Understanding the user experience of customer service chatbots: An experimental study of chatbot interaction design

Understanding the user experience of chatbots for customer service is essential to realize the potential of this technology. Such chatbots are typically designed for efficient and effective interactions, accentuating pragmatic quality, and there is a need to understand how to make these more pleasant and engaging, strengthening hedonic quality. One promising approach is to design for more humanlike chatbot interactions, that is, interactions resembling those of skilled customer service personnel. In a randomized experiment (n = 35) we investigated two chatbot interaction design features that may strengthen the impression of a humanlike character: (a) topic-led conversations, encouraging customer reflection, in contrast to task-led conversations, aiming for efficient goal completion, and (b) free text interaction, where users interact mainly using their own words, rather than button interaction, where users mainly interact through predefined answer alternatives. dependent variables were participant perceptions of anthropomorphism and social presence, two key concepts related to chatbot human likeness, in addition to pragmatic quality and hedonic quality. To further explore user perceptions of the interaction designs, the study also included semi-structured interviews. Topic-led conversations were found to strengthen anthropomorphism and hedonic quality. A similar effect was not found for free text interaction, reportedly due to lack in chatbot flexibility and adaptivity. Implications for theory and practice are suggested.publishedVersio

DIY Methods 2022 Conference Proceedings

As the past years have proven, the methods for conducting and distributing research that we’ve inherited from our disciplinary traditions can be remarkably brittle in the face of rapidly changing social and mobility norms. The ways we work and the ways we meet are questions newly opened for practical and theoretical inquiry; we both need to solve real problems in our daily lives and account for the constitutive effects of these solutions on the character of the knowledge we produce. Methods are not neutral tools, and nor are they fixed ones. As such, the work of inventing, repairing, and hacking methods is a necessary, if often underexplored, part of the wider research process. This conference aims to better interrogate and celebrate such experiments with method. Borrowing from the spirit and circuits of exchange in earlier DIY cultures, it takes the form of a zine ring distributed via postal mail. Participants will craft zines describing methodological experiments and/or how-to guides, which the conference organisers will subsequently mail out to all participants. Feedback on conference proceedings will also proceed through the mail, as well as via an optional Twitter hashtag. The conference itself is thus an experiment with different temporalities and medialities of research exchange. As a practical benefit, this format guarantees that the experience will be free of Zoom fatigue, timezone difficulties, travel expenses, and visa headaches. More generatively, it may also afford slower thinking, richer aesthetic possibilities, more diverse forms of circulation, and perhaps even some amount of delight. The conference format itself is part of the DIY experiment

In vivo overexpression of Emi1 promotes chromosome instability and tumorigenesis

Cell cycle genes are often aberrantly expressed in cancer, but how their misexpression drives tumorigenesis mostly remains unclear. From S phase to early mitosis, EMI1 (also known as FBXO5) inhibits the anaphase-promoting complex/cyclosome, which controls cell cycle progression through the sequential degradation of various substrates. By analyzing 7403 human tumor samples, we find that EMI1 overexpression is widespread in solid tumors but not in blood cancers. In solid cancers, EMI1 overexpression is a strong prognostic marker for poor patient outcome. To investigate causality, we generated a transgenic mouse model in which we overexpressed Emi1. Emi1-overexpressing animals develop a wide variety of solid tumors, in particular adenomas and carcinomas with inflammation and lymphocyte infiltration, but not blood cancers. These tumors are significantly larger and more penetrant, abundant, proliferative and metastatic than control tumors. In addition, they are highly aneuploid with tumor cells frequently being in early mitosis and showing mitotic abnormalities, including lagging and incorrectly segregating chromosomes. We further demonstrate in vitro that even though EMI1 overexpression may cause mitotic arrest and cell death, it also promotes chromosome instability (CIN) following delayed chromosome alignment and anaphase onset. In human solid tumors, EMI1 is co-expressed with many markers for CIN and EMI1 overexpression is a stronger marker for CIN than most well-established ones. The fact that Emi1 overexpression promotes CIN and the formation of solid cancers in vivo indicates that Emi1 overexpression actively drives solid tumorigenesis. These novel mechanistic insights have important clinical implications

Hyperdiploid tumor cells increase phenotypic heterogeneity within Glioblastoma tumors

Here we report the identification of a proliferative, viable, and hyperdiploid tumor cell subpopulation present within Glioblastoma (GB) patient tumors. Using xenograft tumor models, we demonstrate that hyperdiploid cell populations are maintained in xenograft tumors and that clonally expanded hyperdiploid cells support tumor formation and progression in vivo. In some patient tumorsphere lines, hyperdiploidy is maintained during long-term culture and in vivo within xenograft tumor models, suggesting that hyperdiploidy can be a stable cell state. In other patient lines hyperdiploid cells display genetic drift in vitro and in vivo, suggesting that in these patients hyperdiploidy is a transient cell state that generates novel phenotypes, potentially facilitating rapid tumor evolution. We show that the hyperdiploid cells are resistant to conventional therapy, in part due to infrequent cell division due to a delay in the G0/G1 phase of the cell cycle. Hyperdiploid tumor cells are significantly larger and more metabolically active than euploid cancer cells, and this correlates to an increased sensitivity to the effects of glycolysis inhibition. Together these data identify GB hyperdiploid tumor cells as a potentially important subpopulation of cells that are well positioned to contribute to tumor evolution and disease recurrence in adult brain cancer patients, and suggest tumor metabolism as a promising point of therapeutic intervention against this subpopulation