Hayate Shimizu

This paper develops a Kantian account of AI-assisted journal submission. Aylsworth and Castro (2024) analyze student use of ChatGPT through duties to oneself, while Sticker (2026) turns to duties owed to others. I develop this second route in relation to journal submission. Drawing on Kant’s Formula of Humanity and his false-promise example, I argue that an author treats an editor or reviewer merely as a means when she knowingly secures evaluative labor by misrepresenting AI involvement in a way that bears on that participant’s decision whether, and on what terms, to provide it. The author thereby uses the participant’s rational activity while bypassing her judgment about supplying it. Deception matters here as the route by which that treatment occurs, which is why the wrong is not reducible to a breach of journal policy: it is measured by what bears on the participant’s judgment, not by what a policy happens to require. The account distinguishes this wrong from openly acknowledged nondisclosure such as anonymous review, and shows that AI assistance is not thereby prohibited when it is honestly represented.

Oxidative stress has been implicated in cardiac arrhythmia, although a causal relationship remains undefined. We have recently demonstrated a marked up-regulation of NADPH oxidase isoform 4 in patients with atrial fibrillation, which is accompanied by overproduction of reactive oxygen species. In this study, we investigated the impact on the cardiac phenotype of NOX4 overexpression in zebrafish. One-cell stage embryos were injected with NOX4 RNA prior to video recording of a GFP-labeled beating heart in real time at 24-31 h post-fertilization. Intriguingly, NOX4 embryos developed cardiac arrhythmia that is characterized by irregular heartbeats. When quantitatively analyzed by an established LQ-1 program, the NOX4 embryos displayed much more variable beat-to-beat intervals. Both the phenotype and the increased ROS in NOX4 embryos were attenuated by NOX4 morpholino co-injection, treatments of the embryos with polyethylene glycol-conjugated superoxide dismutase, or NOX4 inhibitors fulvene-5, 6-dimethylaminofulvene, and proton sponge blue. Injection of NOX4-P437H mutant RNA had no effect on the cardiac phenotype or ROS production. In addition, phosphorylation of calcium/cal-modulin-dependent protein kinase II was increased in NOX4 embryos but diminished by polyethylene glycol-conjugated superoxide dismutase, whereas its inhibitor KN93 or AIP abolished the arrhythmic phenotype. Taken together, our data for the first time uncover a novel pathway that underlies the development of cardiac arrhythmia, namely NOX4 activation, subsequent NOX4-specific NADPH-driven ROS production, and redox-sensitive CaMKII activation. These findings may ultimately lead to novel therapeutics targeting cardiac arrhythmia. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc.