Objective To observe the pain behavioral performance of rats that different sensory nerve fibers were transected,and examine the expression of brain-derived neurotrophic factor(BDNF) in these models.Methods Twenty-four rats were divided into three groups according to random number table method:SUR group,GS group and SHAM group, which received sural nerve transection, gastrocnemius-soleus nerve transection or sham operation respectively.There were 8 rats in every group.The expression of BDNF in the lumbar 5 DRG and spinal dorsal horn were detected,and the types of damaged cells were also observed.Results In GS group, 50% paw-withdrawal thresholds were significantly decreased on the ipsilateral hind paw compared with baseline and with those in SHAM group,and the paw-withdrawal durations in response to the thermal stimulus increased significantly (P＜0.01 ＝.In contrast, no change was found in SUR group(P＞0.05 ).The expression of BDNF in the lumbar 5 DRG ( (37.87 ± 4.23 ) % ) and spinal dorsal horn ( (21.9 ± 3.1 ) % ) was significantly higher in GS group than in SHAM group( ( 17.31 ± 2.12 ) %, ( 12.6 ± 1.3 ) % ), and no significant difference was found between SUR and SHAM groups(P＞0.05 ).FG opposite cells which also expressed BDNF in GS group were more than those in SUR group ( (47.7 ± 1.8) % and (26.7 ± 2.3 ) % ) (P ＜ 0.01 ＝.The percentage in N200 and FG double positive cells to N200 positive cells in GS group was significantly increased in GS group than those in SUR group ( (47.7 ±1.8 ) %, (26.7 ± 2.3 ) % ) (P ＜ 0.01 ＝.Conclusion The data suggest that injury of the sensory nerve innervating skin does not produce hyperalgesia, but injury of the sensory nerve innervating muscle does.Different kinds of neuron were damaged and the differences of BDNF expression is essential for this difference.

BACKGROUND:Alveolar distraction osteogenesis is an important method for treating alveolar bone atrophy, the osteogenesis process and biomechanics play a crucial role in the fol owing implantation and repair. At present, no related experimental studies are found.
OBJECTIVE:To analyze the biomechanical and histological characteristics of alveolar distraction osteogenesis in a canine model.
METHODS:Twelve adult mongrel canines received premolars extraction and alveoloplasty in mandible to establish an atrophy alveolar model. After 3 months, a segmental alveolar osteotomy was performed in the randomly selected unilateral atrophy alveolar and two intra-osseous distractors were placed. After a 7-days latency period, the alveolar ridge was augmented at a rate of 1.0 mm/d for 5 days. After a consolidation of 1, 2, and 3 months, the canines were sacrificed and the specimens of the distracted alveolar bone were harvested for clinical, radiographic, histological and biomechanical analysis.
RESULTS AND CONCLUSION:The alveolar distractors obtained good healing with surrounding tissue. The atrophy alveolar bones were augmented for (4.80±0.50) mm and (5.12±0.47) mm by clinical and radiographic findings immediately after distraction, respectively. The bone trabeculae in the distracted chamber matured from 1 to 3 months of consolidation by histological analysis. The shearing force of alveolar distraction chamber increased from 1 to 3 months. After 3 months’ consolidation, the shearing force of distracted chamber was comparable to host bone. The histological and biomechanical property of distracted alveolar chamber is comparable to host bone after 3 months’ consolidation.

Objective To investigate the role of nitric oxide (NO) in the protective effects of morphine postconditioning against ischemia-reperfusion (I/R)-induced myocardial apoptoais. Methods Sixty pathogen-free SD rats were randomly divided into 4 groups ( n = 15 each) : group Ⅰ sham operation (S) ; group Ⅱ I/R; group Ⅲ morphine postconditioning ( M ) and group Ⅳ M + L-NAME ( non-selective NOS inhibitor). The animals were anesthetized with intraperitoneal pentobarbital 60 mg/kg, tracheostomized and mechanically ventilated. ECG was monitored. Right carotid artery was cannulated for BP monitoring and left jugular vein was cannulated for drug and fluid administration. Myocardial ischemia was induced by 45 min occlusion of left anterior descending coronary artery (LAD) followed by 120 min reperfusion. In group S LAD was exposed but not occluded; in group M morphine 1.25 mg/kg was injected iv over 5 min from 3 min before reperfuaion to 2 min of repeffuaion and in group M + L-NAME L-NAME 10 mg/kg was injected iv at 20 min before myocardial ischemia. Hemodynamic changes were monitored. The animals were killed at the end of 120 min reperfusion and their hearts removed. Myocardial apoptosis was determined by TUNEL technique. The expression of Akt phosphorylation was assessed by Western blotting. The NO content in myocardium was measured by a chemiluminescence detector.Results A large number of TUNEL positive cells (18.4 ± 1.1 ) % were observed in group I/R. Morphine postconditioning exerted a significant anti-apoptotic effect. The number of TUNEL positive cells was reduced to (10.8 ± 1.2)%. The myocardial eNOS phosphorylation expression and NO content were significantly increased in group M as compared with group I/R. The anti-apoptofie effect and increased NO production were significantly reversed by L-NAME. However, pretreatment with L-NAME did not inhibit the phosphorylation of eNOS in group L + M. Conclusion In vivo, morphine postconditioning can significantly reduce I/R-induced myocardial apoptosis through phosphorylation of eNOS and increase in NO production.

Objective To investigate the effect of morphine postconditioning on myocardial ischemiarepedusion(I/R)injury and the role of PI3K/Akt signaling pathway in the effect.Methods Seventy male SD rats weighing 280-330 g aged 16-17 weeks Were randomly divided into 5 groups(n=14 each):group Ⅰ sham operation(S);group Ⅱ I/R;group Ⅲ morphine postconditioning(M);group Ⅳ morphine postconditioning+ wortmannin(W+M);groupV wortmannin(W).Myocardial I/R injury wa.g produced by occlusion of anterior descending branch of left coronary artery for 45 min followed by 120 min reperfusion.In group M and W+M (groupⅢ,Ⅳ)morphine 1.25 mCkg was given iv at 3 min before and 2 min after reperfusion.In group W+M and W(groupⅣ,Ⅴ)wortmannin(a specific PDK inhibitor)15μ/gkg Was given iv at 20 min before ischemia. The animals were sacrificed at the end of 120 min repedusion for assessment of ischemic and infarct area and determination of total and phosphorylated Akt expression in myocardium by Western blot.Results There were no significant differences in the size of ischemic area and total Akt expression among the 5 groups. The infarct area was significantly smaller in group M than in group I/R. The were no significant differenees in the size of infarct area between group 1/R, W + M and W (group Ⅱ , Ⅳ,Ⅴ ). The phosphorylated Akt expression was significantly upregulated in group I/R and M as compared with group S, and was significantly higher in group M than in group I/R.Conclusion The PI3K/Akt signaling pathway activation is involved in the protective effect of morphine posteondifioning on myocardium against I/R injury.

BACKGROUND:Prefabricated customized bone flaps have the advantages of few trauma, good vascularization, ossification with predetermined shape, and can be used to restore bone defects with compromised blood bed.
OBJECTIVE:To establish animal models of mandibular reconstruction with prefabricated, customized bone flaps.
METHODS:After computed tomography scanning of nine rhesus’ head, customized meshes were made. After loading with recombinant human bone morphogenetic protein-2-incorporated demineralized freeze-dried bone al ograft (DFDBA) or coral ine hydroxyapatite (CHA), the constructs were implanted in latissimus dorsi muscle. Meanwhile, segmental mandibular defects were created, and the customized meshes loaded with DFDBA, CHA, or recombinant human bone morphogenetic protein-2-incooperated DFDBA and CHA were implanted in situ. At 13 weeks, prefabricated bone flaps with recombinant human bone morphogenetic protein-2-incorporated DFDBA or CHA were transferred to repair segmental mandibular defects. Clinical and histological analyses were used to evaluate the ossification and vascularization of the prefabricated implants in ectopic and orthotopic sites.
RESULTS AND CONCLUSION:Segmental mandibular defects were successful y restored with prefabricated bone flaps and recombinant human bone morphogenetic protein-2-incorporated CHA in situ, but other segmental mandibular defects remained with recombinant human bone morphogenetic protein-2-incorporated DFDBA, DFDBA and CHA in situ. Moreover, mandibles reconstructed with prefabricated bone flaps revealed more regenerated and homogeneous bone formation than other reconstructions. These findings suggest that the animal model of mandibular reconstruction with prefabricated, customized bone in rhesus monkey is applicable.