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

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

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

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

6 ng human subjects with restorative therapies poststroke.

7 oke if death occurred within the first month poststroke.

8 5 years and 33% (95% CI = 23-46) at 10 years poststroke.

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

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

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

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

13 Poststroke angiogenesis contributes to long-term recover

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

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

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

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

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

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

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

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

22 can be therapeutically targeted to minimize poststroke brain damage.

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

24 can be therapeutically targeted to minimize poststroke brain damage.

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

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

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

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

29 athways that are not specific to traditional poststroke care.

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

31 including insulin resistance, could improve poststroke cognitive function.

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

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

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

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

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

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

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

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

40 Poststroke delirium may frequently be detected provided

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

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

43 Poststroke depression (PSD) has been recognized by psych

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

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

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

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

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

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

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

51 Poststroke depression has been linked to higher mortalit

52 Poststroke depression has been shown in numerous studies

53 Poststroke depression has been shown to increase mortali

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

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

56 Preliminary data on poststroke depression suggest that repetitive transcrani

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

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

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

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

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

62 termine the most accurate tool for detecting poststroke depression.

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

64 Poststroke depressive symptom severity did not correlate

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

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

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

68 Treatment studies for poststroke dysarthria indicate that speech supplementati

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

70 ve neuronal stimulations is dependent on the poststroke environment.

71 y be associated with formative mechanisms of poststroke epileptogenesis.

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

73 Poststroke fatigue is a debilitating symptom and is poor

74 al theories for mechanistic understanding of poststroke fatigue.

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

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

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

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

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

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

81 Poststroke hyperglycemia is common and is associated wit

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

83 A poststroke increase in markers of oxidative injury and n

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

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

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

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

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

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

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

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

92 RHP reduced poststroke leukocyte diapedesis concomitant with a long-

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

94 Poststroke loss and recovery of functions have been incr

95 Remission of poststroke major depression after treatment has been ass

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Poststroke neuronal regeneration is characterized by wav

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

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

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

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

121 significance of mechanical physiotherapy on poststroke outcomes.

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

123 condary prophylaxis, especially in the early poststroke period.

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

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

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

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

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

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

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

131 plasticity seem particularly suited to favor poststroke recovery.

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

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

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

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

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

137 so attenuated neurodegeneration and improved poststroke sensorimotor function.

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

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

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

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

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

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

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

145 e survivors to evaluate the effectiveness of poststroke therapies.

146 Poststroke tissue remodeling results in a compartmentali

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

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

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

150 198 who underwent valve replacement surgery poststroke were available for analysis.

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

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

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

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

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