ライフサイエンスコーパス: cerebral infarct

1 e recurrence of an infarct (stroke or silent cerebral infarct).

2 ad strokes, and 7 had new or enlarged silent cerebral infarcts).

3 d a stroke, and 5 had new or enlarged silent cerebral infarcts).

4 injection to the putamen ipsilateral to the cerebral infarct.

5 n of the spinal cord (SpC) motoneurons after cerebral infarct.

6 ined as a stroke or a new or enlarged silent cerebral infarct.

7 sters and was consistently associated with a cerebral infarct.

8 d even better neuroprotection after an acute cerebral infarct.

9 dementia, including small vessel disease and cerebral infarcts.

10 sclerosis but not neocortical Lewy bodies or cerebral infarcts.

11 rome and secondary necrotizing pneumonia and cerebral infarcts.

12 lized increase in amyloid burden adjacent to cerebral infarcts.

13 d second overt strokes and 11 had new silent cerebral infarcts.

14 Fifty-three (35.8%) subjects had cerebral infarcts.

15 with high dose CsA had significantly reduced cerebral infarcts.

16 re rise, partially because of multiple small cerebral infarcts.

17 Reduction of cerebral infarct (25%) was only noted in intracerebral t

18 the primary CNS complications include silent cerebral infarcts (39% by 18 years), headache (both acut

19 Cerebral infarct accounted for 77 percent of all strokes

20 ed with wild-type littermates, the volume of cerebral infarcts after occlusion of the middle cerebral

21 r every year, and hence to estimate rates of cerebral infarct and cerebral haemorrhage from the total

22 The closely related trends in cerebral infarct and coronary heart disease suggest comm

23 rate, we aimed to estimate secular trends in cerebral infarct and haemorrhage throughout the 20th cen

24 nd its protein to bring about a reduction in cerebral infarct and promote recovery.

25 The volume of cerebral infarct and swelling were determined using an i

26 Gross and microscopic cerebral infarcts and hippocampal sclerosis were also id

27 aluated for the presence and distribution of cerebral infarcts and WMHs.

28 ous adverse events, one in the PRBC-LyoPlas (cerebral infarct) and one in the 0.9% sodium chloride gr

29 Overt stroke, clinically "silent" cerebral infarct, and neurocognitive impairment are freq

30 lament tau-positive (PHFtau) tangle density, cerebral infarcts, and LB pathology.

31 elation of Alzheimer disease (AD) pathology, cerebral infarcts, and Lewy body (LB) pathology to cogni

32 itute on Aging-Reagan criteria), macroscopic cerebral infarcts, and neocortical Lewy body (LB) diseas

33 pal sclerosis, chronic gross and microscopic cerebral infarcts, and transactive response DNA binding

34 graphics, major cardiovascular risk factors, cerebral infarcts, and white matter lesions.

35 lthough it is now accepted that asymptomatic cerebral infarcts are an important cause of dementia in

36 severe type of sickle cell disease), silent cerebral infarcts are found in more than a third of adol

37 Silent cerebral infarcts are the most common neurologic injury

38 S) are at high risk for neurologically overt cerebral infarcts associated with stroke and neurologica

39 blood transfusion therapy experience silent cerebral infarcts at a higher rate than previously recog

40 romote rehabilitation.SIGNIFICANCE STATEMENT Cerebral infarct because of stroke can lead to lasting r

41 ciated with stroke and neurologically silent cerebral infarcts correlated with neuropsychometric defi

42 of improved neurologic function and reduced cerebral infarct, demyelination, P-selectin expression,

43 Every HI-treated rat with a cerebral infarct developed spontaneous epileptiform disc

44 intact sensorimotor cortex contralateral to cerebral infarcts following bFGF treatment.

45 ncrease in brain lactate, but did not affect cerebral infarct growth.

46 ural brain injury, such as stroke and silent cerebral infarcts; however, emerging advanced neuroimagi

47 y reduced the incidence of the recurrence of cerebral infarct in children with sickle cell anemia.

48 iography (MRI and MRA) at exit showed no new cerebral infarcts in either treatment group, but worsene

49 r secondary prevention of strokes and silent cerebral infarcts includes regular blood transfusion the

50 out the 20th century, whereas mortality from cerebral infarct increased to a peak in the 1970s and th

51 ch as glutamate, and neuronal damage after a cerebral infarct is thought to be mediated by excitotoxi

52 Cerebrovascular pathologies, specifically cerebral infarcts, is linked with greater scam susceptib

53 Trends in estimated cerebral infarct mortality closely matched those for cor

54 In the Silent Cerebral Infarct Multi-Center Clinical Trial, we sought

55 episodes, including seizures (n = 2), silent cerebral infarcts (n = 3), cerebral hemorrhage (n = 2),

56 farcts, we tested the hypothesis that silent cerebral infarcts occur among children with SCD being tr

57 Progressive cerebral infarcts occurred in 45% (18 of 40 children) wh

58 on the performance of algorithms segmenting cerebral infarcts on Magnetic Resonance Imaging (MRI).

59 istory of stroke and with one or more silent cerebral infarcts on magnetic resonance imaging and a ne

60 not limited to, moyamoya that often precedes cerebral infarcts or hemorrhage, proliferative retinopat

61 mentia, Braak score, neuroleptic medication, cerebral infarcts, or Lewy bodies.

62 associated with an increased risk of silent cerebral infarct (SCI) and stroke in diabetic patients y

63 Silent cerebral infarct (SCI) is the most common form of neurol

64 trokes, but a high cumulative risk of silent cerebral infarcts (SCI) remained, suggesting that TCD sc

65 We hypothesized that the silent cerebral infarcts (SCI), which affect up to 40% of child

66 ry (ICA) stenosis as risk factors for silent cerebral infarcts (SCIs) in children with sickle cell an

67 Changing to Hydroxyurea [SWiTCH]) or silent cerebral infarcts (Silent Infarct Transfusion [SIT] Tria

68 Hyperbaric oxygen (HBO) reduces cerebral infarct size after middle cerebral artery occlu

69 choline and TMAO generation, directly impact cerebral infarct size and adverse outcomes following str

70 blood flow (CBF) by 40% to 50%, and reduced cerebral infarct size by 32%.

71 tivates complement, increases myocardial and cerebral infarct size in rats subjected to coronary or c

72 ntation of adiponectin significantly reduced cerebral infarct size in WT and APN-KO mice.

73 even days later, severity of hemiparesis and cerebral infarct size were examined.

74 bitors augments cerebral blood flow, reduces cerebral infarct size, and improves neurological functio

75 nt to transmit TMA/TMAO production, heighten cerebral infarct size, and lead to functional impairment

76 Cerebral infarct size, neurological function and mortali

77 tion of MCA patency and consequently reduced cerebral infarct sizes (P < .005).

78 cerebral artery occlusion, we observed that cerebral infarct sizes and fibrin(ogen) deposition in ch

79 Cerebral infarct (stroke) often causes devastating and i

80 on techniques may better detect edema within cerebral infarcts than conventional non-contrast CT (NCC

81 low by laser doppler, P < 0.05), and smaller cerebral infarcts than vehicle-treated controls (70% red

82 ent mice exhibited approximately 50% smaller cerebral infarcts than wild-type mice.

83 We calculated the ratio of cerebral infarct to cerebral haemorrhage from all availa

84 The ratio of cerebral infarct to cerebral haemorrhage increased fourf

85 hese data were used to estimate the ratio of cerebral infarct to haemorrhage for every year, and henc

86 rparts, and this was accompanied by a larger cerebral infarct vol and worse neurological score.

87 +/-14 mm3 vs. 34+/-37 mm3, p<0.02) and total cerebral infarct volume (46+/-28 mm3 vs. 81+/-60 mm3, p<

88 ally, scFv/TM was more effective at reducing cerebral infarct volume and alleviated neurological defi

89 y, quantitative trait locus (QTL) mapping of cerebral infarct volume and collateral vessel number ide

90 oth acute and chronic, significantly reduces cerebral infarct volume and edema, as well as myocardial

91 PNU-120596 significantly reduced cerebral infarct volume and improved neurological functi

92 emia and reperfusion more robustly decreased cerebral infarct volume and improved survival and neurol

93 of the ischemic lesion (2 days), or reduces cerebral infarct volume at 7 days after middle cerebral

94 intravenously after ischemic stroke reduced cerebral infarct volume by 62% (interleukin-10 mRNA) or

95 There was a significant difference in cerebral infarct volume in the OFNE-perfused animals com

96 erately reduced in Il21r-deficient mice, and cerebral infarct volume increased 2.3-fold, suggesting t

97 es over 50% of the variation in postischemic cerebral infarct volume observed between inbred strains.

98 Cerebral infarct volume was analyzed 24 hours after repe

99 Brain edema and cerebral infarct volume were significantly reduced follo

100 rain, decreased mean blood pressure, reduced cerebral infarct volume, and improved neurological defic

101 We measured the rNIF dose-response on cerebral infarct volume, the therapeutic time window, th

102 MCAo 24 h later showed significantly smaller cerebral infarct volumes (150.34+/-30.91 mm(3)) and bett

103 meric mice lacking CD73 in tissue had larger cerebral infarct volumes and more tissue leukosequestrat

104 Measurements of cerebral infarct volumes and neurological behavioral tes

105 e normal, cd39(-/-) mice exhibited increased cerebral infarct volumes and reduced postischemic perfus

106 ccluding suture, GPI 562 was shown to reduce cerebral infarct volumes by 70%.

107 age, n=6) demonstrated significantly smaller cerebral infarct volumes compared with wild-type mice.

108 t aggregation in response to ADP and reduced cerebral infarct volumes in mice following transient mid

109 itiation, of rMCAo was effective in reducing cerebral infarct volumes measured 72 h later.

110 562 exhibited a dose-dependent reduction of cerebral infarct volumes measured by triphenyltetrazoliu

111 ater did not show significant differences in cerebral infarct volumes or clinical neurological outcom

112 -) mice exhibited significantly larger (49%) cerebral infarct volumes than wild-type mice, with conco

113 ta(-/-) mice displayed significantly reduced cerebral infarct volumes, developed significantly less n

114 ophil and platelet accumulation, and reduced cerebral infarct volumes.

115 okes and the clinical significance of silent cerebral infarcts, we tested the hypothesis that silent

116 Cerebral infarcts were associated with highest overall n

117 n days 13 and 15 after aneurysm rupture, new cerebral infarcts were noted in 6 of 19 patients (32%) i