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A demonstration is presented of how automated reasoning tools can be used to check the predictability of a user interface. Predictability concerns the ability of a user to determine the outcomes of their actions reliably. It is especially important in situations such as a hospital ward where medical devices are assumed to be reliable devices by their expert users (clinicians) who are frequently interrupted and need to quickly and accurately continue a task. There are several forms of predictability. A definition is considered where information is only inferred from the current perceptible output of the system. In this definition, the user is not required to

The proinflammatory cytokines interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α) are involved in the corneal inflammatory response and wound healing following corneal injuries. However, the mechanism by which proinflammatory cytokines modulate corneal epithelial wound healing remains unclear. In this study, we found that IL‐1β or TNF‐α was transiently elevated during corneal epithelial wound healing in mice. After corneal epithelial debridement, persistent treatment with IL‐1β or TNF‐α restrained the level of phosphorylated signal transducer and activator of transcription 3 (p‐STAT3) and boosted the level of cell cycle inhibitor p16Ink4a, resulting in impaired corneal epithelial repair. When p16Ink4a was deleted, the p‐STAT3 level in corneal epithelium was enhanced and corneal epithelial wound healing was clearly accelerated. In diabetic mice, IL‐1β, TNF‐α, and p16Ink4a appeared a sustained and strong expression in the corneal epithelium, and p16Ink4a knockdown partially reverted the defective diabetic corneal epithelial repair. Furthermore, immunoprecipitation proved that p16Ink4a interacted with p‐STAT3 and thus possibly suppressed the STAT3 activity. Our findings revealed a novel mechanism that the proinflammatory cytokines modulate corneal epithelial wound healing via the p16Ink4a‐STAT3 signaling.