ライフサイエンスコーパス: motor dysfunction

1 or diagnosis of intensive care unit-acquired motor dysfunction.

2 15T, or M337V TDP-43 transgenes cause severe motor dysfunction.

3 early-onset and progressive neurological and motor dysfunction.

4 A accelerated neurodegeneration and worsened motor dysfunction.

5 inating in both gastrointestinal sensory and motor dysfunction.

6 oning the medial forebrain bundle attenuated motor dysfunction.

7 isease and can be an onset symptom preceding motor dysfunction.

8 e inflammation, decreased nerve function and motor dysfunction.

9 this combination produced dopamine loss and motor dysfunction.

10 erized by severe neurological impairment and motor dysfunction.

11 and visual tests, but not by the severity of motor dysfunction.

12 or cortex were correlated with the extent of motor dysfunction.

13 s of aging including skin, bone, immune, and motor dysfunction.

14 ed that loss of ICC could be responsible for motor dysfunction.

15 CC may be responsible for the development of motor dysfunction.

16 with the persistence of neuropathic pain and motor dysfunction.

17 ng muscarinic blockade were not due to gross motor dysfunction.

18 uting a low GBEF value to an irreversible GB motor dysfunction.

19 totic neurons resulted in symptoms of severe motor dysfunction.

20 opamine synthesis prevents the appearance of motor dysfunction.

21 bit normal hippocampal function but moderate motor dysfunction.

22 ich contributes to parkinsonian activity and motor dysfunction.

23 gra pars compacta (SN) leads to debilitating motor dysfunction.

24 pamine levels, and consequent extrapyramidal motor dysfunction.

25 e characterized by cognitive, behavioral and motor dysfunction.

26 aracteristic neuropathology, and progressive motor dysfunction.

27 retardation, absence of speech, seizures and motor dysfunction.

28 contribute to the clinical manifestations of motor dysfunction.

29 pears rigid and inflexible, exacerbating the motor dysfunction.

30 in HIV-infected subjects with cognitive and motor dysfunction.

31 characterized by loss of myelin and clinical motor dysfunction.

32 progressive multiple sclerosis ameliorating motor dysfunction.

33 se clinical features including cognitive and motor dysfunction.

34 ture, reduced ATP production, and flight and motor dysfunction.

35 udate nucleus were inversely correlated with motor dysfunction.

36 is frequently associated with cognitive and motor dysfunction.

37 nd mild social interaction deficits, but not motor dysfunction.

38 n effects on clinical measures of apathy and motor dysfunction.

39 bute to behavioral deficits in AS, including motor dysfunction.

40 compacta and age-dependent L-DOPA-sensitive motor dysfunction.

41 and communication, stereotypic behaviors and motor dysfunction.

42 cturnal activity but are fertile and show no motor dysfunction.

43 ration independently predicted cognitive and motor dysfunction.

44 xon regeneration often result in devastating motor dysfunction.

45 ated cannabinoid withdrawal, hypothermia, or motor dysfunction.

46 Mecp2-null mice in dopamine deregulation and motor dysfunction.

47 pamine levels, and consequent extrapyramidal motor dysfunction.

48 le atrophy, and debilitating and often fatal motor dysfunction.

49 hic neuronal loss that leads to cognitive or motor dysfunction.

50 r that results in debilitating cognitive and motor dysfunction.

51 neuron loss was observed in cases with major motor dysfunction.

52 elease dopamine formulations) for addressing motor dysfunction.

53 survivors of TBI are cognitive deficits and motor dysfunction.

54 f midbrain dopaminergic neurons resulting in motor dysfunction.

55 educing the risk of cerebral palsy and major motor dysfunction.

56 outputs and thereby contribute to PD-related motor dysfunctions.

57 urodegenerative diseases are associated with motor dysfunction, a powerful readout for the disease.

58 2 in the writhing assay and without inducing motor dysfunction after sc administration in mice.

59 over, mod2B administration markedly improved motor dysfunction and a prolonged lifespan in Sandhoff d

60 Paroxetine attenuated motor dysfunction and body weight loss and improved gluc

61 ient in betaPP survive and breed but exhibit motor dysfunction and brain gliosis, consistent with a p

62 orated multiple RTT-like features, including motor dysfunction and breathing irregularities, in both

63 Although CCI induced significant motor dysfunction and cognitive deficits, no differences

64 Motor dysfunction and cognitive impairment, suggested by

65 ams contribute to altered neural maturation, motor dysfunction and death.

66 e been shown to correlate with cognitive and motor dysfunction and deficits in social behavior.

67 3 protein in Drosophila motor neurons led to motor dysfunction and dramatic reduction of life span.

68 ng neuronal loss, mitochondrial enlargement, motor dysfunction and early death.

69 eads to neurological debilitation, including motor dysfunction and frank dementia.

70 The phenotype includes smooth muscle motor dysfunction and hypertensive sphincter resulting f

71 as to determine whether lack of awareness of motor dysfunction and lack of insight into mental dysfun

72 lated pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity.

73 expression in SCA1 Purkinje neurons improves motor dysfunction and partially restores Purkinje neuron

74 iptomic dysregulation even after substantial motor dysfunction and pathology were observed.

75 lateral sclerosis (ALS), before the onset of motor dysfunction and remains at the high levels through

76 Loss of Pum1 caused progressive motor dysfunction and SCA1-like neurodegeneration with m

77 early lethality and precipitates age-related motor dysfunction and stress sensitivity, that is rescue

78 The disconnect between motor dysfunction and symptoms continues to promote care

79 erative disease characterized by progressive motor dysfunction and the loss of large motor neurons in

80 We examined cognitive and motor dysfunction and the relationship of behavior defic

81 These mice developed motor dysfunctions and progressive neurodegeneration in

82 apoptotic protease activation), behavioral (motor dysfunction), and metabolic (glucose intolerance a

83 sorders characterized by mental retardation, motor dysfunction, and autistic behaviors.

84 roblems, including behavioral abnormalities, motor dysfunction, and dementia.

85 ed with developmental delay, lack of speech, motor dysfunction, and epilepsy.

86 notypes, including developmental regression, motor dysfunction, and learning and memory deficits.

87 at birth, but subsequently developed severe motor dysfunction, and perished at approximately 3 weeks

88 opathic effects including neurodegeneration, motor dysfunction, and premature death.

89 CS all lead to juvenile lethality, profound motor dysfunction, and significantly reduced Na(+) chann

90 cterized by autism, intellectual disability, motor dysfunction, anxiety, epilepsy, recurrent respirat

91 her regions of the brain, and additional non-motor dysfunctions are common.

92 t seek the mechanisms by which cognitive and motor dysfunctions arise from cerebellar degeneration.

93 pha-synuclein (alphaSyn), often resulting in motor dysfunction as exemplified by Parkinson's disease

94 histological evidence of cord damage and in motor dysfunction assessed 4 weeks later.

95 Recent studies suggest that motor dysfunction associated with the chronic nonphysiol

96 5 mg/kg) significantly attenuated neurologic motor dysfunction at 24 h (p<0.01) and 2 weeks (p<0.05)

97 el evidence for the existence of subclinical motor dysfunction at a pre-clinical stage of SCA6.

98 movement test robustly detected significant motor dysfunction at day 1, 3, and 7 post-injury that po

99 ema had significantly greater frequencies of motor dysfunction at follow-up compared with patients in

100 g is initially normal but, with the onset of motor dysfunction, becomes disrupted, accompanied by abn

101 ter injury is often accompanied by orofacial motor dysfunction, but little is known about the structu

102 Dopaminergic dysregulation can cause motor dysfunction, but the mechanisms underlying dopamin

103 he striatum precedes symptoms in a number of motor dysfunctions, but it is unclear whether this is pa

104 hanges in dopamine release may contribute to motor dysfunctions characterizing senescence.

105 ed children suffer from blindness, epilepsy, motor dysfunction, cognitive decline, and premature deat

106 ated with an increased risk of cognitive and motor dysfunction, dementia, depression, and stroke.

107 degenerative disease characterized by severe motor dysfunction due to progressive degeneration of mes

108 Motor dysfunction (e.g., bradykinesia) and motivational

109 e treatment did result in significantly less motor dysfunction, even when no differences in levels of

110 randial colonic tone are reduced, reflecting motor dysfunctions, even in NTC.

111 Limited motor dysfunction (Expanded Disability Status Scale scor

112 atal mice recapitulates SMA-like progressive motor dysfunction, growth impairment, and shortened life

113 ed-G59S mutant dynactin p150(Glued) develops motor dysfunction >8 months before loss of motor neurons

114 Brainstem or motor dysfunction had resolved in 44 of 57 (77%) at 2 mo

115 treatment) remains unknown, although spastic motor dysfunction has been related to the hyperexcitabil

116 nt transgenic rats exhibit L-DOPA-responsive motor dysfunction, impaired striatal dopamine release as

117 NS, and delayed the onset and progression of motor dysfunction, improved body weight gain and surviva

118 n homolog significantly improves Htt-induced motor dysfunction in a fly model of HD.

119 n the severity of neurochemical deficits and motor dysfunction in a primate model of Parkinson's dise

120 ramatically protected from neurotoxicity and motor dysfunction in a striatal-specific model of HD eli

121 tion in early stages and results in moderate motor dysfunction in adulthood.

122 chronic gastric hypersensitivity and gastric motor dysfunction in adults even in the absence of signi

123 rain abnormality that not only contribute to motor dysfunction in autism, but also deficits in social

124 on represents the first neuroimaging data of motor dysfunction in children with autism, providing ins

125 ucidating how these mechanisms contribute to motor dysfunction in conditions such as cerebral palsy a

126 nd identifies key mechanisms contributing to motor dysfunction in conditions such as cerebral palsy a

127 the present study we sought to characterize motor dysfunction in CRPS patients using kinematic analy

128 The spectrum of gastric motor dysfunction in diabetes mellitus continues to be e

129 es depletion of neurotransmitters and severe motor dysfunction in infants and children.

130 ve, late onset neuromuscular disease causing motor dysfunction in men.

131 ingERp57 in the nervous system led to severe motor dysfunction in mice associated with a loss of neur

132 tically protected from neurodegeneration and motor dysfunction in mouse models of HD.

133 receptors contributes to the pathogenesis of motor dysfunction in Parkinson's disease.

134 ta-band oscillations, imbalanced firing, and motor dysfunction in Parkinson's disease.

135 ht have the potential not only to ameliorate motor dysfunction in PD patients but also to modify dise

136 In addition to the well known motor dysfunction in PD patients, cognitive deficits and

137 ss of locus coeruleus neurons contributes to motor dysfunction in PD.

138 mice provides a model for understanding the motor dysfunction in POMA.

139 -12 months, transgenic mice began to display motor dysfunction in rotarod testing.

140 rade axonal transport may critically mediate motor dysfunction in SBMA, but the site(s) where AR disr

141 sgenic mouse model that develops progressive motor dysfunction in the absence of protein aggregation

142 ibitors can significantly delay the onset of motor dysfunction in the SOD1-G93A transgenic mouse mode

143 L-DOPA treatment improves motor dysfunction in these "MitoPark" mice, but this dec

144 The stress-induced motor dysfunction in V408A mice is similar to that of fa

145 c, deletion of Scyl1 was sufficient to cause motor dysfunction, indicating that SCYL1 acts in a neura

146 was to characterize the effect of FLX on the motor dysfunctions induced by a low dose of TBZ (0.75 mg

147 cy (m-/p+) for Ube3a resembles human AS with motor dysfunction, inducible seizures, and a context-dep

148 Motor dysfunction is an important cause of oropharyngeal

149 Assessment of colonic motor dysfunction is rarely done because of inadequate m

150 Motor dysfunction is usually caused by weakness and the

151 a disorder associated with breast cancer and motor dysfunction, is a neuron-specific nuclear RNA bind

152 is effective in the short-term in relieving motor dysfunction, it does not stop the progressive disa

153 lateral sclerosis (ALS), display progressive motor dysfunction leading to paralysis and premature dea

154 f age, the Gigyf2(+/-) mice begin to exhibit motor dysfunction manifested as decreased balance time o

155 ons, underlying diseases, and rectal sensory-motor dysfunction may all contribute to its increased pr

156 Motor dysfunction may also accompany this condition.

157 f ALS-related phenotypes including kyphosis, motor dysfunctions, muscle weakness/atrophy, motor neuro

158 vous system of mice was sufficient to induce motor dysfunction, neurodegeneration, mitochondrial abno

159 earning and memory deficits) and peripheral (motor dysfunction) neurotoxic effects at concentrations/

160 ted loss and atrophy of striatal neurons and motor dysfunction, normalized expression of the striatal

161 azepine, and tamoxifen could also rescue the motor dysfunction of 7-mo-old FTLD-U mice.

162 hat recapitulate the disease progression and motor dysfunction of HD also exhibit sleep and circadian

163 of the subthalamic nucleus in mediating the motor dysfunction of Parkinson's disease and for pioneer

164 procedure that has been shown to reduce the motor dysfunction of patients with advanced Parkinson's

165 y extended lifespan and delayed the onset of motor dysfunction of SOD1 mutants, suggesting that Bax a

166 c diseases frequently experience sensory and motor dysfunctions of the urinary bladder.

167 e any ALS-related disease phenotypes such as motor dysfunction or decreased lifespan.

168 ved vehicle continued to exhibit significant motor dysfunction (P< 0.01).

169 in cortical layer V and spinal ventral horn, motor dysfunction, paralysis, and death.

170 auses motor neuron degeneration, progressive motor dysfunction, paralysis, and death.

171 's disease is a genetic disorder that causes motor dysfunction, personality changes, dementia, and pr

172 tein also exhibit neurodegenerative changes, motor dysfunction, perturbed energy metabolism, and elev

173 oth the hyperactive and hypoactive phases of motor dysfunction preceded the detection of nuclear micr

174 ion of the drug repaglinide delayed onset of motor dysfunction, reduced striatal atrophy, and prolong

175 s associated with increased vulnerability to motor dysfunction secondary to dopamine depletion.

176 chronic gastric hypersensitivity and gastric motor dysfunction seen in FD patients can be modeled in

177 -1 and GlyR alpha2 pre-mRNA may underlie the motor dysfunction seen in POMA.

178 rodegeneration characterized by vision loss, motor dysfunction, seizures, and often early death.

179 stic features of macrocephaly, cognitive and motor dysfunction, subcutaneous and visceral lipomas and

180 MKK7 cKO mice at 8 months showed motor dysfunctions such as weakness of hind-limb and gai

181 t was initiated before or after the onset of motor dysfunction, suggesting a potential for such antid

182 A steady progression of motor dysfunction takes place in Huntington's disease (H

183 y event in SMA and may be a primary cause of motor dysfunction that is amenable to therapeutic interv

184 d that Atp13a2 null mice develop age-related motor dysfunction that is preceded by neuropathological

185 The relation of esophageal motor dysfunction to outcomes from antireflux surgery re

186 In addition, motor dysfunction was markedly accelerated in G93A SOD1

187 Neurotoxicity (primarily grade 1 motor dysfunction) was reported in 14% patients and corr

188 lity solely to the patient's environment and motor dysfunction, we investigate whether a secondary fu

189 tage of disease, Purkinje cell pathology and motor dysfunction were completely reversible.

190 Motor dysfunctions were chiefly associated with the ante

191 ts in the immune system and gastrointestinal motor dysfunctions, whereas in an initial study we showe

192 mplex, with its characteristic cognitive and motor dysfunction, which is caused by HIV itself.

193 f CP, defined as a nonprogressive congenital motor dysfunction with hypertonia or dyskinesia.

194 peats manifested progressive behavioural and motor dysfunction with neuron loss and gliosis in striat

195 fts, resulting in significant improvement in motor dysfunctions without tumor formation.