ライフサイエンスコーパス: stutter

1 on where the TW is intermittently halted or "stuttered".

2 gations of speech production in children who stutter.

3 anguage areas in a group of young people who stutter.

4 ganglia or excessive dopamine in people who stutter.

5 llum in the fluent utterances of persons who stutter.

6 in enabling fluent utterances in persons who stutter.

7 in the speech neural networks of adults who stutter.

8 fluent speech production in individuals who stutter.

9 ; and (2) the high rate of STR amplification stutter.

10 us) are also present in younger children who stutter.

11 ajor perisylvian brain areas in children who stutter.

12 ta examining neural networks in children who stutter.

13 arly phases of symptom onset in children who stutter.

14 and also by deletions that remove the heptad stutter.

15 al premotor cortex was reduced in people who stutter.

16 functional imaging studies in developmental stuttering.

17 at implicate auditory processing problems in stuttering.

18 tudy of children and adults with and without stuttering.

19 anguage tasks designed to evoke or attenuate stuttering.

20 persons who stutter, even in the absence of stuttering.

21 ts in unrelated Cameroonians with persistent stuttering.

22 that may lead to recovery versus persistent stuttering.

23 product of a gene previously associated with stuttering.

24 s in intracellular trafficking in persistent stuttering.

25 disorder, specific language impairment, and stuttering.

26 vity of the circuit might be associated with stuttering.

27 so increased syllable repetitions similar to stuttering.

28 have examined the neural bases of childhood stuttering.

29 en identified in individuals with persistent stuttering.

30 7 children [40 controls (20 females), 37 who stutter (16 females)] between 3 and 10 years of age.

31 cluded 252 individuals exhibiting persistent stuttering, 45 individuals classified as recovered from

32 e hypothesis for signaling across the heptad stutter adjacent to the HAMP domain in methyl-accepting

33 Stuttering affects nearly 1% of the population worldwide

34 erconnect them, differ in young children who stutter (aged 3-9 years) compared with age-matched peers

35 as removal of separated heptads and presumed stutters also resulted in signal reversion.

36 Stuttering, also known as stammering, has been linked to

37 mple method of correction for the effects of stutter and differential amplification on the analysis o

38 %-3.2%) when marker-specific corrections for stutter and differential amplification were performed.

39 perm DNA were largely the consequence of PCR stutter and not mutations.

40 ohorts were studied: 10 right-handed men who stuttered and 10 right-handed, age- and sex-matched non-

41 Thirty-two children (16 stuttering and 16 controls) aged 7-11 years participated

42 and adolescents aged 5 to 17 years (22 with stuttering and 25 without) and 47 adults aged 21 to 51 y

43 ) and 47 adults aged 21 to 51 years (20 with stuttering and 27 without) were recruited between June 2

44 tively correlated with syllables in both the stuttering and control cohorts.

45 The mean (SD) ages of those in the stuttering and control groups were 12.2 (4.2) years and

46 lies, some members of which had nonsyndromic stuttering and in unrelated case and control subjects fr

47 For both stutters and syllables, the brain regions that were corr

48 45 individuals classified as recovered from stuttering, and 19 individuals too young to classify.

49 cal correlates including conduction aphasia, stuttering, and aspects of schizophrenia.

50 the neuroanatomical bases of early childhood stuttering, and possible white matter developmental chan

51 l disorders, including poor vocal imitation, stuttering, and progressive syntax and syllable degradat

52 g-held theories that the brain correlates of stuttering are the speech-motor regions of the non-domin

53 eats (SSRs), sometimes described as genetic 'stutters,' are DNA tracts in which a short base-pair mot

54 luding application of correction methods for stutter artifact and preferential amplification.

55 hich give distinct bands with no increase in stutter artifact on di-, tri-, and tetranucleotide repea

56 allele stacking; and differentiation of PCR stutter artifacts from true alleles.

57 inherent ability of the viral polymerase to stutter at the poly(U) stretch of a viral RNA template d

58 s, is believed to polyadenylate the mRNAs by stuttering at a stretch of five to seven uridine residue

59 e high processivity of the enzyme eliminates stuttering at homopolymer tracts.

60 miting GTP (1 microM) resulted in polymerase stuttering at the 3' margin of the T-run, immediately pr

61 n who stutter demonstrates that in childhood stuttering, atypical functional organization for speech

62 lleles of the STR locus vWA reveals that the stutter band lacks one repeat unit relative to the main

63 main allele band; this is referred to as the stutter band.

64 Sequence analysis of the main and stutter bands for two sample alleles of the STR locus vW

65 , the discrimination of true alleles versus "stutter bands," and the use of radionucleotides in detec

66 trophysiological techniques reveal the often-stuttering behavior of single pores in non-neuronal cell

67 parisons identified other examples of heptad stutters between a HAMP domain and a contiguous coiled-c

68 n GNPTAB occurred in unrelated subjects with stuttering but not in control subjects.

69 er a missense mutation associated with human stuttering causes vocal or other abnormalities in mice.

70 degree of heterogeneity in transmission from stuttering chain data have important applications in dis

71 lamocortical networks develop differently in stuttering children, which may in turn affect speech pla

72 syllable rate were far more extensive in the stuttering cohort than in the control cohort, which sugg

73 namic responses in the group of children who stutter compared to the control group.

74 Our observations suggest a model of "stuttering conduction": repeated action potential stimul

75 nd 10 right-handed, age- and sex-matched non-stuttering controls.

76 reotypy seen in crystallized song, including stuttering, creation, deletion and distortion of song sy

77 connected speech production in children who stutter demonstrates that in childhood stuttering, atypi

78 This spectroscopy study of stuttering demonstrates brainwide neurometabolite altera

79 inuous coiled-coil marked by a heptad repeat stutter discontinuity at the distal boundary of HD2.

80 d the possible neural bases of developmental stuttering during childhood.

81 Therefore, stutter elements may be broadly important for HAMP funct

82 ay be fundamentally different in persons who stutter, even in the absence of stuttering.

83 gyrus and left premotor cortex, children who stutter exhibited deactivation over these left hemispher

84 Children who stutter exhibited significantly reduced fractional aniso

85 te stimulus intensities, showed irregular or stuttering firing patterns.

86 3) fast-firing interneurons (n = 10), and 4) stutter-firing interneurons (n = 14).

87 monstrated that over 60% of burst-firing and stutter-firing interneurons also expressed the calcium-b

88 Moreover, we demonstrate that the burst- and stutter-firing patterns positively correlate with PV(+)

89 purely to impairments in the motor system as stuttering frequency is increased by linguistic factors,

90 uishing technical error due to amplification stutter from somatic STR mutations.

91 the hypothesis that the genetic component to stuttering has significant sex effects.

92 Results showed that children who stutter have attenuated connectivity in neural networks

93 of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postu

94 ed in this disorder, and previous studies of stuttering have identified linkage to markers on chromos

95 f evidence suggest a genetic contribution to stuttering; however, the complex inheritance of this dis

96 tion of one to three heptads plus a presumed stutter, i.e. 1, 2, or 3 x 7 + 4 amino acids, is require

97 Affecting 1% of the general population, stuttering impairs the normally effortless process of sp

98 3 and 332, on the amino-terminal side of the stutter in helix 2B, which is involved in heterotypic as

99 er interaction within the complex involved a stutter in the TACC3 coiled-coil and a proposed novel si

100 t co-segregate with persistent developmental stuttering in a large Cameroonian family, and we observe

101 NPT [EC 2.7.8.15]), that was associated with stuttering in a large, consanguineous Pakistani family.

102 rther intimate neurometabolic aberrations in stuttering in brain circuits subserving self-regulation

103 study indicates a possible partial basis of stuttering in circuits enacting self-regulation of motor

104 ctural connectivity deficits in children who stutter, in interrelated neural circuits that enable ski

105 or linkage of the broader diagnosis of "ever stuttered" (including both persistent and recovered stut

106 -of-function variants, in AP4E1 in unrelated stuttering individuals in Cameroon, Pakistan, and North

107 igher in unrelated Pakistani and Cameroonian stuttering individuals than in population-matched contro

108 Stuttering induced widespread overactivations of the mot

109 Apart from 34 of these patients who had a stuttering infarction and were referred for reperfusion,

110 calcium spikes, whereas X94 GFP+ cells were stuttering interneurons with quasi fast-spiking properti

111 Stuttering is a common and sometimes severe communicatio

112 Stuttering is a common, highly heritable neurodevelopmen

113 Thus stuttering is a disorder affecting the multiple neural s

114 Stuttering is a disorder of unknown cause characterized

115 Our data support the conclusion that stuttering is a disorder related primarily to disruption

116 Developmental stuttering is a neuropsychiatric condition of incomplete

117 Stuttering is a speech disorder long recognized to have

118 Susceptibility to nonsyndromic stuttering is associated with variations in genes govern

119 Though stuttering is manifest in its motor characteristics, the

120 The cause of stuttering is unknown.

121 This stuttering-like behavior started at one month, and impro

122 oning, or relief of myocardial ischemia in a stuttered manner, has been shown to reduce infarct size,

123 t in its motor characteristics, the cause of stuttering may not relate purely to impairments in the m

124 These results support a stuttering mechanism for the polyadenylation of influenz

125 tates from a processive elongation mode to a stuttering mode for polyadenylation to one in which no t

126 distance distribution, as well as a sequence stutter model, in a probabilistic framework to infer rep

127 vocalizations of pups with the human Gnptab stuttering mutation compared to littermate controls.

128 asses exhibited regular firing and irregular stuttering of action potential clusters, tufted cells de

129 and of the narrower diagnosis of persistent stuttering on chromosome 15 (LOD = 1.95 at 23 cM).

130 ed" (including both persistent and recovered stuttering) on chromosome 9 (LOD = 2.3 at 60 cM) and of

131 The existing methods for microsatellite stutter pattern deconvolution required large amount of d

132 we develop a novel method for microsatellite stutter pattern deconvolution.

133 , the relative intensity of each band in the stutter pattern is approximately the same for each allel

134 d quantitatively to predict the shape of the stutter pattern, a prediction borne out by experiment.

135 nted that is used to analyze the overlapping stutter patterns and determine the relative concentratio

136 Due to microsatellite mutations during PCR, stutter patterns may appear in the final PCR product, wh

137 t successfully predicts the general shape of stutter patterns.

138 These "stutter" patterns may overlap in heterozygous alleles an

139 and "dropin" of alleles, and highly variable stutter peak heights.

140 d protein kinase C signaling, which controls stuttering persistent Ca2+ influx, vascular tone, and bl

141 These stuttering persistent Ca2+ sparklets arise from the mole

142 e Ca2+ channels in arterial myocytes produce stuttering persistent Ca2+ sparklets that increase Ca2+

143 eural systems of normal speech from those of stuttering, PET images of brain blood flow were probed (

144 utations in the NAGPA gene in the persistent stuttering phenotype.

145 n on the island of Hawaii and early on had a stuttering problem.

146 results also suggest that the proportion of stutter product relative to the main allele increases as

147 ontaining a typical verses low proportion of stutter product.

148 del as a potential explanation for how these stutter products are generated.

149 (PCR), insertion-deletion mutations produce stutter products differing from the original template by

150 The threshold for detecting 'stutter' products was computed to be four repeats for (C

151 Brain correlates of stutter rate and syllable rate showed striking differenc

152 Stutter-rate correlates, both positive and negative, wer

153 incipal difference between syllable-rate and stutter-rate positive correlates was hemispheric lateral

154 Stuttered reading lacked left-lateralized activations of

155 post-conditioned with 3 or 6 10-s cycles of stuttered reflow.

156 The aetiology of stuttering remains unclear; compared to other neurodevel

157 Additional voxel-based findings in the stuttering sample included higher NAA:Cr and Cho:Cr rati

158 also observed between local metabolites and stuttering severity (r = 0.40-0.52; P = .001-.02).

159 f stuttering, which were diagnosed using the Stuttering Severity Instrument.

160 ciated with stuttering status, age, sex, and stuttering severity.

161 The stutter shape is most easily determined from homozygous

162 fluency or auditory feedback, the people who stuttered showed overactivity relative to controls in th

163 ess dynamic brain function in adults who had stuttered since childhood, regional cerebral blood flow

164 asks suggested that during the production of stuttered speech, anterior forebrain regions-which play

165 s appears to be related to the production of stuttered speech, while activation of right hemispheric

166 ize advances in the genetic investigation of stuttering, speech-sound disorder (SSD), specific langua

167 examine white matter changes associated with stuttering status, age, sex, and stuttering severity.

168 gular-spiking (IR), initially bursting (IB), stuttering (Stu), single-spiking (SS), fast-adapting (FA

169 rCBF patterns in stuttering subjects differed markedly during the formula

170 or function-are disproportionately active in stuttering subjects, while post-rolandic regions-which p

171 The timing of the recovery and stuttering suggest that immature recovering activity of

172 ory processes associated with attenuation of stuttering symptoms.

173 inct and opposing roles in the generation of stuttering symptoms: activation of left hemispheric regi

174 has altered the switch between nonproductive stuttering synthesis and productive initiation during pr

175 Because RpoB3449 demonstrates "wild-type" stuttering synthesis at the mutant galP2 promoter, which

176 etermines other parameters that might affect stuttering synthesis by analyzing a mutant RNAP, RpoB344

177 RpoB3449 has dramatically diminished stuttering synthesis, and consequently, it has increased

178 the galP2 transcript leading to its reduced stuttering synthesis, indicating that the rate of an RNA

179 rase (RNAP) is known to engage nonproductive stuttering synthesis, which is sensitive to the concentr

180 d cells demonstrated a greater propensity to stutter than mitral cells.

181 gs included lower group mean NAA:Cr ratio in stuttering than nonstuttering participants in the right

182 er measures in adults and older children who stutter that were found primarily in major left hemisphe

183 between output helices through heptad repeat stutters that produce packing phase clashes.

184 further characterize the neurophysiology of stuttering through in vivo assay of neurometabolites in

185 ge studies mapped a susceptibility locus for stuttering to chromosome 12 in 46 highly inbred families

186 Prior ascription of a role in stuttering to inferior frontal and superior temporal gyr

187 e text] and infections occur as self-limited stuttering transmission chains.

188 rmittently pausing or "stuttering" TW (i.e., stuttering trap; ST region).

189 second having an intermittently pausing or "stuttering" TW (i.e., stuttering trap; ST region).

190 Stutters were negatively correlated with right-cerebral

191 Stuttering, which disrupts the smooth flow of speech, af

192 Each family contained multiple cases of stuttering, which were diagnosed using the Stuttering Se

193 We analyzed speech from people who stutter with mutations in this pathway and compared it t

194 By contrasting stuttering with fluent speech using positron emission to