马来酸罗格列酮胃漂浮型缓释片的研究

目的：根据流体动力学平衡控释原理（HBS）研制了马来酸罗列酮胃漂浮型缓释片。方法；以体外释放度和漂浮情况为筛选指标，采用单因素考察和正交试验设计相结合， 对胃漂浮缓释片的处方、制备工艺及体外释放条件进行优化筛选；采用γ闪烁照相技术对优化处方的内漂浮情况进行胃内动态观察。结果：马来酸罗格列酮胃漂浮缓释片在释放介质中迅速起漂，持漂时间超过12h,12h达最大累积释放；初步确定在胃内滞留时间达3h以上。结论：优化处方的释放过程符合Higuchi方程，释放机制为异常扩散；胃漂浮片在胃滞时间明显长于普通片。     

脐血铅含量与婴儿神经行为发育的探讨

目的：了解广西地区儿童铅中毒状况，研究铅对婴儿神经发育的影响。方法：选择1020名婴儿，以脐血铅作为铅暴露示标，3月龄时在贝利（Bayley)婴儿发育表上以精神发育指数（MDI）和心理运动发育指数（PDI）为效应示标。结果：血铅≥0．48μmol/L的婴儿其MDI和PDI明显落后于相对低铅组，随着分界线的下移，两组间MDI和PDI差别渐趋缩小，当分界线为0.24μmol/L时，高、低铅组MDI和PDI已不存在统计学差异。结论：当血铅≥0.48μmol/L时，婴儿神经行为发育即可受到不利影响。     

膳食黑米皮抑制高脂诱导的家兔动脉粥样硬化形成及其机制的初步探讨

目的 探讨膳食黑米皮对高脂诱导的家兔动脉粥样硬化形成的影响及其作用机制。方法 24只雄性新西兰大耳白家兔,按体重随机分为3组,分别饲以正常基础饲料、高脂饲料(含96％基础饲料、0.5％胆固醇、3.5％猪油)、黑米皮饲料(含 91％基础饲料、0.5％胆固醇、3.5％猪油、5％黑米皮),实验期为 60d。用图像分析法测定各组家兔主动脉脂质斑块面积,并分析家兔氧化与抗氧化状态。结果 黑米皮实验家兔的主动脉壁斑块面积较高脂组低66%(P<0.001);黑米皮组实验家兔的主动脉壁8-ohdG含量和血清及主动脉壁中MDA水平也低于高脂组(P<0.05 );而红细胞及主动脉壁中SOD水平和血清α-生育酚含量在两个处理组之间差异无显著性。结论 膳食黑米皮可以抑制高脂诱导的家兔动脉粥样硬化形成,其机制可能与之降低机体氧化应激水平及过氧化脂质生成有关。     

经T管窦道网篮取石治疗胆道残余结石

目的：采用非手术方法治疗胆道残余结石，方法：应用介入方法经T管窦道网蓝取石，结果：治疗39例。取得了满意的疗效。成功率达92．3％，结论：经T管窦道网蓝取石治疗胆道残余结石，是一种简便，安全、有效的治疗方法。     

335例术后全身炎症反应综合征的临床分析

【目的】了解手术创伤对术后全身炎症反应综合征 (SIRS)的影响。【方法】搜集外科重症监护室 (SICU) 335例患者的术后资料 ,分析不同手术组SIRS发病率 ;手术时间、失血量与SIRS持续时间的关系 ;SIRS持续时间与术后并发症的关系。【结果】术后SIRS发病率为 75 8% ,大手术高达 92 4 % ;无并发症患者失血量与SIRS持续时间呈正相关 (r1=0 783,P<0 0 1) ,手术时间与SIRS持续时间呈正相关 (r2 =0 398,P <0 0 1) ;随着SIRS持续时间延长 ,并发症发病率显著增高 (P<0 0 5 )。【结论】术后SIRS发生、发展与手术创伤密切相关 ;监测SIRS进程有助于及早发现并发症     

5例胸腰段脊柱前路手术并发症分析

目的：分析胸腰段脊柱前路手术入路并发症，以提高胸腰段脊柱前路手术的水平，方法：对近4年来我科53例胸腰段脊柱前路手术出现的5例并发症进行回顾性分析，探讨并发症发生的原因。结果；本组病例1例发生腹膜后乳糜液漏，1例切口疝，1例气胸，2例深静脉血栓栓塞，经过积极治疗，全部治愈。结论：胸腰段脊柱前路手术并发症的发生大多数和术者对该段解剖知识，手术操作，认识程度和经验有关，可以避免或及早发现。     

抗前列腺增生药SL—89．0519—08的合成

目的：研究治疗前列腺增生的α1－受体拮抗剂SL－89．0519－08的合成路线。方法：以5－氯－2－甲氧基苯胺为原料，经环合，烃化，脱保护基和亲核取代等步骤，合成了目标化合物，同时对原料合成工艺进行了摸索。结果：合成的目标化合物经IR，^1HMNR,EI-MS和HRMS得以确证。结论：该合成工艺和路线适宜工业化生产。     

外科护理文书存在的风险及管理对策

对外科护理文书的风险细节管理中存在的问题进行阐述，提出强化外科护士的法律意识，树立风险源于细节的管理意识，保证护理文书记录的科学性、及时性、准确性及真实性，注重护患沟通，提高护理质量是降低护理风险，避免医疗纠纷发生的关键。     

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.