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Good quality of life is important for healthy ageing. Studies have shown that although information and communication technology can improve older people’s quality of life, their technology acceptance level is rather low. Tangible user interfaces (TUIs) enable people to interact with the digital world through everyday physical objects, thus offering more intuitive digital environments for older people. In this study, we employ a TUI prototype to investigate the relationship between older people’s technology acceptance and quality of life, the changes in these outcome measures after using TUI, and the associations between them. The TUI prototype, Tangible Cup was used by 20 older participants over a period of three months. Data were collected using the technology acceptance model (TAM) questionnaire, the older people’s quality of life (OPQOL) questionnaire and semi-structured interviews. The results showed some positive changes in technology acceptance after the use of Tangible Cup. However, no change in the quality of life was found. While statistically significant correlations between the change in technology acceptance and the change in quality of life were observed, limitations such as small sample size and participants not accurately representing the target population should be noted. Thus, further research is needed to better understand the associations between the change in technology acceptance and the change in quality of life.

No abstract

Student Support Tools Widget, widget as you lead, I am performing well indeed!-Using results from a formative offline study to inform an empirical online study about a learning analytics widget in a collaborative learning environment

The Hippo signaling effector, TEAD1 plays an essential role in cardiovascular development. However, a role for TEAD1 in postmitotic cardiomyocytes (CMs) remains incompletely understood. Herein we reported that TEAD1 is required for postmitotic CM survival. We found that adult mice with ubiquitous or CM-specific loss of Tead1 present with a rapid lethality due to an acute-onset dilated cardiomyopathy. Surprisingly, deletion of Tead1 activated the necroptotic pathway and induced massive cardiomyocyte necroptosis, but not apoptosis. In contrast to apoptosis, necroptosis is a proinflammatory form of cell death and consistent with this, dramatically higher levels of markers of activated macrophages and pro-inflammatory cytokines were observed in the hearts of Tead1 knockout mice. Blocking necroptosis by administration of necrostatin-1 rescued Tead1 deletion-induced heart failure. Mechanistically, genome-wide transcriptome and ChIP-seq analysis revealed that in adult hearts, Tead1 directly activates a large set of nuclear DNA-encoded mitochondrial genes required for assembly of the electron transfer complex and the production of ATP. Loss of Tead1 expression in adult CMs increased mitochondrial reactive oxygen species, disrupted the structure of mitochondria, reduced complex I-IV driven oxygen consumption and ATP levels, resulting in the activation of necroptosis. This study identifies an unexpected paradigm in which TEAD1 is essential for postmitotic CM survival by maintaining the expression of nuclear DNA-encoded mitochondrial genes required for ATP synthesis.