细胞外基质金属蛋白酶诱导因子和基质金属蛋白酶-2在喉癌中的表达

目的　了解细胞外基质金属蛋白酶诱导因子 (EMMPRIN )和基质金属蛋白酶 2 (MMP 2 )在喉癌的表达情况 ,探讨两者表达的关系以及与喉癌浸润和转移的关系。方法　采用免疫组织化学S P法对 47例喉癌和 2 2例正常喉组织中的EMMPRIN和MMP 2的表达情况进行检测。结果　EMMPRIN和MMP 2在喉癌的阳性表达率 (分别为 87.2 %和 91.5 % )明显高于正常喉组织分别为 ( 9.1%和 18.2 % ) ,EMMPRIN和MMP 2的强阳性表达与喉癌的病理分级、临床分期和淋巴结转移情况有关 ;EMM PRIN和MMP 2的表达一致率为 91.5 % ,Kappa值为 0 .614 ,两者表达具有明显的相关性。 结论　EMMPRIN和MMP 2在喉癌有阳性表达 ,表达与喉癌的临床分期和淋巴结转移有关 ,EMMPRIN与MMP 2的产生有密切的关系     

芬太尼透皮贴剂治疗中重度癌痛433例临床观察

目的:进一步评价芬太尼透皮贴剂治疗中、重度疼痛的疗效、安全性及对生活质量的影响,为临床合理用药提供参考资料.方法:采用多中心随机开放方法,对433例中、重度疼痛患者使用芬太尼透皮贴剂进行观察,芬太尼的初始剂量是2.5mg或参照吗啡芬太尼折算表计算,贴膜每3日更换1次,在使用期间根据疼痛情况进行剂量调整,直到患者无痛或基本无痛.结果:可评价患者336例,其癌痛缓解率100%,41.6%的患者第1次使用后未再进行剂量调整,57.3%的患者调整过1～3次.芬太尼的中位剂量7.5mg,其中92.9%患者在2.5～10mg之内.不良反应轻,主要为恶心、便秘、头晕、呕吐、嗜睡、排尿困难等.治疗后生活质量有明显改善.结论:芬太尼透皮贴剂治疗中、重度疼痛的疗效显著,使用方便,不良反应轻,能明显改善患者的生活质量,绝大多数患者的调整次数在3次以内,大多数患者的使用剂量在每3天2.5～10mg.     

上颌窦鳞癌中CyclinD1和CyclinE的表达及其意义

目的检测上颌窦鳞癌、上颌窦内翻性乳头状瘤及上颌窦炎性黏膜中CyclinD1和CyclinE的表达情况,并分析其表达与上颌窦鳞癌临床病理特性之间的关系.方法应用免疫组化方法检测50例上颌窦鳞癌、20例上颌窦内翻性乳头状瘤、10例上颌窦炎性黏膜中CyclinD1和CyclinE的表达情况.结果在上颌窦鳞癌、上颌窦内翻性乳头状瘤及上颌窦炎性黏膜中,CyclinD1阳性表达率分别为10.0%、25.0%和48.0%(P＜0.05);CyclinE阳性表达率分别为20.0%、35.0%和58.0%(P＜0.05).CyclinD1和CyclinE阳性表达率与上颌窦鳞癌患者的性别、T分型无显著相关(P＞0.05).CyclinD1和CyclinE在高、中和低分化的喉癌中阳性表达率组间比较差异无显著性(P均＞0.05).结论在上颌窦炎性黏膜、上颌窦内翻性乳头状瘤及上颌窦鳞癌中,随病变加重,CyclinD1、CyclinE阳性表达率呈逐渐升高的趋势.细胞周期调控网络中,细胞周期调控因子的异常可能是上颌窦鳞癌发生发展的内在原因.     

紫杉醇诱导视网膜母细胞瘤细胞凋亡及对磷酸化Bcl-2的影响

目的：研究紫杉醇(Tax)抑制视网膜母细胞瘤(Rb)细胞生长并诱导其凋亡及磷酸化Bc-2在其中的作用。方法：应用^3H-胸腺嘧啶掺入分析法观察Tax对细胞生长的抑制作用，以DNA片段凝胶电泳分析细胞凋亡，用Western blot分析Tax对磷酸化Bcl-2的影响，用cDNA细胞转染法观察突变型Bcl-2阻断Tax的作用。结果：Tax可明显地抑制Y79细胞的生长，1μmoL／L Tax处理24小时，^3H-胸腺嘧啶掺入率下降达55．43％，Tax可诱导Y79细胞凋亡。在此过程中，Bcl-2被磷酸化。当Y79细胞被转染突变型Bcl-2后，Tax对Y79细胞的作用被阻断。结论：Tax可抑制Y79细胞生长并诱导其凋亡，磷酸化Bcl-2参与其过程。     

p53和p16蛋白在星形细胞瘤中的表达及其意义

 目的　研究 p5 3、p16蛋白在星形细胞瘤中的表达及其意义。 方法　应用S P法检测 5 6例星形细胞瘤 p5 3及 p16蛋白 ,并同时行组间对照。 结果　p5 3蛋白随肿瘤级别增高表达明显增加 ,各级别间差异性显著 (P <0 .0 5 )。而p16蛋白则随级别增高其缺失率增加 ,各级别间差异性显著 (P <0 .0 5 )。结论　p5 3蛋白高表达和p16蛋白的缺失是星形细胞瘤发生和恶变的重要原因之一。p5 3表达增高可能是星形细胞瘤恶变的信号 ,但 p16在星形细胞瘤的发生和恶性化的过程中可能起更重要的作用     

Multiple myeloma regression mediated by bruceantin.

PURPOSE: Bruceantin has been shown to induce cell differentiation in a number of leukemia and lymphoma cell lines. It also down-regulated c-MYC, suggesting a correlation of down-regulation with induction of cell differentiation or cell death. In the present study, we focused on multiple myeloma, using the RPMI 8226 cell line as a model. EXPERIMENTAL DESIGN: The effects of bruceantin on c-MYC levels and apoptosis were examined by immunoblotting, 4',6-diamidino-2-phenylindole staining, evaluation of caspase-like activity, and 3,3'-dihexyloxacarbocyanine iodide staining. The potential of bruceantin to inhibit primary tumor growth was assessed with RPMI 8226 xenografts in SCID mice, and apoptosis in the tumors was evaluated by the terminal deoxynucleotidyl transferase-mediated nick end labeling assay. RESULTS: c-MYC was strongly down-regulated in cultured RPMI 8226 cells by treatment with bruceantin for 24 h. With U266 and H929 cells, bruceantin did not regulate c-MYC in this manner. Apoptosis was induced in the three cell lines. In RPMI 8226 cells, apoptosis occurred through proteolytic processing of procaspases and degradation of poly(ADP-ribose) polymerase. The mitochondrial pathway was also involved. Because RPMI 8226 cells were the most sensitive, they were used in a xenograft model. Bruceantin treatment (2.5-5 mg/kg) resulted in a significant regression of tumors without overt toxicity. Apoptosis was significantly elevated in tumors derived from animals treated with bruceantin (37%) as compared with the control tumors (14%). CONCLUSIONS: Bruceantin interferes with the growth of RPMI 8226 cells in cell culture and xenograft models. These results suggest that bruceantin should be reinvestigated for clinical efficacy against multiple myeloma and other hematological malignancies.     

人前列腺癌细胞PC-3M亚系u-PAR基因表达的分析

目的 为研究与人前列腺癌细胞(PC-3M)侵袭能力相关的靶分子。方法 采用有限稀释法分离单克隆细胞株，并应用单层细胞侵袭等实验鉴定各亚系的体外侵袭能力；借助RT-PCR和免疫组化的方法，分别在转录和翻译水平检测5株侵袭能力不同的PC-3M亚系尿激酶型纤溶酶原激活物受体(u-PAR)的表达。结果 高侵袭亚系u-PAR基因mRNA的表达和蛋白质水平均明显高于低侵袭亚系。结论 PC-3M亚系u-PAR的高表达与其较强的侵袭能力密切相关，而u-PAR可能是抑制高侵袭亚系侵袭效应的一个重要靶分子。     

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。     

Effects of N-acetylcysteine on pulmonary macrophage activity after intestinal ischemia and reperfusion in rats / with invited commentaries

BACKGROUND/AIMS: Intestinal ischemia and reperfusion (I/R) is considered to be a critical and triggering event in the development of distal organ dysfunction after a variety of insults. It appears that activated leukocytes, especially polymorphonuclear granulocytes (PMNs), and reactive oxygen species are important mediators in the process. In the present study, the aim was to evaluate the behavior of pulmonary macrophages, acute lung injury and pulmonary endothelial permeability after intestinal I/R, together with potential alterations in pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity. METHODS: Intestinal ischemia for 40 min was followed by reperfusion for 12 h in the rat. Macrophage uptake of radiolabeled bacteria, levels of pulmonary blood content assessed by radiolabeled red blood cells and pulmonary endothelial permeability of radiolabeled albumin, as well as pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity by the use of scanning electron microscopy and a tracer was evaluated after 12 h reperfusion. Treatment with the free radical scavenger N-acetylcysteine (NAC) administered prior to reperfusion was evaluated. RESULTS: Overactivation of pulmonary macrophages was noted after intestinal I/R, as was a significant decrease in pulmonary blood content. No increase in pulmonary albumin leakage or increase in pulmonary water content was found after intestinal I/R as compared to controls. Treatment with NAC prevented against intestinal I/R-induced overactivation of pulmonary macrophages and a decrease in pulmonary blood content. CONCLUSION: Reactive oxygen species may be involved in the regulation of pulmonary macrophage function and pulmonary circulation after intestinal I/R.