PubMed Health⌕ Search

PubMed · 6597698

Timing analysis of coding and articulation processes in dyslexia.

Abstract

Several investigators have found that the time required to perform serial naming tasks is a good predictor of dyslexia in children. Protracted overall time scores, such as are reported for the Rapid Automatized Naming (RAN) test of Denckla and Rudel, are, by themselves, insufficient to determine the extent to which the performance deficit is cognitive in nature, or is the articulatory consequence of an inability master the quickly changing acoustic formant patterns associated with consonants, as proposed by Tallal. We administered the RAN test to matched groups of dyslexic and normal control children, aged 8 to 11 years. Measurement of speech signal durations was performed by computer. We applied the Gould and Boies algorithm for extracting cognitive preparation time to these data, resulting in a partition of overall RAN test score into coding time and articulation time components. Differential performances between the groups on RAN subtests were examined for effects of postvocalic consonants and semantic load. It was found that both vocalization time and pause time means were significantly longer for the dyslexics on each of the four RAN subtests: objects, colors, numbers, letters. The Gould and Boies analysis showed very little preparation time during speech in both groups, attributing virtually all coding time to pauses, although reanalysis suggested somewhat less. Increased vowel length among the dyslexics occurred on all subtests, but was not maximized on subtests with more numerous postvocalic consonants. Vowel time differences between groups accounted for nearly all of the differences in vocalization time. Profiles were constructed on speech measures which, for each subtest, correctly identified each subject with his group. On the letters subtest it was found that vowel duration alone achieved a perfect discrimination between the dyslexic and control subjects.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S W Anderson, F N Podwall, J Jaffe. 1984. Timing analysis of coding and articulation processes in dyslexia.. https://doi.org/10.1111/j.1749-6632.1984.tb14760.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Prevalence and risk factors for persistent faecal carriage of extended spectrum beta-lactamase producing Escherichia coli in a paediatric community population.

OBJECTIVE: To investigate clinical and microbiological factors associated with persistent faecal carriage of extended spectrum beta-lactamase (ESBL) producing Escherichia coli in infants. METHODS: Between 2010 and 2022, children aged 3 months to 2 years old were sampled in a community setting in France, at two visits, V1 and V2, 3-24 months apart, to screen for prolonged faecal carriage of ESBL-producing E. coli. Patient clinical information and whole genome sequence of each isolate were used for association studies. RESULTS: A total of 4641 children were sampled. 375 (8%) carried an ESBL-producing Enterobacterales, among which 142 of ESBL-producing E. coli carriers were once again sampled at V2 and included in this study. 21.8% (n = 31/142) and 18.4% (n = 16/99) carried the same ESBL-producing E. coli clone for at least 3 and 6 months, respectively. B2 phylogroup, and among which ST131 clones were associated with an increased risk of persistent carriage. Multivariate analysis identified virulence associated genes involved in adhesion (papC/papGII allele and a tia-like gene) and encoding toxin (senB) as major risk factors for persistence. A genome wide association study highlighted the potential role of the frz metabolic operon, known to be involved in enterocytes adhesion/internalisation. CONCLUSION: Main extraintestinal pathogenic E. coli genomic features (phylogenetic background, adhesion properties) are associated with ESBL-producing E. coli gut colonisation persistence in infants, which could potentially lead to an increased risk of febrile urinary tract infection in these patients.

Child↗

Extensive and differential platinum chemotherapy mutagenesis in livers of children.

Childhood cancer survivors often experience late adverse effects that may be linked to chemotherapy mutagenesis. We studied chemotherapy mutagenesis in normal pediatric tissues using duplex sequencing (NanoSeq) to enable the detection of mutations from single DNA molecules. We found that platinum chemotherapeutics increased the mutation burdens of normal pediatric tissues to levels seen in adults. In the liver, platinum agents imparted a tissue-specific mutational signature that was absent from other tissues. Gene-focused duplex sequencing revealed that chemotherapy mutagenesis generates a great diversity of nonsynonymous variants, some of which may have functional potential, such as leukemogenic variants in blood. Our findings demonstrate extensive chemotherapy mutagenesis in normal tissues of children, which may provide a plausible link between chemotherapy exposure and adverse effects in later life.

Child↗

Clinical and immunological characterization of a child with a homozygous TBK1 kinase-domain truncation.

TBK1 is a serine-tyrosine kinase protein that transmits signals from pattern recognition receptors to the NF-κB pathway leading to production of Type 1 Interferons. Mutations in this protein have been associated with arthritis, vasculitis, herpes simplex encephalitis and amyotrophic lateral sclerosis. In the current study, we characterized the functional consequences of a TBK1-variant bearing a truncation in exon 4 and 5 in a patient with poly arthritis resembling juvenile idiopathic arthritis and necrotizing encephalitis. The truncation was associated with reduced TBK1 protein abundance and altered phosphorylation. The variant was associated with increased basal/and or Poly-I: C induced IL-6, TNFα, IL-1β and IL-18 and type 1 Interferon ex vivo. Our findings expand the phenotypic spectrum of TBK1 loss-of-function variants and may provide insight into the management of immune dysregulation in affected patients.

Child↗