腹腔镜手术和开腹手术治疗盆腔炎性包块的比较

目的:探讨腹腔镜手术治疗盆腔炎性包块的可行性及其价值。方法:收集1999年6月至2004年7月间,41例腹腔镜手术治疗的盆腔炎性包块及13例开腹手术病例,比较其住院天数、费用、疾病种类、手术和术后恢复情况。结果:腹腔镜手术和开腹手术相比较,两组手术时间、住院费用及手术费用差异无显著性(P>0.05),腹腔镜组手术并发症、术中出血量少于开腹手术组,术后排气时间、体温恢复到正常时间、血象恢复时间、术后拆线时间、住院时间均短于开腹手术组,差异有显著性(P<0.05)。结论:腹腔镜手术治疗盆腔炎性包块是可行的,具有较好的临床应用价值。     

益气利水化瘀汤治疗心肌缺血62例疗效观察

目的观察自拟益气利水化化瘀汤治疗心肌缺血的疗效。方法120例心肌缺血患者随机单盲分为两组,治疗组62例服用自拟益气利水化瘀汤,对照组服用消心痛治疗,15d为一疗程。结果治疗组症状改善总有效率为90.32%,对照组有效率为50.00%,治疗前后临床症状改善差异有显著性意义(p<0.01);治疗后心电图改善情况治疗组为74.19%,对照组为48.28%,治疗前后心电图改善差异有显著性意义(p<0.05)。结论自拟益气利水化化瘀汤对治疗心肌缺血有确切的疗效。     

中药内外合治溃疡性结肠炎62例临床观察

[目的]观察中药内服配合灌肠治疗慢性溃疡性结肠炎的疗效。[方法]内服自拟健脾补肾汤配合清热燥湿解毒中药保留灌肠。[结果]62例中痊愈28例,占45·16%;好转27例,占43·55%;无效7例,占11·29%。总有效率为88·71%。[结论]中药内服配合灌肠治疗慢性溃疡性结肠炎的疗效确切,能加速溃疡面愈合并可促进和调整机体的免疫功能。     

抑郁症神经生化和神经电生理学研究进展

抑郁症的发病机制复杂,神经生化学理论是迄今最为“肯定”、并被临床药理“充分利用”的,用以阐述抑郁症发病的神经生物学机制,抑郁症的发生不但与去甲肾上腺素(NE)、5-羟色胺(5-HT)水平相关;也可能与多巴胺(DA)、乙酰胆碱(Ach)、神经肽、γ-氨基丁酸(GABA)能系统等多种神经递质及受体的功能紊乱有关,还与内分泌系统和神经营养因子系统等方面的异常有关。同时,抑郁症的发生还可能与神经认知功能的缺损及神经电生理学的改变有关。     

海藻糖在气管低温保存中的保护机制

目的探讨海藻糖在气管低温保存中的保护作用和机制。方法新鲜配制4组保存液，其中：Ⅰ组LPD；Ⅱ组LPD 10％DMSO；Ⅲ组LPD 0．15M海藻糖；Ⅳ组LPD 10％DMSO 0．15M海藻糖。切取SD大鼠气管后立即分别放入含上述4种溶液的冻存管，在程序降温仪降至-80℃后投入液氮中保存。20d后对气管标本进行HE染色和Bcl-2、Pax蛋白检测(免疫组化)，并将其异位移植到Wistar大鼠腹腔，15d后取出移植气管，观察组织学变化。结果4种保存液低温保存气管20d后，Ⅲ组和Ⅳ组气管结构完整，软骨细胞Pax蛋白表达较低，尤其Ⅳ组保存效果最好，同种异体异位移植后生长良好。各组Bcl-2蛋白表达无明显区别。结论在气管低温保存中海藻糖的保护作用主要是通过对软骨细胞的保护实现的，抑制软骨细胞Pax基因的表达是其中的保护机制之一。海藻糖和DMSO合用保护作用更好。     

利用稻瘟霉分生孢子跟踪分离面包海星中的海星皂苷活性成分

目的研究面包海星中的海星皂苷活性成分。方法以稻瘟霉模型进行活性监测，采用多种层析手段和波谱技术对海星皂苷活性成分跟踪分离并鉴定其结构。结果分离获得14个海星皂苷，鉴定了其中12个结构(1～12)，包括7个新的海星皂苷(6～12)。其中大多对稻瘟霉显示活性且对K-562和BEL-7402肿瘤细胞株显示显著或中等强度的细胞毒性，2个皂苷有溶血作用。结论利用稻瘟霉模型对海星皂苷活性成分进行跟踪分离是可行的，该研究也为进一步开发抗肿瘤新药提供了有价值的先导化合物和科学依据。     

LRIC1基因在人星形细胞瘤中的表达与意义(英文)

目的 LRIG1基因是新发现的与果蝇 Kek-1基因同源的人类基因。Kek-1基因编码一种果蝇细胞表面蛋白—kekkon-1蛋白,它可抑制果蝇表皮细胞生长因子受体(EGFR)介导的信号转导。人类 LRIG1蛋白是一种跨膜糖蛋白,胞外区含亮氨酸重复区域和免疫球蛋白样区域。既往的研究显示 LRIG1几乎表达在所有被检测的人类组织中,如前列腺、乳腺、回肠、胃、肺和脑组织等。然而,目前对它在人类组织中的作用仍然未知。本研究的目的是进一步扩大 LRIG1的表达谱,并探讨它在肿瘤中的作用与意义。方法设计、制作 LRIG1 mRNA 寡核苷酸探针,用原位杂交检测 LRIG1 mRNA 在16例不同级别人星形细胞瘤中的表达,并与相应的肿瘤周边组织相比较;原代培养11例星形细胞瘤细胞,用 PCNA 行免疫组化及 LRIG1探针行原位杂交,分析培养细胞 PCNA 表达和 LRIG1表达之间的关系。结果人星形细胞瘤与其周边组织中均有一定程度的 LRIG1表达,肿瘤组织表达 LRIG1的水平较肿瘤周边组织低,这种降低的程度与肿瘤的级别成正比;培养细胞中也有一定程度的 LRIG1表达,其表达的程度与 PCNA 染色呈反比。结论 LRIG1蛋白具有抑制星形细胞瘤生长或增殖的作用,LRIG1的表达下调,可能参与了肿瘤的发生和发展过程。     

婴儿双歧杆菌/胞嘧啶脱氨酶肿瘤靶向性基因治疗系统的构建(英文)

目的构建婴儿双歧杆菌/胞嘧啶脱氨酶靶向性基因治疗系统。方法 PCR 扩增 CD 基因,EcoR Ⅰ,BamH Ⅰ对 CD 基因和 pGEX-1LamdaT 质粒同时进行双酶切,获得4.9 kb、1.3 kh 两个 DNA 片段。T4 DNA 连接酶连接这两个片段构建重组的CD/pGEX-1LamdaT 质粒,然后用电穿孔法将重组质粒转染婴儿双歧杆菌。从阳性转染的婴儿双歧杆菌中提取重组质粒,双酶切后检测切取片段长度,采用 Sanger 双脱氧链终止法对提取的重组质粒中的插入片段进行测序。结果从阳性转染的婴儿双歧杆菌中获得了6.2 kb大小的重组质粒,该质粒经双酶切后,得到了4.9 kb 和1.3 kb 两个长度的片段,其长度分别与 pGEX-1LambdaT 及 CD 基因的长度相同。测序结果显示,提取的重组质粒中插入的基因片段全长及核苷酸序列与 CD 基因完全相同。结论外源性 CD 基因被准确插入 pGEX-1LambdaT 质粒并转入婴儿双歧杆菌中,婴儿双歧杆菌/胞嘧啶脱氨酶靶向性基因治疗系统被成功构建。     

Results of Treating Vertebral Metastases by Percutaneous Vertebroplasty Combined with Interventional Chemotherapy

OBJECTIVE Vertebral metastases are a common manifestation in patients with advanced cancer and treatment is often ineffective. This study was conducted to explore the efficacy of treating vertebral metastases by percutaneous vertebroplasty （PVP） combined with interventional chemotherapy. METHODS Seventy-five patients with vertebral metastases （42 men, 33 women; ages 31-76 years） were divided into 2 groups： 39 cases were treated by PVP combined with chemotherapy （VPCC group）, and 36 cases were treated by PVP alone （VP group）. All procedures were guided by computed tomography （CT） scanning. The results and complications were evaluated by a questionnaire regarding pain and routine follow-up. RESULTS The response rate was significantly higher in the VPCC group than in the VP group （93.0% vs 74.4%, P〈0.05）; total response rates for the VPCC and VP groups were 25.6% and 10.3% respectively. A common complication related to VPCC was transient aggravating pain. CONCLUSION PVP may ameliorate pain, and consolidate the vertebrae of patients with vertebral metastases. Its short-term effect may be enhanced by adding drugs into the bone cement.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.