Designing and Piloting a Tool for the Measurement of the Use of Pronunciation Learning Strategies

What appears to be indispensable to drive the field forward and ensure that research findings will be comparable across studies and provide a sound basis for feasible pedagogic proposals is to draw up a classification of PLS and design on that basis a valid and reliable data collection tool which could be employed to measure the use of these strategies in different groups of learners, correlate it with individual and contextual variables, and appraise the effects of training programs. In accordance with this rationale, the present paper represents an attempt to propose a tentative categorization of pronunciation learning strategies, adopting as a point of reference the existing taxonomies of strategic devices (i.e. O'Malley and Chamot 1990; Oxford 1990) and the instructional options teachers have at their disposal when dealing with elements of this language subsystem (e.g. Kelly 2000; Goodwin 2001). It also introduces a research instrument designed on the basis of the classification that shares a number of characteristics with Oxford's (1990) Strategy Inventory for Language Learning but, in contrast to it, includes both Likert-scale and open-ended items. The findings of a pilot study which involved 80 English Department students demonstrate that although the tool requires considerable refinement, it provides a useful point of departure for future research into PLS

Erratum: The genomic architecture of NLRP7 is Alu rich and predisposes to disease-associated large deletions

NLRP7 is a major gene responsible for recurrent hydatidiform moles. Here, we report 11 novel NLRP7 protein truncating variants, of which five deletions of more than 1-kb. We analyzed the transcriptional consequences of four variants. We demonstrate that one large homozygous deletion removes NLRP7 transcription start site and results in the complete absence of its transcripts in a patient in good health besides her reproductive problem. This observation strengthens existing data on the requirement of NLRP7 only for female reproduction. We show that two other variants affecting the splice acceptor of exon 6 lead to its in-frame skipping while another variant affecting the splice donor site of exon 9 leads to an in-frame insertion of 54 amino acids. Our characterization of the deletion breakpoints demonstrated that most of the breakpoints occurred within Alu repeats and the deletions were most likely mediated by microhomology events. Our data define a hotspot of Alu instability and deletions in intron 5 with six different breakpoints and rearrangements. Analysis of NLRP7 genomic sequences for repetitive elements demonstrated that Alu repeats represent 48% of its intronic sequences and these repeats seem to have been inserted into the common NLRP2/7 primate ancestor before its duplication into two genes

Effects of orthographic forms on second language speech production and phonological awareness, with consideration of speaker-level predictors

Orthographic forms (spellings) can affect pronunciation in a second language (L2); however, it is not known whether the same orthographic form can affect both L2 pronunciation and metalinguistic awareness. To test this, we asked 260 speakers of English-first-language (L1) English speakers, L1 Italian and L2 English sequential bilinguals, and L1 Italian learners of L2 English-to perform word repetition tasks and rhyme judgment tasks for word pairs containing the same consonant or vowel spelled with a letter or a digraph. L1 Italian speakers established a long-short contrast and used consonant and vowel length contrastively in their L2 English, both in production and in an awareness task. This provides evidence for a direct link between the effects of the same orthographic phenomenon on speech production and on metalinguistic awareness. Results were strengthened by combining experimental and qualitative data in the study of orthographic effects. Finally, the results show that proficiency predicts orthographic effects, and that orthographic effect predictors vary in naturalistic and instructed contexts

The genomic architecture of NLRP7 is Alu rich and predisposes to disease-associated large deletions

WOS: 000384088000010PubMed ID: 26956250NLRP7 is a major gene responsible for recurrent hydatidiform moles. Here, we report 11 novel NLRP7 protein truncating variants, of which five deletions of more than 1-kb. We analyzed the transcriptional consequences of four variants. We demonstrate that one large homozygous deletion removes NLRP7 transcription start site and results in the complete absence of its transcripts in a patient in good health besides her reproductive problem. This observation strengthens existing data on the requirement of NLRP7 only for female reproduction. We show that two other variants affecting the splice acceptor of exon 6 lead to its in-frame skipping while another variant affecting the splice donor site of exon 9 leads to an in-frame insertion of 54 amino acids. Our characterization of the deletion breakpoints demonstrated that most of the breakpoints occurred within Alu repeats and the deletions were most likely mediated by microhomology events. Our data define a hotspot of Alu instability and deletions in intron 5 with six different breakpoints and rearrangements. Analysis of NLRP7 genomic sequences for repetitive elements demonstrated that Alu repeats represent 48% of its intronic sequences and these repeats seem to have been inserted into the common NLRP2/7 primate ancestor before its duplication into two genes.Max E. Binz Fellowship from the McGill University Faculty of Medicine; Canadian Institute of Health ResearchCanadian Institutes of Health Research (CIHR) [MOP-86546, PPP-122897]We thank the patients and their family for their cooperation. The authors wish to acknowledge the use of the Sequencing platform of the McGill University and Genome Quebec Innovation Centre. NMPN was supported by a Max E. Binz Fellowship from the McGill University Faculty of Medicine. The study was supported by the Canadian Institute of Health Research grants, MOP-86546 and PPP-122897, to RS

The genomic architecture of NLRP7 is Alu rich and predisposes to disease-associated large deletions

NLRP7 is a major gene responsible for recurrent hydatidiform moles. Here, we report 11 novel NLRP7 protein truncating variants, of which five deletions of more than 1-kb. We analyzed the transcriptional consequences of four variants. We demonstrate that one large homozygous deletion removes NLRP7 transcription start site and results in the complete absence of its transcripts in a patient in good health besides her reproductive problem. This observation strengthens existing data on the requirement of NLRP7 only for female reproduction. We show that two other variants affecting the splice acceptor of exon 6 lead to its in-frame skipping while another variant affecting the splice donor site of exon 9 leads to an in-frame insertion of 54 amino acids. Our characterization of the deletion breakpoints demonstrated that most of the breakpoints occurred within Alu repeats and the deletions were most likely mediated by microhomology events. Our data define a hotspot of Alu instability and deletions in intron 5 with six different breakpoints and rearrangements. Analysis of NLRP7 genomic sequences for repetitive elements demonstrated that Alu repeats represent 48% of its intronic sequences and these repeats seem to have been inserted into the common NLRP2/7 primate ancestor before its duplication into two genes