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Deep learning (DL) techniques have grown in leaps and bounds in both academia and industry over the past few years. Despite the growth of DL projects, there has been little study on how DL projects evolve, whether maintainers in this domain encounter a dramatic increase in workload and whether or not existing maintainers can guarantee the sustained development of projects. To address this gap, we perform an empirical study to investigate the sustainability of DL projects, understand maintainers' workloads and workloads growth in DL projects, and compare them with traditional open‐source software (OSS) projects. In this regard, we first investigate how DL projects grow, then, understand maintainers' workload in DL projects, and explore the workload growth of maintainers as DL projects evolve. After that, we mine the relationships between maintainers' activities and the sustainability of DL projects. Eventually, we compare it with traditional OSS projects. Our study unveils that although DL projects show increasing trends in most activities, maintainers' workloads present a decreasing trend. Meanwhile, the proportion of workload maintainers conducted in DL projects is significantly lower than in traditional OSS projects. Moreover, there are positive and moderate correlations between the sustainability of DL projects and the number of maintainers' releases, pushes, and merged pull requests. Our findings shed lights that help understand maintainers' workload and growth trends in DL and traditional OSS projects and also highlight actionable directions for organizations, maintainers, and researchers. [ABSTRACT FROM AUTHOR]

Introduction: The research examined the antioxidative impact of astragalosides (AST) on experimental acute pancreatitis (AP) in mice. This study aims to assess the correlation between varying doses of astragalosides and superoxide dismutase (SOD) activity in an acute pancreatitis mouse model. By examining the interplay between astragaloside's protective effects and its antioxidant properties, we aim to deepen our understanding of its therapeutic potential in acute pancreatitis., Methods: The AP model in mice was induced by retrograde injection of sodium deoxycholate into the biliary and pancreatic ducts. Serum amylase activity was monitored at various time points following induction. Furthermore, 24 hours post-induction, levels of serum nitric oxide (NO), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content in pancreatic tissue were assessed., Results: The findings of this study illustrated that AST, while exhibiting a protective effect in experimental AP, could effectively lower the elevated serum NO levels, reduce MDA production, and enhance SOD activity in model mice. AST notably reduced MDA levels in the pancreatic tissue of AP mice, underscoring its ability to inhibit membrane peroxidation induced by oxygen free radicals. Furthermore, AST was observed to elevate SOD activity in scavenging oxygen free radicals in pancreatic tissue., Conclusion: These findings suggest that AST enhances recovery in an experimental acute pancreatitis mouse model by exerting antioxidative effects., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Hou, Yu, Xu, Wang, Chen, Tao, Zhang and Zhu.)

Rationale: Systemic sclerosis (SSc) is a chronic and incurable autoimmune disease with high mortality rates, and skin fibrosis is one of distinguishing hallmarks in the pathogenesis. However, macrophage heterogeneity regulating skin fibrosis remain largely unknown. Methods: We established mouse disease model and performed single-cell RNA-sequencing (scRNA-seq) to resolve the dynamic and heterogenous characteristics of macrophages in skin fibrosis, and the role of TREM2-dependent macrophages in the pathological process was investigated using knockout mice and intraperitoneal transferring TREM2 + macrophages combining with functional assays. Results: We show that TREM2-expressing macrophages (TREM2 + MФs) accumulate in injured skin of mice treated by bleomycin (BLM) and human SSc, and their gene signatures and functional pathways are identified in the course of disease. Genetic ablation of Trem2 in mice globally accelerates and aggravates skin fibrosis, whereas transferring TREM2 hi macrophages improves and alleviates skin fibrosis. Amazingly, we found that disease-associated TREM2 + MФs in skin fibrosis exhibit overlapping signatures with fetal skin counterparts in mice and human to maintain skin homeostasis, but each has merits in skin remodeling and development respectively. Conclusion: This study identifies that TREM2 acts as a functional molecule and a major signaling by which macrophage subpopulations play a protective role against fibrosis, and disease-associated TREM2 + MФs in skin fibrosis might undergo a fetal-like reprogramming similar to fetal skin counterparts., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)