RESUMO
Background: Shear wave elastography (SWE) is a novel imaging technique that provides quantitative assessments of tissue stiffness. This non-invasive method offers real-time, quantitative measurements and has been widely applied to various tissues, providing valuable diagnostic insights. Purpose: This study aimed to investigate the feasibility of using SWE to evaluate the stiffness of the lens in patients with age-related cataracts. Materials and methods: A comparative analysis involving 92 patients diagnosed with age-related cataracts and 39 healthy controls was conducted. Lens stiffness was quantified using SWE measurements. The lens nucleus of all participants was graded based on the Lens Opacities Classification System II (LOCS II). Correlations between the stiffness of the lens and age were also analyzed. Results: The study indicates that both the stiffness of the lens and the lens nucleus were significantly higher in patients with age-related cataracts compared to healthy controls (P < 0.001). In patients with age-related cataracts, although lens nucleus stiffness variations across different grades of cataract severity were not statistically significant, all grades displayed increased stiffness relative to healthy controls. Additionally, a significant positive correlation between lens stiffness and age was observed in all participants (P < 0.001). Conclusion: SWE appears to be a promising imaging technique for quantitatively assessing the mechanical characteristics of the lens in patients with age-related cataracts.
RESUMO
Glioma is the most common primary brain tumor in adults with an adverse prognosis and obscure pathogenesis. PICALM interacting mitotic regulator protein (PIMREG) functions as an oncogene in multiple types of cancer, but its function in glioma remains unknown. The Gene Expression Profiling Interactive Analysis 2 (GEPIA2, http://gepia2.cancer-pku.cn/#index) showed that PIMREG expression in the glioma tissues was higher than that in normal brain tissues. Herein, cell counting kit-8 assay and flow cytometry analysis exhibited that overexpression of PIMREG significantly promoted the proliferation of glioma cells and the transition from G1 phase of the cell cycle to S phase. Wound-healing and transwell assays showed that overexpression of PIMREG markedly enhanced the migration and invasion of glioma cells. Western blot analysis revealed that overexpression of PIMREG increased the expression of cyclin D1, cyclin E, Vimentin, matrix metalloproteinase (MMP)-2, and MMP-9, but reduced the expression of E-cadherin. In addition, overexpression of PIMREG activated the ß-catenin signaling pathway, as evidenced by the increased total and nuclear expression of ß-catenin and the up-regulated expression of its downstream target c-myc. Furthermore, immunofluorescence staining further indicated the increased nuclear translocation of ß-catenin in PIMREG-overexpressing cells. However, knockdown of PIMREG exerted opposite effects on glioma cells. Blockade of the ß-catenin signaling by ICG-001 markedly impeded the promoting effects of PIMREG on glioma cell proliferation and invasion. In conclusion, PIMREG acts as a tumor promoter in glioma at least partly via activating the ß-catenin signaling pathway. This study provides new insights into the molecular mechanism for glioma pathogenesis and treatment.