| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-120 |
Sentence |
denotes |
Endothelin receptor antagonism prevents hypoxia-induced mortality and morbidity in a mouse model of sickle-cell disease. |
| T2 |
121-259 |
Sentence |
denotes |
Patients with sickle-cell disease (SCD) suffer from tissue damage and life-threatening complications caused by vasoocclusive crisis (VOC). |
| T3 |
260-442 |
Sentence |
denotes |
Endothelin receptors (ETRs) are mediators of one of the most potent vasoconstrictor pathways in mammals, but the relationship between vasoconstriction and VOC is not well understood. |
| T4 |
443-575 |
Sentence |
denotes |
We report here that pharmacological inhibition of ETRs prevented hypoxia-induced acute VOC and organ damage in a mouse model of SCD. |
| T5 |
576-746 |
Sentence |
denotes |
An in vivo ultrasonographic study of renal hemodynamics showed a substantial increase in endothelin-mediated vascular resistance during hypoxia/reoxygenation-induced VOC. |
| T6 |
747-885 |
Sentence |
denotes |
This increase was reversed by administration of the dual ETR antagonist (ETRA) bosentan, which had pleiotropic beneficial effects in vivo. |
| T7 |
886-1077 |
Sentence |
denotes |
It prevented renal and pulmonary microvascular congestion, systemic inflammation, dense rbc formation, and infiltration of activated neutrophils into tissues with subsequent nitrative stress. |
| T8 |
1078-1166 |
Sentence |
denotes |
Bosentan also prevented death of sickle-cell mice exposed to a severe hypoxic challenge. |
| T9 |
1167-1325 |
Sentence |
denotes |
These findings in mice suggest that ETRA could be a potential new therapy for SCD, as it may prevent acute VOC and limit organ damage in sickle-cell patients. |
| T1 |
0-120 |
Sentence |
denotes |
Endothelin receptor antagonism prevents hypoxia-induced mortality and morbidity in a mouse model of sickle-cell disease. |
| T2 |
121-259 |
Sentence |
denotes |
Patients with sickle-cell disease (SCD) suffer from tissue damage and life-threatening complications caused by vasoocclusive crisis (VOC). |
| T3 |
260-442 |
Sentence |
denotes |
Endothelin receptors (ETRs) are mediators of one of the most potent vasoconstrictor pathways in mammals, but the relationship between vasoconstriction and VOC is not well understood. |
| T4 |
443-575 |
Sentence |
denotes |
We report here that pharmacological inhibition of ETRs prevented hypoxia-induced acute VOC and organ damage in a mouse model of SCD. |
| T5 |
576-746 |
Sentence |
denotes |
An in vivo ultrasonographic study of renal hemodynamics showed a substantial increase in endothelin-mediated vascular resistance during hypoxia/reoxygenation-induced VOC. |
| T6 |
747-885 |
Sentence |
denotes |
This increase was reversed by administration of the dual ETR antagonist (ETRA) bosentan, which had pleiotropic beneficial effects in vivo. |
| T7 |
886-1077 |
Sentence |
denotes |
It prevented renal and pulmonary microvascular congestion, systemic inflammation, dense rbc formation, and infiltration of activated neutrophils into tissues with subsequent nitrative stress. |
| T8 |
1078-1166 |
Sentence |
denotes |
Bosentan also prevented death of sickle-cell mice exposed to a severe hypoxic challenge. |
| T9 |
1167-1325 |
Sentence |
denotes |
These findings in mice suggest that ETRA could be a potential new therapy for SCD, as it may prevent acute VOC and limit organ damage in sickle-cell patients. |