Tong Zhu, Daize Dong, Xiaoye Qu, Jiacheng Ruan, Wenliang Chen, Yu Cheng. Proceedings of the 2025 Conference of the Nations of the Americas Chapter of the Association for Computational Linguistics: Human Language Technologies (Volume 1: Long Papers). 2025.

Background. Diabetic cardiomyopathy is one of the cardiac complications in diabetes patients, eventually resulting in heart failure and increasing morbidity and mortality. Oxidative stress is a critical pathological feature in diabetic hearts, contributing to the development of DCM. Forskolin (FSK) was shown to reduce oxidative stress. This study was aimed at investigating the effects of FSK on diabetic hearts and the relevant molecular mechanisms. Methods. Streptozotocin‐ (STZ‐) induced diabetes in mice was treated with FSK through intraperitoneal injection. Cardiac functions were evaluated by echocardiography. Hematoxylin‐eosin and Masson trichrome staining was employed to determine heart morphological changes and cardiac fibrosis, respectively. Cardiac fibrosis‐related markers were detected by western blot. Superoxide dismutase activity, reduced/oxidized glutathione ratio, and malondialdehyde concentration in left ventricles were determined using respective commercial kits. Results. Abnormal cardiac diastolic dysfunction and cardiac fibrosis were observed in diabetic hearts. FSK treatment significantly improved the cardiac diastolic function and attenuated the abnormal morphological change in diabetic hearts. Moreover, FSK treatment in diabetic mice decreased the expression of fibronectin, collagen I, TGF‐β, and α‐SMA and reduced myocardial fibrosis. Furthermore, we observed that FSK significantly blocked oxidative stress in diabetic hearts. Conclusions. Our study demonstrates that FSK protects against the development of DCM in STZ‐induced diabetes in mice. Our study suggests that FSK might be a potential target for drug development in treating DCM.

Document-level financial event extraction (DFEE) is the task of detecting event and extracting the corresponding event arguments in financial documents, which plays an important role in information extraction in the financial domain. This task is challenging as the financial documents are generally long text and event arguments of one event may be scattered in different sentences. To address this issue, we propose a novel Prior Information Enhanced Extraction framework (PIEE) for DFEE, leveraging prior information from both event types and pre-trained language models. Specifically, PIEE consists of three components: event detection, event argument extraction, and event table filling. In event detection, we identify the event type. Then, the event type is explicitly used for event argument extraction. Meanwhile, the implicit information within language models also provides considerable cues for event arguments localization. Finally, all the event arguments are filled in an event table by a set of predefined heuristic rules. To demonstrate the effectiveness of our proposed framework, we participate the share task of CCKS2020 Task5-2: Document-level Event Arguments Extraction. On both Leaderboard A and Leaderboard B, PIEE takes the first place and significantly outperforms the other systems.

Saturated free fatty acids (FFAs) elevate in metabolic symptom leading to endothelial dysfunction. Cystic fibrosis transmembrane regulator (CFTR) functionally expresses in endothelial cells. The role of CFTR in FFA-induced endothelial dysfunction remains unclear. This study is aimed at exploring the effects of CFTR on palmitate- (PA-) induced endothelial dysfunction and its underlying mechanisms. We found that PA-induced endothelial dysfunction is characterized by a decrease of cell viability, reduction of NO generation and mitochondrial membrane potential, impairment of the tube formation, but an increase of ROS generation and cell apoptosis. Simultaneously, PA decreased CFTR protein expression. CFTR agonist Forskolin upregulated CFTR protein expression and protected against PA-induced endothelial dysfunction, while CFTR knockdown exacerbated endothelial dysfunction induced by PA and blunted the protective effects of Forskolin. In addition, PA impaired autophagic flux, and autophagic flux inhibitors aggravated PA-induced endothelial apoptosis. CFTR upregulation significantly restored autophagic flux in PA-insulted endothelial cells, which was involved in increasing the protein expression of Atg16L, Atg12-Atg5 complex, cathepsin B, and cathepsin D. In contrast, CFTR knockdown significantly inhibited the effects of Forskolin on autophagic flux and the expression of the autophagy-regulated proteins. Our findings illustrate that CFTR upregulation protects against PA-induced endothelial dysfunction by improving autophagic flux and underlying mechanisms are involved in enhancing autophagic signaling mediated by the Atg16L-Atg12-Atg5 complex, cathepsin B, and cathepsin D. CFTR might serve as a novel drug target for endothelial protection in cardiovascular diseases with a characteristic of elevation of FFAs.