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。     

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.     

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。     

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。     

肱骨近端锁定钢板治疗对老年肱骨近端骨折患者Neer肩关节评分及术后并发症的影响

目的 探讨肱骨近端锁定钢板治疗对老年肱骨近端骨折患者Neer肩关节评分及术后并发症的影响.方法 将70例老年肱骨近端骨折作为实验对象,随机分成观察组与对照组,各35例,对照组患者使用普通钢板治疗,观察组患者使用锁定钢板进行治疗,对2组患者进行为期1年的随访.记录比较2组患者手术治疗后的Neer肩关节评分及术后并发症出现情况.结果 观察组患者手术时间(95.3±21.5)min、骨折愈合时间(61.2±26.3)d显著短于对照组手术时间(126.3±31.7)min、骨折愈合时间(91.6±24.8)d(P<0.05),观察组患者术中出血量(145.3±25.6)mL显著少于对照组(197.2±34.1)mL(P<0.05),观察组患者手术满意度(88.6%)显著高于对照组(74.3%)(P<0.05).观察组患者手术后1个月、3个月Neer肩关节评分显著高于对照组,仅在手术后1年,2组患者的Neer肩关节评分差异无统计学意义;对照组患者术后有2例肱骨头缺血性坏死,3例疼痛,观察组患者术后有2例疼痛,没有出现肱骨头缺血性坏死病症.结论 肱骨近端锁定钢板治疗对老年肱骨近端骨折具有更好的效果,具有创伤小、内固定坚强及并发症出现几率小的优点,值得使用与推广.     

PDCD5 Correlates with Disease Activity and IL-17 in Rheumatoid Arthritis

Background Programmed cell death 5 (PDCD5) is a novel apoptotic regulatory gene, which has a promoting effect on apoptosis of various tumor cells. Studies showed that PDCD5 accelerates the apoptosis of synoviocytes in vitro, implying its potential role in the pathogenesis of rheumatoid arthritis (RA). The objective of this study was to examine the expression of PDCD5 in serum and synovial fluid of RA and to determine its effect on the expression of inflammatory cytokine, interleukin-17 (IL-17), as well as the assessment of disease activity in RA. Methods PDCD5 and IL-17 levels in serum and synovial fluid from 18 RA patients and 22 Osteoarthritis (OA) patients were detected by ELISA. The concentrations of serum PDCD5 in 40 healthy people were also detected as control. As disease activity indices, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), and X-ray grading scale were also evaluated. Results The serum and synovial fluid PDCD5 levels in RA patients were significantly higher than those in OA and healthy controls. The serum PDCD5 level was inversely correlated with CRP and ESR. Further, serum PDCD5 level in RF negative group was significantly higher than that in positive group. In addition, PDCD5 level had a negative correlation with IL-17 level both in serum and synovial fluid of RA patients. However, the differences of synovial fluid PDCD5 level in RA patients with different Larsen stages were not detectable. Conclusions These results suggest that PDCD5 might play a role in the pathogenesis of RA. Insufficient apoptosis of FLS and inflammatory cells in RA could possibly cause the increased expression of PDCD5 protein. Meanwhile, PDCD5 level correlated negatively with disease activity indices and IL-17 level, implying it as a potential target in the diagnosis and treatment of RA.     

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.     

泪道再通管植入治疗慢性泪囊炎

目的 评价一次性泪道再通管植入治疗慢性泪囊炎疗效.方法 对28例（28只眼）慢性泪囊炎行一次性泪道再通管植入术,行泪道碘油造影后,经逆行扩张鼻泪管后植入一次性泪道再通管.结果 28只眼27只成功植入了泪道再通管,手术成功率96.4%.术后6个月随访有效率为100%.结论一次性泪道再通管植入治疗慢性泪囊炎操作简单,有效率高.