ライフサイエンスコーパス: asphyxiate

1 wks gestation, and ventilated for >4 hrs or asphyxiated.

2 respiratory pattern was determined in three asphyxiated, awake preterm lambs after cesarean section

3 arate risk-adjusted analysis of drowning and asphyxiated donors was similar to other MOD donors at 30

4 Of the 214 patients who had died, 70 asphyxiated during a laryngeal attack.

5 As a consequence, fillets derived from asphyxiated fish were less stable in terms of oxidative

6 Male Sprague-Dawley rats were asphyxiated for 8 mins and resuscitated.

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

11 Cardiac injury is common in asphyxiated neonates and is associated with matrix metal

12 Asphyxiated neonates often have myocardial depression, w

13 Rationale: Asphyxiated neonates with hypoxic ischemic encephalopath

14 ocardial and cardiac mitochondrial injury in asphyxiated newborn piglets following resuscitation.

15 ed inflations (SIs) improves the recovery of asphyxiated newborn piglets in comparison with coordinat

16 culation with better hemodynamic recovery in asphyxiated newborn piglets in comparison with standard

17 cantly improve cardiovascular performance in asphyxiated newborn piglets.

18 chondrial injury during the resuscitation of asphyxiated newborn piglets.

19 iac function and reduce myocardial injury in asphyxiated newborn piglets.

20 sociated with the risk of adverse outcome in asphyxiated patients with HIE undergoing hypothermia.

21 The lifespan of asphyxiated patients with undiagnosed HAE-C1-INH was on

22 Asphyxiated piglets treated with cyclosporine had lower

23 as a trend toward a larger mortality rate in asphyxiated rats treated with induced hyperthermia at 24

24 Asphyxiated rats with hyperthermia induced at 24 hrs had

25 e were fewer normal-appearing CA1 neurons in asphyxiated rats with hyperthermia induced at 24 hrs vs.

26 he number of normal-appearing CA1 neurons in asphyxiated rats with hyperthermia induced at 48 hrs did

27 Histopathology damage scores in asphyxiated rats with hyperthermia induced at 48 hrs did

28 ed hyperthermia at 24 hrs (9 of 21 died) vs. asphyxiated rats without induced hyperthermia (3 of 21)

29 edicting the individual outcomes of severely asphyxiated term neonates.

30 istent with the diagnosis of Jeune syndrome (Asphyxiating thoracic dysplasia).

31 Short-rib polydactyly syndromes (SRPS) and Asphyxiating thoracic dystrophy (ATD) or Jeune Syndrome

32 ed to human skeletal ciliopathies, including asphyxiating thoracic dystrophy (ATD; also known as Jeun

33 Mutations in IFT80 cause Jeune asphyxiating thoracic dystrophy (JATD) and short rib pol

34 Jeune asphyxiating thoracic dystrophy (JATD) is a skeletal dys

35 Jeune's asphyxiating thoracic dystrophy (JATD) is an autosomal r

36 duals also have the skeletal dysplasia Jeune asphyxiating thoracic dystrophy (JATD).

37 t IFT80 mutations underlie a subset of Jeune asphyxiating thoracic dystrophy cases, establishing the

38 we identify TCTEX1D2 mutations causing Jeune asphyxiating thoracic dystrophy with partially penetrant

39 th the clinical diagnosis of Jeune syndrome (asphyxiating thoracic dystrophy).

40 Jeune asphyxiating thoracic dystrophy, an autosomal recessive

41 solated nephronophthisis and syndromic Jeune asphyxiating thoracic dystrophy.

42 d at 48 hrs did not differ from that in rats asphyxiated without induced hyperthermia (59 +/- 21 vs.

43 at 48 hrs did not differ from those in rats asphyxiated without induced hyperthermia (6.4 +/- 3.0 vs