Although there is a consensus on the instructional potential of Serious Games (SGs), there is still a lack of methodologies and tools not only for design but also to support analysis and assessment. Filling this gap is one of the main aims of the Games and Learning Alliance (http://www.galanoe.eu) European Network of Excellence on Serious Games, which has a focus upon pedagogy-driven SGs. This paper relies on the assumption that the fundamental aspect of SG design consists in the translation of learning goals/ practices into mechanical element of gameplay, serving to an instructional purpose beside that of play and fun. This paper proposes the Learning Mechanics-Game Mechanics (LM-GM) model, which supports SG analysis and design by allowing reflection on the various pedagogical and game elements in an SG. The LM-GM model includes a set of pre-defined game mechanics and pedagogical elements that we have abstracted from literature on game studies and learning theories.Designers and analysts can exploit these mechanics to draw the LM-GM map for a game, so as to identify and highlight its main pedagogical and entertainment features, and their interrelations. The tool may also be useful for teachers to evaluate the effectiveness of a given game and better understand how to implement it in educational settings. A case study is reported to illustrate the framework's support in determining how gameplay and pedagogy intertwine in an SG. Finally, the paper presents the results of two comparative user tests demonstrating the advantages of the proposed model with respect to a similar state-of-the-art framework.

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Abnormality in the P50 auditory-evoked potential gating is an endophenotype associated with schizophrenia. Biochemical and genetic studies have suggested that the alpha 7 nicotinic acetylcholine receptor (nAChR) is involved in this sensory gating deficit. Two related alpha 7 genes (CHRNA7 and CHRNA7-like gene) resulting from a partial duplication (from exon 5 to exon 10) are present in the human genome. Two types of genetic variation, a large deletion and a −2 base-pair deletion in exon 6 resulting in a truncation of the open reading frame, affect specifically the CHRNA7-like gene. We developed a simple multiplex PCR assay on genomic DNA, allowing the quantification of the number of exons 6 and the distinction of all possible exon 6 genotypes. Genotyping of 70 schizophrenic patients and 77 controls showed that carrying at least one −2 bp deletion of exon 6 did not constitute a risk factor for schizophrenia. In contrast, the distribution of genotypes differed significantly between subjects with normal and abnormal P50 ratios, with an over-representation of genotypes carrying at least one −2 bp deletion of exon 6 among subjects exhibiting an abnormal P50 ratio. We thus conclude that the −2 bp deletion within the CHRNA7-like gene is a risk factor for P50 sensory gating deficit. Interestingly, most of the effect came from the non schizophrenic group, which may suggest that in schizophrenic patients other risk factors account for the large proportion of subjects exhibiting an abnormal P50 ratio.

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