ライフサイエンスコーパス: cerebral hypoperfusion

1 induced EEG silence during transient global cerebral hypoperfusion.

2 chieving EEG silence during transient global cerebral hypoperfusion.

3 ative low cardiac output are associated with cerebral hypoperfusion.

4 hat oestradiol augments the PGHS response to cerebral hypoperfusion.

5 ment or otherwise modify the Fos response to cerebral hypoperfusion.

6 us and that it modulates the Fos response to cerebral hypoperfusion.

7 ithout evidence of occlusive vasculopathy or cerebral hypoperfusion.

8 is lost and regained in the setting of acute cerebral hypoperfusion.

9 resulting from intracranial hypertension and cerebral hypoperfusion.

10 oxygen in face of hypocapnia (34% to 53%) or cerebral hypoperfusion (34% to 57%) to compensate for re

11 cells, a rarefaction of brain microvessels, cerebral hypoperfusion, a disrupted blood-brain barrier

12 We hypothesized that estrogen and cerebral hypoperfusion alone would augment Fos abundance

13 Recent data suggest that cerebral hypoperfusion and activation of cerebral ion tr

14 n duration-dependent increase in severity of cerebral hypoperfusion and extension of ischaemic pathol

15 eatment--consistent with possible effects of cerebral hypoperfusion and reperfusion injury.

16 or for dementia since it may lead to chronic cerebral hypoperfusion and stroke.

17 Chronic cerebral hypoperfusion and VaD was induced by bilateral

18 egative neurological consequences of chronic cerebral hypoperfusion and VaD.

19 itive function in an animal model of chronic cerebral hypoperfusion and vascular dementia (VaD).

20 n the present study, we tested the effect of cerebral hypoperfusion and/or estradiol on the expressio

21 anial pressure monitoring alone in detecting cerebral hypoperfusion at the bedside in patients with s

22 demonstrate that CE in DKA is accompanied by cerebral hypoperfusion before treatment and suggest that

23 ts of the posterior cerebral circulation and cerebral hypoperfusion could partially explain the patho

24 ng of intracranial pressure and treatment of cerebral hypoperfusion decrease secondary injury.

25 curacy of intracranial monitoring to predict cerebral hypoperfusion (defined as an oligemic regional

26 In summary, cerebral hypoperfusion either at rest or induced by hypo

27 Our study indicates that a single, mild, cerebral hypoperfusion event produces profound and long

28 mine the independent impact of hypocapnia or cerebral hypoperfusion (following INDO) on cerebral oxyg

29 Cerebral hypoperfusion has previously been associated wi

30 position of alpha-synuclein, (2) OH-mediated cerebral hypoperfusion impairs cognition and (3) the two

31 ell type specific dynamics following chronic cerebral hypoperfusion in mice.

32 question, we developed an oligemic model of cerebral hypoperfusion in the 3xTg-AD mouse model of AD.

33 Although cerebral hypoperfusion in the aged rats was not associat

34 otension (OH) is a common cause of transient cerebral hypoperfusion in the population.

35 ork in this laboratory has demonstrated that cerebral hypoperfusion increases the expression of prost

36 uggested mechanisms for the disorder include cerebral hypoperfusion, inflammation, gene polymorphisms

37 Chronic cerebral hypoperfusion is a major cause of age-related v

38 Cerebral hypoperfusion is among the mechanisms that may

39 Cerebral hypoperfusion is associated with accelerated co

40 Cerebral hypoperfusion is widely implicated in cognitive

41 of the PGHS-2 gene expression in response to cerebral hypoperfusion/ischemia in neurons, we used a ce

42 ucible isoform of this enzyme, is induced by cerebral hypoperfusion/ischemia.

43 ables were significant only in AHF (signs of cerebral hypoperfusion, low serum sodium, chronic obstru

44 the posterior circulation and the associated cerebral hypoperfusion may be a factor in triggering hyp

45 nsible, but recent data instead suggest that cerebral hypoperfusion may be involved and that activati

46 preliminary findings suggest that a relative cerebral hypoperfusion may underlie depression in elderl

47 ted a pilot investigation of whether chronic cerebral hypoperfusion might affect genomic distribution

48 previous studies, demonstrating an effect of cerebral hypoperfusion on the expression of both isoform

49 ar fibrillation, especially with symptoms of cerebral hypoperfusion, should then be considered to be

50 We have previously demonstrated that cerebral hypoperfusion stimulates several physiological

51 Mice that were subjected to prolonged cerebral hypoperfusion stress developed white matter dem

52 implications for pathologies associated with cerebral hypoperfusion such as stroke, dementia and hype

53 All animals acted as controls, and had cerebral hypoperfusion under baseline propofol anesthesi

54 Transient global cerebral hypoperfusion was achieved with bilateral inter

55 perventilatory-induced hypocapnia (and hence cerebral hypoperfusion) was prevented; and (2) that phar

56 Significant increases in the severity of cerebral hypoperfusion were observed after 60 min compar