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1 oglobin [Hb] H disease) or lethal (Hb Bart's hydrops fetalis).
2 unexplained cases of severe neonatal NSHA or hydrops fetalis.
4 efects in the formation of the heart lead to hydrops fetalis and are likely the cause of embryonic le
5 /-) embryos die at midgestation with extreme hydrops fetalis and cardiovascular abnormalities, includ
7 m of GLD with a high incidence of non-immune hydrops fetalis and childhood onset of facial and four l
8 that is characterized by multiple anomalies, hydrops fetalis, and death within the first 8 wk of life
9 linical and electrophysiologic predictors of hydrops fetalis; and 3) to describe the medium-term foll
11 a complicated by ventricular dysfunction and hydrops fetalis carries a significant risk of morbidity
15 of diverse pathological outcomes, including hydrops fetalis, fetal myocarditis, meningoencephalitis,
16 lly relevant thalassemias (hemoglobin Bart's hydrops fetalis, hemoglobin H disease, beta-thalassemia
17 s in 8 group A versus 0 group B (P < 0.007), hydrops fetalis in 8 group A versus 0 group B (P < 0.007
19 re the correction of alpha-thalassemia major hydrops fetalis in transgene-free iPS cells using zinc f
21 etuses with incessant tachycardia and either hydrops fetalis (n=24) or ventricular dysfunction (n=2)
24 h homozygous mutants develop polyhydramnios, hydrops fetalis, spina bifida occulta and osteochondrody
26 nd neonatal deaths associated with nonimmune hydrops fetalis uncovered 2 heterozygous missense varian
27 oss of beta-glucuronidase activity can cause hydrops fetalis, with in utero or postnatal death of the
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