Individual Cognitive Stimulation Therapy (iCST) is a home-based psychosocial intervention for persons living with dementia (PLwDs) whose therapeutic value depends not only on activity content but also on how the session is conducted. Existing digital and voice-based iCST systems can still feel staged, especially around pauses, restarts, and slow endings. We describe a browser-based research prototype that uses continuous, interruptible speech to deliver a short iCST session. A central design move in the prototype is to separate local turn-taking from session-level control: the underlying real-time API manages interruption and exchange timing, while the application manages overall session progression. We describe how a prior formative study, iCST guidance, dementia communication literature, and iterative implementation informed the session arc, the system boundary, and the role-and-prompt structure. We conclude by discussing the design implications, limitations, and future evaluation needs for conducting an iCST session with a real-time voice agent.
Yixiao Li, Ita Daryanti Saragih, Donna M. Fick et al.· International Conference on...· 0 citations
INTRODUCTION Type 2 diabetes (T2D) is a major global health burden with rising prevalence and significant morbidity and mortality. Smoking has been recognized as an independent risk factor for T2D, but the exact underlying mechanisms are not yet fully understood. METHODS We conducted a two-sample Mendelian randomization (MR) study to investigate the effects of smoking behaviors and smoking-related DNA methylation on type 2 diabetes (T2D) risk. This secondary analysis was based on publicly available summary statistics. Smoking traits were obtained from a large meta-GWAS of over 1.2 million individuals of European ancestry. DNA methylation data were derived from the CHARGE Consortium EWAS (n=15907) and mQTLs from the GoDMC (n=27750). T2D outcome data were obtained from a European GWAS including 74124 cases and 824006 controls. Replication was performed in FinnGen (17268 cases, 184778 controls) and BioBank Japan (40250 cases, 170615 controls). Stringently selected genetic instruments were applied, and causal effects were estimated primarily using two-sample MR with inverse-variance weighted analysis, complemented by MR-Egger and weighted median approaches, and further validated by colocalization analysis. RESULTS In our genomic analysis, we presented convincing evidence supporting the association between genetically predicted smoking initiation and an increased susceptibility to T2D. In epigenetic analysis, we identified methylation at 21 smoking-related CpG sites associated with T2D risk. Subsequently, 14 of these CpG sites were validated using the FinnGen dataset, and 12 of them were validated using the BBJ dataset. Furthermore, we observed strong colocalization evidence for four CpG sites, including cg23756272 (BCL2), cg03864215 (KCNJ11), cg09861057 (TDRD10) and cg10672416 (C12orf65), and T2D risk. CONCLUSIONS This research provides novel findings of the impact of smoking on T2D susceptibility, highlighting the role of epigenetic DNA methylation.
Wenhua Li, Yixiao Li, Pan Dong et al.· Tobacco Induced Diseases· 0 citations
