Objective To investigate the possibility of auricle reconstruction assisted by an expander using porous silicon auricle frame.Methods An adult male with average sized,normal ears was selected.The spiral CT scan was used to acquire primitive data of his external ear.Mimics 8.1 and Geomagic studio 12 were used for 3D reconstruction and image processing.Three-dimensional model of auricle 1.4 mm in thickness was created according to the anterior auricular surface data.Finally,a metal model was made according to the 3D model of auricle.By the extrusion method,silicon auricle frame was formed from the metal model.Multiple perforations,1 mm in diameter and 1 mm internal from each other,were then made by a puncher.50 ml kidney tissue expanders were implanted between the panniculus carnosus and the fascia through an incision on the backs of 10 New Zealand white rabbits.The expander was inflated with 20 ml saline weekly,to a total of 160 ml.Maintenance of expansion lasted for a month.The expander was then removed through an incision along the expander near the back.Silicon auricle frame was inserted into the pocket.The reconstructed ears were observed for 6 months postoperation.Whether there were deformations,contractures and extrusions were observed.Results The reconstructed ears were elastic and compressible.No deformation,contracture or extrusion were observed 6 months postoperation.Scaphoid fossa,triangular fossa,helix,antihelix were legible.Conclusions The silicon frame,1.4 mm in thickness manufacted by computer aided design,could stand up to contraction of the overlying expanded flap,and it thus is possible to be used for auricle reconstruction assisted by the expander.

Objective To evaluate the difference of adaptive exposure dose in two digital X-ray imaging systems. Methods Resin phantom and contrast-detail test phantom were used on Cesium iodide and Gadolinium oxide sulfide plate imaging detector DR systems using difference exposure parameters. All entrance surface dose were recorded, Image quality index (IQFinv ) was calculated by CDRAD analysis software. The optimal exposure radiation dose was determined according to the sensitivity and IQFinv. Results There were no significant differences of entrance surface dose between two digital X-ray systems on two different exposure parameters with 70 kV ( P > 0. 05) , while there were significant differences with 125 kV(P < 0.05) . The maximum difference was 28. 57% . The mean IQFinv value of Cesium iodide detector DR and Gadolinium oxide sulfide detector DR with 125 kV and 70 kV were 4. 89 ±1. 01 and 2.47 ±0.25, 5. 10 ±1.05 and 2.38 ±0.43, respectively. There were significant diferences between the two systems under the same exposure parameters (t = 6. 509,10. 158, P < 0. 05). The optimal exposure dose ratio between Cesium iodide and Gadolinium oxide sulfide detector DR system was 1:2. Conclusion According to the IQFinv value, the adaptive exposure parameter can be adjusted to achieve good image quality with low radiation dose on different digital radiography systems.

This study examined the effect of GHRP-6, a known GHSs receptor agonist, on the phosphorylation of cAMP-responsive element-binding protein (CREB) and the underly mechanism. GH3 cells were cultured and subjected to different treatments as follows: GHRP-6, GHRP-6 plus GHRH, phorbol ester (PMA), an activator of PKC, alone or in combination with GHRP-6, Gö6983, a general inhibitor of PKCs, in the presence or absence of GHRP-6, rottlerin, an inhibitor of PKCs, alone or plus GHRP-6. The cells were transiently transfected with PKCsigma-specific siRNA and then treated with GHRP-6. GH level was measured by enzyme-linked immunosorbent assay (ELISA). The expression of phosphor-CREB, PKCsigma, PKCtheta and phosphor-PKCsigma was determined by Western blotting. The results showed that GHRP-6 stimulated GH secretion in both time- and dose-dependent manners and enhanced the effect of GHRH on GH secretion. GHRP-6 was also found to induce CREB phosphorylation. Moreover, GH secretion was enhanced by the PKC activator PMA and reduced by the PKC inhibitors (Gö6983, rottlerin) and knockdown of PKCsigma. PKCsigma could be activated by GHRP-6. It is concluded that PKC, especially PKCsigma, mediates CREB phosphorylation and GHRP-6-induced GH secretion.

Objective:To compare the relative deviation between display value and measured value of entrance surface dose (ESD) at different tube voltages, source-to-image distances and phantom thicknesses, so as to provide the basis for the feasibility of using real-time ESD display value to evaluate the radiation dose and the suitability of exposure parameters.Methods:At two different tube voltages and source-to-image distances, the exposure experiments were carried out using three polyethylene models with surface area of 30 cm×30 cm and thickness of 5 cm, 10 cm and 20 cm, respectively. After each exposure, the ESD display values on DR equipment and the measured values on radiation dose detector were recorded. The Wilcoxon rank sum test was used to compare the difference between them, with the relative deviation of ESD display value calculated using formula.Results:At the same tube voltage and source-to-image distance, the ESD display values were not affected by the thickness of phantom, but the measured value changed with the thickness of the phantom. When the thickness of the phantom was 10 cm and 20 cm respectively, the ESD display value was smaller than the measured value and the difference was statistically significant ( Z=-2.201, -2.203, P<0.05). The thicker mold would lead to the larger relative deviation between display value and measured value. Only when the thickness of mold was 20 cm and source-to-image distance 100 cm, the relative deviation was greater than ±20%. Conclusions:The ESD display value on DR equipment can be used to evaluate the skin incident dose to the examinee, with necessary account taken of the influence of their body thickness.

This study examined the effect of GHRP-6,a known GHSs receptor agonist,on the phosphorylation of cAMP-responsive clement-binding protein(CREB)and the underly mechanism.GH3 cells were cultured and subjected to different treatments as follows: GHRP-6,GHRP-6 plus GHRH,phorbol ester(PMA),an activator of PKC,alone or in combination with GHRP-6,G(o)6983,a general inhibitor of PKCs,in the presence or absence of GHRP-6,rottlerin,an inhibitor of PKCs,alone or plus GHRP-6.The cells were transiently transfected with PKCσ-specific siRNA and then treated with GHRP-6.GH level was measured by enzyme-linked immunosorbent assay(ELISA).The expression of phosphor-CREB,PKCσ,PKCθ and phosphor-PKCσ was determined by Western blotting.The results showed that GHRP-6 stimulated GH secretion in both time-and dose-dependent manners and enhanced the effect of GHRH on GH secretion.GHRP-6 was also found to induce CREB phosphorylation.Moreover,GH secretion was enhanced by the PKC activator PMA and reduced by the PKC inhibitors(G(o)6983,rottlerin)and knockdown of PKCσ.PKCσ could be activated by GHRP-6.It is concluded that PKC,especially PKCσ,mediates CREB phosphorylation and GHRP-6-induced GH secretion.