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1 t neuroprotection occurs before the onset of cerebral hypoxia.
2 mbi affect the vasculature and contribute to cerebral hypoxia.
3 e patterns, including PbtO 2 improvement and cerebral hypoxia.
4 s beneficial in other conditions with global cerebral hypoxia.
5                                              Cerebral hypoxia and ischemia may stimulate neurogenesis
6                                              Cerebral hypoxia and ischemia trigger endogenous protect
7 ted lactate/glucose ratio were observed with cerebral hypoxia and ischemia.
8 mportance lies in the likely exacerbation of cerebral hypoxia and the contribution of such seizure ac
9 dicates ongoing cell injury following severe cerebral hypoxia, and that recovery of oxidative phospho
10 zed rabbits were first subjected to 8 min of cerebral hypoxia by breathing 3% oxygen and then to 8 mi
11 c output, bradycardia further contributes to cerebral hypoxia during CRE.
12                             The mechanism of cerebral hypoxia-induced myoclonic jerks is not known.
13 f memantine for 7 days significantly reduced cerebral hypoxia-induced neurodegeneration in the CA1 of
14                                              Cerebral hypoxia is a major component of immediate and s
15 xpressed in hypoxic brain regions of a mouse cerebral hypoxia-ischaemia (H/I) model.
16 ls of induced hypothermia as treatment after cerebral hypoxia-ischaemia in term newborn infants.
17 xamined whether MIA cooperates with neonatal cerebral hypoxia ischemia to promote ASD-like aberration
18 ic db/db mice suffered less damage following cerebral hypoxia-ischemia (H/I) than male db/db mice.
19 tex displays impaired growth after transient cerebral hypoxia-ischemia (HI) at preterm gestation that
20 hether whole body hypothermia after neonatal cerebral hypoxia-ischemia (HI) could broaden the therape
21                                     Neonatal cerebral hypoxia-ischemia (HI) is the leading cause of d
22 ive was to determine the effects of neonatal cerebral hypoxia-ischemia (HI) on ODP.
23                We have previously shown that cerebral Hypoxia-ischemia (HI) results in activation of
24 cerebrovascular diseases, including neonatal cerebral hypoxia-ischemia (HI).
25 rmal lung function, after induction of acute cerebral hypoxia-ischemia by occlusion of the brachiocep
26                                              Cerebral hypoxia-ischemia caused death of O4+ late OPCs
27                                              Cerebral hypoxia-ischemia causes encephalopathy and neur
28 s study tested the hypotheses that (1) acute cerebral hypoxia-ischemia changes laryngeal adductor, la
29  Our understanding of events associated with cerebral hypoxia-ischemia during cardiopulmonary bypass
30                                    Moreover, cerebral hypoxia-ischemia impaired neurobehavioral perfo
31 with therapeutic hypothermia after transient cerebral hypoxia-ischemia in a piglet model of perinatal
32 nd improved neurological functions following cerebral hypoxia-ischemia in the neonatal rat.
33 campal neurons of neonatal rats subjected to cerebral hypoxia-ischemia in vivo.
34   Bromodeoxyuridine uptake assay showed that cerebral hypoxia-ischemia inhibited proliferation of ste
35 dendrocyte progenitor cells (OPCs) following cerebral hypoxia-ischemia, a previously developed neonat
36                  In various animal models of cerebral hypoxia-ischemia, it is not clear whether neuro
37 ther preterm birth asphyxia or induced acute cerebral hypoxia-ischemia, minute ventilation initially
38 neration by XO as a major cause of damage in cerebral hypoxia-ischemia.
39 Cs and improved neurological functions after cerebral hypoxia-ischemia.
40  intracerebroventricular injection 3 h after cerebral hypoxia-ischemia.
41 n damage in those animals subjected to prior cerebral hypoxia-ischemia.
42 t size in 7-day-old rat pups with an in vivo cerebral hypoxia/ischemia model.
43                                       During cerebral hypoxia or ischaemia, mitochondrial dysfunction
44 bral StO(2) (P = 0.01, d = 0.84), indicating cerebral hypoxia, significantly increased cerebral deoxy
45                                              Cerebral hypoxia was defined as PbtO 2 less than 20 mm H
46                                              Cerebral hypoxia was induced by lowering the FiO2 (0.05-
47 ns such as amyotrophic lateral sclerosis and cerebral hypoxia, which are associated with neuronal GLT
48 ular syncope, with abnormal movements due to cerebral hypoxia, which may be difficult to differentiat