[Analysis of predictors for Frey syndrome after parotidectomy].

Objective:To analysis the data of the patients with parotid tumors, clarify the contributing factors of Frey syndrome, and to evaluate the role of soft tissues membrane SIS in prevention of Frey syndrome after parotidectomy. Method:The data of 95 patients who suffered from parotid tumors and underwent parotidectomy were included in this study. The relationship between the patients' age, sex, tumor location ,tumor size, disease pathology, type of resection, SIS application and the incidence of Frey syndrome were statistically analyzed . Result:The incidence of Frey syndrome after parotidectomy for 95 patients was 25.3%. Age, sex, tumor location and size, disease pathology, type of resection did not appear to be associated with development of Frey syndrome（P>0.05）. SIS application was the only statistically significant factor（P<0.01）, and SIS could prevent Frey syndrome after parotidectomy. Conclusion:Frey syndrome is one of the common complicationsafter parotidectomy. Implantation of SIS is an effective method for prevention of Frey syndrome after parotidectomy.

[Evaluation of therapeutic effect of virtual design for correcting facial asymmetry of skeletal Class â ¢ deformity].

Objective: To establish a computer-aided surgical simulation procedure based on the natural head position(NHP) for orthognathic surgery and to access the effect for correcting facial asymmetry for skeletal Class Ⅲ deformity. Methods: Thirty-five patients(male: 14 and female: 21, mean age: [21.5±2.3] years) of skeletal Class Ⅲ deformity with facial asymmetry were included and divided into virtual group (16 patients) and control group(19 patients). The computer-aided surgical simulation procedure was used in the virtual group and the intermediate and final splints were fabricated using the rapid protyping technique. The traditional model surgery based on plaster casts was used in control group, and the splints were handmade. To evaluate the symmetry, three-dimensional(3D) photos were taken for all the patients before operation and 6 months after operation using the 3dMD face imaging system. Coordinate system was built based on mirror-original alignment method on the 3D photo. Thirteen soft tissue landmarks were marked on each 3D photo. The asymmetry index(AI) of those soft tissue landmarks was calculated. Results: There was no significant difference in the AI values between the two groups before surgery. Sixth month after operation, the mean AI values in the virtual group were (0.81±0.50) mm for subnasale, (1.01±0.80) mm for labiale superius, (1.94±1.30) mm for crista philtri, (1.60±1.20) mm for pogonion and (5.68±2.25) mm for gonion. The mean AI values in the control group were (1.49±1.10) mm for subnasale, (1.79±1.33) mm for labiale superius, (3.52±2.50) mm for crista philtri, (2.79±2.08) mm for pogonion and (8.43±3.94) mm for gonion and those indexes were significantly different between the two groups(P<0.05). There was no significant difference in the AI values of the pronasale, alare, labiale inferius and cheilion between the two groups sixth month after operation. Conclusions: The introduced procedure of the virtual design based on the estimated NHP could more effectively correct the asymmetry deformity for the skeletal Class Ⅲ patients.

Propofol inhibits burn injury-induced hyperpermeability through an apoptotic signal pathway in microvascular endothelial cells.

Recent studies have revealed that an intrinsic apoptotic signaling cascade is involved in vascular hyperpermeability and endothelial barrier dysfunction. Propofol (2,6-diisopropylphenol) has also been reported to inhibit apoptotic signaling by regulating mitochondrial permeability transition pore (mPTP) opening and caspase-3 activation. Here, we investigated whether propofol could alleviate burn serum-induced endothelial hyperpermeability through the inhibition of the intrinsic apoptotic signaling cascade. Rat lung microvascular endothelial cells (RLMVECs) were pretreated with propofol at various concentrations, followed by stimulation with burn serum, obtained from burn-injury rats. Monolayer permeability was determined by transendothelial electrical resistance. Mitochondrial release of cytochrome C was measured by ELISA. Bax and Bcl-2 expression and mitochondrial release of second mitochondrial-derived activator of caspases (smac) were detected by Western blotting. Caspase-3 activity was assessed by fluorometric assay; mitochondrial membrane potential (Δψm) was determined with JC-1 (a potential-sensitive fluorescent dye). Intracellular ATP content was assayed using a commercial kit, and reactive oxygen species (ROS) were measured by dichlorodihydrofluorescein diacetate (DCFH-DA). Burn serum significantly increased monolayer permeability (P<0.05), and this effect could be inhibited by propofol (P<0.05). Compared with a sham treatment group, intrinsic apoptotic signaling activation - indicated by Bax overexpression, Bcl-2 downregulation, Δψm reduction, decreased intracellular ATP level, increased cytosolic cytochrome C and smac, and caspase-3 activation - was observed in the vehicle group. Propofol not only attenuated these alterations (P<0.05 for all), but also significantly decreased burn-induced ROS production (P<0.05). Propofol attenuated burn-induced RLMVEC monolayer hyperpermeability by regulating the intrinsic apoptotic signaling pathway.

Propofol inhibits burn injury-induced hyperpermeability through an apoptotic signal pathway in microvascular endothelial cells

Recent studies have revealed that an intrinsic apoptotic signaling cascade is involved in vascular hyperpermeability and endothelial barrier dysfunction. Propofol (2,6-diisopropylphenol) has also been reported to inhibit apoptotic signaling by regulating mitochondrial permeability transition pore (mPTP) opening and caspase-3 activation. Here, we investigated whether propofol could alleviate burn serum-induced endothelial hyperpermeability through the inhibition of the intrinsic apoptotic signaling cascade. Rat lung microvascular endothelial cells (RLMVECs) were pretreated with propofol at various concentrations, followed by stimulation with burn serum, obtained from burn-injury rats. Monolayer permeability was determined by transendothelial electrical resistance. Mitochondrial release of cytochrome C was measured by ELISA. Bax and Bcl-2 expression and mitochondrial release of second mitochondrial-derived activator of caspases (smac) were detected by Western blotting. Caspase-3 activity was assessed by fluorometric assay; mitochondrial membrane potential (Δψm) was determined with JC-1 (a potential-sensitive fluorescent dye). Intracellular ATP content was assayed using a commercial kit, and reactive oxygen species (ROS) were measured by dichlorodihydrofluorescein diacetate (DCFH-DA). Burn serum significantly increased monolayer permeability (P<0.05), and this effect could be inhibited by propofol (P<0.05). Compared with a sham treatment group, intrinsic apoptotic signaling activation - indicated by Bax overexpression, Bcl-2 downregulation, Δψm reduction, decreased intracellular ATP level, increased cytosolic cytochrome C and smac, and caspase-3 activation - was observed in the vehicle group. Propofol not only attenuated these alterations (P<0.05 for all), but also significantly decreased burn-induced ROS production (P<0.05). Propofol attenuated burn-induced RLMVEC monolayer hyperpermeability by regulating the intrinsic apoptotic signaling pathway.