ライフサイエンスコーパス: brain swelling

1 role for EPCR-binding CIDRalpha1 domains in brain swelling.

2 Rather, it tended to increase brain swelling.

3 and were killed at day-3 for measurement of brain swelling.

4 ich could in turn lead to hypoxic damage and brain swelling.

5 lay an important role in the pathogenesis of brain swelling.

6 eability, T2-weighted MRI revealed edema and brain swelling.

7 -learning models of malarial retinopathy and brain swelling.

8 -inositol did not prevent the development of brain swelling.

9 n, based on the multifactorial mechanisms of brain swelling.

10 mia in patients with acute traumatic diffuse brain swelling.

11 e for: (1) dead-space ECS microdomains after brain swelling; (2) slowed molecular diffusion in the EC

12 as raised intracranial pressure secondary to brain swelling (82%).

13 nimals also had increased infarct volume and brain swelling, accompanied by increased apoptotic neuro

14 Stepwise measures to prevent lethal brain swelling after traumatic brain injury need experim

15 m the vasculature into the parenchyma causes brain swelling and edema.

16 ave shown that intravenous glyburide reduces brain swelling and improves survival.

17 Mild hypothermia reduced ammonia-induced brain swelling and increased intracranial pressure.

18 LPS induced cytotoxic brain swelling and maintained anatomical integrity of th

19 tamine, a tTG inhibitor, reduces ICH-induced brain swelling and neurological deficits.

20 e surgical decompression may prove to impact brain swelling and outcomes.

21 e, or cranial bleeding to control subsequent brain swelling and prevent death.

22 and hemorrhages), followed by inflammation, brain swelling, and brain herniation.

23 ured brain, developing techniques that limit brain swelling, and customizing brain perfusion.

24 e suffering blood-brain barrier dysfunction, brain swelling, and hemorrhaging accompanied by accumula

25 n of granulocytes and activated macrophages, brain swelling, and infarct size.

26 l-Tyr-Val-Ala-Asp-chloromethylketone reduced brain swelling, and N-benzyloxycarbonyl-Asp-Glu-Val-Asp-

27 s neuroprotective effects on infarct volume, brain swelling, and neurological score compared to the v

28 nce imaging (MRI) study in humans identified brain swelling as the most prominent predictor of fatal

29 ilitates the osmotically driven pathological brain swelling associated with stroke and traumatic brai

30 rats, p=0.0016) and a moderate inhibition of brain swelling by FGF-13.

31 Cystamine treatment attenuated ICH-induced brain swelling (day 3: 14.4+/-3.2 vs. 21.4+/-4.0% in veh

32 (RP-1127; glibenclamide) would safely reduce brain swelling, decrease the need for decompressive cran

33 howed blood-brain barrier integrity, reduced brain swelling, decreased function of activated effector

34 sma ammonia levels continued to increase and brain swelling eventually developed.

35 orrhagic transformation, infarct volume, and brain swelling in a rat transient focal ischemia with hy

36 9, and we used it to investigate the role of brain swelling in the pathogenesis of fatal cerebral mal

37 on would have the opposite effect (increased brain swelling) in vasogenic (noncellular) edema because

38 ng brain volume in the survivors who had had brain swelling initially.

39 Brain swelling is a major predictor of mortality in pedi

40 ction in cerebral oxygenation as a result of brain swelling, ischemia, and elevated intracranial pres

41 r therapy of some types of refractory edema, brain swelling, neuroinflammation, glaucoma, epilepsy, c

42 ied, 21 of whom (84%) had evidence of severe brain swelling on MRI at admission.

43 None of the four patients died and none had brain swelling or focal changes according to brain MRI.

44 Aminoguanidine did not affect ischemic brain swelling (p > 0.05).

45 of acute surgical intracranial hematomas and brain swelling, pupillary abnormalities, early hypotensi

46 osmotic stress and ameliorates post-ischemic brain swelling through a simultaneous inhibition of NKCC

47 Recent findings have linked brain swelling to death in cerebral malaria (CM).

48 Here, we provide evidence that brain swelling triggers Ca(2+) signaling in astrocytes a

49 Brain swelling was also markedly reduced compared with v

50 In contrast, evidence of severe brain swelling was seen on MRI in 39 of 143 survivors (2

51 The reduction in infarct volume and brain swelling were associated with improvement of clini

52 hen perfusion-fixed, and infarct volumes and brain swelling were determined.

53 ronal levels, but subcortical infarction and brain swelling were not affected.

54 was evaluated daily, and histopathology and brain swelling were quantified at 3 days.

55 had an accelerated progression of cytotoxic brain swelling, with ICP elevation of 20 +/- 2 mmHg at 1