Objective To compare the effects of flap delay and vascular endothelial growth factor (VEGF) on the viability of the rat dorsal flap. Methods Thirty rats were divided into 3 groups: saline group, flap delay group and VEGF group. The rats in flap delay group underwent flap delay by keeping bipedicle untouched, and the cranial pedicle was cut 7 days later. The rats in VEGF group were given VEGF solution locally when the flaps were elevated in the operation. The ratsin saline group were given saline solution in the same way. Five days after thesingle pedicle flaps were performed, the flap survival rate was measured. Theflap tissues were collected to measure and analyze the microvascular density, diameter and sectional area by immunochemical method. Results The flap survival rate of flap delay group was similar to that of VEGF group andthere is no statistically significant difference(Pgt;0.05). The vascular diameter of flap delay group was much larger than that of saline group and VEGF group, showing statistically significant difference (Plt;0.05). The vascular density of VEGF group was much higher than that of saline group and flap delay group, showing statistically significant difference (Plt;0.05). The vascular sectional area of flap delay group was similar to that of VEGF group(Pgt;0.05). Conclusion The change in the flap after flap delayis manifested as obvious dilatation of microvessels, while the change in the flap after the injection of VEGF is manifested as obvious vascular proliferation. Both flap delay and VEGF can increase the vascular sectional area and the viability of the flap, but the mechanism is different.
Objective To study the mutations at 1 573 fragment of TNF receptor II (TNFR-II) gene in patients with keloid. Methods The tissue DNA was extracted from 22 samples of keloids donated by 22 patients (6 males and 16 females, aged 18-53 years), and all keloids were examined and classified by pathologist. The peri pheral blood DNA was extracted from the same patients as the control. PCR was used to ampl ify the 1 573 fragment of TNFR-II gene from the keloid tissue DNA and peripheral blood DNA. The PCR products were sequenced directly and then compared with the GeneBankdata. Results All the concentration of the extracted DNA in trial were higher than 0.50 μg/μL and the purity (A260/A280) ofthe extracted DNA were higher than 1.5. It closed to the magnitude of the design DNA fragment by agarose gel electrophoresis examining, and corresponded with the test requirement. Mutations at 1 573 fragment of TNFR-II gene were detected in 13 out of 22 keloids. The mutation incidence was 59.1%. Among them, 9 had point mutation at codon 1 663, accounting 40.9%. No TNFR-II gene mutation was detected in all peripheral blood samples. There were significant difference between keloids DNA and peripheral blood DNA (P lt;0.01). The mutations involved point mutation, deletion and insertion as well as multisite and multitype. Conclusion There is a correlation between the mutation at 1 573 fragment of TNFR-II gene and keloid.