Driving continuous improvement

The quality of improvement depends on the quality of leading and lagging performance indicators. For this reason, several tools, such as process mapping, cause and effect analysis and FMEA, need to be used in an integrated way with performance measurement models, such as balanced scorecard, integrated performance measurement system, performance prism and so on. However, in our experience, this alone is not quite enough due to the amount of effort required to monitor performance indicators at operational levels. The authors find that IT support is key to the successful implementation of performance measurement-driven continuous improvement schemes

Remember me

Sermon for All Saints

Affective Videogames and Modes of Affective Gaming: Assist Me, Challenge Me, Emote Me

In this paper we describe the fundamentals of affective gaming from a physiological point of view, covering some of the origins of the genre, how affective videogames operate and current conceptual and technological capabilities. We ground this overview of the ongoing research by taking an in-depth look at one of our own early biofeedback-based affective games. Based on our analysis of existing videogames and our own experience with affective videogames, we propose a new approach to game design based on several high-level design heuristics: assist me, challenge me and emote me (ACE), a series of gameplay "tweaks" made possible through affective videogames

Proline-rich tyrosine kinase 2 mediates gonadotropin-releasing hormone signaling to a specific extracellularly regulated kinase-sensitive transcriptional locus in the luteinizing hormone beta-subunit gene

G protein-coupled receptor regulation of gene transcription primarily occurs through the phosphorylation of transcription factors by MAPKs. This requires transduction of an activating signal via scaffold proteins that can ultimately determine the outcome by binding signaling kinases and adapter proteins with effects on the target transcription factor and locus of activation. By investigating these mechanisms, we have elucidated how pituitary gonadotrope cells decode an input GnRH signal into coherent transcriptional output from the LH β-subunit gene promoter. We show that GnRH activates c-Src and multiple members of the MAPK family, c-Jun NH(2)-terminal kinase 1/2, p38MAPK, and ERK1/2. Using dominant-negative point mutations and chemical inhibitors, we identified that calcium-dependent proline-rich tyrosine kinase 2 specifically acts as a scaffold for a focal adhesion/cytoskeleton-dependent complex comprised of c-Src, Grb2, and mSos that translocates an ERK-activating signal to the nucleus. The locus of action of ERK was specifically mapped to early growth response-1 (Egr-1) DNA binding sites within the LH β-subunit gene proximal promoter, which was also activated by p38MAPK, but not c-Jun NH(2)-terminal kinase 1/2. Egr-1 was confirmed as the transcription factor target of ERK and p38MAPK by blockade of protein expression, transcriptional activity, and DNA binding. We have identified a novel GnRH-activated proline-rich tyrosine kinase 2-dependent ERK-mediated signal transduction pathway that specifically regulates Egr-1 activation of the LH β-subunit proximal gene promoter, and thus provide insight into the molecular mechanisms required for differential regulation of gonadotropin gene expression