ライフサイエンスコーパス: poststroke

1 gia from stroke (mean of 38.8 +/- 24.4 weeks poststroke).

2 ormed in a therapeutic setting up to 3 hours poststroke.

3 ng human subjects with restorative therapies poststroke.

4 oke if death occurred within the first month poststroke.

5 5 years and 33% (95% CI = 23-46) at 10 years poststroke.

6 nctional improvement between 3 and 12 months poststroke.

7 functional and cognitive function at 90 days poststroke.

8 MI), Barthel Index (BI)) from 3 to 12 months poststroke.

9 ty of life outcomes were assessed at 90 days poststroke.

10 habilitative therapies during the first year poststroke.

11 ome of them at 4 to 6 months (chronic phase) poststroke.

12 people with long-standing upper-limb paresis poststroke.

13 were more effective when administered 0-3 h poststroke.

14 ty by reducing infarct volume and decreasing poststroke acidosis.

15 iated with a significantly increased risk of poststroke AF detection.

16 eri-infarct cortex up-regulate HMGB1 at 14 d poststroke, along with an accumulation of endogenous EPC

17 tailed interval [ETI] = 0.78-0.80) at 1 week poststroke and 0.81 (95% ETI = 0.80-0.82) at 2 weeks.

18 erquartile range [IQR] = 1.3-12.8) at 1 week poststroke and 4.2 (IQR = 1.3-9.8) at 2 weeks.

19 istration of recombinant tPA protein 6 hours poststroke and 7 more times at 2 d intervals mitigated w

20 PROMIS) scales were completed within 1 month poststroke and again at 6 months.

21 tors and amantadine to assist motor recovery poststroke and traumatic brain injury, respectively.

22 ng in multiple sclerosis, postpoliomyelitis, poststroke, and in chronic fatigue syndrome.

23 alence and course of PSE over the first year poststroke, and its psychological associations.

24 kably poor neurological recovery and loss of poststroke angiogenesis and oligodendrogenesis.

25 oach to cerebral regeneration: regulation of poststroke angiogenesis and recovery through direct modu

26 Poststroke angiogenesis contributes to long-term recover

27 s recovery was accompanied by an increase in poststroke angiogenesis that was correlated with improve

28 Participants with chronic poststroke aphasia and spoken language comprehension imp

29 nal and ipsilesional tissue in recovery from poststroke aphasia are unclear.

30 Recent treatment studies in poststroke aphasia have shown that intensity of language

31 ndividuals (20 female, 48 male) with chronic poststroke aphasia who completed a three-week language t

32 disorders of speech and language, other than poststroke aphasia.

33 likely to be crucial for speech recovery in poststroke aphasia.

34 performance in neurological scoring and high poststroke-associated mortality.

35 ibuted to large- or small-vessel disease had poststroke atrial fibrillation (AF) detected by an inser

36 Immune histochemistry of murine and human poststroke autoptic brains congruently identified abunda

37 d in vitro, exogenous tPA delivery increased poststroke axonal sprouting of corticobulbar and cortico

38 analysis pipeline visualized and quantified poststroke B cell diapedesis throughout the brain, inclu

39 ke recovery in aged mice can be reversed via poststroke bacteriotherapy following the replenishment o

40 ced after transient focal ischemia modulates poststroke behavioral deficits and brain damage.

41 presently studied whether alpha-Syn mediates poststroke brain damage and more importantly whether pre

42 can be therapeutically targeted to minimize poststroke brain damage.

43 can be therapeutically targeted to minimize poststroke brain damage.

44 s a potential therapeutic target to minimize poststroke brain damage.

45 t for understanding and potentially treating poststroke brain dysfunction.

46 Poststroke brain edema predicts the severity of eventual

47 nge of therapies shows promise for improving poststroke brain repair.

48 ted the cholesterol homeostasis genes in the poststroke brain with Apoe, the highest expressing trans

49 nistic routes of induced neurogenesis in the poststroke brain, using both a forelimb overuse manipula

50 RNAs (LncRNAs), also undergo changes in the poststroke brain.

51 ar control can be induced in the healthy and poststroke brain.

52 ia provide clues regarding language recovery poststroke, but further studies of the role of the ipsi

53 Participants with chronic poststroke CA (n = 23) completed 35 h of iReadMore train

54 ease disparities in access to preventive and poststroke care for dual eligible and minority patients.

55 ntial gap that may be unaddressed in routine poststroke care.

56 athways that are not specific to traditional poststroke care.

57 ysis of therapy effects in participants with poststroke central alexia.

58 from a lesion of the CNS, such as a stroke [poststroke central pain (CPSP)].

59 be useful when considering an ICM in routine poststroke clinical care.

60 with standard diet for 8 weeks to mimic the poststroke clinical situation.

61 and secondary neurodegeneration and prevents poststroke cognitive decline.SIGNIFICANCE STATEMENT Deme

62 and secondary neurodegeneration and prevents poststroke cognitive decline.SIGNIFICANCE STATEMENT Deme

63 including insulin resistance, could improve poststroke cognitive function.

64 significant associations were noted between poststroke cognitive impairment and antihypertensives am

65 Poststroke cognitive impairment and dementia (PSCID) is

66 Poststroke cognitive impairment is common, but the cogni

67 Poststroke cognitive impairment is considered one of the

68 red as a potential approach for treatment of poststroke cognitive impairment.

69 was defined by the change from prestroke to poststroke cognitive testing.

70 l memory, and increased anxiety through 8 wk poststroke compared to wild type (WT) littermates also r

71 ehavioral changes in the (4) healthy and (5) poststroke condition; notably, MI-related enhancement of

72 at directs the rotating lever arm toward the poststroke conformation is almost flat, implying that th

73 r arm in a crystal structure of the presumed poststroke conformation of myosin VI.

74 First, the motor domain attains the poststroke conformation without directing the lever arm

75 s approximately 180 degrees between pre- and poststroke conformations.

76 havioral variance accounted for by simulated poststroke connectomes to that observed in the randomly

77 to determine how this comorbidity may affect poststroke cortical plasticity and thereby functional re

78 neurogenic and non-neurogenic mechanisms of poststroke CSAs.

79 ected gastrocnemius) and were followed up to poststroke d 14.

80 were also associated with a reduced risk of poststroke death or ADL dependency (adjusted odds ratio,

81 Poststroke delirium may be underdiagnosed due to the cha

82 Poststroke delirium may frequently be detected provided

83 orithm is appropriate to the time profile of poststroke delirium.

84 An understanding of the epidemiology of poststroke dementia (PSD) is necessary to inform researc

85 e dementia, with the lowest risk of incident poststroke dementia at a daily consumption level of 3 to

86 icular, cause specific complications such as poststroke dementia or even poststroke depression.

87 d coffee was associated with a lower risk of poststroke dementia, with the lowest risk of incident po

88 ently, there are no available treatments for poststroke dementia.

89 nd tea and the risk of stroke, dementia, and poststroke dementia.

90 n with tea was associated with lower risk of poststroke dementia.

91 Both poststroke depression (hazard ratio=1.13, 95% CI=1.06-1.

92 Poststroke depression (PSD) has been recognized by psych

93 Although poststroke depression (PSD) is a frequent chronic compli

94 in the pooled estimates of the prevalence of poststroke depression (PSD).

95 Seventeen patients with poststroke depression and cognitive impairment who had e

96 onic conditions present at discharge and new poststroke depression and other mental health diagnoses

97 of this study was to evaluate the effect of poststroke depression and other mental health diagnoses

98 ear mortality risk was seen in patients with poststroke depression and other mental health diagnoses

99 easure was the development of major or minor poststroke depression based on symptoms elicited by the

100 e instruments that may help in screening for poststroke depression but none are satisfactory for case

101 tential inequities in clinical management of poststroke depression by gender, race/ethnicity and age

102 Poststroke depression has been linked to higher mortalit

103 Poststroke depression has been shown in numerous studies

104 Poststroke depression has been shown to increase mortali

105 Annual diagnosis and treatment rates for poststroke depression increased from 2003 to 2020 (both

106 Cognitive impairment due to poststroke depression is reversible and can be quantifie

107 the increased mortality risk associated with poststroke depression last longer than the depression it

108 Preliminary data on poststroke depression suggest that repetitive transcrani

109 Patients with poststroke depression were younger, more often white, an

110 Among individuals diagnosed with poststroke depression, 69.8% were prescribed an antidepr

111 , exercise, and SSRIs may reduce symptoms of poststroke depression, but use of SSRIs to prevent depre

112 rate than fluoxetine or placebo in treating poststroke depression, in improving anxiety symptoms, an

113 e function, once improved after remission of poststroke depression, is likely to remain stable over t

114 mong individuals who received a diagnosis of poststroke depression, we estimated treatment rates by g

115 termine the most accurate tool for detecting poststroke depression.

116 l control is associated with the severity of poststroke depression.

117 is common after stroke and may be caused by poststroke depression.

118 s superior to fluoxetine in the treatment of poststroke depression.

119 garding clinical diagnosis and management of poststroke depression.

120 ications such as poststroke dementia or even poststroke depression.

121 Poststroke depressive symptom severity did not correlate

122 ion levels compared to 0-4 years education), poststroke disability (OR, 1.4), and impaired activities

123 us argatroban or eptifibatide did not reduce poststroke disability and was associated with increased

124 ulpability for SES-associated disparities in poststroke disability from poststroke factors to those t

125 gher stroke incidence and experience greater poststroke disability than whites.

126 This cohort study found that higher baseline poststroke disability was associated with increased rate

127 unt for additional individual variability in poststroke disability.

128 ally in Asia for the treatment of asthma and poststroke dizziness.

129 s SeLECT(2.0), may offer better guidance for poststroke driving decisions than generic SFIs.

130 Treatment studies for poststroke dysarthria indicate that speech supplementati

131 acteroidetes were identified as hallmarks of poststroke dysbiosis, which was associated with intestin

132 Thus, our understanding of poststroke edema needs to be revised, and these findings

133 There are few longitudinal studies of poststroke emotionalism (PSE) and our understanding of t

134 ve neuronal stimulations is dependent on the poststroke environment.

135 Lesion locations from 76 patients with poststroke epilepsy (39 [51%] male; mean [SD] age, 61.0

136 Poststroke epilepsy (PSE) is a major complication among

137 psy in a discovery data set of patients with poststroke epilepsy and control patients with stroke.

138 Poststroke epilepsy was defined as at least 1 remote sym

139 successfully captured cases at high risk of poststroke epilepsy.

140 tiseizure medication (ASM) for patients with poststroke epilepsy.

141 een patients treated with different ASMs for poststroke epilepsy.

142 y be associated with formative mechanisms of poststroke epileptogenesis.

143 ins challenging due to the multiple pre- and poststroke factors that determine the deficits and recov

144 ed disparities in poststroke disability from poststroke factors to those that precede presentation.

145 al and neurophysiological changes related to poststroke fatigue and put forward potential theories fo

146 Poststroke fatigue is a debilitating symptom and is poor

147 al theories for mechanistic understanding of poststroke fatigue.

148 ria for PSR: transient worsening of residual poststroke focal neurologic deficits or transient recurr

149 h the potential to enhance cognition and aid poststroke functional recovery.

150 The exposure was poststroke functional status at study baseline, defined

151 OE4 and APOE4 x time, higher cumulative mean poststroke glucose level was associated with a faster de

152 L cholesterol levels, higher cumulative mean poststroke glucose level was associated with faster decl

153 In this cohort study, higher poststroke glucose levels were associated with faster gl

154 have mild to moderate impairments 3-9 months poststroke have substantial improvement in functional us

155 her higher doses of motor therapy in chronic poststroke hemiparesis result in better outcomes, compar

156 Analyzing poststroke human and mouse blood microvessels we have id

157 sociations between ischemic stroke sites and poststroke hyperglycemia (PSH).

158 usion did not benefit patients with moderate poststroke hyperglycemia in a recent trial.

159 Poststroke hyperglycemia is common and is associated wit

160 flammatory EP2 signaling participates in the poststroke immune response.

161 As a result of this balance, poststroke immune responses alter stroke outcomes.

162 that may systemically affect homeostasis in poststroke immune responses, and pinpointed multiple aff

163 of 222 participants who had mild to moderate poststroke impairments were randomly assigned to receive

164 ion model showed that changes within 96-hour poststroke in APOF, APOL1, APMAP, APOC4 (apolipoprotein

165 After severe corticospinal tract damage poststroke in humans, some recovery of strength and move

166 A poststroke increase in markers of oxidative injury and n

167 s, and thus a clinical target for preventing poststroke infection, has also been identified.

168 We found 2 clusters for poststroke infection, one associated with pneumonia in t

169 ty and dysphagia are important predictors of poststroke infection, there is evidence from experimenta

170 nodepression (SIDS) is an essential cause of poststroke infections.

171 pparently attenuated behavioral deficits and poststroke inflammation after middle cerebral artery occ

172 icroglial activation plays a central role in poststroke inflammation and causes secondary neuronal da

173 PET studies until week 6 after stroke reveal poststroke inflammation as a dynamic process that involv

174 Poststroke inflammation was evaluated with flow cytometr

175 al ischemic event is followed by an extended poststroke inflammatory response.

176 erstanding of the dual role of complement in poststroke injury and recovery, and discuss the challeng

177 ic stroke and identify sleep as a window for poststroke intervention that promotes neuroplasticity an

178 Poststroke intravenous transfer of CD8+ TRLs reduced inf

179 er limb impairment during the first 6 months poststroke is 70% of the maximum possible.

180 Late functional improvement poststroke is associated with lower 5-year mortality, in

181 cture-naming errors from 86 individuals with poststroke language impairment (aphasia).

182 We found no evidence that poststroke LDL cholesterol and SBP levels were associate

183 RHP reduced poststroke leukocyte diapedesis concomitant with a long-

184 The basal and poststroke levels of neurotrophic factors (brain-derived

185 Poststroke loss and recovery of functions have been incr

186 Remission of poststroke major depression after treatment has been ass

187 ng and stroke, such that neutrophils in aged poststroke mice showed the greatest impairment in this f

188 els, but this response was not seen in older poststroke mice.

189 Recolonizing germ-free mice with dysbiotic poststroke microbiota exacerbates lesion volume and func

190 sychiatric sequelae, a considerable cause of poststroke morbidity.

191 all identified confounders, women had lower poststroke mortality (HR, 0.79 [95% CI, 0.68-0.91]).

192 l fibrillation was identified in relation to poststroke mortality (P=0.002).

193 effect of other mental health conditions on poststroke mortality has not been examined.

194 Severe obesity is associated with increased poststroke mortality in middle-aged and older adults.

195 own an association of Ala312 fibrinogen with poststroke mortality in subjects with atrial fibrillatio

196 cross-linking processes, is associated with poststroke mortality in subjects with atrial fibrillatio

197 hether antidepressant treatment would reduce poststroke mortality over 9 years of follow-up.

198 ighborhood disadvantage would predict higher poststroke mortality, and neighborhood effects would be

199 ibutors to sex differences in recurrence and poststroke mortality, including social factors, are uncl

200 sm with ischemic stroke, stroke subtype, and poststroke mortality.

201 rs, primarily explained the sex disparity in poststroke mortality.

202 groups pseudorandomly to balance severity of poststroke motor deficits: REGULAR stimulation, BURST st

203 r determined in the acute phase, can predict poststroke motor outcomes at 3 months, especially in pat

204 in aged mice is translated into significant poststroke motor recovery, even when NgR1 blockade is pr

205 Motor imagery (MI) is assumed to enhance poststroke motor recovery, yet its benefits are debatabl

206 gression, are critical for optimizing future poststroke motor rehabilitation clinical trials.

207 CIMT is the first well defined poststroke motor rehabilitation to have identified chang

208 cerebellar dentate nucleus (DN) for chronic, poststroke motor rehabilitation, we collected invasive r

209 e cerebellar dentate nucleus (DN) on chronic poststroke motor rehabilitation, we collected invasive r

210 simulated their prestroke naming ability and poststroke naming impairment in each language, and their

211 a significant portion of the variability of poststroke neglect recovery.

212 of permanent disability remains the goal of poststroke neuro-rehabilitation programs, and new approa

213 with morphologies previously associated with poststroke neuroblasts, but DCX(+) cells coexpressed the

214 h repair; however, the mechanisms regulating poststroke neurogenesis and its functional effect remain

215 Our aim was to explore whether poststroke neurogenesis participates in the development

216 r stroke, the effect of revascularization on poststroke neuroinflammation and the role of anti-inflam

217 This work thus demonstrates that poststroke neuroinflammation contributes to hemorrhagic

218 g targeted complement inhibition to suppress poststroke neuroinflammation in mice with or without con

219 but the role that mTORC1 signaling plays in poststroke neuroinflammation is not clear.

220 These SCFA-producers alleviated poststroke neurological deficits and inflammation, and e

221 onal apoptosis is one of the major causes of poststroke neurological deficits.

222 T2D/obesity impaired poststroke neurological recovery in association with hyp

223 s, and autophagy, which are known to mediate poststroke neuronal death.

224 are potent and proregenerative modulators of poststroke neuronal plasticity at various structural lev

225 Poststroke neuronal regeneration is characterized by wav

226 nctional improvement between 3 and 12 months poststroke occurs in about one in four patients with isc

227 e OPC astrocytic transformation and improves poststroke oligodendrogenesis in mice.

228 tigate the impact of rt-PA delivered 4 hours poststroke onset as well as selective MMP-9 (JNJ0966) +/

229 Poststroke optogenetic stimulations can promote function

230 rward; and second, the lever arm reaches the poststroke orientation by undergoing a rotational diffus

231 m of this study to determine its function in poststroke outcome.

232 ssociation between brain frailty markers and poststroke outcomes after thrombolysis is unclear.

233 physical activity with stroke incidence and poststroke outcomes have not been extensively studied us

234 e of guideline-recommended therapy and worse poststroke outcomes in older patients.

235 ed to chronological age alone, in predicting poststroke outcomes.

236 significance of mechanical physiotherapy on poststroke outcomes.

237 aken to test whether lesions causing central poststroke pain (CPSP) are associated with a specific co

238 Moreover, lesions associated with poststroke pain showed a similar connectivity pattern as

239 ternal capsule (VS/ALIC) in 10 patients with poststroke pain syndrome.

240 degree, college graduates had higher initial poststroke performance in global cognition (1.09 points

241 condary prophylaxis, especially in the early poststroke period.

242 this relationship is seen only in the early poststroke phase.

243 or-related regions in both the early or late poststroke phase.

244 ese areas in only the early and not the late poststroke phase.

245 The optimum level and timing of poststroke physical activity interventions to enhance fu

246 The efficacy and optimization of poststroke physical therapy paradigms is challenged in p

247 vel druggable target for angiogenesis during poststroke progression.

248 ); however, there was a significantly faster poststroke rate of incident cognitive impairment compare

249 Our data support further evaluation of poststroke recanalization in the presence of NOX inhibit

250 after stroke will likely exert influence on poststroke recovery in patients with diabetes.

251 s the therapeutic effect of RXR in improving poststroke recovery in the aged brain.

252 between obesity and type 2 diabetes (T2D) in poststroke recovery is unclear.

253 utility of antidepressants in the process of poststroke recovery should be further investigated.

254 ified that microbiota-derived SCFAs modulate poststroke recovery via effects on systemic and brain re

255 re comprehensive assessments of HRQOL during poststroke recovery.

256 isk of ischemic stroke and negatively impact poststroke recovery.

257 thalamic circuit as an important mediator of poststroke recovery.

258 newborn cells are functionally critical for poststroke recovery.

259 BB recovery and causing BBB leakiness during poststroke recovery.

260 plasticity seem particularly suited to favor poststroke recovery.

261 ence of previous stroke-related deficits (or poststroke recrudescence [PSR]) is an underrecognized an

262 cal framework by which new interventions for poststroke rehabilitation may be developed incorporating

263 cendant role in clinical decision making for poststroke rehabilitation, which remains largely reliant

264 evaluation and possible targets for improved poststroke rehabilitative care.

265 estimate trajectories of cognitive function poststroke relative to a stroke-free cognitive trajector

266 The role of miRNAs in poststroke revascularization has been unexplored and in

267 hout and with adjustment for cumulative mean poststroke SBP and LDL cholesterol levels (-0.05 points/

268 Cumulative mean poststroke SBP and LDL cholesterol levels were not assoc

269 owever, after accounting for cumulative mean poststroke SBP and LDL cholesterol levels, higher cumula

270 Time-dependent cumulative mean poststroke SBP, glucose, and LDL cholesterol levels.

271 T(2.0) score and, to a lesser extent, by the poststroke seizure-free interval (SFI).

272 n integrated health care system (1993-2007), poststroke seizures were identified through electronic s

273 so attenuated neurodegeneration and improved poststroke sensorimotor function.

274 Baseline factors, outcomes, treatments, and poststroke serious adverse events (SAEs) were compared b

275 yline for 12 weeks during the first 6 months poststroke significantly increased the survival of both

276 ndings indicate that the frequently observed poststroke slowing reflects a disruption of corticothala

277 e behaviorally assessed at acute and 3 month poststroke stages using the Scale and Rhythm subtests of

278 ural MRIs were acquired at acute and 6 month poststroke stages.

279 w that the functional state of the DN in the poststroke state and its connectivity with the ipsilesio

280 overy stroke transition after ATP binding to poststroke state apomyosin and that BHC formation is rap

281 le and estimate its thermal fluctuation in a poststroke state as comparable in amplitude to the measu

282 o-cerebellar coherence (CCC) in the chronic, poststroke state may be key to developing novel neuromod

283 tates, postulated to represent prestroke and poststroke states, respectively.

284 AGXT2 variants were not associated with poststroke survival in the Leeds study or were they asso

285 ts, peri-ischemic social isolation decreases poststroke survival rate and exacerbates infarct size an

286 city following stroke.SIGNIFICANCE STATEMENT Poststroke, the remaining neuroanatomy maintains cogniti

287 e survivors to evaluate the effectiveness of poststroke therapies.

288 Poststroke tissue remodeling results in a compartmentali

289 ioid-induced alterations and accelerated the poststroke tissue restoration and functional recovery pr

290 thermore, RAMT(+) rats demonstrated improved poststroke track width (11% wider), stride length (21% l

291 Patients 3 to 6 months poststroke underwent a battery of assessments before rec

292 iology, current rehabilitation therapies for poststroke upper limb paresis have limited efficacy at t

293 ed for the treatment of Alzheimer's type and poststroke vascular-type dementia.

294 of combined MT and NMES therapy in improving poststroke walking speed, spasticity, balance and other

295 198 who underwent valve replacement surgery poststroke were available for analysis.

296 lts with upper extremity paresis >/=6 months poststroke were randomized to one of four dose groups in

297 of this intervention for patients 3-9 months poststroke who were followed-up for the next 12 months.

298 Acute treatment (10 min poststroke) with the JNK inhibitor SP600125 reduced infa

299 uced infarct sizes both 24 hours and 14 days poststroke, with improved behavioral parameters.

300 In contrast, delayed treatment (7 d poststroke) worsened infarction volumes and neurological