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1 arbia and hypoxia, which ultimately leads to asphyxia.
2 o i.v. NaCN (20 microg) and transient (10 s) asphyxia.
3 racteristics induced by repeated episodes of asphyxia.
4 seizures-signs commonly attributed to birth asphyxia.
5 beta 1-null mice die at birth from asphyxia.
6 europrotective effect of cooling after birth asphyxia.
7 a and autoheparinization in drowning-related asphyxia.
8 frequently considered to be caused by birth asphyxia.
9 to 45-minute normocapnic hypoxia followed by asphyxia.
10 None of the patients had birth asphyxia.
11 ve related these reactions to signs of birth asphyxia.
12 , 5% CO(2)), and (d) combined resistance and asphyxia.
13 probe was placed into the peritoneum before asphyxia.
14 tion from anaerobic metabolism during severe asphyxia.
15 eeding (Esbilac; 200 cal.kg(-1).day(-1)) and asphyxia (100% N(2) for 50 seconds followed by cold expo
17 isease; 2) an etiology of arrest drowning or asphyxia; 3) higher pH, and 4) bilateral reactive pupils
18 lion, UR 0.717 million-1.216 million), birth asphyxia (9%, 0.814 million, 0.563 million-0.997 million
20 girl who died of anoxic encephalopathy from asphyxia after the accidental ingestion of fresh hemlock
22 improved treatment prospects for babies with asphyxia and altered understanding of the theory of neur
23 ephalography in rats undergoing experimental asphyxia and analyzed cortical release of core neurotran
26 the treatment of term newborns who sustained asphyxia and exhibit acidosis and/or encephalopathy (wea
27 brain, BDNF may be a potential treatment for asphyxia and other forms of acute injury in the perinata
29 icular fibrillation cardiac arrest and birth asphyxia and tissue plasminogen activator for ischemic s
30 s, preterm birth and low birth weight, birth asphyxia, and intracranial hemorrhage of the newborn sig
31 uses of deaths in 2008 were pneumonia, birth asphyxia, and preterm birth complications, each accounti
32 sepsis, necrotizing enterocolitis, perinatal asphyxia, and the immune thrombocytopenias), aid the pra
38 y of brain injury that occurs not just after asphyxia, but also when cerebral perfusion is impaired d
40 ults suggest that inspiratory resistance and asphyxia cause changes in the baroreceptor reflex which
43 of ischemic stroke in cerebral palsy; birth asphyxia, congenital malformations, placental pathology,
45 ty percent of patients with drowning-induced asphyxia developed overt disseminated intravascular coag
46 ia for 72 hours in infants who had perinatal asphyxia did not significantly reduce the combined rate
49 ldren younger than 5 years, apart from birth asphyxia, for which a level-2 intervention is available.
51 The receptor density (Bmax) in the untreated asphyxia group was decreased compared to control animals
52 In contrast, Bmax in the allopurinol treated asphyxia group was similar to control (1.06+/-0.37); and
53 without seizures), and evidence of perinatal asphyxia (group 1); and those without other evidence of
54 atal morbidity arising from birth hypoxia or asphyxia has not changed significantly in recent years d
56 show that moderate hypothermia within 6 h of asphyxia improves survival without cerebral palsy or oth
59 ctivity was decreased from control following asphyxia in both the untreated and treated animals (47.7
61 help determine the prognosis after suspected asphyxia in term infants, including obstetric informatio
64 ere was no effect of allopregnanolone on the asphyxia induced impairment of the input/output (I/O) cu
66 2 hrs postasphyxia from animals subjected to asphyxia-induced cardiac arrest for 7 or 9 mins (n = 8/g
67 ase in long term potentiation at P5, and the asphyxia-induced increase in IP(3)R1 expression in CA1 p
68 ngle dose of this steroid could reduce birth asphyxia-induced losses in hippocampal function at 5 day
69 ur objective was to test the hypothesis that asphyxia induces bleeding by hyperfibrinolytic dissemina
70 chypnea of the newborn, infective pneumonia, asphyxia, intracerebral hemorrhage, seizure, cardiomyopa
72 hemic brain injury in survivors of perinatal asphyxia is a frequently encountered clinical problem fo
79 udden infant death syndrome (n = 544 [44%]), asphyxia (n = 74 [6.0%]), septicemia (n = 61 [4.9%]), an
80 five of neonatal morbidity, comprising birth asphyxia (n=3), septicaemia (n=1), and neonatal convulsi
86 ased to the 60% level, and he had occasional asphyxia over 10 seconds with no thoracic motion after a
89 he first two groups, cardiac arrest followed asphyxia produced by neuromuscular blockade with and wit
92 esults suggest that the hypoxic component of asphyxia reduces baroreceptor-vascular resistance reflex
93 alformations (aRR, 1.61; 95% CI, 1.43-1.81), asphyxia-related complications (aRR, 1.75; 95% CI, 1.26-
94 death, congenital anomalies (APC = -7.87%), asphyxia-related conditions (APC = -9.43), immaturity-re
95 ed with increased risks of preterm delivery, asphyxia-related neonatal complications, and congenital
98 ss index (BMI) in early pregnancy and severe asphyxia-related outcomes in infants delivered at term (
104 5, 1.6), apnea (RR = 5.8, 99% CI: 5.1, 6.5), asphyxia (RR = 8.5, 99% CI: 5.7, 11.3), respiratory dist
105 (term=39 days) and 1h before inducing birth asphyxia, spiny mice dams were injected subcutaneously (
107 d were subjected to formula feeding and cold asphyxia stress or were delivered naturally and were mot
108 ed but increases in formula feeding and cold asphyxia stress, correlating with induced inducible NO s
109 tus more susceptible to the acute hypoxia or asphyxia that can accompany relatively uncomplicated lab
110 After resuscitation of an infant with birth asphyxia, the emphasis has been on supportive therapy; h
111 dicolegal significance attached to perinatal asphyxia, the neuropathological basis of this condition
112 of environmental factors, particularly birth asphyxia, the specific cause of cerebral palsy remains u
114 ed sham rats (all surgical procedures except asphyxia) treated with induced hyperthermia at 24 hrs (n
115 xia-ischaemia in a piglet model of perinatal asphyxia using clinically relevant magnetic resonance sp
116 oxia-ischemia in a piglet model of perinatal asphyxia using magnetic resonance spectroscopy (MRS) bio
117 ceptor responses to hypoxia, hypercapnia and asphyxia were examined in a superfused in vitro rat caro
118 anglia and thalami of infants with perinatal asphyxia were predictive of worse clinical outcomes.
119 s to alter CBF regulation to hypercapnia and asphyxia, which may put the drug exposed newborn at risk
121 bilical cord produced moderate but sustained asphyxia, which resolved after the end of the compressio
123 sts the hypothesis that repeated episodes of asphyxia will lead to alterations in the characteristics
124 (LV) function after cardiac arrest caused by asphyxia with that of cardiac arrest induced by dysrhyth
125 rmia induced at 24 hrs vs. rats subjected to asphyxia without induced hyperthermia (33 +/- 13 vs. 67
126 thology damage scores than rats subjected to asphyxia without induced hyperthermia (9.3 +/- 1.5 vs. 6
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