We built a joint replacement loosening model based on the original rabbit model of infection and evaluated the performance characteristics of ¹⁸F-FDG and ⁶⁸ Ga-FAPI in evaluating infection and loosening. After surgery, the rabbits were divided into four groups, with six individuals in the control group and 10 each in the aseptic loosening, S. aureus and S. epidermidis groups. PET/CT and serological examination were performed three times at two-week intervals. After the rabbits were euthanized, micro-CT, tissue pathology, pullout tests and scanning electron microscopy (SEM) were performed. The pullout test and SEM showed the feasibility of the aseptic loosening model. ¹⁸F-FDG showed similar performance in the control and loosening groups. The SUVmax of the S. aureus group was consistently higher than that of the S. epidermidis group. As for ⁶⁸ Ga-FAPI, the SUVmax of the control group was lowest in the second week and gradually increased over subsequent weeks. The SUVmax of the loosening group began to exceed that of the control group after the second week. The SUVmax of the S. aureus group in the second week was the lowest among the four groups and increased as the number of weeks increased. The pathology results showed concordance with the performance of PET/CT. Linear regressions between SUVmax and serology showed that ¹⁸F-FDG was positively correlated with CRP and IL-6, while ⁶⁸ Ga-FAPI revealed negative correlations with CRP and IL-6 in the second week and positive correlations in the sixth week. In addition, the SUVmax and MT(target)V of both ¹⁸F-FDG and ⁶⁸ Ga-FAPI were negatively correlated with bone volume/trabecular volume (TV) and bone surface area/TV. In this longitudinal observation, ⁶⁸ Ga-FAPI showed greater sensitivity than ¹⁸F-FDG in detecting diseases, and ⁶⁸ Ga-FAPI had no intestinal or muscular uptake. The MT(target)V of ⁶⁸ Ga-FAPI was larger than that of ¹⁸F-FDG, which meant that ⁶⁸ Ga-FAPI had the potential to define the scope of lesions more accurately. Finally, the SUVmax of ⁶⁸ Ga-FAPI could not differentiate between loosening and infection; further study of the diagnostic criteria is warranted.

Background: Glioblastoma (GBM) is the most malignant glioma, with poor survival rates and prognosis. Several studies have reported the abnormal expression of circular RNAs (circRNAs) and their functions in the malignant biological behavior of GBM. However, such research is still in the preliminary stages, and further study is needed to confirm the therapeutic potential of circRNAs in GBM. Methods: RNA-seq was performed using four tumor tissues from patients with GBM and their adjacent non-tumor brain tissues to screen differentially expressed circRNAs. Fluorescence in situ hybridization assay was used to examine the location of circ_0021350 in glioma cells. In addition, a series of biological function assays were employed to verify the oncogenic role of circ_0021350 in GBM. Quantitative reverse transcription PCR was used to examine circular, micro- (miRNA), and messenger RNA (mRNA) levels. Furthermore, dual-luciferase reporter, RNA pull-down, and RNA binding protein immunoprecipitation assays were applied to verify the interaction between circ_0021350 and its downstream effectors. Results: Circ_0021350 was significantly elevated in GBM tissues and glioma cells. Overexpression of circ_0021350 promoted glioma cell proliferation and metastatic ability; silencing of circ_0021350 had the opposite effect. Mechanistic analysis revealed that circ_0021350 sponged miR-1207-3p to regulate PIK3R3, whose overexpression reversed the reduction in the malignant biological behavior of glioma cells caused by silencing circ_0021350. Conclusion: Our findings suggest that circ_0021350 is an oncogenic circRNA in GBM, and the circ_0021350/miR-1207-3p/PIK3R3 axis may serve as a potential therapeutic target in GBM treatment.