The intricate relationship between dietary habits and cognitive function is gaining increasing attention, with a focus on the gut-brain axis as a modifiable target for intervention. This review synthesizes evidence on the impact of dietary patterns, particularly the Mediterranean diet, plant-based diets, and low-carbohydrate diets, on cognitive health. These diets, rich in antioxidants, anti-inflammatory compounds, and neuroprotective nutrients, are suggested to slow cognitive decline and reduce the risk of neurodegenerative disorders through mechanisms such as reduced inflammation and oxidative stress, and enhanced neurogenesis. The Mediterranean diet has been associated with improved cognitive performance and a delay in cognitive decline in elderly populations. However, challenges in dietary intervention implementation, including adherence and individual variability, remain. Future research must adopt a multidisciplinary approach, incorporating long-term, large-scale, multicenter randomized controlled trials to assess the enduring impacts of various dietary patterns on cognitive function, considering socioeconomic and cultural factors. This review underscores the potential of dietary interventions to prevent and mitigate cognitive impairment, ultimately aiming to improve quality of life.

The pores of vitrified bond diamond grinding wheel play a key role in the grinding process. However, uneven pore distribution and low porosity affect the grinding performance of the wheel significantly. Stereolithography based additive manufacturing provides an effective method to fabricate vitrified bond diamond grinding wheels with a uniform distribution and an interconnected pore structure. The key to high-performance grinding wheel via stereolithography 3D printing lies in the preparation of the slurry with high solid loading, low viscosity and uniform stability. In this study, the dispersion and stability of vitrified bond and diamond slurries were investigated systematically. The effects of resin monomers, surface modifiers, and solid loading on the dispersion, rheological behavior and stability of slurries were studied in detail. Finally, an optimal vitrified bond and diamond slurry for stereolithography based additive manufacturing was obtained, and complex-shaped gyroid triply periodic minimal surface grinding wheel were fabricated. By grinding the SiC ceramics, the material removal rate, grinding temperature, and surface roughness were compared to those achieved using a conventional solid structure grinding wheel. The results show that the gyroid porous grinding wheel can achieve better surface roughness and lower the grinding temperature.

Diabetic nephropathy (DN) is one of the common complications of diabetes and the main cause of end-stage renal disease (ESRD) in clinical practice. Schisandrin A (Sch A) has multiple pharmacological activities, including inhibiting fibrosis, reducing apoptosis and oxidative stress, and regulating immunity, but its pharmacological mechanism for the treatment of DN is still unclear. In vivo, streptozotocin (STZ) and a high-fat diet were used to induce type 2 diabetic rats, and Sch A was administered for 4 weeks. At the same time, protein–protein interaction (PPI) networks were established to analyze the overlapping genes of DN and Sch A. Subsequently, the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to determine the hub pathway. In addition, molecular docking was used to preliminarily verify the affinity of hub proteins and Sch A. Further, H&E staining, Sirius red staining, immunohistochemistry, immunofluorescence, and western blot analysis were used to detect the location and expression of related proteins in DN. This study revealed the multi-target and multi-pathway characteristics of Sch A in the treatment of DN. First, Sch A could effectively improve glucose tolerance, reduce urine microprotein and urine creatinine levels, and alleviate renal pathological damage in DN rats. Second, EGFR was the hub gene screened in overlapping genes (43) of Sch A (100) and DN (2524). Finally, it was revealed that Sch A could inhibit the protein expression levels of EGFR and PTRF and reduced the expression of apoptosis-related proteins, and this effect was related to the modulation of the AKT/GSK-3β signaling pathway. In summary, Sch A has a protective effect in DN rats, EGFR may be a potential therapeutic target, throughout modulating AKT/GSK-3β pathway.

The global incidence of thyroid cancer has increased significantly, and patients with advanced, recurrent, or radioiodine-refractory disease face a severe shortage of effective treatment options. The RET proto-oncogene serves as a key driver in the development of thyroid cancer, and its alterations are closely associated with highly aggressive tumor subtypes. Although the emergence of highly selective RET inhibitors (such as selpercatinib and pralsetinib) has revolutionized the treatment landscape, their complete clinical development pathway, rational combination strategies, and future research priorities still require systematic clarification. Understanding the development trends of these drugs is important for guiding clinical decision-making, optimizing trial design, and accelerating new drug development. We searched 16 clinical trial registries, and identified 18 studies registered up to 21 March 2025. Our analysis revealed that among the 18 eligible trials, the majority were Phase 1/2 studies. Selpercatinib and pralsetinib are the most frequently studied RET inhibitors. Notably, research on next-generation RET inhibitors as monotherapy approaches (e.g., LOXO-260, enbezotinib, SY-5007 and TY-1091) is currently underway. Additionally, combination regimens incorporating these inhibitors with agents such as ¹³¹I, recombinant human thyroid-stimulating hormone (rhTSH), and anti-programmed cell death protein 1 (anti-PD-1) antibodies are becoming an increasingly important area of investigation. While selective RET inhibitors have demonstrated therapeutic potential, concerns regarding drug resistance and toxicity persist. Therefore, future strategies should prioritize the development of next-generation inhibitors and the optimization of combination regimens to improve outcomes for RET -altered thyroid cancer patients.

Objective: Non-SMC condensin II complex subunit D3 (NCAPD3) has recently been demonstrated as a crucial oncogenic factor, nevertheless, the biological role of NCAPD3 in the pathogenesis of breast cancer has not been elucidated. Evidence suggests that targeting ferroptosis can inhibit the progression of breast cancer. Moreover, 2,3,5,4’-Tetrahydroxystilbene-2-O-β-D-glucoside (THSG) could modulate MCF-7 cell proliferation in our previous study. Therefore, we aimed to investigate the potential mechanism by which NCAPD3 mediates ferroptosis in THSG inhibition of T47D cell proliferation by full-length transcriptome sequencing.Methods: Alternative splicing analysis was performed based on full-length transcriptome sequencing and the overlapping genes in differentially expressed transcripts (DETs) and differential alternative splicing (diAS) were obtained. Further, RT-PCR was used to validate the type of alternative splicing. And the hub genes (transcripts) were selected using the bioinformatics analysis, quantitative polymerase chain reaction (qPCR) and Western blotting (WB). Moreover, cell cycle and ferroptosis were assessed using flow cytometry analysis and WB respectively. Mechanically, cell viability and clone formation was detected using Biochemical kit. And siRNA of Ncapd3 was transfected into T47D cells to detect the expression levels of ferroptosis-related proteins (WB) and cell viability (MTT).Results: 40 overlapping transcripts of DETs and diAS were obtained consistent with the analysis of full-length transcriptome sequencing, and Ncapd3 (Ncapd3-203) is key gene (transcript), which was also highly expressed in breast cancer and THSG could inhibit the mRNA and protein expression. Moreover, THSG could induce cell cycle arrest in G2/M stage and reduce ferroptosis-related protein expression (xCT and GPx4). Mechanically, we found that THSG inhibits the cell proliferation and clone formation in T47D cells, and Ncapd3 inhibition could inhibit (xCT and GPx4) proteins expression, which regulated THSG-suppressing effect in T47D cells.Conclusion: THSG could inhibit the proliferation in T47D cells by NCAPD3 -dependent ferroptosis, which provided novel insights into targeted strategy for breast cancer.

Correction on: Zhou Y, Cao J, Zhang S, Sun M, Zhang Y, Li S, Luo Z, Wang P and Xie J (2025) Review and analysis of clinical trials of selective RET inhibitors for the treatment of thyroid cancer. Front. Oncol. 15:1683624. doi: 10.3389/fonc.2025.1683624 Missing affiliation where work was done (Note: adding present affiliations after moving is not permitted.)Affiliation [ ] was omitted from the paper. This affiliation has now been added for author (s)