The oral route is the most preferred route for systemic and local drug delivery. However, the oral drug delivery system faces the harsh physiological and physicochemical environment of the gastrointestinal tract, which limits the bioavailability and targeted design of oral drug delivery system. Innovative pharmaceutical approaches including nanoparticulate formulations, biomimetic drug formulations, and microfabricated devices have been explored to optimize drug targeting and bioavailability. In this review, the anatomical factors, biochemical factors, and physiology factors that influence delivering drug via oral route are discussed and recent advance in conventional and novel oral drug delivery approaches for improving drug bioavailability and targeting ability are highlighted. We also address the challenges and opportunities of oral drug delivery systems in future.

Scar formation is a common outcome of post-injury repair and can compromise both esthetic appearance and physiological function. Fibroblasts are central mediators of this process; their aberrant activation or differentiation into myofibroblasts drives fibrosis and excessive scar tissue accumulation. Nanodrug delivery systems (NDDSs) offer unique opportunities to modulate fibroblast behavior through cell-/microenvironment-guided targeting, controlled release, and stimuli-adaptive designs. Here, we summarize fibroblast biology across scar repair and delineate the mechanistic underpinnings of scar pathogenesis. We then synthesize recent progress in NDDS-enabled interventions for pathological scarring, with an emphasis on how materials design can be matched to fibroblast states and wound-stage cues. By connecting mechanisms to delivery strategies, this review provides a framework to guide the development of scar-minimizing therapies and functional tissue regeneration.

Glioma is the most commonly occurring primary neuroepithelial neoplasm. Long noncoding RNAs (lncRNAs) are emerging as pivotal modulators of gene expression in the immune system and play critical roles in the growth, progression, and immune response of carcinomas. In this study, we performed univariate Cox regression analysis on survival data from TCGA and identified 20 prognostic lncRNAs. Moreover, we revealed that these prognosis-related lncRNAs (PRLnc) were dysregulated in glioma. Furthermore, we constructed a signature based on the expression levels of these prognosis-related lncRNAs based on 13 prognostic lncRNAs, including AGAP2-AS1, CYTOR, MIR155HG, LINC00634, HOTAIRM1, SNHG18, LINC01841, LINC01842, LINC01426, MIR9-3HG, TMEM220-AS1, LINC00641, LINC01270, and LINC01503. The KaplanMeier curves show that high-risk patients had a shorter survival time. Finally, the glioma samples were classified into 2 subgroups based on the median expression of prognosis-related lncRNAs in each sample. In summary, these findings suggest that PRLnc is associated with tumor-infiltrating immune cells in glioma and that subtype 2 patients may respond more positively to immunotherapy.

Diabetic chronic wounds (CWs) represent a recalcitrant, difficult-to-heal pathological condition characterized by an imbalance of the immune microenvironment. Smart composite nanocarriers for immune regulation enable multi-targeted, spatiotemporally controllable synergistic interventions by responding to pathological signals such as reactive oxygen species (ROS), pH, and abnormal enzyme activity, thereby offering a novel pharmaceutical strategy to overcome the limitations of traditional single-target therapies. Artificial intelligence (AI) integrates clinical and biological data to predict healing risks, optimize treatment plans and nanocarrier design, and dynamically adjust strategies based on patient conditions, ensuring precision and personalized therapies. This paper systematically reviews the immunopathological basis of CWs, summarizes the design rationale and functional evolution of immune-modulating smart composite nanocarriers, and discusses an AI-enabled precision therapy framework from an interdisciplinary perspective. It aims to establish a theoretical foundation and research paradigm for constructing programmable drug delivery systems tailored to complex disease microenvironments, facilitating the transition of smart nanopharmacy from material-oriented to system-regulation-oriented approaches, and accelerating the clinically predictable translation of diabetic wound therapies.

AIM: To investigate the feasibility of transfecting the TNF-related apoptosis-inducing ligand (TRAIL) gene into neural stem cells (NSCs) in vitro, and explore whether NSCs retain their proliferative and differentiated activities after transfection. MATERIAL and METHODS: NSCs were obtained from fetal mouse brains, cultured in serum-free medium and identified by immunofluorescence staining. Lentivirus vector solution containing green fluorescent protein (GFP) gene was added to the NSCs based on the multiplicity of infection (MOI). The transfection efficiency of GFP was observed using a fluorescence microscope and detected by flow cytometry. NSCs were transfected with GFP-TRAIL fusion genes mediated by the optimized MOI lentivirus solution. The expression of TRAIL proteins in NSCs was detected by immunofluorescence and Western blot analysis. The differentiation of NSCs were induced and identified by immunofluorescence staining.RESULTS: The optimal MOI value of virus transfection was 10, resulting in a transfection rate was higher than 90%. GFP fluorescence could be observed at 24 hours after transfecting GFP-TRAIL genes into NSCs with an MOI of 10, and reached the maximum value at 72 hours. Immunofluorescence and Western-blot assays confirmed that GFP-TRAIL fusion proteins could be continuously expressed stably. Transfected NSCs could differentiate into neurons and glial cells without any statistically significant difference compared to the non-transfected group. CONCLUSION: Neural stem cells retained their proliferative and differentiated potential after being transfected with the TRAIL gene while sustainably expressing TRAIL protein