Thick malignant melanomas (> 3 mm Breslow) with good clinical outcome: a histological study and survival analysis

Thick malignant melanomas in general tend to have a poor prognosis, but exceptions occur where there may be no further recurrence. The reasons for this difference in clinical behaviour are not fully understood. We have looked at thick malignant melanomas (greater than 3.0 mm) in the East of Scotland that have no evidence of metastasis after a minimum of 6 years follow-up and compared the clinical and histological features with a similar group, associated with histological evidence of metastasis and/or death. Both groups received similar treatment regimes. We have identified 41 patients with thick melanomas in the former group. When compared with the control group, factors found to be significantly different between the two groups were: the nature of the lower margin of the tumour; vascular invasion; and anatomical location.     

X刀治疗脑内病变283例长期随访研究

目的:总结X刀治疗脑内病变的长期随访结果.方法:对283例X刀治疗的脑瘤和脑血管畸形患者进行临床和影像学随访,随访时间为1～8年,平均(2.05±4.66)年.结果:82例转移瘤消失35例(42.7％),缩小28例(34.1％),无变化11例(13.4％),增大8例(9.8％);61例胶质瘤消失10例(16.4％),缩小19例(31.1％),无变化16例(26.2％),增大16例(26.2％);55例动静脉畸形消失29例(52.7％),缩小20例(36.4％),无变化6例(10.9％);17例海绵状血管瘤缩小4例(23.5％),无变化13例(76.5％);35例脑膜瘤消失5例(14.3％),缩小15例(42.9％),无变化13例(37.1％),增大2例(5.7％);12例神经鞘瘤消失3例(25.0％),缩小6例(50.0％),无变化2例(16.7％),增大1例(8.3％);10例生殖细胞瘤消失8例(80.0％),缩小2例(20.0％);11例其他肿瘤消失2例(18.2％),缩小4例(36.4％),无变化4例(36.4％),增大1例(9.0％).影像检查还发现病灶有坏死表现99例,囊性变19例,周边环状强化73例,胶质细胞增生20例,暂时性反应性肿大23例,放射性脑水肿28例.结论:X刀对小型脑肿瘤和血管畸形是一种安全有效的治疗方法,X刀治疗的主要并发症是放射性脑水肿.     

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.     

椎管内原发性孤立性纤维性肿瘤临床病理观察(附2例报告)

目的探讨椎管内孤立性纤维性肿瘤的临床病理特征、诊断和鉴别诊断,以期提高对该肿瘤的诊断水平。方法复习2例椎管内原发性孤立性纤维性肿瘤的临床资料,并观察其组织学特征和免疫组化标记。结果2例患者男、女各1例,年龄分别为23岁和32岁,临床表现为局部神经压迫症状。MRI示椎管内髓外硬膜内占位。组织学特征为梭形、卵圆形细胞呈束状、波浪状或旋涡状排列,富于胶原纤维及伴有分支状薄壁血管。细胞未见异型性和核分裂像。免疫组化示瘤细胞Vimentin( ),CD34( ),CD99( ),Bcl-2( ),AACT(-),Actin(-),S-100(-),EMA(-),GFAP(-),CD68(-),CD117(-),SMA(-),NF(-)。结论椎管内原发性孤立性纤维性肿瘤是一种罕见的肿瘤,诊断主要依靠病理形态学及免疫组化,并应与椎管内的其他梭形细胞肿瘤鉴别。     

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.