缺氧诱导因子-1α表达与大肠腺癌细胞增殖及血管形成的关系

目的探讨缺氧诱导因子1α(HIF1α)在大肠腺癌组织中的表达及其与细胞增殖、血管形成的关系。方法应用免疫组织化学方法检测20例正常大肠组织、60例大肠腺癌组织中HIF1α、增殖细胞核抗原(PCNA)蛋白表达及微血管密度(MVD),并分析HIF1α表达与PCNA、MVD的相关性。结果HIF1α蛋白在大肠腺癌中的阳性表达率为73.3%(44/60),其阳性表达与大肠腺癌淋巴结转移、Dukes分期有关,其阳性表达率淋巴结转移组(89.3%,25/28)显著高于无淋巴结转移组(59.4%,19/32)(P<0.05),并随肿瘤分期的升高而增高。HIF1α表达与PCNA、MVD呈正相关(γ=0.647,P<0.01和γ=0.655,P<0.01)。结论HIF1α在大肠腺癌组织中表达水平明显上调,并与肿瘤细胞增殖、血管形成密切相关,提示它可能在大肠癌的发生发展过程中起重要作用。     

63例宫颈腺癌临床治疗和预后分析

目的:了解影响宫颈腺癌预后的相关因素,探讨宫颈腺癌比较理想的治疗方法.方法:对天津医科大学附属肿瘤医院1980年1月至2000年1月间收治的63例宫颈腺癌进行分析,占同期宫颈癌的4.65%,并随机选取同期治疗的80例宫颈鳞癌作为对照进行比较.患者平均发病年龄53.7岁,绝经后患者占55.6%.主要症状为阴道不规则出血和/或白带增多.其中Ⅰ期17例,Ⅱ期33例,Ⅲ期13例.20例采用单纯放射治疗,43例采用放射治疗与手术相结合的综合治疗.结果:收治的宫颈腺癌占宫颈癌的比例从80年代的3.5%(38/1087)上升至90年代的7.36%(34/462),其5年总的生存率为56.9%(33/63-5),低于同期宫颈鳞癌5年生存率.单纯放疗组5年生存率50%;手术放疗组5年生存率为60.5%,两组间无统计学差异.行根治性手术的Ⅰ、Ⅱ期患者5年生存率为80%,而行全宫切除的同期患者5年生存率仅为39.3%,但二者差异尚无统计学意义.宫颈肿瘤≥4cm和＜4cm者5年生存率分别为34.3%(12/35)和60.7%(17/28)具有明显差异(P＜0.05).Ⅰ、Ⅱ期5年生存率62%(31/50),而Ⅲ期5年生存率为7.7%(1/13),二者差异显著(P＜0.01).结论:宫颈腺癌的发病比例呈上升趋势,宫颈腺癌的预后与临床分期、肿瘤大小、治疗方式关系密切.以根治性手术为主的综合治疗是宫颈腺癌的主要治疗方法.     

吉西他滨联合顺铂与去甲长春碱联合顺铂治疗老年晚期非小细胞肺癌临床分析

目的观察比较吉西他滨联合顺铂(GP方案)与去甲长春碱联合顺铂(NP方案)治疗老年晚期非小细胞肺癌的疗效、生存期及毒副反应.方法对61例经病理或细胞学证实的晚期非小细胞肺癌老年患者(年龄＞70岁)随机分为两组,GP方案组30例,NP方案组31例.GP组:吉西他滨1000 mg/m2,静脉滴注,第1,8天;顺铂80～100 mg/m2,静脉滴注,第1天.NP组:去甲长春碱25 mg/m2,静脉滴注,第1,8天;顺铂用法及剂量同GP组.两组均21 d为一周期,每例患者治疗两周期以上.结果 GP组总有效率40.0%,1年生存率为34.8%,中位生存期9.3个月;NP组总有效率38.7%,1年生存率30.0%,中位生存期为8.8个月.两组间总有效率、1年生存率比较差异均无显著性(P=0.58,P=0.51).最常见的毒副反应为骨髓抑制,GP组Ⅲ～Ⅳ度血小板减少发生率显著高于NP组(P=0.016),而NP组Ⅲ～Ⅳ度白细胞减少发生率显著高于GP组(P=0.01).结论吉西他滨联合顺铂与去甲长春碱联合顺铂治疗老年晚期非小细胞肺癌疗效肯定,毒性均可耐受.两方案疗效差异无显著性.     

全髋关节置换术的并发症及其处理(三)全髋置换术后脱位

全髋关节置换术后的髋脱位无论对病人还是对医生，都是一个警示信号。为什么出现脱位?是翻修还是保守治疗?保守治疗措施?关节脱位是否影响内植物的使用寿命?本文通过文献回顾对上述问题进行分析，包括脱位机制、脱位方向和术后脱位时间。     

全髋关节置换术的并发症及其处理(五)全髋关节置换术后的转子区问题

全髋关节置换(THR)手术时采用转子截骨有助于显露髋关节，但是存在不愈合及截骨块移位的风险。临床统计显示，初次全髋置换手术发生转子骨折者1．9％，翻修术为1．8％。转子骨折和截骨对THR术后的结果可能产生负面影响，特别是初次行THR术后。一旦骨折或截骨后不愈合，患者常常出现跛行。不愈合的处理十分困难，需要进行假体翻修术和固定。     

Lamivudine for the prevention of hepatitis B virus reactivation in hepatitis B s-antigen seropositive cancer patients undergoing cytotoxic chemotherapy.

PURPOSE: For cancer patients receiving cytotoxic chemotherapy, hepatitis B virus (HBV) reactivation is a well described complication resulting in varying degrees of liver damage. The objectives of this study were to assess the efficacy of the antiviral agent lamivudine in reducing the incidence of HBV reactivation and diminishing morbidity and mortality of cancer patients with chronic HBV infection during chemotherapy. PATIENTS AND METHODS: Two groups were compared in this nonrandomized study. The prophylactic lamivudine group consisted of 65 patients in a phase II study who were treated with lamivudine before and until 8 weeks after discontinuing chemotherapy. The historical controls consisted of 193 consecutive patients who underwent chemotherapy without prophylactic lamivudine. Significant prognosticators for the development of HBV reactivation were determined based on data from the controls. Potential confounding factors were identified between the two groups. The outcomes were compared. RESULTS: In the controls, lymphoma and anthracycline usage were factors identified to be associated with reactivation. The two groups were comparable in most baseline characteristics, although in the prophylactic lamivudine group, there were significantly more patients with lymphoma and receiving anthracyclines. In the prophylactic lamivudine group, there was significantly less HBV reactivation (4.6% v 24.4% in the controls; P <.001), fewer incidences of hepatitis (17.5% v 44.6%; P <.0001) that were less severe (4.8% v 18.7%; P =.0005), and less disruption of chemotherapy (15.4% v 34.6%; P =.0029). The reduction in overall mortality was not statistically different. CONCLUSION: Prophylactic lamivudine significantly reduced the incidence of HBV reactivation and the overall morbidity of cancer patients undergoing chemotherapy.     

Expression of hepatoma-derived growth factor is a strong prognostic predictor for patients with early-stage non-small-cell lung cancer.

PURPOSE: Hepatoma-derived growth factor (HDGF), which is unrelated to hepatocyte growth factor, can stimulate DNA synthesis and cell proliferation on entering the nucleus. We hypothesize that HDGF plays an important role in biologic behavior of early-stage non-small-cell lung cancer (NSCLC). PATIENTS AND METHODS: Ninety-eight patients with pathologic stage I NSCLC who underwent curative surgery were studied. Immunohistochemistry was used to determine the expression level of HDGF in the tumor specimens. The intensity of the protein staining and percentage of stained tumor cells were used to determine a labeling index. Statistical analyses, all two-sided, were performed to determine the prognostic effect of HDGF expression levels on clinical parameters and outcomes. RESULTS: The mean +/- standard deviation HDGF labeling index in the 98 tumors was 185 +/- 41. Patients whose tumors had higher HDGF indexes (>/= 185) had a significantly poorer probability of overall survival at 5 years after surgery than did those with lower HDGF indexes (0.26 v 0.82; P <.0001). Similarly, the 5-year disease-specific and disease-free survival probabilities were lower in those with higher HDGF indexes (0.42 v 0.92, and 0.34 v 0.71; P <.0001 and P =.0008; respectively). Multivariate analysis indicated that HDGF level was an independent predictor of overall, disease-specific, and disease-free survivals. CONCLUSION: Overexpression of HDGF is common in early-stage NSCLC. The expression level in tumor cells is strongly correlated with poor overall, disease-specific, and disease-free survivals, suggesting HDGF may be a powerful prognostic marker for patients with early-stage NSCLC.     

一种新型增殖型腺病毒治疗肝癌的体外研究

目的评价增殖腺病毒 CNHK500对肝癌细胞的治疗效果。方法利用病毒增殖实验、细胞活力实验(MTT)、蛋白印迹分析来检测增殖病毒 CNHK500在端粒酶阳性的肝癌细胞株 HepGⅡ、Hep3B、SMMC7721及正常细胞中选择性增殖和溶解细胞的特性。结果 CNHK500感染人肝癌细胞株 HepGⅡ、Hep3B、SMMC7721细胞后大量增殖,在感染后96小时增殖倍数分别为52000、396984.9和632911.3倍,同野生型5型腺病毒(wtAd5)类似。然而在正常细胞中,CNHK500的增殖能力较 wtAd5大大减弱,感染96小时后仅增殖3.1～100倍,而 wtAd5却高达3160～17357倍。MTT 实验观察到在肝癌细胞 HepGⅡ和 Hep3B 中,感染后第7天达到半数杀伤的 MOI 值(IC50)分别为2和0.01,而在正常成纤维细胞 BJ 细胞中却高达1000。在常氧情况下,用蛋白印迹可在肿瘤细胞中检测到腺病毒 E1A 蛋白的表达,但在正常细胞却检测不到。E1B 蛋白仅在缺氧条件下(0.1%O_2)的肿瘤细胞中表达。结论实验结果表明 CNHK500能有效地选择性在肝癌细胞中增殖、复制、杀伤,而在正常细胞中增殖和溶解细胞能力却大大减弱。联合治疗基因,CNHK500可能为肝癌的治疗提供一种新的策略。     

兔眼辐射损伤后角膜和晶体上皮细胞DNA含量的定量分析

利用改良Feulgen染色和图像分析技术对不同剂量6 0 Coγ射线 (0、 10、 2 0和 30Gy)和照后不同时间 (3、 15天和 1、 3、 6个月 )的兔眼角膜和晶体上皮细胞的DNA含量进行了定量分析。结果表明 ,各剂量组DNA含量的MOD和IOD值降低 ,与对照组相比均有明显差异 (p<0 0 1) ,提示辐射能引起角膜及晶体上皮细胞核中DNA含量发生规律性变化 ,因此角膜及晶体上皮细胞DNA含量测定可以作为眼辐射损伤的指标之一 ,为其诊断提供实验依据。