ABSTRACT
Background Programmed necrosis is closely related to the occurrence and development of neurodegenerative diseases, but whether lead causes programmed cell necrosis has not been reported. Objective This experiment is designed to probe into the function of programmed necrosis and the effect of its inhibitor on lead-induced microglia (BV2 cell) injury. Methods The BV2 cells at logarithmic growth phase were treated with 0, 1, 5, 10, 25, 50, 100, and 200 μmol·L−1 lead acetate for 12, 24, 36, and 48 h, respectively, and methylthiazolyldiphenyl-tetrazolium bromide (MTT) was used to determine cell viability. After treatment with 0, 25, 50, and 100 μmol·L−1 lead acetate for 24 h, enzyme-linked immunosorbent assay, Western blotting, and flow cytometry were used to determine the expressions of tumor necrosis factor-α (TNF-α), receptor-interacting protein kinase 3 (RIPK3), receptor-interacting protein kinase 1 (RIPK1), and mixed lineage kinase domain-like protein (MLKL) in the cells, and the effect of RIPK1 inhibitor Nec-1 pretreatment on lead-induced BV2 cell injury . Results The BV2 cell viability decreased with higher lead concentration (r12 h=−0.995, r24 h=−0.984, r36 h=−0.983, r48 h=−0.981, all P<0.01) and time extension (only for 5 μmol·L−1 lead acetate, r=−0.994, P<0.01). Compared with the control group, the BV2 cell viability decreased at the same exposure time when the concentration of lead was above 10 μmol·L−1 (P<0.01). Compared with the control group, the expressions of RIPK1 and MLKL were increased in the 25, 50, and 100 μmol·L−1 lead groups (P<0.05 or 0.01), accompanied by an increase in the contents of inflammatory cytokine TNF-α, especially in the 100 μmol·L−1 lead group, the increment was the highest (P<0.01). The expression levels of p-RIPK1 and p-MLKL in BV2 cells were both increased when the concentration of lead acetate was above 50 μmol·L−1 (P<0.01). In addition, pretreatment with Nec-1 increased the cell viability rate and decreased the necrosis and late apoptosis rate of BV2 cells exposed to lead compared with corresponding lead exposure groups (P<0.05). Conclusions Lead can reduce BV2 cell viability, increase necrosis rate, and up-regulate the expressions of RIPK1, RIPK3, amd MLKL, and the phosphorylation levels of RIPK1 and MLKL. The RIPK1 inhibitor Nec-1 has an intervention effect on lead-induced damage in BV2 cells, indicating that programmed necrosis may play a role in lead neurotoxicity.
ABSTRACT
Objective: To evaluate 3D imaging technology in the preoperative evaluation of breast conserving surgery. Methods: A ret-rospective analysis was conducted using clinical data from 38 patients who underwent breast conserving surgery that was assisted by 3D imaging technology in Xiaogan Hospital Affiliated to Wuhan University of Science and Technology from April 2017 to January 2019. All 38 patients underwent 3.0-T breast magnetic resonance imaging (MRI) examination before surgery, and 3D reconstruction of virtu-al images was constructed through 3D modeling of medical digital imaging and communication (DICOM) data. The predicted resected tissue volume was compared with the volume of the actual resected specimen, and the surgical margin and postoperative aesthetics of the breast conserving surgery were evaluated. Results: The reconstructed 3D model clearly displayed the anatomical structures of the breast, tumor, gland, and blood vessels, and their relationship in 3D spaces. The goodness of fit of the 3D model to the practical sit-uation was 97.4% (37/38). In terms of the resection tissue volume, there was no significant difference between the predicted results (PRTV) and actual results (ARTV) [(61.7 ± 20.1) mL vs. (65.1 ± 20.7) mL, P>0.05]. There was a strong positive correlation between ARTV and PRTV (P<0.01). One patient underwent supplementary secondary surgery, resulting in an incidence of 2.6% (1/38). The postopera-tive satisfaction for breast conserving surgery was 100% (38/38). Conclusions: 3D imaging technology clearly displays the anatomical relationship between breast tumor and surrounding tissues, and correctly assesses breast volume, guiding surgical resection.