ライフサイエンスコーパス: stuttering

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

2 tudy of children and adults with and without stuttering.

3 ts in unrelated Cameroonians with persistent stuttering.

4 that may lead to recovery versus persistent stuttering.

5 product of a gene previously associated with stuttering.

6 s in intracellular trafficking in persistent stuttering.

7 disorder, specific language impairment, and stuttering.

8 vity of the circuit might be associated with stuttering.

9 have examined the neural bases of childhood stuttering.

10 so increased syllable repetitions similar to stuttering.

11 en identified in individuals with persistent stuttering.

12 functional imaging studies in developmental stuttering.

13 at implicate auditory processing problems in stuttering.

14 anguage tasks designed to evoke or attenuate stuttering.

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

16 Stuttering affects nearly 1% of the population worldwide

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

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

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

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

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

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

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

24 45 individuals classified as recovered from stuttering, and 19 individuals too young to classify.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 This spectroscopy study of stuttering demonstrates brainwide neurometabolite altera

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 Stuttering induced widespread overactivations of the mot

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

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

60 Stuttering is a common and sometimes severe communicatio

61 Stuttering is a common, highly heritable neurodevelopmen

62 Thus stuttering is a disorder affecting the multiple neural s

63 Stuttering is a disorder of unknown cause characterized

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

65 Developmental stuttering is a neuropsychiatric condition of incomplete

66 Stuttering is a speech disorder long recognized to have

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

68 Though stuttering is manifest in its motor characteristics, the

69 The cause of stuttering is unknown.

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

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

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

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

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

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

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

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

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

79 These stuttering persistent Ca2+ sparklets arise from the mole

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

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

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

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

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

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

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

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

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

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

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

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

92 rCBF patterns in stuttering subjects differed markedly during the formula

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

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

95 ory processes associated with attenuation of stuttering symptoms.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 By contrasting stuttering with fluent speech using positron emission to