ライフサイエンスコーパス: cerebral infarction

1 s 1 grade 5 treatment-related adverse event (cerebral infarction).

2 eases (e.g., angina pectoris, heart failure, cerebral infarction).

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

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

5 s with nontraumatic intracranial bleeding or cerebral infarction.

6 with nontraumatic intracranial hemorrhage or cerebral infarction.

7 re potentially progressive and can result in cerebral infarction.

8 atens oxygen delivery increasing the risk of cerebral infarction.

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

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

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

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

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

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

15 ts of decompressive craniectomy in malignant cerebral infarction.

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

17 rexpressing transgenic mice are resistant to cerebral infarction.

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

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

20 the NADPH oxidase catalytic subunit NOX5 in cerebral infarction.

21 t oxLDL may influence the pathophysiology of cerebral infarction.

22 l cord injury and bladder overactivity after cerebral infarction.

23 s the only independent predictor for delayed cerebral infarctions.

24 g vessel diameter is insufficient to prevent cerebral infarctions.

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

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

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

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

29 cessful reperfusion (>=modified Treatment in Cerebral Infarction 2b) was 80.0% (32 of 40).

30 in recanalization (modified Thrombolysis-In-Cerebral-Infarction 2b-3), good clinical outcome (modifi

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

32 Cerebral infarction after 6 hours of ischemia, as evalua

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

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

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

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

37 Since both cerebral infarction and coronary heart disease are cause

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

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

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

41 g during SAH was associated with the risk of cerebral infarction and poor outcome at discharge and fo

42 ia during SAH is associated with the risk of cerebral infarction and poor outcome at discharge and fo

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

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

45 We report the first case of coinciding cerebral infarction and venous sinus thrombosis unveilin

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

47 Seventeen cerebral infarctions and 14 intracerebral hemorrhages oc

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

49 e the incidence of clinically silent embolic cerebral infarctions and associated risk factors followi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Large cerebral infarctions are major predictors of death and s

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

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

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

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

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

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

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

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

73 3 years old, 53.7% men) with acute (<1-week) cerebral infarction due to significant (>50%) stenosis o

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

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

76 NIHSS) score at day 2, expanded Treatment in Cerebral Infarction (eTICI) score, and modified Rankin S

77 predictors of FPE (expanded Thrombolysis in Cerebral Infarction [eTICI] 2c-3) and modified FPE (mFPE

78 giographic end points (Expanded Treatment in Cerebral Infarction [eTICI] score of 2b50 or greater wit

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

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

81 Thrombolysis in cerebral infarction grade 2b and 3 (TICI) was achieved i

82 eperfusion based on modified Thrombolysis in Cerebral Infarction grade 2b or greater (90.9% [8474 of

83 ed as failed (final modified Thrombolysis in Cerebral Infarction grade of 0 or 1) or partial (grade 2

84 A final modified Thrombolysis in Cerebral Infarction grade of 2b or 3 was associated with

85 fusion according to modified Thrombolysis in Cerebral Infarction grade, and sICH.

86 uccessful reperfusion (modified Treatment in Cerebral Infarction >=2b) and 90-day functional independ

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

88 gamma, are associated with increased risk of cerebral infarction, heart attack, and reduced cardiac e

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

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

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

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

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

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

95 We characterized cerebral infarction in children with tuberculous meningi

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

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

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

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

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

101 axis also participated in the progression of cerebral infarction in the mouse model of ischemic injur

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

103 Progression of WMLs and cerebral infarctions in FD is mainly related to age, sex

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

105 , a lower chance of modified Thrombolysis in Cerebral Infarction (mTICI) grade 2b to 3 reperfusion (a

106 ed to analyze final modified thrombolysis in cerebral infarction (mTICI) scores, periprocedural compl

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

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

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

110 ischemia-reperfusion model, thereby reducing cerebral infarction, neuronal apoptosis and preserving B

111 Nonhemorrhagic cerebral infarction occurred in 86% of participants with

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

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

114 Cerebral infarction occurs in one quarter of all childre

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

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

117 farction; and 12 versus seven had new silent cerebral infarction on imaging.

118 tal myocardial infarction; or (4) new silent cerebral infarction on imaging.

119 Cerebral infarction on magnetic resonance imaging (MRI)

120 se events, including one cardiac arrest, one cerebral infarction, one intracranial haemorrhage, one P

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

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

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

124 TEs, myocardial infarction or ischemia, and cerebral infarction or ischemia.

125 ants with some comorbidities and evidence of cerebral infarction or more than 4 microbleeds or areas

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

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

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

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

130 n the adjusted analysis, rates of procedural cerebral infarction (p = 0.188), ventriculostomy-related

131 potential pharmacological interventions for cerebral infarction prevention.

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

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

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

135 % (P < 0.05) and 34% (P < 0.05) reduction in cerebral infarction, respectively, along with decreased

136 eline covariates, including cerebral oedema, cerebral infarction, respiratory failure, hydrocephalus

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

138 essful reperfusion (extended Thrombolysis in Cerebral Infarction scale score 2b-3) on first and final

139 ighting analysis, a modified Thrombolysis in Cerebral Infarction Scale score of 2b or 3 was associate

140 the occurrence of a modified Thrombolysis in Cerebral Infarction Scale score of 2b or 3) and outcome

141 grade 2b50-3 on the extended thrombolysis in cerebral infarction scale) of an occlusion in the V4 seg

142 ission to determine the prevalence of silent cerebral infarction (SCI), defined as magnetic resonance

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

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

145 essful reperfusion (modified Thrombolysis in Cerebral Infarction score >=2b), discharge mRS score, or

146 antial reperfusion (modified Thrombolysis in Cerebral Infarction score 2b or 3), and symptomatic intr

147 antial reperfusion (modified Thrombolysis in Cerebral Infarction score 2b-3), ambulatory status, glob

148 ful recanalisation (expanded Thrombolysis In Cerebral Infarction score of 0-2a) or risk of reocclusio

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

150 essful reperfusion (modified Thrombolysis in Cerebral Infarction score of 2b or higher).

151 tion was defined as extended Thrombolysis in Cerebral Infarction score of 2b or higher.

152 reperfusion was defined as a Thrombolysis in Cerebral Infarction score of 2b/2c/3 on the completion a

153 ome was the rate of expanded Thrombolysis In Cerebral Infarction score of 2c or 3 (eTICI 2c/3; ie, sc

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

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

156 arization (good to excellent thrombolysis in cerebral infarction scores) and shift toward better outc

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

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

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

160 Focal cerebral infarction (stroke) due to unilateral occlusion

161 24 [SD]) who were suspected of having acute cerebral infarction (symptom duration, 2.8 days +/- 2.7)

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

163 troke, caused by vessel blockage, results in cerebral infarction, the death of brain tissue.

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

165 For cerebral infarction, the relative risk during pregnancy,

166 0-2, recanalisation success (thrombolysis in cerebral infarction (TICI) >=2b) and symptomatic intrace

167 ecanalization according to the Thrombosis in Cerebral Infarction (TICI) scale and functional independ

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

169 Secondary outcomes included thrombolysis in cerebral infarction (TICI) scores (2b-3 or 3), symptomat

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

171 sful reperfusion, defined as thrombolysis in cerebral infarction (TICI) scores of 2b to 3, 90-day mor

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

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

174 lar disease (ischemic or hemorrhagic stroke, cerebral infarction, transient ischemic attack, carotid

175 f cervical vascular disorders (ie, aneurysm, cerebral infarction, transitory cerebral ischemia) and c

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

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

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

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

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

181 Cerebral infarction volumes were quantitated from histop

182 In the brain, cerebral infarction was significantly smaller in both EM

183 Cerebral infarction was visualized by TTC staining on da

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

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

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

187 % stenosis in the carotid ipsilateral to the cerebral infarction, which is designated as the symptoma

188 The most common serious adverse event was cerebral infarction, which occurred in four (5%) of 80 p

189 ) children had mild disease and 19 (63%) had cerebral infarctions, which were commonly acute (n = 9,

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

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

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