Search

Technology and digital management have been introduced into the service industry and have gradually changed the lifestyle of consumers. With the popularization of automation systems and the shortage of human resources, the development and application of self-ordering kiosks have become more important in the restaurant industry. The purpose of this study is to evaluate the usability of the interface of self-ordering kiosks, propose and validate an interface design scheme, and generalize suggestions and reference directions for the interface design of self-ordering kiosks in fast food restaurants. The results of this study show that users preferred the specific design more, were more focused on the presented information, and understood the customization options better. In customization tasks, the number of errors for this design was significantly lower than the others. In post-task usability testing, including the System Usability Scale (SUS), Net Promoter Score (NPS), and subjective user perception questionnaires, the specific design had the best scores. Combining the findings and conclusions of this study, we propose relevant references and suggestions for future research on the interface of self-ordering kiosks, which are expected to help improve user experience and interface operation efficiency.

Background: The most common B-cell cancers, chronic lymphocytic leukemia/lymphoma (CLL), follicular and diffuse large B-cell (FL, DLBCL) lymphomas, have distinct clinical courses, yet overlapping “cell-of-origin”. Dynamic changes to the epigenome are essential regulators of B-cell differentiation. Therefore, we reasoned that these distinct cancers may be driven by shared mechanisms of disruption in transcriptional circuitry. Methods: We compared purified malignant B-cells from 52 patients with normal B-cell subsets (germinal center centrocytes and centroblasts, naïve and memory B-cells) from 36 donor tonsils using >325 high-resolution molecular profiling assays for histone modifications, open chromatin (ChIP-, FAIRE-seq), transcriptome (RNA-seq), transcription factor (TF) binding, and genome copy number (microarrays). Findings: From the resulting data, we identified gains in active chromatin in enhancers/super-enhancers that likely promote unchecked B-cell receptor signaling, including one we validated near the immunoglobulin superfamily receptors FCMR and PIGR. More striking and pervasive was the profound loss of key B-cell identity TFs, tumor suppressors and their super-enhancers, including EBF1, OCT2(POU2F2), and RUNX3. Using a novel approach to identify transcriptional feedback, we showed that these core transcriptional circuitries are self-regulating. Their selective gain and loss form a complex, iterative, and interactive process that likely curbs B-cell maturation and spurs proliferation. Interpretation: Our study is the first to map the transcriptional circuitry of the most common blood cancers. We demonstrate that a critical subset of B-cell TFs and their cognate enhancers form self-regulatory transcriptional feedback loops whose disruption is a shared mechanism underlying these diverse subtypes of B-cell lymphoma. Funding: National Institute of Health, Siteman Cancer Center, Barnes-Jewish Hospital Foundation, Doris Duke Foundation.