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Sökning: WFRF:(Kirk J) > (2000-2004)

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  • Torstensson, Niklas, et al. (författare)
  • Mimicked accents : Do speakers have similar cognitive prototypes?
  • 2004
  • Ingår i: Proceedings of the 10th Australian International Conference on Speech Science & Technology. - : Australian Speech Science & Technology Association Inc.. ; , s. 271-276
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • There are several possible situations in which perpetrators might want to disguise their voices in order to avoid identification and to deflect the search for them to another person or group of individuals. One possible manner that can be used for voice disguise is the adoption of another accent. This paper examines the mimicking of the British-English Swedish accent, that is mimicking of the Swedish spoken by native British English speakers, by native Swedish speakers. It was found that the speakers selected similar and prominent features of the British-English Swedish accent in their first spontaneous recordings, and that the mimicked accent was impacted upon at word and suprasegmental level after having listened to a native speaker.
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  • van Kuilenburg, André B P, et al. (författare)
  • Novel disease-causing mutations in the dihydropyrimidine dehydrogenase gene interpreted by analysis of the three-dimensional protein structure
  • 2002
  • Ingår i: Biochemical Journal. - : Portland Press Ltd.. - 0264-6021 .- 1470-8728. ; 364:Pt 1, s. 157-163
  • Tidskriftsartikel (refereegranskat)abstract
    • Dihydropyrimidine dehydrogenase (DPD) deficiency is an autosomal recessive disease characterized by thymine-uraciluria in homozygous deficient patients. Cancer patients with a partial deficiency of DPD are at risk of developing severe life-threatening toxicities after the administration of 5-fluorouracil. Thus, identification of novel disease-causing mutations is of the utmost importance to allow screening of patients at risk. In eight patients presenting with a complete DPD deficiency, a considerable variation in the clinical presentation was noted. Whereas motor retardation was observed in all patients, no patients presented with convulsive disorders. In this group of patients, nine novel mutations were identified including one deletion of two nucleotides [1039-1042delTG] and eight missense mutations. Analysis of the crystal structure of pig DPD suggested that five out of eight amino acid exchanges present in these patients with a complete DPD deficiency, Pro86Leu, Ser201Arg, Ser492Leu, Asp949Val and His978Arg, interfered directly or indirectly with cofactor binding or electron transport. Furthermore, the mutations Ile560Ser and Tyr211Cys most likely affected the structural integrity of the DPD protein. Only the effect of the Ile370Val and a previously identified Cys29Arg mutation could not be readily explained by analysis of the three-dimensional structure of the DPD enzyme, suggesting that at least the latter might be a common polymorphism. Our data demonstrate for the first time the possible consequences of missense mutations in the DPD gene on the function and stability of the DPD enzyme.
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