Handing over objects is a collaborative task that requires participants to synchronize their actions in terms of space and time, as well as their adherence to social standards. If one participant is a social robot and the other a visually impaired human, actions should favorably be coordinated by voice. User requirements for such a Voice-User Interface (VUI), as well as its required structure and content, are unknown so far. In our study, we applied the user-centered design process to develop a VUI for visually impaired humans and humans with full sight. Iterative development was conducted with interviews, workshops, and user tests to derive VUI requirements, dialog structure, and content. A final VUI prototype was evaluated in a standardized experiment with 60 subjects who were visually impaired or fully sighted. Results show that the VUI enabled all subjects to successfully receive objects with an error rate of only 1.8%. Likeability and accuracy were evaluated best, while habitability and speed of interaction were shown to need improvement. Qualitative feedback supported and detailed results, e.g., how to shorten some dialogs. To conclude, we recommend that inclusive VUI design for social robots should give precise information for handover processes and pay attention to social manners.

The SARS-CoV-2 pandemic not only resulted in millions of acute infections worldwide, but also caused innumerable cases of post-infectious syndromes, colloquially referred to as long COVID. Due to the heterogeneous nature of symptoms and scarcity of available tissue samples, little is known about the underlying mechanisms. We present an in-depth analysis of skeletal muscle biopsies obtained from eleven patients suffering from enduring fatigue and post-exertional malaise after an infection with SARS-CoV-2. Compared to two independent historical control cohorts, patients with post-COVID exertion intolerance had fewer capillaries, thicker capillary basement membranes and increased numbers of CD169+ macrophages. SARS-CoV-2 RNA could not be detected in the muscle tissues, but transcriptomic analysis revealed distinct gene signatures compared to the two control cohorts, indicating immune dysregulations and altered metabolic pathways. We hypothesize that the initial viral infection may have caused immune-mediated structural changes of the microvasculature, potentially explaining the exercise-dependent fatigue and muscle pain.

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