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.     

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.     

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.     

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.     

术后不同时间应用双膦酸盐对骨质疏松性转子间骨折愈合的影响

目的 探讨术后不同时间应用双膦酸盐对骨质疏松性转子间骨折愈合的影响.方法 回顾性分析我院2009年1月至2014年10月收治的346例骨质疏松性转子间骨折病人的临床资料.根据术后应用双膦酸盐类药物的时间不同分为1周组(术后1周内开始用药,158例)、1月组(术后1周至1个月内开始用药,86例)和3月组(术后1～3个月内开始用药,102例).对比分析三组病人的骨折愈合情况、平均愈合时间、Harris髋关节评分、手术前后腰椎(L1～4)骨密度值变化及术后并发症情况等.结果 1周组、1月组和3月组的骨折正常愈合的比例(91.77％、91.86％和95.10％)、平均骨折愈合时间[(14.68±3.04)周、(15.22±2.46)周、(14.54±2.88)周]、髋关节Harris评分[(88.27±12.94)分、(86.36±13.16)分、(87.69±11.98)分]比较,差异均无统计学意义(P均>0.05).术后3、6个月时,3月组的腰椎骨密度值[(0.7187±0.1084)g/cm2、(0.7604±0.1225)g/cm2]均低于1周组[(0.7606±0.0855)g/cm2、(0.8027±0.1090)g/cm2]和1月组[(0.7533±0.1103)g/cm2、(0.7961±0.0881)g/cm2],差异均有统计学意义(P均<0.05);1周组腰椎骨密度值在术后3个月时即显著高于术前,而1月组、3月组则在术后6个月时才较前一次有明显升高.三组病人胃肠道反应、发热、肌肉或关节疼痛、再发骨折、内固定松动或移位、内固定感染、断钉等术后并发症的差异没有统计学意义(P均>0.05).结论 骨质疏松性转子间骨折术后不同时间应用双膦酸盐类药物不影响骨折的愈合,而术后早期应用双膦酸盐类药物可以更快地提升病人的骨密度.     

肩关节解剖学因素与肩袖修补术后关节僵硬的相关性分析

目的探讨肩关节解剖学因素与肩袖修补术后关节僵硬的相关性。方法回顾性分析2016年3月至2021年12月于民航总医院骨科行肩袖修补术的肩袖损伤患者212例, 男97例、女115例, 年龄(58.87±9.69)岁(范围41～72岁)。根据术后3个月是否发生关节僵硬分为僵硬组与无僵硬组。采用患者肩关节CT三维重建测量并计算所有患者术前及术后第1天临界肩关节角(critical shoulder angle, CSA)、肩峰指数(acromial index, AI)、肩峰外侧角(lateral acromion angle, LAA), 收集术前和术后3个月肩关节活动度(前屈、外展、外旋)及年龄、性别、病程、体质指数、肩袖肌腱脂肪浸润程度、肩袖撕裂程度、缝合方式、术前是否并发僵硬。比较两组解剖因素及临床特征的差异, 将差异有统计学意义的指标纳入二分类变量logistic回归分析。绘制受试者工作特征(receiver operating characteristic, ROC)曲线评估与术后关节僵硬相关因素的预测效能。结果僵硬组43例, 无僵硬组169例。两组年龄、性别、病程、体质指数、肩袖...     

锁定钢板治疗桡骨远端不稳定骨折97例临床研究

目的：探讨锁定钢板治疗桡骨远端不稳定骨折的临床疗效。方法：选取桡骨远端不稳定骨折患者88例,在桡骨远端掌侧自掌长肌腱桡侧进入,切断部分旋前方肌显露骨折端及移位的骨块,整复桡骨远端不稳定骨折复位。也可于相应背侧切口协助复位牵引结合撬拨矫正桡骨干骺端畸形,恢复桡骨长度、茎突高度、掌倾角、尺偏角、关节面平整、关节面解剖位置,安放合适的T型锁定加压铜板并且锁定螺钉行远端骨折块固定。根据患者病情劝导其做适当的恢复性和功能性的锻炼。结果：术后尽量保持掌倾角（11．0±5．0）°,尽量保持平均尺偏角（16．0±3．0）°。纠正桡骨短缩和腕关节脱位情况,固定无松动、无再移位,骨折处无感染和神经损伤。结论：应用锁定钢板治疗桡骨远端不稳定骨折疗效较满意。     

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

目的 观察放射线联合p53基因及内皮抑素治疗C57BL/6小鼠前列腺癌皮下移植瘤的效果,并初步探讨其作用机制。方法 建立C57BL/6小鼠前列腺癌皮下移植瘤模型。随机分成5组:空白组(A)、放射组(B)、放射线联合p53基因组(C)、放射线联合内皮抑素组(D)及放射线联合p53基因和内皮抑素组(E)。第1天C、E组瘤内注射p53基因腺病毒(1×1vp),第1~14天D、E组每日1次腹腔注射内皮抑素(1.5mg/kg)。第4天B、C、D、E组小鼠肿瘤区单次照射(6 MV X线D_T 15Gy)。每日测量肿瘤体积;检测各组肿瘤标本P53、Ki67及血管内皮生长因子(VEGF)的表达及微血管密度值(MVD)。结果 4个治疗组的肿瘤生长速度均低于空白组(P=0.000),其中E组生长最慢(P<0.05)。免疫组织化学结果:4个治疗组P53的表达均明显低于空白组(P=0.000);4个治疗组Ki67的表达均高于空白组,但变化趋势不同:B、C组Ki67的表达值接近,均随时间的推移而逐渐升高(P=0.000),D、E组的表达则呈现波动性;第5天时E组VEGF的表达最低(P<0.05);肿瘤生长过程中各组MVD值均持续升高,C、D、E 3组MVD值在各时间均高于空白组(P<0.05)。结论 放射线联合p53基因及内皮抑素的抑瘤效果优于单独放射治疗及放射线联合p53基因或内皮抑素。三者均有自己的作用机制,但相互之间可以互相影响。     

类风湿关节炎患者程序化死亡基因5与肿瘤坏死因子-α的表达及其相关性分析

目的 检测类风湿关节炎(RA)及骨关节炎患者血清、滑液中程序化死亡基因(PDCD)5及肿瘤坏死因子(TNF)-α的表达水平,并分析PDCD5与TNF-α表达的相关性,初步探讨PDCD5在RA发病机制中的作用.方法 选取2009年12月至2010年8月50例患者(其中RA 26例,骨关节炎24例),采用酶联免疫吸附试验(ELISA)法检测血清、滑液中PDCD5及TNF-α的含量,统计学分析采用t检验及Pearson直线相关分析.结果 血清中,RA患者的PDCD5含量显著高于骨关节炎患者[(37±33)与(13±14) pg/ml,P＝0.02];滑液中,RA患者的PDCD5含量也显著高于骨关节炎患者[(37±26)与(11±7)pg/ml,P＜0.01].TNF-α在RA患者血清中的含量与骨关节炎患者比较差异无统计学意义(P=0.122),但其在RA患者滑液中的含量显著高于骨关节炎患者(P=0.037).PDCD5与TNF-α在RA及骨关节炎患者的血清中均呈负相关(r=-0.55,P=0.004;r=-0.51,P=0.012),PDCD5与TNF-α在RA患者的滑液中也呈负相关(r=-0.49,P=0.012),但在骨关节炎患者的滑液中无相关(r=-0.353,P=0.09).结论 PDCD5与TNF-α是RA重要的凋亡调控因子,在RA的发生发展过程中发挥重要作用.     

血友病患者全膝置换围手术期的凝血因子替代治疗

背景：世界血友病协会的治疗指南明确表示,关节置换应当在保证患者凝血因子活性的情况下进行。目的：观察血友病关节炎患者行人工膝关节置换围手术期凝血因子替代治疗的安全性和有效性。方法：1997/2006在血液内科的配合下,围手术期行凝血因子Ⅷ和Ⅸ活性水平监测,根据指南制定常规流程,进行因子Ⅷ（冻干人凝血因子Ⅷ）或因子Ⅸ（凝血酶原复合物）的替代治疗,对4例血友病关节炎患者共6个膝关节行人工膝关节置换治疗。结果与结论：围手术期应用凝血因子进行常规替代治疗,血友病患者围手术期出血量与类风湿关节炎和骨关节炎患者差异无显著性意义（P=0.885）。置换后早期3个膝关节出现关节内血肿或肌肉出血,其中1例患者因凝血因子抑制性抗体形成,导致1侧膝关节置换后伤口裂开,行扩创清理后,伤口愈合良好。4例患者6个膝关节置换后没有晚期感染、假体松动、移位和断裂等并发症发生。所有4例患者置换前膝关节KSS评分平均28.2分,功能评分平均35分。置换后KSS评分85.2分,功能评分87分,与普通类风湿关节炎和骨关节炎膝关节置换后评分相似,但平均住院天数延长约3倍,住院费用为普通膝关节置换的2.5~3倍。结果显示凝血因子的替代治疗和凝血因子水平监测是保证血友病关节炎行人工膝关节置换最后成功的关键。