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1 wks gestation, and ventilated for >4 hrs or asphyxiated.
2 respiratory pattern was determined in three asphyxiated, awake preterm lambs after cesarean section
7 hether neuronal autophagy in the thalamus of asphyxiated human newborns or P7 rats is enhanced and re
8 ce, likely reflecting decreased formation of asphyxiating mucus plugs; and 3) in Scnn1b-Tg mice, neut
9 baby with respiratory distress syndrome, an asphyxiated neonate, and a baby with severe sepsis of a
10 scular dysfunction occurs in the majority of asphyxiated neonates and has been suggested to be a majo
13 ocardial and cardiac mitochondrial injury in asphyxiated newborn piglets following resuscitation.
14 ed inflations (SIs) improves the recovery of asphyxiated newborn piglets in comparison with coordinat
15 culation with better hemodynamic recovery in asphyxiated newborn piglets in comparison with standard
21 as a trend toward a larger mortality rate in asphyxiated rats treated with induced hyperthermia at 24
23 e were fewer normal-appearing CA1 neurons in asphyxiated rats with hyperthermia induced at 24 hrs vs.
24 he number of normal-appearing CA1 neurons in asphyxiated rats with hyperthermia induced at 48 hrs did
26 ed hyperthermia at 24 hrs (9 of 21 died) vs. asphyxiated rats without induced hyperthermia (3 of 21)
29 Short-rib polydactyly syndromes (SRPS) and Asphyxiating thoracic dystrophy (ATD) or Jeune Syndrome
30 ed to human skeletal ciliopathies, including asphyxiating thoracic dystrophy (ATD; also known as Jeun
35 t IFT80 mutations underlie a subset of Jeune asphyxiating thoracic dystrophy cases, establishing the
36 we identify TCTEX1D2 mutations causing Jeune asphyxiating thoracic dystrophy with partially penetrant
40 d at 48 hrs did not differ from that in rats asphyxiated without induced hyperthermia (59 +/- 21 vs.
41 at 48 hrs did not differ from those in rats asphyxiated without induced hyperthermia (6.4 +/- 3.0 vs
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