局部进展期鼻咽癌同期放化疗卡培他滨联合顺铂剂量递增的Ⅰ期临床研究

Objective To decrease radiation induced toxicities especially mucostis in patients with locally advanced nasopharyngeal carcinoma( NPC ) who underwent concurrent radiochemotherapy, the maximum tolerated dose and dose limited toxicities of capecitabine combination with cisplatin were observed. Methods From Aug 2006 to Oct 2007, 24 patients with intensity modulated radiotherapy(IMRT) and concurrent chemotherapy with capecitabine and cisplatin for nasopharyngeal carcinoma(stages Ⅲ-Ⅳ) were enrolled in this study. There were four dose-level groups of Capecitabine[625-1250 mg/(m2 ·d) , d1-14]and fixed cisplatin dose[20 mg/(m ·d) ,d1-5) ]MRI and CT scan were used for evaluation of tumor shrinkage. Treatment related toxicities were evaluated according to the common toxicity criteria( NCI-CTC Version 3.0). Results The acute side-effects include Grade 3 or Grade 4 mucosal toxicity(lasting for at least 5 d) and Grade 3 or Grade 4 non-mucosal toxicity were evaluated. Group 625 mg/m2 and Group 825 mg/m2 had none, Group 1000 mg/m2 had 6 patients and Group 1250 mg/m2 had 3 patients for mucosal toxicity, which were the main dose-limited toxicity and relevant to the dose of capecitabine apparently( P < 0. 05 ). There was also a trend of increase by the dose level of capecitabine for other toxicities. The median follow-up time for all patients was 28. 5 months. The locoregional recurrence occurred in 2 patients and distant metastasis in 2 patients. Two-year overall survival rate and locoregional control rate were 100% and 91.7%, respectively.Complete response and partialresponse were found on MRI or CT scan in patients of 29. 2% at the end of treatment and 83. 3% after three months, respectively. Conclusions The combination regimen of capecitabine and cisplatin is safe and effective according to the preliminary result. Toxicities related to radiochemotherapy for NPC were significantly associated with the dose level of chemotherapy.     

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.     

医院协会在行业管理中的作用

医院协会是医院行业管理组织,以行业自律和维权为主体开展工作。作为政府、医院和患者的桥梁,医院协会要认清形势,明确目标,准确定位,科学有效地开展工作,推动卫生事业发展。     

肿瘤浸润淋巴细胞对直肠癌术前放疗预后的影响

目的 探讨直肠痛肿瘤组织内术前放疗后浸润淋巴细胞(TIL)数量改变对预后的影响.方法 搜集近8年余接受30 Gy分10次12 d完成的术前放疗的直肠癌患者107例,分析TIL分级与术前放疗后病理消退程度及预后关系.结果 直肠癌放疗前TIL 1级75例,2级16例,3级16例,4级0例,术前放疗后TIL 1级19例,2级43例,3级35例,4级10例.放疗后病理消退分级1级36例,2级57例,3级14例.单因素分析发现放疗前及放疗后TIL对局部病理消退影响有统计学意义(X2=36.80,P<0.01;X2=14.00,P<0.01);术前放疗后癌巢内TIL及病理消退对预后影响显著(X2=24.00,P<0.01;X2=12.17,P<0.01).Logistic多元分析提示放疗后TIL与病理消退关系密切(X2=8.05,P<0.01).结论 放疗前及放疗后TIL与直肠癌术前放疗局部病理消退相关.直肠癌术前放疗后癌巢TIL是影响生存预后的因素之一.     

苏云金杆菌以色列变种漂浮块剂防制城市小型滋生地中致倦库蚊和白纹伊蚊幼虫效果评价

目的：观察苏云金杆菌以色列变种漂浮块剂的稳定性及防制蚊幼虫效果。方法：生物测定及小型滋生地现场试验。结果：该块剂在水中可持续漂浮１４天，且不出现松散现象。其对致倦库蚊的ＬＤ５０为０．４２７８ｍｇ／ｍｌ；现场试验结果显示：在３．４ｍ２水池中，用５、１０、２０ｇ／ｍ２剂量，２４小时时致倦库蚊幼虫下降率分别为９４．５％、９１．８％和１００％，持效分别为１１、１３、１７天。相同剂量２４小时白纹伊蚊幼虫死亡率均为１００％，持效分别为６、８、１２天     

论新教师入职初期如何进行角色转变

新教师刚剐步入高校这一高等教育群体往往会面临很多角色转变方面的困惑,为了快速适应新环境,本文对新教师入职初期如何进行角色转变进行了归纳和总结。     

中药材贮藏期虫蛀现象的研究现状

中药材在贮藏过程中,受自身性质及外界贮藏因素的影响,容易发生虫蛀现象。虫蛀后的中药材,轻则影响外观,降低消费者的购买力;重则影响品质,降低其药用价值,并产生虫体、排泄物及分泌物等杂质,严重污染中药材。该研究对影响中药材虫蛀发生的相关因素和虫蛀后的成分变化进行文献整理,对预防虫蛀发生的养护措施进行系统总结,首次对可应用于中药材贮藏过程中的虫蛀发生检测技术进行综述。在贮藏过程中,虫蛀的发生是生物因素(害虫的来源、种类和虫口密度等)、内在因素(水分、化学成分和自身的新陈代谢等)和环境因素(温度、相对湿度和环境含氧量等)共同作用的结果。虫蛀发生后,中药材所含的成分含量存在明显的变化。通过对中药材入库前的严格检查、入库后的定期养护及采用恰当的贮藏养护方法,可降低虫蛀发生率,提高中药材的保存完好率。中药材的贮藏养护是保证质量的关键环节,通过科学规范的贮藏,严格执行操作管理规范,就能降低被虫蛀的风险,保证中药材的品质。     

补骨脂肝毒性及减毒研究进展

补骨脂是临床常用中药,相关药理研究发现补骨脂具有免疫调节、抗肿瘤、消炎抗菌和促进骨生长等作用。随着中医药事业的发展,近年来有关补骨脂引发肝毒性的相关案例报道引起了广泛关注。文章综述了补骨脂肝毒性的临床报道以及相关的毒理性研究,重点关注补骨脂引发肝毒性的相关成分和机制,总结临床应用中针对补骨脂增效减毒的炮制及中药配伍,为临床上补骨脂的合理用药及毒理学研究提供参考。     

醒脑静与纳络酮合用治疗肺性脑病120例临床研究

目的　探讨醒脑静与纳络酮合用治疗肺性脑病的疗效及安全性。方法　 12 0例肺性脑病患者 ,随机分为对照组 , 和治疗组。对照组 34例 ,常规治疗给予氧疗、抗感染、解痉平喘、排痰、应用呼吸兴奋剂。对照组 4 0例 ,常规治疗基础加用纳络酮。治疗组 4 6例 ,在对照组治疗的基础上加用醒脑静与纳络酮观察。治疗前后分别记录病人的神志和血气分析结果。结果　对照组 显效 6例 ,有效 18例 ,无效 10例 ,总有效率 70 .5 9%。对照组 显效 8例 ,有效 2 2例 ,无效 10例 ,总有效率 75 %。治疗组显效 12例 ,有效 32例 ,无效 2例 ,总有效率 95 .6 5 %。治疗组与对照组对比差异有显著意义 (P <0 .0 5 )。结论　醒脑静与纳络酮联合应用 ,能缩短病人的清醒时间 ,降低 Pa(CO2 ) ,提高 Pa(O2 )和 p H值 ,无明显副作用