Critical size defect in the canine mandible.

OBJECTIVE: The purpose of this study was to determine the minimum size defect in a canine mandible that would not spontaneously heal during the dog's natural life (the critical size defect). STUDY DESIGN: Sixteen adult female mongrel dogs underwent continuity resection on both sides of the mandible to create bilateral defects. In 8 dogs, mandibular defects ranging from 5 to 20 mm were created with periosteal resection. In the other 8 dogs, mandibular defects ranging from 30 to 60 mm were created preserving the periosteum. The dogs were then killed at 6 months and the defects examined using radiographs and histologic analysis. RESULTS: When the periosteum was removed, mandibular defects greater than 15 mm failed to heal across the entire defect. However, when the periosteum was preserved, mandibular defects needed to be greater than 50 mm in order to fail to heal. CONCLUSION: The critical size defect in a canine mandible model is 15 mm when the periosteum is removed and 50 mm when the periosteum is preserved.     

手术治疗125例分化性甲状腺癌的5年随访结果分析

目的：探讨甲状腺全切除术在治疗分化性甲状腺癌中的临床应用价值。方法：采用我院1988年1月～2001年5月甲状腺全切除术或甲状腺侧叶切除加峡部切除术治疗分化性甲状腺癌125例,对其手术并发症发生、局部复发、转移情况及术后5年生存率进行回顾性对比分析。结果：甲状腺全切除术术后并发症发生率高于甲状腺侧叶切除加峡部切除术组;局部复发、转移率低于侧叶切除加峡部切除术组;5年生存率两组无显著性差异。结论：甲状腺全切除术是治疗甲状腺癌有效的手术方式,但应掌握手术指征,改进、提高手术技术,减少并发症。     

虚拟现实技术在枢椎椎弓根螺钉精确植入中的应用研究

目的探索以虚拟现实技术为基础的枢椎椎弓根螺钉置人方法。方法选取8具成人颅一颈椎标本，采用改良四柱式定位框架固定于枕颈，使颅-颈-肩形成统一刚体，保持空间位置恒定，CT薄层扫描获取枢椎三维定位信息，采用Aero—Tech立体定向手术规划系统三维建模，设计安全、可视化、个体化的虚拟置钉路径，反复虚拟演示验证钉道安全后，导向弓把持下置人导向钢针，复查CT评价置钉的准确性。结果16个枢椎椎弓根置钉过程中，方向出现偏差（横突孔突破）1个，失败率为6．25％。结论目标椎弓根的容积三维重建、置钉路径可视化设计和虚拟演示，使操作过程简单、直观而精确，不需要线形和角性参数的测量；加上导向抓持装置提供的稳定性，使该技术具有很好的临床应用前景。     

Discussing options between patients and health care professionals in genetic diagnosis: ethical and legal criteria

The specific characteristics of genetic data lead to ethical-legal conflicts in the framework of genetic diagnosis. Several international organisations, including UNESCO and the Council of Europe, have enacted rules referring to the use of genetic information. This paper discusses possible legal and ethical criteria that could be used in genetic testing.     

放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.