ライフサイエンスコーパス: motor function

1 mulation (DBS) within circuits that modulate motor function.

2 networks necessary for proper cognitive and motor function.

3 s, glial activation, and progressive loss of motor function.

4 l memory, visual-motor integration, and fine motor function.

5 vement cannot readily decouple, compromising motor function.

6 with vitamin A on intelligence, memory, and motor function.

7 lts that questioned the importance of D2R in motor function.

8 i on the brain in relation to motivation and motor function.

9 lamic development, and thereby cognitive and motor function.

10 bers, synaptic plasticity, and cognitive and motor function.

11 cant for basic and clinical understanding of motor function.

12 s of P-loop residues in bacteriophage lambda motor function.

13 illustrating a role for TMEM184b in sensory-motor function.

14 f cerebellar Purkinje cells and a decline in motor function.

15 P binding, and the influence of mechanics on motor function.

16 its are critical modulators of cognitive and motor function.

17 reased anxiety, but had no overall change in motor function.

18 neurons resulting in a catastrophic loss of motor function.

19 , surviving animals did not exhibit abnormal motor function.

20 specific oscillatory dynamics are related to motor function.

21 uced recovery in both neuronal structure and motor function.

22 This loss greatly affects full recovery of motor function.

23 tion, memory, executive function, and visual-motor function.

24 o disease onset and diminished cognitive and motor function.

25 ipheral axons, leading to deficits in distal motor function.

26 erapy-induced ongoing pain without impairing motor function.

27 whereas enhanced expression of VEGF improves motor function.

28 1C to bind Rab6A at both ends, but not KIF1C motor function.

29 on in the brain followed by deterioration in motor function.

30 ear mHTT changed in parallel with decreasing motor function.

31 injury, disease or aging results in impaired motor function.

32 remaining neuronal population and restoring motor function.

33 of the compensatory mechanisms that maintain motor function.

34 icant improvements in vulnerable tissues and motor function.

35 hetic applications aiming to recover loss of motor function.

36 isual ability as well as mobility and visual motor function.

37 opment and degeneration in adulthood impairs motor function.

38 ral ischemia, as well as muscle strength and motor function.

39 deficits in APP/PS1, without altering gross motor function.

40 43, markedly increased survival and improved motor function.

41 on of Kv2.1 expression and an improvement in motor function.

42 ting cognitive development, respiration, and motor function.

43 rategies to achieve tunable and controllable motor function.

44 in brain 9cRA levels and greater recovery in motor function.

45 uces signatures of brain injury and impaired motor function.

46 g silencer (ISS) improves SMN expression and motor function.

47 STN transmission and patterning and improved motor function.

48 nction, episodic memory, working memory, and motor function.

49 eration, alpha-syn aggregates and normalized motor function.

50 tor function and a ladder test to study fine motor function.

51 a range of conformational changes, blocking motor function.

52 branches and dendrites leading to decreased motor function.

53 ly-specific insertions in modulating kinesin motor function.

54 genic networks responsible for two different motor functions.

55 transcriptional regulation to cognitive and motor functions.

56 eech without compromising other cognitive or motor functions.

57 e brain degeneration and results in improved motor functions.

58 highest levels of associative, cognitive and motor functions.

59 tem, demonstrating a critical influence over motor functions.

60 fluence over a myriad array of cognitive and motor functions.

61 3B, but differentially influence how the two motors function.

62 were reading (44% [95% CI, 42%-48%]), visual motor function (38% [95% CI, 36%-42%]), visual informati

63 ndent learning and memory deficits, restores motor function after brain trauma, and decreases brain l

64 nt therapies can lead to partial recovery of motor function after neurological injury.

65 ects promoted axon regeneration and improved motor function after SCI.

66 ern-sensitive spinal plasticity and improves motor function after spinal injury or during neuromuscul

67 erated, there was no decline in cognitive or motor functioning after one year of follow-up.

68 ed on an open-field grid test to study gross motor function and a ladder test to study fine motor fun

69 motor symptoms, selective deletion worsened motor function and accelerated the onset of paralysis.

70 In view of the fundamental aspects of motor function and behavior that depend on the firing of

71 in improved performance in multiple tests of motor function and behavior.

72 onths with progression, correlations between motor function and biomarkers, and hazard ratios analyze

73 cular or respiratory function in addition to motor function and can be performed by trainees with som

74 altered basal ganglia activity disrupt both motor function and cognition.

75 ioral functions such as anxiety, depression, motor function and cognitive function at various acute/s

76 or Afg3l2, exhibits a progressive decline in motor function and displays dark degeneration of Purkinj

77 sized that dorsal striatal p11 might mediate motor function and drug responses in parkinsonian mice.

78 ch was started at disease onset, ameliorated motor function and extended survival.

79 es showed significantly improved recovery of motor function and gait.

80 The relationship between motor function and MR-based structural measurements was

81 ders can lead to permanent loss of voluntary motor function and muscle paralysis.

82 t striatal pathway, which may be relevant in motor function and neurodegenerative diseases.

83 fiber thickness and muscle growth, improves motor function and overall growth and increases lifespan

84 ar junction, delayed disease onset, improved motor function and preserved motor neurons as well as ne

85 -specific caveolin-1 overexpression improves motor function and preserves memory in mice subjected to

86 ally, the PI3K inhibitor wortmannin improved motor function and prolonged lifespan of the Mtm1-defici

87 bilitative training after stroke can improve motor function and promote topographical reorganization

88 the initial membrane depolarization improved motor function and Purkinje neuron morphology in the SCA

89 ressive motor neuron disease causing loss of motor function and reduced life expectancy, for which li

90 fective NMJs might contribute to the loss of motor function and represent a potential therapeutic tar

91 n rural Bangladesh we examined cognitive and motor function and scholastic achievement in a cohort of

92 IBS pathophysiology since they regulate gut motor function and stool consistency, and targeted 5-HT4

93 In addition, motor function and survival were assessed.

94 ) mouse model of ALS (G93A SOD1) would alter motor function and survival.

95 cell activation that precedes the decline of motor function and the onset of hindlimb paralysis.

96 ion is required for regulation of cerebellar motor function and vocal communication, likely through d

97 structure of the plug domain in MotB affects motor functions and allows cells to swim through media o

98 at one end, regions serving primary sensory/motor functions and at the other end, transmodal regions

99 -generated PA in the regulation of kinesin-1 motor functions and breast cancer metastasis and suggest

100 , and may thus participate in the control of motor functions and cognitive processing that are impair

101 -deficient (Nrros(-/-)) mice show defects in motor functions and die before 6 months of age.

102 Appoptosin transduction impaired multiple motor functions and exacerbated neuropathology in tau-tr

103 e overall fundamental contribution of D2R in motor functions and explains some of the side effects el

104 oring its space of parameters and associated motor functions and found that, depending on effective c

105 llum regulates Purkinje cell development and motor functions and vocal communication, demonstrating e

106 ems develop the capacity to coordinate their motor functions and, in turn, if the red nucleus/rubrosp

107 pted alpha-synuclein expression, deficits in motor function, and alterations in neurochemical effects

108 imaging findings, namely cognitive function, motor function, and brain volume (global and regional).

109 the cortex that are essential for language, motor function, and memory, and tractography can reveal

110 life five abcd1 mutants demonstrate impaired motor function, and overall survival to adulthood of het

111 ischemic limb perfusion, capillary density, motor function, and their amputation.

112 f the afferent mechanisms underlying healthy motor function, and their disruption in neurological con

113 e peripheral nervous system is essential for motor function, and uncontrolled SC proliferation occurs

114 unctional domains (reading, mobility, visual motor function, and visual information processing) at ba

115 unctional domains (reading, mobility, visual motor function, and visual information processing) at ba

116 within the thalamus, impaired cognitive and motor functions, and affected self-reports of mood/drug

117 aduodenal leucine on eating, gut hormone and motor functions, and blood glucose in humans.

118 sis, however, experience no deterioration in motor functions, and some can still grasp with their par

119 for Gpr88 in the regulation of cognitive and motor functions, and support its relevance to the pathop

120 These deficits in motivation and motor function are associated with alterations in cortic

121 rotozoa, though modulatory aspects of myosin motor function are distinct.

122 Many cognitive and motor functions are enabled by the temporal representati

123 hysiological deficits, causing impairment in motor function, are largely unknown.

124 ied types of CIMT have beneficial effects on motor function, arm-hand activities, and self-reported a

125 were examined on the subsequent recovery of motor function as assessed by climbing and flight assays

126 The Myo1c motor functions as a cargo transporter supporting variou

127 reational activity intervention in improving motor function, as measured by WMFT.

128 a key role in anxiety-related behaviors and motor function, as well as brain bioenergetics, in a mou

129 is correlated with improved neurological and motor function, as well as with preservation of neuronal

130 found a gene-dosage effect on cognitive and motor function at 15 months of age, as the TgTDP-25(+/+)

131 hereafter and had no impact on cognitive and motor function at 2 y.

132 ntal disability at 18 months and may improve motor function at 5 years.

133 regulation of UNC-104 significantly improves motor function at advanced ages and also mildly extends

134 ights into both filopodia formation and MYO6 motor function at endosomes and at the plasma membrane.

135 rgic neurons in SNpc, and improvement in the motor function at the behavior level of PD mice.

136 How this motor functions at a mechanistic level during motility a

137 tryptamine and vinorelbine enhance regain of motor functions, axonal regrowth, motor neuron survival

138 piratory and muscle physiology, which impact motor function behaviours.

139 o the effects of age and oxidative stress on motor function between 7 and 35 days of age.

140 omponents represent expressions of different motor functions, both pertinent to the control of bipeda

141 tACS can modulate perception, cognition, and motor function but the underlying neural mechanism is po

142 presents a promising intervention to improve motor function by decreasing neuromotor noise after perf

143 study were to assess the effects produced on motor function by different DMD genotypes and early init

144 no or only mild gross motor deficits (Gross Motor Function Classification in MLD level 0 or 1) and a

145 rtality, loss of gross motor function (Gross Motor Function Classification in MLD), loss of any langu

146 ment III cognitive score less than 70, Gross Motor Function Classification System (GMFCS) level of 3

147 d modifiable lifestyle factors for all Gross Motor Function Classification System (GMFCS) levels (I-V

148 ommunication devices for people with limited motor function.Clinical Trial No: NCT00912041.

149 nergy and endocrine homeostasis, sensory and motor functions, cognition, and attention, which are all

150 h diverse psychological processes, including motor function, cognitive control, affect, and social co

151 tment of symptomatic mice with ASO7 improved motor function compared to saline-treated mice.

152 with lower capillary density and poorer limb motor function compared with wild type littermates.

153 tion and preceded physiologically measurable motor function decline.

154 , as evidenced by differences in the rate of motor function decline.

155 riata of transgenic R6/2-J2 HD mice as their motor function declined.

156 ing human pathology, none displayed profound motor function defects.

157 nd point, 1-month overall response regarding motor function defined as improvement or no further prog

158 Thirty-day postinjury motor function determined by CatWalk (Noldus Information

159 FTY720 significantly reduced the deficit of motor function, diminished the loss of tyrosine hydroxyl

160 TORC1 blockade reduced lesion size, improved motor function, dramatically decreased production of pro

161 Explanations for the improved motor function during RBD episodes are evaluated in ligh

162 that the deleterious effects of oxidation on motor function early in life are the result of a singula

163 Human motor function emerges from the interaction between the

164 d risk of poor executive function and visual motor function, even if not detected clinically, and may

165 s Off) on working memory (F=0.75, p=0.39) or motor function (F=0.22, p=0.69) when performed under sin

166 hortly after exposure (30 min), and impaired motor functions (falls: +83%; time top: -43%; time botto

167 etained 50% more neurons and maintained full motor function far beyond the lifespan of mice fed ad li

168 Gross motor function, feeding method, energy intake, and HPA l

169 ys likely contribute to the recovery of hand motor function following spinal cord injury (SCI).

170 within the central nervous system to restore motor function following spinal cord injury, the role of

171 splantation-related mortality, loss of gross motor function (Gross Motor Function Classification in M

172 ease (PD) patients experience loss of normal motor function (hypokinesia), but can develop uncontroll

173 Although motor function impairment occurs in all patients with AS

174 teral parietal cortices also correlated with motor function improvement, consistent with the increase

175 vivo effect on the lifespan, body weight and motor function in a mouse HD model.

176 Here, we show tunable rescue of motor function in a mouse model of PD, following transpl

177 moter screen, prolongs survival and improves motor function in a mouse model of spinal muscular atrop

178 We find that S107 is able to restore motor function in aging Drosophila to young levels, and

179 omoting mechanisms can substantially improve motor function in ALS and importantly, that augmenting v

180 key factor in the detrimental outcome of the motor function in amyotrophic lateral sclerosis.

181 PDE4 inhibitors significantly improved motor function in Cln3(Deltaex7/8) mice, attenuated glia

182 g the idea that the age-dependent decline in motor function in Drosophila requires FK506-BP2 function

183 re, FliL does not play a significant role in motor function in E. coli.

184 ent a novel therapeutic target for improving motor function in humans with paralysis due to spinal co

185 ular, might be a good approach for enhancing motor function in instances where neuromuscular communic

186 Motor function in mammalian species depends on the matur

187 The prognosis for recovery of motor function in motor complete spinal cord injured (SC

188 r symptoms and/or delay the deterioration of motor function in movement disorders by blocking aberran

189 , and may help optimize therapies to restore motor function in patients with neuromuscular disorders

190 alyses suggest that olesoxime might maintain motor function in patients with type 2 or type 3 SMA ove

191 ry outcomes in intervention trials targeting motor function in populations with chronic stroke.

192 ed significant improvements in life span and motor function in Ppt1(-/-) mice.

193 so participate in maintaining a low level of motor function in severely impaired patients.

194 The ability to improve motor function in spinal cord injury patients by reactiv

195 its correlation to brain atrophy, as well as motor function in the 18-week-old N171-82Q HD mice.

196 n reactivate the spinal CPGs and improve the motor function in the absence of descending supraspinal

197 acological treatment acutely restored normal motor function in the ataxic mice.

198 In patients, reduced motor function in the right upper and lower limb was ass

199 Although both isoforms had ill effects on motor function in transgenic flies and decreased neurite

200 riod, attenuating inflammation and improving motor function in vivo.

201 npp5f-null mice exhibit enhanced recovery of motor functions in both open-field and rotarod tests.

202 mechanisms associated with visceral pain and motor functions in health and functional gastrointestina

203 rotransmitters, and continuous impairment of motor functions in MPTP-intoxicated mice.

204 zed striatal neurotransmitters, and improved motor functions in MPTP-intoxicated mice.

205 cance of lobules implicated in cognitive and motor functions in normal subjects.

206 r, perceptions, emotions, innate drives, and motor functions in species ranging from flies to nonhuma

207 rming experiments to assess the integrity of motor functions in the intact spinal cord and the cord t

208 , an important modulator of both sensory and motor functions in the mammalian spinal cord, originates

209 Myosin-Ic (Myo1c), a nonprocessive actin motor, functions in a variety of exocytic events, althou

210 Both motors function in P-cell nuclear migration, but dynein,

211 ioral performance, including both memory and motor functions, in FIV(+) animals.

212 ersive learning as well as markedly affected motor function including disordered coordination.

213 the VT4R was identified in nuclei related to motor function, including the oculomotor complex and mot

214 entiation of subsets of CThPN specialized in motor function, indicating that Fog2 coordinates subtype

215 uctuations while leaving basic cognitive and motor functions intact.

216 ion, a R502P amino acid substitution, on the motor function is unclear.

217 ance, yet its impact on human cardiac myosin motor function is unclear.

218 The capacity to coordinate sensory and motor functions is demonstrated in awake, behaving rats,

219 t the role of the subthalamic nucleus in non-motor functions is needed.

220 was used to identify lobules associated with motor function, language, executive function, memory, ve

221 t pan-neural loss of Rai1 causes deficits in motor function, learning, and food intake.

222 xpectedly, none of these approaches improved motor function, lifespan and motoneuron survival.

223 s and near point of convergence (NPC) ocular-motor function may be useful in delineating traumatic br

224 groups in functional domains 1 and 2 of the Motor Function Measure (MFM D1 + D2) assessed in the ful

225 ing ischemic stroke, ubqln Tg mice recovered motor function more rapidly than did the WT mice.

226 sive manganese accumulation was the impaired motor function observed in the Zip14 KO mice.

227 uting the largest effect of a tubulin PTM on motor function observed to date.

228 in all eight survivors, but deterioration of motor function occurred in the majority (n = 5).

229 and 5 years conferred an additional gain in motor function of 3 units/year (1.3 raw units) up to age

230 lopodial tips was hampered by the diminished motor function of a dimeric construct of the shaker-1 mu

231 iguingly S1P completely stops the decline of motor function of HD model mice even after the onset of

232 The motor function of the spinal cord requires the computati

233 exocytosis in MB neurons and alters specific motor functions of 1-year-old male mice.

234 tention control are also seen on lower level motor functions of dexterity and strength-by examining r

235 echanisms in appetite regulation include the motor functions of the stomach, such as the rate of empt

236 tance of ERK/MAPK signaling in governing the motor functions of the striatal direct and indirect path

237 This intervention reduced the impairment in motor function on forced tasks, such as rotarod and trea

238 wn of alpha-synuclein by ~35% did not affect motor function or cause degeneration of nigral dopaminer

239 How specific myosin variants alter motor function or clinical expression of disease remains

240 tation program did not significantly improve motor function or recovery beyond either an equivalent o

241 induce motor neuron degeneration, defects in motor function, or altered survival.

242 on any secondary peripheral nerve or central motor function outcome, or on cognitive function or clin

243 ia, with evidence of clinical improvement of motor function over time in the surviving patient.

244 faster and more complete recovery of forepaw motor function (P < 0.05).

245 ed (p=0.002), executive function (p<0.0001), motor function (p<0.0001), and working memory (p=0.001).

246 the domains of episodic memory (p=0.03) and motor function (p=0.02).

247 cedented increase in life span with improved motor function, persistent GALC expression, nearly norma

248 lowered ER stress and prevented the loss of motor function, providing proof of principle that small

249 blood draw, clinical assessment of strength, motor function, quality of life, and adverse effect asse

250 ge (r = 0.29, P = .04 for cortical GMV), and motor functioning (r >/= 0.29, P < .05 for all tissues).

251 nt Test of Neuromuscular Disorders) scale of motor function (ranging from 0 to 64, with higher scores

252 d RR, 2.32; 95% CI, 1.17 to 4.59) and visual motor function (RD, 0.03; 95% CI, 0.01 to 0.06 and RR, 3

253 study, we observed a significant spontaneous motor function recovery 14 to 28 days after spinal cord

254 dependent fear learning and memory, improved motor function recovery, and decreased brain lesion volu

255 antly increased and decreased, respectively, motor function recovery.

256 and improve outcome, as reflected by better motor function, reduced brain lesion volume, and diminis

257 PPAR-delta using the agonist KD3010 improved motor function, reduced neurodegeneration and increased

258 ing leads to pathway-specific alterations in motor function, reduced neuronal excitability, and the i

259 We assessed motor function regularly for 6 months after stroke and t

260 bserved during RBD episodes exhibit improved motor function, relative to baseline states during wake

261 The inhibition of small intestinal motor function represents a novel mechanism by which exe

262 dverse effects on brain regions that control motor function, resulting in tremor, rigidity, and gait

263 cts of liraglutide versus placebo on gastric motor functions, satiation, satiety, and weight in obese

264 Infant motor function scales (Test of Infant Motor Performance

265 Motor function scores (MFS) and compound muscle action p

266 ones (p<0.0001), improvements in CHOP-INTEND motor function scores (p=0.0013), and increased compound

267 t includes 11 items assessing fine and gross motor function, sensation, and balance to produce a tota

268 deficits in mitochondrial bioenergetics and motor function.SIGNIFICANCE STATEMENT The present work p

269 d disability scale evaluating fine and gross motor function, strength, sensation, and balance.

270 e in structures with a more direct impact on motor function, such as deep layers of the contralateral

271 measured by total time to complete the Wolf Motor Function Test (WMFT) at the end of the 2 week inte

272 was 12-month change in log-transformed Wolf Motor Function Test time score (WMFT, consisting of a me

273 r Extremity and Lower Extremity scales, Wolf Motor Function Test, Action Research Arm Test, Ten-Meter

274 est of Neuromuscular Disorders (CHOP-INTEND) motor function test, and compound motor action potential

275 Progress was assessed by monthly sensory and motor function tests during routine clinic visits and wi

276 achievement of motor milestones, and better motor function than in historical cohorts.

277 likely to be alive and have improvements in motor function than those in the control group.

278 mulation of D1 receptors is known to enhance motor function, the global effect of D2 receptor (D2R) s

279 rior zone was associated preferentially with motor function, the middle zone with cognitive control,

280 d change from baseline of two assessments of motor function: the motor milestones portion of the Hamm

281 intensely investigated in relation to their motor functions, they are also consistently reported in

282 tants completely restores the sensitivity of motor function to both age and oxidative stress, support

283 achine interfaces (BMIs) aim to restore lost motor function to people with neurological deficits by d

284 l known to play a key role in the control of motor function via balanced output from the indirect (iS

285 Motor function was altered, and specific effects were fo

286 hologically, the improvement in lifespan and motor function was associated with a reduction in brain

287 hibitory control, cognitive flexibility, and motor functioning was applied at baseline and one year a

288 At 1 month, overall response rates regarding motor function were 87.2% after 4 Gy x 5 and 89.6% after

289 on, executive function, visual function, and motor function were assessed at 4.5 years.

290 Disruptions in motor function were associated with increases in cerebel

291 IQ, language, and motor function were measured at 7 years.

292 ne induction in adulthood, deficits in gross motor function were seen in NeuroAR mice, but not MyoAR

293 pectively.General intelligence or memory and motor functions were not affected by antenatal or newbor

294 ectrical stimulation can promote recovery of motor function when applied late after injury and that m

295 sed on a well-supported theory of cerebellar motor function, which ascribes to the cerebellum a role

296 a promising PD therapeutic target to improve motor function while reducing l-dopa-induced dyskinesias

297 cted effect of ageing on episodic memory and motor function with advanced stages of HIV infection sug

298 ced dramatic and synergistic improvements in motor function with an unprecedented increase in life sp

299 kinson's disease (PD) patients and linked to motor function, with beta activity considered antikineti

300 ed important insights, dissecting collective motor functions within living cells still remains challe