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1  disorders such as articulation disorder and stuttering.
2 anguage tasks designed to evoke or attenuate stuttering.
3  persons who stutter, even in the absence of stuttering.
4 icospinal tract, as previously implicated in stuttering.
5 autosomal dominant inheritance of persistent stuttering.
6 so increased syllable repetitions similar to stuttering.
7 dysfunction, both of which are implicated in stuttering.
8 red insights into genetic factors underlying stuttering.
9 sosomal pathway proteins have been linked to stuttering.
10 nique insight into the brain regions causing stuttering.
11 progression and persistence of developmental stuttering.
12 d circuitry contribute to the many facets of stuttering.
13 amily with an autosomal dominantly inherited stuttering.
14 e a chaperone protein in the pathogenesis of stuttering.
15 tions and silent pauses reminiscent of human stuttering.
16 -based network was relevant to developmental stuttering.
17 tudy of children and adults with and without stuttering.
18 ts in unrelated Cameroonians with persistent stuttering.
19  that may lead to recovery versus persistent stuttering.
20 product of a gene previously associated with stuttering.
21 s in intracellular trafficking in persistent stuttering.
22  disorder, specific language impairment, and stuttering.
23 vity of the circuit might be associated with stuttering.
24  have examined the neural bases of childhood stuttering.
25 en identified in individuals with persistent stuttering.
26 eficits in interhemispheric communication in stuttering.
27  functional imaging studies in developmental stuttering.
28 at implicate auditory processing problems in stuttering.
29 cluded 252 individuals exhibiting persistent stuttering, 45 individuals classified as recovered from
30  a distinct timing mechanism compared to non-stuttering adults.
31                                              Stuttering affects approximately 1 in 100 adults and can
32                                              Stuttering affects nearly 1% of the population worldwide
33                                              Stuttering, also known as stammering, has been linked to
34                      Thirty-two children (16 stuttering and 16 controls) aged 7-11 years participated
35  and adolescents aged 5 to 17 years (22 with stuttering and 25 without) and 47 adults aged 21 to 51 y
36 ) and 47 adults aged 21 to 51 years (20 with stuttering and 27 without) were recruited between June 2
37  show a potential link between developmental stuttering and changes in the gut microbiota, laying the
38 tively correlated with syllables in both the stuttering and control cohorts.
39           The mean (SD) ages of those in the stuttering and control groups were 12.2 (4.2) years and
40 lies, some members of which had nonsyndromic stuttering and in unrelated case and control subjects fr
41 ed beat, suggesting a potential link between stuttering and non-speech rhythm perception.
42 WS), however, data supporting a link between stuttering and poorer auditory rhythm discrimination has
43 these quantitative measures in developmental stuttering and provides new evidence of microstructural
44  45 individuals classified as recovered from stuttering, and 19 individuals too young to classify.
45 cal correlates including conduction aphasia, stuttering, and aspects of schizophrenia.
46 the neuroanatomical bases of early childhood stuttering, and possible white matter developmental chan
47 l disorders, including poor vocal imitation, stuttering, and progressive syntax and syllable degradat
48 spiking, rapidly adapting spiking, transient stuttering, and transient slow-wave bursting) and 4 stea
49 g-held theories that the brain correlates of stuttering are the speech-motor regions of the non-domin
50 sily through ICD-10 diagnosis codes, whereas stuttering as a speech phenotype was coded in only 12% o
51 bidities enriched in individuals affected by stuttering as predicting features and imputing stutterin
52 s, is believed to polyadenylate the mRNAs by stuttering at a stretch of five to seven uridine residue
53 e high processivity of the enzyme eliminates stuttering at homopolymer tracts.
54 miting GTP (1 microM) resulted in polymerase stuttering at the 3' margin of the T-run, immediately pr
55 n who stutter demonstrates that in childhood stuttering, atypical functional organization for speech
56 trophysiological techniques reveal the often-stuttering behavior of single pores in non-neuronal cell
57 n GNPTAB occurred in unrelated subjects with stuttering but not in control subjects.
58 inically ascertained sample of developmental stuttering cases validate our GWAS findings in PheML-imp
59 er a missense mutation associated with human stuttering causes vocal or other abnormalities in mice.
60 degree of heterogeneity in transmission from stuttering chain data have important applications in dis
61 lamocortical networks develop differently in stuttering children, which may in turn affect speech pla
62 syllable rate were far more extensive in the stuttering cohort than in the control cohort, which sugg
63         Our observations suggest a model of "stuttering conduction": repeated action potential stimul
64 nd 10 right-handed, age- and sex-matched non-stuttering controls.
65 reotypy seen in crystallized song, including stuttering, creation, deletion and distortion of song sy
66                   This spectroscopy study of stuttering demonstrates brainwide neurometabolite altera
67 d the possible neural bases of developmental stuttering during childhood.
68 te stimulus intensities, showed irregular or stuttering firing patterns.
69 single study cohort with acquired neurogenic stuttering following stroke (n = 20, 13 males/seven fema
70  published literature of acquired neurogenic stuttering following stroke (n = 20, 14 males/six female
71 purely to impairments in the motor system as stuttering frequency is increased by linguistic factors,
72 ered by speech-language pathologists reduced stuttering frequency.
73 the hypothesis that the genetic component to stuttering has significant sex effects.
74 of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postu
75 ed in this disorder, and previous studies of stuttering have identified linkage to markers on chromos
76  into module iteration, also referred to as "stuttering", have been derived through in vivo and in vi
77                              The etiology of stuttering, however, remains enigmatic.
78 f evidence suggest a genetic contribution to stuttering; however, the complex inheritance of this dis
79 t association between grey matter volume and stuttering impact for adults with persistent development
80      Affecting 1% of the general population, stuttering impairs the normally effortless process of sp
81        Theoretical accounts of developmental stuttering implicate dysfunctional cortico-striatal-thal
82 he first neuroimaging study of developmental stuttering in a family with autosomal dominant inheritan
83 t co-segregate with persistent developmental stuttering in a large Cameroonian family, and we observe
84 NPT [EC 2.7.8.15]), that was associated with stuttering in a large, consanguineous Pakistani family.
85 rther intimate neurometabolic aberrations in stuttering in brain circuits subserving self-regulation
86  study indicates a possible partial basis of stuttering in circuits enacting self-regulation of motor
87  exhibit atypical vocalizations analogous to stuttering in humans.
88 T (p.Pro270Ser) variant that segregated with stuttering in the family.
89 act for adults with persistent developmental stuttering in the left posteroventral putamen, extending
90 n Broca's area and the striatum underpinning stuttering in these individuals.
91  validated the genetic risk of self-reported stuttering in two independent datasets.
92 -of-function variants, in AP4E1 in unrelated stuttering individuals in Cameroon, Pakistan, and North
93 igher in unrelated Pakistani and Cameroonian stuttering individuals than in population-matched contro
94                                              Stuttering induced widespread overactivations of the mot
95    Apart from 34 of these patients who had a stuttering infarction and were referred for reperfusion,
96  calcium spikes, whereas X94 GFP+ cells were stuttering interneurons with quasi fast-spiking properti
97 s improved expressive language skills, and a stuttering intervention delivered by speech-language pat
98 76) evaluating the Lidcombe Program of Early Stuttering Intervention delivered by speech-language pat
99                                              Stuttering is a common and sometimes severe communicatio
100                                              Stuttering is a common neurodevelopmental disorder that
101                                              Stuttering is a common speech disorder that interrupts s
102                                              Stuttering is a common, highly heritable neurodevelopmen
103                                Developmental stuttering is a complex neurodevelopmental disorder char
104                                Developmental stuttering is a condition of speech dysfluency, characte
105                                         Thus stuttering is a disorder affecting the multiple neural s
106                                              Stuttering is a disorder of unknown cause characterized
107         Our data support the conclusion that stuttering is a disorder related primarily to disruption
108                                Developmental stuttering is a highly heritable, common speech conditio
109                                              Stuttering is a neurodevelopmental condition characteriz
110                                Developmental stuttering is a neuropsychiatric condition of incomplete
111                                Developmental stuttering is a speech disorder characterized by disrupt
112                                              Stuttering is a speech disorder long recognized to have
113               Susceptibility to nonsyndromic stuttering is associated with variations in genes govern
114                                   Typically, stuttering is characterized by speech sounds, words or s
115                                     Although stuttering is highly heritable and enriched within famil
116                                       Though stuttering is manifest in its motor characteristics, the
117                                 The cause of stuttering is unknown.
118 plex interplay between a novel iterative or "stuttering" KS-AT didomain (MmpF), the multidomain modul
119                                         This stuttering-like behavior started at one month, and impro
120 ude that lesions causing acquired neurogenic stuttering map to a common brain network, centred to the
121 ing to test whether lesions causing acquired stuttering map to a common brain network.
122 t in its motor characteristics, the cause of stuttering may not relate purely to impairments in the m
123                      These results support a stuttering mechanism for the polyadenylation of influenz
124 ediated pore closure occurred via a complex 'stuttering' mechanism.
125 tates from a processive elongation mode to a stuttering mode for polyadenylation to one in which no t
126 eport serves as the first interrogation of a stuttering module from a trans-AT subfamily PKS that is
127 ents in vitro and in E. coli, the "split-and-stuttering" module was shown to catalyze up to five elon
128  vocalizations of pups with the human Gnptab stuttering mutation compared to littermate controls.
129  vocalization defects in mice carrying human stuttering mutations in Gnptab derive from abnormalities
130                Here we show that other human stuttering mutations introduced into this mouse gene, Gn
131 ith two age and sex matched controls without stuttering (n = 14).
132 d (iii) adults with persistent developmental stuttering (n = 20, 14 males/six females, 18-43 years).
133 PFWE < 0.05), resulting in a common acquired stuttering network across both stroke datasets.
134                   Within the common acquired stuttering network, we found a significant association b
135 ature dataset, we found that lesions causing stuttering occurred in multiple heterogeneous brain regi
136                                              Stuttering occurs in early childhood during a dynamic ph
137 asses exhibited regular firing and irregular stuttering of action potential clusters, tufted cells de
138  and of the narrower diagnosis of persistent stuttering on chromosome 15 (LOD = 1.95 at 23 cM).
139 ed" (including both persistent and recovered stuttering) on chromosome 9 (LOD = 2.3 at 60 cM) and of
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 ady states (non-adapting spiking, persistent stuttering, persistent slow-wave bursting, and silence).
144 eural systems of normal speech from those of stuttering, PET images of brain blood flow were probed (
145    This finding was shown to be specific for stuttering (PFWE < 0.05) and reproducible in our indepen
146 nical cohort of patients with stroke-induced stuttering (PFWE < 0.05), resulting in a common acquired
147 oci on chromosomes 1 and 4 that map with the stuttering phenotype.
148 utations in the NAGPA gene in the persistent stuttering phenotype.
149                    The mechanisms underlying stuttering priapism are complex, and involve dysregulati
150 ), non-ischaemic (high-flow or arterial) and stuttering priapism.
151 n on the island of Hawaii and early on had a stuttering problem.
152  However, the cellular mechanisms leading to stuttering remain unknown.
153                             The aetiology of stuttering remains unclear; compared to other neurodevel
154 bus pallidus was associated with more severe stuttering (rho = 0.86, P = 0.01).
155 ared and distinct genetic variants impacting stuttering risk within sex and ancestry groups.
156 levance of our population-based analysis for stuttering risk.
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 ize advances in the genetic investigation of stuttering, speech-sound disorder (SSD), specific langua
162 uttering as predicting features and imputing stuttering status as the outcome variable.
163 examine white matter changes associated with stuttering status, age, sex, and stuttering severity.
164 gular-spiking (IR), initially bursting (IB), stuttering (Stu), single-spiking (SS), fast-adapting (FA
165                             rCBF patterns in stuttering subjects differed markedly during the formula
166 or function-are disproportionately active in stuttering subjects, while post-rolandic regions-which p
167               The timing of the recovery and stuttering suggest that immature recovering activity of
168 twork with symptom severity in developmental stuttering suggests a shared neuroanatomy across aetiolo
169 ory processes associated with attenuation of stuttering symptoms.
170 inct and opposing roles in the generation of stuttering symptoms: activation of left hemispheric regi
171 has altered the switch between nonproductive stuttering synthesis and productive initiation during pr
172    Because RpoB3449 demonstrates "wild-type" stuttering synthesis at the mutant galP2 promoter, which
173 etermines other parameters that might affect stuttering synthesis by analyzing a mutant RNAP, RpoB344
174         RpoB3449 has dramatically diminished stuttering synthesis, and consequently, it has increased
175  the galP2 transcript leading to its reduced stuttering synthesis, indicating that the rate of an RNA
176 rase (RNAP) is known to engage nonproductive stuttering synthesis, which is sensitive to the concentr
177 gs included lower group mean NAA:Cr ratio in stuttering than nonstuttering participants in the right
178 e-wide association analyses of self-reported stuttering that were stratified by sex and ancestry, as
179  further characterize the neurophysiology of stuttering through in vivo assay of neurometabolites in
180 ance, focusing on movement disorders such as stuttering, tics and freezing of gait.
181  various neurological disorders ranging from stuttering to aphasia; however, the underlying neural me
182 ge studies mapped a susceptibility locus for stuttering to chromosome 12 in 46 highly inbred families
183                Prior ascription of a role in stuttering to inferior frontal and superior temporal gyr
184 end infections in novel hosts, sometimes, in stuttering transmission chains that die out, and rarely,
185 e text] and infections occur as self-limited stuttering transmission chains.
186 rmittently pausing or "stuttering" TW (i.e., stuttering trap; ST region).
187  second having an intermittently pausing or "stuttering" TW (i.e., stuttering trap; ST region).
188 ic firing responses are greatly increased in stuttering type neurons under blocking their Kv1 channel
189 nvestigated the neuroanatomical substrate of stuttering using three independent datasets: (i) case re
190 e four-generation family in which persistent stuttering was inherited in an autosomal dominant manner
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 n alterations that are most likely linked to stuttering, while spontaneous recovery appears related t
194        We further show genetic similarity of stuttering with autism, depression and impaired musical
195                               By contrasting stuttering with fluent speech using positron emission to
196          To identify individuals affected by stuttering within our EHR, we built a PheCode-driven Gin

 
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