Production of tense marking in successive bilingual children: when do they converge with their monolingual peers?

Children with English as a second language (L2) with exposure of 18 months or less exhibit similar difficulties to children with Specific Language Impairment in tense marking, a marker of language impairment for English. This paper examines whether L2 children with longer exposure converge with their monolingual peers in the production of tense marking. 38 Turkish-English L2 children with a mean age of 7;8 and 33 monolingual age-matched controls completed the screening test of the Test of Early Grammatical Impairment (TEGI). The L2 children as a group were as accurate as the controls in the production of -ed, but performed significantly lower than the controls in the production of third person –s. Age and YoE affected the children’s performance. The highest age-expected performance on the TEGI was attested in eight and nine year-old children who had 4-6 YoE. L1 and L2 children performed better in regular compared to irregular verbs, but L2 children overregularized more than L1 children and were less sensitive to the phonological properties of verbs. The results show that tense marking and the screening test of the TEGI may be promising for differential diagnosis in eight and nine year-old L2 children with at least four YoE.

Manifesting carriers of Xp21 muscular dystrophy; lack of correlation between dystrophin expression and clinical weakness.

Ten females presenting with muscle weakness and a raised serum creatine kinase revealed abnormalities in the expression of dystrophin in their muscle biopsies and were diagnosed as manifesting carriers of Xp21 Duchenne/Becker muscular dystrophy. Seven cases, aged 3-22 yr at the time of biopsy, had a variable proportion of dystrophin-deficient fibres and an abnormal expression on immunoblot. These were confidently diagnosed as manifesting carriers. Results in the remaining three cases, aged 8-10 yr, were less clear-cut. Dystrophin expression on immunoblots was slightly reduced and some unevenness and reduction of immunolabelling was seen on sections, but dystrophin-deficient fibres were not a feature of these cases. The weakness in the ten carriers ranged from minimal to severe and there was no correlation between the degree of weakness and the number of dystrophin-deficient fibres. Two minimally weak girls had a high proportion of dystrophin-deficient fibres. Our results show that analysis of dystrophin expression is useful for the differential diagnosis of carriers of Xp21 dystrophy and autosomal muscular dystrophy, but that dystrophin expression does not correlate directly with the degree of clinical weakness.