1995
DOI: 10.1016/0002-9378(95)91325-4
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Intrauterine growth restriction in infants of less than thirty-two weeks' gestation: Associated placental pathologic features

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Cited by 298 publications
(180 citation statements)
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“…We examined the distributions of placental vascular findings and constructs in term placentas as a means of determining what might be considered ''normal.'' Often studies of placental vascular pathology compare subgroups of preterm births (16,20,32,33), use high-risk term placentas as the reference group (1), or are conducted in teaching hospitals where patient populations overrepresent high-risk pregnancy conditions, even among term deliveries. Ten of the original 39 findings in our vascular scoring scheme were removed because they showed poor intrarater reliability.…”
Section: !1 þmentioning
confidence: 99%
“…We examined the distributions of placental vascular findings and constructs in term placentas as a means of determining what might be considered ''normal.'' Often studies of placental vascular pathology compare subgroups of preterm births (16,20,32,33), use high-risk term placentas as the reference group (1), or are conducted in teaching hospitals where patient populations overrepresent high-risk pregnancy conditions, even among term deliveries. Ten of the original 39 findings in our vascular scoring scheme were removed because they showed poor intrarater reliability.…”
Section: !1 þmentioning
confidence: 99%
“…Placentas from pregnancies complicated by FGR are smaller and have significantly increased maternal and fetal vascular lesions compared to placentas from normal pregnancies with appropriate for gestational age neonates (AGA) 115,116 . Maternal vascular lesions were detected in about 50% of placentas from pregnancies complicated with FGR at term, compared to only 20% in normal pregnancies, while fetal vascular lesions were observed in 11%…”
Section: Fetal Growth Restrictionmentioning
confidence: 99%
“…the outer cell layer bathed by maternal blood) [9,[14][15][16]. Pathological up-regulation of PAI-1 levels in syncytiotrophoblasts [14,15] is suggested to promote increased intervillous fibrin deposition and placental infarction (villous collapse) noted in pregnancies associated with preeclampsia (PE) [14][15][16][17][18]. A direct role of PAI-1 in TNF-α-mediated inhibition of trophoblast migration and invasion was demonstrated using PAI-1 blocking antibodies in villous explants from first trimester placenta and a trophoblast cell line [19,20].…”
Section: Introductionmentioning
confidence: 99%