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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
16 rm birth (28%), severe infections (26%), and asphyxia (23%).
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
19               These results demonstrate that asphyxia activates a brainstorm, which accelerates prema
20  girl who died of anoxic encephalopathy from asphyxia after the accidental ingestion of fresh hemlock
21                                              Asphyxia alone did increase blood pressure (+7.0 +/- 1.1
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
24 th cow's milk-based formula and subjected to asphyxia and cold stress to develop NEC.
25                              The patient had asphyxia and cyanosis confirmed by medical staff when hi
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
28 ntial of brain cooling for epilepsy, stroke, asphyxia and other neurological diseases.
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
33 ia (FiCO2 = 7.5%), hypoxia (FiO2 = 12%), and asphyxia (apnea for 1 min).
34                                Deaths due to asphyxia as well as following acute poisoning with sever
35 Heart Association care in a porcine model of asphyxia-associated VF cardiac arrest.
36                                    Perinatal asphyxia at term remains a significant cause of infant d
37            The combination of resistance and asphyxia both reduced gain and displaced the curve to hi
38 y of brain injury that occurs not just after asphyxia, but also when cerebral perfusion is impaired d
39                                        Birth asphyxia can cause moderate to severe brain injury.
40 ults suggest that inspiratory resistance and asphyxia cause changes in the baroreceptor reflex which
41 rol group) or exposed to 7.5 min of in utero asphyxia, causing acidosis and hypoxia.
42                   During reventilation after asphyxia, CBF increased more in cocaine than in control
43  of ischemic stroke in cerebral palsy; birth asphyxia, congenital malformations, placental pathology,
44                                        Birth asphyxia constitutes a major global public health burden
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
47 3) complications of delivery (uterine atony, asphyxia, emergency Cesarean section).
48                           After 7 minutes of asphyxia, followed by VF, 20 female 3-month-old swine ra
49 ldren younger than 5 years, apart from birth asphyxia, for which a level-2 intervention is available.
50 associated with accidents, cardiac events or asphyxia, generally had normal pH.
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
55  effects in the newborn, including perinatal asphyxia, hypoxia, and hypercapnia.
56 show that moderate hypothermia within 6 h of asphyxia improves survival without cerebral palsy or oth
57 aluated using farmed rainbow trout killed by asphyxia in air or percussion.
58                   Following severe perinatal asphyxia in both humans and rats, thalamic neurons displ
59 ctivity was decreased from control following asphyxia in both the untreated and treated animals (47.7
60                      The role of intrapartum asphyxia in neonatal encephalopathy and seizures in term
61 help determine the prognosis after suspected asphyxia in term infants, including obstetric informatio
62                    Hypercapnia, hypoxia, and asphyxia increased contralateral phrenic burst amplitude
63                                  With severe asphyxia induced by complete cord occlusion for 10 min,
64 ere was no effect of allopregnanolone on the asphyxia induced impairment of the input/output (I/O) cu
65           Rats were then subjected to 20 min asphyxia-induced cardiac arrest followed by 30 min cardi
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
71                                    Perinatal asphyxia, intraventricular hemorrhage and stroke are com
72 hemic brain injury in survivors of perinatal asphyxia is a frequently encountered clinical problem fo
73                 Moderate cooling after birth asphyxia is associated with substantial reductions in de
74                                              Asphyxia is the most common cause of death after avalanc
75                                    Perinatal asphyxia is the most important cause of acute neurologic
76 -six rabbits were submitted to 13 minutes of asphyxia, leading to cardiac arrest.
77 athing disorders with repetitive episodes of asphyxia may adversely affect heart function.
78                                 In a porcine asphyxia model, we characterized the hemodynamic, volume
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
81                All cases of drowning-induced asphyxia (n=49) were compared with other patients with c
82                     Events such as perinatal asphyxia, near drowning, respiratory arrest, and near su
83                    With either preterm birth asphyxia or induced acute cerebral hypoxia-ischemia, min
84 ed before causation is ascribed to perinatal asphyxia or other aetiologies.
85  newborn (OR = 1.10; 95% CI, 1.02-1.19), and asphyxia (OR = 1.34; 95% CI, 1.03-1.75).
86 ased to the 60% level, and he had occasional asphyxia over 10 seconds with no thoracic motion after a
87 cantly correlated with the features of birth asphyxia, particularly a history of seizures.
88 irth-weight, congenital anomalies, perinatal asphyxia, postsurgical, and sepsis categories.
89 he first two groups, cardiac arrest followed asphyxia produced by neuromuscular blockade with and wit
90                With no evidence of trauma or asphyxia, profound accidental hypothermia with cardiac a
91 ned a clinically relevant model of perinatal asphyxia providing intrapartum hypoxia in rats.
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
96 at full term and was partly mediated through asphyxia-related neonatal complications.
97 y in full-term children was mediated through asphyxia-related neonatal morbidity.
98 ss index (BMI) in early pregnancy and severe asphyxia-related outcomes in infants delivered at term (
99                              Risks of severe asphyxia-related outcomes in term infants increase with
100     Sham-operated piglets (n=8) underwent no asphyxia-reoxygenation.
101 s myocardial injury in newborn piglets after asphyxia-reoxygenation.
102                 Preterm birth and term birth asphyxia result in brain injury from inadequate oxygen d
103         Moderate hypothermia after perinatal asphyxia resulted in improved neurocognitive outcomes in
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 (
106                                              Asphyxia stimulates a robust and sustained increase of f
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
113 bjected to 7-min (n = 14) and 9-min (n = 14) asphyxia times.
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
120                                              Asphyxia, which occurs during obstructive sleep apnoeic
121 bilical cord produced moderate but sustained asphyxia, which resolved after the end of the compressio
122                                     In fact, asphyxia, which was the most stressful, induced a higher
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
127 fter the initiation of hypothermia for birth asphyxia would result in further improvement.

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