Pitfalls in TRAP assay in routine detection of malignancy in effusions

Telomerase has been found to be reactivated in a majority of cancers but is inactive in most somatic cells. Our principal goal was to determine the potential use of the telomeric repeat amplification protocol (TRAP) assay as marker for malignancy in cytological effusions. The simple selection criterion was the cytological diagnosis, and routine samples were classified into malignant (58 samples) and nonmalignant (233 samples). Of the malignant samples, 44/58 (76%) were positive by TRAP assay. Of the 14 telomerase-negative cytology-positive samples, RNA integrity was poor in 9, indicating suboptimal sample conservation for molecular analysis. In 3 of the remaining 5 samples with a negative TRAP assay, a high number of malignant cells was observed, and these cells might have been telomerase-negative. Thus, the sensitivity of TRAP assay for the presence of malignant cells was about 76%. In the cytologically nonmalignant effusions, the presence of telomerase activity was observed in 24% (55/233). Of these, 6% were highly suspicious for malignancy, 9% were doubtful, and 9% were cytologically nonmalignant effusions confirmed by a follow-up of 12 mo or more. According to these data, the specificity of the TRAP assay to detect tumor cells in effusions ranged only between 82-91%. Our results indicate that, although the TRAP assay is positive in 6-15% of putative malignant effusions, the relatively high number of TRAP false-negative and false-positive cases renders this test unsuitable for routine diagnostic purposes.     

实验性豚鼠炎性胸膜腔积液模型的建立

目的：建立一种炎性胸膜腔积液（简称胸液）的动物模型。方法：选择40只豚鼠分为8组,第1－7组为试验组,第8组为对照组,试验组每只左胸膜腔内注入1％角叉菜胶（carrageenan)0.8-1.0ml,分批处死观察。结果：胸液于1天内已经出现,2－3天积液量最多,胸液中中性粒细胞计数及病理切片中胸膜、肺的炎性改变亦达高峰,以后胸液逐渐吸收,第7天开始出现胸膜纤维化与粘连,第10天时明显,14天呈现胸膜包裹。结论：角叉菜胶是一比较理想的胸膜腔致炎剂;该动物模型的建立,为胸液的进一步研究提供了有用的工具。     

高频超声引导下胸腔积液置管引流

胸腔积液临床常见,少量积液常无症状,中大量积液可致患者出现呼吸困难、无法平卧等表现,需通过胸腔穿刺置管引流及时加以缓解。胸腔积液穿刺引流不仅可用于临床治疗,还可辅助诊断不明原因胸腔积液。在超声直视下操作置管可提高穿刺成功率[1-2]。本研究观察高频超声在辅助引导置管引流胸腔积液中的效果。     

Cytokines and fibrinolytic enzymes in tuberculous and parapneumonic effusions

Tuberculous (TB) pleurisy and parapneumonic effusion (PPE) are common causes of pleural fibrosis. The mechanisms underlying fibrin deposition may be different since involved inflammatory cells are distinct. In this study, we measured various cytokines and fibrinolytic enzymes and compared the differences between the two effusions. PPE was further divided into noncomplicated PPE and complicated PPE/empyema subgroups. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, macrophage inflammatory protein (MIP)-1beta, monocyte chemoattractant protein (MCP)-1, plasminogen activator inhibitor type 1 (PAI-1) and tissue type plasminogen activator (tPA) were measured using enzyme-linked immunosorbent assays. Significantly higher values of PAI-1, PAI-1/tPA ratio, IL-1beta, IL-8 and MIP-1beta and significantly lower values of TNF-alpha, IL-6 and MCP-1 were observed in PPE/empyema than in TB effusions. Compared to noncomplicated PPE, complicated PPE/empyema had significantly higher levels of TNF-alpha, IL-1beta, IL-8 and MIP-1beta. TB pleurisy patients who had higher effusion levels of TNF-alpha, IL-1beta and IL-8 were predisposing to residual pleural thickening. The underlying mechanisms of fibrin formation and deposition between the two effusions studied (PPE/empyema and TB pleurisy) could not be fully explained by the results of the present study. More studies are needed to explore this further.     

胸水细胞端粒酶活性检测对良恶性胸腔积液的鉴别诊断价值

目的：探讨胸水细胞端粒酶活性对良、恶性胸腔积液的鉴别诊断价值。方法：用改良的PCR-ELISA法检测37例恶性、32例良性胸水细胞端粒酶活性,并与胸水细胞学、癌胚抗原（CEA）诊断结果进行比较。结果：37例恶性胸腔积液中有26例端粒酶活性阳性（26/37）,阳性率为70.27%,高于良性胸腔积液中端粒酶海性表达（2/32,P＜0.01);端粒酶活性检测诊断恶性胸水敏感性为70.27%,特异性为93.75%,与胸水细胞学诊断符合率为54.05%;其敏感性高于胸水CEA诊断结果（敏感性为51.35%)。结论：胸水细胞端粒酶活性检测作为细胞学检查的辅助手段能提高恶性胸水的诊断率,有助于良、恶性胸腔积液的鉴别诊断。     

高聚金葡素联用顺铂治疗恶性胸水64例疗效观察

目的 :观察生物反应调节剂高聚金葡素 (HASL)加顺铂 (DDP)联用治疗恶性胸水的疗效。方法 :将 64例恶性胸水患者男 4 0例 ,女 2 4例 ,随机分为 2组 ,治疗组选用HASL +DDP ,对照组单用DDP进行比较。结果 :胸水减少 ,治疗组有效率 82 .3 % ,对照组有效率 60 %。结论 :HASL联用DDP能有效控制恶性胸水 ,提高患者生存质量 ,减轻化疗药物毒副作用 ,值得临床推广应用。     

B超引导下穿刺诊治心包积液的价值

①目的 探讨B超引导下心包穿刺诊治心包积液的价值。②方法 对38例心包积液病人行B超检查,并在B超引导下进行46次心包穿刺。③结果 46次心包穿刺术中首次穿刺成功45次,成功率97.8%;1例首次穿刺失败改变穿刺方向后再次穿刺成功。④结论 B超检查对心包积液的诊断、指导穿刺和选择治疗方法等有重要价值。     

恶性胸腔积液对晚期非小细胞肺癌预后的影响

目的 探讨恶性胸腔积液对晚期非小细胞肺癌（ＮＳＣＬＣ）预后生存的影响。方法 根据临床分期及有无胸腔积液将患者分为三组,用生存统计中的Ｋａｐｌａｎ－Ｍｅｉｅｒ表法做出三组生存曲线并比较显著性。结果 无胸腔积液的ⅢＢ期患者的生存与有胸腔积液的ⅢＢ期患者及Ⅳ期肺癌患者的生存期比较有显著性差异,而ⅢＢ期有胸腔积液的肺癌患者的生存期与Ⅳ期患者的生存期比较无显著性差异。在单因素及多因素预后分析中,胸腔积液均为     

非感染性肺底积液的X线诊断分析

目的 :探讨肺底积液X线诊断的准确性。方法 :回顾性分析 42例非感染性肺底积液的X线征象。结果 :肺底积液的主要X线表现是假膈征、心淹征、双膈影征和变换体位液体弥散征象。结论 :熟悉肺底积液的X线诊断和鉴别诊断 ,对肿瘤患者胸膜转移的早期诊断、及时治疗有重要意义。     

Effect of platelet-activating factor on secretion of mucous glycoprotein from chinchilla middle ear epithelial cells in vitro

Platelet-activating factor (PAF) is a naturally occurring phospholipid that acts as a pleiotropic mediator and mediates cell-cell reactions under physiological and pathological conditions. Recently, it has been shown that PAF is a strong secretagogue of mucous glycoprotein in the airways, suggesting its role in mucous glycoprotein secretion and the pathogenesis of otitis media with effusion. In the current study, we examined the effect of PAF on mucous glycoprotein secretion in cultured chinchilla middle ear epithelial cells. PAF at 1 M significantly stimulated mucous glycoprotein secretion from cultured chinchilla middle ear epithelial cells. This action was concentration-dependent, with secretions reaching near maximum when the cells were incubated with PAF at 100 M. In a time-dependent study, PAF demonstrated an initial rapid stimulation of mucous glycoprotein secretion, followed by a gradual increase thereafter. A six-fold increase was seen in the first 2 h compared with controls. Cycloheximide, a protein synthesis inhibitor, demonstrated an inhibitory effect on PAF-stimulated mucous glycoprotein secretion in this study. These findings suggest that PAF plays an important role in the pathogenesis of otitis media with effusion by stimulating mucous glycoprotein secretion in vitro.Supported by NIH grant P0I-D000133 from the National Institute on Deafness and Other Communication Disorders.