ライフサイエンスコーパス: carotid occlusion

1 of brain ischemia and 4 were excluded due to carotid occlusion.

2 peripheral artery disease, and contralateral carotid occlusion.

3 ge test results will do well after permanent carotid occlusion.

4 fered carotid stenting for the prevention of carotid occlusion.

5 ing a cohort of 45 symptomatic patients with carotid occlusion.

6 redicted stroke in patients with symptomatic carotid occlusion.

7 accurately predicts stroke in patients with carotid occlusion.

8 l disease, and 28 (12%) having contralateral carotid occlusion.

9 may be an unusual presentation of impending carotid occlusion.

10 ct injury, and to 12.3 +/- 5.6 mmol/L before carotid occlusion.

11 t (velocity 4 m/sec) injury followed by sham carotid occlusion.

12 ham operated or subjected to 5 min bilateral carotid occlusion.

13 eptides in response to muscle contraction or carotid occlusions.

14 mice were subjected to two vessel (bilateral carotid) occlusion (2VO) or 2VO plus systemic hypotensio

15 teral hemispheric stroke following permanent carotid occlusion after the superficial temporal artery

16 The impact injury alone and bilateral carotid occlusion alone caused minimal neuronal loss in

17 n gerbils were submitted to 30 min bilateral carotid occlusion and 2 h of reperfusion at 37 degreesC

18 One of them underwent permanent carotid occlusion and did not develop any delayed ischem

19 In patients with chronic carotid occlusion and increased OEF, increased CBV may i

20 f normothermic forebrain ischemia (bilateral carotid occlusion and MABP=30 mmHg) and allowed to recov

21 end of the cut tibial nerve, brief repeated carotid occlusions and carotid sinus nerve stimulations

22 prespecified subgroups of age, contralateral carotid occlusion, and baseline surgical risk.

23 ina, previous ipsilateral CEA, contralateral carotid occlusion, and other severe comorbid illnesses.

24 ipsilateral stroke and TIA in patients with carotid occlusion, and to a lesser extent in asymptomati

25 (108.2 +/- 1.4 mm Hg) was unaffected by the carotid occlusions, and was similar among animals and co

26 pact injury followed by 40 mins of bilateral carotid occlusion; and c) 2.5-mm deformation impact (vel

27 sec) injury followed by 40 mins of bilateral carotid occlusion; b) sham impact injury followed by 40

28 Brief carotid occlusions caused a release of irNPYs from the l

29 Only the brief carotid occlusions caused a similar increase in MABP and

30 > or =60% ACS in patients with contralateral carotid occlusion (CCO).

31 A new carotid occlusion during annual monitoring with carotid

32 iewed data from 81 patients with symptomatic carotid occlusion enrolled in a prospective study of hae

33 During global cerebral ischemia induced by carotid occlusion, flow to all regions was reduced by ne

34 Using rats with unilateral carotid occlusion followed by hypoxia at postnatal day 7

35 duces delayed post-ischemic (5 min bilateral carotid occlusion) hippocampal CA1 neuronal degeneration

36 After a single 6-min bilateral carotid occlusion, histological damage was evident in th

37 of developing an infarct following permanent carotid occlusion in the course of brain surgery.

38 Carotid occlusions induced c-Fos-ir expression in the ar

39 We have found that transient carotid occlusion induces a wide variation in histologic

40 The risk of progression to carotid occlusion is well below the risk of carotid sten

41 Preventing carotid occlusion may not be a valid indication for sten

42 n dioxide in air in 107 patients with either carotid occlusion (n = 48) or asymptomatic carotid steno

43 sk patients such as those with contralateral carotid occlusion or bilateral severe stenosis.

44 N attenuated the cardiovascular responses to carotid occlusions, or altered the pattern of release of

45 in the whole group (P: < 0.00001) and in the carotid occlusion (P: = 0.019) and carotid stenosis (P:

46 cle 1 h before (but not 6 h after) bilateral carotid occlusion prevented the ischemia-induced decreas

47 sed in cases with demonstrated contralateral carotid occlusion, prior cerebrovascular accident (CVA),

48 Bilateral carotid occlusion produces extensive neuronal damage in

49 occlusion, 5 minutes of transient bilateral carotid occlusion (purported to cause negligible adenosi

50 These patients with symptomatic carotid occlusion should not be discouraged from air tra

51 The St. Louis Carotid Occlusion Study (STLCOS) demonstrated that incre

52 Records from the Carotid Occlusion Surgery Study (COSS), a randomised tri

53 ese patients underwent permanent therapeutic carotid occlusion; three patients had subsequent infarct

54 nt for both MRP-14 and CD36 failed to reduce carotid occlusion times, indicating that CD36 is require

55 Seventy-seven patients with symptomatic carotid occlusion travelled by aeroplane to a single PET

56 les River Laboratories to 5 min of bilateral carotid occlusion under continuous striatal temperature

57 of cerebral hemodynamics, 110 patients with carotid occlusion underwent (a) positron emission tomogr

58 ly enhanced with antecedent coronary-but not carotid-occlusion versus controls.

59 ereas DNase or FVII knockdown had no effect, carotid occlusion was abrogated with RNase or FXII knock

60 Transient carotid occlusion was elicited with a hydraulic occluder

61 tolerance group, in which a 2-min bilateral carotid occlusion was followed 3 days later by a 6-min i

62 of stroke in patients with symptoms and with carotid occlusion was repeated by substituting a count-b

63 sustained attention that persisted until the carotid occlusion was reversed.

64 Both muscle contractions and carotid occlusions were performed 3, 6 and 12 h after th

65 ines a subgroup of patients with symptomatic carotid occlusion who are at high risk for subsequent st

66 cost-effective in patients with symptomatic carotid occlusion who have increased OEF.

67 In the past two decades unilateral carotid occlusion with 8% hypoxia has been used to study

68 ult rats were exposed to 10 min of bilateral carotid occlusion with simultaneous hypotension.