乳腺癌患者血清Leptin和VEGF的表达

目的：研究瘦素（Leptin）、血管内皮生长因子（VEGF）在乳腺癌患者血清中的表达，探讨其在乳腺癌诊断中的意义。方法：选择乳腺癌患者36例，乳腺良性增生病变患者31例，另选56例健康女性作为对照。分别用放射免疫分析（RIA）和酶联免疫吸附试验（ELISA）测定这些患者术前血清Leptin、VEGF。结果：正常对照组与良性病变组、乳腺癌组Leptin存在明显差异，正常对照组与乳腺癌组，良性病变组与乳腺癌组VEGF存在明显差异。乳腺癌患者术前血清Leptin、VEGF含量与有无淋巴结转移具有相关性。结论：乳腺癌患者术前血清Leptin、VEGF可作为鉴别乳腺良恶性肿瘤有无转移的指标。     

新型血管吻合用支架对血管内膜的影响

目的：研制一种可溶性血管内支架辅助血管断端吻合，并检测该支架在血管吻合的过程中对血管内膜的影响。方法：选用高纯度低分子量明胶为主要原料制备血管吻合用支架，利用该支架进行血管吻合操作，观察支架对血管内膜的作用，并从超微结构方面进行研究。结果：明胶类可容性血管内支架表面光滑，在血管吻合的过程中不会对血管壁造成损伤；与同类支架相比具有明显的优势。结论：明胶类可溶性血管内支架具有光滑的外表面，适合于进行血管吻合操作。     

脑动静脉畸形血管重构的分子生物学机制

脑动静脉畸形存在活跃的血管重构,本文就其重构的分子生物学机制作一综述。     

Histamine differentially interacts with tumor necrosis factor-α and thrombin in endothelial tissue factor induction: the role of c-Jun NH2-terminal kinase

BACKGROUND: Histamine plays an important role in vascular disease. Tissue factor (TF) expression is induced in vascular inflammation and acute coronary syndromes. OBJECTIVES: This study examined the effect of histamine on tumor necrosis factor-alpha- (TNF-alpha-) vs. thrombin-induced endothelial TF expression. METHODS AND RESULTS: Histamine (10(-8)-10(-5) mol L-1), TNF-alpha (5 ng mL-1), and thrombin (1 U mL-1) induced TF expression in human endothelial cells. Although TF expression by TNF-alpha and thrombin was identical, histamine augmented TNF-alpha-induced expression 7.0-fold, but thrombin-induced expression only 2.6-fold. Similar responses occurred with TF activity. The H1-receptor antagonist mepyramine abrogated these effects. Differential augmentation by histamine was also observed at the mRNA level. Histamine-induced p38 activation preceded a weak second activation to both TNF-alpha and thrombin. Histamine-induced c-Jun NH2-terminal kinase (JNK) activation was followed by a strong second activation to TNF-alpha, and less to thrombin. Selective inhibition of this second JNK activation by SP600125 reduced TF induction to histamine plus TNF-alpha by 67%, but to histamine plus thrombin by only 32%. Histamine augmented TNF-alpha- and thrombin-induced vascular cell adhesion molecule 1 (VCAM-1) expression to a similar extent. Consistent with this observation, VCAM-1 induction to TNF-alpha and thrombin was mediated by p38, but not by JNK. CONCLUSIONS: Histamine differentially augments TNF-alpha- vs. thrombin-induced TF expression and activity, which is mediated by the H1-receptor, occurs at the mRNA level, and is related to differential JNK activation.     

New approach to management of intraaortic balloon pumps in patients with peripheral vascular disease: Case reports of four patients requiring urgent IABP insertion

Four selected cases of emergent IABP insertion in PV patients are presented. After angiographic documentation of critical iliac stenosis, conservative peripheral angioplasty was performed prior to IABP insertion. No patient experienced a peripheral ischemic event associated with IABP use. © 1992 Wiley-Liss, Inc.     

Analysis of Vascular Endothelial Growth Factor (VEGF) and a receptor subtype (KDR/flk-1) in the liver of rats exposed to riddelliine: a potential role in the development of hemangiosarcoma

Riddelliine alters hepatocellular and endothelial cell kinetics and function including stimulating an increase in hepatocytic vascular endothelial growth factor (VEGF) in the absence of increased serological levels of VEGF (Nyska etal. 2002). The objective of this study was to further assess hepatic VEGF and KDR/flk-1 synthesis and expression by hepatic cells under riddelliine treatment conditions. Forty-two male F344/N rats were dosed by gavage with riddelliine (0, 1.0, and 2.5 mg/kg/day) for 6 weeks. Seven animals/group were sacrificed after 8 consecutive daily doses; remaining rats were terminated after 30 daily doses, excluding weekends. Hepatic tissues were evaluated by immunohistochemistry and in situ hybridization. The results showed that VEGF mRNA expression was observed in control and treated animals; however, qualitative differences were noted. Treated animals exhibited VEGF mRNA in clustered, focal hepatocytes and bile duct epithelium, whereas VEGF mRNA in hepatocytes from vehicle control rats was distributed evenly across all hepatocytes. Results evaluating the distribution of the VEGF cognate receptor, KDR/flk-1 showed that randomly distributed, rare sinusoidal endothelium, including those demonstrating karyomegaly and cytomegaly expressed KDR/flk-1. Phosphorylation of KDR/flk-1 at pTyr996 and pTyr1054/1059, but not pTyr951, was also detected, evidence that endothelial cell KDR/flk-1 was activated. These results suggest that both hepatocytes and endothelial cells are targets of riddelliine-induced injury. We speculate that damage to both populations of cells may lead to dysregulated VEGF synthesis by hepatocytes and activation of KDR/flk-1 by endothelium leading to the induction of sustained endothelial cell proliferation, culminating in the development of hepatic hemangiosarcoma.     

Gadolinium-based balloon angioplasty for pulmonary artery stenosis in an infant with a right isomerism.

We report here the first described case of utilizing gadolinium-based contrast material as the contrast agent during a catheter intervention treatment for pulmonary artery stenosis. The patient, a male infant with complex heart disease associated with a right isomerism, had a history of severe allergic reaction to iodine-containing contrast agents. A combination of digital subtraction angiography and a gadolinium contrast agent, however, provided us with good-quality images both before and after balloon angioplasty without any associated complications. This method should therefore be considered as an alternative angiographic procedure in children with a high risk of iodine-related allergic complications.     

肝脏单形性上皮样血管平滑肌脂肪瘤的影像表现

目的提高对肝脏单形性上皮样血管平滑肌脂肪瘤（HMEA）影像表现的认识和诊断准确率。方法对经手术病理证实的4例HMEA进行回顾性分析，讨论影像表现和病理之间的联系。结果4例HMEA中，2例误诊为肝细胞癌，1例误诊为局灶性结节增生，1例诊断正确。影像表现主要为：（1）平扫呈等低或等稍高密度的HMEA2例，强化模式呈“快进慢出”。病理特点足瘤内有丰富的窦隙状薄壁分隔微血管网，无分化成熟的脂肪细胞，1例伴厚壁的血管。（2）平扫呈低密度或低信号的HMEA2例，强化模式呈“快进快出”，中央可见粗大的动脉。病理特点为瘤中央有畸形粗大厚壁的动脉，无脂肪细胞夹杂其间。结论HMEA影像表现与病理结构直接相关，根据影像表现结合临床资料可对该病作出初步诊断，但确诊仍依赖病理组织学检查。