Fujian Medical University (Chinese: 福建医科大学) is a university located in Fuzhou, Fujian, China. Fujian Medical University was founded in 1937, named Fujian Provincial Medical Vocational School at that time. The name of the school was changed to Fujian Provincial Medical College in 1939 and was called Fujian Medical College in 1949. In 1969, after merging with Fujian Chinese Traditional Medical College and the medical department of Huaqiao University, Fujian Medical University was founded and moved to Quanzhou, Fujian. It was moved back to Fuzhou in 1978. The name of the school was changed back to Fujian Medical College in 1982 and then changed back to the present name in April 1996.
Accurate and generalizable pathological segmentation is essential for clinical deployment. However, existing methods remain challenged by cross-center domain shifts and ambiguous tissue boundaries, often relying on spurious domain-specific correlations and producing unreliable predictions in structurally complex regions. To address these issues, we propose the Causal-Evidential Generalization Network (CaEG-Net) for pathological image segmentation, which draws on ideas from causal inference and Dempster-Shafer evidence theory. Specifically, we incorporate a Causal Constraint Mechanism to mitigate spurious correlations through sample reweighting, thereby promoting the learning of domain-invariant morphological features. Furthermore, we design an Evidential Boundary Constraint module to model pixel-level uncertainty and suppress unreliable boundary responses in ambiguous regions, enabling more accurate boundary delineation. Extensive experiments on six datasets, including four public benchmarks and two in-house clinical datasets, demonstrate that CaEG-Net achieves superior segmentation performance in comparison to existing methods. The code was released at https://github.com/Bonjour-492/CaEG-Net.
Blueberries are highly susceptible to postharvest softening, oxidative damage, and microbial decay. In this study, gelatin/Sargassum fusiforme polysaccharide/carbon dots (gelatin/SFP/CDs) composite coating was applied to blueberries, which were then stored at 25 °C and 50–55% relative humidity for 12 days. The preservation mechanism was investigated from quality, physiological, and transcriptional perspectives. During 12-day storage, gelatin/SFP/CDs-coated blueberries exhibited lower decay incidence, darkening, weight loss, pH increase, and bacterial proliferation, while maintaining higher firmness, soluble solids content, titratable acidity, and commercially acceptable rate. Physiological analyses showed that gelatin/SFP/CDs coating delayed cell wall degradation by preserving cell wall polysaccharides and suppressing enzymes involved in cell wall degradation. Meanwhile, it alleviated oxidative stress by reducing reactive oxygen species (ROS) accumulation and enhancing antioxidant capacity. Transcriptomic analysis further revealed that gelatin/SFP/CDs regulated genes involved in cell wall metabolism, ROS generation, antioxidant defense, and the ascorbate–glutathione cycle. These findings suggest that gelatin/SFP/CDs coating delays blueberry senescence through suppressing cell wall degradation and alleviating ROS accumulation.
CD3 ligand 1 (CD3L1, ITPRIPL1), an emerging immune checkpoint, sustains immune privilege in the testis and facilitates tumor immune evasion. Targeting CD3L1 with a monoclonal antibody demonstrates potent antitumor activity in preclinical models and spontaneous tumors in companion animals. In an ongoing clinical trial, anti-CD3L1 therapy unexpectedly activated tumor-associated macrophages (TAMs) within the tumor microenvironment (TME), surpassing its anticipated role in T-cell reactivation. Mechanistic studies identified neuropilin-2 (NRP2) as the primary receptor on macrophages and uncovered the CD3L1-NRP2 axis as a critical driver of immunosuppressive M2 TAM polarization. Strikingly, in T-cell-deficient osteosarcoma models, anti-CD3L1 treatment reprogrammed TAMs toward an anti-tumor M1 phenotype, suppressing tumor progression. Clinical data corroborated these findings, revealing profound TME remodeling in advanced solid tumors. Our results elucidate a dual role for CD3L1 in immune evasion, mediated through both T-cell suppression and macrophage polarization, and highlight anti-CD3L1 as a multifaceted therapeutic strategy that enhances antigen presentation via TAM modulation.
BackgroundRomidepsin is a class I-selective histone deacetylase (HDAC) inhibitor indicated for the treatment of adult patients with cutaneous T-cell lymphoma (CTCL) who have received at least one prior systemic therapy and for adult patients with relapsed or refractory peripheral T-cell lymphoma (PTCL). Despite its clinical use, large-scale safety data remain limited. This study leverages the FDA Adverse Event Reporting System (FAERS) database to characterize romidepsin-associated adverse events (AEs) in real-world settings, aiming to enhance clinical risk management.MethodsData from the FAERS database, spanning from January 2014 to March 2025, served as the basis for this analysis. To evaluate the association between romidepsin and AEs, multiple disproportionality analyses were employed, including the reporting odds ratio (ROR), the proportional reporting ratio (PRR), the Bayesian confidence propagation neural network (BCPNN), and the multi-item gamma Poisson shrinker (MGPS).ResultsWithin the specified reporting period, 17,448,626 AE reports were recorded in the FAERS database, of which 1,285 events were associated with romidepsin. Based on four calculation methods, 101 preferred terms (PTs) related to romidepsin were determined. Common AEs included thrombocytopenia, pyrexia, anemia, electrocardiogram QT prolonged, and infections, aligning with the drug label. In addition, some unanticipated major AEs were detected, including cardiotoxicities beyond QT prolongation (acute cardiac failure, atrial fibrillation, sinus tachycardia, mitral valve incompetence, and bundle branch block left) alongside other significant AEs: hepatic failure, amenorrhea, mental status changes, glomerular filtration rate decreased, embolism, and retinal detachment.ConclusionThis study provides a systematic evaluation of AEs associated with romidepsin, confirming its established safety profile and identifying several emerging safety concerns in a real-world setting. These findings offer valuable insights to assist clinicians and pharmacists in better-managing romidepsin’s safety.
Endotoxin is one of the chemical substances that cause acute liver injury (ALI), which become a common health problem worldwide. Lactic acid bacteria (LAB) have emerged as a promising candidate for attenuating endotoxin-induced ALI. Lactiplantibacillus plantarum FJG2627 is a LAB isolated from traditional pickles with excellent probiotic effects. In this study, the protective functions of L. plantarum FJG2627 against ALI caused by lipopolysaccharides (LPS) in mice were investigated. Administration of L. plantarum FJG2627 significantly reduced serum ALT, AST, and pro-inflammatory factors (IL-1β and IL-6), while markedly increased the anti-inflammatory factor (IL-10). Additionally, administration of L. plantarum FJG2627 increased the abundance of beneficial bacteria such as Adlercreutzia, and reduced that of pathogenic bacteria such as Bilophila. Non-targeted metabolomics revealed that L. plantarum FJG2627 intervention altered metabolic pathways related to glucose (including galactose metabolism, etc.) and amino acid metabolisms (including histidine metabolism, etc.) in ALI mice. In summary, L. plantarum FJG2627 exerts a significant protective effect on LPS-induced ALI by controlling oxidation, suppressing inflammatory mediators, modulating intestinal microbial communities, and liver metabolites. L. plantarum FJG2627 has the potential to be developed as a food-grade Lactobacillus for safeguarding against liver damage.
