ライフサイエンスコーパス: post-stroke

1 and (ii) at a chronic stage (after 9 months post stroke).

2 onths following stroke (on average <3 months post-stroke).

3 with lacunar stroke; 24% had MCI or dementia post stroke.

4 er-extremity (UE) motor function in patients post stroke.

5 as at 24 h, confirmed histologically at 48 h post stroke.

6 ith HT, had MRI indices of hemorrhage at 3 h post stroke.

7 P<0.01) to neuroprotection seen up to 7 days post stroke.

8 ar thrombectomy improves outcomes at 90 days post stroke.

9 ed improved behavioral recovery at one month post-stroke.

10 gesterone was given starting at 3, 6 or 24 h post-stroke.

11 urogenesis were performed for up to 3 months post-stroke.

12 ioneurogenesis when given no later than 12 h post-stroke.

13 ation and non-leaky blood vessels by 10 days post-stroke.

14 tions between arm function and use in humans post-stroke.

15 not enhance motor recovery in patients early post-stroke.

16 70% of their initial impairment by 3 months post-stroke.

17 received treatment via a femoral vein at 4 h post-stroke.

18 hemic cell damage analyzed at 6, 24 and 48 h post-stroke.

19 mals at 1 day, 2 days and weekly for 6 weeks post-stroke.

20 These rats were sacrificed at 24, or 48, h post-stroke.

21 important role in the recovery of movements post-stroke.

22 earning effects with tDCS and motor practise post-stroke.

23 available for measuring upper limb function post-stroke.

24 igated the effects of tDCS on motor learning post-stroke.

25 ents with heterogeneous lesions at 1-2 weeks post-stroke.

26 ety and quality of life (QoL), up to 5 years post-stroke.

27 ears; 7 female; 3 multiple sclerosis [MS]; 6 post-stroke; 1 post-traumatic).

28 s fugax and transient ischemic attack (45%), post-stroke (7%), global ischemia (10%), and asymptomati

29 12 hemiparetic patients (7.3 +/- 4.0 months post-stroke, age 26-75 years, six male/six female) acros

30 nd DMS D1-neurons, contributing to increased post-stroke alcohol-seeking and relapse.

31 Rats were killed at 22 days post-stroke and brains extracted for evaluation of infar

32 ns of acute stroke care on one year survival post-stroke and determined the size of the effect across

33 ical activity levels are reduced immediately post-stroke and remain below recommended levels for heal

34 d V in the dorsolateral prefrontal cortex of post-stroke and vascular dementia and, of mixed and Alzh

35 tein SMI31 immunoreactivity was increased in post-stroke and vascular dementia compared with post-str

36 etermine their temporal course up to 90 days post-stroke, and explore their utility as an early diagn

37 The molecular signals for post-stroke angiogenesis begin within hours of initial c

38 had neuroprotective properties and enhanced post-stroke angiogenesis, a key component of brain repai

39 The overlap in molecular signaling between post-stroke angiogenesis, neurogenesis and axonal sprout

40 The Continue or Stop Post-Stroke Antihypertensives Collaborative Study (COSSA

41 = 0.04), poor cognitive outcome (P = 0.03), post-stroke anxiety (P = 0.04) and post-stroke depressio

42 as 'goath') are commonly seen in persisting post-stroke aphasia and are thought to signal impairment

43 In this study, 17 patients with chronic post-stroke aphasia performed inner speech tasks (rhyme

44 rrors were obtained from 64 individuals with post-stroke aphasia, who also underwent high-resolution

45 and neuroimaging data from individuals with post-stroke aphasia.

46 twork, with residual language performance in post-stroke aphasia.

47 rd of all ischaemic strokes, even more after post-stroke atrial fibrillation monitoring.

48 e mechanisms aimed at mitigating the risk of post-stroke autoimmune complications driven by adaptive

49 inical utility as a prognostic biomarker for post-stroke BBB complications, and are likely elevated e

50 elevated early in patients who later develop post-stroke BBB disruption due to the presence of an inv

51 of any of these 16 genes are predictive for post-stroke blood brain barrier (BBB) disruption.

52 At day 7 post-stroke, both immediate and delayed intracerebral tr

53 he acute and sub-acute/chronic phases in the post-stroke brain.

54 es phagocytosis during the recovery phase in post-stroke brains and suggests that CD36 plays a repara

55 Because lesions at this site can produce the post-stroke central pain syndrome, this finding supports

56 tory substances may be beneficial in chronic post-stroke conditions, while multimodal imaging can be

57 possibility that asymmetric walking patterns post-stroke could be remediated utilizing the split-belt

58 of crossbridge force generation and faster (post-stroke) crossbridge detachment by negative strain.

59 grees before reaching the orientation in the post-stroke crystal structure, consistent with previous

60 es was increased by >2-fold in subjects with post-stroke demented compared to post-stroke non-demente

61 s in the white matter that would distinguish post-stroke demented from post-stroke non-demented subje

62 ed Cambridge Cognition Examination scores in post-stroke demented subjects.

63 nd temporal white matter were not greater in post-stroke demented versus post-stroke non-demented sub

64 or Alzheimer pathology in the development of post stroke dementia.

65 significantly changed between patients with post-stroke dementia and post-stroke patients with no de

66 Post-mortem brain tissues from post-stroke dementia and post-stroke patients with no de

67 d with dementia and executive dysfunction in post-stroke dementia and vascular dementia.

68 decreased neuronal volumes in subjects with post-stroke dementia and vascular dementia.

69 evalence and risk factors for pre-stroke and post-stroke dementia are conflicting.

70 ble data on the prevalence and predictors of post-stroke dementia are needed to inform patients and c

71 risk factors may be of benefit in preventing post-stroke dementia in the general population.

72 The strong association of post-stroke dementia with multiple strokes and the progn

73 who survive stroke develop delayed dementia (post-stroke dementia), with most cases being diagnosed a

74 vascular dementias, multi-infarct dementia, post-stroke dementia, subcortical ischaemic vascular dis

75 and place were more strongly associated with post-stroke dementia.

76 d for factors associated with pre-stroke and post-stroke dementia.

77 to identify risk factors for pre-stroke and post-stroke dementia.

78 Post stroke depression (PSD) is one of the most common c

79 = 0.03), post-stroke anxiety (P = 0.04) and post-stroke depression (P = 0.02).

80 as been thought to be effective for treating post-stroke depression (PSD).

81 Recent investigations indicate that post-stroke depression and social impairment are cross-c

82 model replicates multiple features of human post-stroke depression and thus provides a new model for

83 Clinical correlates of post-stroke depression include severity of physical and

84 Post-stroke depression is a frequent chronic and recurre

85 rhaps the most compelling reason to identify post-stroke depression, however, is its substantial impa

86 ollow-up, neurovascular thrombectomy reduced post-stroke disability and improved health-related quali

87 triever thrombectomy reduced the severity of post-stroke disability and increased the rate of functio

88 Post-stroke domain V administration increased VEGF level

89 Such proposed therapies for post-stroke dysphagia have required confirmation of phys

90 Based on evidence from the post-stroke dysphagia neurostimulation literature, these

91 ion have demonstrated therapeutic promise in post-stroke dysphagia when applied contralaterally.

92 ulate cortical swallowing neurophysiology in post-stroke dysphagia with therapeutic effects which are

93 Other post-stroke emotional/behavioral disorders include mania

94 nd to antidepressant drug therapy, the other post-stroke emotional/behavioral disorders need to be ev

95 d, whereas C3a receptor deficiency decreased post-stroke expression of GAP43 (P < 0.01), a marker of

96 Our current findings suggest that post-stroke fatigue (1) is a problem of movement speed (

97 we investigated the long-term prevalence of post-stroke fatigue in patients with a young transient i

98 The pathophysiology of post-stroke fatigue is poorly understood although it is

99 Post-stroke fatigue negatively influences short-term fun

100 citability is associated with high levels of post-stroke fatigue.

101 excitability is lower in patients with high post-stroke fatigue.

102 both would be influenced by the presence of post-stroke fatigue.

103 hemisphere is a viable therapeutic target in post-stroke fatigue.

104 The post-stroke free-energy minimum is higher and is formed

105 to improve the accuracy of predictability in post-stroke functional impairment.

106 eflects the tension loss due to the original post-stroke heads executing a reverse power stroke.

107 ts and 17 subjects with chronic (> 6 months) post-stroke hemiplegia participated in the study.

108 dy was performed to sonographically evaluate post-stroke hemiplegic shoulders and explore possible re

109 y after major stroke, resulting in so-called post-stroke hypertension.

110 a novel multivariate approach of predicting post-stroke impairment of speech and language from the i

111 BSc2118 was intrastriatally injected 12 h post-stroke in mice that had received normal saline or r

112 inhibition of neurogenic innervation limits post-stroke infection.

113 on preserved NK cell function and restrained post-stroke infection.

114 0 +/- 17 years, range 28-87 years) underwent post stroke language assessment with the Revised Western

115 Although ED1(+) cells decreased by 7-14 days post-stroke, large numbers of Iba1(+) cells persisted in

116 seline and having AF first diagnosed >7 days post-stroke (late AF) was highly associated with recurre

117 Greater post-stroke left hemisphere network fragmentation and hi

118 Univariate post-stroke lesion-behavior mapping is a particularly po

119 ice were associated with greater deficits in post-stroke locomotor functions.

120 Although post-stroke (<or=1 year) dementia rates were heterogeneo

121 ntrol groups, and negatively associated with post-stroke lymphocyte counts.

122 = 13.2 years, range = 23.1-77.0 years; time post-stroke: mean = 49.2 months, standard deviation = 55

123 = 12.2 years, range = 17.2-80.1 years; time post-stroke: mean = 55.6 months, standard deviation = 62

124 he type of task used in motor rehabilitation post-stroke might be less relevant, as long as it is int

125 Post-stroke mortality is higher among residents of disad

126 The forward (pre-stroke to post-stroke) motion has an approximately 4.5 k(B)T (wher

127 Post-stroke movement disorders can manifest in parkinson

128 ution of structural brain damage, defined as post-stroke necrosis or cortical disconnection.

129 Furthermore, SDF1 and Ang1 promote post-stroke neuroblast migration and behavioral recovery

130 , we report here critical check-points about post-stroke neurogenesis after cortical infarcts, import

131 nal knockdown leads to a specific deficit in post-stroke neurogenesis through impaired migration of n

132 tion in the subventricular zone and impaired post-stroke neurogenesis.

133 bjects with post-stroke demented compared to post-stroke non-demented subjects (P = 0.026) and by 11-

134 e not greater in post-stroke demented versus post-stroke non-demented subjects.

135 would distinguish post-stroke demented from post-stroke non-demented subjects.

136 hese, 6/28 (21%) were continent at six weeks post-stroke or discharge.

137 hite matter changes, which may contribute to post-stroke or small vessel disease dementia.

138 The pathological substrates associated with post-stroke or vascular dementia are poorly understood,

139 h, and it develops a 24 degrees twist in the post-stroke orientation.

140 how its alpha-helical neck in either pre- or post-stroke orientations, little is known about the tran

141 ically as a tool for the control for central post-stroke pain and neuropathic facial pain.

142 Lesions of 10 patients with central post-stroke pain of thalamic origin and 10 control patie

143 fying patients at risk of developing central post-stroke pain of thalamic origin early after thalamic

144 Central post-stroke pain of thalamic origin is an extremely dist

145 ally implicated in the generation of central post-stroke pain of thalamic origin.

146 s put patients at risk of developing central post-stroke pain of thalamic origin.

147 o three additional lesion syndromes: central post-stroke pain, auditory hallucinosis, and subcortical

148 Using a representative post-stroke patient as an example, this article reviews

149 subjects to be reduced by 30-40% compared to post-stroke patients with no dementia and controls.

150 t-stroke and vascular dementia compared with post-stroke patients with no dementia and correlated wit

151 tween patients with post-stroke dementia and post-stroke patients with no dementia groups or ageing c

152 brain tissues from post-stroke dementia and post-stroke patients with no dementia were derived from

153 In post-stroke patients with spasticity of the biceps brach

154 ent should be continued during the immediate post-stroke period is unclear.

155 as sensitized to MBP but did not survive the post-stroke period.

156 s in patients and healthy controls to assess post-stroke plasticity.

157 ot affect the incidence of algorithm-defined post-stroke pneumonia (71 [13%] of 564 patients in antib

158 adverse events were infections unrelated to post-stroke pneumonia (mainly urinary tract infections),

159 noted no differences in physician-diagnosed post-stroke pneumonia between groups (101 [16%] of 615 p

160 Algorithm-defined post-stroke pneumonia could not be established in 129 (1

161 axis cannot be recommended for prevention of post-stroke pneumonia in patients with dysphagia after s

162 The primary outcome was post-stroke pneumonia in the first 14 days, assessed wit

163 Post-stroke pneumonia is associated with increased morta

164 Post-stroke prognoses are usually inductive, generalizin

165 Here, we sought to establish how applicable post-stroke prognostic models, trained with monolingual

166 ge 5-112) and ending at a mean of 426.6 days post-stroke (range 170-917).

167 collection beginning at a mean of 36.9 days post-stroke (range 5-112) and ending at a mean of 426.6

168 een shown to be necessary and sufficient for post-stroke recovery in rodents.

169 mising therapeutic target, but their role in post-stroke recovery remains controversial.

170 ndition tended to have the greatest relative post-stroke recovery.

171 may have important clinical implications for post-stroke recovery.

172 Post-stroke rehabilitation has also, naturally, focused

173 right or left hemisphere lesions to enhance post-stroke rehabilitation interventions.

174 ould be consistent with their involvement in post-stroke reorganization.

175 ts suggest the involvement of these areas in post-stroke reorganization.

176 glia migration that may have implications in post stroke repair.

177 y ECG monitoring in the 7 days and 12 months post-stroke, respectively.

178 Histological analysis at 3 days post-stroke revealed that only those ischemic animals tr

179 of the primary somatosensory (S1) cortex in post-stroke sensory discrimination and 2) To determine t

180 and 2) To determine the relationship between post-stroke sensory discrimination and structural integr

181 however, the neural structures that support post-stroke sensory function have not been described.

182 icity genes were differentially expressed in post-stroke SI mice.

183 One day post-stroke, slight increases in both ED1(+) and Iba1(+)

184 ributed pattern of activation was evident in post-stroke subjects with a positive correlation between

185 we performed clinicopathological studies in post-stroke survivors, who had exhibited greater frontal

186 e matter and cognitive impairment in elderly post-stroke survivors.

187 Three days post-stroke, there was marked infiltration and aggregate

188 up had significantly better behavior at 6/10 post-stroke time points as compared to Saline+Saline.

189 jects had a cognitive assessment at 3 months post stroke to exclude dementia, and had an MRI scan (n=

190 Importantly, post-stroke treatment (3 h after MCAo) was still effecti

191 ifferent anatomical structures in supporting post-stroke upper limb motor recovery and points towards

192 e little data on whether functional recovery post-stroke varies among hospitals.

193 Z image analysis took into account potential post-stroke volume loss.

194 phere stroke patients, each more than a year post-stroke when first assessed-testing each patient's s

195 12.4 years, 20 females, 56.81 +/- 63 months post-stroke) with minimal motor and cognitive impairment