Inhibition of anchorage-independent growth and lung metastasis of A549 lung carcinoma cells by IkappaBbeta

To evaluate the role of the NF-kappaB signaling pathway in oncogenic transformation, we expressed IkappaBbeta, a specific inhibitor of NF-kappaB, in two human lung adenocarcinoma cell lines, A549 and H441. Expression of IkappaBbeta significantly reduced NF-kappaB activation induced by cotransfection with p65/RelA or TNF-alpha and abrogated the basal NF-kappaB activity in A549 cells. Transfection of IkappaBbeta into A549, H441 and K-ras-transformed NIH3T3 cells suppressed anchorage-independent growth as measured by colony formation in soft agar. Anchorage-independent growth of vector-transfected A549 cells in reduced serum could be enhanced by both EGF and IGF-I. In contrast, only EGF but not IGF-I could induce anchorage-independent growth of IkappaBbeta-expressing A549 cells, suggesting that the IGF-I signaling pathway regulating growth and survival may be blocked by IkappaBbeta. Interestingly, expression of IkappaBbeta suppressed growth of A549 cells in low serum in vitro without affecting in vivo growth subcutaneously in nude mice. However, metastatic growth of IkappaBbeta-expressing A549 cells in the lungs of nude mice was significantly inhibited. These results provide evidence that NFkappaB plays an important role in anchorage-independent growth and metastatic growth of lung carcinoma cells.     

Induction of tumor suppression and glandular differentiation of A549 lung carcinoma cells by dominant-negative IGF-I receptor

Overexpression or activation of insulin-like growth factor I receptor (IGF-IR) has been observed in many human cancers including breast, lung, colon and gastric carcinomas. We demonstrate that inhibition of the endogenous insulin-like growth factor I receptor by stable expression of a dominant-negative IGF-IR represses the transforming activity in vitro and tumorigenicity of human lung carcinoma cells A549 in vivo. The suppression of tumorigenicity in nude mice is correlated with the induction of glandular differentiation. In addition, functional inhibition of the endogenous receptor dramatically increases the sensitivity of A549 cells to a variety of apoptotic signals including UV irradiation and proteasome inhibitors. These effects are due to the formation of a stable heterocomplex of the dominant-negative receptor with the endogenous wild type receptor which reduces the kinase activity of the latter by twofold. Thus, inhibition of the IGF-IR signaling pathway not only suppresses tumorigenicity but also enhances sensitivity to apoptosis-inducing agents. Antagonizing IGF-IR signaling by promoting tumor differentiation and enhancing sensitivity to apoptotic death are potential cancer therapeutic approaches.     

低能量He-Ne激光氧液对肺炎的临床应用

目的探讨低能量Ｈｅ－ＮＥ激光氧液治疗肺炎患儿的价值。方法激光氧液以１０％葡萄糖３～５ｍｌ／ｋｇ体重,Ｈｅ－Ｎｅ激光功率３毫瓦,氧流量２升／分钟,照射时间８分钟配制而成,静脉滴注速度每分钟３０～４０滴,每日５０～１００ｍｌ,３～５天为一疗程。结果对１９９７年１月～１９９９８年１０月住院期间胸片证实的２５６例肺炎患儿与对照组比较有显著性差异（Ｐ＜０．０１）。结论此法对肺炎患儿治疗操作简易,正确可信。     

慢性肾炎NK细胞活性的研究

目的　研究红细胞对慢性肾炎NK细胞活性的作用。方法　检测了 49例患者和 15例健康人NK细胞活性、红细胞C3b受体花环率 (RCR)、红细胞免疫复合物花环率 (RICR)及血红蛋白 (Hb)的含量。结果　慢性肾炎患者NK细胞活性、RCR水平显著低于正常对照 (P <0 .0 5、P <0 .0 1) ,RICR水平显著高于正常对照 (P <0 .0 1) ;慢性肾炎患者NK细胞活性与RCR、Hb呈正相关 ,与RICR呈负相关。结论　红细胞对慢性肾炎NK细胞活性有明显活化作用 ,作用机制与红细胞胞浆中的NK细胞增强因子及红细胞膜免疫功能有关     

选择性门奇断流加贲门周围腹膜化治疗食管胃底曲张静脉出血21例

采用选择性门奇断流加贲门周围腹膜化治疗食管胃底曲张静脉出血２１例。手术方法为脾切除和仅切断进入胃和食管的出血性门静脉分支，对食管、胃外的门奇交通支予以保护，断流后利用胃底部包绕贲门和食管下段，使贲门周围腹膜化以阻止新生血管重新长入和避免再出血。经３个月至３．５ａ随访，仅１例再出血，无肝性脑病发生，患者的生活质量明显提高。结果提示该方法是治疗门脉高压症食管胃底曲张静脉出血的一种较好的措施。     

不宜切除小肝癌射频与射频联合全身化疗的随机对照初步研究

目的 研究射频联合化疗治疗不宜切除小肝癌的临床安全性以及对肝癌原位复发率的影响。方法 ≤3cm不宜切除的原发性肝癌患者38例,其中27例1年随访资料完整。根据射频与射频联合全身化疗的随机分组方案入选标准,射频组12例,射频联合全身化疗组15例。在超声引导下行多电极射频治疗。化疗方案为：表阿霉素50mg,d1,3,静推;顺铂40mg,d1,3,静滴;氟脲嘧啶500mg,d1,2,3,静滴。观察患者术后1,4,7d的肝功能、血常规和并发症,术后1,6,12个月复查GT(增强),评价两组患者治疗的安全性及原位复发率。结果 两组射频术后1个月,均无原位复发。射频联合全身化疗组6,12个月的原位复发率较单射频组明显下降,差异有显著性。两组均无严重并发症,肝功能、血常规变化差异无显著性。结论 对≤3cm不宜切除的原发性肝癌患者,射频联合全身化疗是安全的,并能降低肝癌原位复发率。     

静脉补铁和口服补铁对肾性贫血的治疗比较

目的　比较静脉和口服补铁对血液透析患者铁缺乏和贫血的治疗效果。方法　选择 41例维持性血液透析患者 ,平均透析时间 10 .3± 8.8个月 ,每周透析 2～ 3次。试验前检查每位患者的血红蛋白、血球压积、RBC、血清铁(SI)、血清铁蛋白 (SF)、转铁蛋白 (Tf)、转铁蛋白受体 (sTfR)、前白蛋白 (Pro Alb)和C反应蛋白 (CRP)。HCT <3 3 %作为贫血的指标 ,将患者随机分入静脉补铁组和口服补铁组 ,静脉补铁组 19例。给予枸橼酸铁 5 0mg透析后输入 ,共 10次 ,口服补铁组 2 2例 ,给予硫酸亚铁 60 0mg/d。两组病人都给予促红细胞生成素 60 0 0U/周 ,6周后两组重复检查上述指标。结果　试验结束时静脉补铁组各铁参数指标明显高于口服补铁组 ,Tf(2 .2 1± 0 .77vs1.75± 0 .2 5g/L ,P <0 .0 0 1) ;sTfR(1.2 2±0 .68vs 0 .78± 0 .19mg/L ,P <0 .0 1) ;SF(4 96.13± 3 0 6.5 7vs2 79.2± 2 0 6μg/L ,P <0 .0 0 1) ,SI(14 1.6± 5 8.7vs60 .6± 19.1μg/dl,P<0 .0 0 0 1) ;静脉补铁组贫血改善较口服组好 ,HCT上升值 (0 .0 5 4± 0 .0 5 0vs0 .0 3 7± 0 .0 40 )和Hb上升值 (13 .8± 14 .9vs6.9± 9.1P <0 .0 0 1)有明显差异 ;将两组病人治疗前后血红蛋白、血球压积的变化值 ,与治疗前后各铁参数变化值作相关分析 ,发现转