Application value of contrast-enhanced ultrasonography in the treatment of uterine fibroids by high-intensity focused ultrasound ablation: A retrospective study.

PURPOSE: To determine efficacy and safety of contrast-enhanced ultrasonography (CEUS) in high-intensity focused ultrasound (HIFU) ablation of uterine fibroids (UFs). METHODS: We retrospectively reviewed women undergoing HIFU ablation for UFs between June 2018 and January 2020. Before and after HIFU, patients underwent CEUS and magnetic resonance imaging (MRI) examinations. The relationship between CEUS features and ablation rate was analyzed. The time-intensity curves on CEUS were measured before and after HIFU ablation, and compared with those obtained using MRI. Adverse reactions were recorded. RESULTS: A total of 64 patients were included. The immediate HIFU ablation rate significantly differed between low-, iso-, and high-enhancement UFs (87.2% ± 1.6%, 83.3% ± 2.1%, and 72.9% ± 3.1%, respectively; p < 0.05). On CEUS, the peak time of the time-intensity curve was significantly longer after treatment than before treatment (32.2 ± 9.7 and 26.7 ± 9.4 s, respectively; p < 0.05). Peak intensity was significantly lower after treatment than before treatment (13.7 ± 7.5 and 30.9 ± 11.2 dB, respectively; p < 0.05). All measurements were comparable between CEUS and MRI. The most common peri- and post-procedure adverse reaction was pain, which was temporary. CONCLUSION: CEUS could dynamically and safely evaluate the immediate effects of the HIFU ablation of UFs.

Upstream stimulatory factor 2 (USF2) induced upregulation of triggering receptor expressed on myeloid cells 1 (TREM1) promotes endometritis by regulating toll-like receptor (TLR) 2/4-nuclear factor-kappaB (NF-κB) signaling pathway.

Triggering receptor expressed on myeloid cells 1 (TREM1) participates in the development of endometritis. This study aims at identifying the effects and interaction of TREM1 and upstream stimulatory factor 2 (USF2) in endometritis by using a model of lipopolysaccharide (LPS)-induced human endometrial epithelial cells (HEnEpCs). ELISA was performed to determine the levels of interleukin (IL)-6, IL-1ß, and tumor necrosis factor (TNF-α) after LPS stimulation. TREM1 and USF2 expression was examined with RT-qPCR and Western blot. The JASPAR database was employed to predict the binding site between USF2 and TREM1, which was confirmed by luciferase reporter and chromatin immunoprecipitation assays. After TREM1 overexpression, IL-6, IL-1ß, and TNF-α expression was detected by ELISA. Next, the binding of TREM1 to toll-like receptor (TLR) 2/4 was examined with co-immunoprecipitation. Then, proteins in TLR2/4-nuclear factor-kappaB (NF-κB) signaling in HEnEpCs under LPS condition were assessed by Western blot or immunofluorescence before and after TREM1 knockdown. Finally, TLR2 or TLR4 was silenced to explore whether intervene TLR2/4-NF-κB signaling pathway could rescue TREM1-overexpression-induced inflammation in LPS-induced HEnEpCs. Results revealed that upregulated TREM1 was observed in LPS-challenged HEnEpCs. Next, USF2 was found to have transcriptionally active TREM1 expression. Additionally, USF2 knockdown decreased the levels of IL-6, IL-1ß, and TNF-α, whereas this effect was rescued after TREM1 overexpression. Besides, TREM1 could bind to TLR2/4 to regulate NF-κB signaling. Moreover, the intervention of TLR2/4-NF-κB signaling pathway rescued TREM1-overexpression-induced inflammation in LPS-stimulated HEnEpCs. Collectively, USF2 promotes endometritis by upregulating TREM1, thereby activating TLR2/4-NF-κB pathway.