Aim This study aimed to develop a novel tumor-bearing tissue phantom model that can be used for US/CT/MR-guided tumor puncture and thermal ablation.Methods The phantom model comprised two parts: a normal tissue-mimicking phantom and a tumor-mimicking phantom. A normal tissue phantom was prepared based on a polyacrylamide gel mixed with thermochromic ink. Moreover, a spherical phantom containing contrast agents was constructed and embedded in the tissue phantom to mimic a tumor lesion. US/CT/MR imaging features and thermochromic property of the phantom model were characterized. Finally, the utility of the phantom model for imaging-guided microwave ablation training was examined.Results The tumor phantom containing contrast agents showed hyper-echogenicity, higher CT numbers, and lower T2 signal intensity compared with the normal tissue phantom in US/CT/MR images. Consequently, we could locate the position of the tumor in US/CT/MR imaging and perform an imaging-guided tumor puncture. When the temperature reached the threshold of 60 °C, the phantom exhibited a permanent color change from cream white to magenta. Based on this obvious color change, our phantom model could clearly map the thermal ablation region after thermotherapy.Conclusions We developed a novel US/CT/MR-imageable tumor-bearing tissue model that can be used for imaging-guided tumor puncture and thermal ablation. Furthermore, it allows visual assessment of the ablation region by analyzing the obvious color change. Overall, this phantom model could be a good training tool in the field of thermal ablation.
Atherosclerosis remains a major cause of morbidity and mortality worldwide. Intraplaque neovascularization critically promotes atherosclerotic progression and instability. Vascular endothelial growth factor A (VEGFA) stimulates aberrant microvessel growth in plaques by inducing endothelial cell proliferation and migration. Pigment epithelium-derived factor (PEDF) potently inhibits VEGFA-dependent neovascularization. This study introduces a thermosensitive hydrogel (PFSgel) developed from poloxamer 407 (F127) and sodium alginate (SA) to deliver PEDF locally to atherosclerotic lesions. The PFSgel demonstrated a suitable liquid-solid transition at body temperature (37°C), then forming a stable 3D network structure after SA gelling with the Ca 2+ in the physiological environment which contributed to the character of controlled release. Rheological analysis confirmed its phase transition temperature of 28.7°C and notable self-healing properties, making it ideal for dynamic vascular environments. In vitro experiments showed that PFSgel could suppress VEGFA-induced endothelial cells’ proliferation and migration through modulation of CD31 and MMP-2/MMP-9 signaling. Notably, in vivo degradation test validated the controlled release pattern of PFSgel. In Apoe-deficient atherosclerotic mice, ultrasound-guided PFSgel injection onto the abdominal aorta enabled gradual in situ release of encapsulated PEDF. This effectively reduced plaque burden, neovascularization, and luminal stenosis, even with exogenous VEGFA administration. Histological analyses confirmed reduced lipid deposition, plaque area, and neovascularization within plaques. Overall, this novel in situ -forming PEDF delivery platform enables targeted suppression of pathological neovascularization via CD31 and MMP-2/MMP-9 pathways, representing a promising approach to stabilize high-risk plaques by intervening against VEGFA-dependent neovascularization.