ライフサイエンスコーパス: ischemic lesion

1 r and extravascular fibrin deposition in the ischemic lesion.

2 aneurysm treatment, clinical vasospasm, and ischemic lesion.

3 ine whether induction of apoptosis alters an ischemic lesion.

4 referentially localized to nuclei within the ischemic lesion.

5 sults in a 50% decrease in the volume of the ischemic lesion.

6 functional outcome and reduced spread of the ischemic lesion.

7 function after cell transfer into an area of ischemic lesion.

8 ed increased migration of neutrophils to the ischemic lesion.

9 BBB leakage, hemorrhagic transformation, and ischemic lesions.

10 s associated with either overt CVA or silent ischemic lesions.

11 s might contribute to secondary expansion of ischemic lesions.

12 on their effect on neurologic recovery from ischemic lesions.

13 rtic arch type were predictive for bilateral ischemic lesions.

14 ing of the brain revealed no evidence of new ischemic lesions.

15 P = .028) and chronic (P = .009) subcortical ischemic lesions.

16 mined improvement of symptoms and/or digital ischemic lesions.

17 P(C) in neuronal soma within the penumbra of ischemic lesions.

18 rNIF treatment delays the maturation of the ischemic lesion (2 days), or reduces cerebral infarct vo

19 t reduction in the incidence of new cerebral ischemic lesions (45.2% vs. 87.1%, p = 0.001).

20 tent and respiratory function or the size of ischemic lesion after HLI, despite reducing blood flow.

21 subacute stroke patients with a subcortical ischemic lesion and 12 age-matched control subjects were

22 Newly born immature neurons migrate into the ischemic lesion and differentiate into mature parvalbumi

23 ociated with a decrease in the volume of the ischemic lesion and improved neurological outcome follow

24 eactivity was mainly present adjacent to the ischemic lesion and in the non-ischemic cortex.

25 endpoints were the number and volume of new ischemic lesions and major adverse cardiovascular and ce

26 ed imaging (DWI) is sensitive to small acute ischemic lesions and might help diagnose transient ische

27 oid angiopathy (CAA) is also associated with ischemic lesions and vascular cognitive impairment.

28 ted with significant increase in the size of ischemic lesion, approximately 2-fold increase in the nu

29 erred, as opposed to those at high risk when ischemic lesions are left untreated, thus confirming res

30 requently due to cerebral ischemia, and such ischemic lesions are more frequently located at the leve

31 The clinical implications of ischemic lesions are not yet fully understood.

32 tude and delayed the appearance of the total ischemic lesion area and largely prevented TUNEL stainin

33 ea in the 40-min group, but had no effect on ischemic lesion area in the 60-min group.

34 The ischemic lesion as defined by EI exhibited ischemic cell

35 -1beta immunoreactive cells increased in the ischemic lesion as early as 15 min and peaked at 1 h to

36 Cerebral microvessels expressed tie 1 in the ischemic lesion as early as 2 h after MCA occlusion.

37 Finally, both the volume of the ischemic lesion as well as inducible nitric oxide syntha

38 y endpoint was the incidence of new cerebral ischemic lesions assessed by diffusion-weighted magnetic

39 MR imaging confirmed the presence of ischemic lesions associated with mild MPO-mediated enhan

40 ase activity remains in the periphery of the ischemic lesion at 24 and 48 h, where it can contribute

41 ssels containing tie 1 mRNA decreased in the ischemic lesion at 8 h after MCA occlusion.

42 d ameboid-like microglia were present in the ischemic lesion between 2 to 10 h of reperfusion.

43 , has been reported to be protective against ischemic lesions, but effects of OPN on vascular functio

44 ist BSF-208075 (ambrisentan) could reduce an ischemic lesion by modulation of leukocyte-endothelium i

45 Detection of coronary ischemic lesions by fractional flow reserve (FFR) has be

46 e III were significantly associated with new ischemic lesions; calcified lesions were negatively asso

47 Ischemic lesion determination by ADC was more accurate i

48 amined these parameters after focal cortical ischemic lesions distal from the SVZ in adult rats.

49 n of the glutaminase in central areas of the ischemic lesion does not involve significant proteolytic

50 ted in substantial temporal averaging of the ischemic lesion during the early phase, but was clearly

51 to identify factors predictive for cerebral ischemic lesions during embolic protected CAS.

52 n abnormality (smaller) may be predictive of ischemic lesion enlargement.

53 After 1 week of sildenafil treatment, the ischemic lesion exhibited two significantly different re

54 ic tolerance and decreases the volume of the ischemic lesion following MCAO in wild-type and tPA-defi

55 n of neuroserpin decreases the volume of the ischemic lesion following MCAO.

56 n the map-ISODATA calculated at 6 weeks, the ischemic lesion for each animal was divided into two spe

57 Compared with nonischemic lesions, ischemic lesions had smaller MLD (1.3 vs. 1.7 mm, p = 0.

58 anges in brain areas remote from the initial ischemic lesion, i.e., diaschisis.

59 terizing the spatiotemporal evolution of the ischemic lesion in a permanent middle artery occlusion (

60 diffusion and perfusion MRI reveals an acute ischemic lesion in about 60% of TIA patients.

61 (DWI) is frequently used for identifying the ischemic lesion in focal cerebral ischemia, the understa

62 lly investigate the long-term response of an ischemic lesion in rat brain to the administration of si

63 ly formed capillaries at the boundary of the ischemic lesion in rats (n=12) treated with hMSCs compar

64 In the subcortex, E2 treatment prevented the ischemic lesion in the 30-min group, reduced lesion area

65 localized to the outer boundary zone of the ischemic lesion in the cortex and striatum, and in most

66 oid cells were present throughout the entire ischemic lesion in the infarct zone from 70-166 h of rep

67 was performed for evaluation of new cerebral ischemic lesions in 728 (86.9%) of 837 consecutive patie

68 e agent citicoline on the growth of cerebral ischemic lesions in a double-blind placebo-controlled st

69 factors, and temporal profile of concurrent ischemic lesions in patients with acute primary intracer

70 erformance for noninvasive identification of ischemic lesions in stable patients with suspected or kn

71 of magnetic resonance imaging (MRI)-measured ischemic lesions in the brain.

72 atients having moderate-to-severe unilateral ischemic lesions in the frontal motor cortical areas.

73 tivity were observed in the ischemic and non-ischemic lesions in the mouse brain.

74 The clinical relevance of these acute ischemic lesions is not fully understood, but ablation-r

75 Conclusion Subcortical white matter ischemic lesion locations and severity of ultrastructura

76 n 1 year after transplantation; small vessel ischemic lesions, malignancy, or non-Aspergillus fungal

77 a, and upregulation of the PAI-1 gene in the ischemic lesion may foster fibrin deposition through sup

78 icroangiopathic basis for the association of ischemic lesions, microhemorrhages, and strokes in human

79 ion, discrimination, and reclassification of ischemic lesions of intermediate stenosis severity.

80 aphy angiography (CTA) for identification of ischemic lesions of intermediate stenosis severity.

81 e of transient ischemic attack/stroke or new ischemic lesions on cerebral diffusion-weighted magnetic

82 revious observations suggested that multiple ischemic lesions on diffusion-weighted imaging (DWI) are

83 At baseline, ischemic lesions on diffusion-weighted imaging (DWI) wer

84 determine the significance of perioperative ischemic lesions on functional outcome.

85 ity of 0.89 in detecting significant hypoxic-ischemic lesions on postnatal day 21.

86 tissue resulted in up to 58.4% reduction in ischemic lesion over controls at the site of Adv/SLPI ex

87 A time-dependent enlargement of an ischemic lesion over the course of 24 h was observed and

88 acute lesions, P = .088; chronic subcortical ischemic lesions, P = .085).

89 nt study, we combined IN-1 treatment with an ischemic lesion (permanent middle cerebral artery occlus

90 bral edema is a sequela of large hemispheric ischemic lesions, presumably as an extension of the init

91 Mild ischemic lesions, primarily in the form of PVL, occur in

92 We investigated the effect of small cortical ischemic lesions, produced by intracerebral injection of

93 Ischemic lesion recurrence was defined as any new lesion

94 ntally lesioned animals revealed a bilateral ischemic lesion restricted to the hippocampus.

95 These findings indicate that small ischemic lesions restricted to adult cerebral cortex can

96 ndent, and provided exclusive information on ischemic lesion reversibility.

97 ice, this cotreatment significantly improved ischemic lesion size and neurological outcome.

98 cts of estrogen and testosterone on cerebral ischemic lesion size induced by middle cerebral artery (

99 Ischemic lesion size was measured using computed tomogra

100 tween plasma testosterone concentrations and ischemic lesion size was observed.

101 The total ischemic lesion (sum of areas with lacking and intermedi

102 were localized to the inner boundary of the ischemic lesion surrounding the infarct zone at 46 of re

103 Thermal-ischemic lesions (TCL) of sensorimotor cortex, which ind

104 ET-1 and ET-3 produced large ischemic lesions that were restricted to those cortical

105 ble to determine the location of the hypoxic-ischemic lesions, their extent and evolution.

106 Of the six patients with focal ischemic lesions, three had foci of contraction band nec

107 vascular risk factors and the association of ischemic lesions to distinctive behavioral symptoms.

108 Neurological evaluation and ischemic lesion (TTC stain) were assessed at 24 hours of

109 a glucose was also inversely correlated with ischemic lesion volume (beta = -0.006; P < .04).

110 From baseline to week 12, ischemic lesion volume [all values mean (SE)] expanded b

111 <0.05) reduced BBB leakage, brain edema, and ischemic lesion volume compared with rats treated with t

112 The primary assessment was progression of ischemic lesion volume from baseline to 12 weeks as meas

113 lated and induced SDs increase significantly ischemic lesion volume in vivo, supporting the hypothesi

114 /kg s.c.) of haloperidol reduces by half the ischemic lesion volume induced by a transient middle cer

115 number of studies showing enlargement of the ischemic lesion volume ranged from 12 (43%) of 28 at or

116 Neurological deficits, gross hemorrhage and ischemic lesion volume were measured.

117 ective in reducing neurological deficits and ischemic lesion volume without increasing hemorrhagic tr

118 emia, and computed tomography measurement of ischemic lesion volume.

119 study blood brain barrier (BBB) leakage and ischemic lesion volume.

120 Ischemic lesion volumes assessed over 15-minute interval

121 at substantial enlargement of human cerebral ischemic lesion volumes can occur beyond the first 6, 12

122 d with rats treated with tPA alone, although ischemic lesion volumes were the same in both groups bef

123 Ischemic lesion was evaluated by 2,3,5-triphenyltetrazol

124 No ischemic lesion was localized on echography; a poor corr

125 e of [(11)C]PK11195 vs [(18)F]DPA-714 in the ischemic lesion was similar (core/contralateral ratio: 2

126 Neurological evaluation and ischemic lesion were assessed 24 h after reperfusion.

127 diagnostic odds ratio (DOR) for detection of ischemic lesions were 0.89 [95%confidence interval (CI),

128 New ischemic lesions were found in 32.8% of patients.

129 Compared with control subjects, ischemic lesions were significantly more likely to be in

130 to 0.84] cm(3), p = 0.0001) of new cerebral ischemic lesions were significantly reduced by proximal

131 ng or intussusception at the boundary of the ischemic lesion, which closely corresponded to elevated

132 atin and rht-PA blocked the expansion of the ischemic lesion, which improved neurological function co

133 sal ganglia, and spinal cord diffuse clastic ischemic lesions with calcifications; glomeruloid vascul

134 variables was performed correlating sites of ischemic lesions with PSH.

135 rebleeding, amount of blood on CT scan, and ischemic lesion within 72 hours from subarachnoid hemorr

136 these multiple lesions was the recurrence of ischemic lesions within a week after a clinically sympto

137 formance correlated with presence of chronic ischemic lesions within the interhemispheric tracts and