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.     

苦碟子注射液治疗突发性聋疗效的观察

目的:探讨苦碟子注射液治疗突发性聋的效果。方法:随机将120例患者分为两组,治疗组60例,予以苦碟子注射液治疗;对照组60例,予以低分子右旋糖酐联合复方丹参注射液治疗。结果:治疗组治疗耳聋、耳鸣总有效率分别为88.33%、82.86%,对照组分别为68.33%、62.50%,治疗组耳聋、耳鸣总有效率均明显高于对照组(P<0.05)。结论:苦碟子注射液治疗突发性聋疗效好且安全可靠,无明显不良反应。     

RNA干扰基因敲除MAGE-1在恶性胶质瘤U87细胞中的初步研究

目的：通过构建抑制MAGE-1的短片段双链核糖核酸（siRNA）表达载体，鉴定其在人恶性胶质瘤细胞系U87细胞中对MAGE．1基因表达的干涉作用。方法：化学合成2对编码短发夹RNA序列的靶向MAGE—1基因寡核苷酸链，克隆至经BglⅡ、HindⅢ双酶切的pSUPER载体上，重组构建核糖核酸干扰（RNAi）质粒载体。利用RT-PCR、流式细胞术和荧光显微镜，检测经稳定转染后胶质瘤U87细胞中MAGE-1的表达，以了解siRNA的干涉效果。结果：重组构建的pSUPER—MAGE—1载体经双酶切、电泳及插入基因片段序列分析，表明寡核苷酸链成功地插入至预计位点，且序列与预期完全一致。稳定转染后G418筛选出的U87多克隆细胞MAGE-1的表达经RT—PCR、流式细胞术和荧光显微镜检测，2对siRNA均有较明显的干扰作用。结论：载体的成功构建并能对U87细胞中的MAGE—1分子进行RNAi，为进一步研究MAGE—1在肿瘤中的作用，分析基因功能，展开肿瘤基因治疗奠定了基础。     

甲睾酮对小鼠生殖系统发育及生精功能的影响

目的 探讨甲睾酮对雄性小鼠精子的产生及生殖器官的影响.方法 将48只昆明小白鼠随机分为4组,每组12只,每天分别向各组灌胃甲睾酮16 mg/kg,32 mg/kg,64 mg/kg 和等量蒸馏水(对照组),连续10 d.结果 与对照组比较,甲睾酮16 mg/kg组精子活率最高为66.22%(P<0.05);甲睾酮64mg/kg组睾丸指数、精子畸形率、精子密度都极显著和显著地升高(P<0.01和P<0.05),且睾丸组织有较明显的病理学损伤.结论 适量甲睾酮能提高精子活率,大剂量使精子活率降低且畸形率升高.     

斑驳病一家系

斑驳病是一种罕见的常染色体显性遗传病。临床典型特征是先天性白发和白斑。先证者女,2岁3个月,额、腹及双下肢白斑和白色额发2年余。其父亲亦有白色额发和白斑,家族成员共3代19人,患病6人,年龄最小2岁,最大72岁。每代均有成员发病,男3例,女3例,符合常染色体显性遗传。     

妇女叶酸增补中需要关注的问题

妇女围孕期增补叶酸能够有效预防神经管缺陷等疾病的发生。随着对叶酸研究的不断深入，叶酸补充中出现了诸多问题。本文简要综述了叶酸在服用方式以及基础和临床研究中出现的值得讨论、已经引起关注和需要进一步研究探讨的问题，并提出了深入研究叶酸可能的发展趋势。     

使用便携式微量输液泵持续输注氟尿嘧啶的临床观察及护理

目的：探讨使用便携式微量输液泵在肿瘤化疗中持续输注氟尿嘧啶的应用效果。方法：选取我科2006年3月-2008年7月96例癌症化疗病人按入院先后顺序分为对照组和实验组,每组48例。对照组采用传统的化疗方式,采用浅静脉留置针直接从外周静脉输注氟尿嘧啶（5-Fu）连续5天,每天维持6-8小时。实验组采用浅静脉留置针连接便携式微量输液泵持续泵入氟尿嘧啶（5-Fu）120h～135h,两组均以21天为1个周期,观察两组病人化疗毒副反应发生情况。结果：实验组化疗毒副反应发生率明显低于对照组,平均住院时间明显缩短,两组比较差异有统计学意义（P〈0.01）。结论：使用便携式微量输液泵持续泵入氟尿嘧啶能减轻病人的毒副反应,缩短住院时间,提高肿瘤病人生活质量,有效减轻护士的工作负担。     

心脾综合征的多普勒超声心动图诊断

目的:探讨多普勒超声心动图对心脾综合征的诊断价值,分析其心脏伴随畸形漏诊及误诊原因,提高对心脾综合征诊断的准确率。方法:本文总结了221例心脾综合征患儿的超声检测结果,并与其心血管造影或磁共振检查结果进行对照。结果:超声心动图诊断为心脾综合征与心导管或磁共振结论符合者199例(占90.0%),诊断不符合者22例(占10.0%)。结论:多普勒超声心动图可以较准确地诊断心脾综合征,但对其心脏伴随畸形检出的准确率尚待进一步提高。     

肥胖类型与脑卒中亚型的相关性研究

目的探讨肥胖类型与脑卒中亚型的相关性。方法将573例急性脑卒中患者分为脑出血组126例,脑梗死组447例,脑梗死组再分为脑血栓形成组(215例)和腔隙性脑梗死组(232例),另外选择277例无脑卒中者为对照组。测量腰围、臀围和体重,计算体重指数和腰臀比(WHR),分析肥胖参数与脑卒中各亚组的关系。结果脑卒中各亚组与对照组肥胖发生率差异无显著性意义(P>0.05);各组WHR明显大于对照组(P<0.05)。WHR增大明显增加脑卒中各亚组的危险性(P<0.05);女性腹围增大患腔隙性脑梗死危险性升高(P<0.05);男性体重增加患脑出血的危险性升高(P<0.01)。结论腹型肥胖是脑出血、脑血栓形成和腔隙性脑梗死的危险因素之一。