In the present study, we reconstructed upper airway and soft palate models of 3 obstructive sleep apnea-hypopnea syndrome（OSAHS） patients with nasal obstruction. The airflow distribution and movement of the soft palate before and after surgery were described by a numerical simulation method. The curative effect of nasal surgery was evaluated for the three patients with OSAHS. The degree of nasal obstruction in the 3 patients was improved after surgery. For 2 patients with mild OSAHS, the upper airway resistance and soft palate displacement were reduced after surgery. These changes contributed to the mitigation of respiratory airflow limitation. For the patient with severe OSAHS, the upper airway resistance and soft palate displacement increased after surgery, which aggravated the airway obstruction. The effcacy of nasal surgery for patients with OSAHS is determined by the degree of improvement in nasal obstruction and whether the effects on the pharynx are beneficial. Numerical simulation results are consistent with the polysomnogram（PSG） test results, chief complaints, and clinical findings, and can indirectly reflect the degree of nasal patency and improvement of snoring symptoms, and further,provide a theoretical basis to solve relevant clinical problems.
Shen YuYing-Xi LiuXiu-Zhen SunYing-Feng SuYing WangYin-Zhe Gai
The effect of disturbed flow on the mass trans- fer from arterial surface to flowing blood was studied nu- merically, and the results were compared with that of our previous work. The arterial wall was assumed to be vis- coelastic and the blood was assumed to be incompressible and non-Newtonian fluid, which is more close to human arte- rial system. Numerical results indicated that the mass trans- fer from the arterial surface to flowing blood in regions of disturbed flow is positively related with the wall shear rates and it is significantly enhanced in regions of disturbed flow with a local minimum around the reattachment point which is higher than the average value of the downstream. There- fore, it may be implied that the accumulation of cholesterol or lipids within atheromatous plaques is not caused by the reduced efflux of cholesterol or lipids, but by the infiltration of the LDL （low-density lipoprotein） from the flowing blood to the arterial wall.
