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1 malities (but not placental insufficiency or intrauterine growth retardation).
2 birth weight OR small for gestational age OR intrauterine growth retardation).
3 xia during early embryogenesis can result in intrauterine growth retardation.
4 or very low birth weight, preterm birth, and intrauterine growth retardation.
5 I: 1.93, 8.21) hazard villages suffered from intrauterine growth retardation.
6 ing and treating human pregnancy failure and intrauterine growth retardation.
7 ernal interface results in pre-eclampsia and intrauterine growth retardation.
8 cerebellar hypoplasia, immunodeficiency, and intrauterine growth retardation.
9 mbryonic lethality, neural tube defects, and intrauterine growth retardation.
10 ow birth weight may be due to the effects of intrauterine growth retardation.
11 ll neonates were healthy with no evidence of intrauterine growth retardation.
12 sed preterm delivery (23% vs. 6%, p = 0.03), intrauterine growth retardation (21% vs. 0%, p < 0.0001)
13 those described in diabetes-exposed embryos: intrauterine growth retardation (31.1%), caudal regressi
14 al duplication for 6q24 and characterized by intrauterine growth retardation and insulin dependence.
15 elopmental disorder characterized by extreme intrauterine growth retardation and multiple organ abnor
18 infrequently, with surviving progeny showing intrauterine growth retardation and reduced fertility.
21 In one group of 42 patients with unexplained intrauterine growth retardation and subsequent short sta
22 lities in glucose tolerance in children with intrauterine growth retardation and Turner syndrome; how
23 ne, but not lighter use, was associated with intrauterine growth retardation, and exposure in late pr
25 d to complications such as preterm delivery, intrauterine growth retardation, and preeclampsia; howev
26 sistent, statistically significant effect on intrauterine growth retardation associated with any of t
27 that mice lacking LBP-1a expression develop intrauterine growth retardation at embryonic day 10.5, c
28 pression in the placenta was associated with intrauterine growth retardation but not with preterm del
29 ormone therapy in a dose-dependent manner in intrauterine growth retardation children; the magnitude
30 ients from 4 kindreds, all of whom displayed intrauterine growth retardation, chronic neutropenia, an
31 us (TNDM) is a rare disease characterized by intrauterine growth retardation, dehydration, and failur
32 a (DC) characterized by bone marrow failure, intrauterine growth retardation, developmental delay, mi
33 y represent a useful therapeutic approach to intrauterine growth retardation due to placental vascula
34 me potential for a slightly elevated risk of intrauterine growth retardation during the second and th
35 utosomal recessive disorder characterized by intrauterine growth retardation, dwarfism, microcephaly
36 was characterized by ID, ASD, microcephaly, intrauterine growth retardation, febrile seizures in inf
39 roducts) was related to an increased risk of intrauterine growth retardation in four regions of a Mar
42 everal epidemiologic studies have shown that intrauterine growth retardation is a risk factor for the
43 petence in adolescence and hypothesized that intrauterine growth retardation is associated with a low
45 (T) from 30 to 90 days of gestation leads to intrauterine growth retardation (IUGR) and increased pre
46 ancy contributes to low birth weight through intrauterine growth retardation (IUGR) and preterm deliv
50 To address this, we developed a model of intrauterine growth retardation (IUGR) in the rat that l
51 elin-1 promoter results in a murine model of intrauterine growth retardation (IUGR), which is rescued
53 nd third trimesters were not associated with intrauterine growth retardation, low birth weight, or pr
56 diabetes, premature rupture of membranes or intrauterine growth retardation or small size for gestat
57 eterm labor (OR = 2.7, 95% CI: 1.2, 5.7) and intrauterine growth retardation (OR = 3.3, 95% CI: 1.2,
58 umans, placental insufficiency can result in intrauterine growth retardation, perinatal death and spo
59 tnk2(-/-) mice exhibited a maternal-specific intrauterine growth retardation phenotype that resulted
60 Approximately 10 percent of infants with intrauterine growth retardation remain small, and the ca
61 e immunization decreased fetal infection and intrauterine growth retardation, shortened maternal vire
62 tinine increase in urinary caffeine, risk of intrauterine growth retardation was essentially unchange
63 ose intolerance and exhibited no significant intrauterine growth retardation, whereas rat IGFBP-1 tra
64 hyrin in a very low birth weight infant with intrauterine growth retardation who did not respond to p
65 mutation minute (Mnt) in the mouse leads to intrauterine growth retardation with paternal transmissi
66 ed genetic background-specific lethality and intrauterine growth retardation, without evidence of a g
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