血管内皮细胞生长因子对肾小球内皮细胞通透性的影响

目的 :观察血管内皮细胞生长因子 (VEGF)对肾小球内皮细胞通透性的影响 ,并与脐静脉内皮细胞进行比较分析。　 方法 :采用二室弥散系统检测内皮细胞通透性。肾小球内皮细胞 (MGEC)和人脐静脉内皮细胞(HUVEC)接种于细胞培养嵌套的微孔滤膜 (孔径 0 4 5 μm)上 ,待细胞生长融合后 ,加入不同浓度的VEGF作为处理因素 ,以生物素标记的牛血清白蛋白 (biotin BSA)作为通透性指示剂 ,采用ELISA方法检测不同时间段biotin BSA通过细胞单层的百分数。　 结果 :正常培养条件下 ,生长在滤膜上的MGEC和HUVEC单层的通透性没有明显差异。VEGF可显著增加MGEC和HUVEC的通透性 ,呈剂量和时间依赖性。 1μg/LVEGF作用 12h可使MGEC对白蛋白的通透率增加近 2 5 % (0 31± 0 0 3vs 0 2 5± 0 0 3) ;VEGF浓度达 10 μg/L始显著增加HUVEC通透性 (0 2 8± 0 0 7vs0 2 1± 0 0 4 ) ,且远小于MGEC通透性增加的幅度 (P <0 0 1) ;VEGF浓度达 5 0 μg/L时 ,其增加内皮细胞通透性的作用基本达到饱和。 5 0 μg/LVEGF作用 0 5h即可使MGEC和HUVEC的蛋白通透率分别增加 10 0 % (0 12± 0 0 2vs0 0 6± 0 0 1)和 6 0 % (0 0 8± 0 0 3vs0 0 5± 0 0 1) ,并至少持续到 12h。　 结论 :首次在体外直接证实了VEGF具有增加MGEC     

Rebalanced hemostasis in patients with idiopathic thrombocytopenic purpura

Previous laboratory and clinical data have shown evidence for the concept of rebalanced hemostasis in liver disease. We evaluate whether this concept of rebalanced hemostasis can be applied in patients with idiopathic thrombocytopenic purpura (ITP). Twenty patients with ITP (platelet count?<?100?×?10⁹ /l) who visited our hospital were enrolled. We measured the von Willebrand factor (vWF) antigen levels and performed native blood thromboelastography (TEG) to evaluate the hemostasis. As a subgroup analysis, we compared patients with elevated vWF levels with those with normal levels. Bleeding symptoms of the patients were followed up for 6 months. The mean (SD [IQR]) platelet count was 44.23?×?10⁹ /l (25.78 [27.00–60.50]). The following TEG parameters were within the normal range in most patients (number of patients with a normal value): clotting time (17), clot formation time (17), α-angle (15), maximum clot formation (10), and maximum lysis (12). The mean (SD) vWF antigen level (%) was 163% (80). There were eight patients (40%) with elevated vWF antigen levels [218% (104) vs. 126% (19), p?=?0.007, elevated vs. normal patients, respectively]. Those with elevated vWF antigen levels were older [58 year (10) vs. 40 year (13), p?=?0.004] and had a longer disease status [67 months (39) vs. 33 months (25), p?=?0.028]. Although the platelet count was not different, the CFT was shorter [287 (104) vs. 561 (291), p?=?0.042] and the α-angle was larger [49 (6) vs. 34 (15), p?=?0.033] in those with elevated vWF antigen levels. There were no patients with major bleeding events during the follow-up period. Four patients showed minor bleeding events (n?=?1 vs. n?=?3, elevated vs. normal patients, respectively). We found that the vWF antigen level was elevated and the TEG profiles were better in older ITP patients with longer disease statuses. Patients with ITP appeared to achieve a rebalance hemostasis through an elevation of their plasma vWF antigen levels and hemostatic changes that promote thrombosis. Measuring the vWF antigen levels and performing TEG analysis can help determine the treatment strategy in ITP patients.     

血管内皮生长因子对培养内皮细胞合成一氧化氮的影响

目的 :探讨血管内皮生长因子 （VEGF） /血管渗透因子 （VPF）对内皮细胞 （EC）分泌一氧化氮 （NO）的影响。方法 :将培养的人脐静脉内皮细胞 （HUVEC）随机分为 6组 （n=6 /组 ） :1正常对照组 ;2 VEGF 1ng/ m l;3VEGF 10ng/ m l;4VEGF 10 0 ng/ m l;5低氧组 ;6低氧组 +VEGF 10 0 ng/ m l。采用硝酸还原酶法测定培养液中的 NO2 - ,NO3 -的含量以反映 NO水平。结果 :VEGF促进正常 EC分泌 NO,在一定浓度范围内呈剂量依赖性 ;低氧损伤 EC,使其分泌 NO减少 ;VEGF 10 0 ng/ ml预处理可保护 EC免受低氧损害 ,保持正常分泌 NO的功能。结论 :VEGF能够调节 EC的功能 ,为其促血管形成作用中 EC分裂、增殖、迁移奠定物质基础     

Melatonin prevents human pancreatic carcinoma cell PANC-1-induced human umbilical vein endothelial cell proliferation and migration by inhibiting vascular endothelial growth factor expression

Abstract: Melatonin is an important natural oncostatic agent, and our previous studies have found its inhibitory action on tumor angiogenesis, but the mechanism remains unclear. It is well known that vascular endothelial growth factor (VEGF) plays key roles in tumor angiogenesis and has become an important target for antitumor therapy. Pancreatic cancer is a representative of the most highly vascularized and angiogenic solid tumors, which responds poorly to chemotherapy and radiation. Thus, seeking new treatment strategies targeting which have anti‐angiogenic capability is urgent in clinical practice. In this study, a co‐culture system between human umbilical vein endothelial cells (HUVECs) and pancreatic carcinoma cells (PANC‐1) was used to investigate the direct effect of melatonin on the tumor angiogenesis and its possible action on VEGF expression. We found HUVECs exhibited an increased cell proliferation and cell migration when co‐cultured with PANC‐1 cells, but the process was prevented when melatonin added to the incubation medium. Melatonin at concentrations of 1 μm and 1 mm inhibited the cell proliferation and migration of HUVECs and also decreased both the VEGF protein secreted to the cultured medium and the protein produced by the PANC‐1 cells. In addition, the VEGF mRNA expression was also down‐regulated by melatonin. Taken together, our present study shows that melatonin at pharmacological concentrations inhibited the elevated cell proliferation and cell migration of HUVECs stimulated by co‐culturing them with PANC‐1 cells; this was associated with a suppression of VEGF expression in PANC‐1 cells.     

非霍奇金淋巴瘤患者sVEGF和sbFGF水平的变化及临床意义

目的:研究非霍奇金淋巴瘤(NHL)患者血清血管内皮生长因子(sVEGF)及血清碱性成纤维细胞生长因子(sbFGF)水平与临床特征的关系,探索其临床意义.方法:ELISA法检测36例不同病期NHL患者sVEGF、sbFGF水平,并收集临床资料,进行统计分析.结果:NHL患者sVEGF、sbFGF水平明显高于对照组(均P＜...     

血管内皮生长因子调节内皮祖细胞生物学功能

目的研究血管内皮生长因子（VEGF）对体外培养骨髓源性内皮祖细胞（EPCs）数量及增殖、迁移、黏附功能的影响及机制初探。方法密度梯度离心法获取骨髓单个核细胞,FITC-荆豆凝集素I、DiI-乙酰化低密度脂蛋白荧光双染鉴定。单个核细胞培养7d后分为对照组和VEGF干预组。VEGF干预组加入不同浓度VEGF（25,50,75,100μg／L）培养48h,分别采用四氮唑溴盐比色法、改良的Boyden小室和黏附能力测定观察EPCs的增殖、迁移和黏附能力。RT—PCR法半定量检测VEGF对EPCs内皮型一氧化氮合酶（eNOS）mRNA表达的影响。硝酸还原酶法比色测定VEGF对EPCs分泌一氧化氮的影响。结果VEGF可浓度依赖性地增加EPCs数量并明显促进EPCs的黏附、迁移和增殖能力,与对照组比较差异显著。VEGF可上调EPCseNOSmRNA的表达,促进EPCs分泌一氧化氮。结论VEGF可能通过上调EPCseNOSmRNA的表达影响EPCs部分生物学功能。     

Serum levels of platelet-derived growth factor-BB and vascular endothelial growth factor as prognostic factors for patients with fulminant hepatic failure

Background and Aims: In animal models for acute liver injury, the administration of some angiogenic factors such as vascular endothelial growth factor (VEGF) and granulocyte‐colony stimulating factor (G‐CSF) are shown to reduce liver injury and improve liver proliferative capacity. The aim of the present study was to assess the role of angiogenic factors in fulminant hepatic failure (FHF). Methods: Serum levels of nine angiogenic factors (angiopoietin‐2, follistatin, G‐CSF, hepatocyte growth factor [HGF], interleukin‐8, leptin, platelet‐derived growth factor [PDGF]‐BB, platelet endothelial cell adhesion molecule‐1 and VEGF) were measured using the Bio‐Plex Protein Array System in 30 patients, 17 of whom were diagnosed with FHF, 13 with acute hepatitis (AH), and 20 controls. Results: Serum levels of PDGF‐BB and VEGF were lower in FHF patients than AH patients and controls (PDGF‐BB; 2050 ± 1572 pg/mL vs 4521 ± 2419 pg/mL vs 8506 ± 5500 pg/mL, VEGF; 39 ± 38 pg/mL vs 144 ± 122 pg/mL vs 205 ± 121 pg/mL). By using univariate logistic regression models, serum levels of PDGF‐BB and VEGF were associated with poor outcomes. Serum PDGF‐BB levels were strongly correlated with serum VEGF levels (r = 0.70). Furthermore, serum PDGF‐BB levels were significantly correlated with platelet counts (r = 0.79), PT activity (r = 0.37) and D.Bil/T.Bil ratio (r = 0.50), while serum VEGF levels were significantly correlated with platelet counts (r = 0.68) and PT activity (r = 0.38). Conclusions: We consider that serum levels of PDGF‐BB and VEGF are worth investigating as biomarkers for predicting outcomes of FHF patients.     

哮喘大鼠支气管肺泡灌洗液中血管内皮生长因子和血小板源性生长因子的变化及缬沙坦的干预

目的观察血管内皮生长因子（VEGF）和血小板源性生长因子（PDGF）在哮喘大鼠支气管肺泡灌洗液（BALF）中的变化,探讨两者与哮喘气道重塑的关系以及缬沙坦的干预作用。方法50只Wistar大鼠随机分成5组,每组10只：A组（正常对照组）、B组（哮喘组）、C组[15mg／（kg·d）缬沙坦]、D组[30mg／（kg·d）缬沙坦]和E组[50mg／（kg·d）缬沙坦]。分别观察各组肺组织切片的病理改变,用酶联免疫吸附法（EHSA）检测各组大鼠BALF中VEGF和PDGF的水平。结果哮喘大鼠肺组织出现了气道重塑的病理改变;与A组比,B组BALF中VEGF和PDGF水平显著增高（P〈0．01）,与B组比,缬沙坦干预后的C组、D组和E组BALF中VEGF和PDGF均显著减少（P〈0．05或P〈0．01）。结论VEGF和PDGF在哮喘大鼠BALF中浓度增高,可能参与了哮喘发病和气道重塑过程。缬沙坦能明显降低哮喘大鼠BALF中VEGF和PDGF的水平,有助于改善哮喘大鼠气道重塑的病理生理过程,其作用机理还有待进一步研究。     

Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas

Endostatin, a cleaved fragment of collagen XVIII, is a potent endogenous angiogenesis inhibitor. Elevated serum endostatin levels have been recently reported in patients with various types of neoplasms. The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various pituitary adenoma types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels. Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with pituitary adenomas (20 somatotropinomas, 3 corticotropinomas, 6 prolactinomas and 42 clinically nonfunctioning pituitary adenomas – CNFPAs) and compared with levels from age-matched controls. In 35 patients postoperative immunohistochemical investigations were performed. Serum endostatin concentrations were significantly higher in all pituitary adenoma types, except for prolactinomas (somatotropinomas: 124 ± 16; p < 0.02, corticotropinomas: 157 ± 42; p < 0.02, prolactinomas: 141 ± 37; p > 0.05, CNFPAs: 169 ± 11 ng/ml; p < 0.000005 vs 73 ± 10 ng/ml in controls). There was a significant positive correlation between endostatin and VEGF serum levels in patients with pituitary adenomas (r = +0.322; p = 0.006). In the control group a significant negative correlation xbetween circulating endostatin and VEGF was found (r = −0.653; p = 0.00975). The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization of pituitary adenomas. Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence of pituitary tumors.     

Characterization of platelet glycoproteins and platelet/endothelial cell antibodies in patients with thrombotic thrombocytopenic purpura

Platelets and sera from 12 patients with thrombotic thrombocytopenic purpura (TTP) and 12 healthy normal control subjects were examined. As determined by quantitative flow cytometry, prior to plasma exchange therapy platelet surface glycoprotein (GP) Ib levels were similar in TTP patients and normal controls (mean 20 188 and 20 226 molecules/platelet, respectively). Platelets from patients with TTP did, however, have significantly reduced levels of GPIIb/IIIa prior to plasmapheresis (mean 36 348 v 52 505 molecules/platelet in controls; P = 0.0004) and of GPIV (mean 13 321 v 26 212 molecules/platelet in controls; P = 0.0002). An increase in activated platelets, as determined by CD62 expression, was observed in 82% of patients. Increased platelet-associated immunoglobulins and/or complement was also seen in approximately 60% of the patients. In general, with return of platelet counts to normal levels following seven plasmaphereses, the above abnormalities were reversed, although often not to normal levels. Western blot analysis indicated the presence of antibodies reactive to platelet GPIV (88 kD) in 70% of pretreatment sera from patients with TTP; a similar band was observed in 80% of patient sera against microvascular endothelial cells. Immunofluorescence microscopic examination indicated the presence of antibody in pretreatment sera from patients with TTP to microvascular (73%) and large vessel (36%) endothelial cells. As measured by an indirect flow cytometric assay, pretreatment sera from 55% of patients with TTP were reactive with large vessel endothelial cells and 100% reacted with microvascular endothelial cells; reactivity was significantly greater against the microvascular endothelial cells (P = 0.0048) and was reduced following plasma exchange therapy. These results indicate abnormalities in platelet glycoprotein expression in TTP and suggest that anti-platelet and anti-endothelial cell antibodies play a role in the thrombocytopenia and vasculitis characteristic of this disorder.     

Poor outcome in disseminated intravascular coagulation or thrombotic thrombocytopenic purpura patients with severe vascular endothelial cell injuries

Various hemostatic and vascular endothelial cell markers were measured in patients with disseminated intravascular coagulation (DIC), non-DIC, or thrombotic thrombocytopenic purpura (TTP) and in healthy volunteers to examine the relationships between the hemostatic abnormalities or vascular endothelial cell injuries and the patients' outcomes. Although the plasma levels of soluble fibrin monomer, thrombin-antithrombin complex, plasmin-plasmin inhibitor complex, and D-dimer were significantly increased in the DIC patients, there were no significant differences in these markers between the DIC patients who survived and those who died, suggesting that these markers might not be directly related to the patient outcome. The plasma thrombomodulin (TM) levels in the DIC and TTP patients were significantly higher than those in the healthy volunteers, and the plasma TM levels in the patients who died were significantly higher than those in the patients who survived. These findings showed that the TM level reflected the outcome, and that the outcome of the diseases underlying DIC and TTP might depend on vascular endothelial cell injuries. The plasma protein C and antithrombin activities were markedly reduced in the DIC, non-DIC, and TTP patients who died compared to those who survived. These findings suggest that reduced plasma antithrombin and protein C activities are useful markers of systemic vascular endothelial injuries. Although the plasma tissue factor (TF) levels were significantly increased in the DIC patients, there was no significant difference in the plasma TF levels between the DIC patients who died and those who survived. In conclusion, we found that the outcome of the diseases underlying DIC and TTP is related to vascular endothelial cells, and that plasma TM, antithrombin, and protein C are useful markers for systemic vascular endothelial cell injury. Am. J. Hematol. 58:189–194, 1998. © 1998 Wiley-Liss, Inc.     

COPD患者血清胎盘生长因子水平的研究

目的探讨慢性阻塞性肺疾病（COPD）患者血清胎盘生长因子在发病机制中的作用。方法采用酶联免疫吸附试验法检测COPD组42例和对照组42例血清胎盘生长因子水平,并与COPD患者FEV1占预计值％和COPD严重程度进行相关分析。结果COPD组血清胎盘生长因子水平高于对照组（28．30±14．30pg／ml vs 6．8±3．12pg／ml,P〈0．01）。COPD组FEV1占预计值％与血清胎盘生长因子水平呈负相关（r=-0．52,P〈0．01）。COPD病情严重程度与血清胎盘生长因子水平正相关（r=0．61,P〈0．01）。结论COPD组血清胎盘生长因子水平高于对照组,且与COPD的严重程度呈正相关。胎盘生长因子在COPD发病机制中起一定作用。     

去甲斑蝥素对多发性骨髓瘤细胞周期和血管内皮细胞生长因子的影响

目的 探讨去甲斑蝥素(NCTD)抗骨髓瘤效应的机制.方法 利用流式细胞术检测不同浓度NCTD作用24h后细胞周期的改变,Western blot检测CDK1、cyclin A和cyclin B1的改变,免疫组化和RT-PCR测定血管内皮细胞生长因子(VEGF)的表达.结果 经NCTD处理24h后,随着NCTD浓度增加,G2/M期细胞明显增加,S期细胞明显减少,呈剂量依赖性;NCTD以剂量依赖的方式抑制cyclin B1、CDK1和cyclin A的表达;NCTD以剂量依赖的方式抑制VEGF mRNA和蛋白的表达.结论 NCTD对U266细胞有抗增殖和促凋亡作用,其作用机制可能与调节细胞周期和抑制VEGF的表达有关.     

慢性特发性血小板减少性紫癜患者血清转化生长因子-β1测定的意义

目的探讨血清转化生长因子-β1（TGF-β1）在慢性特发性血小板减少性紫癜（ITP）中的临床意义。方法采用双抗体夹心酶联免疫吸附法（ELISA）检测38例初治慢性ITP患者治疗前后血清中TGF-β1水平。结果慢性ITP患者治疗前TGF-β1水平明显高于对照组（P〈0．01）。经治疗缓解后血清TGF-β1水平与治疗前比较明显下降（P〈0．01）。未缓解者TGF-β1水平与初诊患者比较差异无统计学意义（P〉0．05）。TGF-β1水平与血小板数呈负相关（r=-0．342,P〈0．05）,与巨核细胞数呈正相关（r=0．409,P〈0．01）。结论TGF-β1参与了慢性ITP的发病,检测TGF-β1水平变化有助于对慢性特发性血小板减少性紫癜患者病情的判断,可作为疗效观察的辅助指标。     

非小细胞肺癌患者血清血管内皮生长因子、血小板衍生生长因子和表皮生长因子受体测定的临床意义

目的 探讨血清血管内皮生长因子(vascular endothelial growth factor,VEGF)、血小板衍生生长因子(platelet-derived growth factor,PDGF)和表皮生长因子受体(epidermal growth factor receptor,EGFR)测定在非小细胞肺癌(non-small cell lung cancer,NSCLC)诊断和预后判定中的意义.方法 采用双抗体夹心ABC-ELISA法测定31例NSCLC患者及30名健康者血清VEGF、PDGF和EGFR的含量.结果 NSCLC患者血清VEGF、PDGF和EGFR测定值均高于健康对照组(P值均＜0.01).血清VEGF、PDGF和EGFR测定值与NSCLC病理分型无关(P值均＞0.05),与远处转移有关,远处转移组的测定值高于未转移组(P＜0.05～0.01).NSCLC患者血清VEGF与PDGF测定值之间呈显著正相关(r=0.641,P＜0.01),血清VEGF和EGFR测定值呈正相关(r=0.369,P＜0.05).结论 检测血清VEGF、PDGF和EGFR水平对NSCLC的诊断和预后判定具有一定价值.     

Suppression of growth of pancreatic cancer cell and expression of vascular endothelial growth factor by gene silencing with RNA interference

OBJECTIVE: To explore the anti‐angiogenesis and tumor cell growth suppressive effects resulted from gene silencing by RNAi in BxPC‐3 human pancreatic cancer cells. METHODS: The designation and transfection of vascular endothelial growth factor (VEGF)‐siRNA lentivirus was carried out in vitro. Real‐time PCR and western blot were conducted to measure the expression levels of VEGF mRNA and protein. Flow cytometry was employed to evaluate cell apoptosis and cell death. A lactate dehydrogenase (LDH) assay was used to assess the cytotoxicity of VEGF‐siRNA. A 3‐(4, 5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide (MTT) assay was used to picture the cellular growth. For the in vivo study, BxPC‐3 cells were injected subcutaneously into nude mice to form xenografts. The mice were divided into three groups according to the intervention used. The control group, the negative control group and the knockdown group of mice were injected with saline, an empty lentivirus vehicle and lentivirus carrying VEGF‐siRNA, respectively. None of the mice died during the study. When these mice were killed, the xenografts were collected and the tumor sizes of the different groups were compared. Finally, immunohistochemistry was used to assess the VEGF expression level and microvascular density. RESULTS: After the transfection of VEGF‐siRNA lentivirus, the cellular expression of VEGF mRNA decreased to 50% of the control and the VEGF protein in the BxPC‐3 cells decreased to 30% of the control. Apoptosis and cell death increased after transfection of the VEGF‐siRNA lentivirus. The LDH assay showed high cytotoxicity induced by VEGF‐siRNA lentivirus transfection. The MTT assay showed slower cellular growth in the knockdown cells. Tumor growth suppression was observed in nude mice that had received the VEGF‐siRNA lentivirus transfection, and the tumor sizes of the xenografts in this group were clearly smaller than those in other two groups. VEGF expression and microvascular density were significantly decreased. CONCLUSION: Vascular endothelial growth factor gene silencing via VEGF‐siRNA can effectively inhibit the production of VEGF and exert an anti‐angiogenesis and tumor cell growth suppressive effect both in vitro and in vivo.     

低氧对培养心肌细胞表达和分泌血管内皮生长因子的影响

目的　探讨低氧对心肌细胞血管内皮生长因子 (VEGF)表达的影响。方法　采用Kuwabara等并加以改进的方法对心肌细胞进行低氧培养 ,并于低氧培养的即刻、2 4、4 8h分别测定培养液中的氧分压。使用逆转录聚合酶链反应 (RT PCR)、免疫组织化学和酶联免疫吸附测定 (ELISA)法分别检测低氧培养的不同时间点VEGFmRNA及VEGF蛋白的表达和分泌。结果　与常规培养相比 ,简易低氧培养培养液氧分压降至 5 8mmHg ,并于 3个时间点保持这一水平 (P >0 .0 5 )。从mRNA水平和蛋白水平我们检测到VEGF表达的增加 ,于低氧培养 2 4h达峰值 ,培养液中的峰值浓度为 (72 4 .6 7± 5 6 .87)pg ml。结论　低氧促进心肌细胞表达VEGFmRNA、VEGF蛋白和分泌该蛋白     

Clinical significance of vascular endothelial growth factor in patients with primary lung cancer

OBJECTIVE: Vascular endothelial growth factor (VEGF) is an angiogenesis factor closely associated with the growth and metastasis of malignant tumours. METHODOLOGY: In the present study, we measured plasma VEGF levels in 20 normal subjects (N), 35 patients with benign lung diseases (B), 28 patients with untreated advanced lung cancer (NT) and 10 patients with treated lung cancer (T). In addition, we measured the VEGF levels in pleural effusions from five patients with primary lung cancer and two patients with active infectious diseases. Vascular endothelial growth factor was measured by ELISA. RESULTS: The mean (+/-SD) plasma VEGF level in NT patients (160.8 +/- 177.4 pg/mL) was fivefold higher than that in other patient groups (T, 17.7 +/- 4.9 pg/mL; B, 28.3 +/- 17.6 pg/mL) and the N group (14.9 +/- 7.0 pg/mL; P < 0.01). Vascular endothelial growth factor from lung cancer pleural effusions (17 526.0 +/- 22 498.2 pg/mL) was 25-fold higher than that from patients with active infectious diseases (665.5 +/- 259.0 pg/mL). CONCLUSIONS: Plasma VEGF may be a good clinical indicator for the assessment of primary lung cancer and pleural effusion VEGF in primary lung cancer is higher than pleural effusion VEGF in patients with inflammatory diseases.