Virtual human technologies are now being widely explored as therapy tools for mental health disorders including depression and anxiety. These technologies leverage the ability of the virtual agents to engage in naturalistic social interactions with a user to elicit behavioural expressions which are indicative of depression and anxiety. Research efforts have focused on optimising the human-like expressive capabilities of the virtual human, but less attention has been given to investigating the effect of virtual human mediation on the expressivity of the user. In addition, it is still not clear what an optimal task is or what task characteristics are likely to sustain long term user engagement. To this end, this paper describes the design and evaluation of virtual human-mediated tasks in a user study of 56 participants. Half the participants complete tasks guided by a virtual human, while the other half are guided by text on screen. Self-reported PHQ9 scores, biosignals and participants' ratings of tasks are collected. Findings show that virtual-human mediation influences behavioural expressiveness and this observation differs for different depression severity levels. It further shows that virtual human mediation improves users' disposition towards tasks. CCS CONCEPTS• Human-centered computing → User studies; • Applied computing → Health informatics; • Computing methodologies → Artificial intelligence.

Suppressor of cytokine signalling (SOCS) 3 is an essential regulator of cytokine signalling, and in turn its expression is tightly regulated. Data from overexpression studies in cell lines suggest that SOCS2 regulates SOCS3 protein degradation, by forming a molecular bridge to an E3 ubiquitinligase complex. Whether this regulation is relevant in primary cells is unknown. In this study, we utilized Socs2 −/− mice to examine the role of SOCS2 in modulating SOCS3 expression and degradation, and its impact on IL-2 and IL-6 signalling in primary haemopoietic cells. Both biochemical and biological analyses demonstrated unperturbed SOCS3 expression and cytokine signalling in the absence of SOCS2. Our results suggest that SOCS2 is not a physiological regulator of SOCS3 expression and action in primary haemopoietic cells.

No abstract