脑星形细胞瘤中血管内皮生长因子表达与肿瘤血管形成的关系

目的 研究脑星形细胞肿瘤中血管内皮生长因子(VEGF)蛋白的表达及其与微血管密度(MVD)间的相关性。方法 采用免疫组织化学S—P法检测60例脑星形细胞肿瘤中VEGF蛋白的表达，计数肿瘤MVD，分析其意义及两者间的相关性。结果 VEGF总阳性率为63．3％(36／60例)，其中Ⅱ、Ⅲ、Ⅳ级星形细胞瘤中VEGF阳性率分别为42．1％(8/19例)、71．4％(20／28例)、76．9％(10／13例)。间变性星形细胞瘤和多形性胶质母细胞瘤明显高于弥漫性星形细胞瘤(P＜0．05)；在Ⅱ、Ⅲ、Ⅳ级肿瘤各级别间MVD的差异有显著性(P＜0．05)，而且肿瘤从低度恶性向高度恶性转变过程中，微血管形态由窦状扩张为主变为以芽状和细索状为主，而球状血管丛仅出现在胶质母细胞瘤中。VEGF表达与肿瘤MVD呈正相关(P＜0．05)。结论 联合检测VEGF、MVD可作为判断脑星形细胞瘤恶性潜能的重要生物学指标，同时对了解肿瘤血管形成机制有一定意义。     

肾细胞癌中血管内皮生长因子的表达

目的 探讨肾癌组织中血管内皮生长因子的表达及其与肾癌生物学行为的关系。方法 应用单克隆鼠抗-VEGF抗体通过免疫组化SP法研究肾癌中血管内皮生长因子的表达。结果 60例肾癌组织中35例(58.3％)血管内皮生长因子阳性。血表达与组织学分级(P<0.05)和TNM分期(P<0.05)均明显相关。 结论 血管内皮生长因子表达对肾癌生物学行为有重要影响,设法抑制血管内皮生长因子有望成为肾癌治疗的另一有效方法。     

一种基于血管内皮细胞损伤的大鼠局灶性脑梗死模型

目的：建立一种因血管内皮细胞损伤而诱导的大鼠局灶性脑梗死模型。方法：取S—D大鼠11只，分离左侧颈总动脉、颈外动脉和颈内动脉。结扎左颈外动脉远心端，夹闭左翼腭动脉和颈总动脉，经颈外动脉逆行插管并缓慢注入月桂酸钠至颈内动脉系统，造成大脑中动脉血管内皮细胞受损。结果：从模型动物的行为表现、梗死灶形态学和病理学进行考察，10只大鼠均产生一定程度的脑梗死表现，造模成功率为90．9％。结论：该模型的稳定性和重复性较好，能在大脑中动脉的供血区产生恒定的梗死灶，适合进行脑缺血损伤的有关实验研究。     

应用结合于内皮细胞的尿激酶预防血栓形成

提纯出受损伤内皮细胞的特异性抗原，再用免疫学方法制得相应抗体，并把它与尿激酶形成结合物。在人工造成血管内皮细胞损伤的动物中，分别用尿激酶结合物、单纯特异性抗体处理，各组动物处死后进行形态学观察。结果显示：在未用尿激酶结合物处理的动物血管内和使用结合物处理的血管内，血栓形成的程度有明显的差别，前者明显，后者轻微。这种方法既能预防血栓形成，又不会产生继发性出血的危险。     

CT增强扫描在评价NSCLC血管生成中的临床意义

目的　探讨非小细胞肺癌 (NSCLC)血管内皮生长因子 (VEGF)的表达水平与CT增强程度的关系 ,从影像学角度评价肿瘤血管生成在肺癌诊断、治疗及淋巴结转移中的临床价值。方法　对 30例NSCLC病人进行动态螺旋CT扫描 (SCT) ,测量病灶增强幅度 ,并利用免疫组化技术检测VEGF。对病灶增强值、VEGF阳性表达及淋巴结转移情况进行统计学分析。结果　 30例肺癌病人CT增强值均数为 (36 .2 8± 6 .41 )HU ,VEGF阳性表达 2 1例 ,阴性表达 9例。VEGF在中晚期的阳性表达高于早期病人 (Ρ<0 .0 5) ,淋巴结转移组高于非淋巴结转移组 (Ρ <0 .0 5) ;癌灶增强值与VEGF阳性表达、肿瘤分期及淋巴结转移亦呈正相关。结论　NSCLC的CT增强程度能够反映肿瘤的血管生成 ,并与淋巴结转移密切相关 ,有助于肺癌的诊断、TNM分期 ,而且可以从肿瘤分子生物学行为方面补充目前肺癌分期方法的不足     

Association of Vascular Endothelial Growth Factor Expression with Tumor Angiogenesis and with Early Relapse in Primary Breast Cancer

Angiogenesis is an independent prognostic indicator in breast cancer. In this report, the relationship between expression of vascular endothclial growth factor (VEGF; a selective mitogen for endothelial cells) and the microvessel density was examined in 103 primary breast cancers. The expression of VEGF was evaluated by immunocytochemical staining using anti-VEGF antibody. The microvessel density, which was determined by immunostaining for factor VIII antigen, in VEGF-rich tumors was clearly higher than that in VEGF-poor tumors ( P <0.01). There was a good correlation between VEGF expression and the increment of microvessel density. Furthermore, postoperative survey demonstrated that the relapse-free survival rate of VEGF-rich tumors was significantly worse than that of VEGF-poor tumors. It was suggested that the expression of VEGF is closely associated with the promotion of angiogenesis and with early relapse in primary breast cancer.     

Effects of L-Tetrahydropalmatine on NOSⅢ Gene Expression in Hypoxia and Cultured Porcine Cerebral Arterial Endothelial Cells during Reoxygenation

L- Tetrahydropalmatine (L- THP) ,a kind of al-kaloid extracted from traditional Chinese medicineRhizoma corydalis,posseses sedative,analgesic andhypnotic effects.Recently,it has been demonstratedthat L- THPalso had calcium- antagonistic and antiar-rythmic effects.Studies showed that L- THP had aprotective effect on acute focal and global cerebral is-chemia- reperfusion injury[1,2 ] .Many studies provedthat the production of NO wasincreased significantlyduring ischemia- reperfusion.The o…     

Fluid shear induced endothelial cell detachment from glass - influence of adhesion time and shear stress

In this study, human umbilical vein and human saphenous vein endothelial cells were seeded on glass and exposed to fluid shear in a parallel-plate flow chamber. Cell retention, morphology and migration were studied as a function of shear stress and of adhesion time prior to exposure to shear. Three-hour and 24-h adhesion times gave rise to comparable cell retention values after 2 h of flow for both cell types. Cell retention decreased from 85 to 20% as shear stress increased from 88 to 264 dynes cm⁻² (8.8 to 26 Pa). Mean spreading areas decreased after the onset of flow, but subsequently stabilized to plateau values, which were smaller at higher shear stresses. Shape factors increased faster to higher values as cells were exposed to higher shear stresses, without any obvious preference in orientation of the cells with respect to the direction of flow. Migration was unidirectional with flow and linear with time. Migration was faster for cells which had adhered for 24 h than for cells which had adhered for 3 h and was accompanied by the presence of fibrillar structures left behind on the surface upstream of migrating cells. It is concluded that after 3 h adhesion to glass, cells have adhered with an adhesion strength that does not substantially increase during the next 21 h. However, during this time changes in cell-substratum interactions seem to occur judging by the differences in, e.g., migration rates.     

TGFβ-1 regulation of VEGF production by breast cancer cells

Background: Angiogenesis is essential for tumor growth and metastasis. Vascular endothelial growth factor (VEGF) is the most potent angiogenic factor identified to date. TGFβ-1 acts as an indirect angiogenic agent. Methods: VEGF and TGFβ-1 were measured in the serum of breast cancer patients and agematched controls and in tumor tissue of cancer patients by ELISA. VEGF protein and mRNA expression by breast tumor cell lines were examined, and the effect of TGFβ-1 on VEGF production in these cells was assessed. Results: VEGF levels were significantly higher (P=.03) in the serum of patients with breast cancer compared to age-matched controls. A positive correlation was found between serum (r=0.539) and tumor tissue (r=0.688) levels of VEGF and TGFβ-1. Metastatic MDA-MB-231 breast cancer cells produce more VEGF than do the primary BT474 cells. TGFβ-1 significantly (P<.05) increased production of VEGF. Conclusions: Breast cancer cells constitutively produce VEGF protein and mRNA. There is a relationship between VEGF and TGFβ-1 levels in breast cancer patients, and TGFβ-1 regulates VEGF expression by breast cancer cells. Presented at the 50th Annual Cancer Symposium of the Society of Surgical Oncology, Chicago, Illinois, March 20–23, 1997.     

Kupffer cell depletion in vivo results in preferential elimination of IgG aggregates and immune complexes via specific Fc receptors on rat liver endothelial cells.

In the present study we have investigated the clearance kinetics and tissue distribution of monomeric (m) IgG and soluble aggregates of IgG (AIgG) and immune complexes (IC) in normal and Kupffer cell (KC) depleted rats. In normal rats, clearance of mIgG occurred in a biphasic manner with a first half-life (T1/2) (T1) of 36.3 +/- 6.3 min and a second T1/2 (T2) of 168.4 +/- 4.7 min. AIgG composed of 20-27 IgG molecules per aggregate were cleared significantly faster than mIgG with a T1 of 2.5 +/- 0.1 min and a T2 of 32.5 +/- 5.6 min. KC depletion did not have a significant effect on the clearance rate of mIgG (T1: 33.4 +/- 8.9 min; T2; 159.5 +/- 12.5 min), while clearance of AIgG was delayed significantly with T1 4.8 +/- 0.7 min and T2 41.2 +/- 3.2 min. Eight minutes after injection, 77% of AIgG was found in the liver in normal rats while 62% was found in the liver of KC-depleted rats. Double immunofluorescence studies indicated that AIgG in the liver was associated with KC and endothelial cells (EC) in normal rats. In KC-depleted rats, AIgG was strongly associated with EC. A similar staining pattern was observed when IgG-immune IC were administered. The clearance of AIgG in KC-depleted rats was inhibited fully by pre-administration of high concentrations of IgG but not by pretreatment with IgA. asialofetuin (ASFe) or ovalbumin (OVA). Aggregated F(ab')2IgG was cleared with a comparable rate to mIgG from the circulation, again suggesting Fc gamma receptor-mediated elimination of AIgG by EC. There was a reduced degradation of AIgG in rats depleted of KC as compared with normal rats. These data suggest binding and degradation of AIgG by EC in vivo.