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1 al vascular leakage would be associated with brain swelling.
2  role for EPCR-binding CIDRalpha1 domains in brain swelling.
3 eability, T2-weighted MRI revealed edema and brain swelling.
4 -learning models of malarial retinopathy and brain swelling.
5                Rather, it tended to increase brain swelling.
6  and were killed at day-3 for measurement of brain swelling.
7 h accompanying fluid egress, may cause fatal brain swelling.
8 ich could in turn lead to hypoxic damage and brain swelling.
9 lay an important role in the pathogenesis of brain swelling.
10 -inositol did not prevent the development of brain swelling.
11 n, based on the multifactorial mechanisms of brain swelling.
12 mia in patients with acute traumatic diffuse brain swelling.
13 ater influx, which led to cellular edema and brain swelling.
14 increases their volume, which contributes to brain swelling.
15 e for: (1) dead-space ECS microdomains after brain swelling; (2) slowed molecular diffusion in the EC
16 as raised intracranial pressure secondary to brain swelling (82%).
17 nimals also had increased infarct volume and brain swelling, accompanied by increased apoptotic neuro
18          Stepwise measures to prevent lethal brain swelling after traumatic brain injury need experim
19        The mechanisms linking sequestration, brain swelling and death remain poorly understood.
20 m the vasculature into the parenchyma causes brain swelling and edema.
21 cific deletion of SUR1-TRPM4 or NCX1 reduced brain swelling and improved neurological function in mic
22 ave shown that intravenous glyburide reduces brain swelling and improves survival.
23     Mild hypothermia reduced ammonia-induced brain swelling and increased intracranial pressure.
24 ed during a traffic accident and had diffuse brain swelling and intraocular hemorrhage.
25                        LPS induced cytotoxic brain swelling and maintained anatomical integrity of th
26 tamine, a tTG inhibitor, reduces ICH-induced brain swelling and neurological deficits.
27 e surgical decompression may prove to impact brain swelling and outcomes.
28 e, or cranial bleeding to control subsequent brain swelling and prevent death.
29 e compared with adult TBI, including diffuse brain swelling and so-called second impact syndrome.
30  and hemorrhages), followed by inflammation, brain swelling, and brain herniation.
31 ured brain, developing techniques that limit brain swelling, and customizing brain perfusion.
32        The mechanisms linking sequestration, brain swelling, and death remain poorly understood.
33                    Associations between LFL, brain swelling, and death suggest that the rapid accumul
34 e suffering blood-brain barrier dysfunction, brain swelling, and hemorrhaging accompanied by accumula
35 n of granulocytes and activated macrophages, brain swelling, and infarct size.
36 l-Tyr-Val-Ala-Asp-chloromethylketone reduced brain swelling, and N-benzyloxycarbonyl-Asp-Glu-Val-Asp-
37 s neuroprotective effects on infarct volume, brain swelling, and neurological score compared to the v
38 nce imaging (MRI) study in humans identified brain swelling as the most prominent predictor of fatal
39 ilitates the osmotically driven pathological brain swelling associated with stroke and traumatic brai
40 nonperfusion were not associated with severe brain swelling but with neurological deficits, suggestin
41 on-perfusion were not associated with severe brain swelling, but with neurological deficits, suggesti
42 rats, p=0.0016) and a moderate inhibition of brain swelling by FGF-13.
43                                              Brain swelling causes morbidity and mortality in various
44   Cystamine treatment attenuated ICH-induced brain swelling (day 3: 14.4+/-3.2 vs. 21.4+/-4.0% in veh
45 (RP-1127; glibenclamide) would safely reduce brain swelling, decrease the need for decompressive cran
46 howed blood-brain barrier integrity, reduced brain swelling, decreased function of activated effector
47        We found an age-dependent decrease in brain swelling during acute cerebral malaria, and brain
48 sma ammonia levels continued to increase and brain swelling eventually developed.
49 re still incompletely understood, but severe brain swelling identified by magnetic resonance imaging
50 ses, hypodense oedema in 6/31 (19.6%) cases, brain swelling in 1/31 (3.2%) cases, and no parenchymal
51 orrhagic transformation, infarct volume, and brain swelling in a rat transient focal ischemia with hy
52 ue to vascular congestion, may contribute to brain swelling in cerebral malaria.
53 eet could be targeted to reduce postischemic brain swelling in stroke patients.
54 9, and we used it to investigate the role of brain swelling in the pathogenesis of fatal cerebral mal
55  candidate pathology contributing to diffuse brain swelling in this age group.
56 on would have the opposite effect (increased brain swelling) in vasogenic (noncellular) edema because
57 ng brain volume in the survivors who had had brain swelling initially.
58                                              Brain swelling is a major predictor of mortality in pedi
59                                              Brain swelling is associated with death from cerebral ma
60  cerebral malaria, but it is unclear whether brain swelling is caused by cerebral edema or vascular c
61                                              Brain swelling is linked to the influx of water into per
62 ction in cerebral oxygenation as a result of brain swelling, ischemia, and elevated intracranial pres
63 r therapy of some types of refractory edema, brain swelling, neuroinflammation, glaucoma, epilepsy, c
64 ied, 21 of whom (84%) had evidence of severe brain swelling on MRI at admission.
65  None of the four patients died and none had brain swelling or focal changes according to brain MRI.
66       Aminoguanidine did not affect ischemic brain swelling (p > 0.05).
67 8.58, 95% CI = 2.56-29.08, respectively) and brain swelling (P < .05).
68 3.78 and 8.58, 2.56-29.08 respectively), and brain swelling (p<0.05).
69 of acute surgical intracranial hematomas and brain swelling, pupillary abnormalities, early hypotensi
70 id barrier breakdown showed correlation with brain swelling (r(2): 0.55, P < .01) and RMCBS score (r(
71 ar hemoglobin concentrations correlated with brain swelling score determined by MRI (r = 0.37, P = 0.
72 lobin concentration and its correlation with brain swelling suggested that excess blood volume, poten
73 osmotic stress and ameliorates post-ischemic brain swelling through a simultaneous inhibition of NKCC
74                  Recent findings have linked brain swelling to death in cerebral malaria (CM).
75               Here, we provide evidence that brain swelling triggers Ca(2+) signaling in astrocytes a
76                                              Brain swelling was also markedly reduced compared with v
77                    At autopsy, when present, brain swelling was more often diffuse and bilateral amon
78              In contrast, evidence of severe brain swelling was seen on MRI in 39 of 143 survivors (2
79          The reduction in infarct volume and brain swelling were associated with improvement of clini
80 hen perfusion-fixed, and infarct volumes and brain swelling were determined.
81 ronal levels, but subcortical infarction and brain swelling were not affected.
82  was evaluated daily, and histopathology and brain swelling were quantified at 3 days.
83  had an accelerated progression of cytotoxic brain swelling, with ICP elevation of 20 +/- 2 mmHg at 1