently no curative treatment, and only childbirth and delivery of the placenta, usually prematurely, alleviate the mother's symptoms. |
| T4 |
370-454 |
Sentence |
denotes |
Placental insufficiency plays a central role in the pathophysiology of preeclampsia. |
| T4 |
370-454 |
Sentence |
denotes |
Placental insufficiency plays a central role in the pathophysiology of preeclampsia. |
| T5 |
455-565 |
Sentence |
denotes |
Abnormal placentation during the first trimester leads to defective remodeling of the uterine vascularization. |
| T5 |
455-565 |
Sentence |
denotes |
Abnormal placentation during the first trimester leads to defective remodeling of the uterine vascularization. |
| T6 |
566-817 |
Sentence |
denotes |
This results progressively in placental hypoperfusion, which induces trophoblast dysfunction and the release in maternal circulation of trophoblastic factors leading to an excessive inflammatory response, endothelial dysfunction and glomerular damage. |
| T6 |
566-817 |
Sentence |
denotes |
This results progressively in placental hypoperfusion, which induces trophoblast dysfunction and the release in maternal circulation of trophoblastic factors leading to an excessive inflammatory response, endothelial dysfunction and glomerular damage. |
| T7 |
818-1052 |
Sentence |
denotes |
Among these factors, the most important is sFlt-1, which is a soluble form of the VEGF and PlGF receptor. sFlt-1 binds to free VEGF and PlGF in the maternal circulation, thus reducing their bioavailability for their membrane receptor. |
| T7 |
818-1052 |
Sentence |
denotes |
Among these factors, the most important is sFlt-1, which is a soluble form of the VEGF and PlGF receptor. sFlt-1 binds to free VEGF and PlGF in the maternal circulation, thus reducing their bioavailability for their membrane receptor. |
| T8 |
1053-1154 |
Sentence |
denotes |
The result is inhibition of the effects of VEGF and PlGF on maternal endothelial cells and podocytes. |
| T8 |
1053-1154 |
Sentence |
denotes |
The result is inhibition of the effects of VEGF and PlGF on maternal endothelial cells and podocytes. |
| T9 |
1155-1268 |
Sentence |
denotes |
The sFlt-1/PlGF ratio reflects the circulating angiogenic balance and is correlated with severity of the disease. |
| T9 |
1155-1268 |
Sentence |
denotes |
The sFlt-1/PlGF ratio reflects the circulating angiogenic balance and is correlated with severity of the disease. |