ライフサイエンスコーパス: gait

1 other in ways that lead to a chimpanzee-like gait.

2 etist subjects simultaneously observed their gait.

3 ough most participants adopted an asymmetric gait.

4 erminants and pathophysiology of freezing of gait.

5 res and their roles in controlling speed and gait.

6 length (SL), and stride speed (SS) of human gait.

7 nt for the added energy cost of pathological gait.

8 (LA) that stiffens the foot and aids bipedal gait.

9 the model to adopt a slower, "heel-walking" gait.

10 atory) and fast (escape-type) locomotion and gait.

11 fies the magnitude of deviations from normal gait.

12 ological testing conditions occurring during gait.

13 rm the basis for improved DBS strategies for gait.

14 ecrease the threshold to express freezing of gait.

15 aturally adopted a less effortful asymmetric gait.

16 mpanzee gait as well as an exaggerated human gait.

17 t; no patient maintained a fully independent gait.

18 eaths to strides at any speed, intensity, or gait.

19 to filter the parameter space for plausible gaits.

20 ving-and can transfer this learning to novel gaits.

21 ing semi-terrestrial/terrestrial quadrupedal gaits.

22 at stem tetrapods may have used transitional gaits(5,11) during the initial stages of land exploratio

23 The most common abnormalities seen were gait (54%) followed by coordination (39%) and strength (

24 The most common abnormalities seen were gait (54%), followed by coordination (39%) and strength

25 Chronic pulmonary disease and gait abnormalities were more common among adults with HT

26 rongly associated with pulmonary disease and gait abnormalities.

27 ention, leading to maladaptive and disabling gait abnormalities.

28 ctively, and 5.21 (1.50, 18.07; p=0.009) for gait abnormalities.

29 Virtual reality can be used to study gait adaptability in response to discordant sensorimotor

30 However, it is unclear if gait adaptation is driven by unilateral or bilateral mec

31 generated simulations of walking to predict gait adaptations due to these deficits.

32 Intriguingly, both visible gait alterations and neuroanatomical abnormalities throu

33 We performed laboratory-based gait analyses on 24 persons with medication-refractory E

34 Clinical gait analysis attempts to provide, in a pathological con

35 3-D gait analysis is the gold standard but many healthcare c

36 Our experimental gait analysis of locomotor kinematics across 42 individu

37 l disability, who completed the 6MWT wearing gait analysis system.

38 ed to pain (von Frey stimulation and CatWalk-gait analysis), anxiety (elevated plus maze, EPM) and de

39 ng wearable sensor data and particularly for gait analysis, which provides important biomarkers in mu

40 n the human body are too invasive for use in gait analysis.

41 t allow gait-deviation perception in amputee gait and (2) whether there are differences in observatio

42 uding grip strength, motor coordination, and gait and also related defects in neuromuscular junction

43 also been described for functional paresis, gait and balance disorders.

44 potential of stimulation of ChIs to restore gait and balance, and to prevent falls in PD.SIGNIFICANC

45 s, and vertigo and a 1-day history of wobbly gait and bilateral lower extremity paresthesia without c

46 Gait and cognition were assessed at the year 30 examinat

47 e association of cumulative BP exposure with gait and cognition.

48 xposure from young adulthood to midlife with gait and cognitive function in midlife.

49 om young to midlife is associated with worse gait and cognitive performance in midlife.

50 nt evidence of higher metabolic rates (erect gait and endothermy), as part of a major resetting of te

51 rtiary hospital, who agreed to assessment of gait and grip.

52 ody size during culture and emulate the body gait and locomotion of animals reared on agar.

53 th spontaneous Kcnn2 mutations show abnormal gait and locomotor activity, tremor and memory deficits,

54 ed to establish longitudinal trajectories of gait and model the latency between impaired gait and PD

55 eted, long-term-infected mice display severe gait and motor problems, in contrast to the wasting and

56 erations in emotionality, possibly affecting gait and movement variables.

57 nces in cerebellar granule cell circuitry on gait and other aspects of locomotion.

58 gait and model the latency between impaired gait and PD diagnosis.

59 Physical examination, with a focus on gait and posture, along with radiographical assessment a

60 The command functions for gait and speed are symmetric, implying that a separate u

61 o execute basic locomotor functions, such as gait and speed.

62 ing similarity between biological locomotion gaits and the evolution of phase patterns in coupled osc

63 sion about which Crocodylia use asymmetrical gaits and why persists, impeding reconstructions of loco

64 , feeding difficulties, spasticity or ataxic gait, and abnormal brain MRI.

65 e positioned to integrate movement cues with gait, and as ChI loss has been associated with falls in

66 hermia, defective spatial learning, impaired gait, and supraspinal nociception.

67 ve motor output and give rise to freezing of gait as clinical endpoint.

68 in humans in ways that both mimic chimpanzee gait as well as an exaggerated human gait.

69 s observed between functional and subjective gait assessments and MS status.

70 Several functional and subjective gait assessments were performed.

71 length post-stroke, which may contribute to gait asymmetries impairing patients' mobility.

72 t, a set of standardized measures to capture gait asymmetries in relevant mouse models and patients,

73 Our objective was to assess gait asymmetry (GA) and bilateral coordination of gait (

74 The relationship between spatiotemporal gait asymmetry and walking energetics is currently under

75 s demonstrated by their better perception of gait asymmetry.

76 minant role in shaping the energetic cost of gait asymmetry.

77 was the medial-lateral body sway and spatial gait asymmetry.

78 minant role in shaping the energetic cost of gait asymmetry.

79 We then generated a gait at self-selected walking speed; quantitative compar

80 We first generated gaits at prescribed speeds between 0.50 m/s and 2.00 m/s

81 cheinker syndrome, typically presenting with gait ataxia and painful dysaesthesiae in the legs evolvi

82 pture both shared and specific signatures of gait ataxia and provide a quantitative foundation for ma

83 of proprioception; this loss leads to severe gait ataxia, spinal deformities, and respiratory insuffi

84 f parkinsonism including freezing and failed gait automatization, and non-motor deficits including in

85 nd motor function, leading to impairments in gait, balance, and manual dexterity.

86 asymmetry (GA) and bilateral coordination of gait (BCG), among pwMS during the six-minute walk test (

87 s seems intuitive: with one leg constrained, gait becomes asymmetric.

88 ed step) rather than maintaining a symmetric gait (bilateral short/long steps).

89 e association of cumulative BP exposure with gait, but not with cognitive function in midlife.

90 o mechanical perturbations that affect their gait by changing their motor control strategy.

91 ch makes developing devices that assist both gaits challenging.

92 ateral behavioral phenotype characterized by gait changes and decreased activity.

93 ; recent cross-sectional studies showed that gait characteristics are potential prodromal markers for

94 r with other prodromal markers, quantitative gait characteristics can play an important role in ident

95 In conclusion, we identified a subset of gait characteristics for accurate early classification o

96 ques to determine the optimal combination of gait characteristics to discriminate people with PD and

97 lower back; 14 validated clinically relevant gait characteristics were quantified.

98 Gait characteristics were selected using different ML ap

99 Progression of age can influence gait characteristics.

100 s in the spinal cord and the other providing gait control by targeting commissural and long propriosp

101 ggesting a causal role of the STN in dynamic gait control.

102 ications such as detecting which part of the gait cycle causes increased metabolic cost in patients.

103 ies in gait phases and co-contraction of one gait cycle in patients with lumbar disc herniation (LDH)

104 The gait cycle was divided into four phases by the heel stri

105 n of balance during specific portions of the gait cycle, providing valuable biofeedback for targeted

106 tor area and premotor cortex interrupted the gait cycle, while posterior parietal cortex tracked obst

107 the least metabolically economic part of the gait cycle.

108 urthermore, SVS-COP coupling depended on the gait-cycle-phase with peaks corresponding to periods of

109 ions affecting the step length over multiple gait cycles.

110 main targets for brainstem inputs adjusting gait (Danner et al., 2017).

111 Understanding balance and gait deficits in vestibulopathy may help improve clinica

112 5b prevented subtle gait deficits in WT alphaS mice and the PD-like resting

113 In addition, these mice developed motor and gait deficits with underlying muscle atrophy, similar to

114 an be attributed to slow speeds and which to gait deficits.

115 for early identification and remediation of gait deficits.

116 te all strains displaying similar functional gait-deficits after injury.

117 Macrophage induces L13a/GAIT-dependent translational silencing of inflammatory g

118 such as muscular atrophy, synovitis, posture-gait deterioration, and reactive bone formation in a pat

119 n angle at maximum extension (r = 0.83), and Gait Deviation Index (GDI), a comprehensive metric of ga

120 cipal components demonstrated that the major gait deviation of amputees was the medial-lateral body s

121 he informative kinematic features that allow gait-deviation perception in amputee gait and (2) whethe

122 on average the accuracy rate in identifying gait deviations between PT and PTS was similar and bette

123 vement: observing another person adapt their gait did not result in significantly faster learning.

124 Despite clearly visible gait differences, direct comparison of locomotor kinemat

125 CI] 0.23-0.69) and KIR3DL1*002/HLA-Bw4i from gait difficulties (p (c) = 0.05, OR = 0.62, 95% CI 0.44-

126 Postural instability and gait difficulties (PIGDs) represent debilitating disturb

127 ination and electrodiagnostic testing showed gait-difficulties, absent tendon reflexes, decreased joi

128 lar atrophy was severe, and they had posture-gait disorder with accompanying osteopaenia.

129 The prognosis was mainly related to gait disorder, as we showed that beyond 20 years of dise

130 iovascular side effects and improved spastic gait disorders after brain injury in a disease model.

131 Fourteen patients with functional gait disorders and 17 healthy control subjects walked on

132 e motor learning in patients with functional gait disorders and probe whether abnormal postural mecha

133 tation potential in patients with functional gait disorders and related disorders (e.g. fear of falli

134 ients, which persisted in 1 at 4 months; and gait disturbance in 13 patients, which persisted in 2 at

135 Adverse events included speech and gait disturbances, weakness on the treated side, and dys

136 Running is thought to be an efficient gait due, in part, to the behavior of the plantar flexor

137 We recapitulated reported findings on insect gait dynamics and demonstrated LEAP's applicability for

138 Gait dynamics were concurrently recorded using smartphon

139 ATEMENT In persons with Parkinson's disease, gait dysfunction and the associated risk for falls do no

140 ersons with Parkinson's disease (PD) exhibit gait dysfunction, postural instability and a propensity

141 Improvements in gait dystonia decreased from 20.9% at 1 year to 16.2% at

142 rs were analysed as possible contributors to gait effects.

143 ation of RNA-binding complex, and subsequent GAIT element-mediated translational silencing.

144 lysis suggests the presence of the potential GAIT elements in the 3'UTRs of several of these mRNAs.

145 Quantifying multiple gait features (eg, speed, variability, and asymmetry) un

146 nd clinicians must be skilled in identifying gait features through observation to assess motor defici

147 Individuals with freezing of gait (FoG) due to Parkinson's disease (PD) have small an

148 Freezing of gait (FOG) in Parkinson disease (PD) often occurs during

149 Freezing of gait (FoG) in Parkinson's disease involves deficient ant

150 vitro friction testing, as well as via human-gait force-plate measurements.

151 PH were studied with regard to cognitive and gait functions before and after drainage of 40-50ml of C

152 trol directed by ribosomal protein L13a and "GAIT" (Gamma Activated Inhibitor of Translation) element

153 Hence asymmetrical gaits have benefits other than velocity capacity that ex

154 hair stand test, falls efficacy, freezing of gait, health-related quality of life (EuroQol EQ-5D), Ge

155 The impact of environmental load on gait, however, was not as pronounced, with increased loa

156 disease (PD) often occurs during steering of gait (i.e., complex gait), which is thought to arise fro

157 rsolateral prefrontal cortex correlated with gait impairment (i.e., reduced stride length) in the FOG

158 ation Index (GDI), a comprehensive metric of gait impairment (r = 0.75).

159 ohorts with predominant postural instability-gait impairment and with predominant tremor revealed asy

160 tive deficits, overall functional status and gait impairment gradually stabilized.

161 ve provided information on the mechanisms of gait impairment.

162 Gait impairments are among the most common and disabling

163 econd most common neurodegenerative disease; gait impairments are typical and are associated with inc

164 Gait impairments in persons with multiple sclerosis (pwM

165 nt to establish clear links between specific gait impairments, their underlying mechanisms, and disea

166 development of DBS strategies to ameliorate gait impairments.SIGNIFICANCE STATEMENT We tested whethe

167 was robust to all deficits, finding a stable gait in all cases.

168 rneurons is manifested, leading to a hopping gait in hindlimbs.

169 anslational approach captures asymmetries of gait in mice and patients.

170 Most lizards walk and run with a sprawling gait in which the limbs are partly advanced by lateral u

171 egardless, we recorded usage of asymmetrical gaits in 7 species of Crocodyloidea (crocodiles); includ

172 erences between asymmetrical and symmetrical gaits in Crocodylia: asymmetrical gaits involved greater

173 comparisons between able-bodied and impaired gait, including which pathological behaviors can be attr

174 lking speed, both of which are indicators of gait instability.

175 nnels taking all sub-phases of physiological gait into account.

176 ymmetrical gaits in Crocodylia: asymmetrical gaits involved greater size-normalized stride frequencie

177 step times and step lengths of healthy human gait is adapted during split-belt treadmill walking and

178 evious work indicates that adaptation during gait is context dependent, and perturbations altering lo

179 Results show that gait is more asymmetric and less coordinated as the dise

180 Nonetheless, gait is not routinely assessed quantitatively but is des

181 tric and economical; hemiparetic and amputee gait is often asymmetric and requires more energy.

182 arger Crocodylia use relatively less extreme gait kinematics consistent with steeply decreasing athle

183 can reliably and accurately assess adaptive gait kinematics in healthy and low vision subjects.

184 can accurately and reliably assess adaptive gait kinematics in subjects with central vision loss, ol

185 and are yet to be explained by morphology or gait kinematics.

186 gnificant difference was found for flagellar gait kinematics.

187 with postoperative range of motion (ROM) and gait kinematics.

188 Fifteen patients had gait loss, and 6 had respiratory failure.

189 RELMs indicated that gait (lower pace) deviates from that of non-PDC approxim

190 cognitive (p<0.001), depression (<0.05) and gait (<0.001) ratings.

191 But it is also possible that asymmetric gait may be adopted if it is energetically optimal under

192 Kinematic gait measures (trunk displacement, step timing, gait vel

193 the acceptance and usability of quantitative gait measures as outcomes in future disease-modifying cl

194 eds largely provided reasonable estimates of gait measures at self-selected speeds.

195 pose of our study was to investigate healthy gait mechanics at extremely slow walking speeds.

196 egression analysis to compare left and right gait metrics within a condition.

197 The sensor is also capable of extracting gait motions from pelvis.

198 Here we quantitatively examine plausible gaits of the stem amniote Orobates pabsti, a species tha

199 switches between actuation profiles for both gaits, on the basis of estimated potential energy fluctu

200 ce metabolic power by adopting an asymmetric gait (one short/long step, one preferred step) rather th

201 Selected gait parameters and movement patterns related to spontan

202 were also higher, when tested under dynamic gait parameters compared to static conditions, which may

203 el, caused progressive impairment of several gait parameters consistent with cerebellar dysfunction f

204 affects hip adduction, but neither of these gait parameters dramatically affects the other in ways t

205 plicitly determine trends in spatio-temporal gait parameters during treadmill walking.

206 n used to study adaptation of spatiotemporal gait parameters in relation to energetics, but it remain

207 increased cognitive load impacted a range of gait parameters such as step time and step time variabil

208 Mean and variability of spatiotemporal gait parameters were calculated during the first and fif

209 ng after DBS were global (ie, related across gait parameters).

210 Our methods for quantifying gait pathology with commodity cameras increase access to

211 thers displayed only mild alterations of the gait pattern and no signs of cerebellar defects.

212 on conditions according to the physiological gait pattern.

213 balance and also showed less variability in gait patterns.

214 te adaptive learning that transfers to novel gait patterns.

215 participants naturally adopted an asymmetric gait People may prefer to walk asymmetrically to minimiz

216 tion how clinical experience influences PT's gait perception and to seek the key kinematic features t

217 symptomatic head trauma would predict worse gait performance, particularly during dual task conditio

218 investigate lower-limb muscle activities in gait phases and co-contraction of one gait cycle in pati

219 al muscle weakness and atrophy, resulting in gait problems and difficulties with basic motor coordina

220 eloping cognitive impairment, depression and gait problems over the next 4 years.

221 cognitive impairment, depression, sleep and gait problems.

222 nd other clinical signs, along with separate gait profiles.

223 g, and daily living) enhanced sensitivity of gait quantification.

224 implicit motor learning has implications for gait rehabilitation potential in patients with functiona

225 28) improved significantly in cognitive and gait-related functions after CSF drainage.

226 se (n = 34) did not improve in cognitive and gait-related functions after CSF drainage.

227 ut mice exhibit reliable deficits on several gait-related variables when their velocity of ambulation

228 providing valuable biofeedback for targeted gait retraining.

229 Both groups modified gait similarly, but older adults walked with shorter and

230 ether there are differences in observational gait skills between PT and individuals with less clinica

231 LM (0.07 kg; 95% CI: 0.01, 0.14; P = 0.029), gait speed (0.05 m/s; 95% CI: 0.00, 0.11; P = 0.042), mu

232 eline NM-MRI correlated with slower baseline gait speed (346 of 1807 substantia nigra-ventral tegment

233 CI], 5.2-23.9), 2.6 times the odds of a slow gait speed (95% CI, 1.4-4.8), and 3.2 times the odds of

234 A model with gait speed and all covariates had comparable predictive

235 changes in appendicular lean mass (aLM) and gait speed and also 6-y incidence of mobility limitation

236 d Cox proportional hazards models (including gait speed and daily walking time as measures of physica

237 This study aimed to evaluate whether gait speed and grip strength predicted clinical outcomes

238 lly in black women, but not over 6 y or with gait speed decline.

239 e that NM-MRI is sensitive to variability in gait speed in patients with LLD, suggesting this non-inv

240 Gait speed increased by .03 m/s from the no research gro

241 In summary, gait speed is an easily obtained "vital sign" that accur

242 nd post-L-DOPA differences in processing and gait speed measures, depressive symptoms, and reported s

243 wing measured by the Digit Symbol test and a gait speed paradigm.

244 gressiveness/type, every 0.1-m/s decrease in gait speed was associated with higher mortality (HR, 1.2

245 Among frailty components, slow gait speed was associated with incident DM and borderlin

246 Gait speed was measured using the 10-meter walk test, en

247 aLM and gait speed were measured at baseline and at 3 and 6 y.

248 Changes in gait speed were not different between treatment groups (

249 ary study outcomes were changes in mobility (gait speed) and accrual of white matter hyperintensity v

250 anges in physical capability (grip strength, gait speed, and physical activity), sensory function (si

251 dopamine availability, increased processing/gait speed, and relieved depressive symptoms.

252 As the number of researchers increased, gait speed, cadence, and stride length increased, and st

253 exercise on any measures of muscle strength, gait speed, dynamic balance, reaction time, or blood lip

254 mental activities of daily living (IADL) and gait speed, may be an important pretransplant assessment

255 line NM-MRI and treatment-related changes in gait speed, processing speed, or depression severity (al

256 s often accompanied by slowed processing and gait speed.

257 xhaustion, decreased grip strength, and slow gait speed.

258 e was not associated with changes in aLM and gait speed.

259 ts with depression has slowed processing and gait speeds.

260 Because gait studies are typically performed at faster speeds, l

261 reated mice in both open field and kinematic gait studies.

262 ts") used by mammals; including asymmetrical gaits such as galloping and bounding.

263 t have granted stress-releasing benefits via gait-synchrony and mutual-touch.

264 lar task performance, and for the late swing gait target, a decrement in manipulative accuracy was ob

265 leg pass through early, mid, and late swing gait targets.

266 Mean 'final' gait termination EMG activity (right gastrocnemius) was

267 ndicate that humans will adopt an asymmetric gait that is associated with an energy reduction and sug

268 gs show that humans will adopt an asymmetric gait that is associated with an energy reduction and sug

269 ical condition that features a marked ataxic gait that progressively worsens over time.

270 ly must animals choose the correct speed and gait, they must also adapt to changing conditions and qu

271 have a positive effect in patients with SCI: gait training by means of non-invasive, surface function

272 Manual gait training was used as an exemplary case, as it requi

273 learn new walking patterns without bilateral gait training, as stepping with one leg can facilitate a

274 or proprioception at the knee and the ataxic gait typical of HSAN III.

275 following leg loss, some animals changed the gaits used during escape maneuvers, and/or recruited the

276 ull range of quadrupedal footfall patterns ("gaits") used by mammals; including asymmetrical gaits su

277 P=0.011 and 0.005, respectively), and higher gait variability (P=0.018 and 0.001, respectively).

278 se in cognitive load can result in increased gait variability and slower overall walking speed, both

279 Gait variability was not associated with the clinical ve

280 ased walking speed correlated with increased gait variability, indicating global gait worsening in af

281 Patients had slower gait velocities in the Before trials (P < 0.05) but were

282 We observed an increase in gait velocity during After trials towards normal values

283 The trend to normalization of gait velocity following a period of implicit motor learn

284 Although trunk and gait velocity locomotor after-effects were present in bo

285 t measures (trunk displacement, step timing, gait velocity), EMG responses, and subjective measures o

286 The association between cumulative BP and gait was moderated by WMH burden (interaction P<0.05).

287 assessment in their own homes, during which gait was monitored while they walked normally and while

288 ccurs during steering of gait (i.e., complex gait), which is thought to arise from executive dysfunct

289 echanical power during the push-off phase of gait, which can offer advantages over passive prostheses

290 r results: the model adopted a "toe-walking" gait with excessive hip and knee flexion during stance.

291 rmone secretion and one of a severe steppage gait with limb pain, both of which resolved.

292 tion from their visual assessment of patient gait with the patient's communicated perceptions and pre

293 Quantification of gait with wearable technology is promising; recent cross

294 ifferences in tandem walking in persons with gait worsening as compared with those without worsening

295 ncreased gait variability, indicating global gait worsening in affected participants.

296 Global gait worsening occurred in 25% of participants with unil

297 rticipants experienced clinically meaningful gait worsening.

298 y 30% slower in participants who experienced gait worsening.

299 ere similar in participants with and without gait worsening.

300 ce may be more likely to experience post-DBS gait worsening; the percentage of tandem missteps at bas