Elicitation techniques for the evaluation of speech under stress: Towards a framework for use in a controlled environment

Existing work in Computer Science and Electronic Engineering demonstrates that Digital Signal Processing techniques can effectively identify the presence of stress in the speech signal. These techniques use datasets containing real or actual stress samples i.e. real-life stress such as 911 calls and so on. Studies that use simulated or laboratory-induced stress have been less successful and inconsistent. Pervasive, ubiquitous computing is increasingly moving towards voice-activated and voice-controlled systems and devices. Speech recognition and speaker identification algorithms will have to improve and take emotional speech into account. Modelling the influence of stress on speech and voice is of interest to researchers from many different disciplines including security, telecommunications, psychology, speech science, forensics and Human Computer Interaction (HCI). The aim of this work is to assess the impact of moderate stress on the speech signal. In order to do this, a dataset of laboratory-induced stress is required. While attempting to build this dataset it became apparent that reliably inducing measurable stress in a controlled environment, when speech is a requirement, is a challenging task. This work focuses on the use of a variety of stressors to elicit a stress response during tasks that involve speech content. Biosignal analysis (commercial Brain Computer Interfaces, eye tracking and skin resistance) is used to verify and quantify the stress response, if any. This thesis explains the basis of the author’s hypotheses on the elicitation of affectively-toned speech and presents the results of several studies carried out throughout the PhD research period. These results show that the elicitation of stress, particularly the induction of affectively-toned speech, is not a simple matter and that many modulating factors influence the stress response process. A model is proposed to reflect the author’s hypothesis on the emotional response pathways relating to the elicitation of stress with a required speech content. Finally the author provides guidelines and recommendations for future research on speech under stress. Further research paths are identified and a roadmap for future research in this area is defined.

Identification and characterization of innate immune receptor substrates of γ-secretase enzyme complex

The γ-secretase protease complexes and associated regulated intramembrane proteolysis play an important role in controlling receptor-mediated intracellular signalling events, which have a central role in Alzheimer’s disease, cancer progression and immune surveillance. It has previously been reported that the Interleukin-1 receptor, type 1, (IL-1R1) is a substrate for regulated intramembrane proteolysis, mediated by presenilin (PS)-dependent γ-secretase activity. The aims of this project were twofold. Firstly, to determine the conservation of regulated intramembrane proteolysis as a physiological occurrence amongst other cytokine receptors. In this regard, similar to IL-1R1, we identified the Tumour necrosis factor receptor type 1 (TNFR1) and the Toll like receptor 4 (TLR4) as novel γ-secretase substrates. Secondly, given that the diversity of signalling events mediated by the IL-1R1, TLR4 and TNFR1 are spatially segregated, we investigated the spatial distribution, subcellular trafficking and subcellular occurrence of regulated intramembrane proteolysis of IL-1R1, TLR4 and TNFR1. Using dynasore an inhibitor of clathrin-dependent receptor endocytosis, both ectodomain shedding and γ-secretase-mediated cleavage of IL-1R1 were observed post-internalization. In contrast, TNFR-1 underwent ectodomain shedding at the cell surface followed by endosomal γ-secretase-mediated cleavage. Furthermore, immortalised fibroblasts from PS1-deficient mice showed impaired γ-secretasemediated cleavage of IL-1R1 and TNFR1, indicating that both are cleaved by PS1-and not PS2-containing γ-secretase complexes. Subcellular fractionation and immunofluorescence studies revealed that the γ-secretase generated IL-1R1 ICD translocates to the nucleus on IL-1β stimulation. These observations further demonstrate the novel PS-dependent means of modulating IL-1β, LPS and TNFα- mediated immune responses by regulating IL-1R1/TLR4/TNFR1 protein levels within the cells.