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

5 sters and was consistently associated with a cerebral infarct.

6 d even better neuroprotection after an acute cerebral infarct.

7 sclerosis but not neocortical Lewy bodies or cerebral infarcts.

8 rome and secondary necrotizing pneumonia and cerebral infarcts.

9 lized increase in amyloid burden adjacent to cerebral infarcts.

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

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

12 with high dose CsA had significantly reduced cerebral infarcts.

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

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

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

16 Cerebral infarct accounted for 77 percent of all strokes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 Silent cerebral infarcts are the most common neurologic injury

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Cerebral infarct size, neurological function and mortali

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

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

67 Cerebral infarct (stroke) often causes devastating and i

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

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

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

71 The ratio of cerebral infarct to cerebral haemorrhage increased fourf

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

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

74 +/-14 mm3 vs. 34+/-37 mm3, p<0.02) and total cerebral infarct volume (46+/-28 mm3 vs. 81+/-60 mm3, p<

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

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

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

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

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

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

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

82 Cerebral infarct volume was analyzed 24 hours after repe

83 Brain edema and cerebral infarct volume were significantly reduced follo

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

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

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

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

88 Measurements of cerebral infarct volumes and neurological behavioral tes

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

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

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

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

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

94 562 exhibited a dose-dependent reduction of cerebral infarct volumes measured by triphenyltetrazoliu

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

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

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

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

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

100 Cerebral infarcts were associated with highest overall n