ライフサイエンスコーパス: cerebral infarction

1 atens oxygen delivery increasing the risk of cerebral infarction.

2 ormed within the first 7 days after onset of cerebral infarction.

3 s with nontraumatic intracranial bleeding or cerebral infarction.

4 with nontraumatic intracranial hemorrhage or cerebral infarction.

5 re potentially progressive and can result in cerebral infarction.

6 d (DW) magnetic resonance (MR) imaging after cerebral infarction.

7 res according to the presence or size of new cerebral infarction.

8 ition due to its utility in the diagnosis of cerebral infarction.

9 dies report a 7% to 14% prevalence of silent cerebral infarction.

10 (SCA), resulting in overt stroke and silent cerebral infarction.

11 creased the odds of dementia, independent of cerebral infarction.

12 ts of decompressive craniectomy in malignant cerebral infarction.

13 ed to summary measures of AD pathology or to cerebral infarction.

14 rexpressing transgenic mice are resistant to cerebral infarction.

15 nd Hess grade, age, history of diabetes, and cerebral infarction.

16 that bind to CD36 and are elevated in acute cerebral infarction.

17 t oxLDL may influence the pathophysiology of cerebral infarction.

18 l cord injury and bladder overactivity after cerebral infarction.

19 ia (SCA) carry a 200-fold increased risk for cerebral infarction.

20 s the only independent predictor for delayed cerebral infarctions.

21 g vessel diameter is insufficient to prevent cerebral infarctions.

22 n multiple brain regions and the presence of cerebral infarctions.

23 c heart disease (HR 0.80 [95%CI 0.72-0.87]), cerebral infarction (0.62 [0.52-0.73]), heart failure (0

24 oses included subarachnoid hemorrhage (60%), cerebral infarction (23%), intracerebral hemorrhage (11%

25 he HSP70tg mice were still protected against cerebral infarction 24 hours after permanent focal ische

26 rst-ever strokes occurred, of which 225 were cerebral infarctions, 42 were intracerebral hemorrhages,

27 Cerebral infarction after 6 hours of ischemia, as evalua

28 me had a significant effect on the degree of cerebral infarction after experimental stroke in adult f

29 hondrial function and causes exacerbation of cerebral infarction after ischemia.

30 dent on new protein synthesis, contribute to cerebral infarction after transient focal ischemia in th

31 The excess risk of cerebral infarction among CNS tumor survivors increases

32 Since both cerebral infarction and coronary heart disease are cause

33 The risks of both cerebral infarction and intracerebral hemorrhage are inc

34 ned pathogenic role in delayed maturation of cerebral infarction and NMDA receptor-targeted neuroprot

35 subarachnoid haemorrhage, and often leads to cerebral infarction and poor neurological outcome.

36 riage increasing the rates of myocardial and cerebral infarction and renovascular hypertension by 9%

37 thesized that removal of CB would exacerbate cerebral infarction and stroke-related behavioral defici

38 There were 10 cerebral infarctions and 1 intracerebral hematoma in the

39 Seventeen cerebral infarctions and 14 intracerebral hemorrhages oc

40 egnancy-related strokes), and there were 175 cerebral infarctions and 48 intracerebral hemorrhages th

41 cologically) had MR imaging documentation of cerebral infarction, and all had consistent, acquired ne

42 ry hypertension (PAH), stroke, myocardial or cerebral infarction, and cancer.

43 is associated with cerebrovascular disease, cerebral infarction, and cognitive dysfunction.

44 ese results reveal that arterial thrombosis, cerebral infarction, and hemostasis in mice efficiently

45 /-) mice display decreased hepatocyte death, cerebral infarction, and renal injury relative to wild-t

46 h subsequent risks of myocardial infarction, cerebral infarction, and renovascular hypertension, cons

47 9) times the rates of myocardial infarction, cerebral infarction, and renovascular hypertension, resp

48 ncrease later risk of myocardial infarction, cerebral infarction, and renovascular hypertension.

49 regnancy for incident myocardial infarction, cerebral infarction, and renovascular hypertension.

50 nance imagining (MRI)-documented evidence of cerebral infarction, and the remaining 31 patients had n

51 entified 27 98 myocardial infarctions, 40 53 cerebral infarctions, and 1269 instances of renovascular

52 neurological deficit, cognitive impairment, cerebral infarctions, and angiographic large-vessel invo

53 ntation, less frequently had MRI evidence of cerebral infarctions, and less frequently needed therapy

54 Animal models of cerebral infarction are crucial to understanding the mec

55 The volume of cerebral infarction, as well as the associated neurologi

56 ocomotor activity in stroke rats and reduced cerebral infarction at 2 d after MCAo.

57 liposomes significantly (P < 0.01) decreased cerebral infarction (by 62%) compared to the equivalent

58 at the SOD1 enzyme does not appear to affect cerebral infarction, cerebral edema nor the mitochondria

59 al closure of patent foramen ovale (PFO) for cerebral infarction (CI) or transient ischemic attack (T

60 , GPx-3((-/-)) mice had significantly larger cerebral infarctions compared with wild-type mice and pl

61 t of clinical stroke and silent radiographic cerebral infarction complicating open surgical aortic va

62 fter mild, but not severe, ischemic insults, cerebral infarction develops slowly and may be treatable

63 t-Hess grade, aneurysm size, rebleeding, and cerebral infarction due to vasospasm.

64 tegies is valuable in reducing perioperative cerebral infarctions during CEA.

65 ransferase, or cytochalasin D showed smaller cerebral infarctions following MCA occlusion.

66 OS-deficient; eNOS(-/-)) mice develop larger cerebral infarctions following middle cerebral artery (M

67 ion of total homocysteine after nondisabling cerebral infarction had no effect on vascular outcomes d

68 ent cardiovascular (ischaemic heart disease, cerebral infarction, heart failure, peripheral vascular

69 included brain death in 358 patients (7.9%), cerebral infarction in 161 patients (3.6%), seizures in

70 induced carotid artery thrombosis as well as cerebral infarction in a postischemic stroke model.

71 f timing and duration of mild hypothermia on cerebral infarction in a rat model of reversible focal i

72 h normalized ischemic leukosequestration and cerebral infarction in CD39-deficient mice.

73 of the EP2 receptor significantly increased cerebral infarction in cerebral cortex and subcortical s

74 ding to decreased BBB disruption and reduced cerebral infarction in mice after transient focal cerebr

75 ur results showed that the subacute phase of cerebral infarction in patients was characterized by the

76 e shown that hyperbaric oxygen (HBO) reduced cerebral infarction in rat middle cerebral artery occlus

77 re both well tolerated and effective against cerebral infarction in rodent models via a dual alloster

78 y a central rather than a subsidiary role in cerebral infarction in the gyrencephalic brain.

79 llow-up MRIs of the brain; only 1 had silent cerebral infarction in the same location as the previous

80 oxicity and apoptosis in the pathogenesis of cerebral infarction induced by focal ischemic insults.

81 ing transient ischemic attack (n = 2), small cerebral infarction (n = 2), and cranial nerve palsy (n

82 racts (n = 4), deep vein thrombosis (n = 3), cerebral infarction (n = 2), headache (n = 2), and myelo

83 arction [n = 1], pulmonary embolism [n = 2], cerebral infarction [n = 1], ruptured thoracic [n = 1],

84 Nonhemorrhagic cerebral infarction occurred in 86% of participants with

85 embolic adverse events, mainly myocardial or cerebral infarction, occurred in 7 percent of rFVIIa-tre

86 mild hypothermia has been shown to attenuate cerebral infarction occurring after transient focal isch

87 Cerebral infarction occurs in one quarter of all childre

88 The increased SI of subacute cerebral infarction on DW images reflects not only a sho

89 The overall SI of cerebral infarction on DW images was significantly highe

90 Cerebral infarction on magnetic resonance imaging (MRI)

91 Patients who had cerebral infarction or cerebral haemorrhage and were hyp

92 The incidence of stroke (cerebral infarction or intracranial hemorrhage) was comp

93 unilateral brain damage (focal lesion) from cerebral infarction or intraparenchymal haemorrhage, usi

94 iagnostic performance for predicting delayed cerebral infarctions or poor Glasgow Outcome Scale score

95 were not associated with risk of any stroke, cerebral infarction, or intracerebral hemorrhage.

96 aorta or a bronchial artery, or vasospastic cerebral infarction, or the cause was unestablished.

97 erebral vasculopathy was associated with new cerebral infarction (overt or silent; relative risk = 12

98 potential pharmacological interventions for cerebral infarction prevention.

99 e month of inset was analysed separately for cerebral infarction, primary intracerebral haemorrhage,

100 lso protects against occlusive thrombosis or cerebral infarction,providing new insights into both Rho

101 The incidence of cerebral infarction ranges from 70% to 100% in mice with

102 % (P < 0.05) and 34% (P < 0.05) reduction in cerebral infarction, respectively, along with decreased

103 raphic reperfusion (score on Thrombolysis in Cerebral Infarction scale of grade 2-3) during the endov

104 injury in sickle cell anemia (SCA) is silent cerebral infarction (SCI).

105 Silent cerebral infarctions (SCIs) are known to occur in the pr

106 zation defined as a modified Thrombolysis in Cerebral Infarction score of 2b or 3 at the end of all e

107 as a score of 2b or 3 on the Thrombolysis in Cerebral Infarction score.

108 s assessed with angiographic Thrombolysis in Cerebral Infarction scores at the end of the procedure (

109 ration of neutrophils and macrophages at the cerebral infarction site were reduced in pristane-treate

110 ddle cerebral artery (MCA) ligation, reduced cerebral infarction size and enhanced locomotor activity

111 s presenting with hemiparesis resulting from cerebral infarction sparing the primary motor cortex, an

112 Focal cerebral infarction (stroke) due to unilateral occlusion

113 24 [SD]) who were suspected of having acute cerebral infarction (symptom duration, 2.8 days +/- 2.7)

114 better image quality and detection of acute cerebral infarction than does echo-planar MR imaging.

115 nimals revealed similar extent and degree of cerebral infarction, the MSF-treated ischemic animals sh

116 For cerebral infarction, the relative risk during pregnancy,

117 on was assessed by using the Thrombolysis in Cerebral Infarction (TICI) scale.

118 nmasked core laboratory, was thrombolysis in cerebral infarction (TICI) scores of 2 or greater reperf

119 of substantial reperfusion (Thrombolysis in Cerebral Infarction [TICI] 2b-3).

120 Recanalization (defined as Thrombolysis in Cerebral Infarction [TICI] score 2b-3) and collateral st

121 s brain regions within 1-2 hr, and decreased cerebral infarction (up to approximately 40%) in a dose-

122 tery thrombosis, but experienced significant cerebral infarction using a stroke model with middle cer

123 neck tumor survivors were hospitalized for a cerebral infarction (versus 0.06% expected).

124 CNS tumor survivors were hospitalized for a cerebral infarction (versus 0.1% expected), whereas at a

125 ome compared with control mice, with reduced cerebral infarction volumes noted even when the blocking

126 Cerebral infarction volumes were quantitated from histop

127 Cerebral infarction was visualized by TTC staining on da

128 en, tangle density, Lewy bodies, and chronic cerebral infarction were derived.

129 An elevated Cho/Cr ratio and cerebral infarction were independently associated (P = .

130 ty for Thoracic Surgery database, and silent cerebral infarctions were detected in more than half of

131 volvement to varying degrees of retinopathy, cerebral infarction with calcium depositions, nephropath

132 on of neurofibrillary pathologic changes and cerebral infarction with cognition proximate to death.

133 onhemorrhagic, 6 intracranial hemorrhages, 3 cerebral infarctions with hemorrhagic conversion, and 4