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While both Japanese and English have a grammatic al form denoting the progressive, the two forms (te-iru & be+ing) interact differently with the inherent semantics of the verb to which they attach (Kindaichi, 1950; McClure, 1995; Shirai, 2000). Japanese change of state verbs are incompatible with a progressive interpretation, allowing only a resultative interpretation of V+ te-iru, while a progressive interpretation is preferred for activity predicates. English be+ing denotes a progressive interpretation regardless of the lexical semantics of the verb. The question that arises is how we can account for the fact that change of state verbs like dying can denote a progressive interpretation in English, but not in Japanese. While researchers such as Kageyama (1996) and Ogihara (1998, 1999) propose that the difference lies in the lexical semantics of the verbs themselves, others such as McClure (1995) have argued that the difference lies in the semantics of the grammatical forms, be+ing and te-iru. We present results from an experimental study of Japanese learners’ interpretation of the English progressive which provide support for McClure’s proposal. Results indicate that independent of verb type, learners had significantly more difficulty with the past progressive. We argue that knowledge of L2 semantics-syntax correspondences proceeds not on the basis of L1 lexical semantic knowledge, but on the basis of grammatical forms.
Background: Alzheimer's disease is a common debilitating dementia with known heritability, for which 20 late onset susceptibility loci have been identified, but more remain to be discovered. This study sought to identify new susceptibility genes, using an alternative gene-wide analytical approach which tests for patterns of association within genes, in the powerful genome-wide association dataset of the International Genomics of Alzheimer's Project Consortium, comprising over 7 m genotypes from 25,580 Alzheimer's cases and 48,466 controls.
Principal findings: In addition to earlier reported genes, we detected genome-wide significant loci on chromosomes 8 (TP53INP1, p = 1.4×10−6) and 14 (IGHV1-67 p = 7.9×10−8) which indexed novel susceptibility loci.
Significance: The additional genes identified in this study, have an array of functions previously implicated in Alzheimer's disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimer's disease.