Fluorescent silica nanoparticles (FSNPs) can provide high-intensity and photostable fluorescent signals as a probe for biomedical analysis. In this study, FSNPs hybridized with aggregation-induced emission (AIE) luminogens (namely FSNP-SD) were successfully fabricated by a surfactant-free sol-gel method. The FSNP-SD were spherical, monodisperse and uniform in size, with an average diameter of approximately 100 nm, and emitted strong fluorescence at the peak of 490 nm. The FSNP-SD selectively stained the cytoplasmic regions and were distributed in the cytoplasm. Moreover, they can stay inside cells, enabling the tacking of cells over a long period of time. The intracellular vesicles and multinucleated cells were increase gradually with the rise of FSNP-SD concentration. Both cell viability and survival only lost less than 20% when the cells were exposed to the high concentration of 100 μg/mL FSNP-SD. Additionally, the cell apoptosis and intracellular ROS assay indicated that FSNP-SD had no significant toxic effects at the maximum working concentration of 80 μg/mL. This study demonstrated that the FSNP-SD are promising biocompatible fluorescent probes for living cell imaging.

Gastric inflammatory myofibroblastic tumor (IMT) is a rare mesenchymal neoplasm of intermediate biological potential, with adult cases being particularly uncommon. We report a 64-year-old man with an incidentally detected gastric mass that was preoperatively suspected to be a gastrointestinal stromal tumor (GIST). The relevant literature on adult gastric IMT was also reviewed. Complete surgical resection with negative margins (R0 resection) remains the mainstay of treatment, whereas patients with confirmed ALK rearrangements may benefit from ALK inhibitor therapy. Histopathological confirmation and long-term surveillance are essential because of the potential for recurrence and occasional aggressive behavior.

Biliary tract diseases are frequently associated with chronic cholestasis, cholangiocyte injury, inflammation, and fibrotic remodeling. Persistent injury and dysregulated repair may create a microenvironment that promotes the development of cholangiocarcinoma (CCA). CCA is an aggressive and highly heterogeneous biliary malignancy shaped by the interplay among bile acid dysregulation, inflammatory signaling, oxidative and nitrative stress, metabolic adaptation, stromal remodeling, and therapeutic resistance. Curcumin, a major bioactive polyphenol derived from Curcuma longa, and related curcumin-based compounds have been investigated in preclinical studies for their anti-inflammatory, antioxidant, antifibrotic, and antitumor properties. Available evidence suggests that native curcumin, its analogs and derivatives, and formulation-based interventions may modulate signaling pathways involved in chronic biliary injury and CCA progression, including NF-κB, Nrf2/HO-1, and TGF-β/Smad signaling. However, the therapeutic application of native curcumin is limited by poor aqueous solubility, low oral bioavailability, rapid metabolism, and inadequate tissue-specific delivery. This review critically evaluates curcumin-based interventions across non-malignant biliary injury and established CCA, with emphasis on their proposed mechanisms, delivery strategies, evidence limitations, and translational barriers. Current evidence remains predominantly preclinical, and curcumin-based interventions should therefore be regarded as experimental candidates rather than established therapies.