白细胞介素-18在治疗冠心病合并心力衰竭变化的研究

目的：分析白细胞介素-18（IL-18）的水平在冠心病合并心力衰竭治疗前后的变化。方法：采用酶联免疫法（ELISA）检测人血浆IL-18,冠心病合并心衰患者106例,对照组31例。结果：冠心病合并心衰患者血浆IL-18水平高于正常对照组（P〈0.05）,心衰治疗后血浆IL-18水平显著降低（P〈0.05）。结论：IL-18可能参与冠心病合并心衰的发生发展过程。     

第五届全国中西医结合虚证与老年医学学术会议纪要

第五届全国中西医结合虚证与老年医学学术会议纪要第五届全国中西医结合虚证与老年医学学术交流会于１９９６年１１月４日～７日在湖北省宜昌市举行。现将本次会议学术交流的内容简单介绍如下。虚证理论研究上海医科大学沈自尹教授等通过对神经—内分泌—免疫网络功能的检...     

白细胞介素2基因转染肿瘤细胞体外生物学特性的研究

将人IL-13基因导入肿瘤细胞观察其对小鼠体内肿瘤生长的抑制作用.P815是强致癌性的DBA/2小鼠肥大细胞瘤,将含人IL-13cDNA的质粒载体以磷酸钙共沉淀法导入P815K系,择出一分泌IL-13能力为40ng(每10~6细胞/每24小时)的亚克隆,同法制备分泌鼠IL-2能力为2.2ng的p815 IL-2细胞,及人IL-13分泌量为700ng的CHO IL-13细胞.p815 IL-13细胞一侧肋腹皮下接种同系DBA/2小鼠(每鼠5×10~5细胞),观察到肿瘤的短暂生长,其后出现完全性肿瘤排斥,第25～32天时,绝大多数小鼠肿瘤完全消失;p815 IL-2细胞接种小鼠出现相似过程,而亲本p815细胞接种后肿瘤持续生长至巨大肿瘤.60～70天后给     

人天然白介素－2治疗恶性肿瘤的Ⅱ期临床观察

目的评价人天然白介素－２（ＩＬ－２）治疗恶性肿瘤的效果。方法采用ＩＬ－２加淋巴因子激活的杀伤细胞（ＬＡＫ细胞）全身输注治疗１４例实体瘤（恶性黑素瘤４例，肾癌２例，原发性肝癌和肠癌各３例，恶性淋巴瘤和恶性腮腺混合瘤各１例）和胸腹腔内注入治疗１０例癌性胸腹水（胃癌４例，卵巢癌２例，肠癌、乳腺癌、胰腺癌和肺癌各１例）。结果实体瘤缓解率为２１．４％（３／１４），胸腹水缓解率为７０％（７／１０）。不良反应有发热（＜３９℃）３例；恶心１例；肾功能障碍１例，停药后恢复正常。结论人天然ＩＬ－２具有一定的抗肿瘤作用。     

Serum soluble interleukin-2 receptors and tumor necrosis factor-α in hematological malignancies of childhood

The levels of soluble interleukin-2 receptors (sIL-2R) and tumor necrosis factor (TNF) were determined in the serum of 61 children with hematological malignancy, including 20 patients with leukemia and 16 with lymphoma in active state of malignancy, and 20 patients with leukemia and 5 with lymphoma in complete remission. In addition, serum samples from 15 healthy children were used as controls. It was found that the mean serum levels of sIL-2R and TNF were significantly increased in active malignancy (207.0±17.1 pmol/L for sIL-2R; 209.7±35.0 pg/mL for TNF) compared to the remission status and normal controls (P<0.001). No such difference was observed between leukemia and lymphoma groups. It was concluded that serum sIL-2R and TNF are of potential value in the diagnosis and follow up of patients with neoplastic diseases.     

康乐霉素对豆蔻酰佛波醇乙酯和伊屋诺霉素诱导淋巴细胞增殖的作用(英文)

目的:比较康乐霉素C(Kan)和环孢素(Cyc)对十四酰佛波醇乙酯(TPA)和伊屋诺霉素(IM),及刀豆球蛋白A(Con A)诱导淋巴细胞增殖的作用。方法:氚掺入或MTT法测细胞增殖;钼酸盐染料比色法测钙调磷酸酶(CN)活性。结果:Kan(8,40,80和400nmol·L~(-1))竞争性抑制TPA和IM刺激的脾细胞增殖。Cyc浓度增加,对TPA和IM刺激的脾细胞增殖中IM变化的增殖作用抑制较强。Kan和Cyc抑制Con A刺激的脾富集T-细胞增殖,IL-2拮抗Cyc作用较强;Kan抑制CN活性的作用较Cyc弱。结论:Kan竞争性抑制TPA和IM活化的细胞增殖,而Cyc抑制IM活化作用较强。     

Phase I clinical trial with IL-2-transfected xenogeneic cells administered in subcutaneous metastatic tumours: clinical and immunological findings

Various studies have emphasized an immunodepression state observed at the tumour site. To reverse this defect and based upon animal studies, we initiated a phase I clinical trial of gene therapy in which various doses of xenogeneic monkey fibroblasts (Vero cells) genetically engineered to produce human IL-2 were administered intratumorally in 8 patients with metastatic solid tumours. No severe adverse effect was observed in the 8 patients analysed during this clinical trial even in the highest dose (5 yen 107 cells) group. This absence of toxicity seems to be associated with rapid elimination of Vero-IL-2 cells from the organism. Indeed, exogenous IL-2 mRNA could no longer be detected in the peripheral whole blood 48 hours after Vero-IL-2 cell administration. In addition, we did not find any expression of exogenous IL-2 mRNA in post-therapeutic lesions removed 29 days after the start of therapy. A major finding of this trial concerns the two histological responses of two treated subcutaneous nodules not associated with an apparent clinical response. The relationship between local treatment and tumour regression was supported by replacement of tumour cells by inflammatory cells in regressing lesions and marked induction of T and natural killer cell derived cytokines (IL-2, IL-4, IFNg ...) in post-therapeutic lesions analysed 28 days after the start of Vero-IL-2 administration. Gene therapy using xenogeneic cells as vehicle may therefore present certain advantages over other vectors, such as its complete absence of toxicity. Furthermore, the in vivo biological effect of immunostimulatory genes, i.e IL-2-, may be potentiated by the xenogeneic rejection reaction.     

Activity of growth factors in the IL-6 group in the differentiation of human lung adenocarcinoma

The role of the interleukin-6 (IL-6) group of cytokines in differentiation of two lung adenocarcinoma cell lines has been examined using induction of alkaline phosphatase and expression of surfactant protein A. Oncostatin M was the most active and potent for alkaline phosphatase in A549 cells, with IL-6 having similar activity but less potency. Neither cytokine induced alkaline phosphatase in NCI-H441 cells, although induction was obtained with lung fibroblast-conditioned medium. Surfactant protein A was induced in NCI-H441 cells by conditioned medium and dexamethasone and, to a much lesser extent, by oncostatin M or IL-6. Induction of alkaline phosphatase and surfactant protein A were both dexamethasone-dependent, though some induction of surfactant protein A was obtained with interferon-alpha in the absence of dexamethasone. The activity present in lung fibroblast-conditioned medium suggests paracrine control, but this appears not to be due to oncostatin M or IL-6 as disabling antibodies to either cytokine were not inhibitory, and, although alkaline phosphatase was induced in A549 by both cytokines, it was only induced by conditioned medium in NCI-H441 cells. Furthermore, surfactant protein A was induced in H441 by conditioned medium to a much greater extent than by oncostatin M or IL-6. These data demonstrate that cytokines of the IL-6 group have potential as differentiation inducers in lung adenocarcinoma cells and that there is an equivalent paracrine factor(s) in lung fibroblast conditioned medium. As the production of this factor by fibroblasts is not enhanced by glucocorticoid, although the response of the target cell is, it would appear to be distinct from the fibrocyte pneumocyte factor previously described by Post et al 1984.     

Effect of a fluorinated pyrimidine on cachexia and tumour growth in murine cachexia models: relationship with a proteolysis inducing factor

The fluorinated pyrimidine nucleoside, 5'-deoxy-5-fluorouridine (5'-dFUrd) has been shown to effectively attenuate the progress of cachexia in the murine adenocarcinomas MAC16 and colon 26 as well as in the human uterine cervical carcinoma xenograft, Yumoto. Although concomitant inhibition of tumour growth was observed in all three models this was not sufficient to account for the preservation of body weight. An attempt has been made to correlate the anti-cachectic activity of 5'-dFUrd with the presence of a tumour produced proteolysis-inducing factor (PIF), thought to be responsible for the development of cachexia in the MAC16 model. Two variants of colon 26 adenocarcinoma were employed, clone 20 which produces profound cachexia, and clone 5 which produces no change in body weight in recipient animals. Mice bearing the colon 26, clone 20 variant showed evidence for the presence of PIF in tumour, serum and urine, while there was no evidence for the presence of PIF in tumour or body fluids of mice bearing the clone 5 tumours. Treatment of animals bearing the clone 20 variant with 5'-dF Urd led to the disappearance of PIF from the tumour, serum and urine concomitant with the attenuation of the development of cachexia. The human cervical carcinoma, Yumoto, which also induced cachexia in recipiant animals, showed expression of PIF in tumour, serum and urine in control and vehicle-treated mice, but was absent in mice treated with 5'-dFUrd. Thus in these experimental models cachexia appears to be correlated with the presence of PIF.