IL-2激活的TIL对自体肿瘤细胞的杀伤活性及其与LAK细胞活性的比较

肿瘤浸润性淋巴细胞(TIL)经白细胞介素2(IL-2)体外培养后具有很强的体内外抗肿瘤作用,且有一定的靶细胞特异性,其抗肿瘤效果强于淋巴因子激活的杀伤细胞即LAK细胞(P<0.01)。从瘤体中新鲜分离到的TIL对自体肿瘤细胞的杀伤活性极低,经IL-2体外培养后,其杀伤活性逐渐增高,以培养至7～25d的杀伤活性最强,这与IL-2使TIL分泌3种抗癌淋巴因子包括IL-2、IFN-γ、淋巴毒素(LT)增加有关。体外培养25d后,TIL的抗肿瘤活性下降,实验表明这与培养过程中TIL的Lyt-2~+细胞(Tc)减少而L3T4~+细胞(T_H)增多有关。TIL经冻存复苏和IL-2体外培养后仍保持很强的抗肿瘤活性,冻存前后比较未见显著差异(P>0.05),这为间断地运用TIL治疗复发性、晚期肿瘤提供了一条可行的途径。     

肺癌患者血清肿瘤特异生长因子检测及临床意义

目的 :研究TSGF在肺癌诊断、疗效判定中的临床应用价值。方法 :利用生化比色法测定了 18例肺良性病变患者 ,2 4例肺癌患者及 9例肺癌患者治疗后血清中TSGF水平。结果 :肺癌患者未经治疗前其血清TS GF水平及阳性率明显高于肺良性病变患者 ,其敏感性为 75 .0 % ,特异性为 77.8%。经有效化学治疗后肺癌患者血清TSGF明显下降。结论 :血清TSGF检测对肺癌的诊断、疗效观察有较重要的意义。     

青海地区1204例口腔颌面部肿瘤,囊肿,瘤样病变分析

本文对青海地区1204例口腔颌面部肿瘤、囊肿、瘤样病变的病变部位、性质、年龄及性别进行分析。结果为良性肿瘤634例（52．66％），以血管瘤和涎腺混合瘤最多见。恶性肿瘤232例（1．27％），以鳞状细胞癌居第一位，平均患病年龄48岁，随年龄增长，逐年递增。囊肿306例（25．41％），多发生在去下腺。瘤样病变32例（2．66％），多为牙龈瘤。本组良性肿瘤女性高于男性，血管瘤居第一位。良恶性肿瘤之比为2．73∶1，与国内有关报道略有不同。     

Software compensation improves the analysis of heterogeneous tumor samples stained for multiparameter DNA flow cytometry

Background: High concentrations of propidium iodide (PI), in combination with fluorescein isothiocyanate (FITC) and R-phycoerythrin (RPE) used for multiparameter DNA flow cytometry (FCM), cause spectral cross-talk into the green fluorescence channel (FL1). We have evaluated the use of post-acquisition software compensation (N-Color Compensation) in order to correct this spectral cross-talk caused by PI. Method: Cell mixtures were prepared consisting of keratin 8/18 FITC labeled, keratin 8/18 RPE labeled, and unlabeled MCF-7 breast carcinoma cells. DNA was stained with PI (100 μM). Post-acquisition software compensation was applied to correct the spectral cross-talk of PI fluorescence. Secondly, the distribution of the Ki-67 (FITC) protein during the cell cycle (PI) of SiHa cervical carcinoma cells (no software compensation) was compared to the Ki-67 expression pattern of SiHa cells, simultaneously stained for keratin 8 (RPE), after applying software compensation. Finally, software compensation was used to compare the relative levels of PCNA and p53 expression in two clinical ovarian cancer ascites specimens, stained for PCNA or p53 (FITC), keratin 8/18 (RPE), and DNA (PI), with a known p53 status (positive and negative, respectively). Results: The Ki-67 cell cycle-dependent pattern of a triply stained sample (Ki-67 (FITC), keratin 8 (RPE), and DNA (PI)) is restored after software compensation and the results are comparable to the Ki-67 distribution of a sample stained solely for Ki-67 and DNA. P53 expression could only be resolved after using software compensation in the p53 positive ovarian ascites (OA) sample. Conclusions: We conclude that software compensation is a robust and reliable post-acquisition method for the correction of RPE/PI spectral cross-talk, permitting better identification of weakly expressed proteins in heterogeneous clinical tumor samples stained for multiple cellular antigens and DNA using PI.     

脑囊虫病患者脑脊液中一氧化氮及肿瘤坏死因子α水平研究

目的　探讨脑囊虫病患者各期脑脊液中的一氧化氮 (NO)、肿瘤坏死因子α(TNF α)的变化规律及它们在脑囊虫病中的作用机制。方法　检测 4 9例明确诊断并依据MR分期 ,单发脑实质内囊虫的脑囊虫病患者和 2 0名对照者脑脊液中NO、TNF α水平。结果　NO在脑囊虫病的Ⅰ期显著降低而TNF α水平呈显著升高 ,NO、TNF α于Ⅱ期、Ⅲ期 (整个退变死亡期 )均表现为高水平 ,Ⅳ期恢复正常 ,NO和TNF α存在高度正相关关系。结论　在单发脑实质内囊虫病中NO、TNF α可能参与杀虫作用 ,其免疫调节与杀虫机制存在着动态平衡 ,参与感染控制     

胆囊结石及癌变过程中肿瘤坏死因子可溶性受体的变化

目的　探讨可容性肿瘤坏死因子受体 (sTNFR)在胆囊结石及癌变过程中的变化。方法　用双抗体夹心酶联免疫法对 5 3例胆囊结石 ,9例胆囊癌及 11例正常对照者血清及胆法中的sTNFR水平进行检测。结果　血清及胆汁中sTNFR水平胆囊癌组为 (2 .63± 0 .5 6) μg/L、(10 .0 2± 3 .2 3 ) μg/L较胆石症组 (1.2 5± 0 .3 6) μg/L、(2 .81± 0 .93 ) μg/L及对照组 (0 .95± 0 .19)μg/L、(1.83± 0 .5 4) μg/L均显著升高 (P <0 .0 1)。胆囊黏膜从典型增生、非典型增生到胆囊癌的发展过程中sTNFR在血清 (1.11± 0 .2 8、1.5 3± 0 .3 2、2 .63± 0 .5 6)及胆汁中 (2 .5 0± 0 .81、3 .42±0 .87、10 .0 2± 3 .2 3 )逐级增高 (各组间P <0 .0 5 )。胆汁中sTNFR水平在胆囊癌Ⅰ～Ⅲ期 (8.3 6±2 .60 )与Ⅳ～Ⅴ期 (13 .3 3± 4.46)间差异有显著性 (P <0 .0 0 1) ,肿瘤直径≥ 2cm组 (12 .10± 2 .3 2 )与 <2cm组 (7.42± 2 .10 )间差异有显著性 (P <0 .0 5 )。胆汁中TNFR水平明显高于其对应的血清水平 ,两者之间呈正直线相关 (r =0 .875 ,P <0 .0 0 1)。胆囊癌术后血清sTNFR水平显著下降。结论　sTNFR参与胆囊结石致癌的过程 ,与胆囊癌的临床生物学特点密切相关。     

参附注射液对肠缺血-再灌注大鼠肿瘤坏死因子α的影响

目的观察肿瘤坏死因子α(TNF-α)在大鼠肠缺血-再灌注损伤过程中的作用及参附注射液对TNF-α的影响,探讨参附注射液防治肠缺血-再灌注损伤机制。方法 SD大鼠随机分为肠缺血-再灌注组(IR组)、参附注射液预处理组(SF组)和假手术组(C组)。采用阻断肠系膜上动脉(SMA)的方法制造肠缺血-再灌注模型。分别测定各组动物血浆、肠组织TNF-α含量及血液动力学变化;光镜观察肠粘膜损伤情况。结果IR组再灌注后MAP下降,与C组和SF组比有显著性差异(P<0.01);SF组肠粘膜损伤程度减轻,与IR组比有显著性差异(P<0.01);SF组血浆及肠组织TNF-α水平降低,与IR组比有显著性差异(P<0.01)。结论参附注射液可明显防治大鼠肠缺血-再灌注导致的肠粘膜损伤,这种作用可能是通过抑制TNF-α的释放实现的。     

Enzyme-linked Immunosorbent Assay of Pro-gastrin-releasing Peptide for Small Cell Lung Cancer Patients in Comparison with Neuron-specific Enolase Measurement

Our previous study demonstrated that pro-gastrin-releasing peptide(31–98), or ProGRP, is a specific tumor marker in patients with small cell lung carcinoma (SCLC). Using a newly developed, highly sensitive enzyme-linked immunosorbent assay (ELISA) for ProGRP, we analyzed 1,446 samples including those obtained from 478 lung cancer patients to evaluate the clinical usefulness of this ELISA. Several properties indicated that ProGRP is a useful tumor marker for SCLC. First, ProGRP was specifically elevated in SCLC patients. In non-SCLC patients and patients with non-tumorous lung diseases, its serum level was very rarely elevated. Secondly, ProGRP was a reliable marker, in terms of the marked elevation of serum ProGRP levels in SCLC patients. Thirdly, serum ProGRP levels were elevated in SCLC patients even at a relatively early stage of this disease. Fourthly, changes in the serum ProGRP level showed an excellent correlation with the therapeutic responses in SCLC patients. Neuron-specific enolase (NSE) is accepted as a tumor marker of SCLC patients. With the aim of comparing ProGRP and NSE as tumor markers for SCLC patients, we measured serum NSE levels in all samples collected in the present study. We found that ProGRP was superior to NSE in terms of sensitivity, specificity and reliability. Therefore, we consider that ProGRP can play a major role as a clinical tumor marker for SCLC patients.     

恶性肿瘤局部淋巴结树突状细胞免疫组化研究

本文采用S-100蛋白为免疫学标记，对34例恶性肿瘤局部淋巴结内树突状细胞进行免疫组化定量研究。结果按S-100蛋白阳性细胞数目多少分为增多（7例）、减少（20例）及正常（7例）3组，统计学分析增多组均值（164.4个/mm^2)明显高于对照组（58.3个/mm^2)；减少组均值（16.5个/mm^2)组显低于对照组；而正常组均值（69.8个/mm^2)与对照组无显著差异。     

Vascular cell adhesion molecule-1 modulation by tumor necrosis factor in experimental allergic encephalomyelitis

Anti-tumor necrosis factor (TNF) antibodies inhibit passively transferred experimental allergic encephalomyelitis (EAE) in SJL mice. The possibility that this occurs through interference in TNF's upregulation of endothelial cell adhesion molecules was investigated. Expression of both vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on spinal cord vessels increased during EAE. The upregulation of VCAM-1 was markedly reduced or prevented by anti-TNF treatment. Leukocytic infiltration was 15-fold lower in anti-TNF-treated than diseased animals. Spinal cord endothelial expression of VCAM-1, though not ICAM-1 or fibronectin, positively correlated with the extent of T cell, B cell or monocyte infiltration in each animal.