A novel three-dimensional-printed paranasal sinus-skull base anatomical model.

PURPOSE: A novel precision three-dimensional (3D)-printed paranasal sinus-skull base anatomical model was generated with a commercial grade desktop 3D printer. A specific page-turning pattern was employed in this model, to display the internal spatial structure of the paranasal sinus. METHODS: The CT image data of paranasal sinus were imported into the Mimics software to construct a 3D digital paranasal sinus-skull base model. Then, the model was sliced in the coronal position and loaded into the 3D printer to print each slice of the paranasal sinus-skull base model at a ratio of 1:1 in size. Based on CT image data, nine senior doctors assessed the simulation and accuracy of the anatomical structure features of the paranasal sinus-skull base, and the advantages and educational value of the 3D printing model using a seven-point Likert scale. RESULTS: A life-like 3D paranasal sinus-skull base structural model was successfully printed, with its internal spatial details clearly displayed. Nine senior doctors all thought that the profile of the printed anatomical structure was similar to that displayed by CT scan; however, the model provided more 3D spatial visual information. In addition, the model was considered to be of great value in the anatomy teaching and complicated surgery of the paranasal sinus-skull base, which had a material cost of only 3 dollars. CONCLUSIONS: The 3D printed paranasal sinus-skull base model has 3D visual functions, which provides a novel tool for anatomical studies on paranasal sinus, resident training, pre-surgical education and surgical planning.

[Impact of fenofibrate on NO and endothelial VCAM-1 expression in hyperlipidemic rats].

OBJECTIVE: To investigate the mechanism of hyperlipidemia- and imflammation-induced functional impairment of the endothelium. METHODS: The experiment was conducted using 3 groups of rats fed for 20 weeks with standard chow (control group), high-fat diet and high-fat diet with daily fenofibrate treatment (10 mg/kg, starting since the fifth week), respectively. After 4 and 20 weeks of feeding, respectively, serum lipid level and NO concentration were measured in the rats, and the epithelial vascular cell adhesion molecule-1 (VCAM-1) expression and cell adhesiveness to the aortic endothelium were observed. RESULTS: Compared with the control group, the rats with hyperlipidemia induced by long-term high-fat diet feeding showed lower NO concentration and increased leukocyte accumulation on the endothelial surface, exhibiting also stronger and more extensive endothelial expression of VCAM-1. In contrast, the hyperlipidemic rats with fenofibrate treatment shoed significantly decreased VCAM-1 expression and leukocyte adhesion with recovery of the NO level. CONCLUSION: NO deficiency and activation of inflammation are involved in vascular impairment in rats with high-fat diet-induced hyperlipidemia, and fenofibrate can effectively prevent atherosclerosis by restoring NO concentration and down-regulating VCAM-1 expression in these rats.