腔内技术治疗高龄及高危良性前列腺增生的应用(附283例报告)

目的:探讨和总结腔内治疗技术在高龄和高危良性前列腺增生(BPH)患者中应用的安全性、有效性和治疗经验。方法:采用腔内治疗技术,包括经尿道等离子体前列腺电切术(transurethral plasmakinetic resectionof prostate,PKRP)和经尿道前列腺电切术(transurethral resection of the prostate,TURP),治疗高危(包括合并肾积水、肾功能不全、心功能不全、脑梗塞、慢性呼吸功能障碍、中重度贫血、糖尿病、膀胱肿瘤等疾病或腺体>80 g)、高龄(年龄>70岁)BPH患者283例,其中TURP组112例,PKRP组171组。结果:所有患者术后随访1~30个月。TURP组的国际前列腺症状评分(IPSS)、生活质量评分(QOL)和残余尿量(RUV)由术前的(27.5±2.8)分、(5.5±1.0)分和(75.0±20.0)ml下降至术后的(5.8±1.2)分、(1.0±0.5)分和(8.0±3.0)ml,而最大尿流率(Qmax)由术前的(6.5±2.0)ml/s上升至术后的(18.5±1.5)ml/s(P均<0.05);PKRP组的IPSS、QOL和RUV由术前的(28.2±2.2)分、(5.5±1.0)分和(80.0±20.0)ml下降至术后的(5.4±1.6)分、(1.0±0.5)分和(7.0±3.0)ml,而Qmax由术前的(6.8±2.1)ml/s上升至术后的(20.0±1.5)ml/s(P均<0.05)。两组的治疗效果之间的差异无统计学意义(P>0.05),而PKRP组术后并发症发生率较TURP组少(P<0.05)。结论:年龄在70岁以上伴有心肺、脑肾等重要脏器合并症的高龄及高危BPH患者,经腔内技术治疗,特别是以PKRP治疗,在全面的围手术期准备护理、熟练的手术操作、有效控制手术时间及术后密切监护、加强护理的情况下,具有出血少、安全性高、并发症少、疗效确切等优点。     

经骶尾直肠节段切除治疗直肠绒毛状腺瘤

目的 探讨经骶尾直肠节段切除手术在直肠中下段病变中的应用.方法 回顾性分析6例直肠绒毛状腺瘤经骶尾部手术治疗的临床资料.结果 术后病理检查示直肠绒毛状腺瘤5例,直肠绒毛状腺瘤癌变1例(侵及黏膜下层).6例均未发生直肠瘘、切口感染等并发症.5例获随访2个月至3年,未见肿瘤复发.结论 经骶尾部入路手术途径,具有术野清楚、暴露良好、操作简单、创伤小和并发症少等优点,适用于节段切除直肠病变.     

原发性胃恶性淋巴瘤的临床诊治分析

目的 探讨原发性胃恶性淋巴瘤（PGML）的诊断、治疗与预后.方法 回顾分析2000年～2008年收治的29例经术后病理确诊为原发性胃恶性淋巴瘤的临床资料.结果 29例患者中仅6例术前经胃镜活检确诊,所有患者均行手术治疗,26 例患者术后辅以化疗,手术切除率为89.7%.免疫组化证实B细胞型淋巴瘤27例,T细胞型淋巴瘤2例.25例获得随访,5年生存率为56%,其中Ⅰ期＋Ⅱ期5年生存率为61.9%（13/21）;Ⅲ＋Ⅳ期5年生存率为25 %（1/4）.结论 PGML临床表现无特异性,容易漏诊.胃镜活检是术前诊断该病的主要方法,手术切除联合应用化疗是治疗PGML的重要手段.免疫组化及临床分期对PGML的分类以及判断预后有重要意义.     

内皮素，一氧化氮在内毒素血症大鼠胃粘膜损伤中的作用

目的：观察内皮素－1（ET－1）、一氧化氮（NO）在内毒素血症胃粘膜扣伤中的作用。方法：应用内毒素血症胃粘膜损伤模型分别观察血浆、胃粘膜中ET－1、NO含量变化,以及胃粘膜血流（GMBF）、胃粘膜损伤面积的变化。结果：内毒素血症时ET－1含量增加、NO含量减少,特异性内皮素受体ETAR阻滞剂（BQ123）、NO前体L－精氨酸（L－Arg）能减轻内毒素血症时胃粘膜损伤的程度。一氧化氮合酶阻滞剂N^G－硝基－L－精氨酸甲酯（L－NAME）加重了该模型胃粘膜的损伤。结论：内源性ET－1／NO失衡参与了内毒素血症时胃粘膜损伤病理过程。纠正内源性ET－1／NO失衡,通过改善了GMBF,减轻胃粘膜损伤。     

粒细胞-巨噬细胞集落刺激因子基因修饰的树突状细胞疫苗增强体外抗肿瘤免疫效应

Objective To investigate if granulocyte-macrophage colony stimulating factor (GM-CSF) gene-modified dendritic cells ( DC) enhance antitumor immunity in vitro. Methods Mice were injected with chemokine ligand 3 (CCL3) via the tail vein. Fresh B220-CD11c+ cells were sorted from the peripheral blood mononuclear cells (PBMCs) and cultured into DCs by cytokines. DCs were transfected with AdGM-CSF gene at different ratios of multiplicity of infection ( MOI) to determine the optimal gene transfection conditions, and the expression of GM-CSF was detected after transfection. The variation of GM-CSF gene-modifiedDCs were analyzed by morphological examination, phenotype analysis, and mixed lymphocyte reaction (MLR). DCs were loaded with gastric cancer antigen obtained by freezing and thawing method. The killing effect of DCs vaccine-stimulated T lymphocytes on gastric cancer cells was assessed by MTT assay. INF-γ production was determined with the INF-γ ELISA kit. Results B220- CD11c+ cells increased obviously after CCL3 injection. The ELISA results showed that after GM-CSF gene modification, DCs could produce high level of GM-CSF. When DCs were transfected with AdGM-CSF gene at MOI equal to 100, the GM-CSF level in culture supematants reached saturation [(130.00±12.61) pg/ml]. After GM-CSF gene-modification, DCs tend to be more maturated as detected by morphological observation and phenotype analysis. At the same time, the capacity of activating the proliferation of allogeneic T lymphocytes was enhanced greatly. T lymphocytes stimulated by DCs transfected with GM-CSF gene showed a specific killing effect on gastric carcinoma cells and produced high level of INF-γ[ ( 1245. 00±13. 75) pg/ml].Conclusion After GM-CSF gene modification, DCs can produce high level of GM-CSF, which tend to be more maturated, and the capacity of activating the proliferation of allogeneic T lymphocytes is enhanced greatly. GM-CSF gene modified DCs can induce specific CTL to target tumor cells in vitro.     

拟Smac促凋亡多肽的合成及其生物活性的初步研究

目的探讨拟Smac多肽的合成及其对膀胱癌细胞的促凋亡生物活性。方法应用固相多肽合成技术,合成具有细胞膜穿透性SmacN7融合多肽,经RP-HPLC纯化、纯度分析,用质谱仪定性鉴定;通过荧光显微镜观察细胞凋亡形态、细胞增殖抑制率测定及流式细胞仪分析,研究其对低剂量丝裂霉素C诱导的膀胱癌T24细胞的凋亡促进作用。结果 可穿透性融合多肽SmacN7产物峰纯度达95％以上,分子量为3278．08,质谱鉴定结果与合成预期结果完全一致;50-500 μg／L SmacN7作用12-48h,肿瘤细胞出现典型的凋亡形态学改变;随着SmacN7浓度的增加或作用时间的延长,细胞增殖抑制率出现明显增加,药物作用12h、24h、48h后增殖抑制率分别为（9．62±1．07）％～（61．48±1．15）％、（24．17±1．02）％～（72．86±1．68）％、（43．24±1．15）％～（84．91±1．74）％;肿瘤细胞凋亡率也明显增加,分别为（6．12±1．16）％～（49．81±2．11）％、（13．47±1．15）％～（64．54±2．27）％、（28．91±1．08）％～（82．36±2．19）％。结论 固相合成的拟Smac融合多肽SmacN7为高纯度的目的肽,能够稳定地转入细胞内且利用率高,并有明显促进低剂量丝裂霉素C诱导的膀胱癌T24细胞凋亡的生物活性,为进一步研究膀胱肿瘤的生物治疗积累了有价值的资料。     

25例胃间质瘤的CT表现及其诊断价值

目的分析胃间质瘤（GST）的CT表现,探讨CT对其临床诊断价值。方法回顾性分析经手术病理证实的25例GST患者的CT及相关临床资料。结果GST的CT表现为软组织肿块,肿块向胃腔内、外或同时向腔内外突出,肿块的密度均匀或不均匀伴有大小不等,形态不一;增强后,肿块均匀强化或不规则强化,可见中心坏死及远处转移灶。本组病例中良性7例,肿块直径多数小于5cm,边界较清楚,CT显示多为均匀强化;恶性13例,肿块直径多数大于5cm,边界欠清楚,CT显示为不规则强化,肿块内有坏死表现或转移灶。结论CT可清楚显示肿块的外部形态、内部改变及其与周围脏器的关系,对GST的定位定性诊断及鉴别诊断具有重要价值。     

Effect of Smac on TRAIL-induced apoptosis of prostate cancer cell line PC-3 and the molecular mechanism

The effect of Smac gene on the TRAIL-induced apoptosis of the prostate cancer cell line PC-3 and the molecular mechanism were investigated. The Smac gene was transfected into PC-3 cells under the induction of liposome. The intrinsic Smac gene expression was detected by Western blotting. After treatment with TRAIL as an apoptosis inducer, in vitro cell growth activity was as-sayed by MTT colorimetry. The apoptosis rate of PC-3 cells was determined by annexin Ⅴ-FITC and propidium iodide staining flow cytometry. The expression of cellular XIAP and caspase-3 genes was examined by Western blotting. Smac-transfected cells (PC-3/Smac group) had significantly in-creased Smac protein level as compared with PC-3 controls (P<0.01). After induction with 100-200 ng/mL TRAIL for 12-36 h, cellular proliferation rate in PC-3/Smac group was significantly lower than in PC-3 controls (P<0.05). After induction with 100 ng/mL TRAIL for 24 h, the apoptosis rate in PC-3/Smac group was significantly enhanced as compared with that of PC-3 controls (P<0.05). Ac-cordingly, the XIAP expression level was down-regulated significantly (P<0.05) and caspase-3 sub-unit P20 was up-regulated significantly (P<0.05). It is suggested that the over-expression of cellular Smac can inhibit inhibitor of apoptosis proteins (IAPs), enhance caspases activity and the apoptosis rate of PC-3 cells induced by TRAIL, which may provide a useful experimental basis for prostate cancer therapy.     

真核表达质粒pcDNA3.1(+)-rmCGβ的构建和鉴定

目的 构建恒河猴绒毛膜促性腺激素β亚基(macaca mulatta chorionic gonadotrophin β subunit,rmCGβ)基因真核表达质粒pcDNA3.1(+)-rmCGβ,并了解该质粒能否在真核细胞中表达.方法 通过PCR扩增rmCGβ的全段基因cDNA,应用基因工程技术将扩增的cDNA克隆至PGM-Teasy,测序后插入pcDNA3.1(+)真核表达质粒,构建重组真核表达质粒pcDNA3.1(+)-rmCGβ,经限制内切酶酶切分析及测序鉴定正确后,用脂质体转染技术转染B16细胞,通过RT-PCR扩增出B16/pcDNA3.1(+)-rmCGβ细胞株中rmCGβ全段基因cDNA.结果 经4轮PCR,成功扩增出rmCGβ的cDNA全长基因,酶切和测序证明正确构建了真核表达质粒pcDNA3.1(+)-rmCGβ,通过RT-PCR方法 证实该质粒能在B16真核细胞中正确表达.建立了稳定的细胞株B16/pcDNA3.1(+)-rmCGβ.结论 成功克隆和构建了rmCGβ的真核表达质粒载体pcDNA3.1(+)-rmCGβ,为进一步研究rmCGβ的新功能和免疫治疗奠定了基础.     

尿脱落细胞增殖细胞核抗原mRNA检测在膀胱癌诊断中的应用价值

目的探讨尿脱落细胞增殖细胞核抗原(PCNA)mRNA检测在膀胱癌诊断中的应用价值。方法收集32例膀胱癌、52例泌尿系统良性疾病患者和10例健康志愿者清晨中、后段尿液,采用RT-PCR法检测尿脱落细胞PCNAmRNA表达,并与尿脱落细胞学检查结果比较。结果PCNAmRNA诊断膀胱癌的特异性为64%,低于尿脱落细胞学检测的88%(P<0.05),敏感性为100%,高于尿脱落细胞学检测的69%(P<0.01)。膀胱良性疾病患者、Ⅰ、Ⅱ、Ⅲ级膀胱癌患者尿脱落细胞PCNAmRNA表达强度分别为0.5128±0.0307、0.5153±0.0402、0.6560±0.0626、0.8657±0.0266。膀胱良性疾病患者与Ⅰ级膀胱癌患者间差异无统计学意义,与Ⅱ、Ⅲ级膀胱癌患者间差异有统计学意义(P<0.05)。膀胱癌患者尿脱落细胞PCNAmRNA表达强度随膀胱癌分级增加而升高(P<0.05)。浸润性膀胱癌患者尿脱落细胞PCNAmRNA表达强度高于浅表性膀胱癌患者(P<0.01),分别为0.8040±0.0807、0.5595±0.0447。结论尿脱落细胞PCNAmRNA检测在膀胱癌早期诊断、常规筛查以及术后复发监测中具有潜在的应用价值。