TP、MVD在人脑星形胶质细胞瘤中的表达及意义

目的探讨脑星形胶质细胞瘤组织胸苷磷酸化酶（TP）和微血管密度（MVD）的表达及其与星形细胞瘤的病理分级关系。方法选取病例50例，记录病例年龄、性别、组织学类型、病理分级。正常脑组织病例5例，鼠抗人单克隆抗TP抗体选取乳腺炎石蜡标本1例（阳性对照）。鼠抗人单克隆抗CD34抗体选取扁桃体炎石蜡标本1例（阳性对照）。将上述符合条件病例蜡块每例切片3张，利用免疫组化技术SP法检测它们TP、CD34的表达。结果5例正常尸检脑组织TP表达均阴性（-）；高级别星形胶质细胞瘤TP阳性表达率及微血管密度（MVD）值明显高于低级别星形胶质细胞瘤（WHOⅠ-Ⅱ级）（P〈0．05）。且口表达与MVD明显正相关（r=0．692，P〈0．05）。结论TP及MVD可以作为星形胶质细胞瘤恶性程度病理分级及判定预后的参考指标。     

Macromolecular contrast media. A new approach for characterising breast tumors with MR-mammography

Summery The value of macromolecular contrast agents (MMCM) for the characterization of benign and malignant breast tumors will be demonstrated in this review. Animal studies suggest a high potential of MMCM to increase the specificity of MR-mammography. The concept of tumor differentiation is based on the pathological hyperpermeability of microvessels in malignant tumors. MMCM show a leak into the interstitium of carcinomas, whereas they are confined to the intravascular space in benign tumors. Capabilities and limitations of the MMCM-prototype. Albumin-Gd-DTPA, for breast tumor characterization will be summarized and compared to the standard low molecular weight contrast agent Gd-DTPA. Initial experience with new MMCM, such as Dendrimers, Gd-DTPA-Polylysine and MS-325 will be outlined. The potential of “blood-pool“-iron oxides, such as AMI-227 for the evaluation of tumor microvascular permeabilities will be discussed.      

显微血管减压术治疗老年人神经性高血压的疗效分析

目的 探讨显微血管减压术治疗老年人神经性高血压的疗效。方法 回顾性分析手术治疗的老年脑神经疾病692例，其中236例前有神经性高血压，包括三叉神经痛179例，面肌痉挛48例，舌咽神经痛9例，均行脑神经显微血管减压术治疗。结果 236例中治愈145例（61.4%），显效36例（15.3%），有效23例（9.7%)，无效32例（13.6%）；208例得到平均74个月随访，有133例治愈，30例显效，18例有效，27例无效。结论 异常血管袢压迫脑神经根及延髓，长期疼痛刺激和情绪紧张是神经性高血压的病因，行该区的显微血管减压是治疗神经性高血压的有效方法。     

颅内动脉瘤术中多普勒超声应用研究(附32例报告)

目的应用经颅多普勒(TCD)超声在颅内动脉瘤术中监测载瘤动脉血流速度变化.方法对32例颅内动脉瘤患者使用微血管多普勒(MVD)超声进行术中检测,记录载瘤动脉血流速度的变化,观察术后脑缺血性并发症.结果发现有缺血性并发症组血流速度较无并发症组明显加快(P<0.05),而两组在术前血流速度并无显著性差异(P>0.05).结论将MVD及TCD应用于术中监测载瘤动脉血流动力学变化有一定临床意义.     

Microvascular Involvement in Cardiac Pathology

Abnormalities of the microvasculature are centrally involved in the pathogenesis of some forms of heart disease, but in others are consequences of it. Microvascular abnormalities may contribute to the progression of viral myocarditis and Chagas' disease. Focal abnormalities may occur early in some cardiomyopathies and do occur later in most types of myocarditis. The thickening of arteriolar walls in chronic hypertension is likely to contribute significantly to the impairment of coronary haemodynamics associated with adaptive ventricular hypertrophy and the consequent diminution of coronary reserve, increasing diffusion distances and failure of angiogenesis to compensate. However, the resulting myocyte necrosis stimulates inflammatory angiogenesis. When ischemic myocyte injury becomes irreversible there is a concomitant loss of capacity for reperfusion, the no-reflow phenomenon. Less severe temporary ischemia reduces the proportion of functional capillaries. Multiple mechanisms are involved in this microvascular stunning, including: reperfusion injury; leukocyte activation, adhesion and accumulation; and impaired endothelium-dependent vasodilation. Many of the microvascular changes are those of the inflammatory response to cell death and form part of a final common pathway in myocarditis, cardiomyopathy, cardiac hypertrophy and failure, and ischemic heart disease. Stimulation of angiogenesis prior to myocyte necrosis in hypertrophy and control of leukocyte activity in ischemic heart disease could minimize myocyte loss.     

Intraoperative management to prevent cerebrospinal fluid leakage after microvascular decompression: dural closure with a “plugging muscle” method

Our objective is to present surgical techniques used for the prevention of cerebrospinal fluid leakage after microvascular decompression (MVD). From January 1996 to February 2006, microvascular decompression for hemifacial spasm or trigeminal neuralgia was performed in 678 consecutive patients. In order to achieve watertight dural closure, several pieces of muscle were interposed between the dura when the dura was sutured; the dura was stitched with the addition of muscle pieces to plug the dural defect. In cases where the mastoid air cell system was opened, bone wax was used to seal the opened surface of the cavity, and a muscle patch was applied for the secondary sealing. The cranioplasty was performed using polymethylmethacrylate (PMMA) bone cement. Only 2 (0.29%) of 678 patients, who underwent MVD followed by dural closure using several muscle pieces to plug the potential dural defect, suffered from CSF leaks. Both were treated with lumbar subarachnoid drainage; neither patient required a lumbar peritoneal shunt or a revision operation. A watertight dural closure with the addition of muscle pieces in a “plugging” fashion, along with sealing the opened surface of the mastoid cavity using bone wax and cranioplasty using bone cement, provides a simple and effective technique for the prevention of CSF leakage after MVD.     

贲门癌组织环氧化酶-2和血管生成因子的表达及其与血管生成的关系

目的:探讨环氧化酶-2(COX-2)和血管生成因子(VEGF)在贲门癌组织中的表达及其与肿瘤血管生成的关系.方法:免疫组化法检测贲门癌手术切除标本46例和癌旁正常黏膜标本21例中COX-2,VEGF表达.采用抗CD34抗体标记微血管内皮细胞,计算微血管密度(MVD).分析COX-2,VEGF表达与MVD和贲门癌主要临床病理特征的相关性.结果:贲门癌组织COX-2,VEGF阳性表达率、MVD值显著高于癌旁正常黏膜的(80.4% vs 14.3%,x~2=26.22,P<0.01;76.1% vs 19.1%,x~2=19.28,P<0.01:31.95±3.87 vs 16.28±1.55,t=17.76,P<0.01).COX-2,VEGF表达、MVD值与肿瘤临床TNM分期和淋巴结转移密切相关,TNM分期中Ⅲ Ⅳ期的贲门癌组织中COX-2,VEGF表达率、MVD值显著高于Ⅰ Ⅱ期的(90.3% vs 60.0%,x~2=5.91,P<0.05;96.8% vs 46.7%,x~2=16.13,P<0.01;33.43±3.34 vs 28.90±3.08,t=4.42,P<0.01).伴有淋巴结转移的贲门癌组织中COX-2,VEGF表达率,MVD值显著高于无淋巴结转移的(94.1% vs 41.7%,x~2=15.51,P<0.01:91.2% vs 50.0%,x~2=9.56,P<0.01;33.53±3.21 vs 27.48±1.03,t=6.38,P<0.01).Spearman等级相关分析表明,COX-2,VEGF表达与MVD呈显著正相关(r= 0.823:r=0.892,P<0.01).结论:COX-2,VEGF异常表达及其诱导的血管生成在贲门癌的侵袭和淋巴结转移中起重要作用.     

肝细胞肝癌与局灶性结节性增生微血管的免疫组化染色比较

目的比较肝细胞癌(HCC)和局灶性结节性增生(FNH)微血管密度、微血管形态及结构的差异。方法对64例HCC和15例FNH组织作免疫组化染色，标记CD34、CD31、Ⅷ因子、UEA-Ⅰ及α-SMA等抗原并进行比较。结果血管内皮细胞抗原标记CD34、CD31、Ⅷ因子及UEA-Ⅰ在HCC及FNH组织中均有不同程度表达，微血管计数(MVD)显示HCC及FNH两者间无明显差别。微血管周细胞标记α-SMA在HCC及FNH组织中表达有显著差别，在HCC中分布稀疏而散在，在FNH中则广泛并呈网状。结论HCC及FNH中常用的内皮细胞抗原标记的表达以及MVD无差异。两者组织中微血管的结构存在差别。     

三叉神经痛微血管减压术的手术疗效分析

目的探讨微血管减压术（MVD）治疗原发性三叉神经痛（ITN）的手术疗效，总结不同类型责任血管的处理技巧。方法回顾性分析125例接受MVD的ITN的临床资料。对手术操作的要点进行介绍。结果术中见124例三叉神经根部有接触或压迫的血管，占99．2％，最常见的责任血管是小脑上动脉（SCA，占68％）其次为小脑前下动脉（AICA，占30．4％）。动脉性责任血管占96．8％，岩上静脉作为责任血管占8．8％。所有病例均有效（100％），总治愈率为96．8％。结论微血管减压是治疗三叉神经痛安全、微创、有效的方法。提高显微外科操作技巧，不遗漏责任血管，是提高手术疗效和减少并发症的关键。     

强化三维损毁梯度回波序列在三叉神经痛微血管减压术前评价中的作用

目的 研究强化三维损毁梯度回波序列(3D-SPGRI)在三叉神经痛微血管减压(MVD)术前评价和病例选择中的作用.方法 33例三叉神经痛患者行高分辨率强化3D-SPGRI及三维脑血管成像(3D-MRA)扫描,观察三叉神经出脑干段神经及邻近血管关系,并与MVD术中观察结果 对比.结果 33例患者中29例显示与疼痛侧别一致的神经血管接触或压迫并行显微手术减压,手术证实,其中27例MR图像符合术中所见,所有手术患者术后疼痛完全缓解.结论 3D-SPGRI结合3D-MRA能够清晰显示脑池段三叉神经及其邻近血管,为MVD术前评价、病例选择、判断预后提供有价值的信息.