Xiaoran Lu

Enhancing algorithmic transparency is a pivotal issue in the ethics of artificial intelligence. From a phenomenological perspective, algorithmic transparency comprises two dimensions: the openness and visibility of algorithmic systems and the subject’s cognitive engagement with understanding the operational logic and theoretical underpinnings of algorithms. Consequently, algorithmic transparency should be reframed as a cognitive issue, with education serving as the central pathway for enhancing cognitive capacity. Unlike traditional educational paradigms that prioritize knowledge transmission, phenomenological pedagogy emphasizes intuitive experience and cultivation of critical thinking, enabling learners to achieve deeper understanding and foster the construction of knowledge. This approach not only underscores the practical value of phenomenological pedagogy in advancing algorithmic transparency but also highlights that such transparency depends not merely on public disclosure of algorithmic information but on learners’ experiential intuition and reflective analysis. Compared to purely technical solutions, improving transparency through the enhancement of learners’ cognitive comprehension of algorithms offers distinct and transformative advantages.

© 2015 The Authors.In the heart, augmented Ca 2+ fluxing drives contractility and ATP generation through mitochondrial Ca 2+ loading. Pathologic mitochondrial Ca 2+ overload with ischemic injury triggers mitochondrial permeability transition pore opening and cardiomyocyte death. Mitochondrial Ca 2+ uptake is primarily mediated by the mitochondrial Ca 2+ uniporter. Here, we generated mice with adult and cardiomyocyte-specific deletion of Mcu, which produced mitochondria refractory to acute Ca 2+ uptake, with impaired ATP production, and inhibited MPTP opening upon acute Ca 2+ challenge. Mice lacking Mcu inthe adult heart were also protected from acute ischemia-reperfusion injury. However, resting/basal mitochondrial Ca 2+ levels were normal in hearts of Mcu-deleted mice, and mitochondria lacking MCU eventually loaded with Ca 2+ after stress stimulation. Indeed, Mcu-deleted mice were unable to immediately sprint on a treadmill unless warmed up for 30min. Hence, MCU is a dedicated regulator of short-term mitochondrial Ca 2+ loading underlying a"fight-or-flight" response that acutely matches cardiac workload with ATP production.